19.2 Cardiac Muscle and Electrical Activity

Cardiac Muscle Tissue

Cardiac muscle tissue drives the heart's continuous pumping action. Its unique structural features allow millions of individual cells to contract as a unified whole, and its built-in electrical system keeps the heart beating without any conscious effort.

Structural Features of Cardiac Muscle

Cardiac muscle cells (cardiomyocytes) differ from skeletal muscle fibers in several important ways. They're shorter and wider than skeletal muscle cells, with ventricular cardiomyocytes measuring roughly 100 μm long and 10–25 μm wide. Their branching shape increases the surface area available for cell-to-cell connections and force generation.

Intercalated discs are the specialized junctions that connect adjacent cardiomyocytes end-to-end. They contain three key components:

• Gap junctions allow ions to flow directly between cells, electrically coupling them so an impulse can spread rapidly from one cell to the next
• Desmosomes act like rivets, providing mechanical strength so cells don't pull apart during forceful contractions
• Fascia adherens anchor actin filaments to the cell membrane, transmitting contractile force efficiently between cells

The myocardium, the middle and thickest layer of the heart wall, is composed of this cardiac muscle tissue. Like skeletal muscle, it contains sarcomeres, the repeating contractile units responsible for the actual shortening of the cell.

High mitochondrial content is another defining feature. Mitochondria occupy roughly 30–40% of a cardiomyocyte's volume. That's because the heart relies almost entirely on oxidative phosphorylation (aerobic ATP production) to fuel its nonstop contraction-relaxation cycle.

Autorhythmicity sets cardiac muscle apart from all other muscle types. Specialized pacemaker cells in the SA and AV nodes have unstable resting membrane potentials that spontaneously drift toward threshold and depolarize on their own. This means the heart generates its own rhythm without requiring signals from the nervous system.

Electrical Activity of the Heart

The heart's conduction system is a network of specialized cells that initiate and distribute electrical impulses in a precise sequence, ensuring the atria contract before the ventricles and that ventricular contraction is coordinated from apex to base.

Components of the Cardiac Conduction System

The pathway of an electrical impulse through the heart follows this order:

1. Sinoatrial (SA) node — the primary pacemaker, located in the right atrium near the superior vena cava opening. It has the fastest intrinsic depolarization rate (~60–100 bpm), so it sets the pace for the entire heart.
2. Atrioventricular (AV) node — positioned in the interatrial septum near the tricuspid valve. It receives the impulse from the SA node and deliberately delays transmission (~0.1 s). This delay gives the atria time to finish contracting and fill the ventricles before ventricular contraction begins.
3. Bundle of His — carries the impulse rapidly from the AV node into the interventricular septum, where it splits into the left and right bundle branches.
4. Purkinje fibers — the terminal branches that fan out through the ventricular walls. They conduct impulses extremely fast, enabling the ventricles to contract in a coordinated wave from the apex upward toward the base. This bottom-to-top pattern efficiently ejects blood into the great arteries.

Ion Movements in Cardiac Cells

The action potential in a contractile cardiomyocyte is much longer than in skeletal muscle, and that difference is critical for heart function. Here's how it unfolds:

• Resting membrane potential sits around $-90 \text{ mV}$, maintained mainly by open $K^+$ leak channels and the high intracellular $K^+$ concentration.
• Phase 0 (Rapid depolarization): Voltage-gated $Na^+$ channels open, allowing a fast influx of $Na^+$. The membrane potential shoots toward approximately $+30 \text{ mV}$.
• Phase 1 (Initial repolarization): $Na^+$ channels inactivate and a brief outward $K^+$ current causes a small dip in voltage.
• Phase 2 (Plateau): This is what makes cardiac action potentials unique. $Ca^{2+}$ ions flow in through L-type calcium channels while $K^+$ outflow is reduced. These opposing currents hold the membrane in a depolarized state for 200–400 ms, sustaining contraction far longer than in skeletal muscle.
• Phase 3 (Repolarization): L-type $Ca^{2+}$ channels close and delayed rectifier $K^+$ channels open, allowing $K^+$ efflux to restore the resting potential. The $Na^+/K^+$ ATPase pump also helps re-establish ion gradients.
• Phase 4 (Resting): The cell returns to $-90 \text{ mV}$ and awaits the next impulse.

