Difference between revisions of "Heart Failure - Pathophysiology"

Revision as of 16:13, 22 March 2011

Introduction

The heart pumps unoxygenated blood from the venous circulation into the lungs where it is oxygenated. Newly oxygenated blood then travels to the left atria and ventricle where it is pumped into the arterial circulation to meet the oxygen demands of the body. Heart Failure is a condition that begins when the heart is unable to pump enough blood (cardiac output) at normal filling pressures to meet the body’s requirements. Heart Failure is the end result of heart disease (heart abnormality). Under normal circumstances the heart can adapt to moderate increases of pressure or volume using its functional reserve capacity.

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.

Factors affecting cardiac output include:

Preload. Preload is the end-diastolic volume and when this increases so does the systolic function of the myocardium based on the Frank-Starling Law.

Afterload: Refers to the resistance the left ventricle encounters as it ejects blood into the peripheral circulation. Depends upon many variables; for example ventricular volume, arterial tone etc. In the failing heart, in order to maintain blood pressure with reduced cardiac output the peripheral resistnace and so the afterload has to increase contractility, heart rate, distensibility and synergy of contraction.

Heart failure can affect the right ventricle, the left ventricle, or both ventricles (biventricular). Clinical signs are characteristic and can help determine which ventricle is affected.

Mechanisms of failure

Myocardial failure e.g Dilated cardiomyopathy. Causes a failure in contractility.

Volume overload e.g. Valve regurgitation and shunts (PDA). Initial response based on the Frank-Starling Law and stroke volume increases as preload increases and enables the heart to expel the extra blood. Ultimately the heart decompensates and the chamber enlarges. Fluid will build up in the compartment preceding it. For example, failure of the left atrium in this manner due to mitral regurgitation leads to pulmonary oedema.

Pressure overload e.g. aortic stenosis or systemic overload. Increase afterload so heart muscle hypertrophies. The abnormally thick myocardium may predispose to diastolic failure and arrhythmias.

Compliance failure e.g. Cardiac tamponade. Prevents adequate relaxation of the ventricles and don't allow sufficient filling. Results in diastolic failure.

Abnormal rate/rhythm e.g sustained bradycardia leads to a low output failure.

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 failre 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 lung crackling on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly comressing the left main stem bronchus. In right sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive Hepato-jugular reflux and pleural effusion.

Compensatory Mechanisms

Renin-angiotensin-aldosterone system;

Causes sodium and water retention by the kidney as well as vasoconstriction.

Sympathetic nervous system

Decreased blood pressure stimulates release of noradrenaline. Increase heart rate and contractility by the efect on beta-receptors. Peripheral vasoconstriction is activated by its action on alpha-receptors. Sinus arrhythmias are abolished. Increased heart rate and rhythm imposed by the sympathetic nervous system increases the hearts oxygen consumption. As diastole is shortened the time available for blood to enter the coronary circulation is also shortened, decreasing blood flow to the myocardium. Resulting myocardial hypoxia may cause arrhythmias.

Myocardial hypertrophy

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.

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.

