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A Chamber with a View: The Size of the Right Ventricle during Cardiopulmonary Resuscitation

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Van Haren, Frank

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Lippincott Williams & Wilkins

Abstract

Cardiac arrest (CA) is a condition frequently encountered by emergency and critical care physicians. Despite advances in aspects of acute resuscitation over the last decades, survival from CA remains poor. There is a well-described association between the mechanism of CA and the outcome of initial resuscitation. The outcome is better when the initial rhythm is a sustained ventricular tachyarrhythmia, compared with patients who have pulseless electrical activity (PEA) or patients who present with or proceed to asystole. It is essential to recognize potentially reversible and/or treatable causes of CA in the subgroup of patients with PEA or asystole. Survival following CA in this subgroup is unlikely unless a reversible cause can be found and treated effectively (1). Unfortunately, of the main potentially reversible underlying causes of CA, only three may be definitively diagnosed at the bedside using existing standard monitoring and point-of-care investigations: hypoxia, hypothermia, and hypo/hyperkalemia (2). The remaining causes require a combination of clinical assessment, a high index of suspicion, and additional investigations: severe hypovolemia, tamponade, pulmonary embolism (PE), coronary thrombosis, tension pneumothorax, and toxin-related arrest. There is a clear need for better bedside diagnostic tools which are readily available and have acceptable sensitivity and specificity to diagnose or rule out reversible causes of CA. Echocardiography has become a widely used tool for physicians in critical care settings (3). How could the application of echocardiography help clinicians in the specific setting of CA? Extrapolating from accepted applications of echocardiography in other clinical scenarios, potential causes of CA that could be diagnosed using echocardiography include tamponade, coronary artery disease, PE, and hypovolemia. Echocardiography may also be used to detect cardiac standstill and complete absence of motion, independent of electrical activity noted on the monitor, which may have important prognostic implications (4). The 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations suggest that if echocardiography can be performed without interfering with standard advanced cardiovascular life support protocol, it may be considered as an additional diagnostic tool (5). Several studies have examined the use of ultrasound during CA to detect potentially reversible causes, as well as for prognostication during CA (6, 7). A number of protocols and algorithms have been proposed to facilitate a structured approach to the use of ultrasound during cardiopulmonary resuscitation (CPR), often combining echocardiography with ultrasound of the pleura, lungs, and abdomen (8–10). However, as the International Liaison Committee on Resuscitation (ILCOR) correctly points out, it remains unclear if the addition of ultrasound during CPR improves patient outcomes or even increases the likelihood of return of spontaneous circulation (ROSC) (5). For example, in a randomized controlled trial investigating the use of echocardiography during CPR in adult patients with PEA, compared with no use of echocardiography, the occurrence of ROSC for at least 10 seconds was not different between the two groups (11). Importantly, adequate image acquisition during CPR may be challenging, as well as the correct interpretation of findings, because diagnostic references are obtained from patients who are not in CA. A relevant example is the diagnosis of massive PE based on the finding of right ventricular (RV) dilation and left ventricular (LV) flattening. In this issue of Critical Care Medicine, Aagaard et al (12) report on a rigorously conducted animal study, in which they describe the magnitude of RV dilation as measured by echocardiography in three different CA models in pigs: PE, hypoxia, and primary arrhythmia. They confirmed the hypothesis that the RV becomes more dilated during resuscitation from CA caused by PE compared with the other causes. However, the RV was dilated in all groups, and the absolute difference was only 7–9 mm

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Critical Care Medicine

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2099-12-31