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Degenerative Mitral Valve Disease

2016-10-17T16:15:21Z

Lwilkie: /* References */

{{OpenPagesTop}}
Also known as: '''''MVD — Mitral Valve Disease — Mitral Insufficiency — Mitral Endocardiosis — Myxomatous Mitral Valve Disease (MMVD) — Endocardiosis — Mitral Regurgitation — Chronic Valvular Disease'''''

== Introduction ==
Myxomatous degeneration of the mitral valve is the most common acquired cardiac disease in the dog. Degenerative mitral valve disease (DMVD) is a progressive disease and subtle changes in valve structure precede the development of clinically significant disease. The aetiology of DMVD is unknown. Genetic predisposition for development of the disease is likely, however the inheritance is complex.

The '''mitral apparatus''' consists of the mitral '''valve leaflets''', valve '''annulus''', '''chordae tendinae''' and '''papillary muscles'''. The mitral valve leaflets are known as '''anterior''' and '''posterior''' leaflets. In the normal dog, these are thin, translucent structures that are anchored to the papillary muscles by chordae tendinae. Both papillary muscles (anterior and posterior) arise from the left ventricular free wall. The mitral valve prevents the backflow of blood from the left ventricle to the left atrium during systole. In early systole, when left ventricular pressure exceeds left atrial pressure, the mitral valve leaflets close. In normal dogs, the chordae tendinae tether the leaflets to prevent them prolapsing into the left atrium. When the mitral valve is incompetent, there is ''regurgitation'' of blood from the left ventricle to the left atrium. Mitral regurgitation may be mild, with no clinical consequence, or may be severe. The severity of mitral regurgitation is determined primarily by the size of the orifice, that results from incomplete apposition of the mitral valve leaflets, and the relationship between left ventricular and left atrial systolic pressures. Mitral regurgitation causes an increase in left atrial pressure, which over time can lead to left atrial dilation. In diastole, the left ventricle is filled by both pulmonary venous return and blood that has been regurgitated into the left atrium. Therefore, both the left atrium and left ventricle become volume overloaded. This may result in '''ventricular dilation and eccentric hypertrophy'''. In severe cases, increased left ventricular and left atrial filling pressures may result. This leads to an increase in pulmonary venous pressure and may result in [[Heart Failure, Left-Sided|left-sided congestive heart failure]].

==Signalment==

Degenerative mitral valve disease tends to affect middle-aged and older dogs, particularly males. The disease more commonly affects small breed dogs, with Cavalier King Charles Spaniels, Chihuahuas, Boston Terriers, Poodles, Pomeranians and Bull Terriers being predisposed. The disease is also recognized in large breed dogs.

==History and Clinical Signs==
Animals may remain asymptomatic for years, the disease is usually clinically silent until it is advanced.

In most affected dogs, DMVD does not cause clinical signs and the disease is detected by the auscultation of a cardiac murmur at routine health checks.

In cases where DMVD becomes clinically significant, a '''cough''' is usually the first clinical sign noticed by the owner. The coughing is likely of multifactorial aetiology and may be related to pulmonary oedema, stimulation of the juxtapulmonary (J) receptors that are associated with pulmonary capillaries and detect increases in pulmonary venous pressure, compression of a mainstem bronchi by an enlarged left atrium and concurrent airway disease. Occasionally, '''syncope''' is the first sign of clinically significant DMVD. This may occur due to arrhythmias or on exertion where mitral regurgitation limits stroke volume and therefore cardiac output.

== Diagnosis==
===Physical Examination===
* Systolic murmur with point of maximal intensity over the left apex. Murmur grade is usually correlated with severity of mitral regurgitation, severe regurgitation causes a loud murmur.
* Mid-systolic click, associated with mitral prolapse. In many dogs, clicks are a precursor to mitral regurgitation.

Other findings will depend on the stage of disease. Crackles may be detected on thoracic auscultation in patients with pulmonary oedema, resulting from [[Heart Failure, Left-Sided|left-sided congestive heart failure]]. Abdominal palpation is usually normal, but ascites and hepatomegaly may be present when there is concurrent [[Heart Failure, Right-Sided|right-sided congestive heart failure]].

Primary respiratory disease, such as chronic bronchitis, is also common in older small breed dogs. It is important to distinguish between the patient with clinically significant respiratory disease and incidental DMVD from the patient with clinically significant DMVD. Respiratory sinus arrhythmia, indicating vagal influence on heart rate and rhythm, is usually not present in severe cardiac disease. In contrast, sinus arrhythmia is usually preserved or accentuated when respiratory disease is the cause of clinical signs.

===Diagnostic Imaging===
====Radiography====
Early in the course of DMVD, thoracic radiographs will be normal. As the disease progresses, cardiomegaly will become apparent. There may be evidence of left atrial enlargement, with or without dorsal displacement of the trachea and narrowing of the mainstem bronchus. Pulmonary venous distension may be observed if there is increased pulmonary venous pressure. Interstitial pulmonary oedema may precede alveolar pulmonary oedema. Evidence of [[Heart Failure, Right-Sided|right-sided congestive heart failure]] may be present in severe cases, radiographic findings include distension of the caudal vena cava, hepatomegaly, ascites and pleural effusion.

====Echocardiography====
* Thickened mitral valve leaflets
* Prolapse of mitral valve leaflets into the left atrium during systole
* Tricuspid leaflets may also be affected, though usually not as severely as the mitral valve
* Increased diastolic left ventricular diameter
* Hyperdynamic left ventricle
* Colour Doppler jet of mitral regurgitation
*(Flail leaflet)

Thickening of the mitral valve leaflets is usually diffuse, but most pronounced at the leaflet edges. With myxomatous degeneration, the mitral valve becomes stiffer and distorted. The conformation of the valve remains constant throughout the cardiac cycle. Normally, the mitral valve leaflets do not extend beyond a line across the mitral annulus in systole. In dogs with DMVD, the mitral leaflets prolapse towards the left atrium during systole. Colour Doppler can be used to demonstrate the jet of mitral regurgitation. The size of the jet is related to the severity of mitral regurgitation. Most mitral regurgitation jets in DMVD are eccentric.

The more severe the DMVD, the greater the degree of left ventricular and left atrial dilation.

Fractional shortening may be increased (hyperynamic left ventricle). This is because, in the setting of mitral regurgitation, impedance to ventricular emptying is reduced (blood can be ejected into the low pressure left atrium)and end-diastolic ventricular stretch is increased by the addition of the regurgitant fraction, increasing the force of contraction.

A serious complication of DMVD is '''chordae tendinae rupture''', resulting in a 'flail leaflet' and acute worsening of mitral regurgitation. A leaflet segment typically 'flails' back into the left atrium during systole.

'''Left atrial rupture''' is a major complication of DMVD. Left atrial endocardial and endomyocardial splits are usually multiple and may heal or perforate the atrial wall, causing haemopericardium or an acquired atrial septal defect depending on their depth and location.

===Electrocardiogram (ECG)===
Electrocardiography is primarily used to diagnose arrhythmias, but can provide evidence of chamber enlargement. Most arrhythmias in DMVD are supraventricular in origin and occur secondary to left atrial stretch. Ventricular arrhythmias may develop in association with left ventricular dilation and fibrosis.

* P-mitrale: wide P waves in leads II, III and aVF, indicates left atrial enlargement

===Laboratory Tests===
Pro-brain natriuretic peptide ('''NT-proBNP''') concentration is associated with severity of DMVD. Elevated NT-proBNP levels are useful in discriminating patients with respiratory distress caused by heart failure from those with primary respiratory tract disease.

==Staging==
Staging according to American College of Veterinary Internal Medicine (ACVIM) is as follows:
* '''Stage A''': Dog predisposed to the development of DMVD
* '''Stage B''': Subclinical disease
** ''B1'': Without cardiac remodeling
** ''B2'': With cardiac remodeling
* '''Stage C''': Current or prior clinical signs
* '''Stage D''': Refractory heart failure

== Treatment ==
===Stage B===
There is no therapy demonstrated to be beneficial in dogs with stage B1 disease.

The results of the EPIC study demonstrated that administration of '''Pimobendan''' to dogs with stage B2 disease resulted in prolongation of the asymptomatic phase of disease by approximately 15 months. Dogs receiving Pimobendan were around 33% less likely to go into congestive heart failure or suffer a cardiac death than those not receiving the drug. Pimobendan appears safe and well-tolerated.

Based on findings of the EPIC study, dogs with typical mitral valve murmurs of grade III/VI or higher should be investigated to look for evidence of cardiomegaly. If cardiomegaly is apparent, then the dog may benefit from starting Pimobendan, as opposed to the 'watch and wait' approach that was previously recommended.

===Stage C===
Medical management is intended to alleviate clinical signs and prolong life.

'''Furosemide''' is a potent first-line diuretic that can be administered orally or parenterally, depending on the clinical status of the patient. Most patients with congestive heart failure secondary to DMVD require lifelong diuretic therapy.

The addition of an '''ACE inhibitor''' is considered standard therapy. The benefits of ACE inhibitors are related to their vasodilator action and also protecting the heart from the detrimental effects of RAAS activation.

'''Pimobendan''' is phosphodiesterase inhibitor and calcium sensitiser that is both a ''positive inotrope'' and ''vasodilator'' (inodilator). A randomized clinical trial (QUEST) demonstrated a survival benefit associated with Pimobendan administration, when evaluated relative to treatment which was considered at that time to be the gold standard; benazepril. Use of triple therapy with furosemide, an ACE inhibitor and Pimobendan is recommended. When financial or compliance concerns limit the therapeutic choices, evidence suggests that Pimobendan is superior to an ACE inhibitor.

Aldosterone may contribute to the development of myocardial fibrosis. Complete suppression of RAAS is generally not achieved by ACE inhibition alone. Therefore the addition of '''Spironolactone''' may be beneficial.

Surgical mitral valve repair in dogs is currently being performed. However, availability is limited by the expense, required expertise and cardiopulmonary bypass facilities.

===Stage D===
If congestive heart failure signs are not controlled by high doses of Furosemide, addition of a thiazide and Spironolactone should be considered. Together these drugs have a synergistic action, by providing sequential nephron blockade, allowing lower doses of the individual agents.

==Monitoring and Follow Up==
For dogs in stage B, owners should be made aware of signs of congestive heart failure. In dogs with Stage B2 disease where congestive heart failure is imminent, it is useful to give the owner Furosemide to administer if the dog develops signs of respiratory distress. Owners of Stage B2 and Stage C dogs should be educated on how to measure sleeping respiratory rate and should begin recording this regularly.

The frequency of follow-up examinations is dependent on the severity of disease and owner compliance. For dogs with preclinical disease, rechecks can be recommended every 6-12 months depending on the severity of mitral regurgitation and cardiac remodeling. Following hospitalization for control of acute congestive heart failure, dogs should receive a follow up examination within 2 weeks to check for resolution of clinical signs, hydration status, electrolytes and renal function. For dogs in stage C with stable disease, re-checks can be every 3-6 months.

== Prognosis ==

Asymptomatic patients may live for many years. Dogs with stage B2 disease have a median of 27 months before developing congestive heart failure. Once heart failure occurs, life expectancy is usually around 6-12 months, although some patients remain stable for longer. Risk factors for progression include severity of valvular lesions, increased age and male gender. Risk factors for onset of congestive heart failure include severity of mitral regurgitation, left atrial enlargement and elevated NT-proBNP. Development of complications such as atrial fibrillation or chordae tendinae rupture are associated with a poor prognosis.

