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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 mm Hg until a state of shock was obtained, as defined by arterial p H ≤ 7.2 and base deficit ≤-15 mmol/L. Simultaneous ABG and VBG were obtained at 3 minute intervals. Comparisons of p H, base deficit, p CO2, 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 shockstatus and euthanized; no unexpected loss occurred. Significant differences were noted between baseline and shock states in blood gases for the following parameters: p H 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 m Eq/L vs-17.8 ± 2.2 m Eq/L) and venous blood gasses(-0.8 ± 3.8 m Eq/L vs-15.3 ± 4.1 m Eq/L, P < 0.05). p CO2 trends(baseline to shock) demonstrated a decrease in arterial blood(40.0 ± 9.1 mm Hg vs 28.9 ± 7.1 mm Hg) but an increase in venous blood(46.0 ± 10.1 mm Hg vs 62.8 ± 15.3 mm Hg), although these trends were non-significant. For calculated arteriovenous differences between baseline and shock states, only the p CO2 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 p CO2 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 mm Hg until a state of shock was obtained, as defined by arterial p H ≤ 7.2 and base deficit ≤ -15 mmol / L. Simultaneous ABG and VBG were obtained at 3 minute intervals. Comparisons of p H , base deficit, p CO2, and arteriovenous (av) 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 shockstatus and Significant differences were noted between baseline and shock states in blood gases for the following parameters: p H 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 m Eq / L vs -17.8 ± 2.2 m Eq / L) and venous blood gasses (-0.8 ± 3.8 m Eq / L vs -15.3 ± 4.1 m Eq / L, P <0.05). p CO2 trends (baseline to shock) demonstrated a decrease in arterial blood (40.0 ± 9.1 mm Hg vs. 28.9 ± 7.1 mm Hg) but an increase in venous blood (46.0 ± 10.1 mm Hg vs 62.8 ± 15.3 mm Hg), although these trends were non-significant. For calculated arteriovenous differences between baseline and shock states, only the p CO2 difference was shown as 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 p CO2 av difference during hemorrhage, reflective of poor tissue oxygenation, may be a better indicator of impending shock.