Heart Failure - Pathophysiology

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 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:

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.
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

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.
Arrhythmias.

Compliance failure

E.g. Cardian tamponade.

Prevent 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.

Low systemic blood pressure.
Exercise intolerance.
Pallor.
Tachycardia.
Weak femoral pulses.
Pre-renal failre and azotaemia.

Backward-Congestive failure

Clinical signs are different for each side:

Left sided failure

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

Jugular distension.
Hepatomegaly and splenomegaly.
Ascites.
Positive hepato-jugular reflux.
Pleural effusion.

Compensatory Mechanisms

Renin-angiotensin-aldosterone system

Sodium and water retention by the kidney.
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.