Ventilatory responses to hypercapnia during tetracaine spinal anesthesia

The effect of spinal anesthesia with hyperbaric tetracaine with epinephrine on resting ventilation and on ventilatory responsiveness to CO2 rebreathing was studied in 10 unpremedicated patients. Resting end-tidal PCO2 (PETCO2) decreased from 37 +/- 3 mmHg (mean +/- SD) to 34 +/- 2 mmHg after induction of spinal anesthesia (p less than 0.05). Minute ventilation (VE) and occlusion pressure (P0.1) at PETCO2 = 55 mmHg increased during spinal anesthesia from 32.0 +/- 12.9 to 40.2 +/- 17.0 l/min and from 5.0 +/- 1.8 to 8.6 +/- 4.7 cmH2O, respectively. The magnitude of the increase in VE during spinal anesthesia correlated inversely with age. Spinal anesthesia was not associated with significant changes in vital capacity, maximal inspiratory pressure, or the slopes of the lines relating VE or P0.1 to PCO2. These results show increased ventilatory responsiveness to CO2 (a parallel leftward shift of the CO2 response curve) with tetracaine spinal anesthesia.     

Comparative analysis of the hemodynamic and respiratory parameters during laparoscopic versus open living donor nephrectomy: an experimental model

Increased intrabdominal pressure induced by pneumoperitoneum induces modifications in cardiovascular and respiratory systems. The aim of the study was to analyze the hemodynamic and respiratory modifications produced by pneumoperitoneum during living donor nephrectomy in a porcine experimental model. Twenty pigs underwent left nephrectomy, 10 by laparoscopy and 10 by an open approach. The following parameters were measured: mean arterial pressure (MAP), central venous pressure, cardiac output (CO), systemic vascular resistance (SVR), end tidal CO2 (ETCO2), minute volume (MV), respiratory airway pressure (RAP), and "compliance." Both groups were monitored for cardiac and respiratory systems at basal, 5, 30, and 60 minutes as well as postsurgery. The comparative analysis demonstrated increased CO with a higher difference at 30 minutes (4.33 +/- 0.73 vs 8.54 +/- 1.26 L/min, P < .001); decreased SVR (1118.81 +/- 302.52 vs 663.37 +/- 81.45 dinas x s x cm(-5), P < .001), and elevated MAP among the laparoscopic group (66.5 +/- 11.52 vs 80.25 +/- 2.49 mm Hg, P = .004). Analysis of respiratory modifications showed an initial increase in ETCO2 (44.3 +/- 2.6 vs 54.1 +/- 12.56 mm Hg, P < .035) and a higher MV administered (5.6 +/- 0.1 vs 7.01 +/- 0.96 L/min, P = .03) to the laparoscopy group. An increased RAP was observed at 5 minutes (22.11 +/- 2.76 vs 28.8 +/- 3.68 mm Hg, P < .001), in the laparoscopic group and lower levels of "compliance" at the same moment in that group (16 +/- 1.66 vs 14.9 +/- 4.07 cm H2O). Laparoscopic nephrectomy caused an increase in CO and MAP and decreased SVR. Likewise there were elevations of RAP, ETCO2, and MV and a slight decrease in the "compliance."     

Laparoscopic genitourinary surgery utilizing 20 mm Hg intra-abdominal pressure

Traditional practice has dictated that intra-abdominal pressure during laparoscopy be kept at or below 15 mm Hg to minimize the risk of cardiovascular and pulmonary complications. This study was undertaken to determine if maintaining an intra-abdominal pressure of 20 mm Hg could be utilized safely during genitourinary laparoscopy. We reviewed the intraoperative records of 76 consecutive patients undergoing various endoscopic urologic procedures at an intra-abdominal pressure of 20 mm Hg to assess physiologic changes and complications. The records were examined for operating time, minute ventilation (MV), end-tidal CO2 (ETCO2), and peak inspiratory pressure (PIP), which were compared with the preinsufflation values. Also, in the first 39 patients, initial insufflation volumes were recorded at 15 mm Hg and then again when pressure was raised to 20 mm Hg. The mean operating time was 186 +/- 90 min. There was an average 22% increase in the sufflated volume when the pressure was elevated from 15 to 20 mm Hg. To maintain a suitable ETCO2, the anesthesiologist needed to increase the MV an average of 2.9 +/- 2.0 L/min. Increases in ETCO2 (average 4.5 +/- 4.6 mm Hg) and PIP (6.9 +/- 3.6 mm Hg) were noted. In two cases, the intra-abdominal pressure had to be decreased from 20 to 15 mm Hg because of inability to maintain an acceptable ETCO2. Subcutaneous emphysema was noted in three patients, which resolved spontaneously within 24 hr. In one patient, asymptomatic pneumomediastinum was noted after a 6-hr procedure. Intra-abdominal insufflation can be safely maintained at 20 mm Hg in most patients. This higher pressure improves maintenance of the pneumoperitoneum.     

