Electrocardiography & Cardiac Muscle Physiology

Electrocardiography Basics

• An electrocardiogram (ECG) is a graphic record of overall heart electrical activity—​a composite of all nodal and contractile-cell action potentials occurring at a given instant, not a tracing of a single cell’s action potential.
• Electrical currents generated by the heart spread through body fluids and are detectable at the skin by surface electrodes.
• Standard clinical setup = 12-lead ECG:
– 3 bipolar limb leads (measure voltage differences between either two arms or an arm and a leg).
– 9 unipolar leads (augmented limb + pre-cordial/chest leads).
• Collectively, the 12 leads furnish a comprehensive, three-dimensional view of cardiac electrical events.

Principal ECG Waves & Deflections

• A normal tracing displays three immediately recognizable deflections:

1. P wave
   – Duration ≈ 0.08\,\text{s}.
   – Represents depolarization spreading from the sinoatrial (SA) node across both atria.
   – Atrial contraction begins ≈ 0.1\,\text{s} after the wave’s onset.
2. QRS complex
   – Average duration ≈ 0.08\,\text{s}.
   – Reflects ventricular depolarization; always precedes ventricular systole.
   – Complex morphology arises from continuously shifting depolarization vectors through thick ventricular walls; timing varies slightly with ventricular size disparity.
3. T wave
   – Duration ≈ 0.16\,\text{s}.
   – Caused by ventricular repolarization.
   – Lower amplitude & broader spread than QRS because repolarization is slower.
   – Atrial repolarization occurs simultaneously with the QRS complex and is therefore hidden.

Intervals & Segments

• P–R (or P–Q) interval
– ≈ 0.16\,\text{s} from onset of atrial depolarization to onset of ventricular depolarization (first visible Q, if present).
– Encompasses atrial depolarization/​contraction plus conduction through AV node, AV bundle, bundle branches, and Purkinje fibers.
• S–T segment
– Denotes the plateau phase of ventricular myocyte action potentials when the entire ventricular myocardium is depolarized.
• Q–T interval
– ≈ 0.38\,\text{s} from beginning of QRS to end of T wave: covers entire period of ventricular depolarization and repolarization.

Electrical–Mechanical Coupling Timeline (Figure-based Ordering)

1. SA-node-initiated atrial depolarization → P wave.
2. Depolarization completes; impulse delayed at AV node (flat line after P wave).
3. Ventricular depolarization begins at apex → QRS complex; simultaneous atrial repolarization.
4. Ventricular depolarization ends; ventricles fully excited (isoelectric segment after QRS).
5. Ventricular repolarization starts at apex → T wave.
6. Ventricular repolarization completes; heart electrically quiet until next cycle.

Contractile Cardiac Muscle Action Potential (Figure 18.15)

• Resting membrane potential ≈ -90\,\text{mV}.

1. Rapid depolarization
   – Fast voltage-gated \text{Na}^+ channels open.
   – Membrane voltage reverses to ≈ +30\,\text{mV}.
   – Channels inactivate rapidly, ending Na⁺ influx.
2. Plateau phase
   – Depolarization opens delayed slow \text{Ca}^{2+} channels allowing extracellular \text{Ca}^{2+} influx.
   – Few \text{K}^+ channels are open ⇒ prolonged depolarization (≈ 200\,\text{ms}).
   – Cytosolic \text{Ca}^{2+} triggers cross-bridge cycling; mechanical tension develops & peaks near plateau end.
3. Repolarization
   – \text{Ca}^{2+} channels inactivate; voltage-gated \text{K}^+ channels open.
   – Rapid \text{K}^+ efflux restores resting potential; \text{Ca}^{2+} pumped back into sarcoplasmic reticulum & extracellular space.

Functional Consequences of the Plateau

• Extended action potential (≈ 200\,\text{ms}) & contraction (≈ 200\,\text{ms}) versus skeletal muscle AP (≈ 1–2\,\text{ms}) & twitch (≈ 15–100\,\text{ms}).
• Guarantees:
– Sustained, forceful ventricular contraction → efficient blood ejection.
– Long absolute refractory period prevents tetanic contractions, ensuring chambers refill before next beat.

Pacemakers & Rhythm Modification

• Failure of atrial impulses to reach ventricles (e.g., AV block) may necessitate implantable artificial pacemakers.
– Devices “recouple” atria & ventricles, adjust pacing to physical activity, and can relay diagnostic data remotely.
• Intrinsic conduction sets basic rhythm, but autonomic innervation fine-tunes it:
– Sympathetic (accelerator)
• Origin: cardioacceleratory center, medulla oblongata.
• Preganglionic neurons in spinal cord segments T1–T5 → cervical & upper thoracic sympathetic trunk ganglia.
• Postganglionic fibers traverse cardiac plexus to SA node, AV node, myocardium & coronary arteries.
• Effect: ↑ heart rate and ↑ contractile force.
– Parasympathetic (brakes)
• Origin: cardioinhibitory center → dorsal vagus nucleus.
• Vagus nerve (cranial X) carries inhibitory fibers; most postganglionic neurons lie in intrinsic cardiac ganglia.
• Fibers project mainly to SA & AV nodes.
• Effect: ↓ heart rate.

Clinical & Physiological Implications

• Temporal precedence – electrical events (depolarization/​repolarization) always occur just before corresponding mechanical events (contraction/​relaxation).
• Deviations in wave shape, interval length, or segment level provide diagnostic clues (e.g., myocardial ischemia elevates/​depresses S–T; prolonged Q–T predisposes to arrhythmias).
• Autonomic imbalance, conduction blocks, or electrolyte disturbances can be identified via characteristic ECG alterations.