Airway Pressure Monitoring May Improve Small Airway Flow, Hemodynamics, and Tissue Oxygenation.

To the Editor:

We would like to congratulate Scales and Kavanagh (1) for their insightful comments reported in the editorial accompanying the study by Grieco and colleagues (2). It is true that research on resuscitation made early gains, but recent progress has been slow because of the dispersion of researchers to aspects other than elucidating the physiology and pathophysiology of cardiac arrest and resuscitation.

Although our understanding of the interaction between chest compression and mechanical ventilation remains limited, expert opinions will probably continue to rely on flawed studies that neither report nor take into consideration, when interpreting the results, the method of postintubation ventilation (self-inflating bag or ventilator), while suggesting simultaneously that early intubation during cardiopulmonary resuscitation (CPR) does not improve, or even decreases, survival (3). Ventilation with a self-inflating bag in intubated patients usually results in excessive ventilation volume and rate, thus aggravating oxygenation and hemodynamics, and surprisingly, it continues to be a major limitation in resuscitation studies.

Cordioli and colleagues (4) demonstrated that ventilation during CPR by using currently recommended chest compression rates takes place entirely below FRC and is associated with negative intrathoracic pressures during decompression. Although the thoracic pump theory is not widely accepted among the resuscitation community, the study of Cordioli and colleagues suggests that both cardiac pump and thoracic pump have a role in forward blood flow and tissue oxygenation. In this context, the study by Grieco and colleagues (2) strengthens the evidence-based notion that the harmony between circulation and ventilation during CPR is critical. Achieving the correct balance between too little and too much ventilation is of major importance for optimizing survival, and theoretically, there must be an intrathoracic pressure limit at which the effect of a thoracic pump should be maximal. Above this limit, intrathoracic pressure would be deleterious, and under this limit, ventilation may not provide adequate blood oxygenation because of small airway closure, increasing pulmonary vascular resistance and impairing pulmonary and systemic blood flow.

Our group has recently shown an association between mean airway pressure and outcome of CPR in mechanically ventilated patients, with a value of 42.5 mbar being associated with return of spontaneous circulation (5). In our patients, simultaneous positive pressure ventilation in time with each chest compression prevented a loss of intrathoracic pressure via the airway, and probably kept the small airways open. In this study, we found no difference in end-tidal carbon dioxide between survivors and nonsurvivors, probably because of the maintenance of flow in small airways and the improvement in minute-volume ventilation during CPR (6). Of note, the rise in intrathoracic pressure in mechanically ventilated patients undergoing CPR is transmitted equally to all intrathoracic structures and squeezes out the pulmonary vessels, which increases forward blood flow, arterial oxygen partial pressure, and aortic pressure. Moreover, as hemodynamics may be aggravated in prolonged CPR because of vascular tone deterioration, the pressing effect of positive pressure ventilation and increased intrathoracic pressure on aortic wall may increase aortic resistance and retrograde volume loading, therefore enhancing the compression-related blood flow (5).

Collectively, the study by Grieco and colleagues and our findings highlight the favorable effects of the thoracic pump and the importance of intubation and mechanical ventilation in patients with cardiac arrest, supporting our deduction that the interplay between ventilation and chest compression during CPR is a key point to optimize outcomes (6). As proper timing of compression and ventilation seems to be the key for improving the circulation, the focus of the resuscitation community must immediately return to the elucidation of the physiology and pathophysiology of cardiac arrest and resuscitation.