Overview
This lecture covers cardiac electrophysiology with a focus on the heart's intrinsic ability (automaticity) to generate action potentials, the cardiac conduction system, cellular communication, phases of action potentials, and muscle contraction.
Cardiac Automaticity and Myocardium Types
- The heart can depolarize and generate action potentials without nervous system input (automaticity).
- Myocardium contains two cell types: nodal (non-contractile, rhythm-setting) and contractile (force-producing).
- Nodal cells include SA node, AV node, AV/bundle of His, right and left bundle branches, and Purkinje fibers.
- Contractile cells contain proteins (actin, myosin, troponin, tropomyosin) and sarcoplasmic reticulum for contraction.
Cardiac Conduction System Pathway
- The SA node (pacemaker) is in the superior right atrium, sets the sinus rhythm (60-80 bpm).
- SA node sends impulses to the left atrium via Bachman’s bundle and throughout the right atrium via internodal pathways.
- All impulses converge at the AV node, which delays conduction by 0.1 sec to allow atrial contraction.
- Delay is due to fewer gap junctions and smaller fiber diameter in the AV node.
- Impulse then passes to the bundle of His, splits into right and left bundle branches, then into Purkinje fibers for ventricular contraction.
Nodal and Contractile Cell Action Potentials
- Nodal cells have unstable resting membrane potential (~-60 mV) due to "funny" sodium channels allowing slow Na+ influx.
- Once threshold (~-40 mV) is reached, L-type Ca2+ channels open, causing rapid depolarization.
- Repolarization occurs as K+ channels open and K+ exits the cell, returning potential to baseline.
- Contractile cells have stable resting membrane potential (~-85 to -90 mV), threshold at ~-70 mV.
- Depolarization (phase 0) via fast Na+ influx; initial repolarization (phase 1) by K+ outflow; plateau (phase 2) as Ca2+ influx balances K+ outflow; repolarization (phase 3) as K+ outflow dominates; resting (phase 4) is maintained by slow K+ leak.
Excitation-Contraction Coupling
- Ca2+ influx during the plateau triggers Ca2+ release from the sarcoplasmic reticulum via ryanodine receptors.
- Ca2+ binds troponin C, shifting tropomyosin to allow actin-myosin cross-bridge formation for contraction.
- Relaxation occurs as Ca2+ is pumped back into the sarcoplasmic reticulum or out of the cell by ATP-dependent pumps and Na+/Ca2+ exchangers.
Cellular Communication and Synchronization
- Gap junctions (made of connexin proteins) allow ion flow between cells, ensuring coordinated contraction.
- Desmosomes provide structural adhesion, combining with gap junctions to form intercalated discs.
- Cardiac muscle cells act as a functional syncytium, contracting together as a unit.
Key Terms & Definitions
- Automaticity — Heart's ability to generate action potentials without external stimuli.
- SA Node (Sinoatrial Node) — Primary pacemaker of the heart, sets sinus rhythm.
- AV Node (Atrioventricular Node) — Delays impulse before it reaches ventricles.
- Bundle of His — Conducts impulses from AV node to bundle branches.
- Purkinje fibers — Fibers distributing impulses through ventricular myocardium.
- Gap Junction — Protein channels enabling ion flow between cardiac cells.
- Desmosome — Protein structures adhering cardiac cells together.
- Intercalated disc — Complex of gap junctions and desmosomes between cardiac cells.
- Plateau phase — Prolonged depolarization in contractile cells due to Ca2+ influx.
Action Items / Next Steps
- Review muscle contraction mechanisms (focus on excitation-contraction coupling).
- Prepare for next lecture: extrinsic regulation of cardiac function (sympathetic and parasympathetic effects).
- Study conduction system anatomy and phases of the cardiac action potential.