Arterial to end-tidal carbon dioxide tensio difference during laparoscopy Magnitude and effect of anaesthetic technique

The relationship between arterial carbon dioxide tension and end-tidal carbon dioxide tension was studied in 25 patients during laparoscopy. Thirteen patients received general anaesthesia and 12 epidural anaesthesia. The overall mean difference between arterial and end-tidal carbon dioxide tensions was 0.44 kPa (95% confidence intervals 0.28-0.60 kPa) which was significantly less than that reported in studies during other procedures. The reasons for this difference are probably associated with the physiological changes induced by CO2 pneumoperitoneum and steep Trendelenburg positioning. The choice of anaesthetic technique did not affect the arterial to end-tidal carbon dioxide tension difference significantly (p greater than 0.9).     

Arterial to end-tidal carbon dioxide tension difference during anaesthesia for tubal ligation

Twenty-nine patients scheduled for postnatal tubal ligation by minilaparotomy under general anaesthesia were studied. Arterial and end-tidal carbon dioxide tensions were determined during anaesthesia. The mean arterial to end-tidal carbon dioxide tension difference was 0.08 kPa (SEM 0.05). Thirty-one percent of the patients had negative values. These results were similar to those observed during Caesarean section. The physiological changes responsible for reduced arterial to end-tidal carbon dioxide values, persist into the postnatal period. It is predicted from the regression analysis of the time between delivery and anaesthesia for tubal ligation and arterial to end-tidal CO2 difference, that the values might return to normal nonpregnant levels by 8 days following delivery.     

Single breath end-tidal Pco2, measurement during high frequency jet ventilation in critical care patients

The relationship between arterial and end-tidal carbon dioxide tensions following a single large breath was investigated in seven critically ill patients receiving high frequency jet ventilation. There was a close correlation (r = 0.989) between arterial and end-tidal carbon dioxide tensions over a wide range (3.29-8.95 kPa). Measurement of the end-tidal carbon dioxide tension following a single large breath may be useful in monitoring the efficiency of high frequency jet ventilation in the elimination of carbon dioxide.     

End-tidal carbon dioxide as an indicator of arterial carbon dioxide in neurointensive care patients

The relationship between the arterial partial pressure of carbon dioxide (Paco2) and the end-tidal carbon dioxide partial pressure (PEtco2) was evaluated in 11 critically ill adult neurointensive care patients during mechanical ventilation. It was hypothesized that the Paco2 to PEtco2 gradient, or P(a-Et)co2, was maintained and that PEtco2 can be used to determine Paco2 accurately in these patients. After approval by the Clinical Investigations Committee, when clinically indicated arterial blood gases (with Paco2) were measured, the PEtco2 was determined from the capnograph (Hewlett Packard 78520A infrared capnometer). The P(a-Et)co2 was evaluated for possible effects from changes in the other monitored hemodynamic and respiratory parameters. Linear regression analysis was used to determine the significance of the relationship between Paco2 and PEtco2 and other assessed variables. Student's t tests were used where applicable. A p value 相似文献   

The effect of increased apparatus dead space and tidal volumes on carbon dioxide elimination and oxygen saturations in a low-flow anesthesia system

STUDY OBJECTIVE: To determine if a large tidal volume (VT), with an unchanged end-tidal carbon dioxide partial pressure (PETco2), could improve arterial carbon dioxide elimination, oxygen saturation (Spo2), and arterial blood oxygenation. DESIGN: Prospective, randomized, clinical study. SETTING: Single university hospital. PATIENTS: 60 ASA physical status I and II patients scheduled for elective urologic or general surgery. INTERVENTIONS: Patients were randomly assigned to one of two treatments: patients in group 1, nondead space (NDS), received a fresh gas flow of 1 L/min without added apparatus dead space volume. Patients in group 2, dead space (DS), received ventilation using an added dead space volume between the Y-piece and tracheal tube. In both groups, patients' lungs were ventilated to a fixed PETco2 value of 33.8 mmHg. Patients in the DS group were ventilated with VTs to maintain an airway plateau pressure (Pplateau) of 0.04 cm H2O/kg over initial plateau pressure. The corrugated tube was then adjusted to maintain a fixed PETco2. MEASUREMENTS: Dead space volumes, PETco2, arterial CO2 tension (Paco2), SpO2, arterial O2 tension (Pao2), VTs, and airway pressures were measured. MAIN RESULTS: Arterial CO2 tension was significantly lower in the DS group, 36 +/- 2.3 mmHg, compared with the NDS group, 37.5 +/- 2.3 mmHg (P < 0.05), and the difference between PETco2 and Paco2 was lower in the DS group than in the NDS group (P < 0.001). Oxygen saturation was 99% +/- 1.0% in the DS group compared with 98.5% +/- 1.5% in the NDS group (P < 0.05). Arterial O2 tension was 13.2 +/- 25.5 mmHg in the DS group and 119.1 +/- 30.2 mmHg in NDS group (not significant). CONCLUSION: Larger VTs, with an unchanged PETCO2 concentration created by an added apparatus dead space volume, improved arterial carbon dioxide elimination.     

