Physiological deadspace during normocapnic ventilation under anaesthesia

Respiratory physiological deadspace (VDphys) during normocapnic ventilation under anaesthesia was studied in 253 patients scheduled for elective non-thoracic surgery. Subjects were ventilated with SERVO 900B ventilator using CO2 analyser 930 (Siemens-Elema Sweden) to adjust minute volume sufficient to maintain end-tidal carbon dioxide fraction (FECO2) around 5.5kPa with normocapnic confirmation using arterial blood gas analysis. VDphys was calculated using Enghoff's modification of Bohr's equation. VDphys and deadspace to tidal volume ratios (VD/VT) in male patients were 142.6 +/- 28.4 ml and 0.37 +/- 0.068 respectively and were significantly higher than that in females (119.4 +/- 35.6 ml and 0.36 +/- 0.067). Males had significantly higher VDphys/mass (2.5 +/- 0.68 ml.kg) compared with females (2.2 +/- 0.54 ml/kg, P < 0.001) but significantly lower body mass index (BMI) (20.67 +/- 3.2 in males and 22.47 +/- 4.1 in females, P < 0.001). VDphys showed positive correlation with weight, height and body surface area (BSA) but VDphys/kg showed negative correlation with BMI. Multiple regression analysis produced a best fit equation for VDphys = 9.7 + 64.3 x BSA + 13.51S where S = 1 for females and 2 for males.     

Analgesia and ventilatory response to CO2 following epidural sufentanil in children

The authors studied the effects of epidural sufentanil (0.75 microgram.kg-1) after urologic surgery in 15 children ranging in age from 4 to 12 yr, and in weight from 14 to 47 kg. The onset and duration of analgesia were 3.0 +/- 0.3 and 198 +/- 19 min, respectively (mean +/- SEM). Side effects included pruritus (3/15), nausea and vomiting (5/15), drowsiness (10/15), and urinary retention (1/11). No apnea was observed. Periosteal analgesia and ventilation were studied in eight of the children (mean age 8.6 +/- 0.8 yr). There was significant periosteal analgesia of the tibia (30, 60, 90, and 120 min after injection) and of the radius (60, 90, and 120 min after injection). Resting respiratory rate and tidal volume did not change during the study. Resting minute-ventilation decreased from 6.3 +/- 0.5 l.min-1 preoperatively to 5.6 +/- 0.6 l.min-1 (P less than 0.05) postoperatively, before epidural sufentanil injection; it did not decrease further after epidural sufentanil. Similarly, end-tidal CO2 tension increased significantly from 37.2 +/- 0.7 mmHg preoperatively to 39.9 +/- 1.2 mmHg (P less than 0.05) postoperatively, before epidural sufentanil; epidural sufentanil did not cause a further significant increase in end-tidal CO2 tension. The slope of the CO2 ventilatory response curve decreased significantly from 1.68 +/- 0.12 l.min-1. mmHg-1 preoperatively to 1.10 +/- 0.13 l.min-1.mmHg-1 (P less than 0.01) postoperatively. There were further significant decreases to 0.68 +/- 0.10 and 0.89 +/- 0.16 l.min-1.mmHg-1 30 and 60 min after epidural sufentanil.(ABSTRACT TRUNCATED AT 250 WORDS)     

Does the anesthetic method influence the postoperative breathing pattern and gas exchange in hip surgery? A comparison between general and spinal anesthesia