{{Learning
|videos = [http://www.cardioacademy.cevalearn.com/en/Programme/Sessions/1-Pathophysiology-of-Mitral-Valve-Disease video on mitral valve disease from Cardio Academy]
|flashcards = [[Endocardial Pathology Flashcards]]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22Mitral+Valve+Dysplasia%22&occuring1=title&rowId=2&options2=OR&q2=%22Mitral+Valve+Disease%22&occuring2=title&rowId=3&options3=OR&q3=%22Mitral+insufficiency%22&occuring3=title&rowId=4&options4=OR&q4=%22endocardiosis%22&occuring4=title&x=36&y=9&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Mitral Valve Dysplasia publications]

[http://www.cabdirect.org/search.html?it=any&q2=%22Mitral+Valve+Disease%22&q1=%22Mitral+Valve+Dysplasia%22&calendarInput=yyyy-mm-dd&q4=%22endocardiosis%22&q3=%22Mitral+insufficiency%22&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&rowId=4&options1=AND&options2=OR&occuring4=title&options3=OR&options4=OR&occuring3=title&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc:(ft+OR+fr+OR+fa+OR+fv+OR+fw+OR+fx+OR+gf+OR+ga+OR+b1+OR+b2+OR+b3+OR+b4+OR+b5+OR+b6)&y=9&x=36 Other MDV Full Text Articles]
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103219945.pdf ''' Myxomatous degenerative mitral valve disease: an update.''' Disatian, S.; Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand, Thai Journal of Veterinary Medicine, 2010, 40, 2, pp 151-157, many ref.]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093114836.pdf ''' Latest information about canine mitral valve disease: results of the QUEST trial.''' Häggström, J.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 188-191, 10 ref. - '''Full Text Article''']

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017845.pdf ''' Treatment of mitral valve disease in dogs.''' French, A.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 107-108]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017847.pdf ''' Prognostic variables in canine mitral valve disease.''' Häggstrom, J.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 112-113, 7 ref.]
}}

==References==
* Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2016) '''Manual of Canine and Feline Cardiology (Fifth Edition)''' ''Saunders''.
* Luis Fuentes, V, Johnson, L.R, Dennis, S. (2010) '''BSAVA Manual of Canine and Feline Cardiorespiratory Medicine (Second Edition)'''
* Boswood, A. et al. Effect of Pimobendan in Dogs with Preclinical Myxomatous Mitral Valve Disease and Cardiomegaly: The EPIC Study - A Randomized Clinical Trial. JVIM, September 2016. DOI: 10.1111/jvim.14586

{{review}}

{{OpenPages}}

[[Category:Cardiovascular_System_-_Degenerative_Pathology]] [[Category:Endocardial_Pathology]] [[Category:Expert_Review]] [[Category:Cardiac_Diseases_-_Cat]] [[Category:Cardiac_Diseases_-_Dog]]
[[Category:Cardiac_Diseases_-_Horse]]
[[Category:Cardiovascular_System_-_Developmental_Pathology]]
[[Category:Cardiology Section]]

Degenerative Mitral Valve Disease

2016-10-17T16:07:54Z

Lwilkie: /* Stage B */

{{OpenPagesTop}}
Also known as: '''''MVD — Mitral Valve Disease — Mitral Insufficiency — Mitral Endocardiosis — Myxomatous Mitral Valve Disease (MMVD) — Endocardiosis — Mitral Regurgitation — Chronic Valvular Disease'''''

== Introduction ==
Myxomatous degeneration of the mitral valve is the most common acquired cardiac disease in the dog. Degenerative mitral valve disease (DMVD) is a progressive disease and subtle changes in valve structure precede the development of clinically significant disease. The aetiology of DMVD is unknown. Genetic predisposition for development of the disease is likely, however the inheritance is complex.

The '''mitral apparatus''' consists of the mitral '''valve leaflets''', valve '''annulus''', '''chordae tendinae''' and '''papillary muscles'''. The mitral valve leaflets are known as '''anterior''' and '''posterior''' leaflets. In the normal dog, these are thin, translucent structures that are anchored to the papillary muscles by chordae tendinae. Both papillary muscles (anterior and posterior) arise from the left ventricular free wall. The mitral valve prevents the backflow of blood from the left ventricle to the left atrium during systole. In early systole, when left ventricular pressure exceeds left atrial pressure, the mitral valve leaflets close. In normal dogs, the chordae tendinae tether the leaflets to prevent them prolapsing into the left atrium. When the mitral valve is incompetent, there is ''regurgitation'' of blood from the left ventricle to the left atrium. Mitral regurgitation may be mild, with no clinical consequence, or may be severe. The severity of mitral regurgitation is determined primarily by the size of the orifice, that results from incomplete apposition of the mitral valve leaflets, and the relationship between left ventricular and left atrial systolic pressures. Mitral regurgitation causes an increase in left atrial pressure, which over time can lead to left atrial dilation. In diastole, the left ventricle is filled by both pulmonary venous return and blood that has been regurgitated into the left atrium. Therefore, both the left atrium and left ventricle become volume overloaded. This may result in '''ventricular dilation and eccentric hypertrophy'''. In severe cases, increased left ventricular and left atrial filling pressures may result. This leads to an increase in pulmonary venous pressure and may result in [[Heart Failure, Left-Sided|left-sided congestive heart failure]].

==Signalment==

Degenerative mitral valve disease tends to affect middle-aged and older dogs, particularly males. The disease more commonly affects small breed dogs, with Cavalier King Charles Spaniels, Chihuahuas, Boston Terriers, Poodles, Pomeranians and Bull Terriers being predisposed. The disease is also recognized in large breed dogs.

==History and Clinical Signs==
Animals may remain asymptomatic for years, the disease is usually clinically silent until it is advanced.

In most affected dogs, DMVD does not cause clinical signs and the disease is detected by the auscultation of a cardiac murmur at routine health checks.

In cases where DMVD becomes clinically significant, a '''cough''' is usually the first clinical sign noticed by the owner. The coughing is likely of multifactorial aetiology and may be related to pulmonary oedema, stimulation of the juxtapulmonary (J) receptors that are associated with pulmonary capillaries and detect increases in pulmonary venous pressure, compression of a mainstem bronchi by an enlarged left atrium and concurrent airway disease. Occasionally, '''syncope''' is the first sign of clinically significant DMVD. This may occur due to arrhythmias or on exertion where mitral regurgitation limits stroke volume and therefore cardiac output.

== Diagnosis==
===Physical Examination===
* Systolic murmur with point of maximal intensity over the left apex. Murmur grade is usually correlated with severity of mitral regurgitation, severe regurgitation causes a loud murmur.
* Mid-systolic click, associated with mitral prolapse. In many dogs, clicks are a precursor to mitral regurgitation.

Other findings will depend on the stage of disease. Crackles may be detected on thoracic auscultation in patients with pulmonary oedema, resulting from [[Heart Failure, Left-Sided|left-sided congestive heart failure]]. Abdominal palpation is usually normal, but ascites and hepatomegaly may be present when there is concurrent [[Heart Failure, Right-Sided|right-sided congestive heart failure]].

Primary respiratory disease, such as chronic bronchitis, is also common in older small breed dogs. It is important to distinguish between the patient with clinically significant respiratory disease and incidental DMVD from the patient with clinically significant DMVD. Respiratory sinus arrhythmia, indicating vagal influence on heart rate and rhythm, is usually not present in severe cardiac disease. In contrast, sinus arrhythmia is usually preserved or accentuated when respiratory disease is the cause of clinical signs.

===Diagnostic Imaging===
====Radiography====
Early in the course of DMVD, thoracic radiographs will be normal. As the disease progresses, cardiomegaly will become apparent. There may be evidence of left atrial enlargement, with or without dorsal displacement of the trachea and narrowing of the mainstem bronchus. Pulmonary venous distension may be observed if there is increased pulmonary venous pressure. Interstitial pulmonary oedema may precede alveolar pulmonary oedema. Evidence of [[Heart Failure, Right-Sided|right-sided congestive heart failure]] may be present in severe cases, radiographic findings include distension of the caudal vena cava, hepatomegaly, ascites and pleural effusion.

====Echocardiography====
* Thickened mitral valve leaflets
* Prolapse of mitral valve leaflets into the left atrium during systole
* Tricuspid leaflets may also be affected, though usually not as severely as the mitral valve
* Increased diastolic left ventricular diameter
* Hyperdynamic left ventricle
* Colour Doppler jet of mitral regurgitation
*(Flail leaflet)

Thickening of the mitral valve leaflets is usually diffuse, but most pronounced at the leaflet edges. With myxomatous degeneration, the mitral valve becomes stiffer and distorted. The conformation of the valve remains constant throughout the cardiac cycle. Normally, the mitral valve leaflets do not extend beyond a line across the mitral annulus in systole. In dogs with DMVD, the mitral leaflets prolapse towards the left atrium during systole. Colour Doppler can be used to demonstrate the jet of mitral regurgitation. The size of the jet is related to the severity of mitral regurgitation. Most mitral regurgitation jets in DMVD are eccentric.

The more severe the DMVD, the greater the degree of left ventricular and left atrial dilation.

Fractional shortening may be increased (hyperynamic left ventricle). This is because, in the setting of mitral regurgitation, impedance to ventricular emptying is reduced (blood can be ejected into the low pressure left atrium)and end-diastolic ventricular stretch is increased by the addition of the regurgitant fraction, increasing the force of contraction.

A serious complication of DMVD is '''chordae tendinae rupture''', resulting in a 'flail leaflet' and acute worsening of mitral regurgitation. A leaflet segment typically 'flails' back into the left atrium during systole.

'''Left atrial rupture''' is a major complication of DMVD. Left atrial endocardial and endomyocardial splits are usually multiple and may heal or perforate the atrial wall, causing haemopericardium or an acquired atrial septal defect depending on their depth and location.

===Electrocardiogram (ECG)===
Electrocardiography is primarily used to diagnose arrhythmias, but can provide evidence of chamber enlargement. Most arrhythmias in DMVD are supraventricular in origin and occur secondary to left atrial stretch. Ventricular arrhythmias may develop in association with left ventricular dilation and fibrosis.

* P-mitrale: wide P waves in leads II, III and aVF, indicates left atrial enlargement

===Laboratory Tests===
Pro-brain natriuretic peptide ('''NT-proBNP''') concentration is associated with severity of DMVD. Elevated NT-proBNP levels are useful in discriminating patients with respiratory distress caused by heart failure from those with primary respiratory tract disease.

==Staging==
Staging according to American College of Veterinary Internal Medicine (ACVIM) is as follows:
* '''Stage A''': Dog predisposed to the development of DMVD
* '''Stage B''': Subclinical disease
** ''B1'': Without cardiac remodeling
** ''B2'': With cardiac remodeling
* '''Stage C''': Current or prior clinical signs
* '''Stage D''': Refractory heart failure

== Treatment ==
===Stage B===
There is no therapy demonstrated to be beneficial in dogs with stage B1 disease.

The results of the EPIC study demonstrated that administration of '''Pimobendan''' to dogs with stage B2 disease resulted in prolongation of the asymptomatic phase of disease by approximately 15 months. Dogs receiving Pimobendan were around 33% less likely to go into congestive heart failure or suffer a cardiac death than those not receiving the drug. Pimobendan appears safe and well-tolerated.

Based on findings of the EPIC study, dogs with typical mitral valve murmurs of grade III/VI or higher should be investigated to look for evidence of cardiomegaly. If cardiomegaly is apparent, then the dog may benefit from starting Pimobendan, as opposed to the 'watch and wait' approach that was previously recommended.

===Stage C===
Medical management is intended to alleviate clinical signs and prolong life.

'''Furosemide''' is a potent first-line diuretic that can be administered orally or parenterally, depending on the clinical status of the patient. Most patients with congestive heart failure secondary to DMVD require lifelong diuretic therapy.

The addition of an '''ACE inhibitor''' is considered standard therapy. The benefits of ACE inhibitors are related to their vasodilator action and also protecting the heart from the detrimental effects of RAAS activation.

'''Pimobendan''' is phosphodiesterase inhibitor and calcium sensitiser that is both a ''positive inotrope'' and ''vasodilator'' (inodilator). A randomized clinical trial (QUEST) demonstrated a survival benefit associated with Pimobendan administration, when evaluated relative to treatment which was considered at that time to be the gold standard; benazepril. Use of triple therapy with furosemide, an ACE inhibitor and Pimobendan is recommended. When financial or compliance concerns limit the therapeutic choices, evidence suggests that Pimobendan is superior to an ACE inhibitor.

Aldosterone may contribute to the development of myocardial fibrosis. Complete suppression of RAAS is generally not achieved by ACE inhibition alone. Therefore the addition of '''Spironolactone''' may be beneficial.

Surgical mitral valve repair in dogs is currently being performed. However, availability is limited by the expense, required expertise and cardiopulmonary bypass facilities.

===Stage D===
If congestive heart failure signs are not controlled by high doses of Furosemide, addition of a thiazide and Spironolactone should be considered. Together these drugs have a synergistic action, by providing sequential nephron blockade, allowing lower doses of the individual agents.

==Monitoring and Follow Up==
For dogs in stage B, owners should be made aware of signs of congestive heart failure. In dogs with Stage B2 disease where congestive heart failure is imminent, it is useful to give the owner Furosemide to administer if the dog develops signs of respiratory distress. Owners of Stage B2 and Stage C dogs should be educated on how to measure sleeping respiratory rate and should begin recording this regularly.

The frequency of follow-up examinations is dependent on the severity of disease and owner compliance. For dogs with preclinical disease, rechecks can be recommended every 6-12 months depending on the severity of mitral regurgitation and cardiac remodeling. Following hospitalization for control of acute congestive heart failure, dogs should receive a follow up examination within 2 weeks to check for resolution of clinical signs, hydration status, electrolytes and renal function. For dogs in stage C with stable disease, re-checks can be every 3-6 months.

== Prognosis ==

Asymptomatic patients may live for many years. Dogs with stage B2 disease have a median of 27 months before developing congestive heart failure. Once heart failure occurs, life expectancy is usually around 6-12 months, although some patients remain stable for longer. Risk factors for progression include severity of valvular lesions, increased age and male gender. Risk factors for onset of congestive heart failure include severity of mitral regurgitation, left atrial enlargement and elevated NT-proBNP. Development of complications such as atrial fibrillation or chordae tendinae rupture are associated with a poor prognosis.