Arterial to end-tidal carbon dioxide tension difference during anaesthesia in early pregnancy

Sixteen patients requiring general anaesthesia for termination of pregnancy by dilatation and evacuation of the uterus were studied. Arterial and end-tidal carbon dioxide tensions were determined during anaesthesia. The mean arterial to end-tidal carbon dioxide tension difference was 0.07 kPa (-0.02-0.16, 5-95 per cent confidence limits). These results were similar to those observed during Caesarean section and those during anaesthesia for post-delivery tubal ligations. The physiological changes such as increased cardiac output, haemodilution, and increased blood volume which manifest by 12 weeks of gestation probably result in a reduced (a-E')PCO2 value.     

Arterial to end-tidal carbon dioxide tension difference in children under halothane anaesthesia

Using blood gas determinations and capnography, the relationship between arterial and end-tidal PCO₂ was investigated in 20 children under halothane anaesthesia with spontaneous respiration. A median arterial to end-tidal carbon dioxide tension difference of 0.66 kPa (5 mm Hg) was found. There was a close correlation between Pa_co2 and the magnitude of the carbon dioxide difference. Our findings may largely be explained by an increase in Vd/Vt (presumably mainly due to a reduction of Vt) causing admixture of dead space air throughout expiration. It is concluded that though end-tidal carbon dioxide does not exactly reflect Pa_co2 capnography may be of value as a monitor of respiration in paediatric anaesthesia at normal or near-normal values of end-tidal carbon dioxide.     

Comparison of the analgesic efficacy and respiratory effects of morphine, tramadol and codeine after craniotomy

Pain after craniotomy remains a significant problem. The effect of morphine and tramadol patient-controlled analgesia (PCA) on arterial carbon dioxide tension is unknown in patients having such surgery. Sixty craniotomy patients were randomly allocated to receive morphine PCA, tramadol PCA or codeine phosphate 60 mg intramuscularly. Baseline values of pain score (0-10), sedation and arterial carbon dioxide tension were recorded at the time of first analgesic administration and at 30 min, 1, 4, 8, 12, 18 and 24 h. Patient satisfaction was assessed at 24 h. There were no differences in arterial carbon dioxide tension or sedation between groups at any time, but in all three groups some patients had rises greater than 1 kPa. Morphine produced significantly better analgesia than tramadol at all time points (p < 0.005) and better analgesia than codeine at 4, 12 and 18 h. Patients were more satisfied with morphine than with codeine or tramadol (p < 0.001). Vomiting and retching occurred in 50% of patients with tramadol, compared with 20% with morphine and 29% with codeine.     

Mechanisms of improvement of respiratory failure in patients with restrictive thoracic disease treated with non-invasive ventilation

BACKGROUND: Nocturnal non-invasive ventilation (NIV) is an effective treatment for hypercapnic respiratory failure in patients with restrictive thoracic disease. We hypothesised that NIV may reverse respiratory failure by increasing the ventilatory response to carbon dioxide, reducing inspiratory muscle fatigue, or enhancing pulmonary mechanics. METHODS: Twenty patients with restrictive disease were studied at baseline (D0) and at 5-8 days (D5) and 3 months (3M). RESULTS: Mean (SD) daytime arterial carbon dioxide tension (Paco(2)) was reduced from 7.1 (0.9) kPa to 6.6 (0.8) kPa at D5 and 6.3 (0.9) kPa at 3M (p = 0.004), with the mean (SD) hypercapnic ventilatory response increasing from 2.8 (2.3) l/min/kPa to 3.6 (2.4) l/min/kPa at D5 and 4.3 (3.3) l/min/kPa at 3M (p = 0.044). No increase was observed in measures of inspiratory muscle strength including twitch transdiaphragmatic pressure, nor in lung function or respiratory system compliance. CONCLUSIONS: These findings suggest that increased ventilatory response to carbon dioxide is the principal mechanism underlying the long term improvement in gas exchange following NIV in patients with restrictive thoracic disease. Increases in respiratory muscle strength (sniff oesophageal pressure and sniff nasal pressure) correlated with reductions in the Epworth sleepiness score, possibly indicating an increase in the ability of patients to activate inspiratory muscles rather than an improvement in contractility.     

