Calibrated pneumoperitoneal venting to prevent N2O accumulation in the CO2 pneumoperitoneum during laparoscopy with inhaled anesthesia: an experimental study in pigs

Nitrous oxide (N2O) accumulates in the CO2 pneumoperitoneum during laparoscopy when N2O is used as an adjuvant for inhaled anesthesia. This may worsen the consequences of gas embolism and introduce a fire risk. In this study, we quantified the pneumoperitoneal gas venting necessary to prevent significant contamination by inhaled N2O. Four domestic pigs (26-30 kg) were anesthetized and ventilated with 66% N2O in oxygen. A CO2 pneumoperitoneum was insufflated and maintained at a pressure of 12 mm Hg. Each animal underwent three experimental conditions, in random sequence, for 70 min each: 1) no pneumoperitoneal leak, 2) leak of 2 L every 10 min (12 L/h), and 3) leak of 4 L every 10 min (24 L/h). Every 10 min, pneumoperitoneal gas samples were analyzed for fractions (FPn) of N2O and CO2. Without leaks, FPnN2O increased continually and reached 29.58% +/- 3.15% at 70 min. With leaks of 2 and 4 L every 10 min (12 and 24 L/h), FPnN2O reached a plateau of <10% after 30 min. We conclude that calibrated pneumoperitoneal venting of 12 or 24 L/h is enough to prevent the constitution of potentially dangerous pneumoperitoneal gas mixtures if venting is constant. IMPLICATIONS: External venting calibrated at four or eight initial pneumoperitoneal volumes per hour with compensation by fresh CO2 is sufficient to prevent nitrous oxide buildup of more than 10% in the pneumoperitoneum during laparoscopy with inhaled general anesthesia if venting is constant.     

腹腔镜中不同膨腹气体对肿瘤细胞体外及动物模型体内生长的比较

目的 :研究不同膨腹气体 :二氧化碳 (CO2 )、氦气 (He)、一氧化二氮 (N2 O)在模拟气腹条件下对肿瘤细胞体外及动物模型体内生长有无影响。方法 :第 1组用MTT法测定人肝癌细胞株SMMC 772 1在CO2 、He、N2 O“气腹”后及对照组 2 4、4 8、72h的比色值。第 2组观察带瘤Wister大鼠在CO2 、He、N2 O“气腹”后肿瘤生长情况和血清谷丙转氨酶 (AST)、谷草转氨酶 (ALT)、碱性磷酸酶 (ALP)和 -谷氨酰转肽酶 (γ -GT)的变化及穿刺点转移情况。结果 :第 1组实验中 ,CO2 组在“气腹”后 4 8h内肿瘤细胞明显增殖 ,而He组肿瘤细胞生长则显著受抑。第 2组实验中 ,CO2 组肿瘤体积、重量及腹水体积均显著增加 ,血清ALT、AST、ALP值显著升高 ,而He组肿瘤体积、重量及腹水体积均显著减少 ,血清ALT、AST、ALP值较低。N2 O组肿瘤体积、重量及腹水体积和血清ALT、AST、ALP值亦较CO2 组减少。 4组穿刺点转移率没有显著差别。结论 :不同膨腹气体引起的肿瘤细胞生长及代谢功能的改变可能与“气腹”后细胞生存环境 ,特别是腹腔内环境的 pH值改变有关。腹腔镜用于恶性肿瘤患者时 ,应注意CO2 对肿瘤细胞和机体可能产生的不良影响 ,可选择He或N2 O代替     

"Low-pressure" laparoscopic cholecystectomy in high risk patients (ASA III and IV): our experience

