Limitations of end-tidal CO2 as an early indicator of central hypovolemia in humans

Objective. This study tested the hypothesis that pulmonary end-tidal CO2 (PETCO2) tracks reductions in central blood volume in human volunteers exposed to progressive central hypovolemia. Methods. Measurements of PETCO2, systolic (SBP), diastolic (DBP), and mean arterial (MAP) blood pressures, heart rate (HR), stroke volume (SV), and respiratory rate (RR) were obtained in 50 healthy human subjects during baseline supine rest and exposure to progressive reductions of central blood volume produced by application of lower body negative pressure (LBNP). Results. As increasing amounts of LBNP were applied, SBP, DBP, MAP, HR, SV, and PETCO2 decreased (p < 0.001). RR was not altered (p = 1.0). The decrease in PETCO2 did not begin to occur until 40% of maximal LBNP was applied. While PETCO2 decreased progressively thereafter, the range of baseline values (28.8-49.2 mmHg) varied more than the reduction in PETCO2 elicited by maximal LBNP (baseline = 40.1 ± 0.6 mmHg; maximal LBNP = 29.8 ± 1.0 mmHg). The earliest significant alteration was observed in SV, which occurred at 20% of maximal LBNP. MAP did not decline significantly until 80% of maximal LBNP was reached. PETCO2 was correlated positively with SV (r2 = 0.87). Conclusions. Although PETCO2tracked decreases in SV in this human model of progressive central hypovolemia, reductions in PETCO2were small relative to the range of baseline values. Thus, monitoring such small reductions in PETCO2 as an early warning of imminent cardiovascular collapse during hemorrhage may not be clinically useful without monitors capable of providing continuous trending.