Heart failure may result from systolic or diastolic dysfunction. Systolic dysfunction results from inadequate myocardial contractile function, usually as a consequence of ischemic heart disease or hypertension. Diastolic dysfunction refers to an inability of the heart to adequately relax and fill, which may be a consequence of massive left ventricular hypertrophy, myocardial fibrosis, amyloid deposition, or constrictive pericarditis. Approximately one half of CHF cases are attributable to diastolic dysfunction, with a greater frequency seen in older adults, diabetic patients, and women. Heart failure may also be caused by valve dysfunction (e.g., due to endocarditis), or may occur following rapid increases in blood volume or blood pressure, even if the heart is normal.
When, the failing heart can no longer efficiently pump blood, there is an increase in end-diastolic ventricular volumes, increased end-diastolic pressures, and elevated venous pressures. Thus, inadequate cardiac output— called forward failure—is almost always accompanied by increased congestion of the venous circulation—that is, backward failure. Although the root problem in CHF typically is deficient cardiac function, virtually every other organ is eventually affected by some combination of forward and backward failure.
The cardiovascular system attempts to compensate for reduced myocardial contractility or increased hemodynamic burden through several homeostatic mechanisms: • The Frank-Starling mechanism. Increased end-diastolic filling volumes dilate the heart and cause increased cardiac myofiber stretching; these lengthened fibers contract more forcibly, thereby increasing cardiac output. If the dilated ventricle is able to maintain cardiac output by this means, the patient is said to be in compensated heart failure. However, ventricular dilation comes at the expense of increased wall tension and magnifies the oxygen requirements of an already-compromised myocardium. With time, the failing muscle is no longer able to propel sufficient blood to meet the needs of the body, and the patient develops decompensated heart failure.
Activation of neurohumoral systems:
Release of the neurotransmitter norepinephrine by the autonomic nervous system increases heart rate and augments myocardial contractility and vascular resistance.
Activation of the renin-angiotensin-aldosterone system spurs water and salt retention (augmenting circulatory volume) and increases vascular tone.
Release of atrial natriuretic peptide acts to balance the renin-angiotensin-aldosterone system through diuresis and vascular smooth muscle relaxation.
Myocardial structural changes, including augmented muscle mass. Cardiac myocytes adapt to increased workload by assembling new sarcomeres, a change that is accompanied by myocyte enlargement (hypertrophy) (
Fig. 11.1
In pressure overload states (e.g., hypertension or valvular stenosis), new sarcomeres tend to be added parallel to the long axis of the myocytes, adjacent to existing sarcomeres. The growing muscle fiber diameter thus results in concentric hypertrophy—the ventricular wall thickness increases without an increase in the size of the chamber.
In volume overload states (e.g., valvular regurgitation or shunts), the new sarcomeres are added in series with existing sarcomeres, so that the muscle fiber length increases. Consequently, the ventricle tends to dilate, and the resulting wall thickness can be increased, normal, or decreased; thus, heart weight—rather than wall thickness—is the best measure of hypertrophy in volume-overloaded hearts.