The insufflation pressure used for laparoscopic cholecystectomy is usually 12-15 mm Hg, and a pneumoperitoneum with carbon dioxide has a significant effect on both cardiovascular and respiratory function. These effects are transient in young, healthy patients, but may be dangerous in ASA III and IV patients with a poor cardiac reserve. This study was designed to assess the feasibility of performing laparoscopic cholecystectomy at 6.5-8 mm Hg insufflation pressure in "high-risk" patients. Thirteen patients, 10 ASA III and 3 ASA IV, with cholelithiasis, were included in this study The insufflation pressure was 6.5-8 mm Hg, with a 10 degrees anti-Trendelenburg position. The cardiovascular and blood gas variables studied were: mean arterial blood pressure, heart rate, respiratory rate, and end-tidal CO2 pressure. The authors reported no conversions and no intra- or postoperative complications. During insufflation heart rate and mean arterial blood pressure increased minimally if compared with laparoscopic cholecystectomy at 12-15 mm Hg. Pa CO2 increased after insufflation (+5 mm Hg), and the end-tidal CO2 pressure gradient was moderate (3.5 mm Hg) and unchanged during surgery. A low-pressure pneumoperitoneum is feasible for laparoscopic cholecystectomy and minimizes the adverse haemodynamic effects of peritoneal insufflation.     

Nitrous oxide pneumoperitoneum revisited

Nitrous oxide has been effectively banned from use in therapeutic laparoscopy because of fear of combustion. These fears rest on two case reports, a misunderstanding of the physical chemistry of nitrous oxide, and lack of information on the presence of flammable colonic gases in the pneumoperitoneum mixture. This study aims to identify the presence and quantify the amount of hydrogen and methane found in the peritoneal cavity during laparoscopic GI procedures, and then to compare the gas concentrations detected with known limits of combustion. Gas standards with known concentrations of hydrogen and methane were placed in polypropylene syringes and analyzed on a mass spectrometer after 1, 2, 3, and 4 h. This established the rate at which these gases would be leached through a polypropylene syringe—the amount of gas lost during transport from the patient to the laboratory. Twenty gas samples were drawn, randomly, 30 min to 2 h following the start of laparoscopic gastrointestinal procedures. The samples were analyzed for hydrogen and methane within 30 min of their aspiration from the abdominal cavity. An inconsequential amount of methane was lost from the polypropylene syringe in 4 h. After 1 h, one-half the hydrogen had leached from the polypropylene syringe. Hydrogen was detected in the pneumoperitoneum of four patients at a concentration ranging from 0.016 to 0.075%. No methane was detected in any sample. For combustion to occur in a nitrous oxide environment, hydrogen or methane must occupy 5.5% of the gas volume. The maximum amount of hydrogen we detected was less than 1/50 of the combustion threshold. After considering these data, and a large clinical experience of gynecologic laparoscopy using electrosurgery in a nitrous oxide pneumoperitoneum, we conclude that nitrous oxide can be safely used for creating a pneumoperitoneum during laparoscopic surgery.Presented as a poster at the annual meeting of Society of American Gastrointestinal Endoscopic Surgeons (SAGES), Phoenix, Arizona, USA, 2–3 April 1993     

Effects of laparoscopic models on anaerobic bacterial growth with bacteroides fragilis in experimentally induced peritonitis

BACKGROUND: Previous reports of recurrent intra-abdominal abcess formation after the laparoscopic treatment of perforated acute appendicitis led us to investigate the possible effects of gas insufflation on the spread of infection. We previously showed that Escherichia coli counts were significantly higher in a laparoscopy group that underwent carbon dioxide (CO2) insufflation than in control and laparotomy groups. The aim of this study is to investigate the effects of intra-abdominal CO2 and nitrous oxide (N2O) insufflation on anaerobic bacterial growth in a rat model. METHODS: A standard strain of Bacteroides fragilis (ATCC 25285) was injected intraperitoneally (1 x 10(6) cfu/mL per kilogram) in 40 Wistar rats under sterile conditions. Forty rats with induced peritonitis were randomly divided into five groups: control, laparotomy, CO2 insufflation, N2O insufflation, and one group without pneumoperitoneum. Eight hours after the intraperitoneal injection of B. fragilis, peritoneal aspirates were obtained and inoculated onto Brucella agar. At the sixteenth hour of induced peritoneal infection (corresponding to hour 8 in the laparoscopy groups) all animals underwent laparotomy; peritoneal aspirates were obtained and inoculated into Brucella agar for bacterial counts. The colonies of B. fragilis were counted manually, and the results were expressed as the mean number of colony-forming units per milliliter. RESULTS: No significant differences in microorganism counts were noted between the study groups before the procedure (p>.05 for all comparisons). We observed a significant increase in the number of bacteria (mean +/- SD) in the CO2 insufflation group between hour 8 and hour 16 of peritoneal contamination. CONCLUSION: The results suggest that CO2 insufflation may promote the growth of intra-abdominal anaerobic bacteria. Such bacterial growth may lead to intra-abdominal abcess formation or cause localized peritonitis to develop into generalized peritonitis. We suggest that laparoscopy without pneumoperitoneum may be preferred in patients with peritonitis.     

