William H Cooke1, Victor A Convertino. 1. U.S. Army Institute of Surgical Research, Fort Sam Houston, Texas, USA. william.cooke@amedd.army.mil
Abstract
BACKGROUND: Noninvasive procedures for predicting progression to hemodynamic instability during induced central hypovolemia in humans were evaluated. The purpose of this study was twofold: (1) to track changes in autonomic function induced by a model of hemorrhage, and (2) to determine whether measures of autonomic function are reliable without strict control of breathing. METHODS: Electrocardiogram, respiratory frequency, and arterial pressure during progressive lower body negative pressure were recorded for 10 subjects, and for a separate sample of 20 subjects during 5-minute periods of spontaneous breathing or controlled-frequency breathing at 15 breaths per minute.. Heart rate variability was calculated in both time and frequency domains. Up and down baroreflex sequences were calculated with linear regression analysis between sequential changes in systolic pressures and accompanying parallel changes in R-R intervals. RESULTS: Heart rate variability (r = 0.92) and up (r = 0.90) and down (r = 0.96) sequences changed in direct inverse relation to decreased central volume as produced by progressive increases in lower body negative pressure, whereas mean arterial pressures remained constant (r = 0.26). Neither heart rate variability nor up and down baroreflex sequences were affected by the mode of breathing. CONCLUSIONS: Analysis of heart rate variability and baroreflex sequences in hemorrhaging patients may provide advance recognition of those at risk for progression to shock. In conjunction with more traditional modes of assessing volume status, tracking early changes in autonomic function may improve resuscitation efforts for the hemodynamic compromised patient.
BACKGROUND: Noninvasive procedures for predicting progression to hemodynamic instability during induced central hypovolemia in humans were evaluated. The purpose of this study was twofold: (1) to track changes in autonomic function induced by a model of hemorrhage, and (2) to determine whether measures of autonomic function are reliable without strict control of breathing. METHODS: Electrocardiogram, respiratory frequency, and arterial pressure during progressive lower body negative pressure were recorded for 10 subjects, and for a separate sample of 20 subjects during 5-minute periods of spontaneous breathing or controlled-frequency breathing at 15 breaths per minute.. Heart rate variability was calculated in both time and frequency domains. Up and down baroreflex sequences were calculated with linear regression analysis between sequential changes in systolic pressures and accompanying parallel changes in R-R intervals. RESULTS: Heart rate variability (r = 0.92) and up (r = 0.90) and down (r = 0.96) sequences changed in direct inverse relation to decreased central volume as produced by progressive increases in lower body negative pressure, whereas mean arterial pressures remained constant (r = 0.26). Neither heart rate variability nor up and down baroreflex sequences were affected by the mode of breathing. CONCLUSIONS: Analysis of heart rate variability and baroreflex sequences in hemorrhagingpatients may provide advance recognition of those at risk for progression to shock. In conjunction with more traditional modes of assessing volume status, tracking early changes in autonomic function may improve resuscitation efforts for the hemodynamic compromised patient.
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