@@ Line 1: / Line 1: @@
-==Introduction==
+== Introduction  ==
-Heart failure occurs when the heart is unable to maintain an adequate perfusion of the body's tissues at normal filling pressures (Nb, shock is an inability to maintain adequate circulation at low filling pressures).
+The heart pumps unoxygenated blood from the venous circulation into the lungs where it is oxygenated. Newly oxygenated blood then travels to the left atria and ventricle where it is pumped into the arterial circulation to meet the oxygen demands of the body. Heart Failure is a condition that begins when the heart is unable to pump enough blood (cardiac output) at normal filling pressures to meet the body’s requirements. Heart Failure is the end result of heart disease (heart abnormality). Under normal circumstances the heart can adapt to moderate increases of pressure or volume using its functional reserve capacity.&nbsp;&nbsp;
 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.
-Factors affecting cardiac output:
+Factors affecting cardiac output include:
-*'''Preload:''' Preload is the end-diastolic volume and when this increases so does the systolic function of the myocardium based on the '''Frank-Starling Law.'''  Stretching of the myocytes engages more actin and myosin within the sarcomere and allows greater force generation.  In a failing heart the Frank-Starling Law fails and stroke volume cannot increase with an increased preload.
+'''Preload.''' Preload is the end-diastolic volume and when this increases so does the systolic function of the myocardium based on the '''Frank-Starling Law.'''
-*'''Afterload:''' Refers to the resistance the left ventricle encounters as it ejects blood into the peripheral circulation.  Depends upon many variables; for example ventricular volume, arterial tone etc.  In the failing heart, in order to maintain blood pressure with reduced cardiac output the peripheral resistnace and so the afterload has to increase.
-*Contractility
-*Heart rate
-*Distensibility
-*Synergy of contraction
-==Mechanisms of failure==
+'''Afterload:''' Refers to the resistance the left ventricle encounters as it ejects blood into the peripheral circulation. Depends upon many variables; for example ventricular volume, arterial tone etc. In the failing heart, in order to maintain blood pressure with reduced cardiac output the peripheral resistnace and so the afterload has to increase contractility, heart rate, distensibility and synergy of contraction.
-===Myocardial failure===
+Heart failure can affect the right ventricle, the left ventricle, or both ventricles (biventricular). Clinical signs are characteristic and can help determine which ventricle is affected.<br>
-E.g Dilated cardiomyopathy.  Causes a failure in contractility.
+<br>
-===Volume overload===
+== Mechanisms of failure  ==
-E.g. Valve regurgitation and shunts (PDA).
+'''Myocardial failure '''e.g Dilated cardiomyopathy. Causes a failure in contractility.
-Initial response based on the '''Frank-Starling Law''' and stroke volume increases as preload increases and enables the heart to expel the extra blood.  Ultimately the heart decompensates and the chamber enlarges.  Fluid will build up in the compartment preceding it.  For example, failure of the left atrium in this manner due to mitral regurgitation leads to pulmonary oedema.
+'''Volume overload&nbsp;'''e.g. Valve regurgitation and shunts (PDA).&nbsp;Initial response based on the '''Frank-Starling Law''' and stroke volume increases as preload increases and enables the heart to expel the extra blood. Ultimately the heart decompensates and the chamber enlarges. Fluid will build up in the compartment preceding it. For example, failure of the left atrium in this manner due to mitral regurgitation leads to pulmonary oedema.
-===Pressure overload===
+'''Pressure overload&nbsp;'''e.g. aortic stenosis or systemic overload.&nbsp;Increase afterload so heart muscle hypertrophies. The abnormally thick myocardium may predispose to diastolic failure and arrhythmias.
-E.g. aortic stenosis or systemic overload.
+'''Compliance failure '''e.g. Cardiac tamponade. Prevents adequate relaxation of the ventricles and don't allow sufficient filling. Results in diastolic failure.
-Increase afterload so heart muscle hypertrophies.  The abnormally thick myocardium may predispose to:
+'''Abnormal rate/rhythm '''e.g sustained bradycardia leads to a low output failure.
-*Diastolic failure.
-*Arrhythmias.
-===Compliance failure===
+<br>
-E.g. Cardian tamponade.
+== Clinical Signs  ==
-Prevent adequate relaxation of the ventricles and don't allow sufficient filling.  Results in diastolic failure.
+==== Forward-Low output failure  ====
-===Abnormal rate/rhythm===
+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 failre and azotaemia.
-E.g. sustained bradycardia leads to a low output failure.
+==== Backward-Congestive failure  ====
-==Clinical Signs==
+Clinical signs are different for each side. In left sided failure signs include dyspnoea and tachypnoea. There may also be lung crackling on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly comressing the left main stem bronchus. In right sided failure there may be jugular distension, hepatomegaly and splenomegaly, ascites, positive [[Hepato-jugular reflux|Hepato-jugular reflux&nbsp;]] and pleural effusion.
-===Forward-Low output failure===
+<br>
-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.
+== Compensatory Mechanisms  ==
-*Low systemic blood pressure.
+==== Renin-angiotensin-aldosterone system;&nbsp; ====
-*Exercise intolerance.
-*Pallor.
-*Tachycardia.
-*Weak femoral pulses.
-*Pre-renal failre and azotaemia.
-===Backward-Congestive failure===
+Causes sodium and water retention by the kidney as well as vasoconstriction.
-Clinical signs are different for each side:
+==== Sympathetic nervous system  ====