We studied the effects of elective hip surgery, performed under either spinal (SA, n = 10) or general anesthesia (GA, n = 10), on breathing pattern and gas exchange. Measurements were made with respiratory inductive plethysmograph and indirect calorimetry in two positions before and after surgery. The method of anesthesia had no effect on the severity of postoperative hypoxemia. Reduced arterial oxygenation (PaO2; P less than 0.001, SA from 12.5 +/- 2.37 kPa to 10.5 +/- 1.38 kPa, GA from 12.5 +/- 2.95 kPa to 10.5 +/- 1.75 kPa) despite increased alveolar ventilation (P less than 0.01; from 2.30 +/- 0.37 l/min to 2.39 +/- 0.43 l/min in SA, 2.27 +/- 0.56 l/min to 2.57 +/- 0.35 l/min in GA) and reduced arterial carbon dioxide partial pressure (PaCO2; SA from 5.20 +/- 0.22 kPa to 4.95 +/- 0.33 kPa, P less than 0.01, GA from 5.07 +/- 0.36 kPa to 4.72 +/- 0.41 kPa, P less than 0.05) indicated maldistribution of ventilation and perfusion. Changes in breathing pattern and gas exchange and differences between the groups were minimal. Minute ventilation, tidal volume and mean inspiratory flow remained unchanged in both groups. The contribution of rib cage to tidal volume increased postoperatively in the supine position (P less than 0.001; SA from 32.6% +/- 10.3 to 46.3% +/- 7.5, GA from 36.5 +/- 16.4 to 48.5% +/- 15.4). CO2 production, oxygen consumption and energy expenditure remained unchanged. The postoperative changes in breathing pattern are related to the operation, not to the type of anesthesia and do not explain the alterations in gas exchange.     

Ventilatory response to CO2 following intravenous ketamine in children

The effects of intravenous ketamine (bolus of 2 mg.kg-1 followed by a continuous infusion at a rate of 40 micrograms.kg-1.min-1) on ventilatory response to carbon dioxide were studied in nine children ranging in age from 6 to 10 yr and in weight from 20 to 48 kg. Ketamine did not affect resting respiratory rate, tidal volume, end-tidal CO2 tension (PETCO2), or minute ventilation. Five minutes after the ketamine bolus, the slope VE/PETCO2 decreased significantly (P less than 0.05) from 1.71 +/- 0.47 to 1.05 +/- 0.23 1.min-1.mmHg-1 (mean +/- SD). After 30 min of continuous iv ketamine infusion, the slope returned to 1.65 +/- 0.44 1.min-1.mmHg-1, a significantly higher value (P less than 0.05) compared with the nadir and not significantly different from control. The minute ventilation at a PETCO2 of 60 mmHg decreased from 824 +/- 98 to 626 +/- 26 ml.kg-1.min-1 5 min after iv ketamine, and remained depressed (640 +/- 125 ml.kg-1.min-1 P less than 0.05) throughout the 30-min ketamine infusion. In addition, the slope VT/PETCO2 and the VT 60 did not change during the study; nonetheless, the slope f/PETCO2 and the f 60 decreased significantly following iv bolus ketamine, and the f 60 remained significantly decreased following ketamine infusion. The authors conclude that clinically useful doses of iv ketamine significantly alter ventilatory control in children.     

Ventilatory consequences of the lateral position and thoracotomy in children

Functional residual capacity (FRC), breath-by-breath compliance of the respiratory system (Crs) and arterial oxygen tension (PaO2) were measured in ten children, two months to nine years of age, during anaesthesia for surgical correction of patent ductus arteriosus or coarctation of the aorta. The children were mechanically ventilated with halothane, nitrous oxide and oxygen. FIO2 was kept constant in each child. After induction of anaesthesia, FRC was 17 +/- 7 ml X kg-1 (mean +/- 1 SD), corresponding to 60 +/- 22 per cent of a predicted awake value. FRC increased to 21 +/- 8 ml X kg-1 (p = 0.0005) when the child was turned to its right side and decreased to 13 +/- 5 ml X kg-1 (p = 0.0003) when the pleura was opened. No significant change in Crs or PaO2 occurred during these manoeuvres. Retraction of the upper lung to visualize the great vessels caused a significant decrease in FRC, Crs, and PaO2. The lowest PaO2 observed during this stage was 70.0 mmHg. After surgery FRC and PaO2 were about the same as before surgery while Crs had decreased from 0.87 +/- 0.18 preoperatively to 0.64 +/- 0.15 ml X cmH2O-1 X kg-1 (p = 0.0069). This study shows that FRC increases when mechanically ventilated children are placed in the lateral position, and that thoracotomy is associated with marked changes in FRC, Crs and PaO2.     

