Overview
This lecture covers the structure and function of cardiac muscle, focusing on action potentials, excitation-contraction coupling, and the key differences between cardiac and skeletal muscle.
Cardiac Muscle Structure & Function
- The heart is a muscular organ made of four chambers: left/right atria and left/right ventricles.
- The heart acts as two separate pumps: right heart (pumps deoxygenated blood to lungs) and left heart (pumps oxygenated blood to tissues).
- Cardiac muscle is involuntary and features automaticity (self-initiated contractions).
- Three cardiac muscle types: atrial muscle, ventricular muscle, and specialized conduction fibers.
- eCardiac muscle has striated actin and myosin like skeletal muscle but functions as a syncytium (contracts as one unit).
- Gap junctions in intercalated discs allow rapid ion diffusion between cells, enabling coordinated contraction.
Cardiac Action Potential
- Divided into phases:
- Phase 4 (Resting, -85 mV)
- Phase 0 (Rapid depolarization, sodium influx)
- Phase 1 (Initial rapid repolarization, potassium exits, chloride enters)
- Phase 2 (Plateau, slow calcium and sodium influx)
- Phase 3 (Rapid repolarization, potassium exits, calcium/sodium channels close)
- Sodium-potassium pump restores ionic gradients after action potential.
- Cardiac action potential lasts much longer than skeletal muscle (prolonged plateau due to slow calcium/sodium channels and decreased potassium permeability).
Refractory Periods
- Absolute refractory period: No new action potential possible (ventricles: 0.25–0.30 s; atria: 0.15 s).
- Relative refractory period: Possible only with strong stimuli (0.05 s).
- Early extrasystoles can occur during the relative refractory period.
Excitation-Contraction Coupling
- Action potential triggers opening of voltage-dependent calcium channels in cell membrane and sarcoplasmic reticulum.
- Calcium influx binds to troponin C, shifting tropomyosin, exposing myosin-binding sites on actin.
- Myosin heads bind actin, hydrolyze ATP, and cause contraction (sarcomere shortens).
- Relaxation occurs when calcium is pumped back by sarcoplasmic reticulum, sodium-calcium, and membrane calcium pumps.
Modulation of Contraction
- Sympathetic stimulation (β1-adrenergic receptors) increases calcium entry, enhancing contraction force.
- Cardiac glycosides (e.g., digitalis) inhibit Na⁺/K⁺ pump, raising intracellular sodium and calcium, thus increasing contraction strength.
Key Terms & Definitions
- Syncytium — A network of cells acting as one functional unit.
- Intercalated discs — Specialized connections with gap junctions between cardiac muscle cells.
- Action potential — Rapid change in membrane voltage causing muscle contraction.
- Plateau phase — Prolonged depolarization due to slow calcium entry.
- Absolute refractory period — Time when no new action potential can occur.
- Troponin C — Protein that binds calcium to initiate contraction.
- β1-adrenergic receptor — Receptor stimulated by adrenaline/noradrenaline to increase heart contraction.
- Cardiac glycosides — Drugs increasing contraction force by inhibiting Na⁺/K⁺ pump.
Action Items / Next Steps
- Prepare for next class: Study the cardiac cycle and details of atrioventricular conduction.
- Recommended reading: Guyton Physiology, 12th edition, and Pathophysiology, 9th edition.