The heart is equipped with a specialized conduction system that ensures the generation and propagation of the electrical impulses required for coordinated myocardial contraction. The sinoatrial (SA) node, located in the right atrium, is the primary physiological pacemaker of the heart and determines the basal heart rate through spontaneous generation of action potentials.
The electrical impulse generated by the SA node propagates through the atria, triggering their contraction, and then reaches the atrioventricular (AV) node, located at the junction between the atria and ventricles. The AV node introduces a physiological delay in conduction, allowing adequate ventricular filling before systole. After the AV node, the impulse is transmitted along the bundle of His and its branches (right and left), then rapidly distributed through the Purkinje fibers, resulting in synchronous ventricular contraction.
Pathological Alterations of Heart Rhythm
Heart rhythm disorders arise from abnormalities in the generation or conduction of cardiac electrical impulses and can manifest as bradyarrhythmias or tachyarrhythmias.
Bradyarrhythmias
Bradyarrhythmias are characterized by a reduction in heart rate (<60 bpm) and may result from impaired automaticity of the SA node or from conduction block at the level of the AV node.
Sinoatrial node dysfunction: decreased ability of the SA node to generate impulses, often due to fibrotic degeneration, ischemia, or pharmacological effects (beta-blockers, calcium channel blockers).
Atrioventricular blocks: delays or interruptions of conduction between atria and ventricles, classified according to severity (first, second, and third-degree AV block).
Tachyarrhythmias
Tachyarrhythmias occur when the heart rate exceeds 100 bpm and may result from increased automaticity, reentry phenomena, or triggered activity.
Increased automaticity: hyperactivation of ectopic pacemakers in response to adrenergic stimuli, ischemia, or electrolyte disturbances.
Electrical reentry: abnormal persistence of electrical activity in closed circuits, responsible for many supraventricular and ventricular tachycardias.
Triggered activity: early or delayed afterdepolarizations that generate abnormal impulses, often associated with digitalis toxicity or congenital syndromes.
Factors Predisposing to Heart Rhythm Disorders
Arrhythmias can be triggered by multiple factors, including structural cardiac abnormalities, metabolic and electrolyte imbalances, myocardial ischemia, and neurovegetative influences.
Structural heart diseases: fibrosis, atrial or ventricular dilation, and valvular diseases can alter electrical conduction.
Electrolyte imbalances: changes in potassium, calcium, and magnesium levels influence myocardial excitability.
Myocardial ischemia: reduced perfusion alters depolarization and promotes ventricular arrhythmias.
Drugs and substances: antiarrhythmics, digitalis, sympathomimetics, and recreational drugs can interfere with cardiac electrical activity.
Conclusions
Heart rhythm disorders represent a heterogeneous group of conditions resulting from alterations in automaticity, conduction, or propagation of electrical impulses. Understanding the physiology of the cardiac conduction system and the pathological mechanisms underlying arrhythmias is fundamental for correct diagnosis and therapeutic management.
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