Cardiopulmonary Resuscitation–associated Lung Edema: The Price to Pay to Get the Heartbeat?

In this issue of the Journal, Magliocca and colleagues (pp. 447–457) reported the new concept of cardiopulmonary resuscitation (CPR)-associated lung edema (CRALE) in a translational study involving swine models and patients who suffered out-of-hospital cardiac arrest (1). Based on systematic computed tomography analysis in both animal experiments and clinical series, the authors accurately described for the first time the lung damages induced by chest compressions during CPR. Lung injury was observed in about one-third of cases, which is in line with the few previously published data in the field (2–4). This CRALE would be a new part of the postresuscitation disease that is nowadays recognized as a specific and complex entity (5). The novelty is that despite a strong rationale supporting the idea that successfully resuscitated patients with cardiac arrest may suffer from authentic lung injury, the concept of postresuscitation disease had been so far essentially considered from a hemodynamic perspective (6). CRALE will be from now on an additional piece of this complex puzzle that must be taken into account in the management of patients with cardiac arrest. These findings are of high clinical value, as some studies previously suggested that acute respiratory distress syndrome after cardiac arrest significantly affects ICU stay and chance of survival (2–4). According to their hypothesis, Magliocca and colleagues observed that this novel syndrome called “CRALE” was much more prone to occur during mechanical compared with manual CPR.

These observations reactivate the controversy regarding the clinical benefit of mechanical chest compressions and raise several questions concerning ventilation strategies during CPR.

Despite cumulating scientific literature, the superiority of mechanical over manual CPR is still a controversial issue (7–9). The clinical benefit in the daily practice, if any, appears modest, and the reasons explaining these results remain matters of debate. Although mechanical CPR does not improve survival in patients with out-of-hospital cardiac arrest, the CRALE could put the boot in by describing a new adverse event. Though Magliocca and colleagues had reported greater hemodynamic support and systemic perfusion generated by mechanical chest compressions compared with manual chest compressions during ambulance transport in a porcine model of CPR (10), the same group provides evidence in the present study that the severity of lung damage was greater in the mechanical chest compressions group. Then does mechanical CPR–related lung injury preclude us to observe the expected hemodynamic benefits? In other words, would the answer be in looking for new ways of improvement of ventilation strategies during and after CPR rather than giving up with this technique?

The accurate description of the mechanisms involved in CRALE reported in the Journal is indeed a promising opportunity to reconsider ventilation during CPR. In its pioneer work, Safar and colleagues reported Vt generated by chest compressions in intubated patients with cardiac arrest was too small to be measured, whereas similar chest compressions generated almost 150 ml in intubated healthy subjects (11, 12). This finding, though unfortunately neglected for years, was certainly the first observation of what was recently reported as “thoracic airway closure.” During CPR, repetitive chest compressions result in a significant reduction in lung volumes below end-expiratory lung volumes that may favor small airways closure and affect gas exchange (13, 14). Interestingly, airway closure has been also recently reported in patients with acute respiratory distress syndrome (15). Thus, CRALE could be the clinical result of the dynamic reduction of lung volumes occurring during CPR. This could partly explain the greater impact of mechanical chest compressions. Interestingly, positive pressure may overcome airway closure and limit lung volume reduction. Whether a ventilation strategy based on moderate positive end-expiratory pressure (PEEP) level during CPR could be able to limit the occurrence of CRALE is an important question to address.

We already know that a systematic Vt reduction limits the occurrence of lung injury after cardiac arrest (2). Additional studies describing lung and chest wall mechanics as well as lung volumes and gas exchanges are needed to complete the description of CRALE to consider specific ventilation strategies in the particular settings of postresuscitation disease. Identifying patients at risk of CRALE is crucial to adapt ventilator settings at the early stage of this syndrome. This is even more important because caregivers are usually afraid to increase PEEP or put the patient prone in the context of postresuscitation care.

The important findings reported by Magliocca and colleagues as well as their previously published works highlight the imperative need to consider both hemodynamics and respiratory mechanics during and after CPR, revisiting heart–lung interactions in patients with cardiac arrest.