End-tidal CO2 monitoring in mitral stenosis patients undergoing closed mitral commissurotomy

Arterial to end-tidal carbon dioxide difference (P(a-E')CO2) was recorded in 20 mitral stenosis patients (group A) for closed mitral commissurotomy and 20 healthy individuals (group B) for elective limb surgery. Mitral stenosis patients showed a greater difference than group B patients. Repeated measurements of P(a-E')CO2 in mitral stenosis patients at various stages of closed mitral commissurotomy not only showed a mean increase from before thoracotomy but there was also no correlation between P(a-E')CO2 before thoracotomy with that after thoracotomy, after commissurotomy or after chest closure. This indicated that end-tidal CO2 monitoring was unsuitable to measure adequacy of ventilation during closed mitral commissurotomy.     

Ventilatory response to CO2 following intravenous and epidural lidocaine

The authors determined the effects of intravenous infusion and epidural administration of lidocaine on the control of ventilation in two groups of eight healthy unpremedicated subjects. In the intravenous group, an injection of 1.5 mg/kg lidocaine was followed by an infusion at a rate of 60 micrograms X kg-1 X min-1 for 30 min. The slope of the ventilatory response to CO2 was significantly increased (P less than 0.05) from its control value (2.65 +/- 1.22 1 X min-1 X mmHg-1 [mean +/- SD]) at the end of the infusion (58%), while plasma lidocaine level was at 3.14 +/- 0.82 microgram/ml. The correlation between individual plasma lidocaine levels and the changes in the slope of the ventilatory response to CO2 was significant (r = 0.58, n = 24, P less than 0.01). In the epidural group, after the administration of 5 mg/kg of lidocaine, the slope of the ventilatory response to CO2 increased significantly (P less than 0.05) from its control value (1.52 +/- 0.75 1 X min-1 X mmHg-1) at 15 (+22%) and 25 min (+42%), while plasma lidocaine levels were at 1.79 +/- 0.42 and 2.22 +/- 0.47 microgram/ml, respectively. In both groups, resting minute ventilation and end-tidal CO2 values remained unchanged. These results suggest that epidural lidocaine has a stimulating effect on the ventilatory control mechanisms that results from the systemic effect of the drug.     

Lung mechanics during upper abdominal surgery

Functional residual capacity (FRC) and breath-by-breath compliance of the respiratory system (Crs) were studied after induction of anaesthesia, after insertion of retractors and after wound closure in patients undergoing upper abdominal surgery via a subcostal (n = 8) or a midline (n = 8) incision. After anaesthesia induction the mean FRC was 1.6 +/- 0.3 l. In the subcostal incision group FRC did not change between the studied stages, but Crs fell after retractor placement from 51 +/- 3 to 43 +/- 5 ml/cmH2O (p less than 0.01). In the midline incision group FRC rose by 21% (p less than 0.01) when the retractors were inserted, but regained outset level after wound closure. Crs in this group did not change significantly after retraction, but after closure of the wound it fell to 44 +/- 6 ml/cmH2O, i.e. less (p less than 0.05) than the outset value (52.6 ml/cmH2O). FRC thus did not decrease in either group, but Crs fell by about 15%. The authors conclude that the known difference in postoperative pulmonary complications between midline vs. subcostal incisions is not caused by the studied intraoperative events.     

