Continuous measurement of cerebral oxygen saturation (rSO 2) for assessment of cardiovascular status during hemorrhagic shock in a swine model

Lais Helena Camacho Navarro, Rodrigo M. Lima, Muzna Khan, Wendy G. Dominguez, Richard B. Voigt, Michael Kinsky, William Mileski, George Kramer

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background: Early trauma care is dependent on subjective assessments and sporadic vital sign assessments. We hypothesized that near-infrared spectroscopy-measured cerebral oxygenation (regional oxygen saturation [rSO 2]) would provide a tool to detect cardiovascular compromise during active hemorrhage. We compared rSO 2 with invasively measured mixed venous oxygen saturation (SvO2), mean arterial pressure (MAP), cardiac output, heart rate, and calculated pulse pressure. Methods: Six propofol-anesthetized instrumented swine were subjected to a fixed-rate hemorrhage until cardiovascular collapse. rSO 2 was monitored with noninvasively measured cerebral oximetry; SvO2 was measured with a fiber optic pulmonary arterial catheter. As an assessment of the time responsiveness of each variable, we recorded minutes from start of the hemorrhage for each variable achieving a 5%, 10%, 15%, and 20% change compared with baseline. Results: Mean time to cardiovascular collapse was 35 minutes ± 11 minutes (54 ± 17% total blood volume). Cerebral rSO 2 began a steady decline at an average MAP of 78 mm Hg ± 17 mm Hg, well above the expected autoregulatory threshold of cerebral blood flow. The 5%, 10%, and 15% decreases in rSO 2 during hemorrhage occurred at a similar times to SvO2, but rSO 2 lagged 6 minutes behind the equivalent percentage decreases in MAP. There was a higher correlation between rSO 2 versus MAP (R =0.72) than SvO2 versus MAP (R =0.55). Conclusions: Near-infrared spectroscopy- measured rSO 2 provided reproducible decreases during hemorrhage that were similar in time course to invasively measured cardiac output and SvO2 but delayed 5 to 9 minutes compared with MAP and pulse pressure. rSO 2 may provide an earlier warning of worsening hemorrhagic shock for prompt interventions in patients with trauma when continuous arterial BP measurements are unavailable.

Original languageEnglish (US)
JournalJournal of Trauma and Acute Care Surgery
Volume73
Issue number2 SUPPL. 1
DOIs
StatePublished - Aug 2012

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Hemorrhagic Shock
Arterial Pressure
Swine
Oxygen
Hemorrhage
Near-Infrared Spectroscopy
Cardiac Output
Cerebrovascular Circulation
Blood Pressure
Oximetry
Vital Signs
Wounds and Injuries
Propofol
Blood Volume
Catheters
Heart Rate
Lung

Keywords

  • cerebral oxygenation
  • Hemorrhage
  • near-infrared spectroscopy
  • trauma

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Surgery

Cite this

Continuous measurement of cerebral oxygen saturation (rSO 2) for assessment of cardiovascular status during hemorrhagic shock in a swine model. / Navarro, Lais Helena Camacho; Lima, Rodrigo M.; Khan, Muzna; Dominguez, Wendy G.; Voigt, Richard B.; Kinsky, Michael; Mileski, William; Kramer, George.

In: Journal of Trauma and Acute Care Surgery, Vol. 73, No. 2 SUPPL. 1, 08.2012.

Research output: Contribution to journalArticle

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abstract = "Background: Early trauma care is dependent on subjective assessments and sporadic vital sign assessments. We hypothesized that near-infrared spectroscopy-measured cerebral oxygenation (regional oxygen saturation [rSO 2]) would provide a tool to detect cardiovascular compromise during active hemorrhage. We compared rSO 2 with invasively measured mixed venous oxygen saturation (SvO2), mean arterial pressure (MAP), cardiac output, heart rate, and calculated pulse pressure. Methods: Six propofol-anesthetized instrumented swine were subjected to a fixed-rate hemorrhage until cardiovascular collapse. rSO 2 was monitored with noninvasively measured cerebral oximetry; SvO2 was measured with a fiber optic pulmonary arterial catheter. As an assessment of the time responsiveness of each variable, we recorded minutes from start of the hemorrhage for each variable achieving a 5{\%}, 10{\%}, 15{\%}, and 20{\%} change compared with baseline. Results: Mean time to cardiovascular collapse was 35 minutes ± 11 minutes (54 ± 17{\%} total blood volume). Cerebral rSO 2 began a steady decline at an average MAP of 78 mm Hg ± 17 mm Hg, well above the expected autoregulatory threshold of cerebral blood flow. The 5{\%}, 10{\%}, and 15{\%} decreases in rSO 2 during hemorrhage occurred at a similar times to SvO2, but rSO 2 lagged 6 minutes behind the equivalent percentage decreases in MAP. There was a higher correlation between rSO 2 versus MAP (R =0.72) than SvO2 versus MAP (R =0.55). Conclusions: Near-infrared spectroscopy- measured rSO 2 provided reproducible decreases during hemorrhage that were similar in time course to invasively measured cardiac output and SvO2 but delayed 5 to 9 minutes compared with MAP and pulse pressure. rSO 2 may provide an earlier warning of worsening hemorrhagic shock for prompt interventions in patients with trauma when continuous arterial BP measurements are unavailable.",
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AU - Navarro, Lais Helena Camacho

AU - Lima, Rodrigo M.

AU - Khan, Muzna

AU - Dominguez, Wendy G.

AU - Voigt, Richard B.

AU - Kinsky, Michael

AU - Mileski, William

AU - Kramer, George

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AB - Background: Early trauma care is dependent on subjective assessments and sporadic vital sign assessments. We hypothesized that near-infrared spectroscopy-measured cerebral oxygenation (regional oxygen saturation [rSO 2]) would provide a tool to detect cardiovascular compromise during active hemorrhage. We compared rSO 2 with invasively measured mixed venous oxygen saturation (SvO2), mean arterial pressure (MAP), cardiac output, heart rate, and calculated pulse pressure. Methods: Six propofol-anesthetized instrumented swine were subjected to a fixed-rate hemorrhage until cardiovascular collapse. rSO 2 was monitored with noninvasively measured cerebral oximetry; SvO2 was measured with a fiber optic pulmonary arterial catheter. As an assessment of the time responsiveness of each variable, we recorded minutes from start of the hemorrhage for each variable achieving a 5%, 10%, 15%, and 20% change compared with baseline. Results: Mean time to cardiovascular collapse was 35 minutes ± 11 minutes (54 ± 17% total blood volume). Cerebral rSO 2 began a steady decline at an average MAP of 78 mm Hg ± 17 mm Hg, well above the expected autoregulatory threshold of cerebral blood flow. The 5%, 10%, and 15% decreases in rSO 2 during hemorrhage occurred at a similar times to SvO2, but rSO 2 lagged 6 minutes behind the equivalent percentage decreases in MAP. There was a higher correlation between rSO 2 versus MAP (R =0.72) than SvO2 versus MAP (R =0.55). Conclusions: Near-infrared spectroscopy- measured rSO 2 provided reproducible decreases during hemorrhage that were similar in time course to invasively measured cardiac output and SvO2 but delayed 5 to 9 minutes compared with MAP and pulse pressure. rSO 2 may provide an earlier warning of worsening hemorrhagic shock for prompt interventions in patients with trauma when continuous arterial BP measurements are unavailable.

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