Brain Tissue Oxygenation during Hemorrhagic Shock, Resuscitation, and Alterations in Ventilation

Manley, Geoffrey T.; Pitts, Lawrence H.; Morabito, Diane; Doyle, Christine; Gibson, Jeffrey B.; Gimbel, Michael L.; Hopf, Harriet W.; Knudson, M. Margaret

doi:10.1097/00005373-199902000-00011

Cited by 71 publications

(48 citation statements)

References 30 publications

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“…Changes in ventilation provided an increase in P btO 2 in the setting of hypoventilation and a decrease in P btO 2 with hyperventilation. 45 Hyperventilation exacerbated the decrease in P btO 2 during experimental hemorrhagic shock. 46 These studies, while showing the feasibility of P btO 2 monitoring, also demonstrated the ill effects of hyperventilation, which had been used as a standard treatment for patients with increased intracranial pressure.…”

Section: Validation Of Cerebral Oxygen Monitoringmentioning

confidence: 94%

“…In a series of normal cats, Zauner et al 44 demonstrated a mean P btO 2 of 42 mm Hg, which decreased by 29% with hyperventilation. Manley et al 45 showed that changes in brain tissue oxygen coincided with the physiological shifts that occur during hemorrhagic shock. Using a swine model, they demonstrated that a decrease in P btO 2 was seen with hemorrhage and recovered with resuscitation.…”

Section: Validation Of Cerebral Oxygen Monitoringmentioning

confidence: 99%

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Brain Tissue Oxygen Monitoring and the Intersection of Brain and Lung: A Comprehensive Review

2016

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SummaryTraumatic brain injury is a problem that affects millions of Americans yearly and for which there is no definitive treatment that improves outcome. Continuous brain tissue oxygen (P btO 2 ) monitoring is a complement to traditional brain monitoring techniques, such as intracranial pressure and cerebral perfusion pressure. P btO 2 monitoring has not yet become a clinical standard of care, due to several unresolved questions. In this review, we discuss the rationale and technology of P btO 2 monitoring. We review the literature, both historic and current, and show that continuous P btO 2 monitoring is feasible and useful in patient management. P btO 2 numbers reflect cerebral blood flow and oxygen diffusion. Thus, continuous monitoring of P btO 2 yields important information about both the brain and the lung. The preclinical and clinical studies demonstrating these findings are discussed. In this review, we demonstrate that patient management in a P btO 2 -directed fashion is not the sole answer to the problem of treating traumatic brain injury but is an important adjunct to the armamentarium of multimodal neuromonitoring.

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Section: Validation Of Cerebral Oxygen Monitoringmentioning

confidence: 94%

Section: Validation Of Cerebral Oxygen Monitoringmentioning

confidence: 99%

Brain Tissue Oxygen Monitoring and the Intersection of Brain and Lung: A Comprehensive Review

2016

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“…Previous experiments in our laboratory using computerized tomography as well as necropsy with gross examination of in-situ brain probes following brain removal have confirmed correct ana- tomic placement using this technique. [19][20][21] A fiberoptic pressure transducer (Camino Laboratories, San Diego, CA) was placed in a 2-mm burr hole 5 mm caudal to the right coronal suture for continuous monitoring of intracranial pressure (ICP). A midline burr hole was placed anterior to the bregma for introduction of a 4-Fr catheter used for collection of venous sagittal sinus blood to monitor cerebral venous oxygen tension (PcvO 2 ) and saturation (ScvO 2 ).…”

Section: Methodsmentioning

confidence: 99%

“…The in-vivo response of the brain oxygen probes was evaluated by increasing the FiO 2 to 1.0, after which an increase in PbrO 2 was observed that was consistent with previous studies. [19][20][21] Once the response to 1.0 oxygen was validated, the FiO 2 was decreased to 0.3 and swine were allowed to stabilize for another 30 minutes. At the completion of each experiment, probes were placed in their respective calibration barrels and observed for return to the calibrated oxygen levels recorded before the experiment began.…”

Section: Methodsmentioning

confidence: 99%

“…A similar effect was observed following resuscitation with shed blood in previous experiments with the same model of hemorrhage. 19 Therefore, this effect may not necessarily be specific to HBOC-201, but may reflect a physiologic change in cerebral autoregulation that occurs following reversal of global brain ischemia. In addition, it has been suggested that increases in tissue oxygen can lead to the generation of free radicals and subsequent tissue injury.…”

