Prystowsky E N
Duke University Medical Center, Durham, North Carolina 27710.
J Clin Pharmacol. 1988 Jan;28(1):6-21. doi: 10.1002/j.1552-4604.1988.tb03095.x.
The PR interval on the electrocardiogram represents the time that it takes an impulse to travel through the atrium and atrioventricular (AV) conduction system to the ventricles. Normally, activation is slowest in the AV node, and variations in PR interval most commonly parallel changes in AV nodal activation time. The AV nodal conduction time and effective refractory period are rate dependent and, in adult humans, are usually prolonged with increasing atrial paced rates. In addition, alterations in autonomic tone effect AV nodal conduction as well as sinus rate. The effect is usually in the same direction but often to different degrees. In patients with normal AV nodal function, parasympathetic and sympathetic tone are balanced at rest, but in patients with abnormal AV conduction, the effect of the parasympathetic system is more marked. Drugs including the slow channel blockers and beta blockers, affect AV nodal function. Slow channel blockers inhibit the slow inward calcium current, which may prolong conduction and refractoriness in the AV node. However, whereas diltiazem and verapamil have been shown to prolong AV nodal conduction and refractoriness in humans, nifedipine, a potent vasodilator, cannot be used in doses large enough to affect the AV node. The increase in PR interval caused by verapamil is minimal, and at doses of less than 480 mg/d, AV block occurs infrequently. When AV block occurs, it is first degree block in most patients, and it is usually asymptomatic. The electrophysiologic effects of diltiazem are similar to those of verapamil. Beta blockers also have a negative dromotropic effect on the AV node. They prolong the AH interval and AV nodal refractory periods and may lengthen the PR interval. The prolonged PR interval rarely results in more than first degree AV block in patients receiving maintenance therapy. In selected patients, combination therapy with a slow channel blocker and a beta blocker rarely causes second-degree AV block.
心电图上的PR间期代表冲动从心房经房室(AV)传导系统至心室所需的时间。正常情况下,房室结的激活速度最慢,PR间期的变化最常与房室结激活时间的变化平行。房室结传导时间和有效不应期与心率有关,在成年人体内,通常随着心房起搏频率的增加而延长。此外,自主神经张力的改变会影响房室结传导以及窦性心律。其影响通常方向相同,但程度往往不同。在房室结功能正常的患者中,静息时副交感神经和交感神经张力平衡,但在房室传导异常的患者中,副交感神经系统的影响更为显著。包括慢通道阻滞剂和β受体阻滞剂在内的药物会影响房室结功能。慢通道阻滞剂抑制缓慢内向钙电流,这可能会延长房室结的传导和不应期。然而,虽然地尔硫䓬和维拉帕米已被证明可延长人体房室结传导和不应期,但强效血管扩张剂硝苯地平无法使用足够大的剂量来影响房室结。维拉帕米引起的PR间期增加很小,在剂量小于480mg/d时,房室传导阻滞很少发生。当发生房室传导阻滞时,大多数患者为一度阻滞,通常无症状。地尔硫䓬的电生理效应与维拉帕米相似。β受体阻滞剂对房室结也有负性传导作用。它们延长AH间期和房室结不应期,可能会延长PR间期。在接受维持治疗的患者中,延长的PR间期很少导致超过一度的房室传导阻滞。在特定患者中,慢通道阻滞剂和β受体阻滞剂联合治疗很少引起二度房室传导阻滞。