Sinoatrial (SA) Node Dysfunction

The normal pacemaker of the heart, termed the sinus (or sinoatrial (SA)) node, is responsible for generating the electrical impulse that triggers the heart to contract and pump blood. Normally the SA node "fires-off" at regular intervals ranging from 40 to 170 discharges/min. This wide range of rates corresponds with the wide activity levels that humans engage in and the wide range in demands for cardiac output. For example, when we sleep we don't need high levels of cardiac pumping of blood and so our heart rate reaches its lowest levels, sometimes as low as 30-40 beats/min. On the other hand, during peak exercise activity, we need all the cardiac output our heart can muster to deliver oxygenated blood to our heart, brain, muscles, and other tissues, and remove waste products such as carbon dioxide. Consequently, under these conditions our sinus rate approaches its maximum achievable level.

Patients with SA node dysfunction often exhibit more than one of the following abnormalities:

• Symptomatic severe sinus bradycardia (sinus rates < 40/min resting while awake (excluding well conditioned athletes)).
• Severe chronotropic incompetence (absence of the expected increase in sinus rate increase during exercise) in association with with symptoms of early fatigue with minimal exertion.
• Significant sinus arrest or sinus pauses, especially in association with symptoms such as fainting or "dizzy" spells.
• Episodes of bradycardia or sinus pauses (as described above) following termination of and/or interspersed with episodes of paroxysmal atrial tachyarrhythmias, especially atrial flutter or atrial fibrillation.

Most cases of sinus node dysfunction is the result of fixed damage to or degeneration of sinoatrial tissue and it is typically seen in the elderly or patients with significant structural heat disease, including coronary artery disease, congestive heart failure, or cardiomyopathy. As mentioned above, it is often associated with atrial tachyarrhythmias such as atrial fibrillation or flutter. In some cases, sinus node dysfunction may be secondary to, or worsened by, medications (see table 1 below) that the patient may be taking for control of other cardiovascular problems, including supraventricular tachyarrhythmias, ventricular tachyarrhythmias, hypertension (high blood pressure), coronary artery disease, or congestive heart failure. It is not unusual to have brief transient episodes of marked sinus bradycardia or symptomatic sinus pauses caused by vasovagal episodes in patients without any fixed conduction system or cardiovascular disease.

Table 1.  Cardiovascular medications that may adversely affecting sinus node function

Clinical diagnosis of sinus node dysfunction is made by correlating suspicious symptoms ("dizziness", fatigue, shortness of breath, etc.) with ECG recordings of dramatically slow heart rates (Figure 1 below), including very slow sinus rates, so-called "slow junctional escape rhythms", and/or prolonged pauses in the heart rate, or inability of the heart rate to increase during exercise or exertion.

Figure 1. Continuous ECG recording (ECG lead V2) showing characteristic ECG findings in patient with symptomatic sinoatrial node dysfunction. PAC = premature atrial contraction.

Treatment for SA node dysfunction includes elimination of any offending medication (Table 1 above), and if necessary, implantation of a pacemaker system. Patients with symptomatic sinus pauses caused by vasovagal episodes rarely need treatment with a pacemaker; instead recurrent problematic episodes may be treatable with lifestyle modification and/or mild medications.