Heart Failure - Pathophysiology

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 atrium 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 resistance 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 doesn't allow sufficient filling therfore 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 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 lung crackling on ausculatation due to pulmonary oedema and a cough due to left cardiomegaly compressing the left main stem 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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