The Postcardiac Arrest Inflammatory Response: Mechanisms and Therapeutic Targets.

Beyond anoxic brain injury and transient myocardial dysfunction, many patients develop a systemic ischemia/reperfusion response with endothelial and microvascular dysfunction, vasoplegia, and immune dysregulation-features that contribute to shock and organ failure.

除了缺氧性脑损伤和短暂的心肌功能障碍外，许多患者还会出现全身性的缺血/再灌注反应，包括内皮和微血管功能障碍、血管舒张和免疫调节失常——这些特征都会导致休克和器官衰竭。

Hemodynamic instability is often mixed with low systemic vascular resistance despite preserved or recovering cardiac output, but management is still largely supportive and centered on achieving a target mean arterial pressure.

尽管心脏输出量保持或正在恢复，但血流动力学不稳定常常与低系统血管阻力混杂在一起，但管理仍然主要是支持性的，并且集中在实现目标平均动脉压上。

An increasing understanding of the central role of inflammation, including gastrointestinal barrier disruption, cytokine release, complement activation, nitric oxide-cGMP signaling, and immune phenotypic heterogeneity has prompted evaluation of targeted adjunctive therapies.

对炎症中心作用的日益了解，包括胃肠道屏障破坏、细胞因子释放、补体激活、一氧化氮-cGMP信号传导和免疫表型异质性，促使了靶向辅助治疗的评估。

However, randomized trials of immunomodulators and other vasoactive strategies have yielded mixed results, reflecting biological heterogeneity and limited phenotypic stratification.

然而，关于免疫调节剂和其他血管活性策略的随机试验结果不一，反映了生物学异质性和有限的表型分层。

This review synthesizes contemporary understanding of the inflammatory and hemodynamic mechanisms underpinning postcardiac arrest syndrome, examines current and emerging pharmacologic strategies, and highlights priorities for future investigation, including mechanistic phenotyping, prospective biobanking, and prospective trial requirements to guide more precise management strategies in postcardiac arrest care.

本综述综合了对心脏停搏后综合征炎症和血流动力学机制的当代理解，审视了当前和新兴的药物治疗策略，并强调了未来研究的优先事项，包括机制表型分型、前瞻性生物样本库建设和前瞻性试验要求，以指导心脏停搏后护理中更精确的管理策略。