high-output heart failure

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Related to high-output heart failure: low output heart failure

heart failure

inability of the heart to maintain cardiac output sufficient to meet the body's needs; it most often results from myocardial failure affecting the right or left ventricle.
backward heart failure a concept of heart failure emphasizing the resultant passive engorgement of the systemic venous system that.
congestive heart failure (CHF) that which occurs as a result of impaired pumping capability of the heart that is not keeping up with the metabolic needs of body tissues and organs; it is associated with abnormal retention of water and sodium. It ranges from mild congestion with few symptoms to life-threatening fluid overload and heart failure. Congestive heart failure results in an inadequate supply of blood and oxygen to the body's cells. The decreased cardiac output causes an increase in the blood volume within the vascular system. Congestion within the blood vessels interferes with the movement of body fluids in and out of the various fluid compartments, so that fluid accumulates in the tissue spaces, causing edema.

There are three general kinds of pathologic conditions that can bring about congestive heart failure: (1) ventricular failure, in which the contractions of the ventricles become weak and ineffective, as in myocardial ischemia from coronary artery disease; (2) mechanical failure of the ventricles to fill with blood during the diastole phase of the cardiac cycle, which can occur when the mitral valve is narrowed, as in rheumatic mitral stenosis, or when there is an accumulation of fluid within the pericardial sac (cardiac tamponade) pressing against the ventricles, preventing them from accepting a full load of blood; and (3) an overload of blood in the ventricles during the systole phase of the cycle. High blood pressure, aortic stenosis, and aortic regurgitation are some of the conditions that can cause ventricular overload.
Compensatory Mechanisms. 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. This results in ventricular hypertrophy and a need for more oxygen. 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. Left-sided heart failure produces dyspnea of varying intensity. 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. In advanced cases, the patient must sit up in order to breathe (orthopnea). 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. beta-blockers are an important adjunct in treatment of heart failure, helping to decrease the sympathetic response. 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. They should also have a plan for regular exercise as tolerated. 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. (SOBOE=shortness of breath on exertion) From Jarvis, 1996.
forward heart failure a concept of heart failure emphasizing the inadequacy of cardiac output as the primary cause.
high-output heart failure that in which cardiac output remains high, associated with conditions such as hyperthyroidism, anemia, and emphysema.
left-sided heart failure (left ventricular heart failure) failure of the left ventricle to maintain a normal output of blood; it does not empty completely and thus cannot accept all the blood returning from the lungs via the pulmonary veins, which become engorged. Fluid seeps out of the veins through the pulmonary capillaries and collects in the interstitial tissue of the lung, causing pulmonary edema that eventually leads to right ventricular heart failure as well.
low-output heart failure that in which cardiac output is diminished, associated with cardiovascular diseases such as coronary artery disease, hypertension, and cardiomyopathy.
right-sided heart failure (right ventricular heart failure) failure of proper functioning of the right ventricle, with subsequent engorgement of the systemic veins, producing pitting edema, enlargement of the liver, and ascites.

high-output heart failure

Cardiology CHF due to an ↑ in circulating blood volume without functional myocardial abnormalities, resulting in a hyperkinetic state; the cardiac pump activity is a function of preload–ventricular end-diastolic fiber tension, myocardial contractility, afterload and heart rate; HOHF may be a physiologic response to such 'insults' as anemia, cor pulmonale, exercise, fever, high humidity, systemic HTN, obesity, pregnancy, emotional stress and temperature extremes, or non-physiologic in Albright's disease–polyostotic fibrous dysplasia, carcinoid syndrome–serotonin-producing usually hepatic metastases, arteriovenous fistulas–trauma, Paget's disease of bone, hemangiomatosis, glomerulonephritis, hemodialysis, hepatic disease–alcohol-related thiamine deficiency ↓ peripheral arterial resistance, hyperkinetic heart syndrome, P vera, thyrotoxicosis–T3 ↑ heart rate, cardiac sensitivity to epinephrine and peripheral vasodilation. Cf Low-output cardiac failure.
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