Intraperitoneal Carbon Dioxide Insufflation andCardiopulmonary FunctionsLaparoscopic Cholecystectomy in Pigs

Hung S. Ho, MD; Robert A. Gunther, PhD; Bruce M. Wolfe, MD

\s=b\We studied the effects of laparoscopic cholecystectomyon respiratory and hemodynamic function in eight adultpigs. Minute ventilation was adjusted to normalize baselinearterial blood gases, then fixed throughout carbon dioxideinsufflation. A metabolic measurement cart recorded totalCO2 excretion, oxygen consumption, and minute ventila-tion. Carbon dioxide pneumoperitoneum was maintained ata constant pressure of 15 mm Hg as cholecystectomy was

performed. After 1 hour of insufflation, CO2 excretionincreased from 115\m=+-\10mL/min to 149\m=+-\9mL/min but O2consumption remained unchanged. The PaCO2 increasedfrom 35\m=+-\2mm Hg to 49\m=+-\3mm Hg and arterial pH fell from7.47\m=+-\0.02to 7.35\m=+-\0.03.Systemic and pulmonary hyper-tension occurred and stroke volume dropped from35.5\m=+-\3.5mL to 28.6\m=+-\2.2mL with compensatory tachy-cardia. Right atrial pressure remained unchanged as inferiorvena cava pressure increased to reflect the intraperitonealpressure. We conclude that CO2 pneumoperitoneum re-sulted in significant transperitoneal CO2 absorption, withsecondary hypercapnia and acidemia. The accumulation ofCO2 was also associated with an increase in systemic andpulmonary arterial pressure. Heart rate increased to com-

pensate for the decreased stroke volume to maintain cardiacoutput.

(Arch Surg. 1992;127:928-933)

Laparoscopie cholecystectomy is a recent, but exciting,. development in the surgical management of chole¬

lithiasis, as it removes the target organ and yet, avoids thetraditional large upper abdominal incision with the asso¬ciated postoperative pain, disability, and slow return towork. Since the first procedure was performed in France in1987, laparoscopie cholecystectomy has become popular inthe United States.1-2 Although the procedure has enjoyed aminimal morbidity similar to that of open cholecyst¬ectomy,2"4 reports on complications with ventilatory status

such as hypercapnia or acidemia have appeared. Criticalanalysis of our experience with the first 381 patients at theUniversity of California Davis Medical Center, Sacra¬mento, and its affiliated hospitals revealed a comparablemortality and morbidity with the open procedure. Techni¬cal complications occurred in 2% of the patients; nontech¬nical complications occurred in 4% of patients. The mostcommon nontechnical complication was atelectasis or

pneumonia in five patients. One patient with a history ofchronic obstructive pulmonary disease experienced severe

hypercapnia following intraperitoneal carbon dioxide in¬sufflation. She was subsequently converted to an openprocedure owing to technical reasons, but the hypercapniapersisted postoperatively, requiring 24 hours of mechan¬ical ventilation.5 Wittgen et al6 also reported that patientswith preoperative cardiac or pulmonary disease experi¬enced significant accumulation of arterial C02 and devel¬opment of acidemia during the C02 insufflation period.One of these patients also required conversion to opencholecystectomy because of refractory acidemia.6 Liu et al7prospectively studied 16 healthy patients undergoing lap¬aroscopie cholecystectomy and found a significant respi¬ratory acidosis during CÓ2 insufflation.

These clinical observations raise our concern for the po¬tential pathophysiologic effects of intraperitoneal C02 in¬sufflation and the resulting high intra-abdominal pressuregenerated on the patient's cardiopulmonary performance.As laparoscopie procedures become more universal andmore applicable in diseases other than cholelithiasis, more

complex and longer procedures such as common bile ductsurgical exploration, antireflux operation, lymph nodedissection, intestinal resection, etc, will be performed. Thismeans a longer duration of C02 insufflation. The patientpopulation may be expected to be much older and withmore marginal cardiopulmonary reserve. As a conse¬

quence, the combination of prolonged C02 insufflation andlimited pulmonary reserve may pose a significant risk forthe patients.

