Heart failure is a chronic condition in which the heart is unable to pump a sufficient volume of blood to supply the body’s oxygen needs. High-output failure results from intolerable increases in oxygen demand, often resulting from thyrotoxicosis, beri-beri, and other conditions and does not reflect underlying heart disease. It will not be further discussed in this article. Low-output failure, or congestive heart failure (CHF), results from various cardiovascular diseases.
CHF is a disease of the elderly; failure in infancy and childhood is almost always the result of the obstruction of efficient outflow of blood from the heart because of diseased valves, whereas in adults intrinsic heart disease is the most frequent finding. Mortality in heart failure shows a bimodal age distribution, with a peak around age 1 year and a continuous rise after age 50. The gap between these peaks reflects the fact that young children either die or have the defect repaired surgically, and patients between 1 and 50 years old are in early stages of disease.
After the initial insult, the inability of the heart to pump blood forward adequately results in the accumulation of blood in the venous circulation (congestion), hence the term congestive heart failure. Venous congestion also occurs in the vessels of the lungs, resulting in pulmonary edema. Fatigue, reduced exercise tolerance, shortness of breath, and generalized hypoxia are the inevitable consequences.
The primary defect is unknown, but viral infections and exposure to toxins such as alcohol are thought to be the cause in some cases. Other known causative factors are ischemic heart disease and myocardial infarction (direct myocardial cell injury) and hypertrophic changes resulting from uncontrolled high blood pressure. Recent research has focused on the role of apoptosis secondary to genetic damage and reversion of energy-generating and contractile proteins in the myocardium to less efficient, fetal forms resulting from the secretion of endogenous growth factors. A weakening of the heart’s force of contraction during systole (systolic dysfunction) may result from one or several of these factors.
Whatever the underlying defect, once pump function falls behind demand, the progression of the disease is almost entirely the result of compensatory mechanisms triggered by physiologic perception of low-volume status. The low-volume status is perceived because the bulk of blood volume is in the venous circulation, waiting to be pumped forward by the failing heart, whereas the body’s volume and pressure sensors are located chiefly in the arterial circulation, downstream from the heart. These compensatory events would be beneficial in a short-term, low-volume situation, but are maladaptive in a long-term situation.
The first compensation is an attempt to maintain blood pressure by raising myocardial pumping force and arterial vasoconstriction through stimulation of the adrenergic division of the autonomic nervous system. In acute blood loss this would be effective, but in the chronic failure situation, the prolonged exposure of the heart to adrenergic neurotransmitters (epinephrine and norepinephrine) results in direct myocardial toxicity, and the prolonged vasoconstriction increases the work the heart must perform in order to overcome the increased resistance to blood flow caused by arterial vasoconstriction. The body attempts to increase blood volume through activation of the kidney-based renin-angiotensin-aldosterone system (RAAS), the effect of which is to generate circulating angiotensin II (a powerful vasoconstrictor) and aldosterone (a mediator of sodium and water retention). The chronic effects of vasoconstriction are the same as those of the activated adrenergic system, but of no less importance is the role of angiotensin II and aldosterone as myocardial growth factors that promote hypertrophy and remodeling of the cardiac muscle mass. Additionally, renal secretion of vasopressin (antidiuretic hormone) is stimulated, resulting in vasoconstriction and conservation of water by the kidneys. A vicious cycle is entered, wherein perceived low blood volume triggers water retention and increased vascular resistance, both of which increase the work of the heart required to move blood. An inexorable deterioration of pump function ensues.
Reduced pump function may also occur as a result of the inability of the heart to relax completely during diastole, which results in incomplete filling for the next pump cycle (diastolic dysfunction). Regardless of the mixture of systolic and diastolic dysfunction, the compensatory changes directed toward maintenance of blood volume are the main forces driving disease progression.
Without treatment, mean survival is 5 years from diagnosis. Progressively worsening pump function and global hypoxia account for 50% of CHF deaths; the other 50% are the result of fatal cardiac arrhythmia provoked by hypoxia, electrolyte disturbances (resulting mainly from activation of the RAAS), and cardiac enlargement.
CHF is the most frequent diagnosis-related group occurring in hospital admissions and accounts for a major portion of patient drug and hospital expenditures and public assistance for medical care. The vast majority of heart transplant surgery is occasioned by advanced CHF. Patients with advanced disease suffer from discomfort, limitation of activity, reduced employment, and early death.
Treatment is presently not directed toward the fundamental defect, since this is unknown in the majority of cases. Older therapies include diuretics to reduce the volume overload and inotropic agents, such as digoxin, that increase the force of myocardial contraction, neither of which has affected mortality. Recently, drugs that interrupt the events of the RAAS (angiotensinconverting enzyme inhibitors such as captopril and enalapril) have not only yielded improved quality of life, but are shown to prolong survival. Beta-adrenergic blockers such as propranolol, metoprolol, and carvedilol have also resulted in extended survival. Both classes of drugs lower blood pressure and so are not tolerated in all patients. Lastly, spironolactone, a competitive antagonist of aldosterone, has recently been shown to improve survival. Present therapy includes all three classes as tolerated, plus diuretics if volume overload is evident, and digoxin if these therapies fail to achieve the desired effect. Future treatments will likely involve genetic manipulation directed toward apoptosis and contractile protein subtypes.
- American Heart (n.d.). Congestive heart failure.
- Retrieved from http://www.americanheart.org/presenter.jhtml?identifier=4585