Alveolar-arterial Oxygen Tension Difference Research Articles

Gradiente alveolo-arterial de O2 en la EPOC con hipercapnia

This study was conducted to assess whether or not calculation of the alveolar-arterial oxygen tension difference (AaPO2) from arterial blood gas measurements, breathing air, is useful to discriminate patients with hypecapnia associated with obstructive lung disease.The effect of different values for the respiratory exchange ratio (R) was also analyzed. We calculated the AaPO2 in 45 patients with chronic airway obstruction and hypercapnia (PaCO2 in 45 mmHg) and hemodynamic stability using the standard alveolar gas equation, PAO2 = PIO2 - PACO2 [FIO2 + (1-FIO2)/R], with R assumed to vary from 0.6 to 1.1 and the simplified alveolar gas equation, PAO2 = PIO2 - PACO2/R, with R assumed to be 0.8. It was considered that a patient was correctly classified when the calculated AaPO2 was greater than predicted AaPO2.When the simplified alveolar gas equation was used, 9 (20%) of 45 patients were misclassified, whereas using the standard equation with R assumed to be 0.8, 41 (91%) of 45 patients were correctly classified. Modification of the value of R only allowed improving the classification of two further patients.We conclude that calculation of the AaPO2 using the standard equation and R = 0.8 can be used to classify hypercapnic COPD patients. This laboratory parameter is of sufficient discriminant value to be used for clinical purposes.

The use of inhaled nitric oxide as adjuvant therapy in patients with burn injuries and respiratory failure.

Inhaled nitric oxide (NO) is a relatively new modality in the management of acute respiratory distress syndrome. The purpose of this study was to examine our experience with inhaled NO in 10 adult patients with burn injuries and acute respiratory distress syndrome-related oxygenation failure. The patients had a mean age of 50 +/- 19 years and a mean burn size of 41% +/- 20% of the total body surface area. Seven patients died and 3 survived. The survivors and nonsurvivors did not differ with respect to age, burn size, pre-NO ventilator settings, or indices of oxygenation including PaO2, oxygen saturation in arterial blood, PaO2/fraction of inspired oxygen (FIO2) ratio, and alveolar-arterial oxygen tension difference. The concentration of NO administered ranged between 5 ppm and 30 ppm. PaO2, oxygen saturation in arterial blood, and the PaO2/FIO2 ratio increased in all patients. Although it was not statistically significant, survivors tended to have a more vigorous and sustained response than non-survivors; this was best exemplified by the change in PFR. During the first hour of therapy, the PaO2/FIO2 ratio increased from 64.3 +/- 12.7 to 231.8 +/- 154.5 in survivors and from 93.9 +/- 44.0 to 161.5 +/- 81.8 in the nonsurvivors. After 12 hours of therapy, the PaO2/FIO2 ratio was 306.2 +/- 333.7 in the survivors and 178.9 +/- 69.9 in the nonsurvivors. There were no complications associated with the use of inhaled NO. Although a stronger early response to NO seems to occur in survivors, we cannot definitely conclude that the early response pattern is predictive of recovery. Nonetheless, we believe that inhaled NO has a useful role in the treatment of patients with burn injuries and severe acute respiratory distress syndrome-related oxygenation failure.

A comparison of indices of respiratory failure in ventilated preterm infants

AIMTo compare indices of respiratory failure in terms of their ability to predict adverse respiratory outcomes in preterm infants. The indices evaluated were: (a) the alveolar-arterial oxygen tension difference (A-aDo2);...

