High output heart failure

Cardiovascular system Decreased peripheral vascular resistance increased heart rate, stroke volume, cardiac output, pulse pressure high-output heart failure increased inotropic and chronotropic effects arrhythmias angina Increased peripheral vascular resistance decreased heart rate, stroke volume, cardiac output, pulse pressure low-output heart failure ECG bradycardia, prolonged PR interval, flat T wave, low voltage pericardial effusion... 

Hypoglycemia, acute renal failure, pulmonary edema, severe anemia, thrombocytopenia, high-output heart failure, cerebral congestion, seizures and coma, and adult respiratory syndrome ... 

After excessive drinking over an extended period of time while eating poorly, a middle-aged man is admitted to the hospital with high output heart failure. Which of the following enzymes is most likely inhibited ... 

Hypersecretion of aldosterone in dogs with a chronic aortic-caval fistula and high output heart failure. CirculMion Res. 14, 471-485 (1964). 

Most of the signs and symptoms of thyrotoxicosis stem from excessive heat production, increased motor activity, and increased activity of the sympathetic nervous system. Eventually, the increased energy expenditure is often associated with weight loss. Cardiac manifestations include tachycardia and bounding pulses older patients or those with underlying heart disease may exhibit angina, arrhythmias (especially atrial fibrillation), and high-output heart failure. 

Heart failure (HF) is defined as the inadequate ability of the heart to pump enough blood to meet the blood flow and metabolic demands of the body.1 High-output HF is characterized by an inordinate increase in the body s metabolic demands, which outpaces an increase in cardiac output (CO) of a generally normally functioning heart. More commonly, HF is a result of low CO secondary to impaired cardiac function. The term heart failure will refer to low-output HF for purposes of this chapter. 

Upon stabilization, placement of a pulmonary artery (PA) catheter may be indicated based on the need for more extensive cardiovascular monitoring than is available from non-invasive measurements such as vital signs, cardiac rhythm, and urine output.9,10 Key measured parameters that can be obtained from a PA catheter are the pulmonary artery occlusion pressure, which is a measure of preload, and CO. From these values and simultaneous measurement of HR and blood pressure (BP), one can calculate the left ventricular SV and SVR.10 Placement of a PA catheter should be reserved for patients at high risk of death due to the severity of shock or preexisting medical conditions such as heart failure.11 Use of PA catheters in broad populations of critically ill patients is somewhat controversial because clinical trials have not shown consistent benefits with their use.12-14 However, critically ill patients with a high severity of illness may have improved outcomes from PA catheter placement. It is not clear why this was... 

Blockers are contraindicated in patients with decompensated heart failure unless it is caused solely by tachycardia (high output). Other contraindications include sinus bradycardia, concomitant therapy with monoamine oxidase inhibitors or tricyclic antidepressants, and patients with spontaneous hypoglycemia. Side effects include nausea, vomiting, anxiety, insomnia, lightheadedness, bradycardia, and hematologic disturbances. 

Lignocaine s clearance by the liver is flow dependent. In heart failure cardiac output may be very low and therefore hepatic blood flow through both the hepatic artery and the portal venous system is also low. This meant a lower extraction of the drug from the blood and accumulation of lignocaine until the high plasma concentration produced the central nervous system toxicity. 

High-output" failure is a rare form of heart failure. In this condition, the demands of the body are so great that even increased cardiac output is insufficient. High-output failure can result from hyperthyroidism, beriberi, anemia, and arteriovenous shunts. This form of failure responds poorly to the drugs discussed in this chapter and should be treated by correcting the underlying cause. 

Measurements of arterial pressure, cardiac output, stroke work index, and pulmonary capillary wedge pressure are particularly useful in patients with acute myocardial infarction and acute heart failure. Such patients can be usefully characterized on the basis of three hemodynamic measurements arterial pressure, left ventricular filling pressure, and cardiac index. One such classification and therapies that have proved most effective are set forth in Table 13-4. When filling pressure is greater than 15 mm Hg and stroke work index is less than 20 g-m/m2, the mortality rate is high. Intermediate levels of these two variables imply a much better prognosis. 

When the heart can no longer pump an adequate supply of blood to meet the metabolic needs of the tissues or in relation to venous return, cardiac failure may ensue. The causes of cardiac failure are complex, but stem from mechanical abnormalities (e.g., pericardial tamponade), myocardial failure (e.g., cardiomyopathy and inflammation), and arrhythmias. In high-output failure, the cardiac output, which may be normal or even higher than normal, is not sufficient to meet the metabolic requirement of the body. Cardiac failure may predispose a patient to congestive heart failure, which is a state of circulatory congestion. Toxic injury, caused by agents such as doxorubicin, the alkaloid emetine in ipecac syrup, cocaine, or ethyl alcohol, is another way by which the functional integrity of the heart may also be compromised. 

In treating the heart failure patient with diuretics, it must always be remembered that cardiac output in these patients is being maintained in part by high filling pressures and that excessive use of diuretics may diminish venous return and thereby impair cardiac output. This issue is especially... 

Correct answer = D. It is important to increase the cardiac output to improve oxygen delivery and thus minimize anaerobic metabolism and improve CNS and renal perfusion. Since this patient apparently does not have a heart condition, such as congestive heart failure, she could benefit from fluid therapy. An inotropic agent, such as dopamine, would lead to an increased cardiac output and dilation of the renal vasculature. [Note At high doses, however, it may constrict the renal beds due to interaction on a receptors.] Antibiotic administration is also important but will not improve the patient s hemodynamics. 

Cardiovascular Disorders and Copper. Sudden cardiac failure has been associated with copper deficiency (91J. There are two attractive mechanisms. First, the coronary arteries and aorta may become weakened from an inability to synthesize elastin due to a decrease in lysyl oxidase activity. Rupture of these major blood vessels has been shown to cause sudden death in animals suffering from copper deficiency. Second, a decrease in cytochrome oxidase activity during copper deficiency Impairs aerobic metabolism of the heart and increases the risk of hypertrophy. Hypertrophy, which may lead to high output congestive heart failure, is exacerbated by hypochromic anemia also caused by copper deficiency. 

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