What are the causes of tachycardia?
The acceleration of impulse generation in the sinoatrial node is regulated by the autonomic nervous system. There are two main groups of causes for sinus tachycardia:
- Activation of the sympathoadrenal system. This occurs during emotional stress, physical exertion, neurosis, hyperthermia, and fever. It also develops during acute arterial hypotension (via activation of afferent signaling from baroreceptors) and in heart failure (due to increased venous return to the right atrium triggering the Bainbridge reflex).
- Reduced parasympathetic nervous system tone. This can result from nerve injury or impaired vagal modulation.
Main types of supraventricular tachycardias
Supraventricular tachycardias (SVTs) are generally not life-threatening arrhythmias (except for atrial fibrillation and flutter in Wolff-Parkinson-White syndrome). The main variants include:
- Sinus tachycardia (tachycardia) — includes physiological, inappropriate, and node-involved re-entry forms. In the re-entry form, the excitation wave circulates involving the sinus node, causing paroxysmal palpitations and syncope.
- Focal atrial tachycardia (ectopic) — characterized by P' waves with a morphology distinct from normal sinus P waves, separated by an isoelectric baseline. The enhanced automaticity mechanism typically exhibits "warm-up" (gradual heart rate acceleration) and "cool-down" (gradual deceleration) phenomena.
- Non-re-entry junctional tachycardia (automatic) — a rare form originating from the AV node or the bundle of His. It does not require atrial or ventricular tissue participation to be sustained. It can be provoked by physical exertion or stress.
- Antidromic AVRT (atrioventricular reciprocating tachycardia) — occurs when the electrical impulse conducts antegrade via an accessory pathway and retrograde via the AV node. It features a wide QRS complex and a high heart rate (150–200 bpm).
Features of inappropriate sinus tachycardia
This condition is more common in young women and tends to follow a persistent course, although the prognosis is generally benign. Patients present with palpitations, chest discomfort, dyspnea, and dizziness.
During evaluation, it is crucial to exclude physiological tachycardia, psychogenic causes, and postural orthostatic tachycardia syndrome (POTS).
Treatment begins with lifestyle modifications: conditioning, increased fluid intake, and avoidance of cardiac stimulants. Pharmacotherapy includes:
- Beta-blockers (can be used long-term, but often require high doses, increasing the risk of side effects).
- Calcium channel blockers (effective doses frequently cause hypotension).
- Ivabradine (a selective $I_f$ current blocker). Evidence for inappropriate sinus tachycardia is limited. It is contraindicated during pregnancy and breastfeeding. Concomitant use with CYP3A4 inhibitors (such as verapamil, diltiazem, clarithromycin, and grapefruit juice) must be avoided.
Ventricular arrhythmias
Ventricular tachycardias include rare inherited arrhythmogenic disorders, such as catecholaminergic polymorphic ventricular tachycardia (CPVT).
It is characterized by adrenergically induced bidirectional and polymorphic ventricular tachycardia. The disease is caused by mutations in the following genes:
- RyR2 (dominant variant, cardiac ryanodine receptor).
- CASQ2 (rare recessive variant, cardiac calsequestrin).
Management involves non-selective $\beta$-blockers, restriction of physical exertion, and left cardiac sympathetic denervation if $\beta$-blockers are not tolerated.
Principles of emergency management
The acute management strategy depends on the width of the QRS complex and the patient's hemodynamic stability:
- In unstable hemodynamics, synchronized direct current cardioversion is the treatment of choice.
- With stable hemodynamics and narrow QRS complexes ($\le$ 120 ms), therapy begins with vagal maneuvers. If ineffective, adenosine is administered as a rapid intravenous bolus (10–20 mg).
- With stable hemodynamics and wide QRS complexes (> 120 ms) in the setting of Wolff-Parkinson-White syndrome or atrial fibrillation, intravenous procainamide is recommended; intravenous propafenone should be considered. Intravenous amiodarone is not recommended in these cases.