Oral acetazolamide in the assessment of (urine-blood)PCO2

Urine-blood (U-B)Pco₂ difference in children is usually assessed following urine alkalinization with oral sodium bicarbonate (NaHCO₃). Since oral NaHCO₃ is often poorly tolerated by children, we compared oral acetazolamide with oral NaHCO₃ in a study of (U-B)Pco₂. In the first phase of the study 14 children and adolescents aged 11.1±3.7 years (mean±SD) were studied. Eight participants had normal kidney function and 6 had disturbed distal acidification capacity. Each child was studied twice, once with oral NaHCO₃ (2.5 mEq/kg) and once with acetazolamide (17±2 mg/kg). All studies were performed according to the standard protocol. Acetazolamide administration resulted in a lower blood pH than NaHCO₃ (7.30±0.03 vs 7.38±0.06,P<0.001) and a lower serum bicarbonate (HCO₃ ^–) concentration (25.1±2.2 mEq/l vs 27.5±2.1 mEq/l,P<0.025). Acetazolamide also resulted in a higher urinePco₂ (81.9±26.2 mm Hg vs 71.6±18.2 mm Hg) than NaHCO₃ (P<0.025). No significant differences between acetazolamide and NaHCO₃ were observed with respect to their effects on urinary pH and HCO₃ ^– concentration, plasmaPco₂ and (U-B)Pco₂. Good linear correlations were found between the effects of acetazolamide and NaHCO₃ on urinePco₂ (r=0.878,P<0.001), and on (U-B)Pco₂ (r=0.795,P<0.01). Using either method of urinary alkalization, children with normal kidney function had urinePco₂ greater than or equal to 80 mm Hg and (U-B)Pco₂ greater than or equal to 30 mm Hg, and those with disturbed acidification capacity had urinePco₂ less than or equal to 70 mm Hg and (U-B)Pco₂ less than or equal to 20 mm Hg. Patient satisfaction with the test, on a scale of 1 (worst) to 5 (best), was 2.6±0.8 for NaHCO₃ and 3.9±0.3 for acetazolamide (P<0.001). Tests with NaHCO₃ lasted 150.9±30.5 min versus 115.7±18.1 min for acetazolamide (P<0.01). In the second phase of the study 8 children, 5 with normal and 3 with abnormal acidification capacity were studied twice with oral acetazolamide. Studies were performed 3 weeks apart. The results showed very good reproducibility of (U-B)Pco₂ in all of the subjects. Oral acetazolamide and NaHCO₃ have similar effects on (U-B)Pco₂ but the diuretic agent shortens the testing time and is easier to administer to children. We conclude that oral acetazolamide could be substituted for NaHCO₃ under certain circumstances in the assessment of (U-B)Pco₂.     

Subcutaneous perfusion before and during surgery in obese and nonobese patients

Hypoxia at the surgical site impairs wound healing and oxidative killing of microbes. Surgical site infections are more common in obese patients. We hypothesized that subcutaneous oxygen tension (P_sqO₂) would decrease substantially in both obese and non‐obese patients following induction of anesthesia and after surgical incision. We performed a prospective observational study that enrolled obese and non‐obese surgical patients and measured serial P_sqO₂ before and during surgery. Seven morbidly obese and seven non‐obese patients were enrolled. At baseline breathing room air, P_sqO₂ values were not significantly different (p = 0.66) between obese (6.8 kPa) and non‐obese (6.5 kPa) patients. The targeted arterial oxygen tension (40 kPa) was successfully achieved in both groups with an expected significant increase in P_sqO₂ (obese 16.1 kPa and non‐obese 13.4 kPa; p = 0.001). After induction of anesthesia and endotracheal intubation, P_sqO₂ did not change significantly in either cohort in comparison to levels right before induction (obese 15.5, non‐obese 13.5 kPa; p = 0.95), but decreased significantly during surgery (obese 10.1, non‐obese 9.3 kPa; p = 0.01). In both morbidly obese and non‐obese patients, P_sqO₂ does not decrease appreciably following induction of anesthesia, but decreases markedly (～33%) after commencement of surgery. Given the theoretical risks associated with low P_sqO₂, future research should investigate how P_sqO₂ can be maintained after surgical incision.     

