The electrical activation of the heart usually originates in the sinus node or sinoatrial node (SA), which is the predominant pacemaker. Another auxiliary pacemaker such as the atrioventricular node (AV), the specialized system of conduction and muscle initiate electrical activation in case of dysfunction or suppression of the sinus node. Auxiliary pacemakers typically discharge at a slower rate and when there is no adequate increase in stroke volume, they can cause tissue hypoperfusion.
The spontaneous activation and contraction of the heart are generated by the specialized tissue found in these anatomical sites. The action potentials of the heart are heterogeneous in different regions. In cells isolated from tissue of the sinus node are different from those recorded in atrial and ventricular myocytes. Cells in the sinus node have a faster depolarization and therefore are the dominant pacemakers in a healthy heart.
Bradycardia results from a failure in the generation or conduction of the electrical impulse. The failure in the generation of the impulse can be the consequence of an automatism attenuated by the delay or deficiency of diastolic depolarization, which is caused by diseases such as the sinus node dysfunction or by drugs (quinine, reserpine, etc). The autonomic nervous system modulates the speed of diastolic depolarization and, consequently, the frequency of discharge of the primary (sinus node) and auxiliary pacemakers. The failure to drive an impulse from the node tissue to the atrial or ventricular myocardium causes bradycardia due to blockage at the exit.
Sinus arrest implies a failure of atrial activation. It may be due to a problem of generation of the impulse in the sinus node or a failure of conduction of the impulse to the atrium, usually there is a pause in the conduction of the nervous stimulus of several seconds, followed by the resumption of a regular rhythm or the appearance of a nodal or idioventricular escape rhythm. It appears frequently in normal individuals during deep sleep; but when it is frequent and associated with escape rhythms it can also indicate the existence of a fibrotic sinus node or that it works in an inadequate way, a syndrome of the diseased node or a medication effect (digoxin, quinidine intoxication, or beta-blockers). Sinus arrest may be asymptomatic or be associated with a recurrent sensation of dizziness or syncope, and the resumption of cardiac impulses may be perceived by the patient in the form of palpitations.
The electrocardiogram shows: absence of P-QRS. The P-P interval that delimits the pause is not equivalent to a multiple of the base P-P interval and is shorter than normal cardiac cycles; it usually ends with a sinus rhythm.
Although there are currently no established cutoff values, pauses of 3 seconds or more are infrequent and justify the implantation of a pacemaker in symptomatic patients. However, it does not appear that pauses of 3 seconds or more predict higher mortality, as indicated by more recent studies. The immediate treatment of a complete sinus arrest is the intravenous administration of atropine or isoproterenol until definitive care can be provided.
1. Rubart M, Zipes DP. Arrhythmias, sudden death and syncope. En: Libby P., Bonow R.O., Mann D.L., Zipes D., editors. Braunwald's Heart Diseae. Filadelfia: Saunders Elsevier;2008. 909-21.
2. Monfredi O, Dobrzynski H, Mondal T, Boyett MR, Morris GM. The anatomy and physiology of the sinoatrial node−a contemporary review. Pacing Clin Electrophysiol. 2010;33:1392-406.
3. Sneddon JF, Camm AJ. Sinus node disease. Current concepts in diagnosis and therapy. Drugs. 1992;44:728-37.
4. Farreras Valentí, P., Rozman, C., Domarus, A. and Lopez, F. (2012). Medicina interna. 17th ed.