We performed this study to address the following ques¬tions: (1) To what extent does the intraperitoneal C02 thatis insufflated eventually get absorbed into the systemiccirculation? (2) Does the C02 pneumoperitoneum lead tosignificant arterial C02 accumulation and acid-basechanges? (3) Are there any hemodynamic changes thatmay be clinically important? We aim to assess these phys-

Accepted for publication March 7, 1992.From the Department of Surgery, University of California at Davis

Medical Center, Sacramento, Calif.Presented at the 99th Scientific Session of the Western Surgical Asso-

ciation, Colorado Springs, Colo, November 19, 1991.Reprint requests to Department of Surgery, University of California

Davis Medical Center, 4301 X St, Room 2310, Sacramento, CA 95817(Dr Wolfe).

iologic changes associated with laparoscopie surgical pro¬cedures to minimize potential morbidity when extendingthese applications to treatment of more complex intra-abdominal abnormalities.

MATERIALS AND METHODSAnimal Preparation

The project was conducted in accordance with the National In¬stitutes of Health Guide for the Care and Use of Laboratory Animals.sEight adult pigs, weighing 27 to 30 kg, were anesthetized with an

intramuscular injection of ketamine hydrochloride (10 to 15 mg/kg). After endotracheal intubation, the anesthesia was maintainedwith intravenous pentobarbital sodium. The animals were placedin a supine position on the operating table with the front and hindlimbs fixed in the abduction position. A respiration pump (model607, Harvard Apparatus Co Ine, Millis, Mass) was used to venti¬late the animals with room air. The appropriate minute ventila¬tion was determined by adjusting the tidal volume and respira¬tory rate to obtain normal arterial blood gas values. The expiredflow was directly connected to a metabolic measurement cart(MMC Horizon System, Beckman Instruments Ine, Schiller Park,111) for continuous measurements of 02 consumption, C02 excre¬

tion, and minute ventilation. The neck, abdomen, and groin wereshaved and prepared with povidone-iodine (Betadine) solutionand draped in sterile fashion. The right internal jugular vein andfemoral vessels were surgically exposed and cannulated withpolyethylene catheters (American Pharmaseal, Glendale, Calif)for measurements of right atrial and interior vena cava venous

pressures, respectively. The right carotid artery was then cannu¬lated to monitor the mean arterial pressure (MAP). A flow-directed pulmonary arterial catheter (Baxter, American EdwardsLaboratories, Irvine, Calif) was also inserted via the internal jug¬ular vein and floated into the pulmonary artery for measurementsof cardiac output, pulmonary arterial wedge pressure (PAWP),and pulmonary arterial pressure (PAP). The catheters were con¬nected to membrane transducers (model 1290A, Hewlett-Packard, Waltham, Mass). Mean systemic arterial pressure,PAWP, PAP, right atrial (central venous pressure [CVP]) pres¬sure, and inferior vena cava venous pressures were recorded witha multichannel, amplified, strip chart recording system (7754BSystem, Hewlett-Packard, Palo Alto, Calif). Cardiac output wasmeasured by the thermodilution technique using room temper¬ature normal saline injectate (10 mL) and a cardiac output com¬

puter (model 9520A, American Edwards Laboratories, Irvine,Calif). All pressures were recorded with the pigs in the supineposition, with the transducers zeroed to the midchest of the an¬imal and calibrated to a mercury standard. Arterial blood gaseswere analyzed by a pH/blood gas analyzer (model 170, CorningMedical, Medfield, Mass).

ProtocolAfter the animals were anesthetized and fully instrumented, a

I- to 2-hour baseline period was observed, when the animals' ar¬terial blood gases were normalized and hemodynamic data werestabilized. The minute ventilation obtained during this baselineperiod was then fixed throughout the rest of the experiment.Laparoscopie cholecystectomy was performed using the four-portal technique, with intraperitoneal C02 flow adjusted intraop-eratively to maintain a constant intra-abdominal pressure of 15mm Hg. Arterial blood gas determinations and hemodynamicmeasurements were obtained every 15 minutes. The fractions ofinspired and expired C02 and 02 gases and minute ventilationwere recorded continuously by the metabolic measurement cartfor calculation of the CO, excretion and 02 consumption. Since thelength of the operations varied considerably, we terminated thestudy at 1 hour of insufflation. No data were obtained during therecovery period.

