Lesson 2: Cardiac Action Potential: Myocyte

Why does the cardiac myocyte action potential have a plateau phase, and why is this essential for cardiac output?

The plateau phase prolongs depolarization via Ca²⁺ influx, allowing sustained contraction and adequate stroke volume ejection. Without the plateau, contraction would be too brief to generate effective cardiac output.

A sodium channel blocker (e.g., lidocaine) is administered. Which phase of the myocyte action potential is most affected and what ECG change may occur?

Phase 0 depolarization is slowed because fast voltage-gated Na⁺ channels generate the upstroke. This may widen the QRS complex due to slowed ventricular conduction velocity.

Which phase of the ventricular action potential has the greatest calcium conductance and why is this clinically important?

Phase 2 has the greatest Ca²⁺ conductance due to activation of slow voltage-gated Ca²⁺ channels. This phase determines myocardial contractility and is targeted by calcium channel blockers.

Compare the ionic mechanisms of Phase 0 in cardiac myocytes versus SA node cells.

Myocyte Phase 0 depends on fast Na⁺ influx, producing rapid conduction. SA node Phase 0 depends on slow Ca²⁺ influx, producing slower conduction velocity.

Why does the slope of Phase 0 correlate with conduction velocity, and which clinical conditions alter it?

A steeper Phase 0 slope reflects faster Na⁺ entry and more rapid impulse propagation. Hyperkalemia, sodium channel blockers, and ischemia decrease the slope and slow conduction.

What ionic movements occur during Phase 1 initial repolarization and why is this phase brief?

Phase 1 involves Na⁺ channel inactivation, Cl⁻ influx, and transient K⁺ efflux. It is brief because Ca²⁺ channel activation rapidly transitions the cell into Phase 2 plateau.

Explain how Phase 2 prolongs the absolute refractory period and why this prevents tetany in the heart.

Sustained Ca²⁺ influx keeps Na⁺ channels inactivated, prolonging the absolute refractory period. This prevents summation of contractions and allows ventricular filling between beats.

Lesson

A patient receives verapamil. Which phase of the ventricular action potential is shortened and what is the physiologic effect?

Phase 2 plateau shortens because Ca²⁺ entry is reduced. This decreases myocardial contractility and oxygen demand.

Why does potassium efflux dominate Phase 3 repolarization despite ongoing calcium influx?

Delayed rectifier K⁺ channels open and K⁺ leaves faster than Ca²⁺ enters, restoring membrane potential toward −90 mV.

How does hyperkalemia alter the cardiac action potential and what dangerous arrhythmias may result?

Elevated extracellular K⁺ reduces resting membrane potential and slows Phase 0 depolarization. This predisposes to conduction blocks and ventricular arrhythmias.

What mechanisms maintain the resting membrane potential during Phase 4?

K⁺ leak channels maintain the resting potential near −90 mV while Na⁺/K⁺-ATPase restores ion gradients by removing Na⁺ and replacing K⁺.

Why is Na⁺/K⁺-ATPase essential after repeated depolarizations?

It removes accumulated intracellular Na⁺ and restores intracellular K⁺ levels, allowing normal action potentials to continue.

How do the absolute and relative refractory periods correspond to action potential phases?

The absolute refractory period spans Phases 0–2 and early Phase 3 when Na⁺ channels are inactivated. The relative refractory period occurs late in Phase 3 when some Na⁺ channels recover.

Why is the ventricular resting membrane potential approximately −90 mV?

High K⁺ permeability through leak channels and Na⁺/K⁺-ATPase activity establish a strongly negative intracellular environment.

Relate each phase of the myocyte action potential to the ECG waveform.

• Phase 0 → QRS complex

• Phase 2 → ST segment

• Phase 3 → T wave

• Phase 4 → TP segment baseline

Why do SA and AV node cells lack a plateau phase and how does this affect cardiac function?

Nodal cells rely on Ca²⁺ depolarization without sustained Ca²⁺ influx, so they lack a plateau. This allows automaticity rather than sustained contraction.

Which anesthetic drugs prolong the cardiac action potential and increase QT interval?

Volatile anesthetics and some antiarrhythmics prolong Phase 3 repolarization by affecting K⁺ channels. This increases risk of torsades de pointes.

Why does myocardial ischemia predispose to arrhythmias based on action potential physiology?

Ischemia alters Na⁺ and K⁺ gradients, slows Phase 0 conduction, shortens action potentials, and creates heterogeneous repolarization that promotes reentry.

Which phase keeps fast sodium channels inactivated and why is this clinically important?

Phase 2 plateau maintains Na⁺ channels inactivated due to sustained depolarization. This prolongs refractoriness and prevents premature ventricular contractions.

Why is calcium influx necessary for cardiac contraction but not skeletal muscle contraction?

Cardiac muscle requires extracellular Ca²⁺ influx for calcium-induced calcium release, whereas skeletal muscle relies primarily on sarcoplasmic reticulum calcium release.