Effects of hypothermia with and without buffering in hypercapnia and hypercapnic hypoxemia

Anesthetized, paralyzed and mechanically ventilated pigs were hypoventilated to extreme hypercapnia (Paco₂=20 kPa) at Fio₂ 0.5, and allotted to receive hypothermia (=31.5˚C) and buffer infusion, (HB–group, n = 6) or to a hypothermic control group (H–group, n = 6). The HB–group had higher arterial pH (7.34 vs 7.09, P < 0.01) and plasma bicarbonate (58.8 vs 35.4 mmol–l^-1, P < 0.01) than the controls, but lower mean pulmonary arterial pressure (MPAP), (16 vs 23 mmHg (2.1 vs 3.1 kPa), P < 0.01) and pulmonary vascular resistance (PVR), (512 vs 699 dyn–s–cm^-5 (5120 vs 6990 μN–s–cm^-5), P < 0.05). Mixed venous Po₂ (Pvo₂) was lower in the HB–group (5.1 vs 6.8 kPa, P < 0.01), as well as serum potassium (2.8 vs 3.7 mmol l^-1, P <0.01) and ionized calcium (1.01 vs 1.29 mmol l^-1, P <0.01). Subsequently, the inspired oxygen fraction (Fio₂) was decreased stepwise (0.3, 0.25, 0.21, 0.15, 0.10) at 30 min intervals. At Fio₂ 0.3, the HB–group had lower Pvo₂ (6.6 vs 7.8 kPa, P <0.01), O₂ half saturation tension (3.6 vs 4.2 kPa, P <0.01), MPAP (17 vs 25 mmHg (2.3 vs 3.3 kPa, P <0.01) and PVR (598 vs 793 dyn–s–cm^-5 (5980 vs 7930 μN–S'cm^-5, P <0.05) compared with the controls, but higher arterial O₂ saturation (95.3 vs. 88.6%, P < 0.01) and O₂ content (17.7 vs 15.7 ml– 100 ml^-1, P <0.05). The groups did not differ in O₂ delivery, in spite of their difference in arterial O₂ content, because of a lower cardiac output in the HB–group (1.6 vs 2.2 l–min^-1, P <0.05). Mixed venous O₂ content, O₂ consumption and O₂ extraction did not differ between groups. Combined use of hypothermia and buffering did not improve survival in hypercapnic hypoxemia as compared to a hypothermic regimen without buffer.     

Improvement of arterial oxygenation by selective infusion of prostaglandin E1 to ventilated lung during one-lung ventilation

Background:One-lung anesthesia provides a better surgical field for thoracic procedures but also impairs the arterial oxygenation and venous admixture. During one-lung ventilation, pulmonary vasoconstriction is assumed to be present within both ventilated and collapsed lungs. We propose that arterial oxygenation could be optimized by offsetting the vasoconstriction within the microcirculation of ventilated lung. Method:In an anesthetized dog model, incremental doses of prostaglandin E₁ (PGE₁) were selectively infused into the main trunk of the pulmonary artery of the ventilated lung after one-lung ventilation for 60 min (PGE₁ group, n=9). Arterial oxygenation and calculated venous admixture (Qs/Qt) was also assessed in a time-course control group (Control group, n =5). During two-lung ventilation (FIO₂: 0.66), arterial PO₂ and venous admixture was 44.22 ± 3.5 kPa and 10.7±2.3%, respectively. One-lung ventilation (FIO₂: 0.66) with left lung collapsed reduced arterial PO₂ to 11.6±1.7 kPa and increased venous admixture to 40.7±5.8% (P<0.001). Venous O₂ tension also decreased from 6.3±0.7 kPa to 5.0±0.6 kPa with a slight increase in mean pulmonary artery pressure and pulmonary vascular resistance (P <0.05). Results: During selective infusion of PGE₁ at a dose of 0.04 to 0.2 μg kg^-1 min^-1, there was a dose-dependent improvement in arterial PO₂ with a parallel reduction of venous admixture during one-lung ventilation. Arterial PO₂ increased to a maximum of 23.0±4.3 kPa, and the venous admixture decreased significantly to a minimum of 27.4±4.2% by PGE₁ at a dose of 0.04-0.4 μg kg^-1 min^-1 (P<0.01). PGE₁ resulted in a small increase in cardiac output and decreases of pulmonary pressure and pulmonary vascular resistance at a relatively high dose of 0.4 μg kg^-1 min^-1 during selective infusion (P<0.05). Conclusion: These results suggest that a selective pulmonary artery infusion of PGE₁ to the ventilated lung within the dose range of 0.04-0.4 μg kg^-1 min^-1 is practical and effective to improve arterial oxygenation and reduce venous admixture during one-lung ventilation.     

