Hyperventilation in response to progressive reduction in central blood volume to near syncope.

INTRODUCTION: There is little evidence to support the usefulness in monitoring respiration during casualty triage and transport as an early indicator of hemorrhage severity and trauma patient outcome. We, therefore, tested the hypothesis that hyperventilation can be elicited by progressive reductions in central blood volume independent of metabolic stimuli.
METHODS: Progressive central hypovolemia was induced in 10 healthy subjects (5 men, 5 women) by applying lower body negative pressure (LBNP). The LBNP protocol consisted of a 5-min controlled rest period (0% LBNP) followed by progressive 5-min chamber decompressions until the onset of hemodynamic decompensation (LBNP(max)). During each LBNP stage, total minute ventilation volume (V(E)), tidal volume (V(T)), respiratory rate, oxygen uptake (Vo2), end-tidal CO2 (E(T)co2), arterial oxygen saturation (S(p)o2), and venous blood pH and lactate were measured.
RESULTS: Compared with baseline, Vo2, S(p)o2, Po2, Pco2, pH, and lactate were unaltered throughout LBNP. V(E) was unaltered through 80% of LBNP tolerance, but increased by 54% during LBNP(max) as a result primarily of elevated V(T), while E(T)Co2 was reduced.
CONCLUSIONS: Increased V(E) at LBNP(max) combined with reduced E(T)co2 in the absence of changes in blood and systemic metabolic stimuli support the hypothesis that severe reductions in central blood volume drive hyperventilation. The endogenous "respiratory pump" may be a protective strategy to optimize cardiac filling in conditions of central hypovolemic hypotension, but its late appearance indicates that respiratory parameters may not be useful as a clinical metric for early prediction of patient outcome during hemorrhage.