CO₂ Oscillation during Cardiopulmonary Resuscitation: The Role of Respiratory System Compliance

To the Editor:

We read with interest the manuscript by Grieco and colleagues entitled “Intrathoracic Airway Closure Impacts CO₂ Signal and Delivered Ventilation During Cardiopulmonary Resuscitation” (1).

The authors conducted a very elegant clinical investigation corroborated by focused experiments in the Thiel cadaver model, describing a peculiar oscillatory capnographic pattern during cardiopulmonary resuscitation (CPR). From the results, it has been speculated that a low oscillating CO₂ during chest compressions is a result of the presence of airway collapse, which obstructs the airflow. However, as mentioned by the authors in the discussion, individual differences in the compliance of the respiratory system (Cpl,rs, including the lungs and the chest wall) could have a great prominence in explaining this finding. For a given pressure applied to the sternum during a chest compression, the gas volume displacement will be directly proportional to the compliance of the respiratory system. Therefore, patients with a lower airway opening index (AOI) may have had lower Cpl,rs. This would also explain the correlation between alveolar ventilation and AOI, because greater ventilation was likely in patients with higher compliance. Interestingly, a greater AOI was observed in patients with a shockable rhythm, who are likely to have a shorter duration of cardiac arrest compared with those with nonshockable rhythms and thus a lesser deterioration in Cpl,rs (2).

We wonder about the correlation between Cpl,rs measured during regular tidal ventilation and AOI.

Although small airway closure might affect the measurement of compliance, this is unlikely during regular tidal ventilation. We accept that a formal “static” measurement of Cpl cannot be obtained during chest compression, but a good estimate would be possible from the delivered Vt, given that a constant inspiratory pressure was applied. Indeed, a reliable value for Cpl,rs can be obtained in the Thiel cadavers.

Respiratory system compliance could also explain the beneficial effects of positive end-expiratory pressure (PEEP). Ventilation resulting from chest compression occurs between FRC and residual volume (3). At this level of lung volume, the pressure–volume curve of normal subjects is less compliant than it is above FRC (4). The application of PEEP would increase the end-expiratory lung volume and cause the chest compressions to “ventilate” the respiratory system in a more compliant part of the pressure–volume curve, leading to greater Vt and greater alveolar ventilation.

Finally, the “circulatory” component of CPR, that is, forward blood flow generated by chest compression, affects end-tidal CO₂ and might potentially affect the subsequent AOI calculation. Indeed, ventilation and hemodynamics are deeply interconnected in the pathophysiology of CPR, as $\stackrel{.}{\text{Q}}$ is the major determinant of CO₂ transport to the lungs. Because $\stackrel{.}{\text{Q}}$ may vary during CPR in relationship to chest compression quality and/or patient’s condition, for example, development of stoned heart for prolonged resuscitation and Cpl,rs modification, the evolving AOI may change over time.

In conclusion, although we believe that the work by Grieco and colleagues does not completely tease out the relative contributions of compliance versus airway closure in the generation of CO₂ oscillation, their findings have tremendous clinical relevance, particularly for the potential benefits of PEEP during CPR, and highlight the importance of more studies on the topic.