Barold S S, Hayes D L
Electrophysiology Institute, Broward General Hospital, Ft Lauderdale, Fla., USA.
Mayo Clin Proc. 2001 Jan;76(1):44-57. doi: 10.4065/76.1.44.
In this review, we discuss the various forms and causes of second-degree atrioventricular (AV) block and the reasons they remain poorly understood. Both type I and type II block characterize block of a single sinus P wave. Type I block describes visible, differing, and generally decremental AV conduction. Type II block describes what appears to be an all-or-none conduction without visible changes in the AV conduction time before and after the blocked impulse. Although the diagnosis of type II block is possible with an increasing sinus rate, absence of sinus slowing is an important criterion of type II block because a vagal surge (generally a benign condition) can cause simultaneous sinus slowing and AV nodal block, which can superficially resemble type II block. The diagnosis of type II block cannot be established if the first postblock P wave is followed by a shortened PR interval or is not discernible. A pattern resembling a narrow QRS type II block in association with an obvious type I structure in the same recording (e.g., Holter) effectively rules out type II block because the coexistence of both types of narrow QRS block is exceedingly rare. Concealed His bundle or ventricular extrasystoles confined to the specialized conduction system without myocardial penetration and depolarization can produce electrocardiographic patterns that mimic type I and/or type II block (pseudo-AV block). All correctly defined type II blocks are infranodal. A narrow QRS type I block is almost always AV nodal, whereas a type I block with bundle branch block barring acute myocardial infarction is infranodal in 60% to 70% of cases. A 2:1 AV block cannot be classified in terms of type I or type II block, but it can be nodal or infranodal. Infranodal blocks require pacing regardless of form or symptoms. The widespread use of numerous disparate definitions of type II block appears primarily responsible for many of the problems surrounding second-degree AV block. Adherence to the correct definitions provides a logical and simple framework for clinical evaluation.
在本综述中,我们讨论二度房室(AV)阻滞的各种形式和病因,以及为何它们仍未得到充分理解。I型和II型阻滞均表现为单个窦性P波的阻滞。I型阻滞表现为可见的、不同的且通常呈递减性的房室传导。II型阻滞描述的是一种似乎为全或无的传导,在受阻冲动前后房室传导时间无明显变化。尽管随着窦性心率增加有可能诊断出II型阻滞,但无窦性心动过缓是II型阻滞的一项重要标准,因为迷走神经兴奋(通常为良性情况)可导致窦性心动过缓和房室结阻滞同时出现,这可能表面上类似于II型阻滞。如果受阻后的第一个P波之后PR间期缩短或无法辨认,则不能确立II型阻滞的诊断。在同一记录(如动态心电图)中,与明显的I型结构相关的类似窄QRS波II型阻滞模式可有效排除II型阻滞,因为两种类型的窄QRS波阻滞同时存在极为罕见。隐匿性希氏束或室性期前收缩局限于特殊传导系统而未穿透心肌并引起去极化,可产生模仿I型和/或II型阻滞的心电图模式(假性房室阻滞)。所有正确定义的II型阻滞均为结下阻滞。窄QRS波I型阻滞几乎总是房室结性的,而伴有束支阻滞(急性心肌梗死除外)的I型阻滞在60%至70%的病例中为结下阻滞。二度房室阻滞不能按I型或II型进行分类,但可为结性或结下性。结下阻滞无论其形式或症状如何均需要起搏治疗。对II型阻滞众多不同定义的广泛使用似乎是围绕二度房室阻滞的许多问题的主要原因。遵循正确的定义可为临床评估提供一个合理且简单的框架。