News - Part 31

Hemodynamic Effects of Oxygen Therapy in Patients With Acute Exacerbations of Chronic Obstructive Pulmonary Disease: ConclusionAn abnormal relationship between Do2 and Vo2 has been reported in states of tissue hypoxia. When normally functioning mechanisms, such as an increase in the oxygen extraction ratio and blood flow, compensate for changes in Do2, Vo2 is independent of supply. Only when Do2 decreases below the so-called critical value do those mechanisms become exhausted, and Vo2 becomes dependent on Do2. Although criticized by some authors who did not find this abnormal relationship when Vo2 is measured by expired gas analysis, rather than calculated by the modified Fick equation, others accept that in certain clinical conditions (such as sepsis, the adult respiratory distress syndrome, pulmonary hypertension, and chronic congestive heart failure), there is an abnormal dependency of Vo2 on Do2 for a wide range of supranormal values of Do2. Since those patients have normal Do2 values, it has been proposed that this dependency phenomenon reveals a covert tissue oxygen debt. It can be postulated that patients with decompensated COPD suffer such an occult oxygen debt that could be demonstrated by increases in Vo2 when Do2 increases.
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Standard treatment of these patients includes the administration of oxygen to increase the oxygen-carrying capacity of the blood. Therefore, defining whether increasing Sa02 in these patients leads to a rise in Vo2 is of great clinical importance in order to determine if the excess oxygen supplied is actually used by the tissues. Degaute et al observed that increasing FIo2 from 0.21 to 0.28 leads, to an increase in Pa02, Pv02, and the coefficient of oxygen delivery (the inverse of the oxygen extraction ratio) and to a decrease in cardiac output. A subgroup of patients with higher Pa02 showed no changes in Do2 and a decrease in cardiac output, whereas those with more severe pulmonary impairment presented an increase in Do2, with no change in cardiac output and greater decreases in the oxygen extraction ratio. Although no Vo2 values are reported, it can be inferred from their data that Vo2 decreased in the group in which Do2 did not change (due to the decrease in the oxygen extraction ratio), and Vo2 possibly remained constant in the group in which Do2 increased, due to the coincident and more marked decrease in the oxygen extraction ratio.
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Hemodynamic Effects of Oxygen Therapy in Patients With Acute Exacerbations of Chronic Obstructive Pulmonary Disease: ResultsChanges 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.
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Hemodynamic parameters, Sa02, and mixed-venous oxygen saturation (SvOJ were measured in all patients once they were monitored as described previously (breathing fractional concentration of oxygen in the inspired gas [FIoJ = 0.21). Those values were taken as the baseline. Then oxygen therapy at an FIo2 sufficient to keep Pa02 above 55 mm Hg was started, and measurements were repeated at 30 min and at 24 and 48 h thereafter. When subsequent measurements were made, a steady state was ensured by a change in respiratory’ and heart rates less than 20 percent, systolic blood pressure less than 15 percent, and Sa02 less 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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Hemodynamic Effects of Oxygen Therapy in Patients With Acute Exacerbations of Chronic Obstructive Pulmonary Disease: Materials and MethodsThe effects of long-term oxygen therapy in patients with COPD are well known. A decrease in pulmonary hypertension accompanied by an improvement in the quality of life and survival rate of these patients has been reported previously; however, the changes in hemodynamic and oxygen transport variables induced by oxygen therapy in patients during acute exacerbations are less well understood.
The reported hemodynamic effects of oxygen therapy during acute exacerbations differ among investigators. Abraham et al found no change in cardiac output. Degaute et al studied 35 patients with acute exacerbations of COPD during the first day of admission after withdrawal of oxygen therapy. These investigators found that reintroduction of oxygen therapy caused a drop in the cardiac output and an increase in oxygen delivery (Do2) due to an improvement in arterial oxygen saturation (Sa02). Pulmonary artery pressure did not change. Lejeune et al, in a series of 17 patients with acute exacerbations of COPD studied during the first 3 days of hospitalization, observed a decrease in cardiac output induced by oxygen therapy, whereas pulmonary vascular resistance did not change.
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