The consequences of oxygen therapy in patients with stable COPD have been previously reported; however.

The consequences of oxygen therapy in patients with stable COPD have been previously reported; however, the hemodynamic changes induced according to oxygen therapy in patients during acute exacerbations of COPD are les well known. To investigate the hemodynamic imports of controlled oxygen therapy in patients with acute exacerbations of COPD shortly after arriving at the hospital, we studied 15 consecutive patients who came to the unforeseen occasion room with acutely decompensated COPD that did not require mechanical ventilation. Patients were monitored with a pulmonary artery catheter and a radial artery catheter. Oxygen uptake was calculated through the modified Fick equation. Arterial and venous life-blood gas levels and hemodynamic parameters were measured while breathing place air (baseline) and after 30 min forward oxygen therapy via face mask. Measurement were repeated after 24 and 48 h The fractional concentration of oxygen in the inspired gas ([FIo.sub.2]) administered was adjusted to continue the [PaO.sub.2] above 55 mm Hg All patients had a [PaO.sub.2] below 45 mm Hg at the beginning of the thought After 30 min of oxygen therapy, there was a significant (p<005) increase in arterial oxygen saturation (from 62 [+ or -] 16 to 87 [+ or -] 9 percent) mixed-venous oxygen compressing (from 25 [+ or -] 5 to 43 [+ or -] 11 mm Hg) and oxygen delivery (from 111 [+ or -] 37 to 193 [+ or -] 89 ml/kg.min). Oxygen uptake did not change significantly (from 41 [+ or -] to 43 [+ or -] 16 ml/kg.min). The oxygen extraction ratio decreased from 375 [+ or -] 101 to 253 [+ or -] 96 percent These changes were maintained during the following 48 h There were no significant changes in cardiac output and systemic vascular resistance. A stretch toward lower values of pulmonary vascular resistance did not reach statistical significance. We decide that oxygen therapy in patients with acute excerbations of COPD that do not require mechanical ventilation increases oxygen delivery without changes in cardiac output or oxygen uptake.

The forces of long-term oxygen therapy in patients with COPD are well known. A decrease in pulmonary hypertension accompanied by means of an improvement in the quality of life and survival rate of these patients has been reported previously;[1-6] however, the changes in hemodynamic and oxygen transport variables induced by means of oxygen therapy in patients during acute exacerbations are les well understood.

The reported hemodynamic issues of oxygen therapy during acute exacerbations differ among investigators. Abraham et al[7] base no change in cardiac output Degaute et al[8] studied 35 patients with acute exacerbations of COPD during the first day of admission after withdrawal of oxygen therapy. These investigators[8] rest that reintroduction of oxygen therapy caused a globule in the cardiac output and an increase in oxygen delivery ([Do.sub.2]) proper to an improvement in arterial oxygen saturation ([SaO.sub.2]). Pulmonary artery press did not change. Lejeune et al,[9] in a series of 17 patients with acute exacerbations of COPD studied during the first 3 days of hospitalization, observ a decrease in cardiac output induced at oxyen therapy, whereas pulmonary vascular resistance did not change.

All of those studies were done in patients during the first not many days of hospitalization, and hemodynamic changes were investigated after withdrawal of oxygen therapy. We designed our thought to investigate the effects of controll oxygen therapy onward hemodynamic parameters in patients with acute excerbations of COPD shortly after arriving at the pressing necessity department, before receiving oxygen therapy.

MATERIALS AND METHODS

We studied 15 consecutive patients (10 male patients; mean age, 62 [+ or -] 7 years) admitted to the necessity department with acutely decompensated COPD befitting to acute bronchitis. The diagnosis of COPD was based forward the patient's history, physical examination, chest x-ray film, arterial posterity gas levels, and ECG. A history of daily expectoration during at least 3 month of the year during at least 2 consecutive years was required for the diagnosis of COPD Eleven patients provided the consequence s of previous pulmonary function proofs showing airway obstruction (ratio of forced expiratory convolution in 1 s over forced vital capacity <60 percent of the predicted value). The chest x-ray film obtained forward admission showed no infiltrates, cardiomegaly, or significant pleural effusions. Four patients were febrile (peripheral temperature above 380 [degrees] C) and became afebrile with the first 36 h in the ICU. The initial white family cell count was [12,245/mm.sup.3] [+ or -] [782/mmsup3] The general condition of all patients improved while in the ICU, allowing discharge after a mean stay of 58 [+ or -] 05 days.

Hemodynamic parameters, [SaO.sub.2], and mixed-venous oxygen saturation ([SVOsub2]) were measured in all patients one time they were monitored as described previously (breathing fractional concentration of oxygen in the inspired gas [FIo.sub.2] = 021) Those values were taken as the baseline. Then oxygen therapy at an [FIo.sub.2] sufficient to preserve [PaO.sub.2] above 55 mm Hg was started, and measurements were repeated at 30 min and at 24 and 48 h thereafter. When succeeding measurements were made, a steady state was ensur from a change in respiratory and heart rates les than 20 percent systolic line pressure less than 15 percent and [SaO.sub.2] les than 3 percent during the previous hour. All patients survived the ICU admission and were transferred to other medical wards when their condition improved.

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