Accuracy of end-tidal carbon dioxide monitoring using the NBP-75 microstream capnometer. A study in intubated ventilated and spontaneously breathing nonintubated patients

Arterial carbon dioxide partial pressure measurements using the NBP-75 microstream capnometer were compared with direct PaCO2 values in patients who were (a) not intubated and spontaneously breathing, and (b) patients receiving intermittent positive pressure ventilation of the lungs and endotracheal anaesthesia. Twenty ASA physical status I-III patients, undergoing general anaesthesia for orthopaedic or vascular surgery were included in a prospective crossover study. After a 20-min equilibration period following the induction of general anaesthesia, arterial blood was drawn from an indwelling radial catheter, while the end-tidal carbon dioxide partial pressure was measured at the angle between the tracheal tube and the ventilation circuit using a microstream capnometer (NBP-75, Nellcor Puritan Bennett, Plesanton, CA, USA) with an aspiration flow rate of 30 mL min(-1). Patients were extubated at the end of surgery and transferred to the postanaesthesia care unit, where end-tidal carbon dioxide was sampled through a nasal cannula (Nasal FilterLine, Nellcor, Plesanton, CA, USA) and measured using the same microstream capnometer. In each patient six measurements were performed, three during mechanical ventilation and three during spontaneous breathing. A good correlation between arterial and end-tidal carbon dioxide partial pressure was observed both during mechanical ventilation (r = 0.59; P = 0.0005) and spontaneous breathing (r = 0.41; P = 0.001); while no differences in the arterial to end-tidal carbon dioxide tension difference were observed when patients were intubated and mechanically ventilated (7. 3 +/- 4 mmHg; CI95: 6.3-8.4) compared to values measured during spontaneous breathing in the postanesthesia care unit, after patients had been awakened and extubated (6.5 +/- 4.8 mmHg; CI95: 5. 2-7.8) (P = 0.311). The mean difference between the arterial to end-tidal carbon dioxide tension gradient measured in intubated and non-intubated spontaneously breathing patients was 1 +/- 6 mmHg (CI95: -11-+13). We conclude that measuring the end-tidal carbon dioxide partial pressure through a nasal cannula using the NBP-75 microstream capnometer provides an estimation of arterial carbon dioxide partial pressure similar to that provided when the same patients are intubated and mechanically ventilated.     

Respiratory dead space under anaesthesia in patients with mitral stenosis.

Physiological deadspace (VDphys) and arterial to end-tidal carbon dioxide tension difference [P(a-E)CO2] were calculated under anaesthesia in 27 patients with mitral stenosis planned for close mitral commissurotomy and in 15 healthy individuals for elective non-thoracic surgical procedures. A square wave inspiratory flow pattern and an end-inspiratory pause (25% and 10% of cycle time respectively) were given with a SERVO 900B ventilator used at respiratory rate of approximately 16 per min. An infra-red CO2 analyser was used to measure CO2 production and end-tidal CO2 concentration. Measurements were made prior to the start of the surgery after a minimum of 10 min of stable ventilation to avoid the effect of surgery. Patients with multiple stenosis had significantly higher VDphys (4.28 +/- 1.02 ml kg-1 as compared to 2.10 +/- 0.52 ml kg-1 in controls, P less than 0.001), higher P(a-E)CO2 [0.43 +/- 0.51 kPa as compared to -0.02 +/- 0.23 kPa, P less than 0.01] and lower respiratory system compliance (Crs). Péco2 was positively correlated with PaCO2 in both groups (P less than 0.01). PaO2 was lower in mitral stenosis patients and P(A-a)O2 negatively correlated to Crs (P less than 0.01).     

Effects of protriptyline on sleep related disturbances of breathing in restrictive chest wall disease.

