Heart Failure - Pathophysiology - Revision history

Lwilkie: /* References */

2016-06-30T10:51:30Z

References

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

2016-06-30T10:27:02Z

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

Lwilkie: /* New York Heart Association Classification */

2016-06-30T10:26:21Z

New York Heart Association Classification

Lwilkie: /* Introduction */

2016-06-30T10:10:51Z

Introduction

Lwilkie: /* Introduction */

2016-06-30T10:02:32Z

Introduction

Lwilkie: /* Myocardial hypertrophy */

2016-06-30T09:59:27Z

Myocardial hypertrophy

Lwilkie: /* Antidiuretic Hormone (ADH) */

2016-06-30T09:57:24Z

Antidiuretic Hormone (ADH)

Lwilkie: /* Compensatory Mechanisms */

2016-06-30T09:49:55Z

Compensatory Mechanisms

Lwilkie: /* Compensatory Mechanisms */

2016-06-30T09:39:42Z

Compensatory Mechanisms

Lwilkie: /* Compensatory Mechanisms */

2016-06-30T09:39:04Z

Compensatory Mechanisms

← Older revision		Revision as of 10:51, 30 June 2016
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	== References ==		== 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''~~	+	* Luis Fuentes, V, Johnson, L.R, Dennis, S. (2010) '''BSAVA Manual of Canine and Feline Cardiorespiratory Medicine (Second Edition)'''
−
−	~~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~~''

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 ===American Heart Association (AHA and American College of Cardiology (ACC)===
-* Stage A: Predisposition for developing cardiac disease
+* 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

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 == Classification  ==
-=== New York Heart Association Classification  ===
+=== Modified New York Heart Association Classification  ===
-Classification of congestive heart failure used in human medicine.
+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 1: No clinical signs but evidence of heart disease
+*Class I: Heart disease with no clinical signs
-*Class 2: Exercise intolerance or dyspnoea
+*Class II: Exercise intolerance
-*Class 3: Marked exercise intolerance
+*Class III: Marked exercise intolerance and dyspnoea
-*Class 4: Cannot exercise, dyspnoea at rest
+*Class IV: Cannot exercise, dyspnoea at rest

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 * '''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  ==

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 * Blood Pressure (BP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
 * Cardiac Output (CO) = Venous Return (VR)
 == Mechanisms of failure  ==

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 === [[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.
+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.

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 ===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.
+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.
 == Classification  ==

← Older revision		Revision as of 09:49, 30 June 2016
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	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.		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)===		===Antidiuretic Hormone (ADH)===

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 == Compensatory Mechanisms  ==
-==== Sympathetic Nervous System  ====
+=== 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]] ====
+=== [[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.