Heart Failure - Pathophysiology

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

Volume overload : Chronic increase in the amount of blood that must be pumped by a given chamber, due to shunting of blood (PDA, VSD), regurgitation of blood ( 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 in Pericardial Effusion, Constrictive Pericarditis and Hypertrophic Cardiomyopathy or 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

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 effect 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 heart's 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.

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

Sample Book Chapters
Publisher	Free chapter	Book	Authors

Congestive Heart Failure in the Dog (part of Congestive Heart Failure in the Cat)

Small Animal Emergency and Critical Care Medicine

Elizabeth Rozanski, John Rush

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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

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