Mechanisms of abnormal automaticity
Pathological automaticity (ectopic activity) can localize to the atria, ventricles, bundle of His, or Purkinje fibers. The fundamental mechanism of this phenomenon is partial depolarization of cardiomyocytes and conduction system cells.
The primary mechanism underlying ectopic impulses is triggered activity, which manifests through two types of afterdepolarization:
- Early afterdepolarization. Develops during phase 3 of the action potential (during repolarization). Certain conditions are required for its occurrence: a slow heart rate, prolongation of the $Q—T$ interval (increased duration of the action potential), and low intracellular potassium ion ($K^+$) levels. A classic clinical example of such a disturbance is torsade de pointes (torsade de pointes) ventricular tachycardia. Etiologically, early afterdepolarization is frequently associated with parasympathetic predominance, such as in neurosis or hypothyroidism.
- Delayed afterdepolarization. Forms after complete repolarization has ended. Unlike early afterdepolarization, it occurs against the background of an accelerated heart rate. The mechanism is driven by calcium ion ($Ca^{2+}$) overload in cardiomyocytes resulting from excessive adrenergic stimulation. Main causes: myocardial hypertrophy, heart failure, cardiac glycoside toxicity, and myocardial reperfusion (e.g., following thrombolytic therapy).
Classification by rhythm source
Depending on where the electrical impulse originates, rhythm disorders are divided into two major categories.
1. Nomotopic arrhythmias The impulse originates in the normal pacemaker — the sinuatrial node, but the frequency or regularity of its generation is disturbed. This group includes:
- Sinus tachycardia.
- Sinus bradycardia.
- Sinus arrhythmia.
- Sick sinus syndrome (SSS), which may clinically manifest as tachycardia-bradycardia syndrome.
2. Heterotopic arrhythmias The impulse is generated outside the sinus node, meaning an ectopic pacemaker is active. The main types of such rhythms:
- Slow atrial rhythm.
- Atrioventricular (junctional) rhythm.
- Idioventricular rhythm.
Special forms of heterotopic disturbances are also distinguished: pacemaker migration, escape beats, and interference-dissociation.
Sinus tachycardia
Sinus tachycardia is defined as an increased rate of impulse generation in the sinuatrial node at rest (typically greater than 100 beats per minute) while maintaining uniform intervals between them. The electrophysiological mechanism involves the acceleration of spontaneous diastolic depolarization of the node cell plasma membrane.
Main causes:
- Activation of the sympathoadrenal system. Observed during emotional stress, physical exertion, neurosis, hyperthermia, and fever. Sympathetic influences are also enhanced during acute arterial hypotension (due to activation of afferent signaling from baroreceptors) and in heart failure. In the latter case, tachycardia occurs due to increased venous return to the right atrium, which triggers the Bainbridge reflex.
- Reduction of parasympathetic nervous system effects, which may result from various types of damage.
Sinus bradycardia
A slower heart rate is associated with opposing mechanisms: enhanced parasympathetic or weakened sympathetic influences.
Enhanced parasympathetic influences are observed during:
- Irritation of vagal nuclei (n. vagus) due to elevated intracranial pressure (meningitis, encephalitis).
- Irritation of vagal nerve endings against the background of increased intraventricular pressure and myocardial tone.
- Reflex influences: pressure on the eyeballs (Aschner-Dagnini reflex), stimulation of the carotid sinus region (Hering reflex), or the solar plexus area.
Decreased sympathoadrenal effects on the heart develop during:
- Neurotic states.
- Damage to brain structures (including the hypothalamus) and conduction pathways.
- Damage to intracardiac ganglia and sympathetic nerve endings directly within the myocardium.
- Reduction of the adrenoreactive properties of the heart itself.
Briefly: answers to topical questions
What ECG features are characteristic of sick sinus syndrome (SSS)?
The following features are most informative for sick sinus syndrome:
- Tachy-brady syndrome — intermittent or persistent sinus bradycardia alternating with sinus tachycardia.
- Transient atrial flutter or fibrillation.
- Slow recovery of sinus rhythm after termination of tachycardia.
- Episodes of sinuatrial node arrest (sinus arrest).
To easily remember the reflex causes of bradycardia, move down the body from top to bottom: eyes (Aschner-Dagnini reflex) → neck (Hering reflex) → abdomen (solar plexus).
Class and exam questions
What is triggered activity, and what types are there?
This is the primary mechanism for ectopic impulse generation, based on partial depolarization of cells. It is subdivided into early (occurring during the repolarization phase) and delayed (occurring after repolarization is complete) afterdepolarization.
What is the fundamental difference between nomotopic and heterotopic arrhythmias?
In nomotopic arrhythmias, the impulse is generated in the normal pacemaker (sinuatrial node), but its rate or regularity is disturbed. In heterotopic arrhythmias, the impulse originates from an ectopic pacemaker located outside the sinus node.
Why does sinus tachycardia develop in heart failure?
In heart failure, venous return to the right atrium increases. This leads to activation of the Bainbridge reflex, stimulation of the sympathoadrenal system, and, consequently, an elevated heart rate.
What else to study on this topic
- Electrophysiological mechanisms of the cardiomyocyte action potential
- Sick sinus syndrome (SSS) and tachycardia-bradycardia syndrome
- Pathogenesis of torsade de pointes (torsade de pointes) ventricular tachycardia
- Special forms of heterotopic rhythms: pacemaker migration and interference-dissociation
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