Document Detail


Refining resuscitation strategies using tissue oxygen and perfusion monitoring in critical organ beds.
MedLine Citation:
PMID:  19204507     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Jennifer J Wan; Mitchell J Cohen; Guy Rosenthal; Iain K Haitsma; Diane J Morabito; Nikita Derugin; M Margaret Knudson; Geoffrey T Manley
Related Documents :
14692477 - Titanium in a hyperbaric oxygen environment may pose a fire risk.
17505757 - Effect of zinc and benzene on respiration and excretion of mussel larvae (perna perna) ...
2378827 - The effect of caput succedaneum on oxygen saturation measurements.
14574577 - Relationship between muscle architectural features and oxygenation status determined by...
10362197 - Relationship between exertional symptoms and functional capacity in patients with heart...
14578217 - Airway inflammation after cessation of exposure to agents causing occupational asthma.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of trauma     Volume:  66     ISSN:  1529-8809     ISO Abbreviation:  J Trauma     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-02-10     Completed Date:  2009-04-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376373     Medline TA:  J Trauma     Country:  United States    
Other Details:
Languages:  eng     Pagination:  353-7     Citation Subset:  AIM; IM    
Affiliation:
Department of Surgery, University of California, San Francisco and the San Francisco Injury Center for Research and Prevention, San Francisco, California, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Brain / metabolism
Disease Models, Animal
Hemodynamics
Monitoring, Physiologic
Muscle, Skeletal / blood supply,  metabolism*
Oxygen / metabolism*
Resuscitation / methods*
Shock, Hemorrhagic / metabolism,  physiopathology,  therapy*
Swine
Thermodilution
Vasoconstrictor Agents / pharmacology
Grant Support
ID/Acronym/Agency:
R49-CCR90369//PHS HHS; T32-GM08258/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Vasoconstrictor Agents; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Early prediction of massive transfusion in trauma: simple as ABC (assessment of blood consumption)?
Next Document:  The relationship of blood product ratio to mortality: survival benefit or survival bias?