The structural, biochemical, and molecular basis for myocardial contractile failure is obscure in many cases.
The molecular and cellular changes in hypertrophied hearts that initially mediate enhanced function may contribute to the development of heart failure. Evidence suggests that loss of myocytes because of apoptosis may contribute to progressive myocardial dysfunction in hypertrophic states. Clearly the geometry, structure, and composition (cells and extracellular matrix) of the hypertrophied heart are not normal. Interestingly, and in contrast to the pathologic hypertrophy just discussed, hypertrophy that is induced by regular strenuous exercise (physiologic hypertrophy) seems to be an extension of normal growth and have minimal or no deleterious effect. Whatever the underlying basis for congestive heart failure, a variety of compensatory mechanisms come into play when the hypertrophied heart can no longer accommodate the increased demand. Ultimately the primary cardiac disease and the superimposed compensatory burdens further encroach on the myocardial reserve.
The degree of structural abnormality does not always reflect the level of dysfunction, and it may be impossible from morphologic examination of the heart to distinguish a damaged but compensated heart from one that has decompensated. To some extent, the right and left sides of the heart act as two distinct anatomic and functional units. All content on this website, including dictionary, thesaurus, literature, geography, and other reference data is for informational purposes only. These stimuli increase the rate of protein synthesis, the amount of protein in each cell, the size of myocytes, the number of sarcomeres and mitochondria, and consequently the mass and size of the heart.
With prolonged hemodynamic overload, gene expression is altered, leading to re-expression of a pattern of protein synthesis analogous to that seen in fetal cardiac development; other changes are analogous to events that occur during mitosis of normally proliferating cells.
Most often associated with dividing cells, apoptosis may represent an aborted response to pathophysiologic stimuli that reactivate the fetal growth program in cardiac myocytes, presumably because such cells are no longer capable of progressing through the cell cycle to mitosis. Then begins the downward slide of stroke volume and cardiac output that often ends in death.
Moreover, many of the significant adaptations and morphologic changes noted in congestive heart failure are distant from the heart and are produced by the hypoxic and congestive effects of the failing circulation on other organs and tissues. It ranges from mild congestion with few symptoms to life-threatening fluid overload and heart failure. Tell a friend about us, add a link to this page, or visit the webmaster's page for free fun content.
The response is also accompanied by selective up-regulation of several immediate early response genes and embryonic forms of contractile and other proteins. In contrast, in valvular heart disease, increased pressure or volume work affects the myocardium globally.
Thus, proteins related to contractile elements, excitation-contraction coupling, and energy use may be significantly altered through production of different isoforms that either may be less functional than normal or may be reduced or increased in amount.
It should not be surprising therefore that sustained cardiac hypertrophy often evolves to cardiac failure. Myocardial hypertrophy itself may become increasingly detrimental because of the increased metabolic requirements of the enlarged muscle mass and the increased wall tension, both major determinants of the oxygen consumption of the heart. At autopsy, the hearts of patients having congestive heart failure are generally characterized by increased weight, chamber dilation, and thin walls, with microscopic changes of hypertrophy, but the extent of these changes varies among patients.

Nevertheless, because the cardiovascular system is a closed circuit, failure of one side cannot exist for long without eventually producing excessive strain on the other, terminating in global heart failure. Congestive heart failure results in an inadequate supply of blood and oxygen to the body's cells. Because adult cardiac myocytes cannot divide, augmentation of myocyte number (hyperplasia) cannot occur. Moreover, wall thickness does not necessarily correlate with the pathologic state; despite its increased mass, a heart in which both hypertrophy and dilation has occurred may have increased, decreased, or normal wall thickness.
The increased myocyte size that occurs in cardiac hypertrophy is usually accompanied by decreased capillary density, increased intercapillary distance, and deposition of fibrous tissue. Alterations of intracellular handling of calcium ions may also contribute to impaired contraction and relaxation.
Besides predisposing to congestive heart failure, left ventricular hypertrophy is an independent risk factor for cardiac mortality and morbidity, especially for sudden death. The other major determinants are heart rate and contractility (inotropic state, or force of contraction). Despite this interdependency, the clearest understanding of the pathologic physiology and anatomy of heart failure is derived from a consideration of each side separately. The decreased cardiac output causes an increase in the blood volume within the vascular system. Additional proposed mechanisms potentiating congestive heart failure include reduced adrenergic drive, decreased calcium availability, impaired mitochondrial function, and microcirculatory spasm.
In an attempt to compensate for inadequate pumping of the heart, the body uses three basic adaptive mechanisms which, though they are effective for a brief period of time, will eventually become insufficient to meet the oxygen needs of the body.
These mechanisms are also responsible for many of the symptoms experienced by the patient with congestive heart failure.First, the failing heart attempts to maintain a normal output of blood by enlarging its pumping chambers so that they are capable of holding a greater volume of blood.
This increases the amount of blood ejected from the heart, but it also leads to fluid overload within the blood vessels and excessive accumulation of body fluids in all of the fluid compartments.Second, the heart begins to increase its muscle mass in order to strengthen the force of its contractions.
Eventually, the coronary arteries can no longer meet the oxygen demands of the enlarged myocardium and the patient experiences angina pectoris owing to ischemia.Third, there is a response from the sympathetic nervous system. The involuntary muscle of the heart is regulated by autonomic, or involuntary, innervation.
In response to failing contractility of the myocardial cells, the sympathetic nervous system activates adaptive processes that increase the heart rate, redistribute peripheral blood flow, and retain urine.
These mechanisms are responsible for the symptoms of diaphoresis, cool skin, tachycardia, cardiac arrhythmias, and oliguria.The combined efforts of these three compensatory mechanisms achieve a fairly normal level of cardiac output for a period of time.
During this phase of congestive heart failure, the patient is said to have compensated CHF. When these mechanisms are no longer effective the disease progresses to the final stage of impaired heart function and the patient has decompensated CHF.Clinical Symptoms. In the early stages, shortness of breath occurs only when the patient is physically active. Later, as the heart action becomes more seriously impaired, the dyspnea is present even when the patient is resting. Attacks of breathlessness severe enough to wake the patient frequently occur during sleep (paroxysmal nocturnal dyspnea).