KL-6, a mucinous glycoprotein, as an indicator of chronic lung disease of the newborn

KL-6 is a mucinous glycoprotein that is preferentially expressed by alveolar type 2 cells. Plasma KL-6 was higher in infants with chronic lung disease (n = 12) than in infants without chronic lung disease (n = 14) on day 0-1, 10, and 30 (P = .04). KL-6 correlated with the alveolar-arterial oxygen tension difference on day 10 and day 30. Plasma KL-6 may be useful as an early marker of chronic lung disease and an indicator of severity. (J Pediatr 2000;137:280-2)

Effects of inhaled nitric oxide 10 ppm in spontaneously breathing horses anaesthetized with halothane

Inhaled nitric oxide, a selective pulmonary vasodilator, is known to improve arterial oxygenation after cardiopulmonary bypass and during acute respiratory distress syndrome in humans. During general anaesthesia with spontaneous ventilation, healthy adult horses develop large alveolar-arterial oxygen tension differences. In this study, we have determined the effects of inhaled nitric oxide (10 parts per million (ppm)) on venous admixture and pulmonary haemodynamics in horses anaesthetized with halothane. Seven adult horses were studied twice in random sequence. After premedication with romifidine 100 micrograms kg-1, anaesthesia was induced with ketamine 2.2 mg kg-1 and maintained with 1.1 MAC (0.95%) of halothane in oxygen. Horses breathed spontaneously. After 65 min, each horse had nitric oxide 10 ppm added to the inspired gas for 20 min (procedure HA + NO) or anaesthesia was continued with halothane in oxygen (procedure HA). Cardiac output, minute ventilation, arterial and mixed venous oxygen and carbon dioxide tensions, and mean pulmonary and carotid arterial pressures were measured for 100 min. Shunt fraction and pulmonary and systemic vascular resistances were calculated. Shunt fraction (SF) and mean pulmonary artery pressure (PPA mean) were not different between the two groups after 65 min of general anaesthesia (HA: SF 0.20 (SD 0.06), PPA mean 45 (8) mm Hg; HA + NO: SF 0.21 (0.04), PPA mean 44 (7) mm Hg) or after 85 min (HA: SF 0.22 (0.07), PPA mean 45 (8) mm Hg; HA + NO: SF 0.20 (0.03), PPA mean 43 (7) mm Hg). There were no significant effects of time or nitric oxide inhalation on any other variable. There was a significant correlation (r = 0.80, P < 0.05) between calculated shunt fraction 65 min after induction of anaesthesia and body weight.

Prediction of hypoxemia and mechanical ventilation after lung resection for cancer

Background. Hypoxemia usually occurs after thoracotomy, and respiratory failure represents a major complication. Methods. To define predictive factors of postoperative hypoxemia and mechanical ventilation (MV), we prospectively studied 48 patients who had undergone lung resection. Preoperative data included, age, lung volume, force expiratory volume in one second (FEV1), predictive postoperative FEV1 (FEV1ppo), blood gases, diffusing capacity, and number of resected subsegments. Results. On postoperative day 1 or 2, hypoxemia was assessed by measurement of PaO 2 and alveolar-arterial oxygen tension difference (A-aDO2) in 35 nonventilated patients breathing room air. The other patients (5 lobectomies, 9 pneumonectomies) required MV for pulmonary or nonpulmonary complications. Using simple and multiple regression analysis, the best predictors of postoperative hypoxemia were FEV1ppo ( r = 0.74, p < 0.001) in lobectomy and tidal volume ( r = 0.67, p < 0.01) in pneumonectomy. Using discriminant analysis, FEV1ppo in lobectomy and tidal volume in pneumonectomy were also considered as the best predictive factors of MV for pulmonary complications. Conclusions. These results suggest that the degree of chronic obstructive pulmonary disease in lobectomy and impairment of preoperative breathing pattern in pneumonectomy are the main factors of respiratory failure after lung resection.

Effect of body position changes on pulmonary gas exchange in Eisenmenger's syndrome.

