Tachycardia

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 of sinus tachycardia:

1. Activation of the sympathoadrenal system. Observed in emotional stress, physical exertion, neuroses, hyperthermia, and fever. It also occurs in acute arterial hypotension (due to activation of afferent impulses from baroreceptors) and in heart failure (as a result of increased blood return to the right atrium and activation of the Bainbridge reflex).
2. Decreased effects of the parasympathetic nervous system. May be a consequence of injury.

Main types of supraventricular tachycardias

Supraventricular tachycardias (SVTs) are mostly not life-threatening arrhythmias (except for atrial fibrillation and flutter in WPW syndrome). Several main variants are distinguished:

• Sinus tachycardia (tachycardia) — includes physiological, non-physiological, and re-entry nodal forms. In the re-entry form (re-entry), the excitation wave circulates involving the sinus node, causing paroxysmal palpitations and syncope.
• Focal atrial tachycardia (ectopic) — characterized by the presence of P' waves differing in morphology from sinus waves, and an isoelectric line between them. The mechanism of enhanced automaticity typically exhibits "warm-up" (gradual increase in HR) and "cool-down" (gradual decrease in HR) phenomena.
• Non-re-entry nodal tachycardia (automatic) — a rare form originating from the AV node or the bundle of His. Its persistence does not require the involvement of the atria or ventricles. It can be triggered by physical exertion or stress.
• Antidromic AVRT (atrioventricular reciprocating tachycardia) — occurs when an impulse circulates antegrade through an accessory atrioventricular pathway and retrograde through the AV node. It is characterized by a wide QRS complex and a high heart rate (150–200 bpm).

Features of non-physiological sinus tachycardia

This condition is more common in young women and tends to have a persistent course, although the prognosis is considered favorable. Patients complain of palpitations, chest pain, shortness of breath, and dizziness.

In diagnostics, it is important to rule out physiological tachycardia, psychogenic causes, and postural orthostatic tachycardia syndrome (POTS).

Treatment begins with lifestyle modifications: exercise, increased fluid intake, and restriction of heart-stimulating medications. Pharmacotherapy includes:

• Beta-blockers (can be used long-term, but often require high doses, which increases the risk of side effects).
• Calcium channel blockers (effective doses often cause hypotension).
• Ivabradine (a selective If current blocker). The evidence base for non-physiological sinus tachycardia is insufficient. Contraindicated during pregnancy and breastfeeding. Concurrent use with CYP3A4 inhibitors (e.g., verapamil, diltiazem, clarithromycin, and grapefruit juice) should be avoided.

Ventricular rhythm disorders

Ventricular tachycardias include rare hereditary arrhythmogenic diseases, such as catecholaminergic polymorphic ventricular tachycardia (CPVT).

It is characterized by adrenergically induced bidirectional and polymorphic ventricular tachycardia. The disease is associated with mutations in genes:

• RyR2 (dominant variant, cardiac ryanodine receptor).
• CASQ2 (rare recessive variant, cardiac calsequestrin).

Treatment involves non-selective $\beta$-blockers, restriction of physical activity, and, in case of $\beta$-blocker intolerance, left cardiac sympathetic denervation.

Principles of emergency therapy

The tactics for terminating an attack depend on the width of the QRS complex and the patient's hemodynamic stability:

• In unstable hemodynamics, the method of choice is synchronized cardioversion.
• In stable hemodynamics and narrow QRS complexes ($\le$ 120 ms), therapy begins with vagal maneuvers. If they are ineffective, adenosine triphosphate (adenosine) is administered intravenously as a bolus at a dose of 10–20 mg.
• In stable hemodynamics and wide QRS complexes (> 120 ms) in the setting of WPW syndrome or atrial fibrillation, intravenous procainamide is recommended; intravenous propafenone should be considered. Intravenous amiodarone in such cases is not recommended.

Class and exam questions

What else to study on this topic

• Bainbridge reflex
• WPW syndrome
• Atrial fibrillation
• Cardiac electrophysiological study (EPS)
• Sympathoadrenal system

Other topics in "Physiology concepts"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.