The effect of insufflation pressure on CO(2) pneumoperitoneum and embolism in piglets

We conducted this study to investigate the effect of insufflation pressure on the pathophysiology of CO(2) pneumoperitoneum and embolism in an infant model. Twenty anesthetized piglets had stepwise intraperitoneal insufflation with CO(2) for 15 min at pressures ranging from 5 to 20 mm Hg. The piglets were ventilated to baseline normocarbia (ETCO(2) = 30 mm Hg, PaCO(2) = 38 mm Hg) before beginning each insufflation. CO(2) was then insufflated IV in 15 of these piglets at the same pressures. There was no reduction of blood pressure or cardiac output with intraperitoneal insufflation, but the stroke volume declined significantly (*P < 0.05) from (mean +/- SE) 10.6 +/- 1.3 mL to 8.5 +/- 1.3* mL and from 10.0 +/- 1.4 mL to 7.2 +/- 1.2* mL at 15 and 20 mm Hg insufflation pressure, respectively. Abdominal insufflation at 5, 10, 15, and 20 mm Hg caused an increase in ETCO(2) to 31.7 +/- 0.8 mm Hg, 35.6 +/- 1.2* mm Hg, 37.5 +/- 1.5* mm Hg, and 40.1 +/- 1.8* mm Hg and in PaCO(2) to 41.1 +/- 1.3* mm Hg, 44.2 +/- 1.4* mm Hg, 49.9 +/- 1.8* mm Hg, and 53.0 +/- 2.1* mm Hg, respectively. In contrast, the ETCO(2)decreased to 19.4 +/- 1.5* mm Hg, 20.4 +/- 1.4 mm Hg, 15.2 +/- 2.1* mm Hg, and 10.6 +/- 2.0* mm Hg with IV insufflation using the same pressures. IV insufflation caused marked hypotension and mortality. As the insufflation pressure increased, the mortality increased (0 in 15, 1 in 15, 1 in 14, and 6 in 13* at 5, 10, 15, and 20 mm Hg; *P < 0.05 vs 0 in 15, 1 in 15, and 1 in 14). This study suggests that although intraperitoneal insufflation up to 20 mm Hg may be tolerated hemodynamically, the lowest possible pressure should be used to reduce hypercarbia. A low insufflation pressure may also prevent mortality from CO(2) embolism. IMPLICATIONS: The lowest pressure possible should be used when inflating the abdomen with CO(2) to perform a laparoscopy in babies. A low pressure allows better ventilation and may prevent mortality if CO(2) is accidentally injected into a vein.     

Endoscopy during laparoscopy

BACKGROUND: Intraluminal endoscopy during laparoscopy can substitute for manual palpation in defining anatomy and pathology, but a potential problem is the persistent bowel distention associated with intraluminal air insufflation. METHODS: To compare the rates of intraluminal absorption, a 30-cm segment of small bowel with an intact vascular supply was insufflated with either air or CO2 during CO2 pneumoperitoneum. Intraluminal pressures and bowel circumferences were monitored after the insufflation was stopped. To study the metabolic and hemodynamic effects of CO2 endoscopy during laparoscopy, the small bowel was insufflated to an intraluminal pressure of 15 mmHg during CO2 pneumoperitoneum. Nitrogen pneumoperitoneum was used to differentiate the effects from intraluminal and peritoneal CO2 insufflation. RESULTS: The intraluminal pressures remained elevated and the bowel distended for the entire 3 h following bowel insufflation with air. Following intraluminal CO2 insufflation, both the intraluminal pressures and the bowel circumferences returned to preinsufflation values within 15 min. Intraluminal CO2 insufflation also led to systemic absorption of CO2 with significant metabolic and hemodynamic changes. These changes were effectively corrected by doubling minute ventilation. CONCLUSIONS: Intraluminal CO2 was absorbed faster than intraluminal air. Although decreased bowel distention is certainly of practical value, endotracheal intubation needs to be done to effectively ventilate the absorbed CO2.     