Calculation and Analysis of DataMetabolic Measurements.—The content of the expired flow

from the animals was measured continuously by the metaboliccart, with the inspired flow consisting of room air. In principle,

170

155

140-

Baseline

-30 -15

Pneumoperitoneum0 15

Time, min30 45 60

Fig 1.—After 1 hour of carbon dioxide insufflation, the excretion ofC02(circles) increased from 115± 10 mL/min to 149±9 mL/min, an increaseof 30% above baseline value (mean±SEM). Oxygen consumption(squares), on the contrary, remained essentially unchanged. Asterisk in¬dicates P<.05 vs baseline, analysis of variance for repeated measure¬ments.

the differences between the inspired and expired amounts of CO^as well as those for 02, are the direct measure of the total bodyexcretion of C02 (VVC02) and total 02 consumption (VV02), re¬

spectively. For VVC02, the following equation applied:VVC02= [F.COj x VJ

-

[FC02 x V,j,where V¡ and Ve are the inspired and expired volume, respec¬tively.

For practical calculation of C02 excretion, we ignored theinspired amount of C02 gas because of its low atmospheric con¬centration, with F,C02 of only 0.03 vol%. Thus, the amount of C02excreted was considered to be the measured amount in theexpired gas:

VVC02=FeC02XVe,where Ft.CO<2 is the fraction of C02 in the expired gas (volumepercent) and V, is the minute ventilation (milliliter per minute).

Hemodynamics.—Stroke volume (SV) was calculated fromcardiac output and heart rate (HR) (SV=CO/HR); pulmonaryvascular resistance (PVR) was calculated from the mean PAP,PAWP, and cardiac output (PVR=[PAP-PAWP]/CO); and totalperipheral resistance (TPR) was calculated from the MAP, rightatrial pressure, and cardiac output (TPR=[MAP-CVP]/CO).Since the animals had a small range of weight among themselves,cardiac output was used instead of cardiac index.

Statistical AnalysisData were reported as mean values±l (SEM), with n=8. Anal¬

ysis of variance for repeated measurements was performed todetermine significant differences. A value less than .05 wasconsidered statistically significant. All statistical analyses were

performed using specific software (StatView II, Abacus ConceptsIne, Berkeley, Calif) on a computer (Macintosh Ilex, Apple Com¬puter Ine, Cupertino, Calif).

RESULTSC02 Homeostasis and Acid-Base Balance

After 1 hour of intraperitoneal C02 insufflation, the to¬tal body excretion of C02 (VVC02) increased from 115±10mL/min to 149±9 mL/min, or by 30% above baseline, withP<.05. Oxygen consumption, however, remained essen¬

tially unchanged, from 152±12 mL/min to 156±10mL/min (Fig 1). Concurrently, there were correspondingchanges in arterial blood gas values. Figure 2 shows thatPaco2 increased by 40% from 34.5±1.5 mm Hg to 48.6±3.2mm Hg (P<.05) and arterial pH fell from 7.47±0.02 to7.35±0.03 (P<.05). The volume percentage of expired C02

50-

40

30 — --15

- "15

— —30-30 45 60

Fig 2.—During carbon dioxide pneumoperitoneum, there was an accu¬mulation ofarterial C02 and development ofacidemia. Paco, increasedby 40%, from 34.5± 1.5 mm Hg to 48.6±3.2 mm Hg, and arterial pHfell from 7.47± 0.02 to 7.35± 0.03. Asterisk indicates P<.05 vs baseline,analysis of variance for repeated measurements; two asterisks, P< .05 vsbaseline, analysis of variance for repeated measurements.

30— -45-30 -15 15 60

28

-30

Fig 3.—Although the cardiac output was essentially unchanged through¬out the carbon dioxide insufflation, the stroke volume dropped from35.5±3.5 mL to 28.6+2.2 mL (asterisk indicates P<.05 vs baseline,analysis ofvariance for repeatedmeasurements). Significant tachycardiadeveloped in the animals to compensate for this.

content was correlated statistically with the changes in ar¬terial blood gas (r2=.977 and .957 for Paco2 and pH, respec¬tively); it increased from 2.94+0.1 vol% to 3.67±0.2 vol%during the same period (P<.05). The ratio of minute ven¬tilation over VVC02, the total volume the lung needs toexpire to excrete 1L of C02 decreased from 42±2 L to 33±2L, indicating that the increased excretion of C02 was notdue to respiratory dysfunction. Furthermore, the 02 con¬sumption remained stable throughout the C02 insufflationperiod, reflecting a respiratory quotient steadily increasingfrom 0.76 ±0.03 to 0.98 ±0.03, again indicating that thesource of increased C02 excretion was not from hyperme-tabolism.