Reduced CO2-elimination during combined high-frequency ventilation compared to conventional pressure-controlled ventilation in surfactant-deficient piglets

Background: Combined high-frequency ventilation (CHFV) combines a conventional low-frequency component with superimposed high-frequency jet pulses. The intention is to overcome the limited CO₂-elimination of high-frequency ventilation, and to decrease airway pressures and enhance hemodynamic performance by reducing the conventional component. The present study was performed to compare the effects of conventional continuous positive-pressure ventilation (CPPV) on gas exchange, airway pressures and cardiac output to those of CHFV at matched minute volume (MV) and mean airway pressure (MPAW). Methods: Sixteen anaesthetised piglets with lavage-induced surfactant deficiency were ventilated with CPPV, with positive end-expiratory pressure (PEEP) set to obliterate the lower inflection point of the inspiratory pressure-volume loop. This setting was compared to CHFV during which 50% of the total MV was applied as superimposed jet pulses of 20 Hz at otherwise unchanged settings, and to CPPV at a PEEP level which was reduced (CPPV_red) until MPAW matched MPAW during CHFV. Gas exchange, airway pressures and hemodynamics were measured after the ventilatory setting had been applied for 20 min. Results: MPAW decreased from (median) 2.7 kPa with CPPV to 2.4 kPa with CHFV (P≤0.05). Peak inspiratory pressure was 3.6 kPa with CPPV, 3.2 kPa with CHFV, and 3.2 kPa with CPPV_red (P≤0.05 for differences to CPPV), respectively. PaCO₂ was comparable during CPPV (5.9 kPa), CPPV_red and CHFV_CO2, while it increased during CHFV (6.8 kPa, (P≤0.05)). Cardiac output did not differ significantly between the settings. Conclusions: In the porcine lavage model, CO₂-elimination is reduced during CHFV compared to CPPV at matched minute volume. At matched mean airway pressure, CHFV fails to reduce peak inspiratory airway pressure and to improve hemodynamic performance compared to CPPV.     

Continuous Measurement of Po2, Pco2 and pH During Total Body Perfusion in Dogs

Continuous measurement of blood P_o2, P_co2, and pH can be made either with intravascular electrodes or with electrodes placed in a flow cuvette. The two methods are reviewed. In this study a system based on the Radiometer flow cuvette was used. The continuous recording was checked at intervals against results obtained by conventional electrode analyses of individual blood samples. The continuous recording and individual checks were virtually identical. Checks on electrode calibration were made after 4–5 hours use, and no significant electrode drift was noted. During perfusion with Rygg-Kyvsgaard bubble-oxygenator, variations in P_o2, P_co2 and pH were measured continuously in dogs to register any changes, which might occur in the transition to and from perfusion, and which would be too rapid for measurement by the single sample technique. Apart from catheterization of the venae cavae through the right atrium the heart was undisturbed. In the first minutes of perfusion marked falls in all three parameters were observed. Oxygen tension fell on average by 168 mmHg, P_co2 by 17.3 mmHg and pH by 0.14. P_co2 rapidly returned to normal values, while pH and P_o2 increased slowly during the period of perfusion, an average of 69 min. Possible explanations of the changes are considered. On discontinuing perfusion P_co2 increased and pH fell. These changes may be partly explicable in terms of increase in dead space. The study indicates that variations in P_o2, P_co2 and pH not detectable by the individual sample technique can be registered by continuous measurement. Thus continuous measurement gives fine control and allows early correction of any disturbances, however rapid, in blood gases and pH.     

The relationship between arterial Po2 and mixed venous Po2 in response to changes in positive end-expiratory pressure in ventilated patients

The response of arterial Po ₂ (P_ao ₂) to airway pressure has been used as a measure of recruitment in mechanically ventilated patients. We hypothesised that mixed venous Po ₂ (P_mvo ₂) directly affects P_ao ₂. Sixteen patients with acute lung injury (ALI, lung injury score ≥ 1) on volume‐controlled mechanical ventilation (F_Io ₂ 0.40) were studied. Positive end‐expiratory pressure (PEEP) was increased and decreased. Incremental PEEP increased median values of P_ao ₂, diminished venous admixture (Q_va/Q_t) and cardiac index, but maintained arterial Pco ₂ and tissue O₂ uptake. These changes were reversed during decremental PEEP. However P_ao ₂ did not increase in 37% of PEEP steps and changes in P_ao ₂ correlated to those in P_mvo ₂ (r_s = 0.45, p < 0.001). Changes in P_mvo ₂ contributed to changes in Q_va/Q_t in determining changes in P_ao ₂ (p < 0.05). P_mvo ₂ may be an independent determinant of P_ao ₂ during mechanical ventilation for ALI, so that dosing PEEP to recruit the lung should not be guided by arterial blood oxygenation alone. Arterial hypoxaemia with increasing PEEP may improve by reducing PEEP (or increasing tissue O₂ delivery), when the fall in P_mvo ₂ is greater than about 0.133 kPa.     