{{Learning
|videos = [http://www.cardioacademy.cevalearn.com/en/Programme/Sessions/1-Pathophysiology-of-Mitral-Valve-Disease video on mitral valve disease from Cardio Academy]
|flashcards = [[Endocardial Pathology Flashcards]]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22Mitral+Valve+Dysplasia%22&occuring1=title&rowId=2&options2=OR&q2=%22Mitral+Valve+Disease%22&occuring2=title&rowId=3&options3=OR&q3=%22Mitral+insufficiency%22&occuring3=title&rowId=4&options4=OR&q4=%22endocardiosis%22&occuring4=title&x=36&y=9&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Mitral Valve Dysplasia publications]

[http://www.cabdirect.org/search.html?it=any&q2=%22Mitral+Valve+Disease%22&q1=%22Mitral+Valve+Dysplasia%22&calendarInput=yyyy-mm-dd&q4=%22endocardiosis%22&q3=%22Mitral+insufficiency%22&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&rowId=4&options1=AND&options2=OR&occuring4=title&options3=OR&options4=OR&occuring3=title&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc:(ft+OR+fr+OR+fa+OR+fv+OR+fw+OR+fx+OR+gf+OR+ga+OR+b1+OR+b2+OR+b3+OR+b4+OR+b5+OR+b6)&y=9&x=36 Other MDV Full Text Articles]
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103219945.pdf ''' Myxomatous degenerative mitral valve disease: an update.''' Disatian, S.; Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand, Thai Journal of Veterinary Medicine, 2010, 40, 2, pp 151-157, many ref.]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093114836.pdf ''' Latest information about canine mitral valve disease: results of the QUEST trial.''' Häggström, J.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 188-191, 10 ref. - '''Full Text Article''']

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017845.pdf ''' Treatment of mitral valve disease in dogs.''' French, A.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 107-108]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017847.pdf ''' Prognostic variables in canine mitral valve disease.''' Häggstrom, J.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 112-113, 7 ref.]
}}

==References==
* Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2016) '''Manual of Canine and Feline Cardiology (Fifth Edition)''' ''Saunders''.
* Luis Fuentes, V, Johnson, L.R, Dennis, S. (2010) '''BSAVA Manual of Canine and Feline Cardiorespiratory Medicine (Second Edition)'''

{{review}}

{{OpenPages}}

[[Category:Cardiovascular_System_-_Degenerative_Pathology]] [[Category:Endocardial_Pathology]] [[Category:Expert_Review]] [[Category:Cardiac_Diseases_-_Cat]] [[Category:Cardiac_Diseases_-_Dog]]
[[Category:Cardiac_Diseases_-_Horse]]
[[Category:Cardiovascular_System_-_Developmental_Pathology]]
[[Category:Cardiology Section]]

Degenerative Mitral Valve Disease

2016-10-17T16:07:23Z

Lwilkie: /* Stage B */

{{OpenPagesTop}}
Also known as: '''''MVD — Mitral Valve Disease — Mitral Insufficiency — Mitral Endocardiosis — Myxomatous Mitral Valve Disease (MMVD) — Endocardiosis — Mitral Regurgitation — Chronic Valvular Disease'''''

== Introduction ==
Myxomatous degeneration of the mitral valve is the most common acquired cardiac disease in the dog. Degenerative mitral valve disease (DMVD) is a progressive disease and subtle changes in valve structure precede the development of clinically significant disease. The aetiology of DMVD is unknown. Genetic predisposition for development of the disease is likely, however the inheritance is complex.

The '''mitral apparatus''' consists of the mitral '''valve leaflets''', valve '''annulus''', '''chordae tendinae''' and '''papillary muscles'''. The mitral valve leaflets are known as '''anterior''' and '''posterior''' leaflets. In the normal dog, these are thin, translucent structures that are anchored to the papillary muscles by chordae tendinae. Both papillary muscles (anterior and posterior) arise from the left ventricular free wall. The mitral valve prevents the backflow of blood from the left ventricle to the left atrium during systole. In early systole, when left ventricular pressure exceeds left atrial pressure, the mitral valve leaflets close. In normal dogs, the chordae tendinae tether the leaflets to prevent them prolapsing into the left atrium. When the mitral valve is incompetent, there is ''regurgitation'' of blood from the left ventricle to the left atrium. Mitral regurgitation may be mild, with no clinical consequence, or may be severe. The severity of mitral regurgitation is determined primarily by the size of the orifice, that results from incomplete apposition of the mitral valve leaflets, and the relationship between left ventricular and left atrial systolic pressures. Mitral regurgitation causes an increase in left atrial pressure, which over time can lead to left atrial dilation. In diastole, the left ventricle is filled by both pulmonary venous return and blood that has been regurgitated into the left atrium. Therefore, both the left atrium and left ventricle become volume overloaded. This may result in '''ventricular dilation and eccentric hypertrophy'''. In severe cases, increased left ventricular and left atrial filling pressures may result. This leads to an increase in pulmonary venous pressure and may result in [[Heart Failure, Left-Sided|left-sided congestive heart failure]].

==Signalment==

Degenerative mitral valve disease tends to affect middle-aged and older dogs, particularly males. The disease more commonly affects small breed dogs, with Cavalier King Charles Spaniels, Chihuahuas, Boston Terriers, Poodles, Pomeranians and Bull Terriers being predisposed. The disease is also recognized in large breed dogs.

==History and Clinical Signs==
Animals may remain asymptomatic for years, the disease is usually clinically silent until it is advanced.

In most affected dogs, DMVD does not cause clinical signs and the disease is detected by the auscultation of a cardiac murmur at routine health checks.

In cases where DMVD becomes clinically significant, a '''cough''' is usually the first clinical sign noticed by the owner. The coughing is likely of multifactorial aetiology and may be related to pulmonary oedema, stimulation of the juxtapulmonary (J) receptors that are associated with pulmonary capillaries and detect increases in pulmonary venous pressure, compression of a mainstem bronchi by an enlarged left atrium and concurrent airway disease. Occasionally, '''syncope''' is the first sign of clinically significant DMVD. This may occur due to arrhythmias or on exertion where mitral regurgitation limits stroke volume and therefore cardiac output.

== Diagnosis==
===Physical Examination===
* Systolic murmur with point of maximal intensity over the left apex. Murmur grade is usually correlated with severity of mitral regurgitation, severe regurgitation causes a loud murmur.
* Mid-systolic click, associated with mitral prolapse. In many dogs, clicks are a precursor to mitral regurgitation.

Other findings will depend on the stage of disease. Crackles may be detected on thoracic auscultation in patients with pulmonary oedema, resulting from [[Heart Failure, Left-Sided|left-sided congestive heart failure]]. Abdominal palpation is usually normal, but ascites and hepatomegaly may be present when there is concurrent [[Heart Failure, Right-Sided|right-sided congestive heart failure]].

Primary respiratory disease, such as chronic bronchitis, is also common in older small breed dogs. It is important to distinguish between the patient with clinically significant respiratory disease and incidental DMVD from the patient with clinically significant DMVD. Respiratory sinus arrhythmia, indicating vagal influence on heart rate and rhythm, is usually not present in severe cardiac disease. In contrast, sinus arrhythmia is usually preserved or accentuated when respiratory disease is the cause of clinical signs.

===Diagnostic Imaging===
====Radiography====
Early in the course of DMVD, thoracic radiographs will be normal. As the disease progresses, cardiomegaly will become apparent. There may be evidence of left atrial enlargement, with or without dorsal displacement of the trachea and narrowing of the mainstem bronchus. Pulmonary venous distension may be observed if there is increased pulmonary venous pressure. Interstitial pulmonary oedema may precede alveolar pulmonary oedema. Evidence of [[Heart Failure, Right-Sided|right-sided congestive heart failure]] may be present in severe cases, radiographic findings include distension of the caudal vena cava, hepatomegaly, ascites and pleural effusion.

====Echocardiography====
* Thickened mitral valve leaflets
* Prolapse of mitral valve leaflets into the left atrium during systole
* Tricuspid leaflets may also be affected, though usually not as severely as the mitral valve
* Increased diastolic left ventricular diameter
* Hyperdynamic left ventricle
* Colour Doppler jet of mitral regurgitation
*(Flail leaflet)

Thickening of the mitral valve leaflets is usually diffuse, but most pronounced at the leaflet edges. With myxomatous degeneration, the mitral valve becomes stiffer and distorted. The conformation of the valve remains constant throughout the cardiac cycle. Normally, the mitral valve leaflets do not extend beyond a line across the mitral annulus in systole. In dogs with DMVD, the mitral leaflets prolapse towards the left atrium during systole. Colour Doppler can be used to demonstrate the jet of mitral regurgitation. The size of the jet is related to the severity of mitral regurgitation. Most mitral regurgitation jets in DMVD are eccentric.

The more severe the DMVD, the greater the degree of left ventricular and left atrial dilation.

Fractional shortening may be increased (hyperynamic left ventricle). This is because, in the setting of mitral regurgitation, impedance to ventricular emptying is reduced (blood can be ejected into the low pressure left atrium)and end-diastolic ventricular stretch is increased by the addition of the regurgitant fraction, increasing the force of contraction.

A serious complication of DMVD is '''chordae tendinae rupture''', resulting in a 'flail leaflet' and acute worsening of mitral regurgitation. A leaflet segment typically 'flails' back into the left atrium during systole.

'''Left atrial rupture''' is a major complication of DMVD. Left atrial endocardial and endomyocardial splits are usually multiple and may heal or perforate the atrial wall, causing haemopericardium or an acquired atrial septal defect depending on their depth and location.

===Electrocardiogram (ECG)===
Electrocardiography is primarily used to diagnose arrhythmias, but can provide evidence of chamber enlargement. Most arrhythmias in DMVD are supraventricular in origin and occur secondary to left atrial stretch. Ventricular arrhythmias may develop in association with left ventricular dilation and fibrosis.

* P-mitrale: wide P waves in leads II, III and aVF, indicates left atrial enlargement

===Laboratory Tests===
Pro-brain natriuretic peptide ('''NT-proBNP''') concentration is associated with severity of DMVD. Elevated NT-proBNP levels are useful in discriminating patients with respiratory distress caused by heart failure from those with primary respiratory tract disease.

==Staging==
Staging according to American College of Veterinary Internal Medicine (ACVIM) is as follows:
* '''Stage A''': Dog predisposed to the development of DMVD
* '''Stage B''': Subclinical disease
** ''B1'': Without cardiac remodeling
** ''B2'': With cardiac remodeling
* '''Stage C''': Current or prior clinical signs
* '''Stage D''': Refractory heart failure

== Treatment ==
===Stage B===
There is no therapy demonstrated to be beneficial in dogs with stage B1 disease.

The results of the EPIC study demonstrated that administration of Pimobendan to dogs with stage B2 disease resulted in prolongation of the asymptomatic phase of disease by approximately 15 months. Dogs receiving Pimobendan were around 33% less likely to go into congestive heart failure or suffer a cardiac death than those not receiving the drug. Pimobendan appears safe and well-tolerated.

Based on findings of the EPIC study, dogs with typical mitral valve murmurs of grade III/VI or higher should be investigated to look for evidence of cardiomegaly. If cardiomegaly is apparent, then the dog may benefit from starting Pimobendan, as opposed to the 'watch and wait' approach that was previously recommended.

===Stage C===
Medical management is intended to alleviate clinical signs and prolong life.

'''Furosemide''' is a potent first-line diuretic that can be administered orally or parenterally, depending on the clinical status of the patient. Most patients with congestive heart failure secondary to DMVD require lifelong diuretic therapy.

The addition of an '''ACE inhibitor''' is considered standard therapy. The benefits of ACE inhibitors are related to their vasodilator action and also protecting the heart from the detrimental effects of RAAS activation.

'''Pimobendan''' is phosphodiesterase inhibitor and calcium sensitiser that is both a ''positive inotrope'' and ''vasodilator'' (inodilator). A randomized clinical trial (QUEST) demonstrated a survival benefit associated with Pimobendan administration, when evaluated relative to treatment which was considered at that time to be the gold standard; benazepril. Use of triple therapy with furosemide, an ACE inhibitor and Pimobendan is recommended. When financial or compliance concerns limit the therapeutic choices, evidence suggests that Pimobendan is superior to an ACE inhibitor.

Aldosterone may contribute to the development of myocardial fibrosis. Complete suppression of RAAS is generally not achieved by ACE inhibition alone. Therefore the addition of '''Spironolactone''' may be beneficial.

Surgical mitral valve repair in dogs is currently being performed. However, availability is limited by the expense, required expertise and cardiopulmonary bypass facilities.

===Stage D===
If congestive heart failure signs are not controlled by high doses of Furosemide, addition of a thiazide and Spironolactone should be considered. Together these drugs have a synergistic action, by providing sequential nephron blockade, allowing lower doses of the individual agents.

==Monitoring and Follow Up==
For dogs in stage B, owners should be made aware of signs of congestive heart failure. In dogs with Stage B2 disease where congestive heart failure is imminent, it is useful to give the owner Furosemide to administer if the dog develops signs of respiratory distress. Owners of Stage B2 and Stage C dogs should be educated on how to measure sleeping respiratory rate and should begin recording this regularly.

The frequency of follow-up examinations is dependent on the severity of disease and owner compliance. For dogs with preclinical disease, rechecks can be recommended every 6-12 months depending on the severity of mitral regurgitation and cardiac remodeling. Following hospitalization for control of acute congestive heart failure, dogs should receive a follow up examination within 2 weeks to check for resolution of clinical signs, hydration status, electrolytes and renal function. For dogs in stage C with stable disease, re-checks can be every 3-6 months.

