Video 2 - Cardiac Conduction & Physiology

Types of Cardiac Muscle Cells

• Contractile (working) myocytes

  • Form the bulk of the atrial & ventricular walls.

  • Physically shorten (contract) to push blood.

• Conducting (autorhythmic) cells

  • Act like biological “wires.”

  • Generate & propagate electrical impulses that synchronize contractile cells.

Direction & Coordination of Contraction

• Atria must squeeze downward → drives blood through AV valves into ventricles.

• Ventricles must squeeze upward → pushes blood toward the pulmonary trunk & aorta, both located superior to ventricles.

• Proper sequencing requires a precisely timed electrical pathway (conduction system).

Cardiac Conduction System (electrical highway)

• SA (Sino-Atrial) Node

  • Located near the entrance of the superior vena cava, in right atrial wall, adjacent to the coronary sinus.

  • Nicknamed the heart’s pacemaker; initiates each heartbeat.

• Atrial pathways

  • Impulse spreads across atrial myocardium, causing atrial depolarization and downward contraction.

• AV (Atrioventricular) Node

  • Wedged between atria & ventricles in the inter-atrial septum.

  • Provides a brief delay, allowing ventricles to finish filling before they contract.

• AV Bundle (Bundle of His) & Bundle Branches

  • Conduct impulse along the interventricular (ventricular) septum.

• Apex

  • Electrical signal reaches the tip of the heart first.

• Purkinje Fibers

  • Ascend along inner ventricular walls → spread through myocardium → trigger upward ventricular contraction.

Sequence recap (cardiac cycle):

1. SA node fires.

2. Impulse sweeps across atria → atrial contraction.

3. Reaches AV node → slight pause.

4. Travels down septum to apex.

5. Spreads up outer ventricular walls → ventricular contraction (blood ejected upward).

Electrocardiogram (ECG / EKG)

• Records summed electrical activity from skin electrodes.

• P wave

  • \text{atrial depolarization}.

• QRS complex

  • \text{ventricular depolarization} (large amplitude because ventricular mass is larger).

  • Masks simultaneous \text{atrial repolarization}.

• T wave

  • \text{ventricular repolarization}.

• Interval between T & next P represents time for ventricular relaxation & filling.

• Languages using “K” for cardio → EKG (e.g.
  German “Kardiogramm”).

Illustrative animation (Wikipedia) shows real-time overlay of ECG trace with propagation of depolarization (purple/yellow) and repolarization (green) in heart chambers.

Cardiac Muscle Physiology (cross-bridge mechanics)

• Identical sliding-filament mechanism to skeletal muscle:

  1. Ca^{2+} binds troponin.

  2. Tropomyosin shifts → exposes myosin-binding sites on actin (orange beads).

  3. Myosin heads form cross-bridges → power stroke → contraction.

• Key difference lies in the action potential shape & ionic movements.

Cardiac Action Potential Characteristics

• Resting membrane potential: V_{rest} = -90\,\text{mV} (vs. -70\,\text{mV} in neurons).

• Threshold: V_{th} = -75\,\text{mV} (≈ +15 mV from rest).

• Depolarization Phase

  • Rapid Na^{+} influx up to +30\,\text{mV}.

  • Na^{+} channels then inactivate.

• Plateau Phase (signature feature)

  • Slow / leaky Ca^{2+} channels open as K^{+} leaves.

  • Influx of Ca^{2+} balances K^{+} efflux → membrane potential stays near 0 mV for ~200 ms (sustained depolarization).

• Repolarization

  • Ca^{2+} channels close; continued K^{+} efflux returns cell to V_{rest}.

• Absolute refractory period ≈ 250–300 ms (much longer than skeletal muscle).

Functional Importance of Plateau & Long Refractory Period

• Prevents tetanic contractions; heart cannot fire again until relaxation nearly complete.

• Guarantees time for ventricular filling between beats.

• Acts as natural rate-limiter so chamber contraction/relaxation cycle ≈ blood-flow demands.

Comparisons & Connections

• Neuron: short 1–2 ms spike → rapid, repeatable firing.

• Skeletal muscle fiber: brief twitch; frequency summation possible → sustained tetanus.

• Cardiac muscle: long plateau ensures one-and-done beat pattern; frequency summation impossible by design.

Practical / Clinical Relevance

• ECG interpretation hinges on understanding which waves map to which electrical events; deviations (e.g.
  prolonged PR, widened QRS) signal conduction blocks or myocardial damage.

• Drugs that alter Ca^{2+} channels (e.g.
  calcium-channel blockers) modify plateau duration → change contractility & rate.

• Artificial pacemakers mimic SA node firing when intrinsic conduction fails.

Study Tip: Practice sketching a standard ECG, labeling P, QRS, T, and mapping each to atrial/ventricular events. Link the ECG timeline to the physical pumping sequence to cement the electrical-mechanical correlation.