Treatment is primarily supportive. For severe cardiotoxicity, such as seen with large ingestions in suicide attempts, cathecholamines with chronotropic activity (dopamine, epinephrine, norepinephrine) should be used. Isoproterenol is effective in this regard but may potentiate vasodilation. Atropine is inconsistently effective.
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Temporary pacing should be considered. Whereas intravenous administration of calcium may improve contractility, this maneuver is less effective in managing heart block or excessive vasodilation. Oral charcoal should be given for acute ingestion. Hemoperfusion, however, is ineffective in clearing these drugs because of their large volume of distribution and high endogenous clearance. Glucagon has been felt to be useful in a few cases. The mechanism is thought to be improvement in myocardial contractility through increased cyclic AMP in myocardial cells.
Are calcium channel antagonists indicated in patients with acute Q-wave myocardial infarctions?
No. Most studies of the calcium channel antagonists have not demonstrated any definitive benefits in patients with acute myocardial infarction. In a meta-analysis of 22 trials, no improvement in mortality, reduction of infarct size, or reduction in incidence of reinfarction was documented. One trial explored administration of verapamil starting 1 week after the acute event and showed a significant reduction in mortality. In another trial, nifedipine was associated with increased mortality and reinfarction rate.
Are calcium antagonists indicated in non-Q-wave myocardial infarctions?
Calcium channel antagonists may have a role in patients without evidence of left ventricular failure. Diltiazem decreases the short term reinfarction rate and the incidence of postinfarction angina but does not improve overall survival. In patients with pulmonary congestion, however, use of diltiazem was associated with increased mortality.
Is there a role for calcium-channel antagonists in the treatment of heart failure due to left ventricular systolic dysfunction?
In general, no. Most studies have not shown sustained clinical benefit. Because of significant negative inotropic effect, calcium channel blockers may, in fact, worsen heart failure due to systolic dysfunction. Even those agents selective for vascular smooth muscle-relaxant effects have competing negative inotropic effects.