Hemodynamic ChangesAs the SV dropped from 35.5±3.5 mL at baseline to

28.6±2.2 mL within 60 minutes of C02 insufflation (P<.05),the HR increased from 157 ± 10 beats per minute to 181 ± 11beats per minute. As a result, cardiac output was essen¬tially unchanged throughout the C02 insufflation period,from 5.1 ±0.3 L/min to 5.1 ±0.4 L/min (Fig 3). The animalsalso experienced an increase in both peripheral and PAPswith the MAP increasing from 81 ±4 mm Hg to 93±5 mmHg (P<.05) and the mean PAP increasing from 17.3±0.7mm Hg to 22.4 ±1.5 mm Hg after 60 minutes of C02 insuf¬flation (Fig 4). Thus, higher vascular resistance developedin the animals in the peripheral and pulmonary circula¬tions. The increase in total peripheral resistance, from15±0.4 mm Hg-min-L-1 to 17.8±1.7 mm Hg-min-L"1(P<.05), was better correlated with Paco2 (R2=.950) thanwith the increases in intra-abdominal pressure caused bythe pneumoperitoneum (r2=.782), as reflected by the infe¬rior vena cava venous pressure. Inferior vena cava venouspressure increased from 5.9±1 mm Hg to 14.1 ±1 mm Hg

(P<.05), closely reflecting the intraperitoneal insufflationpressure, whereas CVP and PAWP remained relatively thesame (Fig 5).

COMMENTThe principles and techniques of laparoscopie surgeryhave been well established in the practice of gynecologyand urology, but it was not until recent technologic

advances in optics and instrumentation and the consumerdemand for minimal-access surgery that a tremendousadvancement of laparoscopie techniques and their appli¬cations in general surgery occurred. Laparoscopie chole¬cystectomy has been received enthusiastically by Ameri¬can surgeons, and by late 1991, it has virtually replaced thetraditional open cholecystectomy in the treatment ofcholelithiasis.2

Laparoscopie cholecystectomy, nevertheless, does havelimitations. The procedure requires intraperitoneal gas in¬sufflation for adequate visualization and successful oper¬ation. Carbon dioxide has been used traditionally becauseof its ability to be quickly absorbed, although other gaseshave been advocated in the past.9 When instilled into theabdominal cavity, the C02 gas would normally diffuseacross the peritoneum, to be carried by the circulation tothe lung where it is excreted. Because C02 is capable ofpenetrating cell membranes and ultimately increasing in-tracellular hydrogen ion concentration, it can exert sys¬temic toxic effects if its excretion is impaired. Transforma¬tion of the gas into bicarbonate or citrate by the enzymaticreactions in the cells can be accelerated, but it cannot sub¬stitute for pulmonary elimination. The excretion of C02follows the simple rule of diffusion-perfusion limitation.As the body responds to the exogenous C02 accumulation,gas exchange at the peritoneal surface and the alveolar

<2

100-

95-

90-

85-

80-

75--30 -15 15 30 45

— 60

23.0-

·£ 21.0-

ou 19.0-<

17.0-

15.0--30

Basel i Pneumoperitoneum-15 0 15

Time, min

30 45

—I60

Fig 4.—Both mean arterial pressure (MAP) and pulmonary arterial pres¬sure (PAP) were elevated during carbon dioxide insufflation, reflectinga response to sympathetic discharge due to high Paco2. Asterisk indicatesP<.05 vs baseline, analysis of variance for repeated measurements; twoasterisks, P<.05 vs baseline, analysis of variance for repeated measure¬ments.

