dromotrope

Dromotropy refers to the effect on the rate of electrical conduction through the heart's conduction system, particularly the atrioventricular (AV) node. A positive dromotropic effect increases conduction velocity, while a negative dromotropic effect slows conduction. In clinical practice, dromotropy is often assessed by changes in the PR interval on an electrocardiogram, which reflects AV nodal conduction time.

Physiologically, dromotropy is influenced by the autonomic nervous system and various pharmacologic agents. Sympathetic stimulation increases AV nodal conduction velocity through beta-adrenergic receptors, producing a positive dromotropic effect. Conversely, parasympathetic (vagal) activity decreases AV nodal conduction via acetylcholine acting on muscarinic receptors, yielding a negative dromotropic effect. Other factors, such as ischemia or electrolyte disturbances, can also modify dromotropy.

Pharmacology and clinical use illustrate the concept. Positive dromotropic agents include certain catecholamines that enhance AV conduction, as well as atropine, which blocks vagal tone and can increase conduction velocity. Negative dromotropic effects are produced by drugs that reduce AV nodal conduction, such as calcium channel blockers (verapamil, diltiazem), adenosine, and digoxin. These agents can be used to control rapid AV conduction during tachyarrhythmias or to protect against excessively fast AV conduction, whereas positive dromotropic agents may be considered in circumstances where slowed AV conduction contributes to bradyarrhythmia or low cardiac output.

In summary, dromotropy describes changes in the speed of electrical impulse propagation through the heart’s conduction pathways, with clinical relevance to the management of rhythm disorders alongside chronotropic and inotropic aspects of cardiac function.