Calcium Channel Blockers (CCBs)

Calcium Channel Blockers inhibit L-type calcium channels in cardiac and vascular smooth muscle.

They reduce intracellular calcium, leading to:

↓ Contractility
↓ Heart rate (some agents)
↓ Afterload

Used in:

Mechanism of Action

CCBs block L-type calcium channels.

Calcium normally:

Enters cardiac myocytes during phase 2
Triggers calcium-induced calcium release
Enables actin-myosin contraction

Blocking calcium entry results in:

Vasodilation
Reduced myocardial contractility
Reduced AV nodal conduction (non-DHP agents)

Two Major Classes

1. Dihydropyridines (DHP)

Primary effect:

Vascular smooth muscle relaxation

Major action:

↓ Systemic Vascular Resistance
↓ Afterload

Common agents:

Used primarily for:

Minimal effect on AV node.

2. Non-Dihydropyridines (Non-DHP)

Primary effect:

Cardiac tissue

Major actions:

↓ Heart rate
↓ Contractility
↓ AV nodal conduction

Agents:

Used for:

Rate control in Dysrhythmias
Angina
Hypertension

Clinical Differences

DHP CCBs:

Strong vasodilators
Can cause reflex tachycardia
Peripheral edema common

Non-DHP CCBs:

Slow AV conduction
Risk of bradycardia
Avoid in HFrEF

Contraindications

Non-DHP CCBs:

Avoid in Heart Failure with Reduced EF
Avoid with beta-blockers (risk of heart block)

DHP CCBs:

Use caution in severe hypotension

Clinical Pearls

All CCBs block L-type calcium channels
DHP = vessels
Non-DHP = heart
Non-DHP slow AV node
DHP reduce afterload
Avoid non-DHP in HFrEF