背景:心脏骤停后综合征(PCAS)在临床实践中提出了多方面的挑战,尽管管理策略有所进步,但其特征是严重的神经系统损伤和高死亡率。PCAS的重要关键方面之一是停搏后肺损伤(PALI),这极大地导致了糟糕的结果。PALI起因于病理生理机制的复杂相互作用,包括胸部按压造成的创伤,肺缺血再灌注损伤,抽吸,和全身性炎症。尽管具有临床意义,PALI的病理生理学仍未完全了解,需要进一步研究以优化治疗方法。
方法:这篇综述全面审查了现有文献,以阐明流行病学,病理生理学,以及PALI的治疗策略。进行了全面的文献检索,以确定研究PALI的临床前和临床研究。综合了这些研究的数据,以全面概述PALI及其管理。
结果:流行病学研究强调了心脏骤停后患者中PALI的大量患病率,多达50%的幸存者经历急性肺损伤。诊断成像模式,包括胸部X光片,计算机断层扫描,还有肺部超声,在识别PALI和评估其严重程度中起着至关重要的作用。病理生理学,PALI包含一系列因素,包括与胸部按压有关的创伤,肺IR损伤,抽吸,全身炎症,它们共同导致肺功能障碍和不良预后。治疗学上,肺保护性通气策略,如低潮气量通气和呼气末正压的优化,已成为PALI管理的基石方法。此外,治疗性低温和针对线粒体功能障碍的新兴疗法有望减轻PALI相关的发病率和死亡率.
结论:PALI代表了心脏骤停后护理的重大临床挑战,需要及时诊断和有针对性的干预措施以改善结果。线粒体相关疗法是PALI的新型治疗策略之一。需要进一步的临床研究来优化PALI管理并增强心脏骤停后护理范例。
BACKGROUND: Post-cardiac arrest syndrome (PCAS) presents a multifaceted challenge in clinical practice, characterized by severe neurological injury and high mortality rates despite advancements in management strategies. One of the important critical aspects of PCAS is post-arrest lung injury (PALI), which significantly contributes to poor outcomes. PALI arises from a complex interplay of pathophysiological mechanisms, including trauma from chest compressions, pulmonary ischemia-reperfusion (IR) injury, aspiration, and systemic inflammation. Despite its clinical significance, the pathophysiology of PALI remains incompletely understood, necessitating further investigation to optimize therapeutic approaches.
METHODS: This review comprehensively examines the existing literature to elucidate the epidemiology, pathophysiology, and therapeutic strategies for PALI. A comprehensive literature search was conducted to identify preclinical and clinical studies investigating PALI. Data from these studies were synthesized to provide a comprehensive overview of PALI and its management.
RESULTS: Epidemiological studies have highlighted the substantial prevalence of PALI in post-cardiac arrest patients, with up to 50% of survivors experiencing acute lung injury. Diagnostic imaging modalities, including chest X-rays, computed tomography, and lung ultrasound, play a crucial role in identifying PALI and assessing its severity. Pathophysiologically, PALI encompasses a spectrum of factors, including chest compression-related trauma, pulmonary IR injury, aspiration, and systemic inflammation, which collectively contribute to lung dysfunction and poor outcomes. Therapeutically, lung-protective ventilation strategies, such as low tidal volume ventilation and optimization of positive end-expiratory pressure, have emerged as cornerstone approaches in the management of PALI. Additionally, therapeutic hypothermia and emerging therapies targeting mitochondrial dysfunction hold promise in mitigating PALI-related morbidity and mortality.
CONCLUSIONS: PALI represents a significant clinical challenge in post-cardiac arrest care, necessitating prompt diagnosis and targeted interventions to improve outcomes. Mitochondrial-related therapies are among the novel therapeutic strategies for PALI. Further clinical research is warranted to optimize PALI management and enhance post-cardiac arrest care paradigms.