CALCIUM CHANNEL-BLOCKING DRUGS
(CLASS 4)
These
drugs, of which verapamil is the prototype, were first intro-duced as
antianginal agents. Verapamil and diltiazem also have antiarrhythmic effects.
The dihydropyridines (eg, nifedipine) do not share anti-arrhythmic efficacy and
may precipitate arrhythmias.
Verapamil
blocks both activated and inactivated L-type calcium channels. Thus, its effect
is more marked in tissues that fire fre-quently, those that are less completely
polarized at rest, and those in which activation depends exclusively on the
calcium current, such as the SA and AV nodes. AV nodal conduction time and
effective refractory period are consistently prolonged by therapeu-tic
concentrations. Verapamil usually slows the SA node by its direct action, but
its hypotensive action may occasionally result in a small reflex increase of SA
rate.
Verapamil
can suppress both early and delayed afterdepolariza-tions and may antagonize
slow responses arising in severely depo-larized tissue.
Verapamil
causes peripheral vasodilation, which may be beneficial in hypertension and
peripheral vasospastic disorders. Its effects on smooth muscle produce a number
of extracardiac effects .
Verapamil’s
cardiotoxic effects are dose-related and usually avoid-able. A common error has
been to administer intravenous vera-pamil to a patient with ventricular
tachycardia misdiagnosed as supraventricular tachycardia. In this setting,
hypotension and ventricular fibrillation can occur. Verapamil’s negative
inotropic effects may limit its clinical usefulness in diseased hearts .
Verapamil can induce AV block when used in large doses or in patients with AV
nodal disease. This block can be treated with atropine and β-receptor stimulants.Adverse
extracardiac effects include constipation, lassitude, nervousness, and
peripheral edema.
The
half-life of verapamil is approximately 7 hours. It is exten-sively metabolized
by the liver; after oral administration, its bio-availability is only about
20%. Therefore, verapamil must be administered with caution in patients with
hepatic dysfunction or impaired hepatic perfusion.
In
adult patients without heart failure or SA or AV nodal dis-ease, parenteral verapamil
can be used to terminate supraventricu-lar tachycardia, although adenosine is
the agent of first choice. Verapamil dosage is an initial bolus of 5 mg
administered over 2–5 minutes, followed a few minutes later by a second 5 mg
bolus if needed. Thereafter, doses of 5–10 mg can be administered every 4–6
hours, or a constant infusion of 0.4 mcg/kg/min may be used.
Effective
oral dosages are higher than intravenous dosage because of first-pass
metabolism and range from 120 mg to 640 mg daily, divided into three or four
doses.
Supraventricular
tachycardia is the major arrhythmia indication for verapamil. Adenosine or
verapamil are preferred over older treatments (propranolol, digoxin,
edrophonium, and vasocon-strictor 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 ven-tricular tachycardia can
cause hemodynamic collapse.
Diltiazem
appears to be similar in efficacy to verapamil in the management of
supraventricular arrhythmias, including rate con-trol in atrial fibrillation.
An intravenous form of diltiazem is avail-able for the latter indication and
causes hypotension or bradyarrhythmias relatively infrequently.
Related Topics
Privacy Policy, Terms and Conditions, DMCA Policy and Compliant
Copyright © 2018-2024 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.