OBJECTIVE: To improve our ability to identify physiologic deterioration caused by critical illness, we applied nonlinear and frequency-domain analytical methods to R-to-R interval (RRI) and systolic arterial pressure (SAP) time series during hemorrhagic shock. DESIGN: Prospective, randomized, controlled trial. SETTING: Animal laboratory of a government research institute. SUBJECTS: Twenty swine (weight 36.4+/-0.11 kg). INTERVENTIONS: Fixed-volume hemorrhage followed by resuscitation; off-line analysis of RRI and SAP data. MEASUREMENTS AND MAIN RESULTS: Anesthetized swine (shock group, n=12) underwent withdrawal of 30 mL/kg blood in 10 mL/kg decrements. A control group (n=8) received maintenance fluids only. Electrocardiogram and arterial pressure waveforms were acquired at 500 Hz. Eight hundred-beat data sets were analyzed at six time points: at baseline, after each blood withdrawal, after lactated Ringer's resuscitation, and after infusion of shed blood. Nonlinear methods were used to estimate the complexity (approximate entropy, sample entropy, Lempel-Ziv entropy, normalized entropy of symbol dynamics), RRI bits per word, and fractal dimension by curve lengths and by dispersion analysis of the RRI and SAP time series. Fast Fourier transformation was used to measure the high-frequency and low-frequency powers of RRI and SAP. Baroreflex sensitivity was assessed in the time domain with the sequence method. Hemorrhagic shock caused decreases in RRI complexity as quantified by approximate entropy, sample entropy, and symbol dynamics; these changes were reversed by resuscitation. Similar but statistically insignificant changes in fractal dimension by curve lengths were seen. RRI high-frequency power decreased with hemorrhagic shock-indicating withdrawal of vagal cardiac input-and was restored by resuscitation. Similar changes in baroreflex sensitivity were seen. Hemorrhagic shock did not affect SAP complexity. CONCLUSIONS: Hemorrhagic shock caused a reversible decrease in RRI complexity; these changes may be mediated by changes in vagal cardiac control. Assessment of RRI complexity may permit identification of casualties with hemorrhagic shock.
OBJECTIVE: To improve our ability to identify physiologic deterioration caused by critical illness, we applied nonlinear and frequency-domain analytical methods to R-to-R interval (RRI) and systolic arterial pressure (SAP) time series during hemorrhagic shock. DESIGN: Prospective, randomized, controlled trial. SETTING: Animal laboratory of a government research institute. SUBJECTS: Twenty swine (weight 36.4+/-0.11 kg). INTERVENTIONS: Fixed-volume hemorrhage followed by resuscitation; off-line analysis of RRI and SAP data. MEASUREMENTS AND MAIN RESULTS: Anesthetized swine (shock group, n=12) underwent withdrawal of 30 mL/kg blood in 10 mL/kg decrements. A control group (n=8) received maintenance fluids only. Electrocardiogram and arterial pressure waveforms were acquired at 500 Hz. Eight hundred-beat data sets were analyzed at six time points: at baseline, after each blood withdrawal, after lactated Ringer's resuscitation, and after infusion of shed blood. Nonlinear methods were used to estimate the complexity (approximate entropy, sample entropy, Lempel-Ziv entropy, normalized entropy of symbol dynamics), RRI bits per word, and fractal dimension by curve lengths and by dispersion analysis of the RRI and SAP time series. Fast Fourier transformation was used to measure the high-frequency and low-frequency powers of RRI and SAP. Baroreflex sensitivity was assessed in the time domain with the sequence method. Hemorrhagic shock caused decreases in RRI complexity as quantified by approximate entropy, sample entropy, and symbol dynamics; these changes were reversed by resuscitation. Similar but statistically insignificant changes in fractal dimension by curve lengths were seen. RRI high-frequency power decreased with hemorrhagic shock-indicating withdrawal of vagal cardiac input-and was restored by resuscitation. Similar changes in baroreflex sensitivity were seen. Hemorrhagic shock did not affect SAP complexity. CONCLUSIONS:Hemorrhagic shock caused a reversible decrease in RRI complexity; these changes may be mediated by changes in vagal cardiac control. Assessment of RRI complexity may permit identification of casualties with hemorrhagic shock.
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