Arrhythmias, diastolic dysfunction and neurohumoral activation in heart failure
THE CONTEXT
Heart failure can reflect impaired filling or abnormal heart rate. Neurohumoral responses initially support circulation but can subsequently worsen myocardial injury and fluid retention.
Heart rate and ventricular filling
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Prolonged tachycardia causes myocardial fatigue.
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In complete heart block, bradycardia limits cardiac output even when stroke volume is normal.
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Constrictive pericarditis is associated with marked fluid retention, peripheral oedema, ascites, pleural effusions and elevated jugular veins.
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Restrictive cardiomyopathy is associated with bi-atrial enlargement, restrictive filling and high atrial pressures; atrial fibrillation may cause deterioration.
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Left ventricular hypertrophy and fibrosis can produce poor diastolic filling despite good systolic function.
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Cardiac tamponade is associated with hypotension, elevated jugular veins, pulsus paradoxus and poor urine output.
Neurohumoral responses
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Activation of the renin–angiotensin–aldosterone system causes vasoconstriction and sodium and water retention, primarily through angiotensin II, which constricts renal and systemic arterioles.
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Activation of the sympathetic nervous system initially supports cardiac output by increasing myocardial contractility and heart rate.
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Prolonged sympathetic stimulation causes cardiac myocyte apoptosis, cardiac hypertrophy and focal myocardial necrosis. It also contributes to vasoconstriction and predisposes to arrhythmias.
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Aldosterone and endothelin-1 further enhance sodium and water retention. Vasopressin, also called antidiuretic hormone, contributes in severe heart failure.
Compensation and oedema
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Atrial dilatation stimulates release of natriuretic peptides, which partly counter aldosterone-mediated sodium conservation; this compensation is overwhelmed in heart failure.
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High left and right atrial pressures cause pulmonary and peripheral oedema. Impaired renal perfusion and secondary hyperaldosteronism compound oedema through sodium and water retention.
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Following myocardial infarction, sympathetic and renin–angiotensin–aldosterone system activation causes hypertrophy of non-infarcted segments.