Effects of carbon dioxide pneumoperitoneum on cerebral hemodynamics in pigs.

Previous studies have shown that laparoscopic interventions are associated with increases in intracranial pressure. However, the consequences on cerebral blood flow (CBF) are unknown. This study investigates the effects of carbon dioxide (CO2) pneumoperitoneum on CBF in pigs. Ten pigs (weight, 20-26 kg) were anesthetized with 1.4% isoflurane and fentanyl (1 microg/kg per minute). Mechanical ventilation (fraction of inspired oxygen = 0.4) was set to maintain normocapnia (end-tidal CO2 tension = 35 mm Hg). Arterial and central venous catheters were placed for measurement of mean arterial blood pressure and central venous pressure. Bilateral internal carotid artery blood flow was measured using two transient time flow probes placed around both carotid arteries (with ligated external carotid arteries). Cortical and subcortical cerebral blood flow was measured using laser Doppler flowmetry. Sagittal sinus pressure was measured via a superior sagittal sinus catheter. After baseline measurements, the peritoneal cavity of the animals was insufflated with CO2 to achieve an intraabdominal pressure of 12-mm Hg. After 10 minutes of stable CO2, pneumoperitoneum measurements were repeated. Increases in central venous pressure (6.3 +/- 2.1 to 11.1 +/- 3.0 mm Hg) and sagittal sinus pressure (8.0 +/- 2.8 to 11.9 +/- 3.0 mm Hg) were noted during CO2 pneumoperitoneum (P < .05). Bilateral internal carotid artery blood flow (46.0 +/- 7.4 vs 47.7 +/- 7.1 mL/100g per minute), cortical CBF (263 +/- 115 vs 259 +/- 158 tissue perfusion units), and subcortical CBF (131 +/- 145 vs 133 +/- 149 tissue perfusion units) did not change during CO2 pneumoperitoneum. The current data show that CO2 pneumoperitoneum increases sagittal sinus pressure without changing CBF. Increases in sagittal sinus pressure are likely related to decreases in cerebral venous drainage caused by increases in intraabdominal pressure.     

Nitrous oxide increases normocapnic cerebral blood flow velocity but does not affect the dynamic cerebrovascular response to step changes in end-tidal P(CO2) in humans.

We sought to clarify the effect of nitrous oxide (N2O) on the immediate responses of cerebral vasculature to sudden changes in arterial carbon dioxide tension in healthy humans. By use of a transcranial Doppler ultrasonography, blood flow velocity in the middle cerebral artery (V(MCA)) was measured during a step increase followed by a step decrease in end-tidal CO2 tension (PET(CO2)) between normo- and hypercapnia while subjects inspired gas mixtures containing 70%O2 + 30% N2 (control) and 70% O2 + 30% N2O (N2O) separately. During the control condition, both step increase and decrease in PET(CO2) produced rapid exponential changes in V(MCA). An increase in V(MCA) produced by the step increase in PET(CO2) was smaller (P < 0.001) and slower (P < 0.001) than a decrease in V(MCA) induced by the step decrease in PET(CO2). These general features of the dynamic cerebrovascular response were not affected by substitution of N2O for N2 in the inspired gases although N2O increased baseline V(MCA) by 15% (P < 0.001) compared with the control condition. We conclude that N2(O) in itself does not affect the dynamic cerebrovascular response to arterial CO2 changes, although it produces static mild cerebral vasodilation. IMPLICATIONS: This study suggests that nitrous oxide does not affect the dynamic cerebrovascular reactivity to acute arterial carbon dioxide (CO2) changes, i.e., exponential changes in cerebral blood flow in response to step changes in alveolar CO2 tension, although it does produce a mild increase in normocapnic cerebral blood flow velocity.     

