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Physiological Properties of the Heart & Cardiac Cycle

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1. Physiological Properties of Cardiac Muscle

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2. Excitability & Action Potential of Cardiomyocytes

Phases of the Ventricular Action Potential

  +20 mV ─────────────┐  Phase 1 (notch)
                      └──────────────────── Phase 2 (plateau)
                                                              \
   0 mV                                                        \ Phase 3
                                                                \
 −90 mV ──┘ Phase 4 (rest)           Phase 0 (upstroke)         └── Phase 4

According to Evaluation, Risk Stratification, and Management of Arrhythmogenic Cardiomyopathy (p. 36): the Ca²⁺ entry through LTCC triggers massive Ca²⁺ release from sarcoplasmic reticulum (SR) via ryanodine receptor type 2, producing systolic Ca²⁺ elevation needed for contraction. Ca²⁺ is subsequently extruded via NCX1 and re-sequestered by SERCA2a to allow diastolic relaxation.

Excitation–Contraction Coupling

• Ca²⁺ influx during Phase 2 acts as a trigger for Ca²⁺-induced Ca²⁺ release (CICR) from SR
• Peak intracellular [Ca²⁺] reaches ~1 µM during systole (vs. 100 nM at rest)
• Troponin C binds Ca²⁺ → removes tropomyosin inhibition → actin-myosin crossbridge cycling → contraction

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3. Automaticity of the Heart

Definition

Ionic Basis of Pacemaker Potentials (SA Node)

According to Harrison's Principles of Internal Medicine, 21st Ed. (p. 6947): Phase 4 spontaneous depolarization in SA nodal cells results from the funny current (I_f / I_h), along with T-type and L-type calcium channels. Phase 0 is the depolarization phase; Phase 3 repolarization results from outward hyperpolarizing K⁺ currents.

SA Node Action Potential vs. Ventricular AP

Gradient of Automaticity (Bathmotropic Hierarchy)

SA Node  →  60–100 bpm   (primary pacemaker)
   ↓
AV Node  →  40–60 bpm    (secondary pacemaker)
   ↓
Bundle of His  →  30–40 bpm
   ↓
Purkinje Fibers / Ventricles  →  20–40 bpm  (tertiary)

• If the SA node fails, the next-fastest pacemaker takes over
• The slower rate of subsidiary pacemakers is due to a slower slope of Phase 4 depolarization (smaller I_f density)
• Overdrive suppression: rapid pacing increases Na⁺/K⁺-ATPase activity → hyperpolarization → suppresses subsidiary pacemakers

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4. Cardiac Cycle and Its Phases

Overview of Phases

SYSTOLE (contraction + ejection, ~0.3 s)

DIASTOLE (relaxation + filling, ~0.5 s)

Pressure–Volume Relationships

   Pressure
      │         Systole
   120│           ╭─────╮
      │          /       \
    80│─────────╮         ╰──────
      │  Filling │         │ ISO relax
      │          ╰─────────╯
      └──────────────────────────── Volume
           EDV ~130 mL    ESV ~50 mL

• End-diastolic volume (EDV): ~130 mL
• End-systolic volume (ESV): ~50 mL

Systolic (Stroke) and Minute Volumes

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5. Relationships Between Excitation, Contraction, and Excitability in Cardiac Cycle Phases

Refractory Periods in Relation to the Action Potential

Temporal Alignment of Events

 ECG:     P──────QRS─────────────────T──────
 AP:              0  1  2   (plateau)  3  4
 Contraction:        ↑ onset      peak ↓  relax
 ARP:             [═══════════════════]
 RRP:                                 [════]
 SNP:                                     []

Why Is ARP So Long in Cardiac Muscle?

• In skeletal muscle, ARP = ~2 ms → tetanus possible
• In cardiac muscle, ARP ≈ duration of mechanical contraction (~250 ms)
• This is due to the prolonged plateau (Phase 2) maintained by I_CaL
• Result: the next stimulus can only arrive after relaxation begins → cardiac tetanus is physiologically impossible

The "Vulnerable Period"

• Corresponds to the peak of the T-wave on ECG
• Falls within the Relative Refractory Period
• A well-timed stimulus (e.g., premature ventricular complex, external shock) hitting during this window can trigger ventricular fibrillation (R-on-T phenomenon)

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Summary Diagram: Integration of All Four Topics

   Automaticity (SA Node Phase 4 depolarization)
          ↓
   Action Potential propagated via conduction system
   (SA node → AV node → Bundle of His → Purkinje fibers)
          ↓
   Cardiomyocyte AP (Phases 0–4): Na⁺ → Ca²⁺ plateau → K⁺ repolarization
          ↓
   Ca²⁺ triggers SR release (CICR) → Cross-bridge cycling → CONTRACTION
          ↓
   ARP covers systole → RRP during early diastole → Full recovery in diastole
          ↓
   Cardiac Cycle: Systole (isovolumetric contraction + ejection)
                + Diastole (isovolumetric relaxation + filling)
          ↓
   SV = EDV − ESV (~70 mL); CO = SV × HR (~5 L/min)

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