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 (etCO₂) and tested two hypotheses: (1) that etCO₂ can distinguish massive PE from hemorrhagic shock and (2) that PE with cardiac arrest reduces etCO₂ 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, etCO₂ 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 etCO₂ occurred coincident with an increase in alveolar dead space fraction in the PE group. In the first minute of ventilation after cardiac arrest, the etCO₂ 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 etCO₂ 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 etCO₂ readings during CPR.