The effects of protriptyline on sleep stage distribution and gas exchange have been assessed in eight patients with nocturnal hypoventilation secondary to restrictive chest wall disease. At a dose of 10-20 mg taken when they retired the total sleeping time was unaltered but the proportion of rapid eye movement (REM) sleep fell from 22% to 12% (p less than 0.05). The total time spent at an arterial oxygen saturation of less than 80% decreased (p less than 0.01) and the magnitude of the fall correlated with the reduction in REM sleep (r = 0.67, p less than 0.05). There was also a reduction in the maximum carbon dioxide tension reached during the night (p less than 0.01). The arterial oxygen tension measured diurnally increased (p less than 0.05) from a median of 8.0 kPa (60 mm Hg) to 9.0 kPa (67.5 mm Hg), but the carbon dioxide tension and base excess were unchanged. Anticholinergic side effects were experienced by most patients but did not limit treatment.     

Effect of propofol and clonidine on cerebral blood flow velocity and carbon dioxide reactivity in the middle cerebral artery

This study was designed to evaluate the effects of propofol alone and propofol-clonidine combination on human middle cerebral artery blood flow velocity (Vmca) and cerebrovascular carbon dioxide (CO2) response by using transcranial Doppler ultrasonography. Mean Vmca in response to changes in arterial partial pressure of CO2 (Paco2) was determined under the following conditions: awake (group 1), propofol anesthesia (group 2), and combined propofol-clonidine anesthesia (group 3). Normocapnic, hypercapnic, and hypocapnic values of heart rate, mean arterial pressure, partial end-tidal CO2 pressure, Paco2, and Vmca were obtained. The mean Vmca in groups 2 and 3 was significantly lower than that in group 1 at each level of Paco2. The calculated Vmca at each level of Paco2 was not different between groups 2 and 3. There was a correlation between Paco2 and Vmca in all groups, but in the anesthetized groups the effect of Paco2 on Vmca was attenuated. The present data demonstrated that clonidine-propofol does not change CO2 reactivity compared with propofol alone, but both anesthetics attenuate cerebral blood flow compared with awake controls.     

Reliability of CO2 measurements from the airway by a pharyngeal catheter in unintubated, spontaneously breathing subjects

Although several short communications have appeared describing attempts to record the concentrations of carbon dioxide (CO₂) from the unintubated airway by a catheter placed in the nose, so far only few reports have documented the reliability of the method. To evaluate the reliability of CO₂ measurements by a catheter in the open, unintubated airway during spontaneous respiration, a 12 CH PVC catheter was forwarded through the nostril to the hypopharynx and connected to a capnograph in nine healthy volunteers. Another capnograph was connected to a tightly fitting face mask and simultaneous CO₂ recordings were attained from the two parts of the airway during normoventilation, hyperventilation and rebreathing. A corresponding blood sample was drawn from the radial artery for blood gas analysis. The configurations of the capnograms recorded from the pharyngeal catheter were similar to those recorded from the face mask. The results were analysed by a multifactor analysis of variance. The carbon dioxide tension ( p CO₂) was significantly influenced by degree of ventilation ( P <0.0001), subject ( P <0.0001), measurement site ( P =0.030) and interaction subject-ventilation ( P =0.015). In spite of the significant influence of the measurement site, the difference between end tidal carbon dioxide tension ( P CO₂(ET)) and carbon dioxide tension in arterial blood ( P CO₂(a)) was small. The mean differences between paired measurements ( p CO₂(ET)- p CO₂(a)) were -0.10 kPa±0.41 kPa (mean±SD) for the catheter and -0.20 kPa ±0.43 kPa for the face mask. The study demonstrates that reliable recordings of CO₂ concentrations during spontaneous respiration can be obtained by a thin catheter positioned in the hypopharynx.     

Ketamine infusion versus isoflurane for the maintenance of anesthesia in the prebypass period in children with tetralogy of Fallot

