AIM: To characterize differences of arterial (ABG) and venous (VBG) blood gas analysis in a rabbit model of hemorrhagic shock. METHODS: Following baseline arterial and venous blood gas analysis, fifty anesthetized, ventilated New Zealand white rabbits were hemorrhaged to and maintained at a mean arterial pressure of 40 mmHg until a state of shock was obtained, as defined by arterial pH ≤ 7.2 and base deficit ≤ -15 mmol/L. Simultaneous ABG and VBG were obtained at 3 minute intervals. Comparisons of pH, base deficit, pCO2, and arteriovenous (a-v) differences were then made between ABG and VBG at baseline and shock states. Statistical analysis was applied where appropriate with a significance of P < 0.05. RESULTS: All 50 animals were hemorrhaged to shock status and euthanized; no unexpected loss occurred. Significant differences were noted between baseline and shock states in blood gases for the following parameters: pH was significantly decreased in both arterial (7.39 ± 0.12 to 7.14 ± 0.18) and venous blood gases (7.35 ± 0.15 to 6.98 ± 0.26, P < 0.05), base deficit was significantly increased for arterial (-0.9 ± 3.9 mEq/L vs -17.8 ± 2.2 mEq/L) and venous blood gasses (-0.8 ± 3.8 mEq/L vs -15.3 ± 4.1 mEq/L, P < 0.05). pCO2 trends (baseline to shock) demonstrated a decrease in arterial blood (40.0 ± 9.1 mmHg vs 28.9 ± 7.1 mmHg) but an increase in venous blood (46.0 ± 10.1 mmHg vs 62.8 ± 15.3 mmHg), although these trends were non-significant. For calculated arteriovenous differences between baseline and shock states, only the pCO2 difference was shown to be significant during shock. CONCLUSION: In this rabbit model, significant differences exist in blood gas measurements for arterial and venous blood after hemorrhagic shock. A widened pCO2 a-v difference during hemorrhage, reflective of poor tissue oxygenation, may be a better indicator of impending shock.
AIM: To characterize differences of arterial (ABG) and venous (VBG) blood gas analysis in a rabbit model of hemorrhagic shock. METHODS: Following baseline arterial and venous blood gas analysis, fifty anesthetized, ventilated New Zealand white rabbits were hemorrhaged to and maintained at a mean arterial pressure of 40 mmHg until a state of shock was obtained, as defined by arterial pH ≤ 7.2 and base deficit ≤ -15 mmol/L. Simultaneous ABG and VBG were obtained at 3 minute intervals. Comparisons of pH, base deficit, pCO2, and arteriovenous (a-v) differences were then made between ABG and VBG at baseline and shock states. Statistical analysis was applied where appropriate with a significance of P < 0.05. RESULTS: All 50 animals were hemorrhaged to shock status and euthanized; no unexpected loss occurred. Significant differences were noted between baseline and shock states in blood gases for the following parameters: pH was significantly decreased in both arterial (7.39 ± 0.12 to 7.14 ± 0.18) and venous blood gases (7.35 ± 0.15 to 6.98 ± 0.26, P < 0.05), base deficit was significantly increased for arterial (-0.9 ± 3.9 mEq/L vs -17.8 ± 2.2 mEq/L) and venous blood gasses (-0.8 ± 3.8 mEq/L vs -15.3 ± 4.1 mEq/L, P < 0.05). pCO2 trends (baseline to shock) demonstrated a decrease in arterial blood (40.0 ± 9.1 mmHg vs 28.9 ± 7.1 mmHg) but an increase in venous blood (46.0 ± 10.1 mmHg vs 62.8 ± 15.3 mmHg), although these trends were non-significant. For calculated arteriovenous differences between baseline and shock states, only the pCO2 difference was shown to be significant during shock. CONCLUSION: In this rabbit model, significant differences exist in blood gas measurements for arterial and venous blood after hemorrhagic shock. A widened pCO2 a-v difference during hemorrhage, reflective of poor tissue oxygenation, may be a better indicator of impending shock.
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