End tidal CO2 is reduced during hypotension and cardiac arrest in a rat model of massive pulmonary embolism

Background: We investigated the effect of massive pulmonary embolism (MPE) on end tidal CO2 (etCO(2)) and tested two hypotheses: (1) that etCO(2) can distinguish massive PE from hemorrhagic shock and (2) that PE with cardiac arrest reduces etCO(2) during resuscitation to a greater extent than arrhythmic cardiac arrest. Methods: Anesthetized, mechanically ventilated rats (N = 10 per group), were subjected to either graded PE latex microspheres), or graded hemorrhagic shock to produce a final mean arterial blood pressure, (MAP) of 40 mmHg; a third group was subjected to surgical/anesthetic control conditions. Cardiac arrest was induced by the following methods: intravenous injection of a large bolus of microspheres in the PE group, aortic puncture in the hemorrhage group, and intravenous tetrodotoxin (TTX) to produce arrhythmic cardiac arrest in the control group. Results: At a MAP of 40 mmHg, etCO(2) was significantly decreased in the PE group (18.3 +/- 1.9 torr) compared with both the hemorrhage (24.3 +/- 1.3) and the control group (35.0 +/- 1.3 torr; ANOVA P < 0.001). The decreased etCO(2) occurred coincident with an increase in alveolar dead space fraction in the PE group. In the first minute of ventilation after cardiac arrest, the etCO(2) was significantly decreased in the PE group (6.5 +/- 0.9) versus both hemorrhage (16,5 +/- 1.1) and TTX (34.2 +/- 2.4 torr). Conclusions: Massive PE with shock decreases the etCO(2) and increases the dead space fraction to a greater extent than hemorrhagic shock at the same MAP. Cardiac arrest from PE is associated with extremely low etCO(2) readings during CPR. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.