Pharmacokinetics and pharmacodynamics of vecuronium (ORG NC 45) in patients with cirrhosis

To evaluate the effect of liver cirrhosis on the pharmacokinetics and the pharmacodynamics of vecuronium, 12 patients with cirrhosis, aged (mean +/- SD) 52 +/- 12 yr, and 14 control patients, 42 +/- 15 yr, undergoing elective surgery under general anesthesia were studied. The simultaneous time courses of the plasma concentration of vecuronium and of the neuromuscular blockade were studied after the administration of a bolus dose of 0.2 mg X kg-1. Vecuronium plasma concentration declined biexponentially in both groups. Vecuronium plasma clearance was reduced significantly (P less than 0.01) from 4.26 +/- 1.38 ml X min-1 X kg-1 in the controls to 2.73 +/- 1.19 ml X min-1 X kg-1 in the patients with cirrhosis. The elimination half-life was 58 +/- 19 min in the controls and was prolonged significantly to 84 +/- 23 min (P less than 0.01) in the patients with cirrhosis. The total apparent volume of distribution was unchanged in patients with cirrhosis (0.253 +/- 0.086 1 X kg-1 vs. 0.246 +/- 0.092 1 X kg-1 in the controls). Cirrhosis caused a prolongation of the neuromuscular blockade induced by vecuronium: the duration of effect from injection to 50% recovery of the twitch height was prolonged by 100% (P less than 0.01) from 62 +/- 16 min in the controls to 130 +/- 52 min in patients with cirrhosis. The recovery rate (TH 25-75) also was prolonged (P less than 0.05) from 21 +/- 7 min in the controls to 44 +/- 18 min in patients with cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Respiratory and sleep patterns during nocturnal infusions of branched chain amino acids

In the awake, normal subject, infusions of branched chain amino acids (BCAA) alter the ventilatory response to CO2. If this effect extends to the sleep state, it could contribute to our understanding of the neurophysiology of the sleep state as well as having clinical utility in ameliorating or preventing apnea syndromes. This study examined the effect of nocturnal BCAA infusion on sleep patterns (as measured by EEG, chest wall motion, Sao2 and end-tidal CO2) in five normal male subjects. Subjects were monitored with a polysomnograph from 21.00 to 7.00. Each subject was studied double-blind in random order on three occasions: a) baseline, no infusion (B); b) control, with normal saline infusion (S); and c) treatment, infusion of BCAA (BCAA). Sleep pattern analysis did not demonstrate any measurable effect of the BCAA infusion. End-tidal CO2 levels during BCAA infusion were lower than during baseline or control nights (mean +/- s.d.; BCAA: 5.8 +/- 0.7 kPa vs. B: 6.9 +/- 0.1 kPa, P less than 0.01 and S: 6.7 +/- 0.4 kPa, P less than 0.05). This study demonstrates that nocturnal BCAA infusions have effects on respiratory control during sleep; further clinical studies are required to determine whether these data have implications for disease states.     

Cerebral blood flow velocity and carbon dioxide vasoreactivity during gamma-hydroxybutyrate/fentanyl anaesthesia in non-neurosurgical patients

In this study the effects of gamma-hydroxybutyrate/fentanyl on cerebral blood flow velocity (CBFV) (as measured in the middle cerebral artery by transcranial Doppler ultrasonography) and on cerebrovascular carbon dioxide reactivity were investigated. Mean CBFV (Vmean) and haemodynamic responses were recorded in 12 non-neurosurgical patients before, during and after induction of general anaesthesia with gamma-hydroxybutyrate (GHB) (20 min constant rate infusion of 100 mg kg-1). Two patients were excluded, one because of bradycardia and the other because of severe myoclonia. During the infusion of GHB, normocapnia was maintained by manually assisting ventilation as necessary. The infusion of GHB did not affect Vmean [awake: 57 +/- 12 cm s-1 (mean +/- SD); 22.5 min: 62 +/- 15 cm s-1, NS difference] or mean arterial blood pressure (MAP) (awake: 97 +/- 12 mmHg; 22.5 min: 89 +/- 10 mmHg, NS). This suggests that cerebral blood flow velocity is unaltered by an anaesthetic dose of GHB. Twenty-five minutes after the start of GHB, fentanyl 3 micrograms kg-1 and vecuronium 0.1 mg kg-1 were given, the trachea was intubated and the lungs were mechanically ventilated to maintain end-tidal PCO2 of 4.6 +/- 0.4 kPa (30 min). At 30 min after the start of the GHB infusion, Vmean and MAP decreased to 38 +/- 10 cm s-1 and 76 +/- 12 mmHg (both P < 0.05 vs 22.5 min) respectively. After adjusting the ventilation to achieve hypocapnia (40 min: end-tidal PCO2 3.5 +/- 0.2 mmHg), Vmean decreased to 29 +/- 7 cm s-1, while MAP did not change. This allowed the relative vasoreactivity (percentage change in Vmean/0.133 kPa change in the end-tidal PCO2 from normocapnia to hypocapnia) to be estimated as 2.7 +/- 1.6% 0.133 kPa-1. This suggests that cerebrovascular response to CO2 during gamma-hydroxybutyrate/fentanyl anaesthesia is maintained.     