13-

-30

Baseline

-15

Pneumoperitoneum- - -1-1-1-1-115 30 45 60

Time, min

Fig 5.—Central filling pressure was not affected. Both right atrial pres¬sure (central venous pressure, circles) and pulmonary arterial wedgepressures (triangles) remained unchanged while inferior vena cava pres¬sure (squares) increased from 5.9± 1 mm Hgto 14.1+1 mm Hg (asteriskindicates P<.01 vs baseline, analysis of variance for repeated measure¬ments), as a reflection of the intraperitoneal pressure.

membrane accelerates, and the patient experiences tac-hypnea and elevated tidal volume to rid the body of theexcess gas. Perfusion is also increased to remove the gasfrom the peritoneal cavity and deliver it to the lung. Intheory, this can be accomplished by an increase in cardiacoutput. If the systemic C02 accumulation is severe enoughto decrease SV, then the patient must compensate byaccelerating the HR, which in part is presumably inducedby sympathetic discharge in response to hypercapnia,10perhaps by direct and chemoreflex actions." Our observa¬tion on vascular resistance changes may be explained inpart by this mechanism. This scenario may put furtherstress on the myocardium. Lastly, since the body storagecapacity for C02 is large (120 L), any excess C02 that can¬not be excreted will be absorbed, mainly by skeletal mus¬cle and bone.12 This will be excreted gradually by the bodypostoperatively, but with a risk of persistent hypercapnia.

Studies of the cardiovascular changes during gyneco¬logic laparoscopie procedures have been carried out exten¬sively in the past, but with most emphasis placed on themechanical effects of the pneumoperitoneum. Increasedintra-abdominal pressure has been implicated in contrib¬uting to hemodynamic instability. Prior studies of the ad¬verse hemodynamic effects of increased intra-abdominalpressure showed impeded venous return by raising venousresistance. Kashtan et al13 investigated the effects of highintra-abdominal pressure on venous return and foundmixed results. Because high intra-abdominal pressure (40mm Hg) also raised MAP, the net effects appeared to be de¬pendent on the right atrial pressure. High intra-abdominalpressure augmented venous return at high central venous

filling pressure and reduced venous return at low or normalCVP.13 We maintained right atrial pressure in our animals

at a normal level before insufflation and found that it re¬

mained unchanged throughout the C02 pneumoperito¬neum. The differences between the two studies were thatthe intra-abdominal pressure in the Kashtan et al study wasmuch higher than the 15 mm Hg intraperitoneal pressurenormally used during laparoscopie cholecystectomy. In ad¬dition, the elevation in intraperitoneal pressures was in¬duced with gas insufflation during laparoscopie cholecys¬tectomy, not with fluid infusion.

Kelman et al14 found the cardiac output and CVP to beprogressively increasing during C02 insufflation withintra-abdominal pressures up to 20 to 30 cm H20 but thendecreasing as the pressure approached 30 to 40 cm H20.Motew et al9 observed an elevation of blood pressure andCVP in 10 women undergoing intraperitoneal C02 insuf¬flation up to a pressure of 20 mm Hg. Further increases inintra-abdominal pressure to 30 mm Hg resulted in slightdepression of cardiac output and CVP.9 Lenz et al15 docu¬mented the correlation between cardiac depression and theamount of intraperitoneal C02 used. None of these reports,however, investigated the relationship between the degreeof C02 absorption and its effects on the cardiovascularsystem. Seed et al16 reported some evidence of absorptionof the gas from the peritoneum, but they concluded that itwas not of sufficient magnitude to affect respiratoryhomeostasis. In this study, cardiac output was maintainedbut SV was markedly reduced during C02 insufflation. Thereduction in SV may be a result of the combination of a C02depressant effect on myocardial contractility17 and an in¬crease in afterload. However, our data suggest that theintra-abdominal pressure of 15 mm Hg created by thestandard laparoscopie cholecystectomy pneumoperito¬neum did not have any significant mechanical effects onvenous return, as the CVP remained essentially un¬

changed. Cardiac output measurements alone may be

misleading in this situation where the depressant effect ofhypercapnia on the myocardium is partially masked by thesympathetic stimulation of high Paco2 on heart rate. In ad¬dition, this study provides evidence that C02 was absorbedfrom the peritoneal cavity during laparoscopie cholecys¬tectomy with secondary hypercapnia and acidemia, thelatter of which also caused cardiac depression.11 Furtherevidence indicating that the increased Paco2 and acidemiaare the result of absorbed C02 is provided by the study ofLeighton et al.18 In a similar pig model, peritoneal C02 in¬sufflation, but not helium insufflation, induced hypercap¬nia, acidemia, and increased pulmonary excretion of C02.Both the study of Leighton et al and our study also showa significant pulmonary hypertension during insufflation.

