Phases of the Cardiac Action Potential
The cardiac action potential is a remarkable dance of ions across the cell membrane, and it's composed of five distinct phases:
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Phase 0 – Rapid Depolarization
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What happens: Voltage-gated sodium (Na⁺) channels open, and Na⁺ floods into the cell.
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Think of it as: The opening act where the spotlight suddenly shines, kicking off the performance.
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Result: The cell’s interior becomes more positive, leading to a rapid upward spike in membrane potential.
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Phase 1 – Initial Repolarization
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What happens: Na⁺ channels close, and potassium (K⁺) channels briefly open, allowing K⁺ to exit.
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Think of it as: A brief pause, adjusting the tempo before the main act.
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Result: A slight drop in membrane potential.
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Phase 2 – Plateau Phase
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What happens: Calcium (Ca⊃2;⁺) channels open, Ca⊃2;⁺ enters the cell while K⁺ continues to leave.
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Think of it as: A captivating solo that holds the audience—prolonging the excitement.
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Result: The membrane potential plateaus, prolonging depolarization.
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Phase 3 – Repolarization
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What happens: Ca⊃2;⁺ channels close, more K⁺ channels open, increasing K⁺ outflow.
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Think of it as: The finale where the energy winds down.
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Result: The cell returns toward its resting negative membrane potential.
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Phase 4 – Resting Membrane Potential
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What happens: The cell is at rest, maintained by the Na⁺/K⁺ ATPase pump.
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Think of it as: Backstage prep for the next performance.
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Result: The cell is ready for the next action potential.
Clinical Connections
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Antiarrhythmic Drugs: Many work by altering ion channel function—Class I drugs block Na⁺ channels, Class IV block Ca⊃2;⁺ channels.
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Electrolyte Imbalances: High potassium levels (hyperkalemia) can affect repolarization, leading to dangerous arrhythmias.
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Ischemia Impact: Reduced oxygen affects ATP production, impairing Na⁺/K⁺ pumps and disrupting resting membrane potential.
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Mohammed Adel Salama
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