Nitrous oxide does not affect automated air tonometry in children

PURPOSE: To evaluate the effects of nitrous oxide on automated air tonometry in the clinical setting. MATERIAL AND METHODS: With approval of the Hospital Ethical Committee and after obtaining informed parental consent, an 8-F tonometry catheter was inserted orogastrically in ten children aged one to three years scheduled for elective surgery with combined regional and general anesthesia. A standardized general anesthesia technique with tracheal intubation was used in all patients and consisted of sevoflurane in oxygen/nitrous oxide (30%/70%; n = 5 patients) or in oxygen/air (FIO(2) 0.3; n = 5 patients). After obtaining steady state gastric CO(2) values (PrCO(2)), fresh gas mixtures were rapidly changed from oxygen/nitrous oxide to oxygen/air (A) or vice versa (B). In addition, balloon pressures were recorded using a pressure transducer. Measurements were performed at intervals of ten minutes with recording of balloon pressures, end-tidal CO(2) (PETCO(2)) and PrCO(2) values. Pr-ETCO(2)-gap were calculated to eliminate influences of changes in PaCO(2). RESULTS: Changing the fresh gas mixture from N(2)O/O(2) to O(2)/air resulted in a decrease of balloon pressure of -10.4% (113.4 +/- 14.7 mmHg to 101.6 +/- 25.0 mmHg). Changing the fresh gas mixture from O(2)/air to N(2)O/O(2) resulted in an increase of balloon pressures of 6.4% (107.6 +/- 19.3 mmHg to 114.0 +/- 20.3 mmHg). During both fresh gas exchange experiments no significant changes (> 0.2 kPa) in calculated Pr-ETCO(2)-gaps were observed. CONCLUSIONS: Based on our in vivo data, nitrous oxide during general anesthesia can be used with automated air tonometry and does not affect air tonometric PrCO(2) reading in clinical practice.     

Apnea and oxygen desaturation following nitrous oxide inhalation

Apnea and desaturation following nitrous oxide inhalation were studied in seven adult volunteers breathing spontaneously. Arterial oxygen saturation (SpO2), end-tidal CO2 concentration in the nasal cavity and respiratory patterns were measured in volunteers breathing air after N2O (50% or 67%) + O2. SpO2 was measured with Biox 3700 and end-tidal CO2 concentration was measured with Normocap, and respiratory patterns were recorded with RESPIGRAPH. After breathing N2O, two volunteers had frequent apnea (greater than 20 sec) accompanied by desaturation (SpO2 less than 90%). The lowest value of SpO2 was 82%. When the apnea occurred, the airway seemed to be open and end-tidal CO2 concentration values were lower than those before N2O inhalation. The authors considered that this kind of apnea was due to several factors, such as hypocapnia caused by hyperventilation during N2O anesthesia, dilution of alveolar O2 and CO2 during N2O excretion, loss of consciousness by N2O, and depression of CO2 ventilatory response by N2O. Inhalation of O2 at high concentrations for five minutes could improve the hypocapnia and prevent the apnea.     

Second gas effect of N2O on oxygen uptake

PURPOSE: The concept of the second gas effect is well known, however, there have been no studies that showed the relationship between alveolar oxygen concentration and arterial oxygen tension (PaO2) after the inhalation of nitrous oxide (N2O) in humans. The purpose of this study was to examine the changes in both end-tidal oxygen fraction (F(ET)O2) and PaO2 after N2O inhalation in patients under general anesthesia. METHODS: Fifteen patients scheduled for elective orthopedic surgery were enrolled in this study. Anesthesia was maintained with the continuous infusion of propofol and with nitrogen (N2) and oxygen (O2) (6 L x min(-1), F1O2, 0.33). In all patients, the lungs were ventilated with a Servo 900C ventilator equipped with a gas mixer for O2, N2O, and N2. After obtaining baseline data, N2 was replaced with N2O maintaining FIO2 constant at 0.33. The changes in fractional concentration of O2, N2O, and N2 were continuously measured using mass spectrometer in a breath-by-breath basis. PaO2 and hemodynamic data were obtained at 1, 5, 10, 30 and 60 min after the start of N2O inhalation. RESULTS: Five minutes after N2O inhalation, F(ET)O2 increased from 0.27+/-0.01 to 0.31+/-0.02 (P<0.01) and PaO2 increased from 172.0+/-22.5 mm Hg to 201.0+/-10.3 mm Hg (P<0.01). These effects produced by N2O were observed for 30 min. CONCLUSIONS: These results confirm the concept of second gas effect of N2O on oxygen uptake in humans and provide evidence that the PaO2 increase correlated with the increase in F(ET)O2 after N2O inhalation.     