In this model, we maintained a fixed minute ventilationthroughout the period of insufflation to approximate theclinical model in which mechanical ventilatory impair¬ment prevents intraoperative adjustment of minute venti¬lation. Intraoperatively, it is imperative that end-tidal vol¬ume C02 content be monitored continuously during C02pneumoperitoneum to allow appropriate adjustments ofminute ventilation to avoid potential hypercapnia and ac¬idemia. Minute ventilation is routinely increased intraop¬eratively as systemic absorption of C02 occurs and end-tidal C02 increases. Patients with impaired pulmonaryfunction may not be able to increase gas exchange sub¬stantially, however, and experience systemic C02 accu¬mulation as occurred in this study. In patients with a his¬tory of cardiopulmonary disease, invasive monitoringdevices such as peripheral and pulmonary arterial cathe¬ters may be indicated. Myocardial work must be assessedby monitoring both SV and HR, not simply measurementsof cardiac output. Transesophageal echocardiogram maybe able to replace invasive pulmonary arterial catheteriza-tion in assessment of cardiac performance, but study inhuman subjects is still pending. Laparoscopie cholecystec¬tomy should be performed as an outpatient procedurewith caution, especially in patients who may have pre¬existing cardiopulmonary disease.

This investigation was supported by training grant2T32GM07860-12 from the National Institutes of Health and grant35747 from the National Institute of Diabetes and Digestive and Kid¬ney Diseases, Bethesda, Md.

References1. Dubois F, Icard P, Berthelots C, Levard H. Coelioscopic cholecystec-

tomy: preliminary report of 36 cases. Ann Surg. 1990;211:60-62.2. The Southern Surgeons Club. A prospective analysis of 1518 laparo-

scopic cholecystectomies. N Engl J Med. 1991;324:1073-1078.3. Arnold DJ, Zollinger RW, Bartlett, RM, et al. 28,261 cholecystectomies

in Ohio. Am J Surg. 1970;119:714-717.4. Scher KS, Scott-Conner CE. Complications of biliary surgery. Am Surg.

1987;53:16-21.5. Wolfe BM, Gardiner BN, Leary BF, Frey CF. Endoscopic cholecystec-

tomy: an analysis of complications. Arch Surg. 1991;126:1192-1198.6. Wittgen CM, Andrus CH, Fitzgerald SD, Baudendistel LJ, Dahms TE,

Kaminski DL. Analysis of the hemodynamic and ventilatory effects of laparo-scopic cholecystectomy. Arch Surg. 1991;126:997-1001.

7. Liu SY, Leighton T, Davis I, Klein S, Lippmann M, Bongard F. Prospec-tive analysis ofcardiopulmonary responses to laparoscopic cholecystectomy.J Laparoendosc Surg.1991;1:241-246.

8. Guide for the Care and Use of Laboratory Animals. Washington, DC:National Institutes of Health; 1985 revised. US Dept of Health and HumanServices publication NIH 86-23.

9. Motew M, Ivankovich AD, Bieniarz J, Albercht RA, Zahed B, Scomme-gna A. Cardiovascular effects and acid-base and blood gas changes duringlaparoscopy. Am J Obstet Gynecol. 1973;115:1002-1012.

10. Rasmussen JP, Dauchot PJ, De Palma RG, et al. Cardiac function andhypercapnia. Arch Surg. 1978;113:1196-1200.

11. Price HL. Effects of carbon dioxide on the cardiovascular system. An-esthesiology. 1960;21:652-663.

12. Farhi LE, Rahn H. Dynamics of changes in carbon dioxide stores. An-esthesiology. 1955;21:604-614.

13. Kashtan J, Green JF, Parsons EQ, Holcroft JW. Hemodynamic effectsof increased abdominal pressure. J Surg Res. 1981;30:249-255.

14. Kelman GR, Swapp GH, Smith I, Benzie RJ, Gordon NL. Cardiac out-put and arterial blood gas tension during laparoscopy. Br J Anaesth.1972;44:1155-1162.

15. Lenz RJ, Thomas TA, Wilkins DG. Cardiovascular changes duringlaparoscopy. Anaesthesia. 1976;31:4-12.

16. Seed RF, Shakespeare TF, Muldoon MJ. Carbon dioxide homeostasisduring anaesthesia for laparoscopy. Anaesthesia. 1970;25:223-231.