OBJECTIVE: To evaluate the use of ketamine in comparison with isoflurane in the maintenance of anesthesia in children with tetralogy of Fallot. DESIGN: Prospective, randomized study. SETTING: University hospital. PARTICIPANTS: Fifty children scheduled for correction of tetralogy of Fallot. INTERVENTIONS: After intubation, patients were assigned randomly to receive 2 different anesthesia maintenance regimens: group I, isoflurane, 0 to 1% plus fentanyl, 0.1 microg/kg/min; group II, ketamine, 0 to 5 mg/kg/h, plus fentanyl, 0.1 microg/kg/min. Isoflurane concentration and ketamine infusion rate were adjusted to maintain arterial pressure within 25% of baseline. Hemodynamic and respiratory parameters were recorded at the end of 4 intervals: T0, before induction of anesthesia; T1, induction to 10 minutes postintubation; T2, 10 minutes postintubation to poststernotomy; and T3, poststernotomy to completion of catheterizations. MEASUREMENTS AND MAIN RESULTS: In comparing group I with group II, significant differences were observed in mean arterial pressure (p < 0.0001), heart rate (p < 0.01), arterial oxygen saturation (p < 0.0001), arterial oxygen tension (p < 0.001), arterial carbon dioxide tension (p < 0.001), arterial pH (p < 0.0001), base excess (p < 0.05), and arterial to end-tidal carbon dioxide tension difference (p < 0.01) at T3. CONCLUSION: The use of ketamine anesthesia is recommended as an alternative maintenance regimen in children undergoing definitive correction of tetralogy of Fallot.     

A model of the ventilatory depressant potency of remifentanil in the non-steady state

BACKGROUND: The C50 of remifentanil for ventilatory depression has been previously determined using inspired carbon dioxide and stimulated ventilation, which may not describe the clinically relevant situation in which ventilatory depression occurs in the absence of inspired carbon dioxide. The authors applied indirect effect modeling to non-steady state Paco2 data in the absence of inspired carbon dioxide during and after administration of remifentanil. METHODS: Ten volunteers underwent determination of carbon dioxide responsiveness using a rebreathing design, and a model was fit to the end-expiratory carbon dioxide and minute ventilation. Afterwards, the volunteers received remifentanil in a stepwise ascending pattern using a computer-controlled infusion pump until significant ventilatory depression occurred (end-tidal carbon dioxide [Peco2] > 65 mmHg and/or imminent apnea). Thereafter, the concentration was reduced to 1 ng/ml. Remifentanil pharmacokinetics and Paco2 were determined from frequent arterial blood samples. An indirect response model was used to describe the Paco2 time course as a function of remifentanil concentration. RESULTS: The time course of hypercarbia after administration of remifentanil was well described by the following pharmacodynamic parameters: F (gain of the carbon dioxide response), 4.30; ke0 carbon dioxide, 0.92 min-1; baseline Paco2, 42.4 mmHg; baseline minute ventilation, 7.06 l/min; kel,CO2, 0.08 min-1; C50 for ventilatory depression, 0.92 ng/ml; Hill coefficient, 1.25. CONCLUSION: Remifentanil is a potent ventilatory depressant. Simulations demonstrated that remifentanil concentrations well tolerated in the steady state will cause a clinically significant hypoventilation following bolus administration, confirming the acute risk of bolus administration of fast-acting opioids in spontaneously breathing patients.     

Hypercapnia Improves Tissue Oxygenation

Background: Wound infections are common, serious, surgical complications. Oxidative killing by neutrophils is the primary defense against surgical pathogens and increasing intraoperative tissue oxygen tension markedly reduces the risk of such infections. Since hypercapnia improves cardiac output and peripheral tissue perfusion, we tested the hypothesis that peripheral tissue oxygenation increases as a function of arterial carbon dioxide tension (Paco2) in anesthetized humans.

Methods: General anesthesia was induced with propofol and maintained with sevoflurane in 30% oxygen in 10 healthy volunteers. Subcutaneous tissue oxygen tension (Psqo2) was recorded from a subcutaneous tonometer. An oximeter probe on the upper arm measured muscle oxygen saturation. Cardiac output was monitored noninvasively. Paco2 was adjusted to 20, 30, 40, 50, or 60 mmHg in random order with each concentration being maintained for 45 min.

Results: Increasing Paco2 linearly increased cardiac index and Psqo2: Psqo2 = 35.42 + 0.77 (Paco2), P < 0.001.     