Effects of hypothermia in hypercapnia and hypercapnic hypoxemia

Anesthetized, paralyzed and mechanically ventilated pigs were hypoventilated to extrene hypercapnia (Paco₂?20 kPa) at Fio₂ 0.5, and allotted to a hypothermic group (31.5 ±0.l°C, n = 6) or a control group (39.6±0.2°C, n = 6). Compared with the controls, the hypothermic animals had higher Pao₂ (19.2 vs 15.6 kPa, P>0.05), Sao₂ (97.2 vs 89.3%), Sv?o₂ (78.7 vs 68.2%), end-tidal 0₂ (34.5 vs 24.8 kPa) and arterial pH (7.01 vs 6.91), (P>0.01), but lower Pv?o₂ (7.0 vs. 10.2 kPa) and Paco₂ (13.2 vs 23.5 kPa), (P>0.01). Hypothermia reduced O₂ delivery (Do₂), O₂ consumption (Vo₂) and CO₂ production by 40–45% (P> 0.05), but O₂ extraction ratio, i.e. VO₂, Do₂-¹. 100 (%), did not differ between groups. Hypothermic animals had lower heart rate (127 vs 223 beats.min-¹, P>0.05) and cardiac output (2.5 vs 3.9 l.min-¹, P>0.01). Subsequently, the inspired oxygen fraction (Fio₂) was decreased stepwise (0.3, 0.25, 0.21, 0.15, 0.10) at 30- min intervals. At Fio₂ 0.3, the hypothermic group had higher Pao₂ (10.0 vs 5.7 kPa), Sao₂ (91.3 vs 28.5%), Pv?o, (5.8 vs 3.4 kPa), Sv?o₂ (70.7 vs 10.3%), end-tidal O₂ (16.7 vs 8.5 kPa), O₂ delivery (344 vs 155 ml.min-¹), arterial pH (7.02 vs 6.94) and systemic vascular resistance (3850 vs 1652 dyn.s. cm-⁵(38500 vs 16520 μN. s. c m-⁵)) compared with the controls (P>0.01), while Paco₂ was lower (12.4 vs 22.7 kPa), as well as O₂ extraction ratio (23 vs 63%) and O₂ half saturation tension (4.3 vs 8.0 kPa) (P>0.01). Except for Pao₂, all differences between groups remained significant at Fio₂ 0.25. The control animals died during Fio₂ 0.25 and 0.21, while all hypothermic animals remained circulatorily stable. One hypothermic animal died after 12 min at Fio₂ 0.15 and the remainder after 6–39 min (mean 22 min) at Fio₂ 0.10. We conclude that hypothermia markedly improves whole-body oxygen balance, cardiovascular stability and survival in hypercapnic hypoxemia.     

Effects of buffering in hypercapnia and hypercapnic hypoxemia

Anesthetized, paralyzed and mechanically ventilated pigs were exposed to extreme hypercapnia (Paco_2-20 kPa) at Fio₂ 0.4 for 480 min, with (n = 6) or without (n = 6) continuous infusion of isotonic buffers (bicarbonate and trometamol). Arterial pH was higher in buffered animals than controls, 7.21 ±0.01 vs 7.01±0.01 (mean ± s.e.mean, P < 0.01). Serum osmolality and Paco₂ did not differ between groups throughout the experiment. The hemodynamic response to hypercapnia was attenuated in the buffered group, who had lower heart rate, 133 ± 6 vs 189±12 min^-1 (P < 0.01), mean arterial pressure (MAP) 109 ± 4 vs 124 ± 4 mmHg (14.5 ± 0.5 vs 16.5 ± 0.5 kPa) (P < 0.05), mean pulmonary arterial pressure 16±1 vs 23 ± 1 mmHg (2.1 ±0.1 vs 3.1 ±0.1 kPa) (P < 0.01), and pulmonary vascular resistance (PVR) 249 ± 21 vs 343 ± 20 dyn s-cm^-5 (2490±210 vs 3430±200 μN-s-cm^-5) (P < 0.01), compared with the control group. Subsequently, both groups were exposed to hypercapnic hypoxemia by stepwise increases in Fio₂ (0.15, 0.10, 0.05) at 30-min intervals, while Fico₂ was kept at 0.2. PVR increased in both groups (P < 0.05) but, except for heart rate, all hemodynamic differences between the groups disappeared during hypoxia. At Fio₂ 0.15, buffered animals had higher arterial oxygen saturation (73 ± 5%) than the controls (55 ± 5%), (P < 0.05). The control animals died after 1–29 min (mean 14 min) at Fio₂ 0.10, while all buffered animals survived Fio₂ 0.10 with stable MAP (122 ± 14 mmHg (16.3 ± 1.9 kPa). The buffered animals died after 4–22 min (mean 15 min) at Fio₂ 0.05. We conclude that buffering to a pH of 7.21 attenuates the observed hemodynamic response in extreme hypercapnia and improves survival in hypercapnic hypoxemia.     

