Attenuation of pneumoperitoneum-induced hypertension by intra-peritoneal lidocaine before pneumoperitoneum in laparoscopic cholecystectomy.
10.12701/yujm.2016.33.2.90
- Author:
Sun Ok SONG
1
;
Hae Mi LEE
;
Sung Soo YUN
;
Hwarim YU
;
Soo Young SHIM
;
Heung Dae KIM
Author Information
1. Department of Anesthesiology and Pain Medicine, College of Medicine, Yeungnam University, Daegu, Korea. hdkim@med.yu.ac.kr
- Publication Type:Original Article
- Keywords:
Hemodynamics;
Lidocaine;
Laparoscopic cholecystectomy;
Pain
- MeSH:
Analgesics;
Anesthesia, General;
Blood Pressure;
Cardiac Output;
Central Venous Pressure;
Cholecystectomy, Laparoscopic*;
Heart Rate;
Hemodynamics;
Humans;
Hypertension*;
Lidocaine*;
Methods;
Pain, Postoperative;
Pneumoperitoneum*;
Stroke Volume;
Vascular Resistance
- From:Yeungnam University Journal of Medicine
2016;33(2):90-97
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: We have previously found that intra-peritoneal lidocaine instillation before pneumoperitoneum attenuates pneumoperitoneum-induced hypertension. Whether this procedure alters patient's hemodynamic status during operation should be determined for clinical application. This study elucidated the possible mechanism of the attenuation of the pneumoperitoneum-induced hypertension by intra-peritoneal lidocaine before pneumoperitoneum. METHODS: Thirty-four patients underwent laparoscopic cholecystectomy (LC) were randomly allocated into two groups. After induction of general anesthesia, 200 mL of 0.2% lidocaine (lidocaine group, n=17), or normal saline (control group, n=17) were sub-diaphragmatically instilled 10 minutes before pneumoperitoneum. The changes in systolic blood pressure, heart rate, central venous pressure, stroke volume, cardiac output, and systemic vascular resistance were compared between the groups. The number of analgesics used during post-operative 24 h was compared. RESULTS: Systolic blood pressure was elevated during pneumoperitoneum in both groups (p<0.01), but the degree of elevation was significantly reduced in the lidocaine group than in the control (p<0.01). However, stroke volume and cardiac output were decreased and systemic vascular resistance was increased after induction of pneumoperitoneum (p<0.05) without statistical difference between two groups. The number of analgesics used was significantly reduced in the lidocaine group (p<0.01). CONCLUSION: These data suggest that intra-peritoneal lidocaine before pneumoperitoneum does not alter patient's hemodynamics, and attenuation of pneumoperitoneum-induced hypertension may be the consequence of reduced intra-abdominal pain rather than the decrease of cardiac output during pneumoperitoneum. Therefore, intra-peritoneal lidocaine instillation before pneumoperitoneum is a useful method to manage an intraoperative pneumoperitoneum-induced hypertension and to control postoperative pain without severe detrimental hemodynamic effects.