Preliminary studies on sleep of patients with congenital heart disease and Eisenmenger's syndrome (ES) at our institution demonstrated nocturnal worsening arterial unsaturation, which appeared to be a body position-related phenomenon. To investigate the potential effect of body position on gas exchange in ES, we carried out a prospective study of 28 patients (mean age, 34.8 +/- 11.7 yr) with established ES due to congenital heart disease. In every patient, arterial blood gases were performed during both sitting and supine positions under three different conditions: room air, while breathing 100% oxygen, and after breathing oxygen at a flow rate of 3 L/min through nasal prongs. Alveolar oxygen pressure (PaO2) for the calculation of alveolar-arterial oxygen tension differences (AaPO2) was derived from the alveolar gas equation using PaCO2 and assuming R = 1. We used paired t test, repeated-measures two-way ANOVA with Bonferroni's test, and regression analysis. From sitting to supine position on room air, there was a significant decrease in PaO2 (from 52.5 +/- 7.5 to 47.5 +/- 5.5 mm Hg; p < 0. 001) and SaO2 (from 86.7 +/- 4.6 to 83.3 +/- 4.9%; p < 0.001), both of which were corrected by nasal O2 (to 68.2 +/- 21 mm Hg and to 92 +/- 4%, respectively, p < 0.005). PaCO2 and pH remained unchanged. The magnitude of the change in PaO2 correlated with the change in AaPO2 on room air (r = 0.77; p < 0.01) but not with the change in AaPO2 on 100% oxygen. It is concluded that in adult patients with ES there is a significant decrease in PaO2 and SaO2 when they change from the sitting to the supine position. A ventilation-perfusion (V/Q) distribution abnormality and/or a diffusion limitation phenomenon rather than an increase in true shunt may be the mechanisms responsible for this finding. The response to nasal O 2 we observed warrants a trial with long-term nocturnal oxygen therapy in these patients.

The alveolar-arterial difference in oxygen tension increases with temperature-corrected determination during moderate hypothermia.

Moderate hypothermia (32-33 degrees C) occurs in anesthetic practice. However, intrapulmonary gas exchange and the effect of temperature correction of blood gases on oxygen and carbon dioxide exchange have not been investigated in these patients. We investigated alveolar-arterial difference in oxygen tension (AaDO2) and arterial to end-tidal difference in carbon dioxide (Pa-ETCO2) during rewarming of eight ASA physical status I patients from hypothermia of 32 degrees C. Anesthesia was maintained with fentanyl/propofol. AaDO2 and Pa-ETCO2 were assessed by analyzing arterial blood gases and saturated water vapor pressure, uncorrected or corrected to actual body temperature. The respiratory quotient (RQ) was measured by calorimetry. After temperature correction of blood gases and water vapor pressure, the AaDO2 was significantly higher at 33 and 32 degrees C compared with 36 degrees C (56 +/- 13 and 64 +/- 14 vs 39 +/- 10 mm Hg; P < 0.05 and P < 0.01). The deterioration of pulmonary oxygen exchange was not detected if arterial blood gases and water vapor pressure were not corrected. The RQ did not change during moderate hypothermia compared with 36 +/-C. The temperature-corrected Pa-ETCO2 was not affected by hypothermia. We conclude that AaDO2 is increased during moderate hypothermia. This is only detected when water vapor pressure and arterial blood gases are corrected to actual body temperature. We investigated intrapulmonary oxygen and carbon dioxide exchange during moderate hypothermia (32 degrees C) in eight patients. If oxygen, carbon dioxide, and water vapor pressure were corrected to actual body temperature, the alveolar-arterial oxygen tension difference was increased during hypothermia. The carbon dioxide tension difference and the respiratory quotient were unaffected by hypothermia.

The Alveolar-Arterial Difference in Oxygen Tension Increases with Temperature-Corrected Determination During Moderate Hypothermia