== Prognosis ==

Asymptomatic patients may live for many years. Dogs with stage B2 disease have a median of 27 months before developing congestive heart failure. Once heart failure occurs, life expectancy is usually around 6-12 months, although some patients remain stable for longer. Risk factors for progression include severity of valvular lesions, increased age and male gender. Risk factors for onset of congestive heart failure include severity of mitral regurgitation, left atrial enlargement and elevated NT-proBNP. Development of complications such as atrial fibrillation or chordae tendinae rupture are associated with a poor prognosis.

{{Learning
|videos = [http://www.cardioacademy.cevalearn.com/en/Programme/Sessions/1-Pathophysiology-of-Mitral-Valve-Disease video on mitral valve disease from Cardio Academy]
|flashcards = [[Endocardial Pathology Flashcards]]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22Mitral+Valve+Dysplasia%22&occuring1=title&rowId=2&options2=OR&q2=%22Mitral+Valve+Disease%22&occuring2=title&rowId=3&options3=OR&q3=%22Mitral+insufficiency%22&occuring3=title&rowId=4&options4=OR&q4=%22endocardiosis%22&occuring4=title&x=36&y=9&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Mitral Valve Dysplasia publications]

[http://www.cabdirect.org/search.html?it=any&q2=%22Mitral+Valve+Disease%22&q1=%22Mitral+Valve+Dysplasia%22&calendarInput=yyyy-mm-dd&q4=%22endocardiosis%22&q3=%22Mitral+insufficiency%22&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&rowId=4&options1=AND&options2=OR&occuring4=title&options3=OR&options4=OR&occuring3=title&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc:(ft+OR+fr+OR+fa+OR+fv+OR+fw+OR+fx+OR+gf+OR+ga+OR+b1+OR+b2+OR+b3+OR+b4+OR+b5+OR+b6)&y=9&x=36 Other MDV Full Text Articles]
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103219945.pdf ''' Myxomatous degenerative mitral valve disease: an update.''' Disatian, S.; Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand, Thai Journal of Veterinary Medicine, 2010, 40, 2, pp 151-157, many ref.]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093114836.pdf ''' Latest information about canine mitral valve disease: results of the QUEST trial.''' Häggström, J.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 188-191, 10 ref. - '''Full Text Article''']

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017845.pdf ''' Treatment of mitral valve disease in dogs.''' French, A.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 107-108]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017847.pdf ''' Prognostic variables in canine mitral valve disease.''' Häggstrom, J.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 112-113, 7 ref.]
}}

==References==
* Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2016) '''Manual of Canine and Feline Cardiology (Fifth Edition)''' ''Saunders''.
* Luis Fuentes, V, Johnson, L.R, Dennis, S. (2010) '''BSAVA Manual of Canine and Feline Cardiorespiratory Medicine (Second Edition)'''

{{review}}

{{OpenPages}}

[[Category:Cardiovascular_System_-_Degenerative_Pathology]] [[Category:Endocardial_Pathology]] [[Category:Expert_Review]] [[Category:Cardiac_Diseases_-_Cat]] [[Category:Cardiac_Diseases_-_Dog]]
[[Category:Cardiac_Diseases_-_Horse]]
[[Category:Cardiovascular_System_-_Developmental_Pathology]]
[[Category:Cardiology Section]]

Degenerative Mitral Valve Disease

2016-10-17T15:53:44Z

Lwilkie: /* Prognosis */

{{OpenPagesTop}}
Also known as: '''''MVD — Mitral Valve Disease — Mitral Insufficiency — Mitral Endocardiosis — Myxomatous Mitral Valve Disease (MMVD) — Endocardiosis — Mitral Regurgitation — Chronic Valvular Disease'''''

== Introduction ==
Myxomatous degeneration of the mitral valve is the most common acquired cardiac disease in the dog. Degenerative mitral valve disease (DMVD) is a progressive disease and subtle changes in valve structure precede the development of clinically significant disease. The aetiology of DMVD is unknown. Genetic predisposition for development of the disease is likely, however the inheritance is complex.

The '''mitral apparatus''' consists of the mitral '''valve leaflets''', valve '''annulus''', '''chordae tendinae''' and '''papillary muscles'''. The mitral valve leaflets are known as '''anterior''' and '''posterior''' leaflets. In the normal dog, these are thin, translucent structures that are anchored to the papillary muscles by chordae tendinae. Both papillary muscles (anterior and posterior) arise from the left ventricular free wall. The mitral valve prevents the backflow of blood from the left ventricle to the left atrium during systole. In early systole, when left ventricular pressure exceeds left atrial pressure, the mitral valve leaflets close. In normal dogs, the chordae tendinae tether the leaflets to prevent them prolapsing into the left atrium. When the mitral valve is incompetent, there is ''regurgitation'' of blood from the left ventricle to the left atrium. Mitral regurgitation may be mild, with no clinical consequence, or may be severe. The severity of mitral regurgitation is determined primarily by the size of the orifice, that results from incomplete apposition of the mitral valve leaflets, and the relationship between left ventricular and left atrial systolic pressures. Mitral regurgitation causes an increase in left atrial pressure, which over time can lead to left atrial dilation. In diastole, the left ventricle is filled by both pulmonary venous return and blood that has been regurgitated into the left atrium. Therefore, both the left atrium and left ventricle become volume overloaded. This may result in '''ventricular dilation and eccentric hypertrophy'''. In severe cases, increased left ventricular and left atrial filling pressures may result. This leads to an increase in pulmonary venous pressure and may result in [[Heart Failure, Left-Sided|left-sided congestive heart failure]].

==Signalment==

Degenerative mitral valve disease tends to affect middle-aged and older dogs, particularly males. The disease more commonly affects small breed dogs, with Cavalier King Charles Spaniels, Chihuahuas, Boston Terriers, Poodles, Pomeranians and Bull Terriers being predisposed. The disease is also recognized in large breed dogs.

==History and Clinical Signs==
Animals may remain asymptomatic for years, the disease is usually clinically silent until it is advanced.

In most affected dogs, DMVD does not cause clinical signs and the disease is detected by the auscultation of a cardiac murmur at routine health checks.

In cases where DMVD becomes clinically significant, a '''cough''' is usually the first clinical sign noticed by the owner. The coughing is likely of multifactorial aetiology and may be related to pulmonary oedema, stimulation of the juxtapulmonary (J) receptors that are associated with pulmonary capillaries and detect increases in pulmonary venous pressure, compression of a mainstem bronchi by an enlarged left atrium and concurrent airway disease. Occasionally, '''syncope''' is the first sign of clinically significant DMVD. This may occur due to arrhythmias or on exertion where mitral regurgitation limits stroke volume and therefore cardiac output.

== Diagnosis==
===Physical Examination===
* Systolic murmur with point of maximal intensity over the left apex. Murmur grade is usually correlated with severity of mitral regurgitation, severe regurgitation causes a loud murmur.
* Mid-systolic click, associated with mitral prolapse. In many dogs, clicks are a precursor to mitral regurgitation.

Other findings will depend on the stage of disease. Crackles may be detected on thoracic auscultation in patients with pulmonary oedema, resulting from [[Heart Failure, Left-Sided|left-sided congestive heart failure]]. Abdominal palpation is usually normal, but ascites and hepatomegaly may be present when there is concurrent [[Heart Failure, Right-Sided|right-sided congestive heart failure]].

Primary respiratory disease, such as chronic bronchitis, is also common in older small breed dogs. It is important to distinguish between the patient with clinically significant respiratory disease and incidental DMVD from the patient with clinically significant DMVD. Respiratory sinus arrhythmia, indicating vagal influence on heart rate and rhythm, is usually not present in severe cardiac disease. In contrast, sinus arrhythmia is usually preserved or accentuated when respiratory disease is the cause of clinical signs.

===Diagnostic Imaging===
====Radiography====
Early in the course of DMVD, thoracic radiographs will be normal. As the disease progresses, cardiomegaly will become apparent. There may be evidence of left atrial enlargement, with or without dorsal displacement of the trachea and narrowing of the mainstem bronchus. Pulmonary venous distension may be observed if there is increased pulmonary venous pressure. Interstitial pulmonary oedema may precede alveolar pulmonary oedema. Evidence of [[Heart Failure, Right-Sided|right-sided congestive heart failure]] may be present in severe cases, radiographic findings include distension of the caudal vena cava, hepatomegaly, ascites and pleural effusion.

====Echocardiography====
* Thickened mitral valve leaflets
* Prolapse of mitral valve leaflets into the left atrium during systole
* Tricuspid leaflets may also be affected, though usually not as severely as the mitral valve
* Increased diastolic left ventricular diameter
* Hyperdynamic left ventricle
* Colour Doppler jet of mitral regurgitation
*(Flail leaflet)

Thickening of the mitral valve leaflets is usually diffuse, but most pronounced at the leaflet edges. With myxomatous degeneration, the mitral valve becomes stiffer and distorted. The conformation of the valve remains constant throughout the cardiac cycle. Normally, the mitral valve leaflets do not extend beyond a line across the mitral annulus in systole. In dogs with DMVD, the mitral leaflets prolapse towards the left atrium during systole. Colour Doppler can be used to demonstrate the jet of mitral regurgitation. The size of the jet is related to the severity of mitral regurgitation. Most mitral regurgitation jets in DMVD are eccentric.

The more severe the DMVD, the greater the degree of left ventricular and left atrial dilation.

Fractional shortening may be increased (hyperynamic left ventricle). This is because, in the setting of mitral regurgitation, impedance to ventricular emptying is reduced (blood can be ejected into the low pressure left atrium)and end-diastolic ventricular stretch is increased by the addition of the regurgitant fraction, increasing the force of contraction.

A serious complication of DMVD is '''chordae tendinae rupture''', resulting in a 'flail leaflet' and acute worsening of mitral regurgitation. A leaflet segment typically 'flails' back into the left atrium during systole.

'''Left atrial rupture''' is a major complication of DMVD. Left atrial endocardial and endomyocardial splits are usually multiple and may heal or perforate the atrial wall, causing haemopericardium or an acquired atrial septal defect depending on their depth and location.

===Electrocardiogram (ECG)===
Electrocardiography is primarily used to diagnose arrhythmias, but can provide evidence of chamber enlargement. Most arrhythmias in DMVD are supraventricular in origin and occur secondary to left atrial stretch. Ventricular arrhythmias may develop in association with left ventricular dilation and fibrosis.

* P-mitrale: wide P waves in leads II, III and aVF, indicates left atrial enlargement

===Laboratory Tests===
Pro-brain natriuretic peptide ('''NT-proBNP''') concentration is associated with severity of DMVD. Elevated NT-proBNP levels are useful in discriminating patients with respiratory distress caused by heart failure from those with primary respiratory tract disease.

==Staging==
Staging according to American College of Veterinary Internal Medicine (ACVIM) is as follows:
* '''Stage A''': Dog predisposed to the development of DMVD
* '''Stage B''': Subclinical disease
** ''B1'': Without cardiac remodeling
** ''B2'': With cardiac remodeling
* '''Stage C''': Current or prior clinical signs
* '''Stage D''': Refractory heart failure

== Treatment ==
===Stage B===
There is no evidence that any therapy slows the progression of asymptomatic disease.
===Stage C===
Medical management is intended to alleviate clinical signs and prolong life.

'''Furosemide''' is a potent first-line diuretic that can be administered orally or parenterally, depending on the clinical status of the patient. Most patients with congestive heart failure secondary to DMVD require lifelong diuretic therapy.

The addition of an '''ACE inhibitor''' is considered standard therapy. The benefits of ACE inhibitors are related to their vasodilator action and also protecting the heart from the detrimental effects of RAAS activation.

'''Pimobendan''' is phosphodiesterase inhibitor and calcium sensitiser that is both a ''positive inotrope'' and ''vasodilator'' (inodilator). A randomized clinical trial (QUEST) demonstrated a survival benefit associated with Pimobendan administration, when evaluated relative to treatment which was considered at that time to be the gold standard; benazepril. Use of triple therapy with furosemide, an ACE inhibitor and Pimobendan is recommended. When financial or compliance concerns limit the therapeutic choices, evidence suggests that Pimobendan is superior to an ACE inhibitor.

Aldosterone may contribute to the development of myocardial fibrosis. Complete suppression of RAAS is generally not achieved by ACE inhibition alone. Therefore the addition of '''Spironolactone''' may be beneficial.

Surgical mitral valve repair in dogs is currently being performed. However, availability is limited by the expense, required expertise and cardiopulmonary bypass facilities.

===Stage D===
If congestive heart failure signs are not controlled by high doses of Furosemide, addition of a thiazide and Spironolactone should be considered. Together these drugs have a synergistic action, by providing sequential nephron blockade, allowing lower doses of the individual agents.

==Monitoring and Follow Up==
For dogs in stage B, owners should be made aware of signs of congestive heart failure. In dogs with Stage B2 disease where congestive heart failure is imminent, it is useful to give the owner Furosemide to administer if the dog develops signs of respiratory distress. Owners of Stage B2 and Stage C dogs should be educated on how to measure sleeping respiratory rate and should begin recording this regularly.

