The Effects of Hyperventilation Prior to CO2 Insufflation During Laparoscopic Cholecystectomy
Keywords
Abstract
Description
The use of laparoscopic techniques has become common in clinical practice. Absorption of carbon dioxide (CO2) from the peritoneal cavity is the potential mechanism for hypercapnia and a rise in the end-tidal carbon dioxide (EtCO2). Mild hypercarbia causes sympathetic stimulation which results in a fivefold increase in arginine vasopressin (AVP), tachycardia, increased systemic vascular resistance, systemic arterial pressure, central venous pressure and cardiac output.1 Severe hypercarbia exerts a negative inotropic effect on the heart and reduces left ventricular function.2 Hemodynamic alterations occur only when the PaCO2 is increased by 30 per cent above the normal levels.
Clearance of CO2 is a function of the adequacy of alveolar ventilation with respect to pulmonary perfusion. Controlled hyperventilation has proved to be superior over spontaneous respiration or controlled normo-ventilation for maintaining normal PCO2 during laparoscopy. During pelvic laparoscopy there was a rapid rise of about 30% in the CO2 load eliminated by the lungs. This quickly reached a plateau and could be compensated by hyperventilation of the lungs with a 30% increase in minute ventilation.
Papadimitriou and co' workers concluded that under sevoflurane anesthesia MAC, prophylactic hyperventilation to ensure mild hypocapnia, (around 33 mmHg) limits the cerebral blood flow velocities enhancing effect of CO2 insufflation, compared with permissive hypercapnia (up to 45 mmHg), during gynecological laparoscopies. However, others advocated that hyperventilation and the head-up position before CO2 insufflation are not sufficient to prevent the CO2-mediated cerebral hemodynamic effects of low-pressure pneumoperitoneum (5-8 mmHg) in children, underwent laparoscopic fundoplication.
Dates
| Last Verified: | 10/31/2010 |
| First Submitted: | 08/11/2010 |
| Estimated Enrollment Submitted: | 08/15/2010 |
| First Posted: | 08/16/2010 |
| Last Update Submitted: | 11/17/2010 |
| Last Update Posted: | 11/18/2010 |
| Actual Study Start Date: | 11/30/2008 |
| Estimated Primary Completion Date: | 07/31/2010 |
| Estimated Study Completion Date: | 08/31/2010 |
Condition or disease
Intervention/treatment
Procedure: Ventilation
Phase
Arm Groups
| Arm | Intervention/treatment |
|---|---|
| Placebo Comparator: The normoventilation group 15 minutes prior to CO2 insufflation, the patients' lungs were ventilated with a tidal volume (TV) of about 8 mL.kg-1 and respiratory rate (R.R) owas adjusted to maintain an end-tidal CO2 (ETCO2) of 4.6-6 kPa throughout the procedure. | |
| Active Comparator: The hyperventilation group 15 minutes prior to CO2 insufflation, the patients' lungs were ventilated with a TV of 8 mL.kg-1 with the adjustment of the R.R to maintain an ETCO2 of 4-4.6 kPa, until the end of anaesthesia. |
Eligibility Criteria
| Ages Eligible for Study | 18 Years To 18 Years |
| Sexes Eligible for Study | All |
| Accepts Healthy Volunteers | Yes |
| Criteria | Inclusion Criteria: - ASA I & II - aged 18-45 years - undergoing elective laparoscopic cholecystectomy Exclusion Criteria: - history of cardiovascular disease - respiratory diseases - neurological disease - renal disease - liver disease - hormonal disease - pregnancy - obesity (defined as a body mass index> 29) - smokers |
Outcome
Primary Outcome Measures
1. haemodynamic percussion response [at 5 and 10 minutes, in supine and Trendelenburg (30° head-down) positions, respectively, before CO2 insufflation and at 15, 30, 45, and 60 min after CO2 insufflation, and at 5 min after desufflation of pneumoperitoneum]
Secondary Outcome Measures
1. other hemodynamic and respiratory parameters [at 5 and 10 minutes, in supine and Trendelenburg (30° head-down) positions, respectively, before CO2 insufflation and at 15, 30, 45, and 60 min after CO2 insufflation, and at 5 min after desufflation of pneumoperitoneum,]
