Calcium Channel Blockers Quiz

Calcium channel blockers target voltage-gated calcium ion channels, including L-type (slow), N-type (neural), and T-type (transient) subtypes. They specifically bind to receptors on the $\alpha1$ subunit of the L-type calcium channels. Binding to these channels results in their inactivation, rendering them closed and preventing calcium influx. This inhibition of calcium entry leads to a decrease in intracellular calcium levels.

Calcium channel blockers are classified into 3 main groups based on their chemical structure: phenylalkylamines, dihydropyridines, and benzothiazepines.

Common side effects of calcium channel blockers include systemic hypotension, peripheral edema, flushing, and headache.

Calcium channel blockers selectively interfere with calcium ion movement across myocardial and vascular smooth muscle cells by inhibiting the movement of calcium ions across specific cell types in the heart and blood vessels.

Voltage-gated calcium ion channels are found in various cell types, including skeletal muscle, vascular smooth muscle, cardiac muscle, neurons, and glandular cells.

30-40 hours

Being extremely lipophilic and ultrashort-acting

Preventing cerebral vasospasm after subarachnoid hemorrhage

Calcium channel blockers affect action potential in cardiac tissues, leading to reduced heart rate, myocardial contractility, and conduction velocity through the atrioventricular node.

Calcium channel blockers are indicated for cardiovascular conditions, vasodilation, hypertension, Raynaud's phenomenon, subarachnoid hemorrhage, and cluster headaches.

Contraindications include conditions dependent on AV conduction, decompensated heart failure, aortic stenosis, and hypotension.

Verapamil, a phenylalkylamine, binds to the L-type channel $\alpha1$ subunit, causing negative inotropic effects on cardiac muscle and moderate vasodilation of coronary and systemic arteries. It is effective in treating supraventricular tachydysrhythmias and vasospastic angina pectoris, and can be used for symptomatic hypertrophic cardiomyopathy, but not for acute myocardial infarction.

Side effects include bradycardia, hypotension, peripheral edema, flushing, and decreased GI motility.

Amlodipine provides anti-ischemic effects comparable to β-blockers, especially in patients with acute coronary syndrome. Combining amlodipine with β-blockers may be more effective in treating myocardial ischemia.

Diltiazem, a benzothiazepine, acts on L-type calcium channels similar to verapamil and has additional effects, such as acting on the sodium-potassium pump and inhibiting calcium-calmodulin binding. It is first-line for treating supraventricular tachydysrhythmias and can be used for the chronic control of essential hypertension. It exerts minimal cardiodepressant effects and is unlikely to interact negatively with β-adrenergic blocking drugs to decrease myocardial contractility. Diltiazem is available as an oral capsule and can be administered IV for the management of angina pectoris. Liver disease may require a reduction in the dosage of diltiazem.

Verapamil and diltiazem have depressant effects on cardiac action potentials and can lead to AV heart block when combined with β-blockers or digoxin in patients with preexisting cardiac conduction abnormalities.

Toxicity due to a calcium channel blocker overdose may be partially reversed with IV administration of calcium or dopamine. Calcium channel blockers can potentiate the effects of depolarizing and nondepolarizing neuromuscular blocking drugs, and verapamil and diltiazem's local anesthetic effects may contribute to this potentiation.

Calcium channel blockers slow the inward movement of $K^+$ ions, potentially leading to hyperkalemia in patients taking verapamil.