| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
Faculty of Medicine of Ribeiro Preto, Department of Pharmacology, University of Sao Paulo, SP, Brazil
To the Editor:
Martineau et al. have reported an interesting case of severe CO2 embolism during endoscopic saphenectomy (1). The CO2 embolism was associated with an increase in systolic pulmonary pressure from 22 to 65 mm Hg. Pharmacologic therapy of this life-threatening condition consisted of an IV infusion of nitroglycerine (up to 83 mg/min) and norepinephrine (20 mg/min), and inhaled epoprostenol (75 mg). The authors claimed that inhaled epoprostenol may have prevented them from using extracorporeal circulation for circulatory support. We believe there is little to support this hypothesis. Indeed, the inotropic effects of norepinephrine and the pulmonary vasodilation caused by nitroglycerin-induced nitric oxide (NO) release could totally account for the immediate hemodynamic improvement observed 5 min after the initiation of treatment (2–4).
Norepinephrine was suggested to enhance the already known beneficial effects of NO during pulmonary embolism (5). In addition, CO2 is rapidly excreted by the lungs, and it follows that the hemodynamic collapse may resolve promptly.
References
Montreal Heart Institute, Montreal, Quebec, Canada
In Response:
We agree with Mr. Dias that we cannot rule out that the noradrenaline and the nitroglycerine were alone responsible for the improvement in the clinical condition of this patient. First, when the CO2 embolism occurred, the patient remained hemodynamically unstable until we added the inhaled epoprostenol; second, we have previously encountered the same problem in another patient and the therapy based only on that nitroglycerine and noradrenaline did not work and we had to return to cardiopulmonary bypass (1); third, our experience with inhaled epoprostenol tends to support such a favorable effect (2); fourth, CO2 embolism can lead to pulmonary hypertension and cardiovascular collapse which may not resolve rapidly when the embolism is severe as demonstrated in an animal model (3). Finally, we have just conducted a randomized controlled trial on inhaled epoprostenol in patients undergoing cardiac surgery with pulmonary hypertension. This trial demonstrated that the onset of the medication corresponded to what we have observed in this patient and that the effect is proportional to the severity of pulmonary hypertension (4). For these reasons, as we mentioned in the Discussion (in our article), "It is possible that the favorable response observed in the treatment of pulmonary hypertension with use of inhaled epoprostenol may have prevented us from using extracorporeal circulation for circulatory support." Nitric oxide could have been used but it was not as readily available in our operating room as inhaled epoprostenol. As a minor detail, the drug dosages reported by Dias are not "nitroglycerine (up to 83 mg/min) and norepinephrine (20 mg/min), and inhaled epoprostenol (75 mg)" but all in µg/min and in µg.
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
