Skeletal muscle acidosis correlates with the severity of blood volume loss during shock and resuscitation.

BACKGROUND Continuous assessment of tissue perfusion and oxygen utilization may allow for early recognition and correction of hemorrhagic shock. We hypothesized that continuously monitoring skeletal muscle (SM) PO2, PCO2, and pH during shock would provide an easily accessible method for assessing the severity of blood loss and the efficacy of resuscitation. METHODS Thirteen anesthetized pigs (25-35 kg) underwent laparotomy and femoral vessel cannulation. Multiparameter fiberoptic sensors were placed in the deltoid (SM) and femoral artery. Ventilation was maintained at a PaCO2 of 40-45 mm Hg. Total blood volume (TBV) was measured using an Evans blue dye technique. Animals were bled for 15 minutes, maintained at a mean arterial pressure (MAP) of 40 mm Hg for 1 hour, resuscitated (shed blood + 2 times shed volume in normal saline) and observed for 1 hour. Four animals served as controls (sham hemorrhage). Blood and tissue samples were taken at each time point. RESULTS Blood loss ranged from 28.5-56% of TBV. SM pH and SM PO2 levels fell rapidly with shock. SM PO2 returned to normal with resuscitation; however, SM pH did not return to baseline. SM PCO2 significantly rose with shock, but returned to baseline promptly with resuscitation. There was a significant correlation between SM pH and blood volume loss at end shock (r2 = 0.73, p < 0.001) and recovery (r2 = 0.84, p < 0.001). Animals (n = 2) whose SM pH did not recover to 7.2 were found to have ongoing blood loss from biopsy sites and persistent tissue hypercarbia despite normal MAP. CONCLUSION Continuous multiparameter monitoring of SM provides a minimally invasive method for assessing severity of shock and efficacy of resuscitation. Both PCO2 and PO2 levels change rapidly with shock and resuscitation. SM pH is directly proportional to lost blood volume. Persistent SM acidosis (pH < 7.2) and elevated PCO2 levels suggest incomplete resuscitation despite normalized hemodynamics.

[1]  H. Hosaka,et al.  Esophageal PCO2 as a monitor of perfusion failure during hemorrhagic shock. , 1997, Journal of applied physiology.

[2]  R. Ivatury,et al.  A prospective randomized study of end points of resuscitation after major trauma: global oxygen transport indices versus organ-specific gastric mucosal pH. , 1996, Journal of the American College of Surgeons.

[3]  B Venkatesh,et al.  A multiparameter sensor for continuous intra‐arterial blood gas monitoring: A prospective evaluation , 1994, Critical care medicine.

[4]  F. Cerra,et al.  The future. Monitoring cellular energetics. , 1996, Critical care clinics.

[5]  W. Shoemaker,et al.  Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients. , 1988, Chest.

[6]  R. Ivatury,et al.  In search of the optimal end points of resuscitation in trauma patients: a review. , 1998, The Journal of trauma.

[7]  R. Schlichtig,et al.  Distinguishing between aerobic and anaerobic appearance of dissolved CO2 in intestine during low flow. , 1994, Journal of applied physiology.

[8]  T. Tønnessen,et al.  PCO2 electrodes at the surface of the kidney detect ischaemia , 1996, Acta anaesthesiologica Scandinavica.

[9]  Wanchun Tang,et al.  Effects of hyper- and hypoventilation on gastric and sublingual PCO(2). , 1999, Journal of applied physiology.

[10]  D. Evans,et al.  A novel approach to monitor tissue perfusion: bladder mucosal PCO2, PO2, and pHi during ischemia and reperfusion. , 1999, Journal of critical care.

[11]  Weil Mh Tissue PCO2 as universal marker of tissue hypoxia. , 2000 .

[12]  Wanchun Tang,et al.  Sublingual capnometry: a new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock. , 1999, Critical care medicine.

[13]  U. Haglund,et al.  Tissue oxygenation in hemorrhagic shock measured as transcutaneous oxygen tension, subcutaneous oxygen tension, and gastrointestinal intramucosal pH in pigs , 1991, Critical care medicine.

[14]  B. Butler,et al.  Comparison of skeletal muscle PO2, PCO2, and pH with gastric tonometric P(CO2) and pH in hemorrhagic shock. , 1999, Critical care medicine.

[15]  R. Goris,et al.  Early detection of shock in critically ill patients by skeletal muscle PO2 assessment. , 1989, Archives of surgery.

[16]  T. Brussel,et al.  Continuous intramucosal PCO2 measurement allows the early detection of intestinal malperfusion. , 1998, Critical care medicine.

[17]  Stephen O. Heard,et al.  Continuous measurement of gut pH with near-infrared spectroscopy during hemorrhagic shock. , 1998, The Journal of trauma.

[18]  A. Furuse,et al.  Skeletal muscle gas tension: indicator of cardiac output and peripheral tissue perfusion. , 1973, Surgery.

[19]  T J Morgan,et al.  Monitoring tissue oxygenation during resuscitation of major burns. , 2001, The Journal of trauma.

[20]  M. Weil,et al.  Redefining ischemia due to circulatory failure as dual defects of oxygen deficits and of carbon dioxide excesses , 1991, Critical care medicine.

[21]  T. Blinman,et al.  Rational manipulation of oxygen delivery. , 2000, The Journal of surgical research.

[22]  F D Moore,et al.  Muscle Surface pH as an Index of Peripheral Perfusion in Man , 1971, Annals of surgery.

[23]  T. K. Hunt,et al.  Subcutaneous tissue oxygen pressure: a reliable index of peripheral perfusion in humans after injury. , 1996, The Journal of trauma.

[24]  F. Moore,et al.  Skeletal muscle pH, P(CO2), and P(O2) during resuscitation of severe hemorrhagic shock. , 1998, The Journal of trauma.

[25]  C. Robertson,et al.  Relationship of brain tissue PO2 to outcome after severe head injury. , 1998, Critical care medicine.

[26]  A. Dubin,et al.  Gastric intramucosal pH as a therapeutic index of tissue oxygenation in critically ill patients , 1992, The Lancet.

[27]  T. J. Morgan,et al.  Subcutaneous oxygen tensions provide similar information to ileal luminal CO2 tensions in an animal model of haemorrhagic shock , 2000, Intensive Care Medicine.

[28]  D. Burris,et al.  Subcutaneous oxygen tension: a useful adjunct in assessment of perfusion status. , 1995, Critical care medicine.

[29]  T. J. Morgan,et al.  Continuous measurement of gut luminal PCO2 in the rat: responses to transient episodes of graded aortic hypotension. , 1997, Critical care medicine.

[30]  E. Moore,et al.  Evolving concepts in the pathogenesis of postinjury multiple organ failure. , 1995, The Surgical clinics of North America.

[31]  J. Puyana,et al.  Directly measured tissue pH is an earlier indicator of splanchnic acidosis than tonometric parameters during hemorrhagic shock in swine , 2000, Critical care medicine.

[32]  B. Butler,et al.  Skeletal muscle PO2, PCO2, and pH in hemorrhage, shock, and resuscitation in dogs. , 1998, The Journal of trauma.

[33]  J. Brantigan,et al.  Tissue gases during hypovolemic shock. , 1974, Journal of applied physiology.

[34]  R. Goris,et al.  Early detection of hemorrhagic hypovolemia by muscle oxygen pressure assessment: preliminary report. , 1983, Surgery.

[35]  R. Cox Influence of chloralose anesthesia on cardiovascular function in trained dogs. , 1972, The American journal of physiology.