These attacks usually are accompanied by coughing and wheezing, and the patient seeks relief by sitting upright. Orthopnea and paroxysmal nocturnal dyspnea are related to congestion of the pulmonary blood vessels and edema of the lung tissues.
They are aggravated by lying down because in the prone position quantities of blood in the lower extremities move upward into the blood vessels of the lungs.Fluid retention is another common symptom of congestive heart failure. In left-sided failure there is higher than normal pressure of blood in the pulmonary vessels.
This increased pressure forces fluid out of the intravascular compartment and into the tissue spaces of the lungs, causing pulmonary edema. Right-sided failure causes congestion in the capillaries of the peripheral circulation and results in edema and congestion of the liver, stomach, legs, and feet, and in the sacral region in bedridden patients.Decreased cardiac output also affects the kidneys by reducing their blood supply, which in turn causes a decrease in the rate of glomerular filtration of plasma from the renal blood vessels into the renal tubules. Sodium and water not excreted in the urine are retained in the vascular system, adding to the blood volume. The diminished blood supply to the kidney also causes it to secrete renin, which indirectly stimulates the secretion of aldosterone from the adrenal gland. Aldosterone in turn acts on the renal tubules, causing them to increase reabsorption of sodium and water, and thus to further increase the volume of body fluids.Treatment. Medical management of congestive heart failure is aimed at improving contractility of the heart, reducing salt and water retention, and providing rest for the heart muscle.
Drugs used to accomplish these goals include digitalis glycosides to slow and strengthen the heartbeat, vasodilators such as nitroprusside and phentolamine to reduce resistance to the flow of blood being pumped from the heart, diuretics to assist in the elimination of water and sodium in the urine, and angiotensin converting enzyme inhibitors to reduce blood pressure, inhibit aldosterone release, and reduce peripheral arterial resistance. Electroconversion of atrial fibrillation enlists the help of the atria to fill the ventricles to maximum capacity.
Biventricular pacing or restoration of cardiac synchrony is helpful for patients with interventricular conduction delay and a wide QRS complex.Patient Care. Hospitalized patients with severe congestive heart failure present problems related to their needs for physical and mental rest, adequate aeration of the lungs and oxygenation of the tissues, prevention of circulatory stasis, maintenance of the integrity of the skin, restoration and maintenance of fluid and electrolyte balances, and adequate nutrition.
The care plan should include frequent monitoring of the vital signs, intake and output, daily weight, serum electrolyte and blood gas levels, and nutritional intake. Patients are placed on sodium-restricted diets and limited fluid intake; they should have a good understanding of the reason for this before leaving the hospital.
Since it is likely that they will continue taking several kinds of medications after returning home, patients or family members should be taught about the pharmacologic action of each drug, the need for taking it exactly as prescribed, any precautions to be taken, and any untoward reactions that warrant notification of the physician, nurse practitioner, or physician's assistant.Clinical portrait of congestive heart failure. The condition ranges from mild congestion with few symptoms to life-threatening fluid overload and total heart failure.CHF results in an inadequate supply of blood and oxygen to the body's cells. Since the left ventricle does not empty completely, it cannot accept blood returning from the lungs via the pulmonary veins.
The pulmonary veins become engorged and fluid seeps out through the veins and collects in the pleural cavity.

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