Calcium Channel Blocker Overdose
First Things First (assess & treat for the following):
- In 2004: 10,513 exposures, 62 fatalities
- Patient may present in shock or with severe bradydysrhythmias—institute ABCs and ACLS protocols as needed.
Physiology of calcium
- Calcium enters myocardial cells via voltage-gated calcium channels.
- Entry triggers intracellular organelles to release calcium to affect excitation-contraction.
- Entry also triggers SA node action potential generation.
- Maintains fatty acid utilization by the myocardium
- Smooth Muscle: Calcium influx maintains tone
- Pancreas: Calcium mediates insulin release
Pathophysiology of calcium channel blockers
- Calcium channel blockers inhibit calcium entry by maintaining Ca channel in the closed position.
- In excess, calcium channel blockers cause toxicity characterized by bradycardia, conduction abnormalities and hypotension.
- Can produce a DKA-like state with insulin deficiency, hyperglycemia, acidemia and shock
- Also antagonize fast sodium channels, causing QRS prolongation
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