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

• Myocardium
  • 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