Heart failure

What it is

Heart failure is the inability of the ventricle to efficiently pump blood throughout the circulation. Ejection fraction sets the two forms. HFrEF, EF ≤35-40%: reduced contractility gives systolic ventricular dysfunction, a lower LVEF and a lower cardiac output. The ventricle is dilated with thin walls, and the extra sound is an S3. HFpEF, EF ≥40-50%: decreased ventricular compliance gives diastolic ventricular dysfunction, reduced ventricular filling and increased diastolic pressure, so cardiac output falls while the LVEF stays normal. The ventricle is hypertrophied with thick walls, and the extra sound is an S4. HFrEF is a weak heart that cannot pump; HFpEF is a stiff heart that cannot relax. Left-sided failure comes from increased left ventricular afterload — arterial hypertension, or outflow obstruction such as aortic stenosis. Right-sided failure comes from increased right ventricular afterload, and its most common cause is left-sided failure. Cardiac output is determined by preload, the volume and pressure of blood in the ventricles at the end of diastole, by afterload, and by myocardial contractility; this is the basis of Starling's Law. In patients without valvular disease, the primary abnormality is impairment of ventricular myocardial function leading to a fall in cardiac output, through impaired systolic contraction, impaired diastolic relaxation, or both. That activates counter-regulatory neurohumoral mechanisms which, in the setting of impaired ventricular function, increase both afterload and preload, so a vicious circle is set up: any additional fall in cardiac output causes further neurohumoral activation and increasing peripheral vascular resistance. Stimulation of the renin-angiotensin-aldosterone system leads to vasoconstriction, sodium and water retention, and sympathetic nervous system activation, mediated by angiotensin II, a potent constrictor of arterioles in both the kidney and the systemic circulation. Sympathetic activation may at first sustain cardiac output through increased myocardial contractility and heart rate, but prolonged stimulation causes cardiac myocyte apoptosis, hypertrophy and focal myocardial necrosis, along with peripheral vasoconstriction and arrhythmias. Sodium and water retention is promoted by aldosterone, by endothelin-1, and in severe heart failure by antidiuretic hormone. Natriuretic peptides are released from the atria in response to atrial stretch and act as physiological antagonists to the fluid-conserving effect of aldosterone.