Electrical Conduction System of the Heart – Study Notes

Electrical components of the heartbeat

There are two distinct components of a heartbeat: electrical (conduction system) and mechanical (pumping/contraction).
Focus of this lecture: the electrical phenomenon, including automaticity (depolarization) and conduction across the heart.
Key question reviewed: what communicates cell-to-cell in the heart? Gap junctions (intercalated discs) enable cell-to-cell conduction.
Concept recap: depolarization and conduction are tied to how ions move across membranes and through channels; this lecture links those concepts to the heart specifically.

Depolarization, repolarization, and the ion basis

When a stimulus arrives, sodium rushes into the cell, causing depolarization: the membrane potential moves from relatively negative inside to more positive as Na+ enters.
During repolarization, potassium exits the cell, causing the membrane to return toward its resting negative state.
In the heart, the depolarization wave travels through cardiac cells, but the timing is different from neurons:
- Conduction is slower in the heart than in neurons; signals propagate through cardiac tissue at roughly 0.5 m/s cell-to-cell via gap junctions.
Absolute vs. relative refractory periods:
- Absolute refractory period: no new depolarization can occur regardless of stimulus.
- After this period, a stimulus can cause another depolarization if the membrane is sufficiently ready (relative refractory period).

Restoring ion gradients: the Na⁺/K⁺ pump

The Na⁺/K⁺-ATPase pump re-establishes the original ion gradients after depolarization:
- It exchanges 3 Na⁺ ions out of the cell for 2 K⁺ ions into the cell.
- This creates a net loss of positive charge from the inside, making the outside relatively more positive and the inside relatively more negative over time.
- Hence, after a depolarization, the “doors” (ion channels) must reset to allow the next cycle.
Simple analogy used in class: if you trade $100 for $200, you end up negative unless you balance the trade; similarly, the pump slowly makes the inside more negative relative to the outside if not balanced by other currents.

Automaticity and the “leaky” heart cells

The heart contains cells that can depolarize on their own (automaticity) without a prompt stimulus.
The rate of spontaneous depolarization depends on the rate of Na⁺ leak into the cell (how leaky the channels are).
Increasing the Na⁺ leak (opening more Na⁺ channels) speeds up reaching threshold and thus speeds up depolarization.
Epinephrine and other circulating hormones can increase the rate of Na⁺ leak, accelerating heart rate.
The professor uses the metaphor of “doors” (Na⁺ channels) that, when opened more, enhance the leak and speed conduction.

The cardiac conduction system anatomy (key components drawn in lectures)

SA node (sinoatrial node): the primary pacemaker; intrinsic rate ~60–100 bpm at rest; sets the heart rate under normal conditions.
AV node (atrioventricular node): secondary pacemaker with an intrinsic rate of ~40–60 bpm; provides the important delay to allow enough ventricular filling before contraction.
AV junction and bundle of His (AV bundle): conducts impulse from AV node to the ventricles; faster conduction continues through the bundle branches.
Bundle branches: right bundle branch and left bundle branch; left bundle subdivides into anterior and posterior branches.
Purkinje fibers: distribute impulse throughout the ventricles to coordinate rapid, synchronized contraction.
Bachmann’s bundle (interatrial tract): helps conduct impulse between the atria; the instructor notes not drawing all internodal tracts in detail but often shows a single internodal tract to represent this pathway.
Perkinje fibers may be shown as a network around the ventricles to illustrate rapid ventricular activation.
Valves, papillary muscles, and chordae tendineae provide the anatomical context for ventricular contraction and valve operation; these structures interact with the timing of depolarization and contraction.

Sequence of electrical spread and mechanical timing

The electrical signal starts at the SA node and spreads through the atria via direct cell-to-cell contact (gap junctions).
Atrial depolarization leads to atrial contraction, which helps move blood from the atria into the ventricles.
The impulse then reaches the AV node, where the conduction slows to allow ventricular filling before ventricles contract.
After AV node delay, the impulse travels down the AV bundle, through the bundle branches, and into the Purkinje system to activate the ventricles nearly simultaneously.
The pattern: electrical signal first through atria, then ventricles; mechanical response (muscle contraction) follows the electrical activation in a coordinated fashion.

Conduction velocity and timing details (illustrative values)

Cell-to-cell conduction velocity through atrial myocardium: approximately $v \,\approx\,0.5\ \text{m/s}$ .
Intrinsic firing rates (inherent automaticity) without brain input:
- SA node: $60 \text{ to } 100\ \text{beats per minute (bpm)}$
- AV node: $40 \text{ to } 60\ \text{bpm}$
The SA node acts as the number one pacemaker; the brain and circulating hormones modulate the rate by altering Na⁺ leakiness.

Autonomic and higher-level control of heart rate

Sympathetic (fight or flight) input increases heart rate by increasing Na⁺ leak and conduction velocity in the conduction system.
Parasympathetic (rest and digest) input decreases heart rate by reducing the rate of spontaneous depolarization.
In a healthy heart, the SA node typically sets the pace, and downstream nodes (AV node, His-Purkinje system) follow unless pathological conditions alter the system.

Practical implications and conceptual connections

Why the SA node is the primary pacemaker: it has the highest intrinsic depolarization rate (resting rate) and provides a normal baseline rhythm.
AV node’s role as a gatekeeper ensures timely ventricular filling by delaying conduction; its slower intrinsic rate reduces the risk of excessively rapid ventricular rates.
If the SA node fails, other pacemaker tissues can take over but with slower rates (e.g., AV node 40–60 bpm), which may be inadequate for physiological demands.
The conduction system must be coupled with mechanical timing to ensure efficient cardiac output (atrial contraction contributes to ventricular filling before ventricles contract).
The interplay of auto depolarization, gap junctions, and autonomic input explains normal variability in heart rate with activity, stress, and hormonal changes.

Key terms and quick references

Automaticity: ability of some cardiac cells to depolarize spontaneously without external stimulus.
Depolarization: movement toward a more positive membrane potential due to Na⁺ influx.
Repolarization: return toward resting negative membrane potential due to K⁺ efflux.
Absolute refractory period: interval when no new depolarization can occur.
Relative refractory period: interval when a strong stimulus may cause a depolarization.
Gap junctions: cell-to-cell connections that allow ionic currents to pass between cardiomyocytes.
Na⁺/K⁺-ATPase pump: exchanges 3 Na⁺ out for 2 K⁺ in, maintaining gradients and contributing to resting potential.
SA node: primary pacemaker of the heart (60–100 bpm).
AV node: secondary pacemaker with intrinsic rate 40–60 bpm; provides delay.
Bundle of His, bundle branches, Purkinje fibers: conduction pathways to ventricles.
Bachmann’s bundle: interatrial conduction pathway.
Epinephrine: circulating hormone that can increase Na⁺ leak and heart rate.

Summary takeaway

The heartbeat’s electrical component relies on automaticity, orderly conduction through a defined pathway, and autonomic modulation to meet physiological demands, all while coordinating the timing of atrial and ventricular contractions to optimize blood flow and cardiac output.