In this retrospective study performed in critically ill CO-poisoned patients treated with rocuronium bromide, propofol, and HBO, we observed both a sustained increase in HR and a transient increase in SBP and ΔBP.
In contrast with these effects, previous hemodynamic anesthesia studies have reported no or little vagolytic effects of rocuronium bromide alone on HR, SBP, and DPB [13–15]. Also, in contrast with these effects and the findings of the present report, propofol has been demonstrated in other anesthesia studies to produce marked decreases in HR, SBP and DBP [16–18]. Likewise, HBO studies in healthy subjects, non-CO-poisoned patients and laboratory animals have also reported marked decreases in HR [7–11], SBP and DBP , as a consequence of hyperbaric oxygen rather than increased pressure per se. In contrast with these effects of rocuronium bromide, propofol and HBO, acute CO-poisoning with carboxyhemoglobin values above 25% has been commonly reported to increase HR [19, 20] as well as, in a more controversial fashion, both SBP and ΔBP . Taken together, these data suggest that CO could appear as a good candidate to explain our findings; however, why these CO effects, if such, increased across treatments i.e. showed long-lasting effects despite HBO therapy is a question that still remains to be elucidated. Based on a previous study that has reported that most of the myocardial dysfunction as evaluated using cardiac biomarkers and ejection fraction measurements (but not hemodynamic parameters) dissipates at 24 hours in CO-poisoned patients , it could be hypothesized that adverse interactions between rocuronium bromide, propofol, HBO, and/or CO could be responsible for the increase in HR, SBP, and ΔBP observed in the present study. However, the individual effects of rocuronium bromide, propofol, and HBO – which all decrease HR, SBP and DBP when given alone – clearly question such a possibility. With no doubt, only a randomized controlled trial adequately designed would be able to identify the actual contribution, if any, of rocuronium bromide, propofol, and/or HBO in the results observed.
Thus, if one assumes that the sustained increase in HR from HBOT1 to HBOT3 as well as the transient increase in SBP and ΔBP from HBOT1 to HBOT2 reported herein are the consequence of CO poisoning, then the decrease in SBP and ΔBP recorded between HBOT2 and HBOT3 could be viewed as a beneficial effect of HBO, which after detoxifying hemoglobin could allow initiating the detoxification of other hemoproteins such as myoglobin whose normal functioning is known to be necessary for effective cardiac output. However, although both SBP and ΔBP showed a general trend toward reduction between HBOT2 and HBOT3, which could indicate as suggested above that HBO had begun to produce its beneficial effects, a careful examination of the patients’ hemodynamic responses revealed that 2 subjects with cardiovascular comorbidities (hypertension and coronary artery disease) still exhibited borderline hemodynamic responses [22–27], with a SBP increase above 140 mmHg and a ΔBP increase near or above 80 mmHg. Taken together with the sustained increase in HR recorded from HBOT1 to HBOT3, these data suggest that the detoxification of myoglobin by HBO could be longer than generally thought, and that more 3 HBOT sessions could be necessary to allow full hemodynamic recovery in CO-poisoned patients or at least some of them.
As the vast majority of the retrospective case-series studies, the present report should be interpreted carefully because of its inherited limitations. This includes the small sample of patients, the lack of information on the duration of the exposure to CO, the uncontrolled delay between the end of the exposure to CO and the first HBOT session, the uncontrolled administration of medication, and the absence of actual post-treatment evaluations that could have indicated that HR, SBP, and ΔBP had finally returned to basal values. However, despite these limitations, we believe that the present study is of actual interest since it is the first one, to the best of our knowledge, to report the hemodynamic effects of HBO in critically ill CO-poisoned patients.
Given the respective effects of rocuronium bromide, propofol, HBO, and CO on the hemodynamic parameters, we conclude as discussed in details above that the increase in HR, SBP and ΔBP observed in the present study is likely to be due to CO, and that more than 3 HBO sessions would be necessary to provide full hemodynamic recovery in CO-poisoned patients. If such, it is likely that HR, SBP, and ΔBP could be used as physiological markers to assess CO detoxification. Monitoring these hemodynamic parameters together with patient outcomes in future prospective clinical studies could document this possibility. With no doubt, further studies are needed to confirm our hypothesis, and lead clinicians to use hemodynamic parameters as a clinical biomarker for CO-poisoning and HBO detoxification.