Pharmacology
Summary
Class IV antiarrhythmics are calcium channel blockers, and are pivotal agents in the management of cardiac arrhythmias. These drugs, specifically the nondihydropyridine variants like diltiazem and verapamil, selectively inhibit the L-type calcium channels. This inhibition profoundly impacts the heart's electrical activity, especially within the SA and AV nodes. By targeting these nodes, Class IV antiarrhythmics effectively prevent rapid heart rates and suppress arrhythmias that originate in the atria.
Their mechanism of action revolves around modulating the nodal action potential, particularly by prolonging phase 4 depolarization, which is calcium-dependent. This modulation results in decreased atrioventricular conduction and a long AV node refractory period, which is beneficial in slowing ventricular response rates during conditions like atrial fibrillation. A noteworthy clinical manifestation of nondihydropyridine CCBs is the prolongation of the PR interval on ECG, a potential indicator of heart block. Class IV antiarrhythmics are especially valuable in managing supraventricular arrhythmias such as atrial fibrillation and flutter.
Lesson Outline
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FAQs
Class IV Antiarrhythmics, primarily non-dihydropyridine calcium channel blockers, act by inhibiting the influx of calcium ions through the L-type calcium channels present in cardiac and vascular smooth muscle cells In the heart, this blockade prolongs phase 4 of the nodal action potential, slowing conduction, especially in the AV node, and leads to a slower refractory period, resulting in a reduced force of cardiac muscle contraction, known as a negative inotropic effect.
Class IV antiarrhythmics, or calcium channel blockers, modulate cardiac action potentials by inhibiting the L-type calcium channels. This inhibition primarily affects the plateau phase of the cardiac action potential. The results in prolongation of phase 4 of the nodal action potential and decreased pacemaker activity, especially in the AV node, as well as a prolonged effective refractory period. This modulation is particularly beneficial in controlling the rate of arrhythmias by limiting the rapid transmission of impulses, especially in conditions like atrial fibrillation.
Non-dihydropyridine calcium channel blockers, such as verapamil and dialtezem, nfluence the ECG by prolonging the PR interval, which reflects a delay in atrioventricular nodal conduction. This action on the AV node may lead to heart block, a condition where the electrical signal is impeded or entirely halted as it travels from the atria to the ventricles.
Non-dihydropyridine calcium channel blockers, such as verapamil and diltiazem, are particularly effective in managing atrial fibrillation because they slow down the conduction through the AV node. By doing so, they reduce the number of atrial impulses reaching the ventricles, thereby controlling the ventricular rate. This is crucial in atrial fibrillation, where rapid atrial impulses can lead to a dangerously fast ventricular rate if not adequately controlled.
Supraventricular tachycardia (SVT) is an arrhythmia characterized by an abnormally fast heart rate that originates from tissues above the ventricles. Class IV Antiarrhythmics, or non-dihydropyridine calcium channel blockers, are effective in managing SVT due to their capacity to decelerate conduction and prolong the refractory period, especially in the SA and AV nodes. By doing so, they help temper the rapid heartbeats and maintain a regular cardiac rhythm.
