Effectors of hypercarbia during experimental pneumoperitoneum.
Hypercarbia occurs during laparoscopy with carbon dioxide (CO2) insufflation. This may be due to increased ventilatory dead space after expansion of the peritoneal cavity with impairment of diaphragmatic excursion, or to increased absorption of CO2 from the peritoneum. To separate these effects, the authors examined the consequences of different insufflating gases and of diminished tissue perfusion on hypercarbia and dead space during pneumoperitoneum. Helium was chosen as an alternate insufflating gas because it is both inert and minimally absorbed. Eight swine (18 to 20 kg) were anesthetized, paralyzed, and mechanically ventilated at constant minute volume. Pneumoperitoneum with helium was maintained at 15 mm Hg for 45 minutes. After desufflation and stabilization for 1 hour, pneumoperitoneum was repeated with CO2. The sequence was again repeated after hemorrhagic shock to constant mean arterial pressure of 50 mm Hg. Data was analyzed by analysis of variance; significance levels are P < 0.01 unless otherwise listed. Arterial PCO2 increased significantly with CO2 insufflation within 15 minutes in normotensive animals and within 30 minutes during hypotension. Arterial pH decrease with CO2 pneumoperitoneum was significant in both groups at 30 minutes. Mixed venous PCO2 also increased with CO2 pneumoperitoneum within 30 minutes. Hypotension did not alter these changes. No significant changes were seen with helium pneumoperitoneum. Neither helium nor CO2 pneumoperitoneum significantly altered dead space. The authors make the following conclusions: 1) Absorption of CO2 from the abdomen during CO2 pneumoperitoneum produces respiratory acidosis, which is not seen with helium insufflation; 2) Pneumoperitoneum does not significantly increase dead space with either gas; 3) Transperitoneal absorption of CO2 is only partly related to perfusion because significant hypercarbia occurs during hemorrhagic shock.
Leighton
T
T
Department of Surgery, Harbor-UCLA Medical Center, UCLA School of Medicine, Torrance.
Pianim
N
N
Liu
S Y
SY
Kono
M
M
Klein
S
S
Bongard
F
F
D000042:Absorption; D000140:Acidosis, Lactic / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology; D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000009:adverse effects* / Q000493:pharmacokinetics; D002302:Cardiac Output / Q000187:drug effects; D005069:Evaluation Studies as Topic; D006339:Heart Rate / Q000187:drug effects; D006371:Helium / Q000009:adverse effects*; D006935:Hypercapnia / Q000097:blood / Q000139:chemically induced* / Q000503:physiopathology; D010535:Laparoscopy / Q000009:adverse effects; D011028:Pneumoperitoneum, Artificial / Q000009:adverse effects* / Q000295:instrumentation / Q000379:methods; D012126:Respiratory Dead Space / Q000187:drug effects; D012771:Shock, Hemorrhagic / Q000097:blood / Q000150:complications / Q000503:physiopathology; D013552:Swine; D013990:Tidal Volume / Q000187:drug effects; D013997:Time Factors; D014018:Tissue Distribution
D002245:Carbon Dioxide; D006371:Helium