Moderate hypothermia (32-33[degree sign]C) occurs in anesthetic practice. However, intrapulmonary gas exchange and the effect of temperature correction of blood gases on oxygen and carbon dioxide exchange have not been investigated in these patients. We investigated alveolar-arterial difference in oxygen tension (AaDO2) and arterial to end-tidal difference in carbon dioxide (Pa-ETCO2) during rewarming of eight ASA physical status I patients from hypothermia of 32[degree sign]C. Anesthesia was maintained with fentanyl/propofol. AaDO2 and Pa-ETCO2 were assessed by analyzing arterial blood gases and saturated water vapor pressure, uncorrected or corrected to actual body temperature. The respiratory quotient (RQ) was measured by calorimetry. After temperature correction of blood gases and water vapor pressure, the AaDO2 was significantly higher at 33 and 32[degree sign]C compared with 36[degree sign]C (56 +/- 13 and 64 +/- 14 vs 39 +/- 10 mm Hg; P < 0.05 and P < 0.01). The deterioration of pulmonary oxygen exchange was not detected if arterial blood gases and water vapor pressure were not corrected. The RQ did not change during moderate hypothermia compared with 36[degree sign]C. The temperature-corrected Pa-ETCO2 was not affected by hypothermia. We conclude that AaDO2 is increased during moderate hypothermia. This is only detected when water vapor pressure and arterial blood gases are corrected to actual body temperature. Implications: We investigated intrapulmonary oxygen and carbon dioxide exchange during moderate hypothermia (32[degree sign]C) in eight patients. If oxygen, carbon dioxide, and water vapor pressure were corrected to actual body temperature, the alveolar-arterial oxygen tension difference was increased during hypothermia. The carbon dioxide tension difference and the respiratory quotient were unaffected by hypothermia. (Anesth Analg 1999;88:538-2)

Inhaled nitric oxide reduces lung fluid filtration after endotoxin in awake sheep.

We studied the effect on lung fluid filtration of 37.6 ppm inhaled nitric oxide (NO) imposed for 1 h 2.5 h after endotoxin in seven awake sheep, with seven control subjects. The effects of NO on the longitudinal distribution of pulmonary vascular resistance (PVR) before and after endotoxin were specifically addressed in six sheep. Following endotoxin, sheep developed respiratory distress; PaO2, the alveolar-arterial oxygen tension difference (AaPO2) and venous admixture (Q S/Q T) changed significantly, as did the pulmonary artery pressure (Ppa), PVR, and lung lymph flow (Q L). Inhaled NO reduced Ppa and PVR by 50%; Q L decreased from 7.8 +/- 0.34 ml/15 min to 4.7 +/- 0.80 ml/15 min (mean +/- SEM), and lymph protein clearance from 4.9 +/- 0.18 ml/15 min to 3.6 +/- 0.75 ml/15 min. Lymph/plasma protein concentration ratio (L/P) increased from 0.63 +/- 0.016 to 0.72 +/- 0.006, concomitant with the decrease in Q L. The L/P - Q L relationships shifted from left, at baseline, to the right during endotoxemia, as did the permeability surface product (PS) isolines. The rightward shift was significantly less in the NO group. Inhaled NO significantly improved PaO2, AaPO2, and Q S/Q T, reduced the increase in pulmonary microwedge pressure back to baseline and decreased upstream and downstream PVR at 3.0 through 4. 0 h. We conclude that, in sheep, inhaled NO reduces lung fluid filtration by decreasing microvascular pressure and apparently also by declining the enhanced microvascular permeability during the late phase of endotoxemia.

Medical computing over the World Wide Web: use of forms and CGI scripts for constructing medical algorithm Web pages.

The development of the World Wide Web has led to an explosion of educational and clinical resources available via the Internet with minimal effort or special training. However, most of these Web pages contain only static information; few offer dynamic information shaped around clinical or laboratory test findings. In this report we show how this goal can be achieved with the design and construction of Medical Algorithm Web Pages (MAWP). Specifically, using Internet technologies known as forms and CGI scripts we demonstrate how one can implement medical algorithms remotely over the Internet's World Wide Web. To use a MAWP, one enters the URL for the site and then enters information according to the instructions presented there, usually by entering numbers and other information into fields displayed on screen. When all the data is entered, the user clicks on the SUBMIT icon, resulting in a new Web page being constructed "on-the-fly" containing diagnostic calculations and other information pertinent to the patient's clinical management. Four sample applications are presented in detail to illustrate the concept of a Medical Algorithm Web page: Computation of the alveolar-arterial oxygen tension difference using the alveolar gas equation; Computation of renal creatinine clearance; drug infusion calculation (micrograms/kilogram/minute); Computation of the renal failure index.