Arterial to end-tidal carbon dioxide tension difference during laparoscopic colorectal surgery

BACKGROUND: Determination of end-tidal carbon dioxide pressure (PET(CO2)) is effective to confirm adequate ventilation, because arterial to end-tidal carbon dioxide tension difference (deltaa-ET(CO2)) does not change normally during operation. But deltaa-ET(CO2) may change during laparoscopic surgery, because peritoneal insufflation of CO2 will increase CO2 production and reduce functional residual volume. Changes in deltaa-ET(CO2) were reported in laparoscopic cholecystectomy with cardiovascular complication, but there is controversy about how deltaaET(CO2) will change in more complicated and long laparoscopic surgery. In this prospective study, we examined changes in deltaa- ET(CO2) during laparoscopic colorectal surgery. METHODS: Fifty patients received combined general and epidural anesthesia. CO2 pneumoperitoneum was initiated after obtaining arterial blood for gas analysis. Mechanical ventilation was used to maintain PET(CO2) at a stable value between 30 and 40 mmHg during the procedure. Arterial blood gas analysis was performed 10, 60, 120 minutes after CO2 insufflation, and 10 minutes after the termination of insufflation. RESULTS: The mean +/- SD for deltaa-ET(CO2) was 5.8 +/- 4.1 before pneumoperitoneum, 7.1 +/- 4.8, 8.1 +/- 5.4, 6. 4 +/- 4.9 in 10, 60, 120 minutes after pneumoperitoneum, and 6.4 +/- 4.9 in 10 minutes after the termination of pneumoperitoneum. deltaa-ET(CO2) increased significantly during pneumoperitoneum, but did not increase further even if CO2 insufflation was longer than 60 minutes. CONCLUSIONS: In laparoscopic colorectal surgery, Pa(CO2) should be checked for at least the first 60 minutes to confirm adequate ventilation.     

The influence of xenon, nitrous oxide and nitrogen on gas bubble expansion during cardiopulmonary bypass

BACKGROUND AND OBJECTIVE: Xenon may have favourable applications in the setting of cardiac surgery. Its advantages include a desirable haemodynamic profile as well as potential cardiac and neuroprotective properties. However, its low solubility may lead to enhanced diffusion into enclosed gas spaces. The purpose of this study was to compare the effects of xenon (Xe), nitrous oxide (N2O) and nitrogen (N2) on gas bubble size during cardiopulmonary bypass (CPB). METHODS: Rats were randomized to receive 70% Xe, 26% oxygen (O2), 4% carbon dioxide (CO2) (xenon group); 70% N2O, 26% O2, 4% CO2 (nitrous oxide group) or 70% N2, 26% O2, 4% CO2 (nitrogen group) during 90 min of normothermic CPB. Small gas bubbles (300-500 microL; n = 12 per group) were injected into a bubble chamber on the venous side of the bypass circuit. After 10 min of equilibration, they were removed for volumetric analysis. RESULTS: The increase in bubble size was 2 +/- 2% with nitrogen, 17 +/- 6% with xenon (P = 0.0192 vs. nitrogen) and 63 +/- 23% with nitrous oxide (P = 0.0001 vs. nitrogen). The nitrous oxide group had significantly increased bubble size compared to the xenon group (P = 0.0001). CONCLUSIONS: During CPB, xenon anaesthesia produced a small increase in gas bubble size compared to nitrogen. Nitrous oxide resulted in significantly larger bubbles compared to both nitrogen and xenon.     