The frequency of follow-up examinations is dependent on the severity of disease and owner compliance. For dogs with preclinical disease, rechecks can be recommended every 6-12 months depending on the severity of mitral regurgitation and cardiac remodeling. Following hospitalization for control of acute congestive heart failure, dogs should receive a follow up examination within 2 weeks to check for resolution of clinical signs, hydration status, electrolytes and renal function. For dogs in stage C with stable disease, re-checks can be every 3-6 months.

== Prognosis ==

Asymptomatic patients may live for many years. Dogs with stage B2 disease have a median of 27 months before developing congestive heart failure. Once heart failure occurs, life expectancy is usually around 6-12 months, although some patients remain stable for longer. Risk factors for progression include severity of valvular lesions, increased age and male gender. Risk factors for onset of congestive heart failure include severity of mitral regurgitation, left atrial enlargement and elevated NT-proBNP. Development of complications such as atrial fibrillation or chordae tendinae rupture are associated with a poor prognosis.

{{Learning
|videos = [http://www.cardioacademy.cevalearn.com/en/Programme/Sessions/1-Pathophysiology-of-Mitral-Valve-Disease video on mitral valve disease from Cardio Academy]
|flashcards = [[Endocardial Pathology Flashcards]]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22Mitral+Valve+Dysplasia%22&occuring1=title&rowId=2&options2=OR&q2=%22Mitral+Valve+Disease%22&occuring2=title&rowId=3&options3=OR&q3=%22Mitral+insufficiency%22&occuring3=title&rowId=4&options4=OR&q4=%22endocardiosis%22&occuring4=title&x=36&y=9&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Mitral Valve Dysplasia publications]

[http://www.cabdirect.org/search.html?it=any&q2=%22Mitral+Valve+Disease%22&q1=%22Mitral+Valve+Dysplasia%22&calendarInput=yyyy-mm-dd&q4=%22endocardiosis%22&q3=%22Mitral+insufficiency%22&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&rowId=4&options1=AND&options2=OR&occuring4=title&options3=OR&options4=OR&occuring3=title&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc:(ft+OR+fr+OR+fa+OR+fv+OR+fw+OR+fx+OR+gf+OR+ga+OR+b1+OR+b2+OR+b3+OR+b4+OR+b5+OR+b6)&y=9&x=36 Other MDV Full Text Articles]
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103219945.pdf ''' Myxomatous degenerative mitral valve disease: an update.''' Disatian, S.; Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand, Thai Journal of Veterinary Medicine, 2010, 40, 2, pp 151-157, many ref.]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093114836.pdf ''' Latest information about canine mitral valve disease: results of the QUEST trial.''' Häggström, J.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 188-191, 10 ref. - '''Full Text Article''']

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017845.pdf ''' Treatment of mitral valve disease in dogs.''' French, A.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 107-108]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017847.pdf ''' Prognostic variables in canine mitral valve disease.''' Häggstrom, J.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 112-113, 7 ref.]
}}

==References==
* Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2016) '''Manual of Canine and Feline Cardiology (Fifth Edition)''' ''Saunders''.
* Luis Fuentes, V, Johnson, L.R, Dennis, S. (2010) '''BSAVA Manual of Canine and Feline Cardiorespiratory Medicine (Second Edition)'''

{{review}}

{{OpenPages}}

[[Category:Cardiovascular_System_-_Degenerative_Pathology]] [[Category:Endocardial_Pathology]] [[Category:Expert_Review]] [[Category:Cardiac_Diseases_-_Cat]] [[Category:Cardiac_Diseases_-_Dog]]
[[Category:Cardiac_Diseases_-_Horse]]
[[Category:Cardiovascular_System_-_Developmental_Pathology]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:45:15Z

Lwilkie: /* References */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.
===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.
===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''', '''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''', '''Amioderone''' should be administered if electric cardioversion is an option. Amioderone increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option, and the rate is >150bpm, then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal echocardiographic findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2016) '''Manual of Canine and Feline Cardiology (Fifth Edition)''' ''Saunders''.
 
Luis Fuentes, V, Johnson, L.R, Dennis, S. (2010) '''BSAVA Manual of Canine and Feline Cardiorespiratory Medicine (Second Edition)'''Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:42:45Z

Lwilkie: /* Small Animals */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.
===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.
===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''', '''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''', '''Amioderone''' should be administered if electric cardioversion is an option. Amioderone increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option, and the rate is >150bpm, then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal echocardiographic findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:42:02Z

Lwilkie: /* Clinical Signs */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.
===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.
===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''', '''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''' '''Amioderone''' should be administered if electric cardioversion is an option. Amioderone increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option, and the rate is >150bpm, then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal echocardiographic findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:41:23Z

Lwilkie: /* Horses */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''', '''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''' '''Amioderone''' should be administered if electric cardioversion is an option. Amioderone increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option, and the rate is >150bpm, then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal echocardiographic findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:41:03Z

Lwilkie: /* Horses */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''', '''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''' '''Amioderone''' should be administered if electric cardioversion is an option. Amioderone increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option, and the rate is >150bpm, then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal echocardiographic findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:40:09Z

Lwilkie: /* Introduction */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''', '''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''' '''Amioderone''' should be administered if electric cardioversion is an option. Amioderone increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option, and the rate is >150bpm, then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal echocardiographic findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:38:51Z

Lwilkie: /* Prognosis */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

In horses it may be detected unexpectedly during an examination of an animal with no history of heart disease. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise.

In cattle it occurs most commonly in animals with abnormalities of the gastrointestinal tract.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''', '''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''' '''Amioderone''' should be administered if electric cardioversion is an option. Amioderone increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option, and the rate is >150bpm, then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal echocardiographic findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:38:12Z

Lwilkie: /* Small Animals */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

In horses it may be detected unexpectedly during an examination of an animal with no history of heart disease. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise.

In cattle it occurs most commonly in animals with abnormalities of the gastrointestinal tract.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''', '''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''' '''Amioderone''' should be administered if electric cardioversion is an option. Amioderone increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option, and the rate is >150bpm, then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal ultrasound findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:36:32Z

Lwilkie: /* Small Animals */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

In horses it may be detected unexpectedly during an examination of an animal with no history of heart disease. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise.

In cattle it occurs most commonly in animals with abnormalities of the gastrointestinal tract.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''':
'''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''':
If '''electrical cardioversion''' is an option, start '''Amioderone'''. This increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option and the rate is >150bpm then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal ultrasound findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:36:00Z

Lwilkie: /* Small Animals */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

In horses it may be detected unexpectedly during an examination of an animal with no history of heart disease. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise.

In cattle it occurs most commonly in animals with abnormalities of the gastrointestinal tract.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).

In '''dogs''' with AF secondary to '''structural heart disease''':
'''Digoxin''' is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as '''Diltiazem''' can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.

In '''dogs''' with '''primary 'lone' AF''':
If '''electrical cardioversion''' is an option, start '''Amioderone'''. This increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option and the rate is >150bpm then rate control is appropriate, using '''beta-blockers''' or '''Diltiazem'''. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]].

In '''cats''', atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is '''Diltiazem'''.

In '''rabbits''', '''Digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as '''Furosemide''' can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure.

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal ultrasound findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:14:30Z

Lwilkie: /* Diagnosis */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

In horses it may be detected unexpectedly during an examination of an animal with no history of heart disease. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise.

In cattle it occurs most commonly in animals with abnormalities of the gastrointestinal tract.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation====
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
In '''dogs''', '''digoxin''', is usually the first line of therapy in slowing conduction through the AV node. The goal is to keep the heart rate between 140 and 160 beats per minute. If the heart rate remains high, a calcium channel blocker such as '''diltiazem or a beta-blocker''' should be used as well.

High-dose '''oral quinidine or electrical cardioversion''' can be used in primary atrial fibrillation cases to convert the heart back to sinus rhythm. This requires experienced personnel, general anaesthesia and special equipment.

In '''cats''', '''diltiazem or atenolol''' are usually the drugs of choice. Digoxin can also be added if the heart rate is still high or there is evidence of heart failure.

In '''rabbits''', '''digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as '''frusemide''' can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure.

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal ultrasound findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:14:10Z

Lwilkie: /* Diagnosis */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

In horses it may be detected unexpectedly during an examination of an animal with no history of heart disease. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise.

In cattle it occurs most commonly in animals with abnormalities of the gastrointestinal tract.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
===Physical Examination===
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
===Electrocardiogram (ECG)===
====Atrial Flutter====
* No P waves
* Regular saw-tooth deflections of baseline
* Ventricular rate variable
* Sudden onset and termination
====Atrial Fibrillation===
* No P waves
* Coarse oscillation of the baseline (F-waves)
* R-R interval irregular and chaotic
===Echocardiography===
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
In '''dogs''', '''digoxin''', is usually the first line of therapy in slowing conduction through the AV node. The goal is to keep the heart rate between 140 and 160 beats per minute. If the heart rate remains high, a calcium channel blocker such as '''diltiazem or a beta-blocker''' should be used as well.

High-dose '''oral quinidine or electrical cardioversion''' can be used in primary atrial fibrillation cases to convert the heart back to sinus rhythm. This requires experienced personnel, general anaesthesia and special equipment.

In '''cats''', '''diltiazem or atenolol''' are usually the drugs of choice. Digoxin can also be added if the heart rate is still high or there is evidence of heart failure.

In '''rabbits''', '''digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as '''frusemide''' can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure.

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal ultrasound findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Atrial Fibrillation & Atrial Flutter

2016-06-30T11:05:57Z

Lwilkie: /* Introduction */

{{OpenPagesTop}}
== Introduction ==
Atrial fibrillation is the commonest pathological dysrhythmia.

'''Atrial Fibrillation (AF):''' Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.

'''Atrial Flutter:''' is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.

Atrial fibrillation can occur in all species when there is '''atrial dilation''' secondary to other cardiac lesions.

In horses it may be detected unexpectedly during an examination of an animal with no history of heart disease. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise.

In cattle it occurs most commonly in animals with abnormalities of the gastrointestinal tract.

==Clinical Signs==
===Horses===
This may be an '''incidental finding''' on clinical examination, especially if the horse is not used for highly athletic activities. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include '''exercise intolerance''', reluctance to exercise or a poor performance during exercise. It can be associated with '''[[Exercise Induced Pulmonary Haemorrhage|exercise induced pulmonary haemorrhage]]''', so this can be a clinical sign of the condition.

===Cattle===
Signs generally relate to the underlying disease process, which in cows can range from '''gastrointestinal diseases''' such as a [[LDA|left-displaced abomasum]], to uterine torsion.

===Small Animals===
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.

Other signs are generally related to the underlying disease process or [[:Category:Heart Failure|'''congestive heart failure''']]. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.

== Diagnosis ==
A full '''history and clinical examination''' may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an '''irregularly irregular heart rhythm''' on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a '''variable pulse quality''' and a variable intensity of heart sounds.
 
An '''electrocargiogram''' (ECG) can be performed for a definitive diagnosis of atrial fibrillation. It will show a '''lack of P waves''' and instead 'F waves'. The ventricular rate is high, the interval between QRS complexes is irregular but the QRS complexes themselves appear normal.

'''Atrial flutter on ECG''' has the following features: the atrial rhythm is regular, at approximately 300-400 beats per minute. P waves are usually discrete P waves or a saw-toothed baseline. Ventricular rhythm and rate generally depend on the atrial rate and AV nodal conduction, but are generally regularly irregular and rapid. It can sometimes mimic atrial fibrillation.

'''Echocardiography and radiography''' may help characterise the type and severity of the heart disease, if present. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.

==Treatment==
===Horse===
In horses where the condition is found without other concurrent heart disease, treatment is with the drug '''quinidine sulphate'''. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.

Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with '''digoxin''', which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe '''side effects''' which can occur with this treatment and they include [[Ventricular Tachycardia|ventricular tachycardia]], [[:Category:Colic in Horses|colic]], diarrhoea and hypotension.

There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.

Horses can also develop atrial fibrillation secondary to '''cardiac disease''', such as [[Mitral Valve Dysplasia|mitral valve insufficiency]], [[Tricuspid Valve Dysplasia|tricuspid valve insufficiency]], or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop '''congestive heart failure''' and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.

===Cattle===
Cattle are not usually treated with an antiarrythmic drug as the heart will '''revert to sinus rhythm''' following the correction of the underlying abdominal disorder.

===Small Animals===
In '''dogs''', '''digoxin''', is usually the first line of therapy in slowing conduction through the AV node. The goal is to keep the heart rate between 140 and 160 beats per minute. If the heart rate remains high, a calcium channel blocker such as '''diltiazem or a beta-blocker''' should be used as well.

High-dose '''oral quinidine or electrical cardioversion''' can be used in primary atrial fibrillation cases to convert the heart back to sinus rhythm. This requires experienced personnel, general anaesthesia and special equipment.

In '''cats''', '''diltiazem or atenolol''' are usually the drugs of choice. Digoxin can also be added if the heart rate is still high or there is evidence of heart failure.