Effects of propofol vs isoflurane on respiratory gas exchange during laparoscopic cholecystectomy

Background : Respiratory function and pulmonary gas exchange are affected in laparoscopic procedures where a pneumoperitoneum is introduced using CO₂. Previous studies have shown differing results concerning pulmonary gas exchange during laparoscopic procedures: Whereas in patients undergoing isoflurane anaesthesia decreases in PaO₂ are demonstrated, this factor remains unchanged in patients undergoing propofol anaesthesia. In the present study, the effects of propofol on pulmonary gas exchange were compared with those of isoflurane in patients undergoing elective laparoscopic cholecystectomy in a prospective randomised manner. Methods : Twenty ASA patients with physical status I and II were divided randomly between isoflurane (IG) and propofol groups (PG). After induction of anaesthesia patients were moderately hyperventilated. Respirator settings remained unchanged during pneumoperitoneum (PP) until 10 min after deflation of the peritoneal cavity. Blood gas analyses were performed at 5 time points: 15 min after induction of anaesthesia (giving pre-PP values), immediately before carbon dioxide insufflation (0 min PP), after both 30 and 60 min of PP and 10 min post PP. Inspiration plateau pressure (P_plat), compliance of the respiratory system, and both ins- and expiratory gas concentrations were continuously recorded by an Ultima V® monitor (Datex Corp., Helsinki, Finland). The difference between arterial and end-tidal CO₂ partial pressure (P(a-et)CO₂) was calculated so as to allow assessment of physiological dead space by the modified Bohr equation. Results : Pulmonary gas exchange differed significantly after 30 min of PP between the IG and the PG. At this time, PaO₂ was 19.5 ± 2.9 kPa (mean ± SD) in the IG and 23.1 ± 1.8 kPa in the PG (P<0.01), whereas PaCO₂ was 5.5 ± 0.37 kPa in the IG and 4.9 ± 0.27 kPa in the PG (P<0.01). These discrepancies remained until after carbon dioxide desufflation. At 10 min post PP, PaO₂ was 18.3 ± 2.6 kPa in the isoflurane group and 21.9 ± 2.2 kPa in the propofol group (P<0.01), whereas PaCO₂ was 5.4 ± 0.46 kPa in the IG and 4.8 ± 0.22 kPa in the PG (P<0.01). During carbon dioxide insufflation the P(a-et)CO₂ increased significantly in the IG from 0.47 ± 0.13 kPa to 0.76 ± 0.37 kPa (P<0.05), while the values in the PG remained constant. Conclusion : This study demonstrates that pulmonary gas exchange in patients with laparoscopic cholecystectomy is affected by the choice of anaesthetic procedure. During and after laparoscopic cholecystectomy using isoflurane as the anaesthetic, the PaCO₂ is significantly higher and the PaO₂ significantly lower than they are with propofol.     

Rectal luminal PrCO 2, measured by automated air tonometry, does not reflect gastric luminal PrCO 2 in children

Rectal luminal regional P_{CO 2} (Pr_{CO 2}) was compared with gastric luminal Pr_{CO 2} measured by automated air tonometry at intervals of 10 min in 20 children aged 6–16 years scheduled for elective surgery under general anesthesia. In 5 patients, measurement of rectal Pr_{CO 2} failed because of catheter-related problems. In the remaining 15 children, aged 10.6 ± 2.5 years, 19 ± 7 paired rectal and gastric Pr_{CO 2} values (n total, 241) were measured. Bias and precision for gastric compared to rectal Pr_{CO 2} was −1.79 kPa and 2.89 kPa. In patients with obvious feces in the rectum, bias (precision) for gastric compared to rectal Pr_{CO 2} was −2.7 kPa (2.6 kPa) and in those with empty rectum, −0.75 kPa (1.42 kPa; t-test; P < 0.001). Based on our in vivo data, rectal luminal Pr_{CO 2}, measured by automated air tonometry, does not reflect gastric luminal Pr_{CO 2} in children. Enteral luminal gas production within feces in the rectum seems to be a major source of this disagreement.     

