Effects of helium-oxygen on intrinsic positive end-expiratory pressure in intubated and mechanically ventilated patients with severe chronic obstructive pulmonary disease
D. Tassaux et al., Effects of helium-oxygen on intrinsic positive end-expiratory pressure in intubated and mechanically ventilated patients with severe chronic obstructive pulmonary disease, CRIT CARE M, 28(8), 2000, pp. 2721-2728
Objective: To test the hypothesis that replacing 70:30 nitrogen: oxygen (Ai
r-O-2) with 70:30 helium:oxygen (He-O-2) can decrease dynamic hyperinflatio
n ("Intrinsic" positive end-expiratory pressure) in mechanically ventilated
patients with chronic obstructive pulmonary disease (COPD), and to documen
t the consequences of such an effect on arterial blood gases and hemodynami
cs.
Design: Prospective, interventional study.
Setting: Medical intensive care unit, university tertiary care center.
Patients: Twenty-three intubated, sedated, paralyzed, and mechanically vent
ilated patients with COPD enrolled within 36 hrs after intubation.
Interventions: Measurements were taken at the following time points, all wi
th the same ventilator settings: a) baseline; b) after 45 mins with He-O-2;
c) 45 mins after return to Air-O-2. The results were then compared to thos
e obtained in a test lung model using the same ventilator settings.
Main Results (mean +/- so):Trapped lung volume and intrinsic positive end-e
xpiratory pressure decreased during He-O-2 ventilation (215 +/- 125 mL vs.
99 +/- 15 mL and 9 +/- 2.5 cm H2O vs. 5 +/- 2.7 cm H2O, respectively; p < .
05). Likewise, peak and mean airway pressures declined with He-O-2 (30 +/-
5 cm H2O vs. 25 +/- 6 cm H2O and 8 +/- 2 cm H2O vs. 7 +/- 2 cm H2O, respect
ively; p < .05). These parameters all rose to their baseline values on retu
rn to Air-O-2 (p < .05 vs, values during He-O-2). These results were in acc
ordance with those obtained in the test lung model. There was no modificati
on of arterial blood gases, heart rate, or mean systemic arterial blood pre
ssure. In 12/23 patients, a pulmonary artery catheter was in place, allowin
g hemodynamic measurements and venous admixture calculations. Switching to
He-O-2 and back to Air-O-2 had no effect on pulmonary artery pressures, rig
ht and left ventricular filling pressures, cardiac output, pulmonary and sy
stemic vascular resistance, or venous admixture.
Conclusion: In mechanically ventilated COPD patients with intrinsic positiv
e end-expiratory pressure, the use of He-O-2 can markedly reduce trapped lu
ng volume, intrinsic positive end-expiratory pressure, and peak and mean ai
rway pressures. No effect was noted on hemodynamics or arterial blood gases
. He-O-2 might prove beneficial in this setting to reduce the risk of barot
rauma, as well as to improve hemodynamics and gas exchange in patients with
very high levels of intrinsic positive end-expiratory pressure. (Crit Care
Med 2000; 28:2721-2728).