Hemodynamic Effects of Oxygen Therapy in Patients With Acute Exacerbations of Chronic Obstructive Pulmonary Disease: Results
Changes in hemodynamic and gas exchange parameters are summarized in Table 1 and Figure 1. The Sa02, Pa02, and Pv02 increased significantly after oxygen therapy. There was no significant change in cardiac output, mean blood pressure, and pulmonary artery pressure. Systemic and pulmonary vascular resistances tended to decrease, but the change did not reach statistical significance. Individual changes in pulmonary artery pressure and pulmonary vascular resistance were highly variable, and no particular relationship was found between disease severity and changes in the pulmonary vasculature after oxygen therapy. Following a significant increase in Do2 due to the increase in Sa02, calculated Vo2 did not change, and the oxygen extraction ratio decreased.
Breathing oxygen-enriched air is an initial and standard treatment for patients with acute respiratory failure due to COPD. Restoration of Pa02 values above 50 to 55 mm Hg to relieve pulmonary vasoconstriction and tissue hypoxia are the accepted goals of oxygen therapy in these patients; however, there are few clinical studies on the effects of oxygen therapy on systemic and pulmonary hemodynamics during acute exacerbations of COPD. The baseline of most previous studies was obtained after withdrawing oxygen administration for variable periods of time once the patients were admitted. In trying to study patients during the acute hypoxic state, our baseline was the hemodynamic and gas-exchange status shortly after arrival at the hospital, before administering oxygen. Like other investigators, we did not find a decrease in pulmonary vascular resistance, although there was a trend toward lower values after oxygen therapy. There are contradictory results as to the changes in cardiac output after oxygen therapy in these patients. The systemic adaptation to hypoxia that includes an augmented cardiac output allowing maintenance of Do2 is likely to be attenuated when Pa02 increases after oxygen administration. In fact, a decrease in cardiac output during oxygen therapy has been reported in patients with decompensated COPD. In those studies, patients were studied once their condition was stable, after withdrawal of oxygen therapy; however, our patients’ baseline was during the acute exacerbation before oxygen therapy. This fact may explain the different hemodynamic changes observed in our study. We found that cardiac output showed a nonsignificant trend toward higher values, probably due to a better Do2 allowing a better myocardial performance.
Table 1 —Hemodynamic and Oxygen Transport Variables After Administering Oxygen by Face Mask to Patients with Acutely Decompensated COPD
|Dataf||Baseline||30 min||24 h||48 h|
|Pa02, mm Hg||36±8||69 ± 26§||79 ± 46§||68±21§|
|Sa02, percent||62 ±16||87 ±9$||90 ±8$||89 ±7$|
|PvO,, mm Hg||25±5||43± 11$||47 ± 16$||39 ±6$|
|Pco2, mm Hg||58± 15||58± 18||59 ±14||55± 16|
|pH||7.38 ±0.67||7.35 ±0.05||7.36±0.05||7.39 ±0.07|
|Heart rate, beats per min||99± 16||95 ± 14||84 ±13$||82 ± 12§|
|Cl, L/m-m2||3.69 ±1.30||3.90± 1.42||3.89 ±1.09||3.72 ±0.95|
|Pra, mm Hg||13 ±7||11 ±7||10±3||7±2|
|Ppaw, mm Hg||13 ±6||15 ±5||17 ±5||13 ±7|
|Ppa, mm Hg||42 ±12||39 ±9||39± 11||32 ±9|
|SVR, dyne*s/cmm2||1,297 ±580||1,012 ±424||1,148 ±322||1,126 ±262|
|PVR, dyne-s/cm*m2||568 ± 165||506 ±212||461 ±121||418 ±121|
|Do2, mlAg-min||11.13 ±3.69||19.28 ±8.92§||18.57 ±8.68§||19.67 ±7.28§|
|Vo2, ml/kg*min||4.1 ± 1.2||4.3± 1.6||3.5±2.0||4.5± 1.9|
|OER, percent||37.5 ±10.1||25.3 ±9.6*||20.4 ± 6.9§||25.2±7.2§|
Figure 1. Changes in selected hemodynamic and oxygen transport variables after administering oxygen to patients with COPD during acute exacerbation. Asterisks indicate p<0.05 for comparison with baseline.