CO2气腹对糖尿病兔胰腺功能影响的实验研究

目的探讨二氧化碳（CO2）气腹对糖尿病兔胰腺功能的影响。方法利用四氧嘧啶制作糖尿病兔模型,建立不同压力气腹,观察气腹前和气腹后0、2、6及12h各时间点血糖、淀粉酶、胰岛素、C肽、胰腺组织SOD活性及MDA含量的变化。结果气腹结束后,血糖、淀粉酶、胰岛素、C肽浓度和MDA含量较气腹前上升（P〈0.05）,SOD活性较气腹前下降（P〈0.05）。气腹结束后12h,10mmHg（1mmHg=0.133kPa）气腹组血糖、淀粉酶、胰岛素、C肽浓度和MDA含量与气腹前比较差异无统计学意义（P〉0.05）,15mmHg气腹组血糖、淀粉酶、胰岛素、C肽浓度和MDA含量仍较气腹前升高（P〈0.05）;SOD活性在2组均未恢复至气腹前水平（P〈0.05）。10mmHg和15mmHg气腹组相应时相之间,血糖和胰岛素变化差异无统计学意义（P〉0.05）,淀粉酶、C肽浓度、MDA含量和SOD活性变化差异有统计学意义（P〈0.05）。结论CO2气腹对糖尿病兔胰腺功能有损伤作用,损伤程度与气腹压力相关,较低的气腹压引起的胰腺损害更易逆转。     

Residual Nitrous Oxide in Operating Room Personnel

The concentrations of nitrous oxide in the blood and end-tidal air of 10 operating-room nurses were assayed by gas chromatography immediately and 1, 2, 5, and 21 h after 3 hours of exposure to an average of 380 ppm of nitrous oxide in operating-room air. In the second trial the nurses' end-tidal air concentrations of nitrous oxide were assayed on Monday, Wednesday, Friday and Sunday morning, and on Sunday afternoon and evening to reveal a possible accumulation of nitrous oxide during a routine week. After cessation of exposure there was a rapid decrease in the blood concentrations of nitrous oxide during the first hour (from 153 +/- 110 microgram/1 to 48 +/- 20 microgram/l at 1 h; means +/- s.d.), followed by a slower decrease. Small amounts (mean +/- s.d.: 18 +/- 6 microgram/l) of nitrous oxide were still measurable on the following morning 21 h after exposure. At 2 or 5 h after exposure there was an increase in blood and end-tidal air concentrations of nitrous oxide in seven and nine nurses, respectively. The end-tidal air concentrations of nitrous oxide were greater on Wednesday (22 +/- 7 microgram/l) than on Monday morning (8.4 +/- 1.5 microgram/l), but on Friday they were similar to those measured on Monday morning. The concentrations measured on Sunday, i.e. 2 days after exposure, were similar (average 15 microgram/l) to those measured during the week. It is concluded that, after cessation of exposure to nitrous oxide, there is a rapid decrease in the concentrations in blood and end-tidal air, but small amounts of nitrous oxide remain in the body for at least 3 days after cessation of exposure.     

A comparison of the hemodynamic and metabolic effects of extraperitoneal carbon dioxide and nitrous oxide insufflation.

BACKGROUND: The aim of the present study was to compare the hemodynamic and metabolic effects of extraperitoneal carbon dioxide (CO(2)) and nitrous oxide (N(2)O) insufflation. MATERIAL AND METHODS: Fourteen dogs were used in the experiment. All the animals were intubated under general anesthesia. A catheter was placed into the right jugular vein for central venous pressure (CVP), pulmonary artery pressure (PAP), pulmonary wedge pressure (PWP), and heart rate (HR) monitorization. End-tidal CO(2) pressure was measured by a capnometer connected to the endotracheal tube. Another catheter was inserted into the left femoral artery for arterial blood gas analysis and blood pressure monitorization. The preperitoneal dissection was made from a 1.5 cm subumbilical incision by using a preperitoneal dissection balloon. A laparoscope was placed in the preperitoneal space and the gas insufflation was kept at a constant pressure of 12 mm Hg throughout the experiment. All the study parameters were measured at the beginning of the insufflation and at every 15 minutes for 1 hour. RESULTS: Mean artery pressure increased with time in both groups, but the increase was only significant in the CO(2) group. PWP, CVP, PAP, and HR increased slightly in both groups, but there was no significant difference between the groups. The end-tidal CO(2) increased in the CO(2) group but decreased from the baseline in the N(2)O group. A significant acidosis was observed in only the CO(2) group. PaCO(2) significantly increased in the CO(2) group; hence, PaCO(2) slightly decreased in N(2)O group. The difference between the groups was significant. CONCLUSIONS: N(2)O insufflation of the extraperitoneal space in dogs avoided the unwanted metabolic and hemodynamic side effects of CO(2) insufflation. Thus, N(2)O insufflation in the extraperitoneal space is a safer alternative to CO(2) insufflation experimentally, and can be preferred especially in patients with cardiac and pulmonary diseases.     