In '''rabbits''', '''digoxin''' has been used anecdotally to slow the heart rate.

In all cases with concurrent severe heart disease and possibly '''congestive heart failure''', efforts to control the disease by using diuretics such as '''frusemide''' can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure.

== Prognosis ==
In '''horses''', the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.

In '''cattle''', prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.

In '''small animals''', cases with primary atrial fibrillation and normal ultrasound findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02642.asp, Atrial fibrillation]
|flashcards = [[Rabbit Medicine and Surgery Q&A 02]] [[Equine Internal Medicine Q&A 12]]
}}

== References ==
Boswood, A (2008) '''Cardiovascular System Study Guide''', ''Royal Veterinary College''.
 
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition), W.B. ''Saunders Company''.
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''', ''University of Liverpool''.
 
Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition), ''Merial''.
 
Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing''.
 
Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) '''Equine Internal Medicine''' (Second Edition), ''Saunders''.
 
Robinson, N.E., Sprayberry, K.A. (2009) '''Current Therapy in Equine Medicine''' (Sixth Edition), ''Saunders Elsevier''.
 
Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition), ''Saunders''.
 
Mazzaferro, E. (2011) '''Blackwell's five minute veterinary consult clinical companion: ECC''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}

[[Category:Altered_Supraventricular_Impulse_Formations]]
[[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Horse]][[Category:Cardiac Diseases - Cat]][[Category:Cardiac Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T10:51:30Z

Lwilkie: /* References */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

The primary determinants of cardiac performance are:
* '''Preload''': The volume of blood or hydrostatic pressure within the ventricles at the end of diastole.
* '''Afterload''': The force that opposes ejection of blood into the peripheral arterial system, of which arterial blood pressure is the primary factor
* '''Contractility''': The ability of the myocardium to function as a pump and eject blood

The '''Frank-Starling''' mechanism states that stroke volume increases in response to increased end-diastolic volume (preload) when all other factors remain constant. Therefore, if a larger volume of blood flows to the ventricle, there is greater wall stretch, causing greater expansion during diastole, which in turn increases the force of contraction and therefore stroke volume (quantity of blood that is pumped into the aorta during systole).

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: concentric and eccentric hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Natriuretic Peptides===
Natriuretic peptides include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The main site of manufacture, storage and release is the myocardium. Under normal circumstances, ANP and BNP are both manufactured by the atrial myocardium. In heart disease, BNP is manufactured predominantly in the ventricular myocardium. Both are released in response to increased chamber wall stress. These hormones counter regulate many of the above mechanisms, causing vasorelaxation and increased sodium loss. However, in congestive heart failure this counter regulatory system is overwhelmed by other vasoconstrictive and sodium retaining mechanisms.

Natriuretic peptides are useful biomarkers of cardiac disease, as levels are elevated in patients with clinically significant disease.

===Antidiuretic Hormone (ADH)===
Release of ADH from the posterior pituitary gland increases absorption of free water in the collecting duct of the nephron. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. In heart failure, there are increased circulating levels of ADH. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

Excess ADH leads to fluid retention, contributing to congestive heart failure, and dilutes total body sodium and chloride leading to hypo-osmolarity. The finding of hyponatraemia and hypochloraemia on blood tests from patients with cardiac disease indicate an advanced stage of disease. Dilutional hyponatraemia (excess free water, rather than a reduction in sodium) is a poor prognostic sign.

== Classification ==

=== Modified New York Heart Association Classification ===

Classification of congestive heart failure modified from human medicine. This is problematic, as cardiac debilitation is not the only factor governing exercise tolerance. This is particularly difficult to apply to cats, which tend to lead a sedentary lifestyle. Furthermore, a normal level of activity is clearly defined for humans (e.g. ability to walk a certain distance), but in veterinary medicine this may be influenced by the breed and lifestyle of the dog.

*Class I: Heart disease with no clinical signs
*Class II: Exercise intolerance
*Class III: Marked exercise intolerance and dyspnoea
*Class IV: Cannot exercise, dyspnoea at rest

===American Heart Association (AHA and American College of Cardiology (ACC)===

* Stage A: Predisposition for developing cardiac disease e.g. Cavalier King Charles Spaniel, Doberman
* Stage B: Structural heart disease, no clinical signs
* Stage C: Structural heart disease, current or prior clinical signs
* Stage D: Refractory heart failure

===International Small Animal Cardiac Health Council (ISACHC)===
The only veterinary-specific clinical classification.

* Class Ia: Structural heart disease, no radiographic or echocardiographic evidence of cardiac enlargement
* Class Ib: Structural heart disease,radiographic or echocardiographic evidence of cardiac enlargement
* Class II: Mild clinical signs
* Class IIIa: Overt clinical signs, death or severe debilitation likely without immediate therapy but homecare possible
* Class IIIb: Overt clinical signs, death or severe debilitation likely and hospitalisation required

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

* Luis Fuentes, V, Johnson, L.R, Dennis, S. (2010) '''BSAVA Manual of Canine and Feline Cardiorespiratory Medicine (Second Edition)'''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Ventricular Septal Defect

2016-06-30T10:50:13Z

Lwilkie: /* References */

{{OpenPagesTop}}
== Introduction ==
[[Image:VSD1.jpg|thumb|right|150px|<center>Ventricular septal defect. Courtesy of A. Jefferies</center>]]
[[Image:VSD2.jpg|thumb|right|150px|<center>Ventricular septal defect. Courtesy of A. Jefferies</center>]]

Ventricular septal defects (VSDs) are the most common congenital cardiac abnormality in large animals and the second most common congenital cardiac abnormality in cats (12-56% of congenital heart disease cases). They less commonly occur in dogs (6-12% of congenital heart disease cases).

The lesion is usually in the '''membranous area''' of the interventricular septum, just below the aortic valve and the septal tricuspid leaflet.

Ventricular Septal Defects can occur alone or in combination with other congenital malformations, such as [[Tetralogy of Fallot]]. Usually blood flows from the higher pressure left ventricle through the VSD to the lower pressure right ventricle during systole. Significant left-to-right shunting causes volume overload of the pulmonary circulation, increasing pulmonary venous return to the left atrium and consequently the left ventricle. This may result in volume overload of the left heart with consequent [[Heart Failure, Left-Sided|left-sided congestive heart failure]] and [[Pulmonary Hypertension|pulmonary hypertension]]. If chronic over-circulation of the pulmonary vasculature occurs, pulmonary hypertension may develop. Pulmonary hypertension causes increased right ventricular pressures and therefore right-to-left shunting during systole may occur; this is known as '''Eisenmenger's syndrome'''. Right-to-left shunting allows deoxygenated blood to enter the systemic circulation, resulting in arterial hypoxaemia and cyanosis.

Small VSDs provide high resistance to flow, as high pressure gradients between the left and right ventricle are maintained. These are known as '''restrictive''' or '''resistive''' VSDs, and are usually of no haemodynamic consequence. Larger VSDs offer little resistance to the shunting of blood and are more likely to result in haemodynamic consequences. Very large, unrestrictive defects cause the pressures in both ventricles to equilibrate and the two ventricles behave as a common pumping chamber. Unless the pulmonary circulation is protected by a stenotic pulmonic valve, the development of pulmonary hypertension is unavoidable.

==Signalment==
Predisposed breeds include the Lakeland Terrier, Cocker Spaniel, French Bulldog and West Highland White Terrier.

== History and Clinical Signs ==

A murmur is usually detected at the first health check, or primary vaccination. Most affected animals are asymptomatic, but large defects can result in [[Heart Failure, Left-Sided|left-sided congestive heart failure]]. Right-to-left shunting can cause stunted growth and exercise intolerance.

== Diagnosis ==
===Physical Examination===
* '''Systolic''' murmur with point of maximum intensity on the '''right''', cranial hemithorax (blood shunts to the right) The murmur can also be detected on the left side, either due to radiation of the primary murmur or the relative pulmonic stenosis caused by the increased blood flow across the pulmonic valve. There may also be a diastolic component to the murmur if aortic regurgitation is present, as a result of the aortic valve prolapsing into the VSD.
* Murmur grade is inversely proportional to the size of the defect, as smaller defects provide more resistance and therefore produce louder murmurs
* Cyanosis may be present with right-to-left shunts
===Thoracic Radiographs===
* Left ventricular enlargement
* Left atrial enlargement
* Right ventricular enlargement
* Pulmonary over-circulation may be present if the left-to-right shunting is significant
===Echocardiography===
* Left atrial dilation
* Left ventricular dilation (eccentric hypertrophy)
* Hyperkinetic left ventricle
* May be able to visualise large defects
* Spectral or colour flow Doppler can be used to interrogate the right ventricular side of the VSD and should demonstrate left-to-right flow
* Velocity of blood flow accross the VSD can be measured, using Doppler, to assess the pressure gradient. High velocity flow is associated with small defects.
* Mitral regurgitation is common
* Aortic regurgitation can occur if the aortic valve prolapses into the VSD

== Management ==

Treatment may be unnecessary, as the defect may close on its own. Treatment is also not necessary for small VSDs that are of no haemodynamic significance.

In severe cases, [[Heart Failure, Left-Sided|congestive heart failure]] should be appropriately managed. The principle palliative surgical procedure described is pulmonary artery anding, in order to protect the pulmonary vascular bed and therefore prevent the development of pulmonary hypertension. Transcatheter closure of VSDs using an Amplatzer device has also been described in a dog.

If significant right to left shunting with resultant '''polycythaemia''' is present, occlusion of the VSD is contraindicated.

== Prognosis ==

In mild to moderate cases the prognosis is excellent. In severe cases, the prognosis is guarded to poor.
{{Learning
|flashcards = [[Cardiovascular Developmental Pathology Flashcards]]
}}

== References ==

Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier.

Saunders, A.B et. al. Hybrid technique for ventricular septal defect closure in a dog using an Amplatzer Duct Occluder II, JVC (2013) 15, 217-224

Bomassi, E. et.al. Signalment, clinical features, echocardiographic findings and outcome of dogs and cats with ventricular septal defects: 109 cases (1992-2013), J Am Vet Med Assoc (2015), July 15; 247(2):166-75

{{review}}

{{OpenPages}}

[[Category:Cardiovascular_System_-_Developmental_Pathology]] [[Category:Expert_Review]] [[Category:Cardiac_Diseases_-_Dog]] [[Category:Cardiac_Diseases_-_Cat]] [[Category:Cardiac_Diseases_-_Horse]] [[Category:Cardiac_Diseases_-_Cattle]] [[Category:Cardiac_Diseases_-_Pig]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T10:27:02Z

Lwilkie: /* American Heart Association (AHA and American College of Cardiology (ACC) */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

The primary determinants of cardiac performance are:
* '''Preload''': The volume of blood or hydrostatic pressure within the ventricles at the end of diastole.
* '''Afterload''': The force that opposes ejection of blood into the peripheral arterial system, of which arterial blood pressure is the primary factor
* '''Contractility''': The ability of the myocardium to function as a pump and eject blood

The '''Frank-Starling''' mechanism states that stroke volume increases in response to increased end-diastolic volume (preload) when all other factors remain constant. Therefore, if a larger volume of blood flows to the ventricle, there is greater wall stretch, causing greater expansion during diastole, which in turn increases the force of contraction and therefore stroke volume (quantity of blood that is pumped into the aorta during systole).

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: concentric and eccentric hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Natriuretic Peptides===
Natriuretic peptides include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The main site of manufacture, storage and release is the myocardium. Under normal circumstances, ANP and BNP are both manufactured by the atrial myocardium. In heart disease, BNP is manufactured predominantly in the ventricular myocardium. Both are released in response to increased chamber wall stress. These hormones counter regulate many of the above mechanisms, causing vasorelaxation and increased sodium loss. However, in congestive heart failure this counter regulatory system is overwhelmed by other vasoconstrictive and sodium retaining mechanisms.

Natriuretic peptides are useful biomarkers of cardiac disease, as levels are elevated in patients with clinically significant disease.

===Antidiuretic Hormone (ADH)===
Release of ADH from the posterior pituitary gland increases absorption of free water in the collecting duct of the nephron. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. In heart failure, there are increased circulating levels of ADH. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

Excess ADH leads to fluid retention, contributing to congestive heart failure, and dilutes total body sodium and chloride leading to hypo-osmolarity. The finding of hyponatraemia and hypochloraemia on blood tests from patients with cardiac disease indicate an advanced stage of disease. Dilutional hyponatraemia (excess free water, rather than a reduction in sodium) is a poor prognostic sign.

== Classification ==

=== Modified New York Heart Association Classification ===

Classification of congestive heart failure modified from human medicine. This is problematic, as cardiac debilitation is not the only factor governing exercise tolerance. This is particularly difficult to apply to cats, which tend to lead a sedentary lifestyle. Furthermore, a normal level of activity is clearly defined for humans (e.g. ability to walk a certain distance), but in veterinary medicine this may be influenced by the breed and lifestyle of the dog.

