ReviewThe pathophysiologies of asphyxial vs dysrhythmic cardiac arrest: implications for resuscitation and post-event management☆
Introduction
Cardiac arrest (CA) is a clinical syndrome defined as the “cessation of cardiac mechanical activity, as confirmed by the absence of signs of circulation” [1]. Cardiac arrest and sudden cardiac death (SCD) are terms used usually to describe primary (cardiogenic) or dysrhythmic CA of cardiac origin. Asphyxial causes of CA are less common in adults and include all processes that critically reduce cellular availability and use of oxygen. Cardiac arrest may be sudden, but unlike cardiac causes, it is not immediate and follows a “prearrest” period characterized by tissue hypoxia and progressive cardiopulmonary dysfunction. However, evidence suggests that CA is not a uniform condition and significant differences exist in the postresuscitation period after CA due to asphyxia or due to cardiac causes with regard to neurologic recovery, myocardial dysfunction, and outcome.
The aim of the present study is to review the literature to summarize and illustrate the differences between asphyxial and dysrhythmic CA concerning pathophysiologic mechanisms in the prearrest period, during CA, and the after the resuscitation period.
Section snippets
Cardiac arrest causes and epidemiology
Cardiac arrest is a leading cause of death with major socioeconomic implications; it affects more than 400 000 individuals annually with poor prognosis and with survival to hospital discharge not exceeding 11% and neurologic status of the survivors not always being optimal [2], [3]. The true incidence of CA/SCD remains unclear, and definitions of CA and SCD are still not standardized.
Cardiac causes of CA are predominant in adults. Ventricular fibrillation (VF) and pulseless ventricular
Differences in pathophysiologic mechanisms
Asphyxial CA is characterized by a prolonged time course and an important prearrest period where hypoxia (defined as critical reduction in arterial oxygen saturation or arterial oxygen tension), and hypercapnia (defined as increases in arterial carbon dioxide tension), progressively advance along with maintained but gradually deteriorating cardiopulmonary function (Fig. 1) [7], [8], [9], [10].
As asphyxia progresses, bradycardia, as a sign of decompensation, and hypotension, in part due to
Postresuscitation period
Successful CPR attempts and ROSC are the first step toward the goal of complete recovery from CA. The term postcardiac arrest syndrome is related to the pathophysiologic process after the whole-body intense ischemia during prolonged CA and the subsequent reperfusion injuries after successful resuscitation [35]. Important factors that affect prognosis include the duration of untreated CA (no-flow phase), the duration and quality of CPR (low-flow phase), the use of vasopressors, and the possible
Therapeutic considerations
Overall differences that exist between asphyxial and dysrhythmic CA result to a different response to therapy. Treatment implications for each of the 2 entities during resuscitation and after ROSC are summarized in Table 3.
The initial steps in CPR followed A-B-C (airway-breathing-circulation), a noteworthy and easy to recall acronym that highlights the importance of delivering rescue breaths to the CA patient. However, as outlined above, most of adults found in CA do not collapse due to primary
Conclusions
As outlined in this review, asphyxia-induced CA differs significantly from primary CA of cardiac origin with regard to pathophysiologic mechanisms, neuropathologic damage, postresuscitation organ dysfunction, and response to therapy. Advances in our understanding of CA and organ injury require high-quality basic research and clinical trials, possibly on a multicenter basis due to infrequent occurrence of asphyxial CA. Better illustration of pathophysiologic mechanisms involved in the process of
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2022, ResuscitationCitation Excerpt :Kiyohara et al. reported a 1-month favourable neurological outcome proportion of 2.8 %.5 Since hypoxic encephalopathy develops in asphyxia OHCA even before it becomes cardiac arrest (CA),7 it is necessary to achieve an early return of spontaneous circulation (ROSC) to obtain a favourable neurological outcome. We previously reported that of 268 patients with choking-induced OHCA who did not achieve ROSC before arrival at a hospital, only one was living independently-one year later.8
Aetiology of resuscitated out-of-hospital cardiac arrest treated at hospital
2022, ResuscitationCitation Excerpt :None of the small number of cases with OHCA due to hanging or neurological aetiologies survived to hospital discharge, which is consistent with previous findings.18,20. Survival after other respiratory causes such as respiratory failure, choking, and asthma was also low, reflecting the impact of prolonged anoxia on neurological outcome.21,22 This study provides an overview of broad categories of precipitating aetiology within a local health network but is limited in interpretation and applicability due to the retrospective design.
Mild therapeutic hypothermia improves neurological outcomes in a rat model of cardiac arrest
2021, Brain Research BulletinCitation Excerpt :Brain injury alone contributes greatly to the overall morbidity and mortality of patients with CA/CPR. Varvarousis et al. (2015) showed that the mechanism of brain injury is different from ventricular fibrillation CA and asphyxia CA. Our research was focused on asphyxial CA and explored the role of MTH in this condition.
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Conflict of interest and funding: None.