Review
The pathophysiologies of asphyxial vs dysrhythmic cardiac arrest: implications for resuscitation and post-event management

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Abstract

Background

Cardiac arrest is not a uniform condition and significant heterogeneity exists within all victims with regard to the cause of cardiac arrest. Primary cardiac (dysrhythmic) and asphyxial causes together are responsible for most cases of cardiac arrest at all age groups. The purpose of this article is to review the pathophysiologic differences between dysrhythmic and asphyxial cardiac arrest in the prearrest period, during the no-flow state, and after successful cardiopulmonary resuscitation.

Methods

The electronic databases of PubMed/Medline, Scopus, and Cochrane were searched for relevant literature and studies.

Results/Discussion

Significant differences exist between dysrhythmic and asphyxial cardiac arrest regarding their pathophysiologic pathways and affect consequently the postresuscitation period. Laboratory data indicate that asphyxial cardiac arrest leads to more widespread postresuscitation brain damage compared with dysrhythmic cardiac arrest. Regarding postresuscitation myocardial dysfunction, few studies have addressed a comparison of the 2 conditions with controversial results.

Conclusions

Asphyxial cardiac arrest differs significantly from dysrhythmic cardiac arrest with regard to pathophysiologic mechanisms, neuropathologic damage, postresuscitation organ dysfunction, and response to therapy. Both conditions should be considered and treated in a different manner.

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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    Conflict of interest and funding: None.

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