1.2 Cardiac Electrophysiology & Conduction System
Key Takeaways
- The SA node is the primary pacemaker with an intrinsic rate of 60-100 bpm.
- The AV node acts as the secondary pacemaker (40-60 bpm) and delays the electrical impulse by ~0.1 seconds to allow atrial kick.
- Purkinje fibers constitute the tertiary pacemaker system (20-40 bpm) and ensure rapid, synchronized ventricular contraction.
- The cardiac action potential involves 5 phases (0-4), primarily driven by the movement of sodium (Na+), potassium (K+), and calcium (Ca2+) ions.
Cardiac Electrophysiology & Conduction System
While the myocardial muscle performs the mechanical work of pumping blood, it is completely dependent on the electrical conduction system to dictate the rate and rhythm of those contractions. Understanding electrophysiology is the core competency required for accurate electrocardiogram (ECG) interpretation.
1. Properties of Cardiac Cells
Cardiac tissue is unique because it possesses four specialized electrical and mechanical properties:
- Automaticity: The ability of pacemaker cells to spontaneously initiate an electrical impulse without external stimulation.
- Excitability (Irritability): The ability of cardiac cells to respond to an electrical stimulus.
- Conductivity: The ability to transmit an electrical impulse from one cell to another via specialized structures called gap junctions (intercalated discs).
- Contractility: The mechanical ability of the muscle fibers to shorten and pump blood in response to an electrical stimulus.
Exam Trap: Automaticity, Excitability, and Conductivity are electrical properties. Contractility is a mechanical property. An ECG measures only electrical activity; it cannot confirm mechanical contraction (which is why a patient can have a normal ECG but no pulse, a condition known as Pulseless Electrical Activity or PEA).
2. The Cardiac Conduction Pathway
The electrical impulse follows a precise anatomical pathway to ensure coordinated contraction of the atria followed by the ventricles.
Sinoatrial (SA) Node
- Location: High in the posterior wall of the right atrium, near the opening of the Superior Vena Cava.
- Function: The heart's primary, natural pacemaker.
- Intrinsic Rate: 60 to 100 beats per minute (bpm).
- Mechanism: Initiates the electrical impulse that spreads across both atria, causing atrial depolarization (represented by the P wave on the ECG).
Internodal Pathways & Bachmann's Bundle
- The impulse travels from the SA node to the AV node via three internodal tracts in the right atrium (Anterior, Middle/Wenckebach, Posterior/Thorel).
- Simultaneously, the impulse is conducted to the left atrium via Bachmann's Bundle, ensuring both atria contract almost simultaneously.
Atrioventricular (AV) Node
- Location: Inferior interatrial septum, near the coronary sinus ostium.
- Function: Acts as an electrical relay station and the "gatekeeper" to the ventricles.
- Crucial Role: The AV node delays the electrical impulse for approximately 0.1 seconds. This delay is hemodynamically vital as it allows the atria time to finish contracting and empty their blood into the ventricles (providing the "atrial kick" which accounts for 15-30% of cardiac output) before ventricular systole begins.
- Intrinsic Rate: 40 to 60 bpm (serves as a backup pacemaker if the SA node fails).
Bundle of His (AV Bundle)
- The impulse travels from the AV node into the Bundle of His, which quickly penetrates the fibrous skeleton of the heart to enter the interventricular septum.
Bundle Branches
- The Bundle of His bifurcates into the Right Bundle Branch (RBB) and the Left Bundle Branch (LBB).
- The RBB travels down the right side of the septum to depolarize the right ventricle.
- The LBB divides further into the Left Anterior Fascicle and the Left Posterior Fascicle to rapidly depolarize the massive left ventricle.
Purkinje Fibers
- Location: Spread throughout the subendocardial surface of both ventricular myocardia.
- Function: Distribute the electrical impulse extremely rapidly to the ventricular muscle cells, ensuring a synchronized, forceful contraction from the apex upward toward the great vessels.
- Intrinsic Rate: 20 to 40 bpm (the final, tertiary backup pacemaker).
3. The Cardiac Action Potential
At the cellular level, electrical impulses are generated by the movement of electrolytes (ions) across the cell membrane. The most critical ions in cardiac electrophysiology are Sodium (Na+), Potassium (K+), and Calcium (Ca2+).
The Resting Membrane Potential
In a resting state, cardiac cells are polarized. The inside of the cell is negatively charged relative to the outside (approximately -90 mV). This is maintained by the Sodium-Potassium pump, which continually pushes Na+ out of the cell and pulls K+ in.
The 5 Phases of the Action Potential (Non-Pacemaker Cells)
| Phase | Name | Cellular Event (Ion Movement) | ECG Correlation |
|---|---|---|---|
| Phase 0 | Rapid Depolarization | Massive influx of Sodium (Na+) into the cell. The cell rapidly becomes positive. | QRS Complex |
| Phase 1 | Early Repolarization | Fast Na+ channels close. Brief outflow of Potassium (K+). | J-point |
| Phase 2 | Plateau Phase | Slow influx of Calcium (Ca2+) balanced by K+ outflow. Triggers actual muscle contraction. | ST Segment |
| Phase 3 | Rapid Repolarization | Calcium channels close. Rapid outflow of Potassium (K+). Cell returns to negative state. | T Wave |
| Phase 4 | Resting Phase | Cell is at resting membrane potential. Na+/K+ pump restores ionic balance. | Baseline (Isoelectric Line) |
4. Refractory Periods
Refractory periods are protective mechanisms preventing the heart from being stimulated too rapidly, which would lead to tetany (continuous contraction without relaxation).
- Absolute Refractory Period (ARP): Encompasses Phase 0, 1, 2, and the first half of Phase 3. During this time, the cardiac cell cannot respond to ANY electrical stimulus, no matter how strong. This prevents fatal arrhythmias.
- Relative Refractory Period (RRP): Occurs during the second half of Phase 3 (the downslope of the T wave). A sufficiently strong stimulus can cause a premature depolarization. This is a vulnerable period (e.g., "R-on-T phenomenon"), which can trigger Ventricular Fibrillation.
What is the primary physiological purpose of the conduction delay at the AV node?
During which phase of the cardiac action potential in non-pacemaker cells is there a significant influx of Calcium (Ca2+) that sustains the plateau phase and triggers mechanical contraction?
If the Sinoatrial (SA) node fails, what is the expected intrinsic firing rate of the Atrioventricular (AV) junctional pacemaker?
Which portion of the cardiac cycle represents the Relative Refractory Period, a vulnerable time when a strong electrical stimulus could trigger a lethal arrhythmia like Ventricular Fibrillation?