TY - JOUR
T1 - Hyperventilation in response to progressive reduction in central blood volume to near syncope
AU - Convertino, Victor A.
AU - Rickards, Caroline A.
AU - Lurie, Keith G.
AU - Ryan, Kathy L.
PY - 2009/12/1
Y1 - 2009/12/1
N2 - Introduction: There is little evidence to support the usefulness in monitoringrespiration during casualty triage and transport as an early indicatorof hemorrhage severity and trauma patient outcome. We, therefore, tested the hypothesis that hyperventilation can be elicited by progressivereductions in central blood volume independent of metabolic stimuli. Methods: Progressive central hypovolemia was induced in 10 healthysubjects (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 untilthe onset of hemodynamic decompensation (LBNPmax). During eachLBNP stage, total minute ventilation volume (V̇E), tidal volume (VT), respiratoryrate, oxygen uptake (V̇O2), end-tidal CO2 (ETCO2), arterial oxygensaturation (SpO2), and venous blood pH and lactate were measured. Results:Compared with baseline, V̇O2, SpO2, PO2, PCO2, pH, and lactatewere unaltered throughout LBNP. V̇E was unaltered through 80% of LBNPtolerance, but increased by 54% during LBNPmax as a result primarily ofelevated VT, while ETCO2 was reduced. Conclusions: Increased V̇E at LBNPmax combined with reduced ETCO2 in the absence of changes inblood and systemic metabolic stimuli support the hypothesis that severereductions in central blood volume drive hyperventilation. The endogenous" respiratory pump "may be a protective strategy to optimize cardiacfilling in conditions of central hypovolemic hypotension, but its late appearanceindicates that respiratory parameters may not be useful as a clinicalmetric for early prediction of patient outcome during hemorrhage.
AB - Introduction: There is little evidence to support the usefulness in monitoringrespiration during casualty triage and transport as an early indicatorof hemorrhage severity and trauma patient outcome. We, therefore, tested the hypothesis that hyperventilation can be elicited by progressivereductions in central blood volume independent of metabolic stimuli. Methods: Progressive central hypovolemia was induced in 10 healthysubjects (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 untilthe onset of hemodynamic decompensation (LBNPmax). During eachLBNP stage, total minute ventilation volume (V̇E), tidal volume (VT), respiratoryrate, oxygen uptake (V̇O2), end-tidal CO2 (ETCO2), arterial oxygensaturation (SpO2), and venous blood pH and lactate were measured. Results:Compared with baseline, V̇O2, SpO2, PO2, PCO2, pH, and lactatewere unaltered throughout LBNP. V̇E was unaltered through 80% of LBNPtolerance, but increased by 54% during LBNPmax as a result primarily ofelevated VT, while ETCO2 was reduced. Conclusions: Increased V̇E at LBNPmax combined with reduced ETCO2 in the absence of changes inblood and systemic metabolic stimuli support the hypothesis that severereductions in central blood volume drive hyperventilation. The endogenous" respiratory pump "may be a protective strategy to optimize cardiacfilling in conditions of central hypovolemic hypotension, but its late appearanceindicates that respiratory parameters may not be useful as a clinicalmetric for early prediction of patient outcome during hemorrhage.
KW - Hemodynamic decompensation
KW - Hemorrhagic shock
KW - Lower body negative pressure
KW - Minute ventilation
KW - Respiratory rate
KW - Tidal volume
UR - http://www.scopus.com/inward/record.url?scp=77649210803&partnerID=8YFLogxK
U2 - 10.3357/ASEM.2598.2009
DO - 10.3357/ASEM.2598.2009
M3 - Article
C2 - 20027847
AN - SCOPUS:77649210803
SN - 0095-6562
VL - 80
SP - 1012
EP - 1017
JO - Aviation Space and Environmental Medicine
JF - Aviation Space and Environmental Medicine
IS - 12
ER -