室性心律失常高风险患者怎么预防？上个腰麻？

2021

01/11

米勒之声

A-

A+

本文由“小麻哥的日常”授权转载

室性心律失常（ Ventricular Arrhythmias ）有室性早搏（ Ventricular Premature Beat ）、室速( Ventricular Tachycardia )、心室颤动（ Ventricular Fibrillation ，简称室颤）。室颤为心室肌快而微弱的收缩或不协调的快速乱颤，其结果是心脏无排血，心音和脉搏消失，心、脑等器官和周围组织血液灌注停止，可导致猝死。室颤是导致心源性猝死的重要原因，突然意外地发生于无循环衰竭基础的原发性室颤，可呈短阵或持久发作，给药及时且治疗恰当的，有长期存活的可能。

围术期一旦发生室颤将严重威胁患者的生命安全，其预防尤为重要。而心脏交感过度兴奋可导致室性心律失常的发生，而腰麻能降低交感张力，那么腰麻能降低术中室性心律失常的发生率吗？来看看来自动物实验的最新研究结果，成果发表在Anesthesiology 杂志上，文章标题为Spinal Anesthesia Reduces MyocardialIschemia-triggered Ventricular Arrhythmias by Suppressing Spinal Cord NeuronalNetwork Interactions in Pigs，该研究认为在猪模型中腰麻可以通过抑制脊髓神经元网络相互作用降低心肌缺血梗死诱发的室性心律失常的发生率。

那是不是碰到室性心律失常高风险患者先给他上个腰麻？期待相关临床试验的开展进一步评估。

摘要译文

猪模型中腰麻通过抑制脊髓神经元网络相互作用降低心肌缺血触发的室性心律失常的发生

※※※※※※背景※※※※※※

心脏交感兴奋导致心室心律失常。脊柱麻醉调节交感输出且有心脏保护作用。然而，它对心脏-脊髓反射、脊髓背角心脏传入神经元和调节交感输出的中间外侧核交感神经元网络相互作用的影响还未可知。作者假设布比卡因腰麻能降低心肌缺血期间交感兴奋所致的心脏神经元活化及背角-背角、背角-中间外侧核神经网络间相互作用，从而减少心室心律失常的发生。

※※※※※※方法※※※※※※

采用64通道高密度穿透性芯片电极，在大白猪（n=9）T2脊髓上同时记录背角和中间外侧核神经元的神经元细胞外信号。在鞘内注射布比卡因后，在心肌缺血和心脏负荷依赖性不稳定期间评估背角和中间外侧核的神经相互作用以及已知的心脏心律失常发生标志物。

※※※※※※结果※※※※※※

心肌脊髓神经元是根据其对心肌缺血和心肌负荷依赖性不稳定的反应来鉴定的。布比卡因腰麻不改变脊髓背角和中间外侧核的心肌神经元的基础活动。注射布比卡因后，心肌缺血反应性活性增加的心肌神经元的百分比降低。心肌缺血和心脏负荷依赖性应激增加了背角和背角之间的短期相互作用（从1189对中的324增加至931对，P<0.0001）以及背角和中间外侧核神经元之间的短期相互作用（从1135对中的11增至69对，P<0.0001）。布比卡因减少了这种神经网络反应及背角-背角（从1189对中的931对减少到38对，P<0.0001）和中间外侧核-背角神经元（从1135对中的69对减少到1对，P<0.0001）之间相互作用的增加幅度。布比卡因腰麻可减少急性缺血时心室肌活化恢复间期的缩短和复极的传播，减少室性心律失常的发生。

※※※※※※※结论※※※※※※

腰麻可减少心肌缺血时脊髓背角-背角和背角中间外侧核心肌神经元网络相互作用。阻断脊髓局部心脏传入传出神经元之间的短期协调，有助于减少心脏交感神经兴奋性和室性心律失常的发生。

原文摘要

SpinalAnesthesia Reduces Myocardial Ischemia-triggered Ventricular Arrhythmias bySuppressing Spinal Cord Neuronal Network Interactions in Pigs

Background: Cardiac sympathoexcitation leads to ventricular arrhythmias.Spinal anesthesia modulates sympathetic output and can be cardioprotective.However, its effect on the cardio-spinal reflexes and network interactions inthe dorsal horn cardiac afferent neurons and the intermediolateral nucleussympathetic neurons that regulate sympathetic output is not known. The authorshypothesize that spinal bupivacaine reduces cardiac neuronal firing and networkinteractions in the dorsal horn-dorsal horn and dorsal horn-intermediolateralnucleus that produce sympathoexcitation during myocardial ischemia, attenuatingventricular arrhythmogenesis.

Methods: Extracellular neuronal signals from the dorsal horn andintermediolateral nucleus neurons were simultaneously recorded in Yorkshirepigs (n = 9) using a 64-channel high-density penetrating microarray electrodeinserted at the T2 spinal cord. Dorsal horn and intermediolateral nucleusneural interactions and known markers of cardiac arrhythmogenesis wereevaluated during myocardial ischemia and cardiac load-dependent perturbationswith intrathecal bupivacaine.

Results: Cardiac spinal neurons were identified based on their responseto myocardial ischemia and cardiac load-dependent perturbations. Spinalbupivacaine did not change the basal activity of cardiac neurons in the dorsalhorn or intermediolateral nucleus. After bupivacaine administration, thepercentage of cardiac neurons that increased their activity in response tomyocardial ischemia was decreased. Myocardial ischemia and cardiacload-dependent stress increased the short-term interactions between the dorsalhorn and dorsal horn (324 to 931 correlated pairs out of 1,189 pairs, P <0.0001), and dorsal horn and intermediolateral nucleus neurons (11 to 69correlated pairs out of 1,135 pairs, P < 0.0001). Bupivacaine reduced thisnetwork response and augmentation in the interactions between dorsalhorn-dorsal horn (931 to 38 correlated pairs out of 1,189 pairs, P < 0.0001)and intermediolateral nucleus-dorsal horn neurons (69 to 1 correlated pairs outof 1,135 pairs, P < 0.0001). Spinal bupivacaine reduced shortening ofventricular activation recovery interval and dispersion of repolarization, withdecreased ventricular arrhythmogenesis during acute ischemia.

Conclusions: Spinal anesthesia reduces network interactions between dorsalhorn-dorsal horn and dorsal horn-intermediolateral nucleus cardiac neurons inthe spinal cord during myocardial ischemia. Blocking short-term coordination betweenlocal afferent-efferent cardiac neurons in the spinal cord contributes to adecrease in cardiac sympathoexcitation and reduction of ventricular arrhythmogenesis.