Sinus tachycardia

ECG: This tracing shows a tachycardia of 170 bpm of sinus origin (1:1 atria/ventricles ratio, atrial activity preceding the positive QRS complex in leads I, II, V5, V6, negative in aVR); probable left ventricular hypertrophy with increase in S wave voltage in V3 and R wave voltage in V5;

Comments: This patient has a sinus tachycardia which is defined as a resting sinus rate greater than 100 bpm. The electrocardiographic diagnosis of sinus tachycardia is straightforward if the tachycardia is not very rapid allowing good differentiation between P waves, QRS complexes and T waves. Sinus P waves precede and control the occurrence of QRS complexes. When the rhythm accelerates beyond a certain rate, the shortening of the diastoles leads to a superposition of P waves and T waves, with the presence of T wave notching as the only electrocardiographic sign revealing atrial activity. Detecting characteristic features suggesting the sinus origin of the atrial activity (positive in leads I, II, V5, V6 and negative in aVR) can thus be difficult. The evolution profile of the heart rate (if the patient is monitored telemetrically) can be very suggestive of sinus tachycardia, if one can detect progressive acceleration and deceleration of the heart rate. The rate rarely exceeds 180 bpm in adults. Tachycardia can lead to moderate ST depression and T wave flattening.

In a majority of cases, tachycardia should not be considered as an actual rhythm disorder but rather as either a physiological response to increased metabolic demand, or a general pathological process (fever, anemia, B1 avitaminosis, hypovolemia, heart failure, cachexia, hyperthyroidism, pulmonary embolism, etc.), or as a physiological (emotion, anxiety, pain, etc.) or pharmacological (sympathomimetic, etc.) stress. In this patient, various factors may explain the presence of a reactive sinus tachycardia (anemia, renal failure, cardiac decompensation, fever, superinfection). In this setting, treatment is not aimed at the tachycardia per se but rather at its causes.

In rare cases, sinus tachycardia is not considered as adaptive and secondary to increased metabolic demand or to drug hyperstimulation, and should hence evoke the diagnosis of inappropriate sinus tachycardia. The mechanisms involved are still poorly defined. The symptomatology is variable but can be very disabling with repeated occurrence of palpitations, dyspnea, limitation of exercise capacity, lipothymia or even syncope. The rate accelerates rapidly for modest exertion and decelerates much more slowly during recovery. If the rate acceleration is essentially postural, a postural orthostatic tachycardia syndrome (thus constituting a different entity) should be investigated. Inappropriate sinus tachycardia mainly involves young, predominantly female patients, sometimes occurring in an anxious psychological setting leading to a large number of consultations. The long-term prognosis of this type of dysautonomy is preserved. Treatment of contributory factors (excessive caffeine intake, stress deconditioning, anxiety) is the first step in its management. Occasionally, given the persistence of symptoms occurring in a setting of sinus tachycardia, the introduction of medical treatment is necessary. Beta-blockers and ivabradine constitute first-line treatments, although their tolerance is not always idyllic. Radiofrequency modulation of the sinus node can be proposed in very exceptional circumstances when confronted with a disabling refractory tachycardia because of a limited success rate and a non-negligible risk of complications.

Take-home message: In a majority of cases, sinus tachycardia should not be considered as a genuine rhythm disorder, but as a physiological response adapted to an increased metabolic need or to a general pathological process.