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Refining Resuscitation Strategies Using Tissue Oxygen and Perfusion Monitoring in Critical Organ Beds

Wan, Jennifer J. MD; Cohen, Mitchell J. MD; Rosenthal, Guy MD; Haitsma, Iain K. MD; Morabito, Diane J. RN, MPH; Derugin, Nikita MA; Knudson, M Margaret MD; Manley, Geoffrey T. MD, PhD

The Journal of Trauma: Injury, Infection, and Critical Care: February 2009 - Volume 66 - Issue 2 - p 353-357
doi: 10.1097/TA.0b013e318195e222
Original Articles

Background: Muscle tissue oxygen monitoring (Pmo2) holds promise as a continuous guide to resuscitation after hemorrhagic shock, but the relationship of muscle tissue oxygen to perfusion has not been described previously. On the other hand, brain tissue oxygen PbrO2 and perfusion as measured by cerebral blood flow (CBF) are already used clinically, especially as guides to vasopressor use in cerebral perfusion targeted therapy in patients with traumatic brain injury. This laboratory study was undertaken to describe the relative contributions of muscle perfusion and arterial oxygen tension (Pao2) to muscle tissue oxygen (Pmo2) levels. Second, we wanted to compare the relationship between muscle oxygen and muscle blood flow (MBF) with simultaneously measured brain tissue oxygen and perfusion during the administration of a vasopressor and during experimental hemorrhagic shock. We hypothesized that muscle perfusion would be an important contributor to Pmo2, thus underscoring the need for optimal fluid resuscitation after shock. We further hypothesized that Pmo2 would decrease even as Pbro2 increased when vasopressor therapy was used.

Methods: Eight pigs were anesthetized, intubated, underwent splenectomies, and were instrumented to monitor Pmo2, MBF, Pbro2, and CBF. Oxygen challenges were performed by increasing Pao2 from 100 to 500 mm Hg during three different experimental phases: baseline, vasopressor administration, and hemorrhage. Mean Pmo2 and MBF were compared at the beginning and end of each experimental phase and correlations between Pmo2, MBF, Pbro2, CBF, and traditional endpoints of resuscitation were investigated.

Results: During oxygen challenges in all phases, Pmo2 increased (31.2 ± 16.6 mm Hg to 56.6 ± 34.1 mm Hg; p < 0.01), whereas MBF did not change significantly (16.4 ± 11.3 mL/100 g/min to 15.4 ± 11.9 mL/100 g/min). On administration of vasopressors, MBF decreased (18 ± 8.8 mL/100 g/min to 5.3 ± 3 mL/100 g/min; p = 0.03), but no change in Pmo2 was detected. During hemorrhage, both Pmo2 and MBF declined (Pmo2: 40 ± 8.8 mm Hg to 7.7 ± 9.6 mm Hg; p = 0.002; MBF: 9.8 ± 5.8 mL/100 g/min to 3.3 ± 2.4 mL/100 g/min; p = 0.046). Both Pmo2 and MBF showed strong relationships with measurements of resuscitation, base deficit (Pmo2 and MBF: p < 0.01), and mean arterial pressure (Pmo2: p < 0.01, MBF: p = 0.02). Like Pmo2 and MBF, Pbro2 and CBF decreased uniformly during hemorrhage. However, on vasopressor administration, CBF and Pbro2 increased significantly, whereas MBF decreased.

Conclusion: Pmo2 and MBF can be monitored simultaneously and continuously and correlate well with measurements of resuscitation. Pmo2 values reflect both local perfusion and arterial oxygen tension. The clinical application of Pmo2 as a continuous endpoint of resuscitation and its relationship to muscle perfusion warrants further study in critically injured patients and these investigations may help to refine resuscitation strategies.

From the Departments of Surgery (J.J.W., M.J.C., D.J.M., M.M.K.) and Neurosurgery (G.R., I.K.H., N.D., G.T.M.), University of California, San Francisco and the San Francisco Injury Center for Research and Prevention, San Francisco, California.

Submitted for publication April 4, 2007.

Accepted for publication November 19, 2008.

Presented at the 38th Annual Meeting of the Western Trauma Association, February 24–March 1, 2008, Squaw Creek, Olympic Valley, California.

Supported by the Center for Disease Control and Prevention #R49-CCR90369 and the National Institute of Health National Research Service Award #T32-GM08258.

Address for reprints: M. Margaret Knudson, MD, Department of Surgery, Ward 3A, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, CA 94110; email:

© 2009 Lippincott Williams & Wilkins, Inc.