Effects of training on the development of exercise-induced arterial hypoxemia in horses

Abstract Objectives To compare the development of exercise-induced arterial hypoxemia in horses before and after training, and to determine whether increases in maximum oxygen uptake (V˙O2max) following training results in a greater degree of exercise-induced arterial hypoxemia. Animals 13 three- to five-year-old Standardbred geldings without clinical signs of respiratory or cardiovascular disorders. Procedure Horses were rested for 4 months prior to commencing a 16-week training program. Arterial blood was collected from the transverse facial artery during standardized exercise tests performed before and after 8 and 16 weeks of training. Variables measured during exercise tests included arterial blood gas tensions and V˙O2max. Training and testing was performed on a treadmill set at a 10% slope. Results Minimum arterial partial pressures of oxygen (PaO2) during exercise decreased from 83.3 ± 1.5 mm of Hg before training to 77.8 ± 1.0 mm of Hg after 16 weeks of training. Maximum arterial oxygen content increased from 239.2 ± 3.1 to 257.9 ± 3.8 ml/L, which resulted from an increase in hemoglobin concentration. The V˙O2max increased by 19% following training. Minimum values of PaO2 and arterial oxygen saturation were significantly correlated with V˙O2max when data from each stage of training were pooled. Calculated values for minimum alveolar oxygen tension decreased after 8 weeks of training, and alveolar ventilation increased at the end of training. Alveolar-arterial oxygen tension difference increased by 4 mm of Hg following training. Conclusions In trained horses, an increase V˙O2max is associated with a decrease in minimum PaO2 during intense exercise and is mostly attributable to an increase in the alveolar-arterial oxygen tension difference. Therefore, interpretation of blood gas data from exercising horses should take into consideration V˙O2max. (Am J Vet Res 1997;58:653–657)

The ventilation-perfusion relation and gas exchange in mitral valve disease and coronary artery disease. Implications for anesthesia, extracorporeal circulation, and cardiac surgery.

Patients with mitral valve disease (MVD) are at greater risk for respiratory complications after cardiac surgery compared with patients with coronary artery disease (CAD). The authors hypothesized that ventilation-perfusion (VA/Q) inequality is more pronounced in patients with MVD before and after induction of anesthesia and during and after surgery when extracorporeal circulation (ECC) is used. In patients with MVD (n = 12) or with CAD (n = 12), VA/Q distribution was determined using the multiple inert gas elimination technique. Intrapulmonary shunt (Qs/Qr) defined as regions with VA/Q < 0.005 [% of total perfusion (Qr)], perfusion of "low" VA/Q areas (0.005 < or = VA/Q < 0.1, [% of Qr]), ventilation of "high" VA/Q regions (10 < or = VA/Q < or = 100 [% of total ventilation VE]), and dead space (VA/Q > 100 [% of VE]) were calculated from the retention/excretion data of the inert gases. Recordings were obtained while patients spontaneously breathed air in the awake state, during mechanical ventilation after induction of anesthesia, after separation of patients from ECC, and 4 h after operation. Qs/Qr was low in the awake state (MVD group, 3% +/- 3%; CAD group, 3% +/- 4%) and increased after induction of anesthesia to 10% +/- 8% (MVD group, P < 0.05) and 11% +/- 7% (CAD group, P < 0.01). Qs/Qr increased further after separation from ECC (MVD group, 24% +/- 9%, P < 0.01; CAD group, 23% +/- 7%, P < 0.01). Similarly, alveolar-arterial oxygen tension difference (PA-aO2) increased from 168 +/- 54 mmHg (anesthetized state) to 427 +/- 138 mmHg after ECC (MVD group, P < 0.01) and from 153 +/- 65 mmHg to 377 +/- 101 mmHg (CAD group, P < 0.01). In both groups, PA-aO2 was correlated with Qs/Qr. Four hours after operation, Qs/Qr had decreased significantly to 8% +/- 6% (CAD group) and 10% +/- 6% (MVD group). PA-aO2 and Qs/Qr showed no significant differences between the CAD and MVD groups. Qs/Qr is the main pathophysiologic mechanism of gas exchange impairment during cardiac surgery for MVD or CAD. Impairment of pulmonary gas exchange secondary to general anesthesia, cardiac surgery, and ECC are comparable for patients undergoing myocardial revascularization or mitral valve surgery.

