Verapamil hemodynamics

Verapamil IV- Do not administer concomitantly with IV -adrenergic blocking agents (within a few hours), because both may depress myocardial contractility and AV conduction ventricular tachycardia (VT), because use in patients with wide-complex VT (QRS 0.12 seconds or more) can result in marked hemodynamic deterioration and ventricular fibrillation atrial fibrillation or atrial flutter associated with an accessory bypass tract. 

Supraventricular tachycardia is the major arrhythmia indication for verapamil. Adenosine or verapamil are preferred over older treatments (propranolol, digoxin, edrophonium, vasoconstrictor agents, and cardioversion) for termination. Verapamil can also reduce the ventricular rate in atrial fibrillation and flutter. It only rarely converts atrial flutter and fibrillation to sinus rhythm. Verapamil is occasionally useful in ventricular arrhythmias. However, intravenous verapamil in a patient with sustained ventricular tachycardia can cause hemodynamic collapse. 

In pulmonary hypertension, both verapamil and nifedipine increase mean right atrial pressure in association with hypotension, chest pain, dyspnea, and hypoxemia the severe hemodynamic upset resulted in cardiac arrest in two patients after verapamil and death in another after nifedipine (54). A patient with pulmonary hypertension also developed pulmonary edema whilst taking nifedipine (55) and another seems to have developed this as an allergic reaction (56). 

Verapamil reversed digoxin-induced splanchnic vasoconstriction in healthy men (243), but this has no direct effect on systemic hemodynamics. 

In another study the acute response to inhaled nitric oxide and high doses of oral nifedipine or verapamil was assessed in 33 consecutive patients with primary pulmonary hypertension (2). Ten patients responded acutely to nitric oxide, nine of whom responded acutely to calcium channel blockers, without any complications. The other 23 patients failed to respond to nitric oxide and calcium channel blockers. In these non-responders there were nine serious adverse effects with calcium channel blockers. There was no clinical or baseline hemodynamic feature that predicted the acute vasodilator response. Long-term oral treatment with calcium channel blockers was restricted to the nine acute responders, and there was a sustained clinical and hemodynamic improvement in only six patients. It was concluded that nitric oxide may be used as a screening agent for safely identifying patients with primary pulmonary hypertension who may benefit from long-term treatment with calcium channel blockers. 

A 61-year-old woman developed profonnd hypotension, bradycardia, oliguria, and multifocal myoclonus after verapamil overdose. Her serum verapamil concentration was 800 ng/ml (1760 nmol/1) (nsnal target range 50-200 ng/ml, 110-440 nmol/1). She was treated with supportive care, vasopressin, dopamine, and calcinm gluconate. After about 60 hours the myoclonus and hemodynamic compromise resolved completely (25). 

Verapamil is both a snbstrate and an inhibitor of CYP3A4, which is inhibited by clarithromycin and erythromycin. Giving these macrolide antibiotics dnring verapamil therapy is likely to rednce the first-pass metabolism of verapamil, increase its systemic availability, and impair its elimination. In patients taking this combination, verapamil should be started in a low dosage and its hemodynamic effects should be monitored closely. 

Buchhorn R, Motz R, Bursch J. Hemodynamic and neuro-hormonal causes of a severe verapamil induced cardiac decompensation in a child after mustard operation. Herz Kreisl 2000 32 74-7. 

Calcium channel antagonists and nitrates also may increase myocardial oxygen supply through coronary vasodilation. Diastolic function also may be improved with verapamil, nifedipine, and perhaps, diltiazem. These effects may vary from those indicated in the table depending on individual patient baseline hemodynamics. 

Calcium chaimel blockers traditionally have been the first-line agents to treat hypertension after transplantation. In addition to their ability to control blood pressure, calcium channel blockers may ameliorate the nephrotoxic effects of CSA, improve renal hemodynamics, decrease the incidence of delayed graft function and development of allograft atherosclerosis, and provide some immunosuppression. Calcium channel blockers, however, also may contribute to gingival hyperplasia that is often associated with CSA-based immunosuppression. CYP 3A4 interactions with CSA and TAC are of concern with this class of medications, particularly with dil-tiazem, verapamil, and nicardipine, and CSA or TAC concentrations must be monitored to ensure proper dosage adjustments. 

The hemodynamic effects of verapamil are reportedly more variable than those elicited by nifedipine. Studies conducted in dogs and humans reveal inotropic and vasodilator effects similar to those of nifedipine except that reflex tachycardia... 

All Ca + channel blockers approved for clinical use decrease coronary vascular resistance and increase coronary blood flow. The dihydropyridines are more potent vasodilators than verapamil, which is more potent than diltiazem. The hemodynamic effects of these agents vary depending on the route of administration and the extent of left ventricular dysfunction. 

Seabra-Gomes R, Rickards A, Sutton R. Hemodynamic effects of verapamil and practolol in man. EurJ Cardiol 916) 4, 79-85. 

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