Protective effects of halothane but not isoflurane against global ischaemic injury in the isolated working rat heart

The effects of equi-anaesthetic concentrations of halothane (HAL) and isoflurane (ISO) on myocardial performance, perfusion, oxygenation and lactate release were studied before, during and after a low-flow, global ischaemic insult in isolated, paced rat left heart preparations. An antegrade perfusion technique was used, where left atrial pressure (LAP) and mean aortic pressure (MAP) could be altered independently of each other. Aortic flow, coronary flow (CF) and PO₂ in venous coronary effluent were continuously recorded and stroke volume, myocardial oxygen consumption (MVO₂) and myocardial oxygen extraction as well as lactate release were calculated. The hearts were exposed for at least ten minutes to the perfusate without (control, n=10) or with HAL (n=10) or ISO (n= 10) at a MAP of 80 mmHg (10.4 kPa) and a LAP of 7.5 mmHg (1.0 kPa). After baseline measurements, MAP was reduced to 25 mmHg (3,2 kPa) for a total of nine minutes. Thereafter MAP was increased to 80 mmHg (10.4 kPa) for another nine minute period. During the whole experimental procedure, LAP was maintained at 7.5 mmHg (1.0 kPa) and heart rate at 325 beats per minute. In the pre-ischaemic control period, MVO₂ was lower with HAL compared to ISO (P<0.05) and control (P<0.05). Stroke volume was also lower with HAL compared to control (P<0.05). During hypoperfusion, lactate release was twice as high in the control group (P<0.0I) and with ISO (P<0.01) compared to HAL. This was accompanied by a lower oxygen extraction with HAL compared to control (P<0.05) and ISO (P<0.05). In the post-ischaemic periods, MVO₂ and stroke volume were lower with HAL compared to ISO and control. There were no significant differences in CF between the groups. We conclude that HAL, but not ISO, exerts a direct protective effect against a glycon'c anaerobic metabolism during low-flow global myocardial ischaemia.     

Larger tidal volume increases sevoflurane uptake in blood: a randomized clinical study

Background: The rate of uptake of volatile anesthetics is dependent on alveolar concentration and ventilation, blood solubility and cardiac output. We wanted to determine whether increased tidal volume (V_T), with unchanged end‐tidal carbon dioxide partial pressure (P_ETCO₂), could affect the arterial concentration of sevoflurane. Methods: Prospective, randomized, clinical study. ASA physical status ² and II patients scheduled for elective surgery of the lower abdomen were randomly assigned to one of the two groups with 10 patients in each: one group with normal V_T (NV_T) and one group with increased V_T (IV_T) achieved by increasing the inspired plateau pressure 0.04 cmH₂O/kg above the initial plateau pressure. A corrugated tube added extra apparatus dead space to maintain P_ETCO₂ at 4.5 kPa. The respiratory rate was set at 15 min^?1, and sevoflurane was delivered to the fresh gas by a vaporizer set at 3%. Arterial sevoflurane tensions (P_asevo), F_isevo, P_ETsevo, P_ETCO₂, P_aCO₂, V_T and airway pressure were measured. Results: The two groups of patients were similar with regard to gender, age, weight, height and body mass index. The mean P_ETsevo did not differ between the groups. Throughout the observation time, arterial sevoflurane tension (mean±SE) was significantly higher in the IV_T group compared with the NV_T group, e.g. 1.9±0.23 vs. 1.6±0.25 kPa after 60 min of anesthesia (P<0.05). Conclusion: Ventilation with larger tidal volumes with isocapnia maintained with added dead‐space volume increases the tension of sevoflurane in arterial blood.     

Gas exchange, metabolic rate and fluid requirements during anaesthesia of acyanotic and cyanotic infants and children with congenital heart malformations

In order to study gas exchange and metabolic rate in anaesthetized children scheduled for corrective cardiac surgery and to find out if chronic hypoxaemia influenced gas exchange and energy expenditure, oxygen consumption (V?O₂) and carbon dioxide elimination (Vdot;co₂) were measured and energy expenditure (E) was calculated. Infants and children whose haematocrit (Hct) was less than 44% and arterial oxygen saturation (Sao₂) on room-air was greater than 93% were classified as acyanotic (group AC, n= 11, weight range 3.7 to 20 kg), and those whose Hct was higher than 44% and Sao₂ less than 93% as cyanotic (group C, n= 14, weight range 3.4 to 24.3 kg). The majority of children in both groups weighed less than the 50th percentile for normal children. There was no difference in V?o₂, V?co₂ and E between the groups. These variables were related to weight according to the following expressions: V?o₂ (ml min^?1) = 6.1 × kg + 21.6, r= 0.95; V?co₂ (ml min^?1) = 5.7 × kg + 2.9, r= 0.96, and E (kcal h^?1) 1.8 × kg + 5.3; E (J h^?1) = 7.6 × kg + 22.3, r= 0.96. Fluid volumes (FV) could be calculated according to the expression: FV (ml h^?1) = 3.0 × kg + 8.7; r= 0.96. Oxygen consumption was 15 to 20% higher in anaesthetized infants and children with congenital heart malformations than in anaesthetized infants and children with normal cardiopulmonary function. Accordingly, energy expenditure and fluid requirements were also higher. This difference was most probably due to an undernutrition in children with congenital heart malformations which resulted in a compensatory hypermetabolism.     

