Abstract
Gastric tonometry correlates with the severity of blood loss during shock. However, tonometry is cumbersome, has a slow response time, and is not practical to apply in the acute resuscitation setting. We hypothesized that subcutaneous tissue (SC) and skeletal muscle (SM) pH, pCO2, and pO2 changes are comparable with changes seen in bowel tonometry during shock and resuscitation. Thirteen male mini-swine (25-35 kg; n = 4 control, n = 9 shock) underwent laparotomy and jejunal tonometry. A multisensor probe (Diametrics Medical, Roseville, MN) was placed in the carotid artery, the chest SC, and the adductor muscle of the leg (SM). PaCO2 was maintained between 40 and 45 mmHg. Shocked animals were hemorrhaged and kept at mean arterial pressure of 40 mmHg. Animals were bled until a reinfusion of >10% of the total shed blood was needed to maintain the mean arterial pressure at 40 mmHg. Animals were resuscitated with shed blood plus 2x shed volume in lactated Ringer's solution (20 min) and were observed for 3 h. The average blood loss was 47.2% +/- 8.7% of calculated blood volume. During the hemorrhagic phase, SM and SC displayed tissue acidosis (r2 = 0.951), tissue hypercapnea (r2 = 0.931), and tissue hypoxia (r2 = 0.748). Overall, pH displayed the best correlation between SM and SC during shock and resuscitation. PCO2 in the jejunum (tonometry), SM, and SC increased during decompensation. However, during resuscitation as tonometric pCO2 normalized, only SC pCO2 decreased to its baseline value, whereas the SM pCO2 decrease tended to lag behind. Bland-Altman analyses demonstrated that the variability of the tissue pH changes in SM and SC are predictable according to the phases of hemorrhage and resuscitation. Changes in tissue pH correlated during bleeding and during resuscitation among SC and SM, and these changes followed the trends in gut tonometry as well. Continuous pCO2 and pO2 monitoring in the SM and SC tissues had significant correlations during the induction of shock only. SM and SC continuous pH and pCO2 monitoring reflect bowel pCO2 values during hemorrhagic shock. The response of these indicators as potential surrogates of impaired tissue metabolism varies among tissues and according to the phases of hemorrhage or resuscitation.
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