TY - JOUR
T1 - Autonomic compensation to simulated hemorrhage monitored with heart period variability
AU - Cooke, William H.
AU - Rickards, Caroline A.
AU - Ryan, Kathy L.
AU - Convertino, Victor A.
N1 - Funding Information:
Supported, in part, by the U.S. Department of Defense, Medical Research and Materiel Command.
PY - 2008/6
Y1 - 2008/6
N2 - OBJECTIVE:: To test the hypothesis that components of heart period variability track autonomic function during simulated hemorrhage in humans. DESIGN:: Prospective experimental laboratory intervention. SETTING:: Human physiology laboratory. SUBJECTS:: A total of 33 healthy, nonsmoking, volunteer subjects (23 men, ten women). INTERVENTIONS:: Progressive lower body negative pressure was applied in 5-min stages until the onset of impending cardiovascular collapse. MEASUREMENTS AND MAIN RESULTS:: The electrocardiogram, beat-by-beat finger arterial pressure, and muscle sympathetic nerve activity from the peroneal nerve were recorded continuously. Pulse pressure was calculated from the arterial pressure waveform and used as an estimate of relative changes of central blood volume. Heart period variability was assessed in both time and frequency domains. Application of lower body negative pressure caused progressive reductions of R-R interval and pulse pressure and progressive increases of muscle sympathetic nerve activity. Arterial pressures changed minimally and late. R-R interval time domain variability measures and spectral power at the high frequency (0.15-0.4 Hz) decreased progressively with lower body negative pressure (p < .001). Both R-R interval high-frequency power and time domain variability measures correlated inversely with muscle sympathetic nerve activity and directly with pulse pressure (all amalgamated R > .88, all p ≤ .001). CONCLUSIONS:: Components of heart period variability track early compensatory autonomic and hemodynamic responses to progressive reduction in central blood volume. Such analyses, interpreted in conjunction with standard vital signs, may contribute to earlier assessments of the magnitude of blood volume loss during hemorrhage.
AB - OBJECTIVE:: To test the hypothesis that components of heart period variability track autonomic function during simulated hemorrhage in humans. DESIGN:: Prospective experimental laboratory intervention. SETTING:: Human physiology laboratory. SUBJECTS:: A total of 33 healthy, nonsmoking, volunteer subjects (23 men, ten women). INTERVENTIONS:: Progressive lower body negative pressure was applied in 5-min stages until the onset of impending cardiovascular collapse. MEASUREMENTS AND MAIN RESULTS:: The electrocardiogram, beat-by-beat finger arterial pressure, and muscle sympathetic nerve activity from the peroneal nerve were recorded continuously. Pulse pressure was calculated from the arterial pressure waveform and used as an estimate of relative changes of central blood volume. Heart period variability was assessed in both time and frequency domains. Application of lower body negative pressure caused progressive reductions of R-R interval and pulse pressure and progressive increases of muscle sympathetic nerve activity. Arterial pressures changed minimally and late. R-R interval time domain variability measures and spectral power at the high frequency (0.15-0.4 Hz) decreased progressively with lower body negative pressure (p < .001). Both R-R interval high-frequency power and time domain variability measures correlated inversely with muscle sympathetic nerve activity and directly with pulse pressure (all amalgamated R > .88, all p ≤ .001). CONCLUSIONS:: Components of heart period variability track early compensatory autonomic and hemodynamic responses to progressive reduction in central blood volume. Such analyses, interpreted in conjunction with standard vital signs, may contribute to earlier assessments of the magnitude of blood volume loss during hemorrhage.
KW - Blood pressure
KW - Central hypovolemia
KW - Lower body negative pressure
KW - Pulse pressure
KW - Remote medical monitoring
KW - Stroke volume
UR - http://www.scopus.com/inward/record.url?scp=45149084689&partnerID=8YFLogxK
U2 - 10.1097/CCM.0b013e3181760d0c
DO - 10.1097/CCM.0b013e3181760d0c
M3 - Article
C2 - 18496361
AN - SCOPUS:45149084689
SN - 0090-3493
VL - 36
SP - 1892
EP - 1899
JO - Critical Care Medicine
JF - Critical Care Medicine
IS - 6
ER -