Maybe. High doses of nifedipine or diltiazem produce reductions in pulmonary artery pressure and pulmonary vascular resistance in some patients. However, no clinical trial of calcium channel antagonists in primary pulmonary hypertension has demonstrated a survival benefit.
A patient with known Wolff-Parkinson-White syndrome presents with atrial fibrillation with a rapid ventricular response. He is given intravenous verapamil, but then becomes hypotensive and develops ventricular fibrillation.
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What is the likely mechanism for this deterioration?
This case illustrates the potential danger of using calcium channel antagonists in patients with accessory bypass tracts who present with atrial fibrillation. Calcium channel antagonists may depress conduction through the AV node and enhance conduction through accessory bypass tracts, resulting in acceleration of the ventricular response. Very rapid ventricular rates may lead to hypotension and syncope and may cause rhythm degeneration to ventricular fibrillation.
The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army or Department of Defense.
Describe the usual pathogenesis of acute myocardial infarction.
Most acute myocardial infarctions are caused by the occlusion of a coronary artery by a thrombus at the site of a ruptured atheromatous plaque. Total occlusion of an infarct-related artery has been seen in up to 87% of patients undergoing cardiac catheterization within 4-6 hours of acute myocardial infarction.