The long plateau phase creates an extended refractory period during which the cell cannot be re-stimulated. This prevents tetanic contractions (sustained, fused contractions) that would stop the heart from filling between beats.

ECG Interpretation and the Cardiac Cycle

An electrocardiogram (ECG) records the electrical activity of the heart from the body surface. Willem Einthoven developed the first practical ECG in the early 20th century, and it remains one of the most widely used diagnostic tools in medicine. Each waveform corresponds to a specific electrical event:

• P wave — represents atrial depolarization (the signal spreading across both atria). Normal duration is less than 0.12 s with amplitude under 2.5 mm. An absent P wave may indicate atrial fibrillation or SA node dysfunction.
• QRS complex — represents ventricular depolarization. Normal duration is less than 0.12 s. Atrial repolarization also occurs during this time but is hidden by the much larger ventricular signal. A widened QRS (>0.12 s) suggests a bundle branch block or ventricular hypertrophy.
• T wave — represents ventricular repolarization. It's typically upright in most leads. Inverted or flattened T waves can indicate myocardial ischemia or electrolyte imbalances.

Key intervals to know:

• PR interval (start of P wave to start of QRS): Measures conduction time from atrial depolarization through the AV node to the start of ventricular depolarization. Normal range is 0.12–0.20 s. A prolonged PR interval signals AV conduction delay (first-degree AV block).
• QT interval (start of QRS to end of T wave): Encompasses total ventricular depolarization and repolarization. Because it varies with heart rate, it's often corrected using Bazett's formula:

$QTc = \frac{QT}{\sqrt{RR}}$

A prolonged QTc (>450 ms in men, >460 ms in women) raises the risk of dangerous ventricular arrhythmias.

The mechanical events of the cardiac cycle (systole and diastole) are driven by these electrical events. The Frank-Starling law governs how forcefully the ventricles contract: the more the ventricular wall stretches during filling (increased preload), the greater the force of the subsequent contraction.

Cardiac Conduction Abnormalities

• Sinus bradycardia — heart rate below 60 bpm originating from the SA node. Common causes include increased vagal tone, beta-blocker medications, and hypothyroidism. Often benign (athletes frequently have resting bradycardia), but severe cases can cause fatigue or dizziness.
• Sinus tachycardia — heart rate above 100 bpm initiated by the SA node. Usually a normal physiological response to exercise, fever, or stress. Pathological causes include anemia and hyperthyroidism. Treatment targets the underlying cause rather than the tachycardia itself.
• Atrioventricular (AV) block — impaired conduction between atria and ventricles, classified by severity:
  • First-degree: PR interval >0.20 s, but every impulse still reaches the ventricles
  • Second-degree: Some P waves are not followed by QRS complexes. Mobitz Type I (Wenckebach) shows progressive PR prolongation before a dropped beat; Mobitz Type II drops beats without warning and is more serious
  • Third-degree (complete): No communication between atrial and ventricular rhythms. The ventricles beat on their own escape rhythm, typically requiring a pacemaker
• Bundle branch block — impaired conduction in the left or right bundle branch, producing a widened QRS complex (>0.12 s). Left bundle branch block (LBBB) is more clinically concerning and may indicate underlying cardiomyopathy or heart disease.
• Atrial fibrillation — rapid, chaotic electrical activity in the atria, with multiple ectopic foci firing at 300–600 impulses per minute. The atria quiver rather than contract effectively, producing an irregularly irregular ventricular rhythm. A major clinical concern is that blood pools in the poorly contracting atria, forming clots that can travel to the brain and cause stroke.