Flumazenil antagonism of midazolam-induced ventilatory depression

Flumazenil, a benzodiazepine antagonist, reliably reverses midazolam-induced sedation; however, its effect on respiratory depression has not been established completely. Twelve healthy volunteers received sufficient midazolam (0.13 +/- 0.01 mg.kg-1 mean +/- SE) to render them unresponsive to verbal command; they then received flumazenil 1.0 mg or placebo (flumazenil vehicle) in a randomized, double-blind fashion. Ventilatory drive was measured before and after administration of midazolam, as well as 3, 30, 60, and 120 min after administration of flumazenil or placebo. Seven to 30 days later, the study was repeated, with subjects receiving placebo or flumazenil (whichever they had not received during their first trial). Midazolam caused significant decreases in the slope of the CO2 response (-29 +/- 5%; P less than 0.005); minute ventilation (VE) at end-tidal CO2 tension (PETCO2) = 46 mmHg (-28 +/- 4%; P less than 0.001), and tidal volume at PETCO2 = 46 mmHg (-44 +/- 4%; P less than 0.005). Three minutes after intravenous administration of flumazenil 1.0 mg, VE46 and tidal volume increased to 108 +/- 6% and 105 +/- 6%, respectively, of their premidazolam values; at the same time after administration of placebo, VE46 and tidal volume remained significantly depressed (between groups, P less than 0.005 for each variable). Thirty minutes later, these variables did not differ between groups, probably because the effects of flumazenil and midazolam were diminishing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of positive end-expiratory pressure on extravascular lung water during the formation of experimental hydrostatic pulmonary oedema

The influence of positive end-expiratory pressure (PEEP) on extravascular lung water measured with the double-indicator dilution technique (EVLWi) has been studied during formation of hydrostatic pulmonary oedema in a canine model. The oedema was created by elevating the mean pulmonary artery pressure (PAP) to 30 mmHg (4.0 kPa) by inflation of a left atrial balloon, and a simultaneous intravenous saline infusion of 15 ml.kg-1.h-1. All dogs were ventilated with zero end-expiratory pressure (ZEEP) until the initial EVLWi had increased by 50%. In one group (n = 5) a PEEP of 10 cmH2O (1.0 kPa) was applied and the dogs were studied for a further 4 h and in the other group (n = 5) ZEEP was maintained throughout the study. During the first 2 h after ZEEP/PEEP application EVLWi increased from 13.7 +/- 2.1 to 20.2 +/- 1.2 ml.kg-1 with ZEEP ventilation and from 13.6 +/- 1.2 to 18.6 +/- 1.9 ml.kg-1 with PEEP ventilation. EVLWi remained unchanged during the last 2 h in both groups. The gas exchange improved with PEEP, arterial oxygen tension increased from 30.4 +/- 8.9 kPa to 38.6 +/- 2.5 kPa (P less than 0.01), and the shunt fraction decreased from 6.0 +/- 3.8% to 1.2 +/- 0.8% (P less than 0.001). There were significant differences (P less than 0.01) in both PaO2 and shunt fraction between the ZEEP and PEEP groups throughout the study. In conclusion, positive end-expiratory pressure improves gas exchange but does not protect against increasing extravascular lung water during the creation of hydrostatic pulmonary oedema.     

