How Does the Heart Beat – Quick Review

Cardiac Muscle Structure and Pump Function

• Spiral fibre orientation "wrings" blood from apex to base.

• Intercalated discs: desmosomes (strength) + gap junctions (electrical sync).

• Two cell types: contractile (99 %) vs autorhythmic (1 %).

• Specialized protein $\text{Troponin-C}$; elevated plasma levels diagnose myocardial infarction.

Dual Circulation & Ventricular Differences

• Right heart → pulmonary circuit; mean pressure $\approx 15\ \text{mmHg}$.

• Left heart → systemic circuit; mean arterial pressure $\approx 93\ \text{mmHg}$.

• Both eject $\approx 5\ \text{L/min}$; left ventricle thicker due to higher resistance.

Pacemaker (Autorhythmic) Cells

• Generate spontaneous action potentials (auto-rhythmicity).

• Pacemaker potential phases:
  • Phase 1: $I_f$ Na⁺ influx + ↓K⁺ efflux → slow depolarisation.
  • Phase 2: T-type $\text{Ca}^{2+}$ channels open → reach threshold.
  • Phase 3: L-type $\text{Ca}^{2+}$ channels open → rapid upstroke.
  • Phase 4: K⁺ channels open, Ca²⁺ channels close → repolarise to $-60\ \text{mV}$.

Conduction Pathway & Intrinsic Rates

• SA node: $70–80\ \text{AP/min}$ (primary pacemaker).

• AV node: $40–60$; Bundle/ Purkinje: $20–40$.

• Route: SA → interatrial & internodal tracts → AV (delay) → Bundle of His → branches → Purkinje → ventricles.

• Fibrous AV ring insulates atria from ventricles ensuring one-way spread.

Contractile Cell Action Potential

• Phase 0: Fast Na⁺ influx.

• Phase 1: Transient K⁺ efflux.

• Phase 2 (plateau): Slow L-type Ca²⁺ influx ≈ K⁺ efflux.

• Phase 3: Ordinary K⁺ channels open → repolarisation.

• Phase 4: Leaky K⁺ channels maintain $-90\ \text{mV}$.

• Long refractory period prevents tetanus.

Excitation–Contraction Coupling

• AP → T-tubules → Ca²⁺ influx via L-type channels.

• Triggers Ca²⁺-induced Ca²⁺ release from SR.

• Ca²⁺ binds troponin → cross-bridge cycling → contraction; removal → relaxation.

Force & Stroke Volume Control

• Intrinsic: Starling law – ↑EDV stretches fibres toward optimal length → ↑stroke volume.

• Extrinsic: Sympathetic ↑Ca²⁺ entry → stronger, faster contractions; Parasympathetic mainly lowers rate.

Autonomic Regulation of Heart Rate

• SA intrinsic firing ≈ $100\ \text{beats/min}$.

• Resting HR (≈ $60–80$) set by dominant vagal tone (test with atropine → HR rises).

• Sympathetic stimulation ↑HR & conduction velocity.

Clinical Notes

• $CO = HR \times SV$: Bradycardia ↓HR → ↓CO → potential hypotension.

• Weakened/dilated heart (e.g., chronic alcohol) ↓contractility → ↓SV, ↓BP.

Cardiac Muscle Structure and Pump Function

• Spiral fibre orientation "wrings" blood from apex to base.

• Intercalated discs: desmosomes (strength) + gap junctions (electrical sync).

• Two cell types: contractile (99 %) vs autorhythmic (1 %).

• Specialized protein $\text{Troponin-C}$; elevated plasma levels diagnose myocardial infarction.

Dual Circulation & Ventricular Differences

• Right heart pulmonary circuit; mean pressure $\approx 15\ \text{mmHg}$.

• Left heart systemic circuit; mean arterial pressure $\approx 93\ \text{mmHg}$.

• Both eject $\approx 5\ \text{L/min}$; left ventricle thicker due to higher resistance.

Pacemaker (Autorhythmic) Cells

• Generate spontaneous action potentials (auto-rhythmicity).

• Pacemaker potential phases:
  

  • Phase 1: $I_f$ Na
    influx + ↓K
    efflux → slow depolarisation.
    

  • Phase 2: T-type $\text{Ca}^{2+}$ channels open → reach threshold.
    

  • Phase 3: L-type $\text{Ca}^{2+}$ channels open → rapid upstroke.
    

  • Phase 4: K
    channels open, Ca²⁺ channels close → repolarise to $-60\ \text{mV}$.

Conduction Pathway & Intrinsic Rates

• SA node: 70\100\ \text{AP/min} (primary pacemaker).

• AV node: 40\60; Bundle/ Purkinje: 20\40.

• Route: SA → interatrial & internodal tracts → AV (delay) → Bundle of His → branches → Purkinje → ventricles.

• Fibrous AV ring insulates atria from ventricles ensuring one-way spread.

Contractile Cell Action Potential

• Phase 0: Fast Na
  influx.

• Phase 1: Transient K
  efflux.

• Phase 2 (plateau): Slow L-type Ca²⁺ influx $\approx$ K
  efflux.

• Phase 3: Ordinary K
  channels open → repolarisation.

• Phase 4: Leaky K
  channels maintain $-90\ \text{mV}$.

• Long refractory period prevents tetanus.

Excitation

Contraction Coupling

• AP → T-tubules → Ca²⁺ influx via L-type channels.

• Triggers Ca²⁺-induced Ca²⁺ release from SR.

• Ca²⁺ binds troponin → cross-bridge cycling → contraction; removal → relaxation.

Force & Stroke Volume Control

• Intrinsic: Starling law – ↑EDV stretches fibres toward optimal length → ↑stroke volume.

• Extrinsic: Sympathetic ↑Ca²⁺ entry → stronger, faster contractions; Parasympathetic mainly lowers rate.

Autonomic Regulation of Heart Rate

• SA intrinsic firing $\approx 100\ \text{beats/min}$.

• Resting HR (\approx \ 60\80) set by dominant vagal tone (test with atropine → HR rises).

• Sympathetic stimulation ↑HR & conduction velocity.

Clinical Notes

• $CO = HR \times SV$: Bradycardia ↓HR → ↓CO → potential hypotension.

• Weakened/dilated heart (e.g., chronic alcohol) ↓contractility → ↓SV, ↓BP.