The spontaneous breathing pattern and work of breathing of patients with acute respiratory distress syndrome and acute lung injury.

BACKGROUND: The spontaneous breathing pattern and its relationship to compliance, resistance, and work of breathing (WOB) has not been examined in patients with acute respiratory distress syndrome (ARDS) or acute lung injury (ALI). Clinically, the ratio of respiratory frequency to tidal volume (f/VT) during spontaneous breathing may reflect adaptation to altered compliance, resistance, and increased WOB. We examined the relationship between f/VT, WOB, and respiratory system mechanics in patients with ARDS/ALI. METHODS: Data from spontaneous breathing trials were collected from 33 patients (20 with ARDS, 13 with ALI) at various points in their disease course. WOB and respiratory system mechanics were measured with a pulmonary mechanics monitor that incorporates Campbell diagram software. Differences between the patients with ARDS and ALI were assessed with 2-sided unpaired t tests. Multivariate linear regression models were constructed to assess the relationship between f/VT and other pulmonary-related variables. RESULTS: Patients with ARDS had significantly lower compliance than those with ALI (24 +/- 6 mL/cm H2O vs 40 +/- 13 mL/cm H2O, respectively, p < 0.001), but this did not translate into significant differences in either WOB (1.70 +/- 0.59 J/L vs 1.43 +/- 0.90 J/L, respectively, p = 0.30) or f/VT (137 +/- 82 vs 107 +/- 49, respectively, p = 0.23). Multivariate linear regression modeling revealed that peak negative esophageal pressure, central respiratory drive, duration of ARDS/ALI, minute ventilation deficit between mechanical ventilation and spontaneous breathing, and female gender were the strongest predictors of f/VT. CONCLUSION: The characteristic rapid shallow breathing pattern in patients with ARDS/ALI occurs in the context of markedly diminished compliance, elevated respiratory drive, and increased WOB. That f/VT had a strong, inverse relationship to peak negative esophageal pressure also may reflect the influence of muscle weakness.

Prognostic value of the pulmonary dead-space fraction during the first 6 days of acute respiratory distress syndrome.

BACKGROUND: The ratio of pulmonary dead space to tidal volume (VD/VT) in acute respiratory distress syndrome (ARDS) is reported to be between 0.35 and 0.55. However, VD/VT has seldom been measured with consideration to the evolving pathophysiology of ARDS. METHODS: We made serial VD/VT measurements with 59 patients who required mechanical ventilation for > or = 6 days. We measured VD/VT within 24 h of the point at which the patient met the American-European Consensus Conference criteria for ARDS, and we repeated the VD/VT measurement on ARDS days 2, 3, and 6 with a bedside metabolic monitor during volume-regulated ventilation. We analyzed the changes in VD/VT over the 6-day period to determine whether VD/VT has a significant association with mortality. RESULTS: VD/VT was significantly higher in nonsurvivors on day 1 (0.61 +/- 0.09 vs 0.54 +/- 0.08, p < 0.05), day 2 (0.63 +/- 0.09 vs 0.53 +/- 0.09, p < 0.001), day 3 (0.64 +/- 0.09 vs 0.53 +/- 0.09, p < 0.001), and day 6 (0.66 +/- 0.09 vs 0.51 +/- 0.08, p < 0.001). CONCLUSION: In ARDS a sustained VD/VT elevation is characteristic of nonsurvivors, so dead-space measurements made beyond the first 24 hours may have prognostic value.

The effects of tidal volume demand on work of breathing during simulated lung-protective ventilation.

BACKGROUND: Lung-protective ventilation (LPV) can result in a ventilator tidal volume (V(T)) below patient V(T) demand, which may elevate work of breathing (WOB). Increasing the ventilator inspiratory flow may not sufficiently reduce WOB, because the patient's flow-time requirements may exceed the ventilator's flow-time delivery pattern. We investigated (1) the effects of V(T) demand on WOB during LPV and (2) which ventilator pattern best reduced WOB while achieving LPV goals. METHODS: A standard WOB lung model simulated assisted breathing. Using 3 ventilators (Hamilton Veolar, Hamilton Galileo, and Dräger Evita 2 dura), we tested volume-control ventilation with a constant flow pattern (VCV-CF), volume-control ventilation with a decelerating flow (VCV-DF), and pressure-control ventilation (PCV). Simulated V(T) demand was increased from 50-125% of the ventilator-delivered V(T) (400 mL) as ventilator inspiratory time (T(I)) was decreased (0.95, 0.80, 0.65, and 0.45 s) relative to simulated T(I) (0.8 s). WOB was measured with a pulmonary mechanics monitor. RESULTS: During VCV-CF and VCV-DF, a V(T) demand of > or = 100% drastically increased WOB, attributable to imposed WOB from the inspiratory valve. Increasing inspiratory flow by using the decelerating flow pattern and/or decreasing T(I) reduced WOB, but generally not to normal levels. "Double-triggered" breaths, with excessive V(T) delivery, often occurred when ventilator T(I) was well below simulated T(I). PCV was most effective in reducing WOB, but V(T) delivery exceeded the LPV target unless T(I) was reduced. CONCLUSIONS: Given our dual goals of reducing both WOB and V(T) during LPV, VCV-DF with relatively brief T(I) appeared to be the best option, followed by PCV with a relatively brief T(I).

Pulmonary dead-space fraction as a risk factor for death in the acute respiratory distress syndrome.

BACKGROUND: No single pulmonary-specific variable, including the severity of hypoxemia, has been found to predict the risk of death independently when measured early in the course of the acute respiratory distress syndrome. Because an increase in the pulmonary dead-space fraction has been described in observational studies of the syndrome, we systematically measured the dead-space fraction early in the course of the illness and evaluated its potential association with the risk of death. METHODS: The dead-space fraction was prospectively measured in 179 intubated patients, a mean (+/-SD) of 10.9+/-7.4 hours after the acute respiratory distress syndrome had developed. Additional clinical and physiological variables were analyzed with the use of multiple logistic regression. The study outcome was mortality before hospital discharge. RESULTS: The mean dead-space fraction was markedly elevated (0.58+/-0.09) early in the course of the acute respiratory distress syndrome and was higher among patients who died than among those who survived (0.63+/-0.10 vs. 0.54+/-0.09, P<0.001). The dead-space fraction was an independent risk factor for death: for every 0.05 increase, the odds of death increased by 45 percent (odds ratio, 1.45; 95 percent confidence interval, 1.15 to 1.83; P=0.002). The only other independent predictors of an increased risk of death were the Simplified Acute Physiology Score II, an indicator of the severity of illness (odds ratio, 1.06; 95 percent confidence interval, 1.03 to 1.08; P<0.001) and quasistatic respiratory compliance (odds ratio, 1.06; 95 percent confidence interval, 1.01 to 1.10; P=0.01). CONCLUSIONS: Increased dead-space fraction is a feature of the early phase of the acute respiratory distress syndrome. Elevated values are associated with an increased risk of death.