Gastrointestinal System

Cardiac Muscle Physiology and Action Potential covers cardiac muscle physiology and action potential for INI CET (AIIMS PG).

Cardiac Muscle vs Skeletal Muscle:

• Cardiac myocytes: Single nucleus, branched, intercalated discs (gap junctions for electrical coupling), shorter AP
• Functional syncytium: Atrial and ventricular muscle contract as units (gap junctions allow rapid spread)
• All-or-none contraction: Heart contracts as a functional syncytium — no summation or tetanus (long refractory period prevents tetanus)

Cardiac Action Potential (Ventricular Myocyte):

• Phase 0: Rapid depolarization — voltage-gated Na⁺ channels (Nav1.5) open → upstroke to +20 mV
• Phase 1: Initial repolarization — transient outward K⁺ current (I_to) → K⁺ efflux
• Phase 2 (Plateau): L-type Ca²⁺ channels open → Ca²⁺ influx (balanced by K⁺ efflux) → prolonged depolarization → prevents summation/tetanus; triggers calcium-induced calcium release (CICR) from SR
• Phase 3: Rapid repolarization — L-type Ca²⁺ channels inactivate; delayed rectifier K⁺ channels (IKr, IKs) open → net K⁺ efflux → restores RMP
• Phase 4: Stable resting potential (–90 mV) in ventricular myocytes; automaticity in pacemaker cells

Pacemaker Potential (SA Node):

• Phase 4 (Pacemaker potential): “Funny current” (I_f — mixed Na⁺/K⁺ inward current) + decreased K⁺ conductance + T-type Ca²⁺ channels → slow diastolic depolarization
• Phase 0: L-type Ca²⁺ channels open → slow calcium-dependent depolarization (no fast Na⁺ channels in SA node)
• Phase 3: Ca²⁺ channels inactivate; K⁺ channels open → repolarization
• Rate: ~60–100 bpm (SA node); slowest phase 4 slope = slower HR

Refractory Periods:

• Absolute refractory period (ARP): No stimulus can fire another AP (Na⁺ channels inactivated) — corresponds to plateau (phase 2) in cardiac muscle
• Relative refractory period (RRP): Stronger-than-normal stimulus can fire another AP
• Effective refractory period (ERP): Time during which a premature stimulus cannot propagate — longer in cardiac than skeletal muscle
• Why no tetanus?: Long plateau (phase 2) → long ARP → prevents re-excitation before contraction ends

Excitation-Contraction Coupling in Heart:

• L-type Ca²⁺ influx (phase 2) → triggers RYR2 on SR → massive Ca²⁺ release (CICR) → actin-myosin cross-bridge cycling → contraction
• Relaxation: Ca²⁺ removed via:
  1. SERCA (80%) → pumps Ca²⁺ back into SR
  2. NCX (15%) → 3Na⁺ in / 1Ca²⁺ out (forward mode) — electrogenic
  3. PMCA (5%) → plasma membrane Ca²⁺-ATPase
• Frank-Starling Law: Increased preload (end-diastolic volume) → increased stroke volume (within physiological limits); due to optimal sarcomere length
• β₁-adrenergic stimulation: ↑cAMP → PKA phosphorylates L-type Ca²⁺ channels → ↑Ca²⁺ influx → ↑inotropy (positive); also phosphorylates phospholamban → ↑SERCA activity → ↑relaxation (lusitropy)

ECG Correlates:

• P wave: Atrial depolarization
• PR interval: AV node conduction delay (0.12–0.20 s)
• QRS complex: Ventricular depolarization
• ST segment: Ventricular plateau (phase 2)
• T wave: Ventricular repolarization (phase 3)
• QT interval: Total ventricular activity (0.35–0.45 s; prolonged → risk of torsades de pointes)

⚡ Exam Tip for INI CET (AIIMS PG): Class IA antiarrhythmics (quinidine, procainamide) block Na⁺ channels → slow phase 0 upstroke → slow conduction. Class III (amiodarone, sotalol) block K⁺ channels → prolong phase 3 → prolong AP and QT. Class II (β-blockers) reduce SA node firing (negative chronotropy) and AV node conduction (negative dromotropy).