Section: Limitationsmentioning

confidence: 99%

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Small-volume Resuscitation with HBOC-201: Effects on Cardiovascular Parameters and Brain Tissue Oxygen Tension in an Out-of-hospital Model of Hemorrhage in Swine

et al. 2002

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Objective: Hemoglobin-based oxygen carriers, such as HBOC-201, offer several potential advantages over conventional resuscitation solutions or banked blood in the acute treatment of hemorrhagic shock. While previous studies with some hemoglobin solutions revealed vasoactive effects resulting in decreased oxygen delivery, these investigations were performed without directly measuring vital tissue oxygenation. The authors tested the hypothesis that a small-volume bolus of HBOC-201 would improve and sustain brain tissue oxygen tension (PbrO 2 ) without adverse effects on cardiovascular endpoints, when used in an acute out-of-hospital hemorrhage model. Methods: Male Yorkshire swine (n = 7) were hemorrhaged to a mean arterial pressure (MAP) of 40 mm Hg while monitoring standard hemodynamic parameters. In addition, Clark-type polarographic probes were directly inserted into brain tissue to measure PbrO 2 . Following institution of high-flow oxygen (FiO 2 = 1.0), resuscitation was performed with a bolus infusion of HBOC-201 (6 mL/kg). Swine were observed for two hours. Results: Cardiac output (CO), MAP, pulmonary artery diastolic pressure (PAD), and PbrO 2 all decreased significantly with hemorrhage (p < 0.05). Immediately following resuscitation with HBOC-201 (mean volume = 239 mL), MAP and CO were restored to 83% and 84% of baseline levels, respectively. PbrO 2 increased significantly after treatment with HBOC-201, surpassing baseline levels by 66%. PAD rose above baseline levels during observation, but this increase was not significantly different from baseline levels (24.0 mm Ϯ 4.1 vs. 22.7 mm Ϯ 7.4). Conclusions: Small-volume resuscitation with HBOC-201 rapidly restored hemodynamic parameters and PbrO 2 following severe hemorrhage without detrimental vasoactive effects and without compromise to directly monitored brain tissue oxygenation. The results of this preliminary study demonstrate that HBOC-201 could potentially improve current resuscitation measures and that further investigations with HBOC-201 are warranted.

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Hemorrhagic Shock and the Microvasculature

Filho

2017

Comprehensive Physiology

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The microvasculature plays a central role in the pathophysiology of hemorrhagic shock and is also involved in arguably all therapeutic attempts to reverse or minimize the adverse consequences of shock. Microvascular studies specific to hemorrhagic shock were reviewed and broadly grouped depending on whether data were obtained on animal or human subjects. Dedicated sections were assigned to microcirculatory changes in specific organs, and major categories of pathophysiological alterations and mechanisms such as oxygen distribution, ischemia, inflammation, glycocalyx changes, vasomotion, endothelial dysfunction, and coagulopathy as well as biomarkers and some therapeutic strategies. Innovative experimental methods were also reviewed for quantitative microcirculatory assessment as it pertains to changes during hemorrhagic shock. The text and figures include representative quantitative microvascular data obtained in various organs and tissues such as skin, muscle, lung, liver, brain, heart, kidney, pancreas, intestines, and mesentery from various species including mice, rats, hamsters, sheep, swine, bats, and humans. Based on reviewed findings, a new integrative conceptual model is presented that includes about 100 systemic and local factors linked to microvessels in hemorrhagic shock. The combination of systemic measures with the understanding of these processes at the microvascular level is fundamental to further develop targeted and personalized interventions that will reduce tissue injury, organ dysfunction, and ultimately mortality due to hemorrhagic shock. Published 2018. Compr Physiol 8:61-101, 2018.

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Brain Tissue Oxygenation during Hemorrhagic Shock, Resuscitation, and Alterations in Ventilation

Cited by 71 publications

References 30 publications

Brain Tissue Oxygen Monitoring and the Intersection of Brain and Lung: A Comprehensive Review

Brain Tissue Oxygen Monitoring and the Intersection of Brain and Lung: A Comprehensive Review

Small-volume Resuscitation with HBOC-201: Effects on Cardiovascular Parameters and Brain Tissue Oxygen Tension in an Out-of-hospital Model of Hemorrhage in Swine

Hemorrhagic Shock and the Microvasculature

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