Cardiac Arrhythmias

Mechanisms of Pathological Automaticity

Pathological automaticity (ectopic activity) can originate in the atria, ventricles, bundle of His, or Purkinje fibers. The fundamental mechanism involves partial depolarization of cardiomyocytes and conduction system cells.

The primary mechanism driving ectopic impulses is triggered activity, which occurs via two types of afterdepolarizations:

• Early afterdepolarizations (EADs). These develop during phase 3 of the action potential (repolarization). Their development requires specific conditions: a slow heart rate, prolongation of the $QT$ interval (increased action potential duration), and low intracellular potassium ($K^+$) levels. A classic clinical example of this disturbance is torsade de pointes. Etiologically, EADs are often linked to enhanced parasympathetic tone, such as in neurosis or hypothyroidism.
• Delayed afterdepolarizations (DADs). These form after complete repolarization has occurred. Unlike EADs, they arise in the setting of an accelerated heart rate. The mechanism is driven by cardiomyocyte overload with calcium ions ($Ca^{2+}$) due to excessive adrenergic stimulation. Key causes include myocardial hypertrophy, heart failure, cardiac glycoside toxicity, and myocardial reperfusion (e.g., following thrombolytic therapy).

Classification by Rhythm Origin

Depending on where the electrical impulse originates, rhythm disturbances are divided into two major groups.

1. Nomotopic Arrhythmias The impulse originates in the normal pacemaker—the sinoatrial node—however, the rate or regularity of its generation is altered. This group includes:

• Sinus tachycardia.
• Sinus bradycardia.
• Sinus arrhythmia.
• Sick sinus syndrome (SSS), which may clinically manifest as tachy-bradycardia syndrome.

2. Heterotopic Arrhythmias The impulse is generated outside the sinoatrial node, meaning an ectopic pacemaker drives the rhythm. The main types include:

• Low atrial rhythm.
• Atrioventricular (junctional) rhythm.
• Idioventricular (ventricular) rhythm.

Special forms of heterotopic disturbances also include wandering pacemaker, escape beats, and AV dissociation with interference.

Sinus Tachycardia

Sinus tachycardia is defined as an increased rate of impulse generation by the sinoatrial node at rest (typically greater than 100 beats per minute) with regular intervals between beats. The electrophysiological mechanism involves an acceleration of spontaneous diastolic depolarization of the plasma membrane in nodal cells.

Main Causes:

1. Activation of the sympathoadrenal system. This occurs during emotional stress, physical exertion, neurosis, hyperthermia, and fever. Sympathetic influence is also enhanced during acute arterial hypotension (mediated by baroreceptor afferent signaling) and in heart failure. In heart failure, tachycardia results from increased venous return to the right atrium, which triggers the Bainbridge reflex.
2. Reduction in parasympathetic nervous system tone, which can result from various forms of neural or tissue damage.

Sinus Bradycardia

A slowed heart rate results from the opposite mechanisms: enhanced parasympathetic tone or diminished sympathetic influence.

Enhanced parasympathetic tone is observed during:

• Irritation of the vagus nerve (n. vagus) nuclei due to elevated intracranial pressure (meningitis, encephalitis).
• Stimulation of vagal nerve endings secondary to increased intraventricular pressure and myocardial tension.
• Reflex stimulation: pressure on the eyeballs (Aschner-Dagnini reflex), manipulation of the carotid sinus bifurcation (Hering's reflex), or stimulation of the solar plexus.

Diminished sympathoadrenal effects on the heart develop during:

• Neurotic states.
• Damage to brain structures (including the hypothalamus) and conduction pathways.
• Injury to intracardiac ganglia and sympathetic nerve endings directly within the myocardium.
• Decreased adrenoreceptor responsiveness of the heart itself.