Bissett J K, Kane J J, de Soyza N, McConnell J, Schmitt N
J Electrocardiol. 1977 Jan;10(1):5-12. doi: 10.1016/s0022-0736(77)80025-3.
An interpolated premature ventricular contraction (PVC) may produce either complete block of the next sinus impulse or depression of A-V nodal conduction with a prolonged A-H interval. When a PVC results in partial depression of a A-V nodal conduction, the effect on subsequent premature atrial stimuli is unknown. The authors have recently observed three patients in which the effect of a premature ventricular stimulus with interpolation on the functional refractory period of the A-V node could be measured. In case one an interpolated PVC sufficient to prolong the A-H interval from 80 to 120 msec was followed by programmed premature atrial stimuli which resulted in no additional A-V nodal delay, and the apparent functional refractory period of the A-V node was reduced from 420 to 330 msec when compared with the atrial extrastimulus technique. In case two a programmed ventricular extrastimulus prolonged the A-H interval in the following sinus beat from 120 to 240 msec; atrial extrastimuli then resulted in only minimal increments in A-V nodal delay and the apparent functional refractory period of the A-V node was reduced from 590 msec. A ventricular extrastimulus in case three increased the resting A-H interval from 60 to 115 msec; conduction of atrial extrastimuli then resulted in a reduction in the functional refractory period of the A-V node from 465 to 400 msec. In each case an interpolated premature ventricular stimulus produced (1) depression of A-V nodal conduction in the ensuing sinus beat A1 and (2) relative facilitation of A-V nodal conduction of a subsequent premature atrial stimulus (A2). The functional refractory period of the A-V node was reduced when compared with the atrial extrastimulus technique alone.
插入性室性早搏(PVC)可能会导致下一个窦性冲动完全阻滞,或使房室结传导受抑制,A-H间期延长。当PVC导致房室结传导部分受抑制时,其对后续房性早搏刺激的影响尚不清楚。作者最近观察到3例患者,可测量插入性室性刺激对房室结功能不应期的影响。病例1中,一个足以使A-H间期从80毫秒延长至120毫秒的插入性PVC之后进行程控房性早搏刺激,未导致额外的房室结延迟,与房性额外刺激技术相比,房室结的表观功能不应期从420毫秒缩短至330毫秒。病例2中,一个程控室性额外刺激使随后窦性搏动的A-H间期从120毫秒延长至240毫秒;随后房性额外刺激仅导致房室结延迟有极小增加,房室结的表观功能不应期从590毫秒缩短。病例3中,一个室性额外刺激使静息A-H间期从60毫秒增加至115毫秒;随后房性额外刺激的传导使房室结功能不应期从465毫秒缩短至400毫秒。在每种情况下,插入性室性刺激均产生了(1)随后窦性搏动A1中房室结传导受抑制,以及(2)随后房性早搏刺激(A2)的房室结传导相对易化。与单独使用房性额外刺激技术相比,房室结的功能不应期缩短。