Cardiac Electrophysiology Study Notes

Cardiac Electrophysiology Study Notes

1. Introduction

• The heart exhibits automaticity, meaning it can intrinsically depolarize itself and trigger action potentials without nervous system input.

• The nervous system (extrinsic innervation) can modulate heart rate and contractility.

Key Concept:
Automaticity = intrinsic ability of the heart to spontaneously depolarize → triggers action potentials → spreads to myocardium → causes contraction.

2. Myocardium Structure

The myocardium has two types of cells:

A. Nodal Cells (Non-contractile)

• Generate automaticity and action potentials.

• Do not contract.

• Key structures:

  • SA node (Sinoatrial node) – primary pacemaker

  • AV node (Atrioventricular node)

  • AV bundle (Bundle of His)

  • Right and Left Bundle Branches

  • Purkinje fibers – specialized conduction fibers in ventricles

Function: Set the rhythm of the heart and conduct electrical impulses.

B. Contractile Cells

• Composed of contractile proteins (actin, myosin, troponin, tropomyosin).

• Contain sarcoplasmic reticulum (SR).

• Generate force to pump blood.

3. Cardiac Conduction System

Flow of Electrical Impulses:

1. SA Node (Pacemaker)

   • Location: Superior right atrium near the superior vena cava.

   • Sets sinus rhythm: ~60–80 bpm (intrinsic rate).

2. Atrial Conduction

   • Bachmann’s bundle: Right atrium → Left atrium.

   • Internodal pathways: Spread impulses within the right atrium.

3. AV Node

   • Location: Base of right atrium near interventricular septum.

   • 0.1-second delay: Allows atrial contraction before ventricular contraction.

   • Reason for delay:

     • Smaller fiber diameter → slower conduction

     • Fewer gap junctions → slower ion flow

4. Bundle of His (AV Bundle)

   • Conducts impulses from AV node → right and left bundle branches.

5. Bundle Branches

   • Right bundle branch → right ventricle

   • Left bundle branch → left ventricle

6. Purkinje Fibers

   • Terminal fibers spreading impulses to ventricular myocardium → ventricular contraction.

Recap of Conduction Sequence:
SA node → Bachmann’s bundle & internodal pathways → AV node (0.1 s delay) → Bundle of His → Right/Left bundle branches → Purkinje fibers → Ventricles contract.

4. Cellular Electrophysiology

A. Nodal Cell Action Potential

1. Resting membrane potential: ~-60 mV (unstable).

2. Depolarization steps:

   • Funny Na⁺ channels: Slowly allow Na⁺ influx → membrane potential rises to -55 mV.

   • T-type Ca²⁺ channels: Open ~-55 mV → Ca²⁺ influx.

   • Threshold (~-40 mV):

     • L-type Ca²⁺ channels open → rapid Ca²⁺ influx → depolarization to ~+40 mV.

3. Repolarization

   • Ca²⁺ channels close → K⁺ channels open → K⁺ exits → membrane repolarizes.

4. Cycle repeats: Funny Na⁺ channels reopen → spontaneous depolarization.

Key Concept: Nodal cells do not require external nervous input to depolarize.

B. Contractile (Myocardial) Cell Action Potential

Phases of Action Potential:

Phase	Description
0	Rapid depolarization: Voltage-gated Na⁺ channels open → Na⁺ influx → membrane potential rises.
1	Initial repolarization: K⁺ channels open slightly, small Ca²⁺ influx → membrane potential drops slightly.
2	Plateau phase: Ca²⁺ influx through L-type channels balanced by K⁺ efflux → sustained depolarization → contraction.
3	Repolarization: Ca²⁺ channels close, K⁺ efflux dominates → returns to resting potential.
4	Resting membrane potential: K⁺ leak channels maintain baseline until next stimulus.

Calcium-Induced Calcium Release:

• Ca²⁺ influx via L-type channels triggers Ryanodine Receptors (RyR2) in SR → massive Ca²⁺ release.

• Ca²⁺ binds troponin C, moves tropomyosin, exposes actin → cross-bridge formation → contraction.

Repolarization & Calcium Removal:

• Ca²⁺ pumped back into SR via Ca²⁺-ATPase (primary active transport).

• Ca²⁺ extruded via Na⁺/Ca²⁺ exchanger (secondary active transport).

5. Intercellular Communication

• Gap junctions: Channels allowing ions to flow between cells → synchronize depolarization.

• Desmosomes: Structural proteins holding cells together during contraction.

• Intercalated discs: Combination of gap junctions + desmosomes, essential for coordinated contraction.

Functional syncytium:

• Cardiac cells contract as a unit due to interconnected gap junctions → synchronized heartbeat.

6. Summary of Key Points

1. Heart exhibits automaticity → can beat without nervous input.

2. SA node = primary pacemaker → sets sinus rhythm (~60–80 bpm).

3. AV node delay (0.1 s) allows atria to empty before ventricles contract.

4. Nodal cells → depolarize via funny Na⁺ channels → T-type & L-type Ca²⁺ channels.

5. Contractile cells → depolarize via Na⁺ influx, plateau with Ca²⁺ influx → repolarize via K⁺ efflux.

6. Calcium-induced calcium release → activates troponin → contraction.

7. Intercalated discs (gap junctions + desmosomes) → synchronized contraction (functional syncytium).

8. Calcium handling restores resting state via ATP-dependent pumps and Na⁺/Ca²⁺ exchangers.