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Linear and nonlinear measures of heart rate variability during isobaric hemorrhagic shock
358
Abstracts
Conclusions: R-R intervals and SAP complexity metrics did not correlate with injury severity, hypoxia, or hypotension in this model. Regulatory input to the cardiovascular system appears to be preserved following Cl2 inhalation injury in anesthetized sheep. Future studies need to be done in conscious models of inhalation injury. doi:10.1016/j.jcrc.2006.10.025 Linear and nonlinear measures of heart rate variability during isobaric hemorrhagic shock A.I. Batchinsky, I.H. Black, T. Kuusela, M. Boehme, J.J. Wang, L.C. Cancio
U.S. Army Institute of Surgical Research, Fort Sam Houston Texas
sympathovagal balance, that is, an increase in the RRI low frequency power/high frequency power ratio. Complex demodulation indicated decreased vagal modulation of the RRI. Thus, vagal withdrawal may mediate loss of entropy in HS. On the other hand, SAP high frequency power increased; this is likely mediated by intrathoracic pressure changes in mechanically ventilated subjects. Comprehensive waveform analysis including both linear and nonlinear methods provides complementary information about physiologic cardiovascular regulation and may better our understanding of the response to HS. doi:10.1016/j.jcrc.2006.10.026
In silico analysis of mechanical ventilation S. Gunna, J.R. Hotchkissa, P. Crookeb
Background: Loss of complexity in the R-R interval (RRI) has been observed during hemorrhagic shock (HS) and is a predictor of outcome in a variety of diseases. Combining linear and nonlinear waveform analyses may reveal additional information about the mechanisms behind such loss of complexity. Objective: The aim of this study was to investigate the response to HS by combining frequency domain, complex demodulation, and nonlinear statistical analyses. Methods: Six pigs were anesthetized with isoflurane, mechanically ventilated, and bled to and maintained at a mean arterial pressure of 40 mm Hg. Ectopy-free 800-beat segments of RRI and systolic arterial pressure (SAP) waveforms were acquired at 500 Hz at baseline and during HS. R-R interval and SAP variability was investigated by frequency domain (fast Fourier transform) and nonlinear and complex demodulation analyses. Results:
RRI Mean arterial pressure RRI approximate entropy RRI sample entropy RRI low-frequency power, normalized RRI LFP/HFP ratio, normalized Baroreflex slope RRI high-frequency power, nonnormalized RRI LFP/HFP ratio, nonnormalized Amplitude of HFP of RRI, by complex demodulation SAP approximate entropy SAP sample entropy SAP total power SAP detrended fluctuations SAP low-frequency power, normalized SAP high-frequency power, nonnormalized Amplitude of HFP of SAP, by complex demodulation
Baseline 483 72
HS 293*** 44***
0.92 0.89 0.04 0.06 0.54 1.8 6 1.4
0.74* 0.66* 0.17** 0.42* 0.15*** 0.17* 42* 0.5*
1.17 1.31 6 1.12 0.03 0.87 2.9
0.82* 0.8** 23*** 1.61*** 0.01* 0.93*** 5.8*
*P b .05; **P b .01; ***P b .001, mixed-model analysis of variance. Changes in other measured variables were insignificant. Conclusions: Hemorrhagic shock led to loss of complexity of cardiovascular regulation as evidenced by decreases in RRI and SAP entropy. These changes were associated with increases in
a
Department of Critical Care Medicine, University of Pittsburgh Department of Mathematics, Vanderbilt University
b
Background: Although it is often a life-saving intervention, mechanical ventilation can also injure the lung, either by overdistending the airspaces or through repetitive end-expiratory collapse and reexpansion. The dynamics governing the response of the lungs to mechanical ventilation are extremely complex. The pulmonary airspaces are accessed via an asymmetrically branching network of airways and often have heterogeneous impedance characteristics. Interactions between local and global impedance parameters and the pattern of pressure or flow applied at the airway opening determine the local distributions of peak airspace strains, end-expiratory volumes, and total ventilation. It is difficult both to predict a priori which ventilatory strategies will prove optimal for a given individual and to identify which approaches should be bsafestQ on a population basis. Objective: The aim of this study was to explore the feasibility of using in silico approaches to identify optimal and nonoptimal ventilatory strategies in the setting of regionally heterogeneous pulmonary mechanics. Methods: We constructed 5 compartment models of the branching pulmonary system subjected to either volume cycled ventilation (VCV) or pressure regulated ventilation (PRV). The elastance and proximate resistances of each compartment can differ. We embedded these models in a Monte Carlo simulation framework in which the compartmental elastances varied over the clinically relevant range (total pulmonary compliance, 0.01-0.06 L/cm H2O; compartmental compliances, 0.002-0.012 L/cm H2O). Each of 2000 impedance configurations was subjected to pressure control ventilation and volume-cycled ventilation at matched levels of minute ventilation. Outcomes included the fraction of configurations experiencing overstrain of at least 1 compartment (end-inspiratory compartmental volume exceeding that corresponding to transpulmonary pressure 30 cm H2O, thus potentially promoting organ damage), and the number of configurations resulting in collapse of at least 1 compartment (compartmental volume falling below that expected at positive endexpiratory pressure 10 cm H2O), thus grossly impairing gas exchange. Multiple ensembles of PRV inputs were assayed, along with the VCV settings that matched inspiratory time and minute ventilation. PRV settings included conventional Inspiration (I):Expiration (E) ratios, inverse ratio ventilation (I:E N1), and bextreme inverse ratioQ ventilation (I:E N5), corresponding to airway pressure release ventilation. Peak inspiratory pressure in PRV was limited to 30 cm H2O. Results: As expected, there was no overdistention in the PRV simulations. For the majority of ventilator settings, there was