Epidural morphine in children: pharmacokinetics and CO2 sensitivity

The effects of epidural morphine (50 micrograms X kg-1) after abdominal and urologic surgery were studied in 20 children ranging in age from 2 to 15 yr and weighing between 9 and 54 kg. The onset and the duration of analgesia were 30 +/- 12 min and 19.5 +/- 8 h, respectively (mean +/- SD). Side effects were pruritus (4/20), nausea and vomiting (8/20), and urinary retention (4/14). No apnea was observed. Ventilation control was studied in seven children. No significant change in resting respiratory variables occurred after both surgery and epidural morphine injection. However, the slope of the ventilatory response to CO2 was significantly (P less than 0.05) decreased after surgery but before morphine, as compared with its preoperative control value (0.84 +/- 0.44 versus 1.51 +/- 0.72 l X min-1 X mmHg-1), and remained low for 22 h after epidural morphine (0.90 +/- 0.57 l X min-1 X mmHg-1). Sixty minutes after morphine injection, the plasma morphine concentration was always less than 12 ng X ml-1 in the seven children studied. Pharmacokinetic parameters were similar to those observed after epidural injection of morphine in adults, except for a shorter terminal half-life (73.8 +/- 41.6 min) attributed to a greater total body clearance of morphine in the children (28.3 +/- 3.4 ml X min-1 X kg-1). It is concluded that epidural morphine provides effective and prolonged analgesia in children after abdominal and urologic surgery and that it is associated with prolonged respiratory depression that requires close monitoring for at least 24 h.     

Comparison of the pharmacokinetics of etomidate in children and in adults

Etomidate pharmacokinetics were compared in 12 children (P group) (age 7 to 13 years, weight 22 to 48 kg) and in 4 adult women (A group) (age 28 to 52 years, weight 46 to 72 kg), A.S.A. 1, undergoing minor non abdominal surgery. They were unpremedicated and anaesthetized with alfentanil 100 micrograms.kg-1, and isoflurane 2 vol % in N2O/O2 (1/1). Etomidate was administered as a bolus: 0.3 mg.kg-1 in adults and 0.4 mg.kg-1 in children. Venous plasma samples were frozen until further etomidate assay with a HPLC technique. In all patients but two children, data were fitted to a three rather than a two compartment model. Differences between groups (mean +/- SD values) included Vdc (P: 0.66 +/- 0.31 l.kg-1; A: 0.27 +/- 0.15 l.kg-1; p less than 0.01), t1/2 pi (P: 5.4 +/- 2.9 min; A: 2.7 +/- 5.7 min; p less than 0.05) and plasma clearance (P: 17.2 +/- 4.6 ml.kg-1.min-1; A: 10.9 +/- 3.3 ml.kg-1.min-1; p less than 0.05). No statistical difference was found between A and P groups for the following parameters: t1/2 alpha (37.1 +/- 12.0 min vs 26.8 + 15.1 min), t1/2 beta (260 +/- 99 min vs 175 +/- 99 min), Vdss (2.5 +/- 1.11.kg-1 vs 2.8 +/- 1.61.kg-1), Vd beta (4.1 +/- 2.41.kg-1 vs 4.0 +/- 2.21.kg-1), and MRT (228 +/- 80 min vs 172 +/- 101 min). No age-related difference was found inside P group with regard to pharmacokinetic parameters. In conclusion, a 30% higher etomidate bolus dosage is required in children than in adults to achieve similar plasma concentrations, due to a higher volume of the initial compartment. In comparison to adults the higher clearance suggests higher maintenance dose requirements in children.     