Large Tidal Volume Ventilation Does Not Improve Oxygenation in Morbidly Obese Patients During Anesthesia

Eight morbidly obese patients (body mass index [BMI] = 46) were studied during general anesthesia and controlled mechanical ventilation. To evaluate the effect of large tidal volume ventilation on oxygenation and ventilation, the baseline 13 mL/kg tidal volume (VT) (calculated by the ideal body weight) was increased in 3 mL/kg volume increments to 22 mL/kg, while ventilatory rate (RR) and inspiratory time (TI) were kept constant. Each volume increment was maintained for 15 min. Gas exchange was assessed by measuring the arterial blood oxygen tensions, and calculating the indices of alveolar-arterial oxygen tension difference [P(A-a)O2] and arterial/alveolar oxygen tension ratio (a/A). Peak inspiratory airway pressure (Ppeak), end-inspiratory airway pressure (Pplateau), and compliance of the respiratory system (CRS) were recorded using the Capnomac Ultima (Datex, Helsinki, Finland) on-line respiratory monitor. Increasing tidal volumes to 22 mL/kg increased the recorded Ppeak (26.3 +/- 4.1 vs 37.9 +/- 3.2 cm H2O, P < 0.008), Pplateau (21.5 +/- 3.6 vs 27.7 +/- 4.3 cm H2O, P < 0.01), and CRS (39.8 +/- 7.7 vs 48.5 +/- 8.3 mL/cm H2O) significantly without improving arterial oxygen tension and resulted in severe hypocapnia. Since changes in arterial oxygenation were small and not statistically significant, mechanical ventilation of morbidly obese patients with large VTS seems to offer no advantage to smaller (13 mL/kg ideal body weight) VTS.

Analysis of the Complications of 6 Brain-dead Patients

Brain death is irreversible coma due to injury of brain hemisphere and brain stem regardless of any treatment. In brain-dead patients, acute respiratory failure frequently results from capillary endothelial damage in the lung and diabetes insipidus and hypothermia occur due to brain stem compression injury. Ultimately, it has been known that the brain-dead patients progress to multiple organ failure. The primary goal of organ donor management is maintenance of optimal physiologic environment for organs prior to recovery. This study is performed for suggesting the guideline of the prediction and management of complications in the brain-dead patient. We analyzed 6 brain-dead patients waiting for organ donation in the intensive care unit. The causes of brain death among the donors consisted of closed head injury in 4 patients, subarachnoid hemorrhage in 1, and drowning in l. AaDO2(alveolar-arterial oxygen tension difference) and PaO2F1O2 (arterial oxygen tension/fractional inspired O2 concentration) were analyzed to demonstrate the progress of respiratory failure. Body temperature, vital signs, urine output, serum osmolality, serum K(+), serum Na(+), AST(aspartate aminotransferase), ALT(alanine aminotransferase), BUN(blood urea nitrogen) and creatinine were also analyzed in all patients. Diabetes insipidus were found in 5 patients and hypothermia in 4 patients. AaDO increased and PaO2/F1O2 decreased in 5 patients with time. Hepato-renal function remained relatively normal during observation. We concluded that brain-dead patients rapidly progressed to acute respiratory failure. It can be suggested that for successeful organ transplantation, organ procurement should be performed as soon as possible after brain death was confirmed.(Korean J Anesthesiol 1995; 29: 718~723)

Reexpansion of atelectasis during general anaesthesia may have a prolonged effect

