MANAGEMENT OF ACUTE HEART FAILURE
Acute
heart failure occurs frequently in patients with chronic failure. Such
episodes are usually associated with increased exertion, emotion, excess salt
intake, nonadherence to medical therapy, or increased metabolic demand
occasioned by fever, anemia, etc. A particularly common and important cause of
acute failure—with or without chronic failure—is acute myocardial infarction.Patients
with acute myocardial infarction are best treated with emergency
revascularization using either coronary angioplasty and a stent, or a
thrombolytic agent. Even with revascularization, acute failure may develop in
such patients. Many of the signs and symp-toms of acute and chronic failure are
identical, but their therapies diverge because of the need for more rapid
response and the rela-tively greater frequency and severity of pulmonary
vascular congestion in the acute form.
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 ventricu-lar filling pressure, and cardiac index. 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.
Intravenous treatment is the rule in acute heart failure. Among
diuretics, furosemide is the most
commonly used. Dopamine or dobutamine are positive inotropic drugs
with prompt onset andshort durations of action; they are most useful in
patients with severe hypotension. Levosimendan
has been approved for use in acute failure in Europe, and noninferiority has
been demonstrated against dobutamine. Vasodilators in use in patients with
acute decompensation include nitroprusside,
nitroglycerine, and nesiritide. Reduction in afterload often improves
ejection fraction, but improved survival has not been documented. A small
subset of patients in acute heart failure will have hyponatremia, presum-ably
due to increased vasopressin activity. A V1a and V2
receptor antagonist, conivaptan, is
approved for parenteral treatment of euvolemic hyponatremia. Several clinical
trials have indicated that this drug and related V2 antagonists (tolvaptan) may have a ben-eficial effect
in some patients with acute heart failure and hypona-tremia. Thus far,
vasopressin antagonists do not seem to reduce mortality.
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