(S-128) Lee, H-W., Sunday 9:15
TITLE: THE EFFECT OF THORACIC EPIDURAL ANESTHESIA ON THE CEREBRAL HEMODYNAMIC RESPONSE TO EXPERIMENTAL HEMORRHAGIC SHOCK MODEL IN DOGS
AUTHORS: Hye-Won Lee, MD,phD1, Hun Cho, MD,PhD1, Hae-Ja Lim, MD,PhD1, Seong-Ho Chang, MD,PhD1, Suk-Min Yoon, MD,PhD1, Kyung Sun, MD,PhD1, Kwang-Je Baek, MD,PhD2
AFFILIATION: 1Korea University, Seoul, Republic of Korea; 2Inha University, Incheon, Republic of Korea.
INTRODUCTION: The effects of thoracic epidural anesthesia(TEA) in experimental hemorrhagic shock model in dogs have been examined (1,2), yet its effect on the cerebral hemodynamic response to hemorrhagic shock has not been studied. The aim of this study is to investigate whether thoracic epidural anesthesia (TEA) affect the cerebral hemodynamic resposnses to experimental hemorrhagic shock.
METHODS: After approval of animal care committee, sixteen dogs were received general anesthesia with enflurane and nitrous oxide. Injection of thoracic epidural saline (control group, n=8) or 0.5% bupivacaine (TEA group,n=8) was followed in 20 min by reducing and maintaining the mean arterial pressure(MAP) to 40 mmHg for 1 h by blood withdrawal (hemorrhagic shock:HS) and then reinfused the withdrawn blood (autotransfusion:AT). Mean arterial pressure (MAP), heart rate(HR), intracranial pressure(ICP) and brain tissue PO2 (PtiO2) were recorded before and 20 min after TEA, immediately after and 1h after blood withdrawal and immediately after and 1 hr after reinfused the withdrawn blood. Arterial and pulmonary artery blood gas analyses and measurements of plasma norepinephrine (NE), epinephrine (EP), lactate and pyruvate were done simultaneously. Oxygen extraction ratio (OER) was calculated. Data were analyzed by repeated measure ANOVA or repeated measure ANOVA on rank followed by Dunnett test. P value<0.05 was considered significant.
RESULTS: MAP and HR decreased after epidural anesthesia (P<0.05). After AT, MAP return to baseline value in the control group, but not in the epidural group. HR increased 1 hr after HS in the control group (P<0.05), but not in the epidural group. ICP, CPP and PtiO2 decreased during HS (P<0.05) and return to the baseline value 1 hr after AT in the control group. In the epidural group, ICP, CPP and PtiO2 decreased during HS and the decreases continued until 1 hr after AT (P<0.05).
Plasma EP, NE, lactate increased significantly 1hr after HS in control group (P<0.05), but not in the epidural group. In the epidural group, EP decreased after epidural anesthesia (P<0.05) and did not return to baseline value after AT. In the control group, severe metabolic acidosis was shown 1 hr after HS (P<0.05), but not in the epidural group. Both in the control group and in the epidural group, OER was increased 1 hr after HS (P<0.05) and the increase was less in the epidural group(P<0.05).
DISCUSSION: These results suggest that TEA interferes with sympathetic compensation response to hemorrhagic shock. However TEA improves peripheral perfusion during hemorrhagic shock by the sympatholytic effect, but does not affect the cerebral hemodynamic response during hemorrhagic shock. The circulatory and cerebral hemodynamic consequences due to hemorrhagic shock would be reversed by blood transfusion effectively but not in TEA. Therefore more circulatory resuscitation would be necessary especially for maintaining the cerebral hemocynamics in the patients with TEA during hemorrhagic shock.
REFERENCES:
1)Anesthesiology 71:952-9, 1989.
2) Anesthesiology 74:303-8, 1991.
3) Acta Anaesthesiol Scand 1995:39:179-85.