Beta Blockers and Calcium Channel Antagonists
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General Principles
Beta-adrenergic antagonists (beta blockers, BBs) and calcium channel antagonists (CCAs) are widely prescribed for hypertension, atrial fibrillation and other dysrhythmias, and noncardiac indications such as essential tremor, migraine prophylaxis, Raynaud’s, and situational anxiety.
Pathophysiology
- BBs antagonize beta-adrenergic receptors in the myocardium and pacemaker system, producing decreased chronotropy and inotropy.
- Sotalol has BB activity and is also an IKr antagonist (class III antidysrhythmic). In overdose, it produces QT prolongation and bradycardia, which creates a high risk for torsades de pointes.
- Propranolol has cardiac sodium channel antagonist properties in overdose and is also lipophilic enough to cross the blood–brain barrier and produce mental status changes and seizures in overdose.
- CCAs inhibit the entry of calcium into cells.
- The non-dihydropyridine CCAs (diltiazem, verapamil) act primarily on cardiac myocytes and cells of the pacemaker system, producing decreased chronotropy and inotropy.
- The dihydropyridine CCAs (amlodipine, nifedipine) act primarily on peripheral vascular smooth muscle, producing vasodilation.
- In significant overdose, all CCAs lose channel selectivity and can affect all types of calcium channels.
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General Principles
Beta-adrenergic antagonists (beta blockers, BBs) and calcium channel antagonists (CCAs) are widely prescribed for hypertension, atrial fibrillation and other dysrhythmias, and noncardiac indications such as essential tremor, migraine prophylaxis, Raynaud’s, and situational anxiety.
Pathophysiology
- BBs antagonize beta-adrenergic receptors in the myocardium and pacemaker system, producing decreased chronotropy and inotropy.
- Sotalol has BB activity and is also an IKr antagonist (class III antidysrhythmic). In overdose, it produces QT prolongation and bradycardia, which creates a high risk for torsades de pointes.
- Propranolol has cardiac sodium channel antagonist properties in overdose and is also lipophilic enough to cross the blood–brain barrier and produce mental status changes and seizures in overdose.
- CCAs inhibit the entry of calcium into cells.
- The non-dihydropyridine CCAs (diltiazem, verapamil) act primarily on cardiac myocytes and cells of the pacemaker system, producing decreased chronotropy and inotropy.
- The dihydropyridine CCAs (amlodipine, nifedipine) act primarily on peripheral vascular smooth muscle, producing vasodilation.
- In significant overdose, all CCAs lose channel selectivity and can affect all types of calcium channels.
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