Dromotropic effect

Dromotropic effect (negative). Glycerin/ ethanol extract of the fresh leaf, adminis-... 

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. 

Despite difficulties in determining the precise mechanism of action of drugs possessing calcium inhibitory activity, these compounds exert potent negative inotropic, chronotropic and dromotropic effects upon cardiac tissues. They are excellent coronary and peripheral vasodilators and preserve myocardial metabolism while preventing mitochondrial swelling during cardiac ischemia. Their antiarrhythmic activity in intact animals and isolated tissue preparations is closely linked to their ability to inhibit the slow inward calcium current, interfere with transmembrane sodium ion flux, and indirect effects. 

Acetylcholine (ACh) decreases the rate of firing of the sinoatrial (SA) node (negative chronotropic effect) and the rate of conduction through the atrioventricular (AV) node and ventricular conduction system (negative dromotropic effect), resulting in bradycardia. The force of contraction of the heart muscle is also reduced (negative inotropic effect), resulting in decreased ejection fraction and decreased cardiac output. 

Norepinephrine affects calcium flux within cardiac muscle tissue and conductive tissue, resulting in a positive inotropic and dromotropic effect. It also increases the rate of firing of the SA node, resulting in an increase in heart rate (positive chronotropic effect). 

Negative chronotropic and dromotropic effects. ACh acts to decrease the rate of spontaneous depolarization of the cells of the SA node, decreasing heart rate. It also acts to decrease the rate of conduction through the atrioventricular (AV) node, through changes in sodium and calcium conductance. 

CARDIOVASCULAR SYSTEM ACh has four primary effects on the cardiovascular system vasodilation, a decrease in cardiac rate (the negative chronotropic effect), a decrease in the rate of conduction in the specialized tissues of the SA and atrioventricular (AV) nodes (the negative dromotropic effect), and a decrease in the force of cardiac contraction (the negative inotropic effect). The last effect is of lesser significance in ventricular than in atrial muscle. Certain of the above responses can be obscured by baroreceptor and other reflexes that dampen or counteract the direct responses to ACh. 

Paroxysmal supraventricular tachycardia (PSVT) verapamil is the dmg of choice due to its dromotropic effect. 

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