End-tidal carbon dioxide measurements in critically ill neonates: a comparison of side-stream and mainstream capnometers

To determine whether end-tidal PCO2 (PETCO2) measurements obtained with two infrared capnometers accurately approximates the arterial PCO2 (PaCO2) in critically ill neonates, simultaneous measurements of PETCO2 were obtained from the distal and proximal ends of the tracheal tube with a sidestream capnometer (Puritan Bennett/Datex--BP/D) and from the proximal end with a mainstream capnometer (Hewlett-Packard-HP) in 20 intubated neonates. Distal sidestream PETCO2 and mainstream PETCO2 correlated with the PaCO2 (r2 = 0.66 and 0.61, respectively) within the range of 26-57 mmHg PaCO2. However, proximal PETCO2 with the sidestream capnometer correlated very poorly (r2 = 0.09) with PaCO2. The slope of the least square regression line for the distal sidestream capnometer, 0.67, was significantly less than that for the mainstream capnometer, 0.78 but both were significantly greater than that for the proximal sidestream capnometer, 0.39 (P less than 0.05). The slope of the regression for the proximal sidestream capnometer did not differ significantly from horizontal. Insertion of the mainstream sensor for the HP capnometer significantly increased the transcutaneous CO2 when compared with preinsertion values. We conclude that both distal sidestream and mainstream capnometry provide accurate estimates of the PaCO2 in critically ill neonates.     

Alteration of the Piglet Diaphragm Contractility In Vivo and Its Recovery after Acute Hypercapnia

Background: The effects of hypercapnic acidosis on the diaphragm and its recovery to normocapnia have been poorly evaluated. The authors studied diaphragmatic contractility facing acute variations of arterial carbon dioxide tension (Paco2) and evaluated the contractile function at 60 min after normocapnia recovery.

Methods: Thirteen piglets weighing 15-20 kg were anesthetized, ventilated, and separated into two groups: a control group (n = 5) evaluated in normocapnia (time-control experiments) and a hypercapnia group (n = 8) in which animals were acutely and shortly exposed to five consecutive ranges of Paco2 (40, 50, 70, 90, and 110 mmHg). Then carbon dioxide insufflation was stopped. Diaphragmatic contractility was assessed by measuring transdiaphragmatic pressure variations obtained after bilateral transjugular phrenic nerve pacing at increased frequencies (20-120 Hz). For each level of arterial pressure of carbon dioxide, pressure-frequency curves were obtained in vivo by phrenic nerve pacing.

Results: In the hypercapnia group, mean +/- SD transdiaphragmatic pressure significantly decreased from 41 +/- 3 to 29 +/- 3 cm H2O (P < 0.05) between the first (40 mmHg) and fifth (116 mmHg) stages of capnia at the frequency of 100 Hz stimulation. The observed alteration of the contractile force was proportional to the level of Paco2 (r2 = 0.61, P < 0.01). Normocapnia recuperation allowed a partial recovery of the diaphragmatic contractile force (80% of the baseline value) at 60 min after carbon dioxide insufflation interruption.     

An Evaluation of Transcutaneous Carbon Dioxide Partial Pressure Monitoring during Apnea Testing in Brain-dead Patients

Background: Diagnosis of brain death usually requires an arterial carbon dioxide partial pressure (Paco2) of 60 mmHg during the apnea test, but the increase in Paco2 is unpredictable. The authors evaluated whether transcutaneous carbon dioxide partial pressure (Ptcco2) monitoring during apnea test can predict that a Paco2 of 60 mmHg has been reached.

Methods: The authors compared Ptcco2 measured with a transcutaneous ear sensor (V-Sign(R) Sensor, Sentec Digital Monitoring System; SENTEC-AG, Therwil, Switzerland) and Paco2 obtained from arterial blood gas measurements in 32 clinically brain-dead patients.

Results: In the first 20 patients, the mean Paco2-Ptcco2 gradient was 0.7 +/- 3.6 mmHg at baseline and 8.7 +/- 7.1 mmHg after 20 min of apnea. Using receiver operating characteristic curve analysis (area under the curve: 0.983 +/- 0.013), the best threshold value of Ptcco2 to predict that a Paco2 of 60 mmHg had been reached was 60 mmHg (positive predictive value: 1.00 [0.93-1.00]). In the following 12 patients investigated with use of this Ptcco2 target value of 60 mmHg, the mean duration of the apnea test (11 +/- 4 vs. 20 +/- 0 min; P < 0.001), hypercapnia (74.0 +/- 4.9 vs. 98.3 +/- 20.0 mmHg; P < 0.001), acidosis (pH: 7.18 +/- 0.06 vs. 7.11 +/- 0.08; P < 0.001), and decrease in arterial oxygen partial pressure (-47 +/- 44 vs. -95 +/- 89; P < 0.05) at the end of the test were reduced as compared with the 20-min apnea test group.