Altitude exposures during commercial flight: a reappraisal.

BACKGROUND: Hypobaric hypoxia during commercial air travel has the potential to cause or worsen hypoxemia in individuals with pre-existing cardiopulmonary compromise. Knowledge of cabin altitude pressures aboard contemporary flights is essential to counseling patients accurately about flying safety. The objective of the study was to measure peak cabin altitudes during U.S. domestic commercial flights on a variety of aircraft. METHODS: A handheld mountaineering altimeter was carried by the investigators in the plane cabin during commercial air travel and peak cabin altitude measured. The values were then compared between aircraft models, aircraft classes, and distances flown. RESULTS: The average peak cabin altitude on 207 flights aboard 17 different aircraft was 6341 +/- 1813 ft (1933 m +/- 553 m), significantly higher than when measured in a similar fashion in 1988. Peak cabin altitude was significantly higher for flights longer than 750 mi (7085 +/- 801 ft) compared to shorter flights (5160 +/- 2290 ft/1573 +/- 698 m). Cabin altitude increased linearly with flight distance for flights up to 750 mi in length, but was independent of flight distance for flights exceeding 750 mi. Peak cabin altitude was less than 5000 ft (1524 m) in 70% of flights shorter than 500 mi. Peak cabin altitudes greater than 8000 ft (2438 m) were measured on approximately 10% of the total flights. CONCLUSIONS: Peak cabin altitude on commercial aircraft flights has risen over time. Cabin altitude is lower with flights of shorter distance. Physicians should take these factors into account when determining an individual's need for supplemental oxygen during commercial air travel.

Therapeutic hypercapnia and ventilation-perfusion matching in acute lung injury: low minute ventilation vs inspired CO2.

STUDY OBJECTIVES: Hypercapnic acidosis has antiinflammatory effects in animal models of acute lung injury (ALI) and improves ventilation-perfusion (V/Q) matching in normal lungs. The effect of hypercapnia on V/Q matching in ALI is conflicting. Hypercapnic acidosis produced by reduced tidal volumes (Vts) was associated with an increased shunt fraction (QS/QT) in patients with ALI compared with control subjects. Vt differences between groups make the assessment of hypercapnic acidosis on V/Q matching difficult. Adding CO2 to the inhaled gas allows the comparison of gas exchange under identical Vt conditions. We hypothesized the presence of hypercapnic acidosis from inspired carbon dioxide (ICD) would improve gas exchange in ALI and would be superior to that of low minute ventilation (LVe) produced by reduced respiratory rate, rather than Vt. DESIGN: University laboratory study of anesthetized New Zealand White rabbits. INTERVENTIONS: Assessment of V/Q relationships using the multiple inert gas elimination technique was performed in 10 saline solution-lavaged animals, which were ventilated with 6 mL/kg Vts and a positive end-expiratory pressure of 8 cm H2O. Each rabbit was studied while it was in eucapnia, followed by hypercapnia (Pa(CO2), 95 to 100 mm Hg) induced by LVe from decreased respiratory rate and by 10% ICD, in random order. MEASUREMENTS AND RESULTS: The Pa(O2) was greater in ICD and LVe compared to eucapnia, but no significant differences in alveolar-arterial oxygen pressure difference or Pa(O2)/fraction of inspired oxygen ratio occurred. LVe statistically reduced the mean V/Q distributions compared with ICD and eucapnia. Log SDs of ventilation and combined retention and excretion curves of the dispersion index were both increased during LVe, indicating the presence of unfavorable changes in ventilation distribution. Neither LVe nor ICD altered the QS/QT. CONCLUSIONS: LVe slightly impairs overall gas exchange and ventilation distribution, but does not increase QS/QT compared with eucapnia and ICD. While ICD does not significantly improve gas exchange, it may be superior to LVe in achieving the antiinflammatory effects of "therapeutic" hypercapnia, since it does not adversely alter gas exchange and has the potential to make the lung more uniformly acidotic.

Hypercapnic acidosis and mortality in acute lung injury.

OBJECTIVE: We tested the hypothesis that hypercapnic acidosis is associated with reduced mortality rate in patients with acute lung injury independent of changes in mechanical ventilation. DESIGN: Secondary analysis of randomized clinical trial data using hypothesis-driven multivariate logistic regression. SETTING: Randomized, multiple-center trial (n = 861) comparing 12 mL/kg to 6 mL/kg predicted body weight tidal volumes previously published by the National Institutes of Health Acute Respiratory Distress Syndrome (ARDS) Network. PATIENTS: Acute lung injury patients enrolled in a randomized, multiple-center trial (n = 861). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The adjusted odds ratio and 95% confidence intervals (CI) for 28-day mortality rate associated with hypercapnic acidosis defined as day 1 pH <7.35 and Pa(CO2) >45 mm Hg were 0.14 (95% CI 0.03-0.70, p = .016) in the 12 mL/kg predicted body weight tidal volume group and 1.18 (95% CI 0.59-2.35, p = .639) in the 6 mL/kg predicted body weight tidal volume group. Other definitions of hypercapnic acidosis spanning a range of magnitudes suggest a dose-response association between hypercapnic acidosis and 28-day mortality in the 12 mL/kg predicted body weight tidal volume group. None of our definitions of hypercapnic acidosis were associated with reduction in 28-day mortality in the 6 mL/kg predicted body weight tidal volume group. CONCLUSIONS: Hypercapnic acidosis was associated with reduced 28-day mortality in the 12 mL/kg predicted body weight tidal volume group after controlling for comorbidities and severity of lung injury. These results are consistent with a protective effect of hypercapnic acidosis against ventilator-associated lung injury that was not found when the further ongoing injury was reduced by 6 mL/kg predicted body weight tidal volumes.

Hypercapnic acidosis is protective in an in vivo model of ventilator-induced lung injury.

To investigate whether hypercapnic acidosis protects against ventilator-induced lung injury (VILI) in vivo, we subjected 12 anesthetized, paralyzed rabbits to high tidal volume ventilation (25 cc/kg) at 32 breaths per minute and zero positive end-expiratory pressure for 4 hours. Each rabbit was randomized to receive either an FI(CO(2)) to achieve eucapnia (Pa(CO(2)) approximately 40 mm Hg; n = 6) or hypercapnic acidosis (Pa(CO(2)) 80-100 mm Hg; n = 6). Injury was assessed by measuring differences between the two groups' respiratory mechanics, gas exchange, wet:dry weight, bronchoalveolar lavage fluid protein concentration and cell count, and injury score. The eucapnic group showed significantly higher plateau pressures (27.0 +/- 2.5 versus 20.9 +/- 3.0; p = 0.016), change in Pa(O(2)) (165.2 +/- 19.4 versus 77.3 +/- 87.9 mm Hg; p = 0.02), wet:dry weight (9.7 +/- 2.3 versus 6.6 +/- 1.8; p = 0.04), bronchoalveolar lavage protein concentration (1,350 +/- 228 versus 656 +/- 511 micro g/ml; p = 0.03), cell count (6.86 x 10(5) +/- 0.18 x 10(5) versus 2.84 x 10(5) +/- 0.28 x 10(5) nucleated cells/ml; p = 0.021), and injury score (7.0 +/- 3.3 versus 0.7 +/- 0.9; p < 0.0001). We conclude that hypercapnic acidosis is protective against VILI in this model.