Effects of lumbar puncture position on arterial blood gases

We observed the changes in partial pressure of arterial oxygen (Pao ₂) and carbon dioxide (Paco ₂) before and during assumption of the lateral position prior to lumbar puncture in 81 patients to investigate whether lung volume decreased and ventilation was suppressed. Pao ₂ significantly decreased while the patients were in the lateral position, while Paco ₂ remained unchanged. There was a negative correlation between the change in Pao ₂ and age [change in Pao ₂ (mmHg)=−0.13×age (years)+4.28,P<0.01]. The fact that closing volume increases with age implies that the decrease in functional residual capacity in the lateral position could have caused the decrease in Pao ₂. It is therefore advisable to continuously monitor arterial oxygenation using a noninvasive monitor, such as a pulse oximeter, while performing spinal or epidural block, especially in elderly patients.     

The Effect of Acute Respiratory Acidosis on the Proportion: Total Splanchnic Perfusion/Cardiac Output, and the Alteration in this Proportion by Two Anaesthetics

Eight dogs were anaesthetized and ventilated. Respiratory acidosis with variations in the pH (range: 7.49 to 7.05) were brought about by changes in the dead space of the apparatus. The pH-related changes in cardiac output (Q), and total splanchnic perfusion (Q_sp1) were studied during anaesthesia with mebumal natrium (NFN) N₂O-O₂-gallamoni jodidum (NFN) (“basic anaesthesia”), and after the addition of 1 % halothane (inspiratory). Similar relationships were demonstrated in the systemic circulation between pH changes and changes in the cardiac output, pulse pressure, and total peripheral resistance during both types of anaesthesia; whereas the pulse frequency and the mean aorti cpressure were not significantly correlated to changes in pH. Q_sp1 was different during the two types of anaesthesia. Under “basic anaesthesia,” the pH-related changes in Q and Q_sp1 were opposite and of varying magnitude. Their mutual relation: the fraction of cardiac output perfusing the splanchnic area, was Q_sp1/Q= -2.28 + 0.34×pH (r = 0.69, N = 28, P<0.001). After the addition of halothane, no correlation could be demonstrated between Q_sp1/Q and changes in pH. The changes in Q and Q_sp1 were in the same direction and of the same relative magnitude, with an average of Q_sp1/Q = 0.21. In agreement with this, no changes could be demonstrated in the total splanchnie resistance (R_sp1) during halothane anaesthesia in relation to the provoked pH changes, while R_sp1 under “basic anaesthesia” showed a slight rise with falling pH in the majority of dogs (six out of eight). The pressure in the portal vein (P_vp) appeared to rise with a falling pH. For both types of anaesthesia, the AP_vp (kPa) = -0.97 × δpH (r = 0.79, N = 34, P<0.001).     

Flexible fibreoptic bronchoscopy via the laryngeal mask

The efficacy of flexible fibreoptic bronchoscopy through the laryngeal mask was investigated in 20 patients under total intravenous anaesthesia with propofol, fentanyl, atropine and suxamethonium. Mask size 4 was used for men and size 3 for women. Ventilation was performed with oxygen in air, F_IO2 0.6. The ventilatory pressures were median 18 (9–40) cmH₂O (1.8 (0.9–3.9) kPa) before the bronchoscope was inserted. When the tip of the bronchoscope was above the vocal cords the ventilatory pressures increased to 22 (10–43) mmHg (2.2(1.0–4.2) kPa) (P<0.001), and when the tip was situated at the mid-tracheal level there was a further increase to 24 (12–50) mmHg (2.4(1.2–4.9) kPa) (P<0.001). Maximal gas leakages were median 1 (0–2) 1/min^-1. PEEP at the mid-tracheal level was 3 (0–7) cmH₂O (0.3(0–0.7) kPa). When 15 min of the procedure had elapsed, Pao₂ was 232 (112–350) mmHg (30.9(14.9–46.6) kPa) and Paco₂ 39 (33–46) mmHg (5.2(4.4–6.1) kPa). The lowest oxygen saturation was median 98 (96–100)% and the highest end-tidal CO₂ 34 (24–41) mmHg (4.5(3.2–5.5) kPa). It was easy to examine the laryngeal opening and a good assessment of vocal cord function was allowed when muscle relaxation ceased. We conclude that flexible fibreoptic bronchoscopy through the laryngeal mask is a safe technique provided that total intravenous anaesthesia is used. It is a valuable alternative to flexible bronchoscopy performed with topical anaesthesia.     