17. Van den Bos GC, Drake AJ, Noble MI. The effect of carbon dioxideupon myocardial contractile performance, blood flow, and oxygen con-

sumption. J Physiol (Lond). 1979;287:149-161.18. Leighton TA, Bongard FS, Liu SY, Lee TS, Klein SR. Comparative car-

diopulmonary effects of helium and carbon dioxide pneumoperitoneum.Surg Forum. 1991;42:485-487.

DiscussionDONALD L. KAMINSKI, MD, St Louis, Mo: The experiment per¬

formed by Dr Wolfe and his associates is directed at the problemof acidosis and hypercarbia that occurs with intraperitoneal C02insufflation. This problem became evident when laparoscopiecholecystectomies began to be performed, and its incidence,although it was real, was not very great. As laparoscopie proce¬dures become extended into other areas, the incidence of thisproblem is going to be much greater. This was evident last weekin our institution during a laparoscopically assisted abdomino-perineal resection in which the period of C02 insufflationapproached 4 hours. This required several periods of lengthy de¬compression to allow the patient's hypercarbia and acidosis toreverse itself.

The study that Dr Wolfe and his associates performed in pigsconfirms the results of other animal and human studies docu¬menting that intraperitoneal C02 gas under pressure is absorbedand produces hypercapnia and acidosis. The experiments thatthey performed used a fixed minute ventilation, and this does notreproduce the clinical situation as the anesthesiologist willincrease the patient's tidal volume and respiratory rate to producea relatively normal Pco2. The purpose of the authors' experimentwas to determine the amount of C02 absorbed. I think as you cansee from their experiments, the amount of C02 absorption is sig¬nificant. Previous studies by researchers in our department dem¬onstrated that only with experimentally produced chronic ob¬structive lung disease does hypercapnia and acidosis occur indogs with C02 pneumoperitoneum if the minute ventilation isincreased to maintain an end-expiratory CO, of 40 mm Hg.

The authors proposed that the hemodynamic changes that theyhave witnessed were produced by C02. This is incorrect. Thesechanges as we have recently reported are identical with pneumo¬peritoneum produced by C02 or by helium. I assume that the he¬modynamic changes being produced are related to the pressurein the peritoneal cavity rather than C02 gas absorption.

We would agree that patients with cardiopulmonary diseaseshould have hemodynamic monitoring, including arterial bloodgases, during protracted periods of laparoscopy with C02. In ourinstitution a prospective trial comparing helium with C02 in pa¬tients with cardiopulmonary disease undergoing laparoscopy isunder way and may answer some of the questions with regard tohow important C02 absorption is.

How relevant do the authors think this clinical problem is? Itoccurs infrequently in patients undergoing laparoscopie chole¬cystectomy. What should you do when it does occur? The ther¬apeutic options are to proceed to an open procedure, to use de¬compression and wait for protracted periods, which in our

experience can take up to 20 minutes, or you can use a differentgas.

KENNETH Waxman, MD, Irvine, Calif: This experiment was

performed in normovolemic pigs. The hemodynamic effects ofpneumoperitoneum are probably very different in the face of hy-povolemia, such as might occur with patients receiving chronicdiuretic therapy or in patients who recently have been acutely ill.The effects of pneumoperitoneum on venous return are, in fact,quite significant in the setting of hypovolemia.

ROBERT F. WILSON, MD, Detroit, Mich: We have had some in¬terest in the problems associated with increased intra-abdominalpressure and with increased Pco2. One of the things that we havenoted clearly is that individuals who are in shock or have been inshock and are bleeding, once the intra-abdominal pressure beginsto get above 20 or 30 mm Hg, can have severe intestinal ischemia.In individuals who may already have a marginal blood supply totheir intestine, this could be a big problem. An increased Pco2 ina lot of patients will not make much difference, but we found thatif our patients who had received massive transfusions were

allowed to have development of an increased Pco2, the mortalityrate rose abruptly. I think that in patients with marginal cardiop¬ulmonary function, it would be very important for the anesthe¬siologist to keep the Pco2 down to normal and this should avoidmany of these difficulties. We have known for a long time that ifthe blood pressure is rising during anesthesia, one of the thingsyou should look for is an increased Pco2, and certainly in theseindividuals, one way to keep the blood pressure down is to keepthe Pco2 down.