Pulmonary atelectasis, as found during general anaesthesia, may be reexpanded by hyper-inflation of the lungs. The purpose of this study was to determine whether such a recruitment is maintained and whether this is accompanied by an improved gas exchange. We studied a consecutive sample of twelve lung healthy adults, scheduled for elective surgery. After induction of intravenous anaesthesia, the lungs were hyperinflated manually. The ventilationperfusion relationship (VA/Q) was estimated with the multiple inert gas method, and in six patients atelectasis was assessed by computed x-ray tomography. The mean pulmonary shunt was 7.5% of cardiac output after induction of anaesthesia and this decreased to 1.0% and 2.8% at 20 and 40 min after the recruitment manoeuvre. Perfusion of poorly ventilated lung regions (low VA/Q), however, increased from 3.7% to 10.6% and 7.8% at 20 and 40 min after the recruitment, respectively. The mean alveolar-arterial oxygen tension difference (PA-aO2) was 14.3 kPa after induction of anaesthesia and 11.1 kPa immediately after recruitment. Forty minutes later PA-aO2 was still 2.0 kPa lower than after induction of anaesthesia (95% confidence interval [CI] 0.3 to 3.8 kPa). PA-aO2 decreased more in obese patients. The mean area of atelectasis decreased from 9.0 cm2 after induction of anaesthesia to 0.1 cm2 immediately after recruitment, and there was a slow increase to 1.9 cm2 (95% CI 0.0 to 3.9 cm2) 40 min later. During general anaesthesia in lung healthy patients, most of the reexpanded atelectatic lung tissue remains inflated for at least 40 min. The recruitment manoeuvre decreases pulmonary shunt, but increases low VA/Q. The net effect on gas exchange is a small reduction of PA-aO2.

Clinical and functional assessment of patients with idiopathic pulmonary fibrosis: results of a 3 year follow-up

The purpose of this study was to analyse the information provided by different techniques used in the assessment of patients with idiopathic pulmonary fibrosis (IPF) and their role in the prediction of lung function decline with the decline. Twenty seven subjects with IPF (55 +/- 14 (mean +/- SD) yrs) were studied at the initial staging. Nineteen of them (70%) were included in a follow-up over 3 yrs (32 +/- 6 months), whilst the remaining 8 patients were lost to follow-up. During the period of the study, 6 of the 19 patients died. A significant correlation between diffusing capacity of the lungs for carbon monoxide (DLCO) (and carbon monoxide transfer coefficient (KCO) = DLCO/alveolar volume (VA)) and the increase in alveolar-arterial oxygen tension difference (A-aPO2) during exercise (delta A-aPO2) was observed at diagnosis (r = -0.58). Despite the treatment with prednisone (1 mg.kg-1 daily during 4 weeks, tapered to an individualized maintenance daily dose of 15-30 mg), the 13 patients controlled throughout the whole period of the study showed a marked impairment in lung volumes; forced vital capacity (FVC) -0.46 +/- 0.09 l, from 69 +/- 16 to 52 +/- 11% of predicted, and total lung capacity (TLC) -0.39 +/- 0.11 l, from 75 +/- 16 to 62 +/- 14%, and in DLCO -0.6 +/- 0.2 mmol.min-1.kPa-1, from 56 +/- 15 to 47 +/- 18%, predicted. By contrast, both mean arterial oxygen tension (PaO2) and A-aPO2 at rest remained unchanged throughout the 3 yrs follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Optimal release time during airway pressure release ventilation in neonatal sheep

To systematically investigate the effect of altering release time during airway pressure release ventilation in a neonatal animal model before and after oleic acid-induced acute lung injury. Prospective, nonrandomized, controlled study with repeated measures. University research laboratory. Eight neonatal sheep (aged < 7 days, weight 5.1 +/- 0.3 kg). Throughout this study, airway pressure release ventilation was performed with an FIO2 of 0.21 at a frequency of 0.5 Hz (30 breaths/min) and an airway plateau pressure set to deliver tidal volumes between 10 and 15 mL/kg with a release time of 1 sec. Release time was changed in decrements of 0.2 sec starting at 1 sec and ending at 0.2 sec at 10-min intervals. Cardio-respiratory profiles were recorded at the end of each interval. The total exhaled respiratory system time constant (tau) was measured by plotting exhaled volume (integration of exhaled air flow) vs. time. Acute lung injury was induced by oleic acid infusion. The protocol was repeated with increased plateau airway pressure to maintain tidal volumes between 10 and 15 mL/kg at a release time of 1 sec. During airway pressure release ventilation at a release time of 1 sec, oleic acid-induced acute lung injury decreased dynamic lung compliance (9.9 +/- 2.2 vs. 7.5 +/- 2.0 mL/cm H2O, p < .01), the expiratory time constant (0.15 +/- 0.04 vs. 0.12 +/- 0.02 sec, p < .05), and mean arterial pressure (80 +/- 5 vs. 62 +/- 12 mm Hg, p < .01). Alveolar ventilation was maintained as long as release times were > 0.4 sec (approximately 3 tau or greater). PaO2 decreased with release times of < 0.3 sec, but the alveolar-arterial oxygen tension difference was unchanged. In this protocol, with higher plateau and mean airway pressures, oleic acid-induced acute lung injury had no effect on the relationship between release time and oxygenation or ventilation. In this neonatal laboratory model, release times that were much shorter than previously reported maintained clinically acceptable oxygenation and ventilation. The optimal duration of the release time is a function of the time constant of the respiratory system. During airway pressure release ventilation, alveolar ventilation was maintained without apparent lung volume loss with release times of between 4 tau and 10 tau.

