The normal pacemaker of the heart, the sinoatrial node, is located in the superior and lateral aspect of the right atrium. Sinus tachycardia occurs when the normal pacemaker of the heart accelerates the heart rate in response to alterations in physiologic conditions. Sinus tachycardia occurs related to increased sympathetic and decreased parasympathetic tone as a normal response to increased physiologic demands (e.g., exercise, fever, anemia) and as an abnormal response to certain pathologic changes (e.g., hyperthyroidism, pheochromocytoma, arterial venous malformation). Various medications and drugs of abuse that increase sympathetic tone or mimic sympathetic output or decrease parasympathetic tone can elevate the resting sinus rate (Table 75-2). Among the common medications that increase the sinus rate are stimulants, decongestants, caffeine, and β-adrenergic agonists. The normal physiologic response to increased metabolic demands and increased sympathetic drive is to increase cardiac output. Cardiac output is augmented
either by increasing the stroke volume or the heart rate (or both). During infancy, the heart is less able to increase stroke volume; therefore, the cardiac output is primarily augmented by an increase in heart rate.

Cardiac causes for sinus tachycardia include any condition that depresses myocardial function (e.g., myocarditis, pericarditis, endocarditis) or increase cardiac output demand including cardiac lesions resulting in congestive heart failure from large left-to-right intracardiac shunts, atrioventricular valve regurgitation, or left ventricular outflow tract obstruction (aortic stenosis or coarctation of the aorta). Inappropriate sinus tachycardia occurs secondary to enhanced automaticity within the sinus node tissue itself as opposed to a secondary effect of external metabolic or pharmacologic stressors. It is a rare form of sinus tachycardia and is a diagnosis of exclusion.

Patients with sinus tachycardia may be asymptomatic or minimally symptomatic with complaints of palpitations or dizziness and lightheadedness with standing. Symptoms depend on the age of the patient and the underlying etiology of the sinus tachycardia.

A 12-lead electrocardiogram (ECG) should be obtained for determination of P-wave axis. During sinus tachycardia, the P-wave axis is 0° to 90° and the QRS complex is narrow, unless there is associated conduction delay (e.g., bundle branch
block or rate dependent aberrancy). There is typically a “warm-up” and “cooldown” periods as well as beat-to-beat variation to the heart rate, although heart rate variability is diminished in most physiologic states resulting in sinus tachycardia.

A thorough physical examination including blood pressure assessment, complete blood cell count, glucose level, thyroid function tests, and 24-hour urine catecholamine studies may be indicated for evaluation of underlying disease processes associated with sinus tachycardia. Often, observing the patient on a monitor for a short period of time helps in the diagnosis.

Treatment of nonphysiologic sinus tachycardia is usually geared toward correction of the underlying abnormality, such as infection, anemia, or hyperthyroidism. In patients diagnosed with inappropriate sinus tachycardia, β-blockers or calcium channel blockers may be considered for rate control.

Automatic (ectopic) atrial tachycardia is an automatic tachycardia that arises from the atrial myocardium at an area outside of the sinus node. It is typically identified on an ECG by an abnormal P-wave axis or P wave with a different morphology from that seen during sinus rhythm on a previous ECG. It can be difficult to distinguish ectopic atrial tachycardia from sinus tachycardia if the ectopic focus is in the high right atrium (near the sinus node) and has a normal P-wave axis. In some instances, the PR interval maybe prolonged or there maybe atrioventricular block as an indicator that there is an ectopic as opposed to sinus tachycardia. Similar to other automatic mechanisms, automatic (ectopic) atrial tachycardia typically has a “warm-up” and “cool-down” phases.