Cerebral haemodynamic and electrocortical CO2 reactivity in pigs anaesthetized with fentanyl,nitrous oxide and pancuronium

Cerebral haemodynamic, metabolic and electrocortical reactivity to alterations in arterial CO₂, tension (PaCO₂) was assessed in seven mechanically ventilated juvenile pigs to test an experimental model designed for cerebral pharmacodynamic and pharmacokinetic studies. The animals were anaesthetized with fentanyl, nitrous oxide and pancuronium and sequentially normo- and hyperventilated over a 100-min period. Five measurements were made at 25-min intervals. The cerebral blood flow (CBF) was measured with the intraarterial ¹³³Xe technique and the cerebral metabolic rate for oxygen (CMRo₂) determined from CBF and the cerebral arteriovenous oxygen content difference. A linear correlation (r = 0.845) was found between CBF and PaCO₂. The cerebrovascular reactivity to hypocapnia (ΔCBF/ΔPaCO₂) was maintained throughout the experimental period and amounted to (95% confidence interval) 9.1 (7.1–11.1) ml · 100 g^-1 · min^-1 · kPa^-1 within the PaCO₂ range 3.3–6.3 kPa. The CMRo₂ was not influenced by hyperventilation. The baseline electroencephalographic (EEG) pattern was stable at normocapnia (mean PaCO₂ 5.6 kPa), whereas spectral values for delta and total average voltage increased significantly (P<0.05) at extensive hypocapnia (3.5 kPa). Maintenance of cerebral CO₂ reactivity and spectral EEG voltage at a stable plasma level of fentanyl is complementary to the cerebral haemodynamic and metabolic stability previously found at sustained normocapnia in this model.     

The effect of pneumoperitoneum and Trendelenburg position on acute cerebral blood flow–carbon dioxide reactivity under sevoflurane anaesthesia

This study compared cerebral blood flow–carbon dioxide (CBF–CO₂) reactivities in the supine and modest Trendelenburg position under pnemoperitoneum during sevoflurane anaesthesia. After induction of anaesthesia in 25 patients, mechanical ventilation was adjusted to increase Paco ₂ from 4.7 (T₁) to 6.0 kPa (T₂) in the supine position, and the change in jugular bulb oxygen saturation was measured as an index of CBF. Then, after establishment of pneumoperitoneum and 30° Trendelenburg position, the CO₂ step and measurement of CBF were repeated. The CBF–CO₂ reactivity was 7.5 (3.3) %.kPa^?1 (% change in jugular bulb oxygen saturation per unit change in Paco ₂) in the supine position and 6.8 (2.3) %.kPa^?1 in the 30° Trendelenburg‐pneumoperitoneum condition (p = 0.086). We conclude that CBF–CO₂ reactivity is unchanged by the modest Trendelenburg position under pneumoperitoneum during sevoflurane anaesthesia.     

Lung function after open versus laparoscopic cholecystectomy

Postoperative lung function and gas exchange were studied in 36 patients after cholecystectomy. Twenty-four of the patients underwent laparoscopic cholecystectomy while the remaining twelve were operated with open technique. Before surgery all patients had normal ventilatory volumes (forced vital capacity, FVC and forced expired volume in 1 s, FEV₁) and normal gas exchange. Two hours postoperativley FVC was reduced to 64±16% (P<0.05) of the preoperative level in the laparoscopic group and to 45±23% (P<0.05) after open cholecystecomy. On the first postoperative day FVC was virtually normal in the laparoscopic patients (77±17% of preoperative level, NS), whereas the open surgery patients still had a decreased FVC (56±13% of preoperative, P<0.05). FEV₁ in the postoperative period followed the same course as FVC. Gas exchange was significantly impaired in the early postoperative period in all patients but no difference between the two groups was found. Two hours postoperatively Pao₂ was reduced to 85% (P<0.05) of preoperative value and Paco₂ had increased by 0.5 kPa (p<0.05). The alveolo-arterial oxygen tension difference (PA-ao₂) had increased by approximately 45% to a mean of 3.7 kPa (P<0.05). On the first postoperative day gas exchange was still significantly impaired in the open surgery patients. Atelectasis detected by computed X-ray tomography of the lungs were found in both groups. However, the amount of atelectasis tended to be smaller in the laparoscopic group than in the open surgery patients. In summary, cholecystectomy irrespective of whether it was performed by open or laparoscopic technique was followed by deterioration in ventilatory function and gas exchange. However, the magnitude of this impairment was less pronounced in laparoscopic cholecystectomy patients than in the open surgery patients which may suggest that this minimal invasive procedure is favourable with respect to postoperative lung function.