Pulmonary effects of body position, PEEP, and surfactant depletion in dogs

The influence of position (sphinx, lateral, supine), surfactant depletion, and different positive end-expiratory pressure (PEEP) on functional residual capacity (FRC), series dead space (VdS) and compliance of the respiratory system (Crs) were evaluated in five dogs. Ventilation homogeneity as measured by an index (multiple breath alveolar mixing efficiency), oxygenation, and cardiovascular hemodynamics were additionally examined. The dogs were anesthetized with halothane, paralyzed, and mechanically ventilated. FRC and VdS were found to be notably large in dogs, 45 +/- 8 ml/kg and 6 +/- 1 ml/kg, respectively. FRC and ventilation homogeneity were improved in the sphinx position (prone position with upright head). Surfactant depletion by lung lavage with 37 degrees C saline caused an immediate and stable decrease in FRC, Crs, and oxygenation (P less than 0.05, respectively) for about 5 h without marked effects on the circulatory system. FRC and VdS increased with increasing PEEP. At the highest PEEP, 10 cmH2O (1 kPa), Crs decreased (P less than 0.05) and ventilation became more uneven, indicating alveolar overdistension.     

Comparison of glucose counterregulation during short-term and prolonged hypoglycemia in normal humans

To compare glucose counterregulatory mechanisms during short-term hypoglycemia and prolonged hypoglycemia, insulin was infused either intravenously (160 mU X M-2 X min) for 10 min or subcutaneously (15 mU X M-2 X min) for 12 h in normal volunteers. With each type of insulin infusion, hypoglycemia (approximately 50 mg/dl) was either allowed to develop or was prevented (control experiments) by the glucose-clamp technique. During prolonged hypoglycemia, both increased glucose production (1.55 +/- 0.05 versus 0.33 +/- 0.14 mg X kg-1 X min in control experiments at 12 h, P less than 0.01) and suppressed glucose utilization (1.55 +/- 0.06 versus 3.17 +/- 0.15 mg X kg-1 X min in control studies at 12 h, P less than 0.01) were involved in counterregulation. During short-term hypoglycemia, only increased glucose production (3.23 +/- 0.33 versus 0.06 +/- 0.03 mg X kg-1 X min in control experiments at 60 min) was involved, since glucose clearance actually increased (3.99 +/- 0.20 versus 2.88 +/- 0.02 ml X kg-1 X min in control experiments at 60 min, P less than 0.01). Estimated portal venous insulin concentrations decreased 40% (basal 24 +/- 3 versus 14 +/- 1 mU/ml at 60 min, P less than 0.01) in the short-term hypoglycemia experiments but remained at basal levels (basal 25 +/- 1 versus approximately 26 microU/min between 1 and 12 h) during prolonged hypoglycemia. Despite the fact that hypoglycemia was more gradually induced in the prolonged hypoglycemia model, peak counterregulatory hormone responses were at least as great as those during short-term hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intraoperative heart rate reduction - alinidine versus metoprolol

In a double-blind randomized protocol the effectiveness of the specific bradycardic agent alinidine (0.6 mg.kg-1 i.v.) was compared to that of the betablocker metoprolol (0.035 mg.kg-1 i.v.). Twenty-four coronary artery disease patients undergoing a bypass procedure with an intraoperative heart rate increase of more than 20% were included. Patients with a concomitant intraoperative mean arterial pressure increase of more than 30% or with an intraoperative wedge pressure higher than 15 mmHg (2.0 kPa) were excluded. After application of alinidine and metoprolol, heart rate decreased significantly (P less than 0.01) in the alinidine group from 88 +/- 19 beats per min to 72 +/- 13 and in the metoprolol group from 82 +/- 16 to 72 +/- 12. Baseline values were not obtained. Compared to the hemodynamic changes in the metoprolol group, the alterations of pulmonary capillary wedge pressure (PCWP) (P less than 0.05), stroke volume index (SVI) (P less than 0.05), left ventricular stroke work index (LVSWI) (P less than 0.01) and right ventricular stroke work index (RVSWI) (P less than 0.05) in the alinidine group were statistically significantly different. PCWP remained unchanged after alinidine and increased in the metoprolol group (1.4 +/- 0.4 to 1.6 +/- 0.4 kPa). In the alinidine group LVSWI (43.1 +/- 15 to 49.2 +/- 18 g-m.m-2), RVSWI (5.1 +/- 4 to 6.6 +/- 3 g-m.m-2) and SVI (37.2 +/- 12.2 to 42.5 +/- 12.8 ml.m-2) increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pressure-controlled inverse ratio ventilation after cardiac surgery.