Intestinal perfusion during pneumoperitoneum with carbon dioxide, nitrogen, and nitric oxide during laparoscopic surgery.

OBJECTIVE: To find out what effect insufflation pressure and type of gas have on intestinal perfusion during pneumoperitoneum. DESIGN: Randomized, controlled, prospective, experimental study. SETTING: University affiliated animal experimental laboratory, Sweden. ANIMALS: Fasted, anaesthetised, domestic pigs of both sexes operated on laparoscopically (n = 7, weight 26-31 kg). INTERVENTIONS: Insufflation of carbon dioxide (CO2), nitric oxide (NO), or nitrogen (N2) at intra-abdominal pressures of 0, 5, 10, 15 and 20 mm Hg. MAIN OUTCOME MEASURES: Cardiac output, portal blood flow, and jejunal mucosal perfusion. RESULTS: Cardiac output decreased during N2 and NO (15, 20 mm Hg) but not during CO2 insufflation because of an accompanying tachycardia. Portal flow decreased during insufflation with N2 and NO (15, 20 mm Hg) and CO2 (20 mm Hg). Jejunal perfusion was reduced during N2 and NO insufflation (5-20 mm Hg) but remained unchanged during CO2 insufflation (5-20 mm Hg). CONCLUSIONS: Insufflation with CO2 maintained jejunal mucosal perfusion, probably as a result of hypercarbia as N2 at equal pressures reduced mesenteric flow. The vasodilator NO provided no haemodynamic benefit.     

Cerebral venous and tissue gases and arteriovenous shunting in the dog.

Cerebral venous blood gas values have been used to indicate brain tissue oxygenation. However, it is not clear how cerebral tissue and venous measures may vary under physiologic conditions caused by arteriovenous shunt. The purpose of this study was to measure brain tissue and local cerebral venous oxygen (PO2) and carbon dioxide (P(CO2)) partial pressure during changes in ventilation and to calculate shunt fraction. Eight dogs were anesthetized with isoflurane. After a craniotomy, a Neurotrend probe (Diametrics Inc., St. Paul, MN) that measures P(O2), P(CO2), pH, and temperature was inserted into brain tissue, and a small vein that drained the same tissue was catheterized. Arterial, cerebral venous, and brain tissue P(O2) and Pco2 were measured during random changes in ventilation to produce five different levels of inspired oxygen (room air, 40%, 60%, 80%, 95%) at each of three different end-tidal Pco2 (20 mm Hg, 40 mm Hg, 60 mm Hg). Arteriovenous shunt was calculated from oxygen and C(O2) content in artery, vein, and tissue, representing capillary. Tissue P(CO2) was 8 mm Hg greater than vein Pco2 during hypocapnia and this difference increased to 20 mm Hg during hypercapnia. Vein P(O2) was 8 mm Hg higher than tissue P(O2) during hypocapnia, and this difference increased to 40 mm Hg during hypercapnia. Shunt fraction increased from 10%-20% during hypocapnia to 50%-60% during hypercapnia. These results show that brain vein and tissue P(O2) and P(CO2) differ because of arteriovenous shunting and this difference is increased as end-tidal P(CO2) increases. IMPLICATIONS: We found, in dogs, that the gradient between brain venous and tissue P(O2) and PCO2 is increased with increased arterial P(CO2). The divergence between tissue and venous gases can be described by arterial to venous shunting.     

