Brief Article
Copyright ©2014 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Crit Care Med. May 4, 2014; 3(2): 55-60
Published online May 4, 2014. doi: 10.5492/wjccm.v3.i2.55
Arterial vs venous blood gas differences during hemorrhagic shock
Kristopher Burton Williams, Ashley Britton Christmas, Brant Todd Heniford, Ronald Fong Sing, Joseph Messick
Kristopher Burton Williams, Ashley Britton Christmas, Brant Todd Heniford, Ronald Fong Sing, Joseph Messick, Department of Surgery, Carolinas HealthCare System, Charlotte, NC 28204, United States
Author contributions: Heniford BT, Sing RF, Messick J designed research; Sing RF, Messick J performed research; Messick J contributed new reagents or analytic tools; Christmas AB, Heniford BT, Sing RF analyzed data; Williams KB, Christmas AB, Heniford BT, Sing RF wrote the paper; Messick J deceased since the completion of this study.
Supported by Carolinas HealthCare System, Department of Surgery, Charlotte, North Carolina, United States
Correspondence to: Ronald Fong Sing, DO, FACS, FCCM, Department of Surgery, Carolinas HealthCare System, 1000 Blythe Boulevard, Charlotte, NC 28203, United States. ron.sing@carolinashealthcare.org
Telephone: +1-704-3551311 Fax: +1-704-3555619
Received: March 1, 2013
Revised: October 19, 2013
Accepted: March 3, 2014
Published online: May 4, 2014
Processing time: 445 Days and 2 Hours
Abstract

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.

Keywords: Hemorrhagic shock; pH; Base deficit; Arterial blood gases; Venous blood gases

Core tip: Recent studies regarding early goal directed therapy and damage control resuscitation have indicated a potential role for calculated arteriovenous pCO2 differences in monitoring resuscitative efforts. In a rabbit model of hemorrhagic shock, we demonstrate significant derangements between arterial and venous blood and, while not a novel concept, explore the potential of central venous pCO2 as an indicator of hemorrhagic shock. Our results demonstrate a widened arteriovenous pCO2 difference is significantly associated with hemorrhagic shock and may be a more reliable indicator of inadequate tissue perfusion and therefore impending circulatory collapse.