-====Left sided failure====
+Decreased blood pressure stimulates release of noradrenaline. Increase heart rate and contractility by the efect on beta-receptors. Peripheral vasoconstriction is activated by its action on alpha-receptors. Sinus arrhythmias are abolished.&nbsp;Increased heart rate and rhythm imposed by the sympathetic nervous system increases the hearts oxygen consumption. As diastole is shortened the time available for blood to enter the coronary circulation is also shortened, decreasing blood flow to the myocardium. Resulting myocardial hypoxia may cause arrhythmias.
-*Dyspnoea and tachypnoea.
-*Lung crackling on ausculatation due to pulmonary oedema.
-*Cough due to left cardiomegaly comressing the left main stem bronchus.
-====Right sided failure====
+=== [[Cardiac Hypertrophy|Myocardial hypertrophy]]  ===
-*Jugular distension.
-*Hepatomegaly and splenomegaly.
-*Ascites.
-*Positive [[hepato-jugular reflux]].
-*Pleural effusion.
-==Compensatory Mechanisms==
+<br>
-===Renin-angiotensin-aldosterone system===
+== Classification  ==
-*Sodium and water retention by the kidney.
+=== New York Heart Association Classification  ===
-*Vasoconstriction.
-===Sympathetic nervous system===
+Classification of congestive heart failure used in human medicine.
-Decreased blood pressure stimulates release of noradrenaline.  Increase heart rate and contractility by the efect on beta-receptors.  Peripheral vasoconstriction is activated by its action on alpha-receptors.
+*Class 1: No clinical signs but evidence of heart disease.
-Sinus arrhythmias are abolished.
+*Class 2: Exercise intolerance or dyspnoea.
+*Class 3: Marked exercise intolerance.
-Increased heart rate and rhythm imposed by the sympathetic nervous system increases the hearts oxygen consumption.  As diastole is shortened the time available for blood to enter the coronary circulation is also shortened, decreasing blood flow to the myocardium.  Resulting myocardial hypoxia may cause arrhythmias.
-===[[Cardiac Hypertrophy|Myocardial hypertrophy]]===
-==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.
+<br>
-==Introduction==
+== References<br> ==
-*The heart pumps unoxygenated blood from the venous circulation into the lungs where it is oxygenated. Newly oxygenated blood then travels to the left atria and ventricle where it is pumped into the arterial circulation to meet the oxygen demands of the body.
-*Heart Failure is a condition that begins when the heart is unable to pump enough blood (cardiac output) at normal filling pressures to meet the body’s requirements. Heart Failure is the end result of heart disease (heart abnormality).
-*Under normal circumstances the heart can adapt to moderate increases of pressure or volume using its functional reserve capacity. During acute episodes of increased volume or pressure load the dilated heart chambers respond by increasing their force of contraction. This is known as the Frank-Starling Phenomenon. However, in chronic conditions the cardiac chambers hypertrophy. Initially these adaptations are beneficial, but eventually the functional reserve mechanisms lead to heart failure.
-*Heart failure can affect the right ventricle, the left ventricle, or both ventricles (biventricular). Clinical signs are characteristic and can help determine which ventricle is affected.
-==Etiology of Heart Failure==
-The five cardiac impairments that cause heart failure are the following:
-===1. Arrhythmias===
-'''Problem'''
-*Irregularity of cardiac rhythm affects cardiac output
-'''Cause'''
-*Tachycardia: Increased heart rate does not allow for adequate cardiac filling during diastole and consequently cardiac output drops
-*Bradycardia: Decreased heart rate lowers cardiac output by limiting the amount of blood pumped per minute
-===2. Diastolic Failure (Restricted Ventricular Filling)===
-'''Problem'''
-*When the heart is unable to relax fully during diastole (to allow for complete ventricular filling) cardiac output drops
-'''Cause'''
-*Hypertrophic Cardiomyopathy (increased thickness of the ventricular myocardium reduces lumen size available for diastolic filling)
-*Dilated Cardiomyopathy (dilation of the cardiac chambers lowers the contraction force and the cardiac output)
-*Pericardial Effusion (increased pressure on the myocardium decreases space for diastolic filling)
-===3. Pressure Overload===
-'''Problem'''
-*Increased pressure in the ventricle causes concentric hypertrophy in an effort to maintain adequate cardiac output. Eventually, high ventricular pressures can result in cardiac failure.
-'''Cause'''
-*Hypertension (Pulmonary and/or Systemic)
-*Outflow tract narrowing (Aortic and/or Pulmonic Stenosis)
-===4. Systolic Failure (Myocardial Failure)===
-'''Problem'''
-*Decreased myocardial contraction during systole causes reduced cardiac output
-'''Cause'''
-*Primary myocardial diseases (e.g. Dilated cardiomyopathy)
-*Complication from another form of heart failure
-===5. Volume Overload===
-'''Problem'''
-*The cardiac ventricles are required to work harder by pumping an increased volume of blood in order to maintain adequate cardiac output. Increased blood volume in the heart causes eccentric hypertrophy in an effort to accommodate the increased blood volume.
-'''Cause'''
-*Shunting Disorders (e.g. PDA)
+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<br>Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (6th edition, volume 2)W.B. Saunders Company<br>Fossum, T. W. et. al. (2007) Small Animal Surgery (Third Edition) Mosby Elsevier<br>Merck &amp; Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial<br>Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier. <br>
-*Valvular Regurgitation
+<br>
-*Anemia
+<br>
+<br>
-[[Category:Heart Failure]][[Category:To_Do_-_Cardiovascular]]
+[[Category:Heart_Failure]] [[Category:To_Do_-_Review]]