*Class I: Heart disease with no clinical signs
*Class II: Exercise intolerance
*Class III: Marked exercise intolerance and dyspnoea
*Class IV: Cannot exercise, dyspnoea at rest

===American Heart Association (AHA and American College of Cardiology (ACC)===

* Stage A: Predisposition for developing cardiac disease e.g. Cavalier King Charles Spaniel, Doberman
* Stage B: Structural heart disease, no clinical signs
* Stage C: Structural heart disease, current or prior clinical signs
* Stage D: Refractory heart failure

===International Small Animal Cardiac Health Council (ISACHC)===
The only veterinary-specific clinical classification.

* Class Ia: Structural heart disease, no radiographic or echocardiographic evidence of cardiac enlargement
* Class Ib: Structural heart disease,radiographic or echocardiographic evidence of cardiac enlargement
* Class II: Mild clinical signs
* Class IIIa: Overt clinical signs, death or severe debilitation likely without immediate therapy but homecare possible
* Class IIIb: Overt clinical signs, death or severe debilitation likely and hospitalisation required

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat '''Volume 2 (Fifth Edition) ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition)'' Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition) ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition) ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T10:26:21Z

Lwilkie: /* New York Heart Association Classification */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

The primary determinants of cardiac performance are:
* '''Preload''': The volume of blood or hydrostatic pressure within the ventricles at the end of diastole.
* '''Afterload''': The force that opposes ejection of blood into the peripheral arterial system, of which arterial blood pressure is the primary factor
* '''Contractility''': The ability of the myocardium to function as a pump and eject blood

The '''Frank-Starling''' mechanism states that stroke volume increases in response to increased end-diastolic volume (preload) when all other factors remain constant. Therefore, if a larger volume of blood flows to the ventricle, there is greater wall stretch, causing greater expansion during diastole, which in turn increases the force of contraction and therefore stroke volume (quantity of blood that is pumped into the aorta during systole).

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: concentric and eccentric hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Natriuretic Peptides===
Natriuretic peptides include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The main site of manufacture, storage and release is the myocardium. Under normal circumstances, ANP and BNP are both manufactured by the atrial myocardium. In heart disease, BNP is manufactured predominantly in the ventricular myocardium. Both are released in response to increased chamber wall stress. These hormones counter regulate many of the above mechanisms, causing vasorelaxation and increased sodium loss. However, in congestive heart failure this counter regulatory system is overwhelmed by other vasoconstrictive and sodium retaining mechanisms.

Natriuretic peptides are useful biomarkers of cardiac disease, as levels are elevated in patients with clinically significant disease.

===Antidiuretic Hormone (ADH)===
Release of ADH from the posterior pituitary gland increases absorption of free water in the collecting duct of the nephron. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. In heart failure, there are increased circulating levels of ADH. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

Excess ADH leads to fluid retention, contributing to congestive heart failure, and dilutes total body sodium and chloride leading to hypo-osmolarity. The finding of hyponatraemia and hypochloraemia on blood tests from patients with cardiac disease indicate an advanced stage of disease. Dilutional hyponatraemia (excess free water, rather than a reduction in sodium) is a poor prognostic sign.

== Classification ==

=== Modified New York Heart Association Classification ===

Classification of congestive heart failure modified from human medicine. This is problematic, as cardiac debilitation is not the only factor governing exercise tolerance. This is particularly difficult to apply to cats, which tend to lead a sedentary lifestyle. Furthermore, a normal level of activity is clearly defined for humans (e.g. ability to walk a certain distance), but in veterinary medicine this may be influenced by the breed and lifestyle of the dog.

*Class I: Heart disease with no clinical signs
*Class II: Exercise intolerance
*Class III: Marked exercise intolerance and dyspnoea
*Class IV: Cannot exercise, dyspnoea at rest

===American Heart Association (AHA and American College of Cardiology (ACC)===

* Stage A: Predisposition for developing cardiac disease
* Stage B: Structural heart disease, no clinical signs
* Stage C: Structural heart disease, current or prior clinical signs
* Stage D: Refractory heart failure

===International Small Animal Cardiac Health Council (ISACHC)===
The only veterinary-specific clinical classification.

* Class Ia: Structural heart disease, no radiographic or echocardiographic evidence of cardiac enlargement
* Class Ib: Structural heart disease,radiographic or echocardiographic evidence of cardiac enlargement
* Class II: Mild clinical signs
* Class IIIa: Overt clinical signs, death or severe debilitation likely without immediate therapy but homecare possible
* Class IIIb: Overt clinical signs, death or severe debilitation likely and hospitalisation required

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat '''Volume 2 (Fifth Edition) ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition)'' Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition) ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition) ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T10:10:51Z

Lwilkie: /* Introduction */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

The primary determinants of cardiac performance are:
* '''Preload''': The volume of blood or hydrostatic pressure within the ventricles at the end of diastole.
* '''Afterload''': The force that opposes ejection of blood into the peripheral arterial system, of which arterial blood pressure is the primary factor
* '''Contractility''': The ability of the myocardium to function as a pump and eject blood

The '''Frank-Starling''' mechanism states that stroke volume increases in response to increased end-diastolic volume (preload) when all other factors remain constant. Therefore, if a larger volume of blood flows to the ventricle, there is greater wall stretch, causing greater expansion during diastole, which in turn increases the force of contraction and therefore stroke volume (quantity of blood that is pumped into the aorta during systole).

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: concentric and eccentric hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Natriuretic Peptides===
Natriuretic peptides include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The main site of manufacture, storage and release is the myocardium. Under normal circumstances, ANP and BNP are both manufactured by the atrial myocardium. In heart disease, BNP is manufactured predominantly in the ventricular myocardium. Both are released in response to increased chamber wall stress. These hormones counter regulate many of the above mechanisms, causing vasorelaxation and increased sodium loss. However, in congestive heart failure this counter regulatory system is overwhelmed by other vasoconstrictive and sodium retaining mechanisms.

Natriuretic peptides are useful biomarkers of cardiac disease, as levels are elevated in patients with clinically significant disease.

===Antidiuretic Hormone (ADH)===
Release of ADH from the posterior pituitary gland increases absorption of free water in the collecting duct of the nephron. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. In heart failure, there are increased circulating levels of ADH. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

Excess ADH leads to fluid retention, contributing to congestive heart failure, and dilutes total body sodium and chloride leading to hypo-osmolarity. The finding of hyponatraemia and hypochloraemia on blood tests from patients with cardiac disease indicate an advanced stage of disease. Dilutional hyponatraemia (excess free water, rather than a reduction in sodium) is a poor prognostic sign.

== Classification ==

=== New York Heart Association Classification ===

Classification of congestive heart failure used in human medicine.

*Class 1: No clinical signs but evidence of heart disease
*Class 2: Exercise intolerance or dyspnoea
*Class 3: Marked exercise intolerance
*Class 4: Cannot exercise, dyspnoea at rest

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat '''Volume 2 (Fifth Edition) ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition)'' Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition) ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition) ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T10:02:32Z

Lwilkie: /* Introduction */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

The primary determinants of cardiac performance are:
* '''Preload''': The volume of blood or hydrostatic pressure within the ventricles at the end of diastole.
* '''Afterload''': The force that opposes ejection of blood into the peripheral arterial system, of which arterial blood pressure is the primary factor
* '''Contractility''': The ability of the myocardium to function as a pump and eject blood

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: concentric and eccentric hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Natriuretic Peptides===
Natriuretic peptides include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The main site of manufacture, storage and release is the myocardium. Under normal circumstances, ANP and BNP are both manufactured by the atrial myocardium. In heart disease, BNP is manufactured predominantly in the ventricular myocardium. Both are released in response to increased chamber wall stress. These hormones counter regulate many of the above mechanisms, causing vasorelaxation and increased sodium loss. However, in congestive heart failure this counter regulatory system is overwhelmed by other vasoconstrictive and sodium retaining mechanisms.

Natriuretic peptides are useful biomarkers of cardiac disease, as levels are elevated in patients with clinically significant disease.

===Antidiuretic Hormone (ADH)===
Release of ADH from the posterior pituitary gland increases absorption of free water in the collecting duct of the nephron. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. In heart failure, there are increased circulating levels of ADH. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

Excess ADH leads to fluid retention, contributing to congestive heart failure, and dilutes total body sodium and chloride leading to hypo-osmolarity. The finding of hyponatraemia and hypochloraemia on blood tests from patients with cardiac disease indicate an advanced stage of disease. Dilutional hyponatraemia (excess free water, rather than a reduction in sodium) is a poor prognostic sign.

== Classification ==

=== New York Heart Association Classification ===

Classification of congestive heart failure used in human medicine.

*Class 1: No clinical signs but evidence of heart disease
*Class 2: Exercise intolerance or dyspnoea
*Class 3: Marked exercise intolerance
*Class 4: Cannot exercise, dyspnoea at rest

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat '''Volume 2 (Fifth Edition) ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition)'' Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition) ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition) ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T09:59:27Z

Lwilkie: /* Myocardial hypertrophy */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: concentric and eccentric hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Natriuretic Peptides===
Natriuretic peptides include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The main site of manufacture, storage and release is the myocardium. Under normal circumstances, ANP and BNP are both manufactured by the atrial myocardium. In heart disease, BNP is manufactured predominantly in the ventricular myocardium. Both are released in response to increased chamber wall stress. These hormones counter regulate many of the above mechanisms, causing vasorelaxation and increased sodium loss. However, in congestive heart failure this counter regulatory system is overwhelmed by other vasoconstrictive and sodium retaining mechanisms.

Natriuretic peptides are useful biomarkers of cardiac disease, as levels are elevated in patients with clinically significant disease.

===Antidiuretic Hormone (ADH)===
Release of ADH from the posterior pituitary gland increases absorption of free water in the collecting duct of the nephron. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. In heart failure, there are increased circulating levels of ADH. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

Excess ADH leads to fluid retention, contributing to congestive heart failure, and dilutes total body sodium and chloride leading to hypo-osmolarity. The finding of hyponatraemia and hypochloraemia on blood tests from patients with cardiac disease indicate an advanced stage of disease. Dilutional hyponatraemia (excess free water, rather than a reduction in sodium) is a poor prognostic sign.

== Classification ==

=== New York Heart Association Classification ===

Classification of congestive heart failure used in human medicine.

*Class 1: No clinical signs but evidence of heart disease
*Class 2: Exercise intolerance or dyspnoea
*Class 3: Marked exercise intolerance
*Class 4: Cannot exercise, dyspnoea at rest

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat '''Volume 2 (Fifth Edition) ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition)'' Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition) ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition) ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T09:57:24Z

Lwilkie: /* Antidiuretic Hormone (ADH) */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: '''concentric''' and '''eccentric''' hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Natriuretic Peptides===
Natriuretic peptides include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The main site of manufacture, storage and release is the myocardium. Under normal circumstances, ANP and BNP are both manufactured by the atrial myocardium. In heart disease, BNP is manufactured predominantly in the ventricular myocardium. Both are released in response to increased chamber wall stress. These hormones counter regulate many of the above mechanisms, causing vasorelaxation and increased sodium loss. However, in congestive heart failure this counter regulatory system is overwhelmed by other vasoconstrictive and sodium retaining mechanisms.

Natriuretic peptides are useful biomarkers of cardiac disease, as levels are elevated in patients with clinically significant disease.

===Antidiuretic Hormone (ADH)===
Release of ADH from the posterior pituitary gland increases absorption of free water in the collecting duct of the nephron. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. In heart failure, there are increased circulating levels of ADH. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

Excess ADH leads to fluid retention, contributing to congestive heart failure, and dilutes total body sodium and chloride leading to hypo-osmolarity. The finding of hyponatraemia and hypochloraemia on blood tests from patients with cardiac disease indicate an advanced stage of disease. Dilutional hyponatraemia (excess free water, rather than a reduction in sodium) is a poor prognostic sign.

== Classification ==

=== New York Heart Association Classification ===

Classification of congestive heart failure used in human medicine.

*Class 1: No clinical signs but evidence of heart disease
*Class 2: Exercise intolerance or dyspnoea
*Class 3: Marked exercise intolerance
*Class 4: Cannot exercise, dyspnoea at rest

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat '''Volume 2 (Fifth Edition) ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition)'' Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition) ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition) ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T09:49:55Z

Lwilkie: /* Compensatory Mechanisms */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: '''concentric''' and '''eccentric''' hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Natriuretic Peptides===
Natriuretic peptides include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The main site of manufacture, storage and release is the myocardium. Under normal circumstances, ANP and BNP are both manufactured by the atrial myocardium. In heart disease, BNP is manufactured predominantly in the ventricular myocardium. Both are released in response to increased chamber wall stress. These hormones counter regulate many of the above mechanisms, causing vasorelaxation and increased sodium loss. However, in congestive heart failure this counter regulatory system is overwhelmed by other vasoconstrictive and sodium retaining mechanisms.

Natriuretic peptides are useful biomarkers of cardiac disease, as levels are elevated in patients with clinically significant disease.

===Antidiuretic Hormone (ADH)===
In heart failure, there are increased circulating levels of ADH. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

== Classification ==

=== New York Heart Association Classification ===

Classification of congestive heart failure used in human medicine.

