When lung compliance is poor such as in patients with pneumonia or bronchiolitis or when there is excess lung fluid for example with pulmonary edema, the critical closing pressure is increased, and lungs become more likely to collapse. During mechanical ventilation, by maintaining the PEEP above the critical closing pressure, alveolar collapse can be prevented [1].
Through a complex series of cardiopulmonary interactions, PEEP can potentially have a direct impact on CO. The blood in the venous system relies on the pressure difference generated by the venous blood, the mean systemic pressure, and the right atrium to promote the forward flow of blood back to the heart. This difference between the mean systemic pressure and the right atrial pressure is the driving force for the preload [16,17,18]. When PEEP is used, the increase in alveolar pressure is transmitted to the entire thorax, potentially increasing the right atrial pressure and thereby reducing the pressure difference between the mean systemic pressure and the right atrial pressure. If the decrease in this pressure gradient is significant enough, it can result in decreased venous return to the heart, decreasing cardiac output [19, 20]. The exact impact that this effect has is questionable, as a study by Jellinek et al. demonstrated that positive pressure increases both the right atrial pressure as well as the mean systemic pressure proportionally, resulting in no change in the mean systolic pressure-right atrium pressure gradient [21]. The use of too much PEEP can over-distend alveoli resulting in mechanical compression of the pulmonary capillaries, increasing the right ventricular (RV) afterload. An increase in the RV afterload can over-distend the RV, causing bowing of the ventricular septum into the left ventricular (LV), thereby further decreasing the volume of the LV, decreasing LV filling, and reducing CO. On the left side of the heart, PEEP can shift the LV pressure-volume curve to the left, indicating a decrease in LV distensibility. Thus, given that during CPR blood flow and venous return are already compromised as optimal CPR generates only 15% to 25% of normal CO [22], these effects of PEEP on CO can potentially diminish an already severely compromised CO.
Conversely, although an inappropriate amount of PEEP can have a detrimental effect on CO, using an appropriate amount of PEEP can potentially augment CO. Increasing the intrathoracic pressure can decrease the LV afterload, thereby improving the CO, especially in the setting of a poorly functioning LV. Additionally, the correct amount of PEEP can optimize peripheral vascular resistance, thereby improving LV preload [1, 19, 20].
The use of PEEP can potentially play a significant role in the ability to ventilate patients receiving CPR. Studies performed by the Cardiac Arrest and Ventilation International Association for Research Group demonstrated that in a cadaver model and a bench model of CPR, as well as in a clinical study analyzing capnograms of intubated patients receiving CPR, intrathoracic airway closure occurs in patients receiving CPR, which can limit ventilation. This airway closure was mitigated by the use of PEEP up to 10 cmH2O, which also caused some degree of ventilation to occur with the oscillations of air generated by the change in intrathoracic pressure that occurs during the compression and decompression phase of chest compressions [23, 24]. The effect that using no PEEP potentially has on oxygenation and DO2 to the tissues during CPR is also unknown.
There are currently no studies directly evaluating the effect of PEEP on CO during CPR. There is also currently no consensus whether or not PEEP should be applied during CPR, and if used, how much PEEP should be applied. The aim of this study was to evaluate the effect of PEEP on CO and DO2 during CPR and to determine the ideal PEEP to maximize DO2 by augmenting both CO and arterial oxygen concentration during CPR.
The results of this study demonstrate that as PEEP is increased from 0 to 20 cmH2O, there is a significant decline in CO and DO2. Increasing the PEEP from 0 to 5 cmH2O results in a slight, statistically insignificant, decrease in CO, and increase in DO2. Further increases in PEEP to 10 cmH2O and above result in significant drops in CO. Even compared with PEEP of 5 cmH2O, PEEP of 10 cmH2O showed a significant decline in CO. For DO2, compared with both PEEP of 0 and 5 cmH2O, once PEEP 15 cmH2O and higher is reached, there is a statistically significant drop in DO2. In evaluating the effect of PEEP on PaO2 during CPR, as PEEP is increased from 0 to 20 cmH2O, there is a significant increase seen in PaO2. Compared with a PEEP of 0 cmH2O, PEEP of 5, 10, and 15 cmH2O all had significantly higher PaO2. Compared with PEEP of 5 cmH2O, only PEEP of 20 cmH2O had a significantly higher PaO2.