BACKGROUND AND OBJECTIVE: Pressure-controlled inverse ratio ventilation was compared with controlled mechanical ventilation in patients after cardiac surgery. METHODS: Ten patients were ventilated after sternal closure using a Siemens Servo 900C ventilator to a target end-tidal PCO2 of 4.0 kPa. They were randomized to receive controlled mechanical ventilation or pressure-controlled inverse ratio ventilation. CO2-based data were recorded on a laptop personal computer, which together with arterial PCO2 permitted measurement of the respiratory dead space. Once measurements were complete the ventilator was switched to the other mode and new measurements taken. RESULTS: PaCO2 and VCO2 were virtually the same in both modes. Peak airway pressure (17.2 +/- 2.7 vs. 20.8 +/- 2.5 cmH2O, P < 0.01) and minute ventilation (4.9 +/- 1.1 vs. 5.3 +/- 1.1 cmH2O, P < 0.01) were less during pressure-controlled inverse ratio ventilation. Physiological dead space fraction (0.39 +/- 0.06 vs. 0.51 +/- 0.05, P < 0.001), airway dead space (56 +/- 15 vs. 81 +/- 15 mL, P < 0.001) and alveolar dead space fraction (0.25 +/- 0.07 vs. 0.31 +/- 0.09, P < 0.01) were all less during pressure-controlled inverse ratio ventilation. There were no differences in heart rate or mean arterial pressure. CONCLUSIONS: The prolonged inspiratory period and pressure-controlled flow pattern of pressure-controlled inverse ratio ventilation reduce the alveolar and airway dead spaces, and give lower peak airway pressures, compared with conventional ventilation, in cardiac surgical patients.     

Variation in arterial to end-tidal CO2 tension differences during anesthesia in the "kidney rest" lateral decubitus position.

The course of arterial to end-tidal carbon dioxide tension difference [P(a-ET)CO2] was evaluated during general anesthesia in 25 patients scheduled for renal surgery performed in the "kidney position." The difference between arterial PCO2 (PaCO2) corrected to body temperature, and end-tidal PCO2 (PETCO2) measured by mass spectrometry was assessed after induction of anesthesia, after placement in the lateral decubitus position with back arched over a kidney bridge ("kidney position"), and every 20 min until the patients were replaced in the supine position at the end of the surgical procedure. Heart rate, arterial blood pressure, and esophageal temperature were simultaneously recorded. After induction of anesthesia, when the patients were lying supine (T1), P(a-ET)CO2 was 4.8 +/- 3.9 mm Hg (mean +/- SD). Placing the patients in the kidney position (T2) induced a significant increase in P(a-ET)CO2 (to 7.9 +/- 3.5 mm Hg; P less than 0.01). These alterations occurred without any significant change in mean arterial blood pressure or heart rate. A progressive increase in mean P(a-ET)CO2 occurred with maintenance of anesthesia; P(a-ET)CO2 reached 8.8 +/- 4.1 mm Hg (P less than 0.05 vs T2) and 8.9 +/- 4.4 mm Hg (P less than 0.05 vs T2) at 65 and 85 min, respectively, after lateral decubitus positioning. Large variations between and within patients were observed. Although stable mean arterial pressure was maintained, these changes were associated with a significant decrease in body temperature. These results demonstrate that P(a-ET)CO2 increases when patients are placed in the kidney position and may vary with the prolongation of anesthesia in this situation.(ABSTRACT TRUNCATED AT 250 WORDS)