What is the Dromotropic Effect and its Role in Cardiac Regulation?
Sympathetic and parasympathetic reflexes exert complex effects on the heart, which can be positive (+) or negative (-). The dromotropic effect is responsible for changing the velocity of excitation conduction.
Along with it, other physiological regulatory effects are distinguished:
- Chronotropic effect — changes in heart rate (HR).
- Inotropic effect — changes in contractility.
- Bathmotropic effect — changes in myocardial excitability.
- Tonotropic effect — changes in myocardial tone.
How Does the Nervous System Regulate Conduction?
- Sympathetic stimulation: Activation of $\beta_1$-adrenergic receptors produces a positive dromotropic effect (accelerated conduction). Simultaneously, myocardial contractility and heart rate increase.
- Parasympathetic stimulation: Enhanced vagal tone (N. vagus) and its cholinergic actions on the heart cause a negative dromotropic effect mediated by acetylcholine. This leads to a substantial decrease in impulse propagation speed throughout the conduction system, particularly at the AV node.
How Do Pharmacological Agents Alter Conduction?
- Non-selective adrenomimetics (e.g., orciprenaline): Stimulate $\beta_1$-receptors, producing a positive dromotropic effect.
- $\beta_1$-adrenergic receptor blockers: Exert a direct inhibitory effect on the heart, causing a negative dromotropic effect, while also decreasing the automaticity of ectopic pacemakers (AV node and Purkinje fibers).
- Cardiac glycosides (digoxin): Suppress conduction through the AV junction.
- Antiarrhythmic drugs: Amiodarone suppresses AV conduction. Quinidine has a complex profile: its direct effect on cardiomyocytes decreases conduction, whereas its vagolytic (anticholinergic) action blocks vagal effects, which accelerates AV conduction and counteracts the direct effect.
What is the Clinical Significance of the Effect?
Modulating conduction velocity is crucial for managing rhythm disorders:
- Therapeutic use of the positive effect: Improving conduction via $\beta_1$-stimulation is used in AV blocks and bradyarrhythmias.
- Therapeutic use of the negative effect: Slowing conduction is utilized in tachy-form atrial fibrillation. For instance, digoxin induces partial conduction block, which normalizes ventricular rate and converts the arrhythmia into a normosystolic form.
- Hazards and Overdose: Excessive slowing of AV nodal conduction can lead to pathological atrioventricular block (up to complete heart block). In complete transverse block caused by high doses of digoxin, the ventricles switch to an autonomous (idioventricular) rhythm driven by bundle of His cardiomyocytes at a rate of 40–60 beats per minute.