I would have preferred if the authors had also put in pleurallines so they could measure simultaneous intrapleural pressuresand correct their filling pressures accordingly. My guess is thatthe filling pressures for the heart were significantly lower thanshown. The increased resistance the heart had to push againstplus the reduced filling probably accounted for many of the he¬modynamic changes that the authors are saying may be due toimpaired cardiac contractility.

RONALD A. HINDER, MD, Omaha, Neb: All of the data presentedwere from pigs with a C02 pneumoperitoneum. It would havebeen useful to have a group of pigs under anesthesia withoutpneumoperitoneum to act as an adequate control to determine theexact influence of the C02 pneumoperitoneum on the datapresented.

Dr Wolfe: I would like to thank the discussants for their com¬ments and questions. Dr Kaminski has raised an important ques¬tion: What is the frequency and severity of the clinical problemthat arises secondary to systemic absorption of C02 associatedwith a pneumoperitoneum? As a clinically manifested problem inlaparoscopie cholecystectomy, hypercarbia and associated aci¬demia have been distinctly uncommon. However, as laparoscopieprocedures are extended to older patients and more lengthy andcomplex operations, we can expect to see an increase in the fre¬quency of hypercarbia and associated acidemia. The finding inthis study of the increase in the volume of C02 excreted of 30%or more demonstrates that unless a patient can increase mechan¬ical ventilation effectively, hypercarbia and acidemia are likely tobe created.

Options for management of hypercarbia intraoperatively are

essentially as Dr Kaminski has indicated: increase minute ven¬tilation as much as possible. If this is ineffective in controlling

hypercarbia, desufflation and possible conversion to open op¬eration, depending on the clinical circumstances, may be nec¬

essary. Investigation into the use of alternative inert gases forthe pneumoperitoneum is an interesting subject that we need,and others are attempting to study. One of the problems withinert gases as opposed to C02 is that formation of bubbleswhen the gas is absorbed is more likely to occur, particularlyfrom a bleeding site, than occurs with a highly soluble anddiffusible gas such as C02. The potential for pulmonary gasembolism is therefore increased, and the role of inert gasesremains uncertain.

The issue of whether the hemodynamic effects observed aredue to compression secondary to the pressure of the pneumo¬peritoneum or the pharmacologie action of the absorbed C02 hasbeen raised by two of the discussants. Our study, as well as thestudy by Leighton et al18 recently reported in Surgical Forum, in¬dicates that the absorbed C02 and not the increased abdominalpressure is responsible for the effects observed (diminished SVand tachycardia). This is based on the lack of change of the fillingpressures of the heart indicating that the hemodynamic changeswere not secondary to diminished venous return secondary topressure effects within the peritoneal cavity. This is consistentwith a study done 10 years ago by Kashtan and Holcroft in our

department. Their study was done in dogs and showed that onlywhen abdominal pressures reached 40 mm Hg or there was con¬comitant hypovolemia did diminished filling pressures of theheart with associated diminished cardiac output occur. Pleuralpressures were not raised by the high intra-abdominal pressure,indicating that the measurement of the filling pressures of theheart by the pulmonary arterial catheter was accurate. In answerto Dr Waxman's question, we have not studied hypovolemia butintend to do so as an important preliminary step before applyingdiagnostic laparoscopy to trauma patients, for example. It is clearthat caution must be exercised in application of our conclusionsin normovolemic animals or patients who have undergone elec¬tive biliary tract operations to patients who have clinicallyimportant hypovolemia. The pressure in this study, as well as inclinical laparoscopie procedures, is generally maintained at nomore than 15 mm Hg. Laparoscopie cholecystectomy can, in fact,be done at 12 to 13 mm Hg, so studies in which pressures of 20,30, or 40 mm Hg have occurred are probably not pertinent.

The fact that increasing Pco2 is associated with increasedmortality could possibly occur as the result of the fact thatPco2 will rise most rapidly in patients with severe cardiorespi-ratory impairment. It would thus require a controlled study todetermine whether the absorption of C02, per se, or associatedrisk factors that lead to the clinical problem would be respon¬sible for the associated cardiac arrhythmias and other compli¬cations that may occur secondary to increasing hypercarbiaand acidemia.