Using the Gaussian mixture model on adjusted means of CO and DO2, there were three groups of homogeneous PEEP that were identified: 0–5, 10–15, and 20 cmH2O. PaO2 was not included in this analysis because even the lowest PEEP had a PaO2 of 154, which is physiologic, representing an oxygen saturation of 100% and is likely adequate for CPR. In addition, the importance of PaO2 is likely to be in the amount of oxygen delivered to the tissues during CPR, making DO2 the more important variable. Based on these results, assuming that the lungs are not acutely ill or poorly compliant, our results demonstrate that the 0–5 cmH2O PEEP group provides optimal CO and DO2, with PEEP of 5 cmH2O providing the highest DO2 overall, with an insignificant difference in CO between PEEP of 0 cmH2O and 5 cmH2O. Thus, based on these results, it appears that PEEP of 5 cmH2O would be the optimal PEEP for ventilating patients during CPR.
This study has a number of limitations. Most CPR studies are done on animals or other non-human models, and the porcine model is commonly used as a model for cardiac arrest because the physiology approximates that of humans [14]. However, it has to be acknowledged that there are differences in cardiovascular physiology between humans and pigs, such as different thorax geometry [24], which makes it an imperfect model for CPR physiology in humans. Also, the outcomes in this study are meant to evaluate cardiovascular parameters during CPR, with the goal of optimizing organ perfusion during CPR. However, there is no evidence that following the conclusions in this study will directly lead to a better outcome in cardiac arrest patients. However, we do feel that to give providers the best chance at successfully resuscitating a patient, CPR must be optimized, and adjusting the PEEP to achieve optimal oxygen delivery is a potential area of optimization. Ideally, these findings should be verified with a proper trial in humans; however, such a trial may be extremely difficult to design and implement. Although CPR is not typically performed with patients on a ventilator, PEEP adjustments can be made through the PEEP valve on a bag-valve-mask device. Finally, the goal of this study was to isolate the effect of PEEP on CO. To accomplish this, slight adjustments were made to optimize physiologic parameters, such as allowing the animal to tolerate 60 min of CPR, which is not typically done when performing CPR on humans. For example, the respiratory rate was higher than the 10 breaths per minute currently recommended during continuous compression CPR to achieve and maintain a physiologic pH prior to and during CPR. Along the same lines, the decision was made to maintain the animal on each PEEP level for 9 min, with 1 min in between to draw the arterial blood gas and reconnect cardiac output monitor to maintain the entire duration of CPR less than 1 h. We felt that if the compressions were to continue for more than an hour, the animals would be less stable for the final PEEP levels, which would introduce another variable into the equation. By keeping the total compression time less than 1 h, we felt that the animal would be able to tolerate the entire course of compressions, whereas extending the overall time of compressions would have risked greater instability towards the end, compared with the beginning. Using a two-way analysis of variance paradigm for the statistical analysis took into account PEEP level as well as time duration in the final analysis. If the animals were unstable for the final PEEP levels, this would have added an additional variable that would have been difficult to account for. In addition, after initiating cardiac arrest and during the 60 s prior to initiation of chest compression, the pigs were ventilated using a PEEP of 5 cmH2O to avoid alveolar collapse prior to the implementation of the study protocol, despite this differing from what occurs in typical cardiac arrest patients, who are not receiving PEEP when they go into cardiac arrest. We feel that these do not detract from the results of this study, as the goal of the study is to look at the effect PEEP has on CO, which this study certainly does.