Arterial carbon dioxide markedly increases during diagnostic laparoscopy in portal hypertensive children

Several factors are responsible for hypercarbia during laparoscopic procedures. This study was undertaken because we observed a sudden increase in PaCO(2) in children with portal hypertension (PHT), which was unusual in healthy children undergoing laparoscopic procedures. Fifty-seven children underwent laparoscopic procedures under general anesthesia and were mechanically ventilated. Arterial blood samples were obtained 5 min after intubation (T(0)), 15 min and 30 min after CO(2) pneumoperitoneum (T(15) and T(30)), 5 min after desufflation (T(end)), and 10 min after extubation (T(ext)) for blood gas analysis. The changes in PaCO(2), pH, and ETCO(2) were statistically significant during the study periods in both groups (P < 0.05). The percentage of PaCO(2) increase between T(0) and T(15) was 11.5% and 20.1%, respectively, in the control group and the PHT group (P < 0.05). This increase reached 36.8% at T(30) in the PHT group, whereas the control group had a 17.2% increase (P < 0.05). ETCO(2) presented similar changes. The variability in base excess, bicarbonate, PaO(2), arterial oxygen saturation, and SpO(2) was not significant in either group (P > 0.05). The PaCO(2) increased remarkably in children with PHT undergoing laparoscopy, with no difference in intrahepatic or extrahepatic origin. Limiting the duration of CO(2) pneumoperitoneum and intraabdominal pressure and adjusting ventilatory variables to accommodate hypercarbia are of the utmost importance for such cases. IMPLICATIONS: We compared children with portal hypertension with systemically healthy children during laparoscopy. The increase in arterial and end-tidal CO(2) was remarkable in children with portal hypertension, regardless of bicarbonate changes. Managing ventilation to accommodate hypercarbia is of the utmost importance for such cases.     

Gastric air tonometry during laparoscopic cholecystectomy: a comparison of two PaCO2 levels

PURPOSE: Pneumoperitoneum can cause disturbances in acid-base balance and splanchnic perfusion. We studied the effect of ventilation on acid-base balance and gastric mucosal tonometric values in patients undergoing laparoscopic cholecystectomy. METHODS: Twenty-four patients (ASA I-II) were randomly allocated into two groups. In the fixed ventilation group, ventilation was constant allowing free increase in PCO2, while in the constant CO2 group end-tidal PCO2 was fixed with ventilatory adjustment. Intraabdominal pressure was limited to 12 mmHg. Arterial acid-base balance, automated air tonometric variables and gastric mucosal to arterial PCO2 gap were determined frequently from anesthesia induction until three hours postoperatively. RESULTS: During pneumoperitoneum, in the fixed ventilation group arterial PCO2 changed from 5.0 +/- 0.2 to 6.6 +/- 0.4 kPa and pH from 7.43 +/- 0.03 to 7.33 +/- 0.04, tonometric PCO2 from 5.1 +/- 0.5 to 6.9 +/- 0.4 and pH from 7.44 +/- 0.04 to 7.33 +/- 0.04. In the constant CO2 group these variables remained at control levels (P < 0.01 between groups). The PCO2 gap remained unchanged without any differences between the groups. In the recovery room all measured variables were within normal range in both groups. CONCLUSION: Despite inter-group differences in arterial and tonometric PCO2 and pH values during CO2 pneumoperitoneum, the patients did not develop splanchnic hypoperfusion detectable by air tonometric method, as indicated by normal PCO2 gap in both groups throughout the study.     

The impact of morbid obesity, pneumoperitoneum, and posture on respiratory system mechanics and oxygenation during laparoscopy

We studied the effect of morbid obesity, 20 mm Hg pneumoperitoneum, and body posture (30 degrees head down and 30 degrees head up) on respiratory system mechanics, oxygenation, and ventilation during laparoscopy. We hypothesized that insufflation of the abdomen with CO(2) during laparoscopy would produce more impairment of respiratory system mechanics and gas exchange in the morbidly obese than in patients of normal weight. The static respiratory system compliance and inspiratory resistance were computed by using a Servo Screen pulmonary monitor. A continuous blood gas monitor was used to monitor real-time PaCO(2) and PaO(2), and the ETCO(2) was recorded by mass spectrometry. Static compliance was 30% lower and inspiratory resistance 68% higher in morbidly obese supine anesthetized patients compared with normal-weight patients. Whereas body posture (head down and head up) did not induce additional large alterations in respiratory mechanics, pneumoperitoneum caused a significant decrease in static respiratory system compliance and an increase in inspiratory resistance. These changes in the mechanics of breathing were not associated with changes in the alveolar-to-arterial oxygen tension difference, which was larger in morbidly obese patients. Before pneumoperitoneum, morbidly obese patients had a larger ventilatory requirement than the normal-weight patients to maintain normocapnia (6.3 +/- 1.4 L/min versus 5.4 +/- 1.9 L/min, respectively; P = 0.02). During pneumoperitoneum, morbidly obese, supine, anesthetized patients had less efficient ventilation: a 100-mL increase of tidal volume reduced PaCO(2) on average by 5.3 mm Hg in normal-weight patients and by 3.6 mm Hg in morbidly obese patients (P = 0.02). In conclusion, respiratory mechanics during laparoscopy are affected by obesity and pneumoperitoneum but vary little with body position. The PaO(2) was adversely affected only by increased body weight. IMPLICATIONS: Morbid obesity significantly decreases respiratory system compliance and increases inspiratory resistance. Increased body weight, and not altered mechanics of breathing, was associated with worse PaO(2) during laparoscopy.     