Abstracts
Conclusions: R-R intervals and SAP complexity metrics did not correlate with injury severity, hypoxia, or hypotension in this model. Regulatory input to the cardiovascular system appears to be preserved following Cl2 inhalation injury in anesthetized sheep. Future studies need to be done in conscious models of inhalation injury. doi:10.1016/j.jcrc.2006.10.025 Linear and nonlinear measures of heart rate variability during isobaric hemorrhagic shock A.I. Batchinsky, I.H. Black, T. Kuusela, M. Boehme, J.J. Wang, L.C. Cancio
U.S. Army Institute of Surgical Research, Fort Sam Houston Texas
sympathovagal balance, that is, an increase in the RRI low frequency power/high frequency power ratio. Complex demodulation indicated decreased vagal modulation of the RRI. Thus, vagal withdrawal may mediate loss of entropy in HS. On the other hand, SAP high frequency power increased; this is likely mediated by intrathoracic pressure changes in mechanically ventilated subjects. Comprehensive waveform analysis including both linear and nonlinear methods provides complementary information about physiologic cardiovascular regulation and may better our understanding of the response to HS. doi:10.1016/j.jcrc.2006.10.026
In silico analysis of mechanical ventilation S. Gunna, J.R. Hotchkissa, P. Crookeb
Background: Loss of complexity in the R-R interval (RRI) has been observed during hemorrhagic shock (HS) and is a predictor of outcome in a variety of diseases. Combining linear and nonlinear waveform analyses may reveal additional information about the mechanisms behind such loss of complexity. Objective: The aim of this study was to investigate the response to HS by combining frequency domain, complex demodulation, and nonlinear statistical analyses. Methods: Six pigs were anesthetized with isoflurane, mechanically ventilated, and bled to and maintained at a mean arterial pressure of 40 mm Hg. Ectopy-free 800-beat segments of RRI and systolic arterial pressure (SAP) waveforms were acquired at 500 Hz at baseline and during HS. R-R interval and SAP variability was investigated by frequency domain (fast Fourier transform) and nonlinear and complex demodulation analyses. Results:
RRI Mean arterial pressure RRI approximate entropy RRI sample entropy RRI low-frequency power, normalized RRI LFP/HFP ratio, normalized Baroreflex slope RRI high-frequency power, nonnormalized RRI LFP/HFP ratio, nonnormalized Amplitude of HFP of RRI, by complex demodulation SAP approximate entropy SAP sample entropy SAP total power SAP detrended fluctuations SAP low-frequency power, normalized SAP high-frequency power, nonnormalized Amplitude of HFP of SAP, by complex demodulation
Baseline 483 72
HS 293*** 44***
0.92 0.89 0.04 0.06 0.54 1.8 6 1.4
0.74* 0.66* 0.17** 0.42* 0.15*** 0.17* 42* 0.5*
1.17 1.31 6 1.12 0.03 0.87 2.9
0.82* 0.8** 23*** 1.61*** 0.01* 0.93*** 5.8*
*P b .05; **P b .01; ***P b .001, mixed-model analysis of variance. Changes in other measured variables were insignificant. Conclusions: Hemorrhagic shock led to loss of complexity of cardiovascular regulation as evidenced by decreases in RRI and SAP entropy. These changes were associated with increases in
a
Department of Critical Care Medicine, University of Pittsburgh Department of Mathematics, Vanderbilt University
b
Background: Although it is often a life-saving intervention, mechanical ventilation can also injure the lung, either by overdistending the airspaces or through repetitive end-expiratory collapse and reexpansion. The dynamics governing the response of the lungs to mechanical ventilation are extremely complex. The pulmonary airspaces are accessed via an asymmetrically branching network of airways and often have heterogeneous impedance characteristics. Interactions between local and global impedance parameters and the pattern of pressure or flow applied at the airway opening determine the local distributions of peak airspace strains, end-expiratory volumes, and total ventilation. It is difficult both to predict a priori which ventilatory strategies will prove optimal for a given individual and to identify which approaches should be bsafestQ on a population basis. Objective: The aim of this study was to explore the feasibility of using in silico approaches to identify optimal and nonoptimal ventilatory strategies in the setting of regionally heterogeneous pulmonary mechanics. Methods: We constructed 5 compartment models of the branching pulmonary system subjected to either volume cycled ventilation (VCV) or pressure regulated ventilation (PRV). The elastance and proximate resistances of each compartment can differ. We embedded these models in a Monte Carlo simulation framework in which the compartmental elastances varied over the clinically relevant range (total pulmonary compliance, 0.01-0.06 L/cm H2O; compartmental compliances, 0.002-0.012 L/cm H2O). Each of 2000 impedance configurations was subjected to pressure control ventilation and volume-cycled ventilation at matched levels of minute ventilation. Outcomes included the fraction of configurations experiencing overstrain of at least 1 compartment (end-inspiratory compartmental volume exceeding that corresponding to transpulmonary pressure 30 cm H2O, thus potentially promoting organ damage), and the number of configurations resulting in collapse of at least 1 compartment (compartmental volume falling below that expected at positive endexpiratory pressure 10 cm H2O), thus grossly impairing gas exchange. Multiple ensembles of PRV inputs were assayed, along with the VCV settings that matched inspiratory time and minute ventilation. PRV settings included conventional Inspiration (I):Expiration (E) ratios, inverse ratio ventilation (I:E N1), and bextreme inverse ratioQ ventilation (I:E N5), corresponding to airway pressure release ventilation. Peak inspiratory pressure in PRV was limited to 30 cm H2O. Results: As expected, there was no overdistention in the PRV simulations. For the majority of ventilator settings, there was