Baseline FiO2 Research Articles

Determination of functional residual capacity (FRC) by multibreath nitrogen washout in a lung model and in mechanically ventilated patients. Accuracy depends on continuous dynamic compensation for changes of gas sampling delay time.

Validation of an open-circuit multibreath nitrogen washout technique (MBNW) for measurement of functional residual capacity (FRC). The accuracy of FRC measurement with and without continuous viscosity correction of mass spectrometer delay time (TD) relative to gas flow signal and the influence of baseline FIO2 was investigated. Laboratory study and measurements in mechanically ventilated patients. Experimental laboratory and anesthesiological intensive care unit of a university hospital. 16 postoperative patients with normal pulmonary function (NORM), 8 patients with acute lung injury (ALI) and 6 patients with chronic obstructive pulmonary disease (COPD) were included. Change of FIO2 from baseline to 1.0. FRC was determined by MBNW using continuous viscosity correction of TD(TDdyn), a constant TD based on the viscosity of a calibration gas mixture (TD0) and a constant TD referring to the mean viscosity between onset and end of MBNW (TDmean). Using TDdyn, the mean deviation between 15 measurements of three different lung model FRCs (FRCmeasured) and absolute volumes (FRCmodel) was 0.2%. For baseline FIO2 ranging from 0.21 to 0.8, the mean deviation between FRCmeasured and FRCmodel was -0.8%. However, depending on baseline FIO2, the calculation of FRC using TDmean and TD0 increased the mean deviation between FRCmeasured and FRCmodel to 2-4% and 8-12%, respectively. In patients (n = 30) the average repeatability coefficient was 6.0%. FRC determinations with TDmean and TD0 were 0.8-13.3% and 4.2-23.9% (median 2.7% and 8.7%) smaller than those calculated with TDdyn. A dynamic viscosity correction of TD improves the accuracy of FRC determinations by MBNW considerably, when gas concentrations are measured in a sidestream. If dynamic TD correction cannot be performed, the use of constant TDmean might be suitable. However, in patient measurements this can cause an FRC underestimation of up to 13%.

Continuous Inhalation of Nitric Oxide From Birth Preserves the Pulmonary Vasoconstrictor Response to Hypoxia in Chronically Ventilated Preterm Lambs• 1614

Chronic lung injury from prolonged mechanical ventilation of preterm lambs inhibits the normal postnatal decrease in pulmonary vascular resistance (PVR) and blunts the vasoconstrictor response to hypoxia (Bland et al, Pediatr Res 39:327A, 1996). These abnormalities of lung vascular tone and reactivity may contribute to impaired respiratory gas exchange that often exists in infants with chronic lung disease (CLD). We previously reported that nitric oxide (NO) inhalation for 1 h reduced PVR in preterm lambs with evolving CLD. To see if continuous NO inhalation from birth might inhibit the pulmonary vascular dysfunction that occurs in this model of CLD, we studied 4 preterm lambs (124± 3 d gestation; term = 147 d) that were mechanically ventilated for 3-4 wks at a respirator rate of 20 breaths/min, tidal volume 10-15 ml/kg, with 5-15 ppm NO and sufficient O2 to keep the PaO2 ≅ 50-90 mmHg. All lambs received surfactant at birth and had surgery for ductus arteriosus ligation and catheter placement to allow weekly assessment of PVR from measurements of pulmonary arterial and left atrial pressures and pulmonary blood flow before and during steady-state hypoxia. Results of these studies were compared with those of similar studies done with 10 lambs of the same gestation that were mechanically ventilated the same way but without NO. After 3 wks of mechanical ventilation, baseline PVR was not significantly different in the 4 lambs that received NO compared with the 10 lambs that did not receive NO (PVR = 44.8 ± 5.4 vs 53.9 ± 21.2 mmHg/(L/sec)/kg, respectively). However, in response to hypoxia (baseline FiO2.28±.09, PaO2 73 ± 3; hypoxia FiO2.17 ±.03, PaO2 35 ± 1), PVR consistently increased from 48.3 ± 2.3 to 74.0 ± 20.0 mmHg/(L/sec)/kg at the end of wk 3 in lambs that received NO from birth, whereas PVR did not increase significantly at the end of wk 3 in chronically ventilated lambs that did not receive NO. When inhaled NO was discontinued for 2-4 h after 3 wks of mechanical ventilation in the 4 NO-treated lambs, PVR increased on average from 50.5 ± 11.7 to 64.5± 18.7 mmHg/(L/sec)/kg. Subsequent hypoxia (FiO2.17 ±.03, PaO2 35 ± 4 mmHg), without inhaled NO, further increased PVR to 87.8 ± 27.2 mmHg/(L/sec)/kg. Thus, continuous nitric oxide inhalation from birth may help to preserve the normal pulmonary vasoconstrictor response to hypoxia and thereby facilitate ventilation-perfusion matching and respiratory gas exchange in chronically ventilated preterm lambs.