Is distal sampling of end-tidal CO2 necessary in small subjects?

The authors compared PaCO2 with end-tidal CO2 (ETCO2) sampled at multiple sites along the endotracheal tube (ETT) in seven anesthetized rabbits (weight, 2.7-3.6 kg) to determine the most convenient, yet accurate, sampling location. Comparisons were made during spontaneous and controlled ventilation with fresh gas flows (FGF) of two and ten times the minute ventilation using a Mapleson D circuit. An Engstrom Eliza analyzer with a continuous sampling rate of 100 ml/min was used to measure ETCO2. A 0.75-mm ID polyethylene tube inserted in the side of the ETT sampled ETCO2 at the distal tip and at the 6-, 12-, and 15-cm marks on the ETT. ETCO2 was also measured at the standard proximal connector. The differences (P less than 0.05) between PaCO2 and ETCO2 at the distal, 6-, 12-, and 15-cm marks were 2.9 +/- 0.4, 3.1 +/- 0.4, 3.6 +/- 0.4, and 4.6 +/- 0.5 mmHg (mean +/- SEM), respectively, and did not change with FGF or mode of ventilation. The difference between PaCO2 and ETCO2 measured at the proximal connector was always large but significantly (P less than 0.05) greater during spontaneous than controlled ventilation (24.2 +/- 1.5 versus 15.0 +/- 1.4 mmHg) and at higher FGF (19.4 +/- 1.3 versus 16.8 +/- 1.6 mmHg). The differences (P less than 0.05) between ETCO2 at the distal tip and ETCO2 at the 6-, 12-, and 15-cm marks were 0.24 +/- 0.07, 0.73 +/- 0.11, and, 1.77 +/- 0.20 mmHg, respectively. This demonstrates that the change in ETCO2 between the distal tip and the 12-cm mark on the ETT is less than 1 mmHg, and that this clinically insignificant difference is independent of FGF and mode of ventilation. The 12 cm-mark is outside of the mouth on a newborn, and sampling ETCO2 at that point, which may be accomplished simply by inserting a small needle in the side of the ETT, may be the most appropriate sampling location.     

Videoendoscopic endotracheal intubation in the rat: a comprehensive rodent model of laparoscopic surgery

BACKGROUND: Peritoneal absorption of CO(2) during abdominal insufflation in laparoscopy may disrupt the acid-base equilibrium and alter the physiological response to stress. Current nonventilated rodent models of laparoscopy do not manage the CO(2) load of pneumoperitoneum, but ventilated surgical rodent models are invasive (tracheotomy) and may independently induce the inflammatory response. MATERIALS AND METHODS: A comprehensive rodent model of laparoscopy was developed. Rats were randomized to receive anesthesia alone, anesthesia plus CO(2) pneumoperitoneum, or anesthesia plus CO(2) pneumoperitoneum with videoendoscopic intubation and mechanical ventilation. Arterial blood-gas analysis was performed at baseline and after 30 min of intervention. RESULTS: Baseline pH, pCO(2), and HCO(3)(-) arterial blood gas parameters were normal for all rats. After 30 min, pCO(2) and pH changed slightly but remained normal among rats receiving anesthesia alone (pCO(2) = 46.5 +/- 1.9; pH = 7.365 +/- 0.009) whereas animals receiving anesthesia plus CO(2) pneumoperitoneum that were dependent on spontaneous respiration for ventilation developed significant hypercarbic acidosis (pCO(2) = 53.2 +/- 1.9, P < 0.05; pH = 7.299 +/- 0.011, P < 0.001). This acidosis was completely corrected with increased minute ventilation in intubated rats receiving mechanical ventilation (pCO(2) = 36.8 +/- 1.5, P < 0.001; pH = 7.398 +/- 0.011, P < 0.001). CONCLUSIONS: CO(2) pneumoperitoneum induces significant hypercarbic acidosis in nonventilated rats. Noninvasive endotracheal intubation is feasible in the rat with videoendoscopic assistance. Our noninvasive rodent model of laparoscopic surgery controls for anesthesia- and capnoperitoneum-related acid-base changes and provides an environment in which the biological response to pneumoperitoneum can be studied precisely.