*Class 1: No clinical signs but evidence of heart disease
*Class 2: Exercise intolerance or dyspnoea
*Class 3: Marked exercise intolerance
*Class 4: Cannot exercise, dyspnoea at rest

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat '''Volume 2 (Fifth Edition) ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition)'' Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition) ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition) ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T09:39:42Z

Lwilkie: /* Compensatory Mechanisms */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: '''concentric''' and '''eccentric''' hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Antidiuretic Hormone (ADH)===
In heart failure, there are increased circulating levels of ADH. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

== Classification ==

=== New York Heart Association Classification ===

Classification of congestive heart failure used in human medicine.

*Class 1: No clinical signs but evidence of heart disease
*Class 2: Exercise intolerance or dyspnoea
*Class 3: Marked exercise intolerance
*Class 4: Cannot exercise, dyspnoea at rest

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat '''Volume 2 (Fifth Edition) ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition)'' Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition) ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition) ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T09:39:04Z

Lwilkie: /* Compensatory Mechanisms */

{{OpenPagesTop}}
== Introduction ==

The heart pumps deoxygenated blood from the venous circulation into the lungs, where it is oxygenated. Newly oxygenated blood travels via the pulmonary veins to the left atrium and left ventricle, where it is ejected via the aorta into the arterial circulation to supply oxygenated blood to peripheral tissue. Heart failure arises when structural or functional abnormalities prevent the heart adequately filling with or ejecting blood, resulting in the inability to meet metabolic needs of peripheral tissue. The cardiovascular system has a large reserve capacity, so overt clinical signs are only seen with severe disease when the heart cannot compensate for the decreased function.

The '''definition of heart failure''' is: a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at a normal filling pressure.

Heart failure can be further classified according to the cause, whether it leads predominantly to underperfusion or congestion (forward or backward failure) and whether the right or left side of the circulation is affected to a greater extent (right-sided failure or left-sided failure). In some cases, biventricular failure may occur.

* '''Forward failure''' (low output failure/cardiogenic shock): underperfusion of the arterial circulation at normal pressure
* '''Backward failure''' (congestive heart failure): adequate output at abnormal pressures, too much fluid in the venous circulation

The most basic equations relating to regulation of circulation are:
* Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
* Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
* Cardiac Output (CO) = Venous Return (VR)

== Mechanisms of failure ==

'''Myocardial failure ''': Failure of myocardial contraction (systolic dysfunction) e.g. [[Dilated Cardiomyopathy|Dilated Cardiomyopathy]]

'''Volume overload ''': Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood ([[Patent Ductus Arteriosus|PDA]], [[Ventricular Septal Defect|VSD]]), regurgitation of blood ([[Endocardiosis| Degenerative Mitral Valve Disease]]), anaemia or increased metabolic demands ([[Hyperthyroidism]]).

'''Pressure overload ''': Increased resistance to chamber emptying. This may be as a result of systemic or pulmonary hypertension, or an outflow obstruction such as [[Aortic Stenosis]] or [[Pulmonic Stenosis]].

'''Abnormal rate/rhythm ''': Compromised cardiac output due to an increased or decreased heart rate. Abnormally fast heart rates (tachycardias) result a shorter diastole, therefore impaired filling and reduced stroke volume. Abnormally slow heart rates (bradycardias) limit cardiac output as a direct consequence of reduced heart rate (CO = HR x SV).

'''Diastolic failure ''': Impaired ventricular filling with normal systolic function. Examples include [[Cardiac Tamponade|cardiac tamponade]] in [[Pericardial Effusion]], [[Pericarditis, Constrictive| Constrictive Pericarditis]] and [[Hypertrophic Cardiomyopathy|Hypertrophic Cardiomyopathy]] or [[Restrictive Cardiomyopathy|Restrictive Cardiomyopathy]]

== Clinical Signs ==

==== Forward-Low Output Failure ====

Decreased blood supply to the lungs and other organs. Left failure results in decreased blood returning to the right and so both sides fail simultaneously and vice versa. There will be low systemic blood pressure, exercise intolerance, pallor, tachycardia, weak femoral pulses and pre-renal failure and [[azotaemia]].

==== Backward-Congestive Failure ====

Clinical signs are different for each side. In left-sided failure signs include dyspnoea and tachypnoea. There may also be pulmonary crackles on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left mainstem bronchus. In right-sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive '''hepato-jugular reflux''' (Press firmly over the liver and abdomen. A positive test is distension of the jugular vein indicating right sided heart failure.) and pleural effusion.

== Compensatory Mechanisms ==
==== Sympathetic Nervous System ====
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].

These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.

==== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ====
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: '''concentric''' and '''eccentric''' hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.

'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.

'''Eccentric hypertrophy''' develops in response to volume overload (increased preload). The sarcomeres replicate in series, leading to elongation of the myocytes, an increase in internal diameter and an approximately normal wall thickness with an overall increase in external diameter of the chamber.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

===Antidiuretic Hormone (ADH)===
In heart failure, there are increased circulating levels of ADH. ADH is usually involved in regulation of osmolality and plays less of a role in regulation of circulating fluid volume. The stimulus for this 'non-osmotic' release of ADH is probably a marked drop in blood pressure. Therefore increased ADH occurs in late stage or severe heart failure.

== Classification ==

=== New York Heart Association Classification ===

Classification of congestive heart failure used in human medicine.

*Class 1: No clinical signs but evidence of heart disease
*Class 2: Exercise intolerance or dyspnoea
*Class 3: Marked exercise intolerance
*Class 4: Cannot exercise, dyspnoea at rest

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761856_sample.pdf
|chaptername = Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)
|book = Small Animal Emergency and Critical Care Medicine
|author = Elizabeth Rozanski, John Rush
|isbn = 9781840761856
}}

== References ==

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat '''Volume 2 (Fifth Edition) ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition)'' Mosby Elsevier''

Merck & Co (2008) '''The Merck Veterinary Manual''' (Eighth Edition) ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition) ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Heart_Failure]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Heart Failure - Pathophysiology

2016-06-30T09:35:04Z

Lwilkie: /* Renin-angiotensin-aldosterone system */

Heart Failure - Pathophysiology

2016-06-30T09:26:16Z

Lwilkie: /* Myocardial hypertrophy */

Heart Failure - Pathophysiology

2016-06-30T09:17:26Z

Lwilkie: /* Myocardial hypertrophy */

Heart Failure - Pathophysiology

2016-06-30T09:07:22Z

Lwilkie: /* Sympathetic Nervous System */

Heart Failure - Pathophysiology

2016-06-30T09:03:11Z

Lwilkie: /* Sympathetic Nervous System */

Heart Failure - Pathophysiology

2016-06-30T08:59:03Z

Lwilkie: /* Compensatory Mechanisms */

Heart Failure - Pathophysiology

2016-06-30T08:49:13Z

Lwilkie: /* Backward-Congestive Failure */

Heart Failure - Pathophysiology

2016-06-30T08:48:48Z

Lwilkie: /* Introduction */

Heart Failure - Pathophysiology

2016-06-30T08:48:07Z

Lwilkie: /* Clinical Signs */

Heart Failure - Pathophysiology

2016-06-30T08:43:01Z

Lwilkie: /* Mechanisms of failure */

Heart Failure - Pathophysiology

2016-06-30T08:41:47Z

Lwilkie: /* Mechanisms of failure */

Heart Failure - Pathophysiology

2016-06-30T08:41:10Z

Lwilkie: /* Mechanisms of failure */

Heart Failure - Pathophysiology

2016-06-30T08:40:46Z

Lwilkie: /* Mechanisms of failure */

Heart Failure - Pathophysiology

2016-06-30T08:21:56Z

Lwilkie: /* Introduction */

Heart Failure - Pathophysiology

2016-06-30T08:21:10Z

Lwilkie: /* Introduction */

Heart Failure - Pathophysiology

2016-06-29T16:25:31Z

Lwilkie: /* Introduction */

Heart Failure, Left-Sided

2016-06-29T16:20:22Z

Lwilkie: /* Description */

==Description==
Left-sided congestive heart failure involves volume overload of the left atrium, pulmonary veins and pulmonary capillaries, manifesting as [[Pulmonary Oedema|pulmonary oedema]].

In both dogs and cats [[Pulmonary Oedema|pulmonary oedema]] is a sign of left-sided congestive heart failure. In the cat pleural effusion may also be a side of left-sided congestive heart failure, whereas in the dog pleural effusion is always a sign of right-sided congestive heart failure. This species difference occurs because a proportion of the visceral pleural surface drains into the pulmonary veins, and this anatomic arrangement is more prominent in cats.

==Causes==

1. Degenerative mitral valve disease

2. Mitral endocarditis

2. Cardiomyopathies

[[Category:Heart_Failure]][[Category:To_Do_-_Cardiovascular]][[Category:To Do - Major]]

Heart Failure, Left-Sided

2016-06-29T16:16:55Z

Lwilkie:

==Description==
Left-sided congestive heart failure involves volume overload of the left atrium, pulmonary veins and pulmonary capillaries, manifesting as pulmonary oedema.

In both dogs and cats pulmonary oedema is a sign of left-sided congestive heart failure. In the cat pleural effusion may also be a side of left-sided congestive heart failure, whereas in the dog pleural effusion is always a sign of right-sided congestive heart failure. This species difference occurs because a proportion of the visceral pleural surface drains into the pulmonary veins, and this anatomic arrangement is more prominent in cats.

==Causes==

1. Degenerative mitral valve disease

2. Mitral endocarditis

2. Cardiomyopathies

[[Category:Heart_Failure]][[Category:To_Do_-_Cardiovascular]][[Category:To Do - Major]]

Heart Failure, Left-Sided

2016-06-29T16:16:31Z

Lwilkie:

==Description==
Left-sided congestive heart failure involves volume overload of the left atrium, pulmonary veins and pulmonary capillaries, manifesting as pulmonary oedema.

In both dogs and cats pulmonary oedema is a sign of left-sided congestive heart failure. In the cat pleural effusion may also be a side of left-sided congestive heart failure, whereas in the dog pleural effusion is always a sign of right-sided congestive heart failure. This species difference occurs because a proportion of the visceral pleural surface drains into the pulmonary veins, and this anatomic arrangement is more prominent in cats.

Causes[edit]

1. Degenerative mitral valve disease

2. Mitral endocarditis

2. Cardiomyopathies

[[Category:Heart_Failure]][[Category:To_Do_-_Cardiovascular]][[Category:To Do - Major]]

Heart Failure, Right-Sided

2016-06-29T16:10:37Z

Lwilkie: /* Signs */

===Description===
Right-sided congestive heart failure results in elevated central venous pressure. Manifestations of right-sided congestive heart failure are species-specific.

===Clinical Signs===

'''Horse & Ox:''' Ventral Abdomen & Brisket oedema

'''Dog:''' Ascites (abdominal effusion), pleural effusion

'''Cat:''' Pleural effusion

===Causes===

1. Left-Sided Heart Failure

2. Cardiomyopathies

3. Pericarditis

4. Hydropericardium

5. Increased Pulmonary Resistance

6. Myocardial Inflammation & Degeneration

7. Valvular Disease

8. Tumours (heart base)

{{unfinished}}
[[Category:To Do - Major]]
[[Category:Heart_Failure]][[Category:To_Do_-_Cardiovascular]]
[[Category:Cardiology Section]]

Heart Failure, Right-Sided

2016-06-29T16:08:31Z

Lwilkie: /* Description */

===Description===
Right-sided congestive heart failure results in elevated central venous pressure. Manifestations of right-sided congestive heart failure are species-specific.

===Signs===

-Edema (See below for species differences)

-Hepatomegaly

-Pleural Effusion

====Species Differences====

'''Horse & Ox:''' Ventral Abdomen & Brisket edema

'''Dog:''' Ascites (abdomenal edema)

'''Cat:''' Hydrothorax (thoracic edema)

===Causes===

1. Left-Sided Heart Failure

2. Cardiomyopathies

3. Pericarditis

4. Hydropericardium

5. Increased Pulmonary Resistance

6. Myocardial Inflammation & Degeneration

7. Valvular Disease

8. Tumours (heart base)

{{unfinished}}
[[Category:To Do - Major]]
[[Category:Heart_Failure]][[Category:To_Do_-_Cardiovascular]]
[[Category:Cardiology Section]]

Heart Failure, Right-Sided

2016-06-29T16:08:14Z

Lwilkie: /* Description */

===Description===
Right-sided congestive heart failure results in elevated central venous pressure. Manifestiations of right-sided congestive heart failure are species-specific.

===Signs===

-Edema (See below for species differences)

-Hepatomegaly

-Pleural Effusion

====Species Differences====

'''Horse & Ox:''' Ventral Abdomen & Brisket edema

'''Dog:''' Ascites (abdomenal edema)

'''Cat:''' Hydrothorax (thoracic edema)

===Causes===

1. Left-Sided Heart Failure

2. Cardiomyopathies

3. Pericarditis

4. Hydropericardium

5. Increased Pulmonary Resistance

6. Myocardial Inflammation & Degeneration

7. Valvular Disease

8. Tumours (heart base)

{{unfinished}}
[[Category:To Do - Major]]
[[Category:Heart_Failure]][[Category:To_Do_-_Cardiovascular]]
[[Category:Cardiology Section]]