Hemodynamic Effects of Oxygen Therapy in Patients With Acute Exacerbations of Chronic Obstructive Pulmonary Disease: Conclusion
An 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.
The mean baseline value of Do2 in our patients was 11.1±3.7 ml/kg*min, and some values fell below what is considered the critical value of Do2 in humans. Despite a significant rise in Do2, Vo2 did not change. This lack of supply-dependence has several explanations. First, patients with COPD may have a normal Do/Vo2 relationship, and compensatory mechanisms keep Vo2 constant despite changes in Do2; however, there have been reports of a pathologic supply-dependent Vo2 manifested by a vasodilatory intervention in patients with pulmonary hypertension, including patients with COPD. Secondly, patients with acutely decompensated COPD may have an occult oxygen debt, that is, one not manifest by increasing Sa02. In fact, there are data to support that oxygen uptake is more limited by convective than diffusive transport. Increasing Do2 by interventions that do not increase blood flow, such as increasing the hematocrit, does not uniformly lead to increases in oxygen uptake. Therefore, it could be that acutely decompensated patients with COPD present an occult oxygen debt that is not manifest after increasing Do2 by increasing Sa02. Since we could not include a control group (ie, patients not given oxygen therapy), it is not possible to establish how much of the observed changes in Do2 and Vo2 were attributable to oxygen therapy and how much to the natural history of this acute illness. It could be that a better control of infection and a decrease in the work of breathing as the effect of treatment takes place would contribute to a decrease in oxygen demand and therefore in Vo2. Nevertheless, our data support the concept that conventional treatment of these conditions and increasing Do2 by means of oxygen therapy do not result in a higher Vo2. This can be due to the absence of a pathologic Dog/Voa relationship in these patients, to a decrease in metabolic demands as the acute illness is controlled, or to the presence of a Vo2 more dependent on blood flow than on global Do2.