Heart rate response to intravenous atropine during propofol anesthesia

During propofol/fentanyl anesthesia, a large percentage of patients have jugular bulb oxygen saturation (SjO(2)) <50%. The incidence is less with isoflurane/N(2)O. We evaluated the effect of N(2)O on SjO(2) during remifentanil-based anesthesia with concurrent propofol or sevoflurane in 20 adults undergoing brain tumor surgery. Anesthesia was randomized: Group 1 (n = 10), target-controlled infusion propofol; and Group 2 (n = 10), thiopental 2-3 mg/kg followed by sevoflurane 0.9% end-tidal. Jugular bulb and arterial blood samples for gas analysis were withdrawn during the administration of oxygen 33% with nitrogen 67% and then with N(2)O 67%. All samples were drawn before surgery and 20 min after the addition of the study gas and with an ETCO(2) 26-28 mm Hg and mean arterial pressure >90 mm Hg. Both groups had similar demographic and physiologic data. In the Propofol group, SjO(2) was 50% +/- 10% with nitrogen and 52% +/- 9% with N(2)O (not significant); in the Sevoflurane group, however, N(2)O 67% increased SjO(2) from 56% +/- 13% to 66% +/- 12% (P < 0.01). This indicates that N(2)O does not reduce the incidence of low SjO(2) values during propofol anesthesia. IMPLICATIONS: This study demonstrates that nitrous oxide can increase jugular bulb venous oxygen saturation when added to sevoflurane/remifentanil anesthesia, but not to propofol/remifentanil anesthesia, in patients with brain tumors.     

The effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during propofol anesthesia

Nitrous oxide (N(2)O) increases cerebral blood flow when used alone and in combination with propofol. We investigated the effects of N(2)O on cerebrovascular CO(2) reactivity (CCO(2)R) during propofol anesthesia in 10 healthy children undergoing elective urological surgery. Anesthesia consisted of a steady-state propofol infusion and a continuous caudal epidural block. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Randomization determined the sequence order of N(2)O (N(2)O/air or air/N(2)O) and end-tidal (ET)CO(2) concentration (25, 35, 45, and 55 mm Hg) using an exogenous source of CO(2). At steady state, three sets of measurements of middle cerebral artery blood flow velocity, mean arterial blood pressure, and heart rate were recorded. A linear preservation of CCO(2)R was observed above 35 mm Hg of ETCO(2), irrespective of N(2)O. A decrease in CCO(2)R to 1.4%-1.9% per millimeters of mercury was seen in the hypocapnic range (ETCO(2) 25-35 mm Hg) with both air and N(2)O. We conclude that N(2)O does not affect CCO(2)R during propofol anesthesia in children. When preservation of CCO(2)R is required, the combination of N(2)O with propofol anesthesia in children would seem suitable. The cerebral vasoconstriction caused by propofol would imply that hyperventilation to ETCO(2) values less than 35 mm Hg may not be required because no further reduction in cerebral blood flow velocity would be achieved.     

Choice of insufflating gas influences on wound metastasisrid=""id=""Presented at the annual meeting of the Society of American Gastrointestinal Endoscopic Surgeons (SAGES), San Antonio, Texas, USA, March 1999

BACKGROUND: Laparoscopic cancer surgery is limited by concerns about port-site metastasis. No study has definitively addressed the behavior and growth of tumor cells after the use of specific laparoscopic gases. METHODS: In athymic rats, 10,000 colon cancer cells were injected intraperitoneally. The rats received either no pneumoperitoneum (pneumo) or pneumo (8 mmHg, 10 min) with carbon dioxide (CO(2)), nitrous oxide (N(2)O), or air. Two full-thickness incisions were made and closed in the upper abdomen of each animal. After 4 weeks, implants were identified grossly at necropsy, and invasiveness was scored according to penetration through the layers of the abdominal wall. RESULTS: Rats receiving pneumo had more frequent implants (p < 0.01) with deeper penetration (p < 0.001) than rats not receiving pneumo. Implants were more common after air pneumo than after CO(2) (p < 0.05) or N(2)O (p = 0.07) pneumo, and were less penetrating after CO(2) pneumo than after air (p < 0.001) or N(2)O (p < 0.05) pneumo. CONCLUSIONS: Carbon dioxide gas may limit the viability and invasiveness of free intraperitoneal tumor cells, as compared with air or N(2)O.