Influence of inspired oxygen concentration on deadspace, respiratory drive, and PaCO2 in intubated patients with chronic obstructive pulmonary disease.

To investigate the response of CO2-retaining chronic obstructive pulmonary disease (COPD) patients to an increase in FIO2 following a period of mechanical ventilation with PaO2 in the normal range. The administration of a high FIO2 to chronic obstructive pulmonary disease (COPD) patients may result in hypercapnia. Recent evidence indicates that the hypercapnia may be due to reversal of preexisting regional hypoxic pulmonary vasoconstriction resulting in a greater deadspace. This effect would be more pronounced in patients whose initial PaO2 was < 60 torr (< 7.9 kPa). Single blinded, prospective study. A medical surgical intensive care until in a tertiary care, teaching hospital. COPD CO2-retaining patients. FIO2 increased to 0.7. Twelve intubated COPD patients weaned from mechanical ventilation were studied both at their baseline FIO2 (0.3 to 0.4), and following a 20-min period of exposure to an FIO2 of 0.7. Mean baseline values were: PaO2 of 85 torr (11.3 kPa), PCO2 of 56 torr (7.5 kPa), deadspace of 73%, and respiratory drive normal, as measured by P0.1. Statistical analysis using the paired Student's t-test showed that the PaO2 increased significantly when the FIO2 was increased to 0.7, but there was no significant change in PaCO2, deadspace, or respiratory drive. These results show that following a period of mechanical ventilation with an FIO2 sufficient to maintain a normal PaO2, a further increase in FIO2 does not result in an increased PaCO2 in this group of CO2-retaining COPD patients.

EFFECT OF SEVERE SMOKE INHALATION INJURY ON SYSTEMIC MICROVASCULAR BLOOD FLOW IN SHEEP

Multiple nonpulmonary organ dysfunction is frequently associated with acute lung injury; however, the mechanisms underlying the pathogenesis of this process are not completely understood. Decreased oxygen delivery to distant organs due to maldistribution of blood flow may be a contributing factor. We examined the effects of acute lung injury induced by smoke inhalation on microvascular blood flow to various organs in sheep. Seven sheep were prepared with arterial, venous, pulmonary artery, and left atrial catheters. After a 5 day recovery period, a tracheostomy was performed, followed by insufflation with 48 breaths of cool cotton smoke. Determination of microvascular blood flow using colored microspheres, standard hemodynamic measures, and blood gas analysis were performed before and at 12 h intervals after smoke inhalation. Animals were resuscitated to maintain left atrial pressure at +/- 2 mmHg of the baseline value and FiO2 was adjusted to maintain Sao2 at > 90%. After 48 h, sheep were killed and an autopsy was performed. Samples of trachea, left ventricle, ileum, colon, spleen, pancreas, and cortex from both kidneys were obtained for determination of microvascular blood flow. Blood flow to the trachea was substantially increased, while blood flow to the kidneys was preserved near baseline levels. Left ventricular blood flow decreased slightly; however, this decline was not statistically significant. Blood flow to ileum, colon, spleen, and pancreas was significantly decreased, particularly at 36 and 48 h after injury. These decreases were independent of changes in cardiac output or systemic oxygen delivery. It is likely that alteration in microvascular blood flow may contribute to the development of nonpulmonary organ dysfunction after acute lung injury.

