Heliox improves hemodynamics in mechanically ventilated patients with chronic obstructive pulmonary disease with systolic pressure variations

Objective: To test the hypothesis that, compared with airoxygen, heliox would improve cardiac performance in mechanically ventilated patients with severe chronic obstructive pulmo- nary disease and systolic pressure variations > 15 mm Hg and to determine clinical variables associated with favorable hemodynamic responses to heliox. Design: A prospective interventional study. Setting: Medical and respiratory intensive care units at a university-affiliated tertiary medical center. Patients. Twenty-five consecutive mechanically ventilated patients with severe chronic obstructive pulmonary disease and acute respiratory failure who had systolic pressure variations >15 mm Hg. Interventions. Respiratory and hemodynamic measurements were taken at the following time with the same ventilator setting: a) baseline; b) after 30 mins with heliox; and c) 30 mins after return to air-oxygen. Measurements and Main Results. Heliox ventilation decreased intrinsic positive end-expiratory pressure (air-oxygen vs. heliox [mean ± So] 13 ± 4 cm H(2)0 vs. 5 ± 2 cm H(2)0, P <.05), trapped lung volume (air-oxygen vs. heliox 362 ± 67 mL vs. 174 ± 86 mL, p <.05), and respiratory changes in systolic pressure variations (Δ PP) (air-oxygen vs. heliox 29 ± 5% vs.13 ± 7%, p <.05). In the ten patients with pulmonary arterial catheters, heliox decreased mean pulmonary arterial pressure, right atrial pressure, and pulmonary arterial occlusion pressure and increased cardiac index. Preheliox Δ PP correlated with the magnitude of reduction in intrinsic positive end-expiratory pressure during heliox ventilation. Age, preheliox Paco(2), and ratio of forced expiratory volume at first second to forced vital capacity correlated inversely, whereas preheliox Δ PP correlated positively with increases in cardiac index. Conclusions. Heliox may be a useful adjunct therapy in patients with severe chronic obstructive pulmonary disease during acute respiratory failure who have persistent intrinsic positive end-expiratory pressure- induced hemodynamic changes despite ventilator management.