Continued pulmonary recovery observed after discontinuing extracorporeal membrane oxygenation.

Extracorporeal membrane oxygenation (ECMO) is a valuable therapy for the treatment of reversible lung disease in neonates. Associated with this treatment, however, are risks for complications that increase with the duration of therapy. We evaluated alveolar-arterial oxygen tension difference P(A-a)O2 pulmonary compliance (CL), and functional residual capacity (FRC) in 20 infants immediately after ECMO was discontinued, and again 24 hours thereafter. We measured CL by pneumotachography and esophageal manometry and FRC by helium dilution. Mean (+/- SEM) values for CL and FRC increased (CL from 0.28 +/- 0.02 to 0.35 +/- 0.03 mL/cmH2O)/kg and FRC from 18.6 +/- 1.4 to 22.2 +/- 1.1 mL/kg; P < 0.05), and P(A-a)O2 and the oxygenation index (OI) decreased (200 +/- 19 to 169 +/- 14 mm Hg and 6.9 +/- 0.44 to 5.4 +/- 0.5, respectively; P < 0.02), over the 24 hour period following ECMO. Nineteen of 20 infants experienced improvement in at least two of these parameters. Improvements were found to be greatest in the infant with the worst lung function immediately after discontinuing ECMO, and in the ten infants who had not received pancuronium bromide for inducing skeletal muscle paralysis, following decannulation from ECMO. These data indicate that improvement in lung function following ECMO will generally continue over the 24 hour period following the termination of cardiopulmonary bypass, and that borderline pulmonary status may not preclude discontinuation of bypass therapy.

Adult respiratory distress syndrome in children: Associated disease, clinical course, and predictors of death

The adult respiratory distress syndrome is a common cause of respiratory failure; however, its incidence, risk factors, course, and mortality rate for children remain incompletely understood. A 24-month surveillance of pediatric intensive care admissions identified 60 children with adult respiratory distress syndrome constituting 2.7% of such admissions, 8% of total days spent in a pediatric intensive care unit, and 33% of deaths. The mortality rate was 62% (confidence interval, 48.2% to 73.9%). Adult respiratory distress syndrome occurred in approximately 12% of children admitted for sepsis, viral pneumonia, smoke inhalation, or drowning. A low incidence (< 3%) was observed in children admitted with pulmonary contusion or multiple trauma. Ongoing changes in measures of pulmonary gas exchange varied with the magnitude of alveolar injury; no differences were associated with the underlying acute disease or lung injury mechanism. Efficiency of oxygenation differed among outcome groups by the second day after onset of adult respiratory distress syndrome. An alveolar-arterial oxygen tension difference > 420 was the best early predictor of death (sensitivity 80%, specificity 87%, positive predictive value 87%, negative predictive value 80%, and odds ratio 26.7). We conclude that adult respiratory distress syndrome behaves clinically as a single disease regardless of the underlying cause; its course and outcome are dependent on the magnitude of alveolar injury. We speculate that strategies for minimizing secondary lung injury may benefit all patients with adult respiratory distress syndrome.