RANDOMIZED TRIAL OF INHALED (INH) VS INTRA VENOUS (IV) STEROID IN VENTILATOR DEPENDENT PRETERM INFANTS. ▴ 1468

We have previously reported that IV steroid reduces the severity of bronchopulmonary dysplasia in very-low birthweight (VLBW) infants (NEJM 1989; 320:1505). However, adverse effects have been reported. The INH route may maximize pulmonary effects while minimizing systemic effects but there have been no studies comparing INH to IV steroids. We are therefore comparing these two routes in preterm (≤ 30 weeks), VLBW (≤1500 grams) infants who are both ventilator (IMV ≥ 15) and oxygen (FiO2 ≥ 0.3) dependent at 12-21 d of age. From July 10, 1994 to December 1, 1995, 55 infants have been randomized to receive either a 42-day tapering course of IV dexamethasone(n=17), or one of two doses (400 μg daily, n=17; 800 μg daily, n=21) of INH beclomethasone. Baseline FiO2, ventilatory pressure (PIP-PEEP), and mean blood pressure were similar between groups. Baseline mean airway pressure was higher in the IV group, in which two infants required high frequency ventilation. Changes in airway pressures (cm H2O) and blood pressure(mm Hg) are shown below (data from the two INH groups are combined since results were similar): Table

N-acetylcysteine Preserves Oxygen Consumption and Gastric Mucosal pH during Hyperoxic Ventilation

Hyperoxic ventilation, used to prevent hypoxemia during potential periods of hypoventilation, has been reported to paradoxically decrease whole body oxygen consumption (VO2). Reduction in nutritive blood flow due to oxygen radical production is one possible mechanism. We investigated whether pretreatment with the sulfhydryl group donor and O2 radical scavenger N-acetylcysteine (NAC) would preserve whole body VO2 and prevent deterioration of oxygenation in gastric mucosal tissue during hyperoxia. Thirty-eight patients, requiring hemodynamic monitoring (radial and pulmonary artery catheters) due to sepsis syndrome, were included in this randomized experiment. All patients exhibited stable clinical conditions (hemodynamics, body temperature, hemoglobin, FIO2 < 0.5). A gastric tonometer was placed to measure the gastric intramucosal pH (pHi), which indirectly assesses nutritive blood flow to the mucosa. Cardiac output was determined by thermodilution and VO2 by cardiovascular Fick. After baseline measurements, patients randomly received either 150 mg.kg-1 NAC (n = 19) or placebo (n = 19) in 250 ml 5% dextrose intravenously over a period of 15 min. Measurements were repeated 30 min after starting NAC or placebo infusion, 30 min after starting hyperoxia (FIO2 = 1.0), and 60 min after resetting the original FIO2. There were no significant differences between groups in any of the measurements before treatment and after the return to baseline FIO2 at the end of the study. NAC, but not placebo infusion, caused a slight but significant increase in cardiac output and decrease in systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

N-acetylcysteine preserves oxygen consumption and gastric mucosal pH during hyperoxic ventilation.

Hyperoxic ventilation, used to prevent hypoxemia during potential periods of hypoventilation, has been reported to paradoxically decrease whole body oxygen consumption (VO2). Reduction in nutritive blood flow due to oxygen radical production is one possible mechanism. We investigated whether pretreatment with the sulfhydryl group donor and O2 radical scavenger N-acetylcysteine (NAC) would preserve whole body VO2 and prevent deterioration of oxygenation in gastric mucosal tissue during hyperoxia. Thirty-eight patients, requiring hemodynamic monitoring (radial and pulmonary artery catheters) due to sepsis syndrome, were included in this randomized experiment. All patients exhibited stable clinical conditions (hemodynamics, body temperature, hemoglobin, FIO2 < 0.5). A gastric tonometer was placed to measure the gastric intramucosal pH (pHi), which indirectly assesses nutritive blood flow to the mucosa. Cardiac output was determined by thermodilution and VO2 by cardiovascular Fick. After baseline measurements, patients randomly received either 150 mg.kg-1 NAC (n = 19) or placebo (n = 19) in 250 ml 5% dextrose intravenously over a period of 15 min. Measurements were repeated 30 min after starting NAC or placebo infusion, 30 min after starting hyperoxia (FIO2 = 1.0), and 60 min after resetting the original FIO2. There were no significant differences between groups in any of the measurements before treatment and after the return to baseline FIO2 at the end of the study. NAC, but not placebo infusion, caused a slight but significant increase in cardiac output and decrease in systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)