Reductions of maximal V02 and exercise tolerance in comparable patients have been described by others. Maximal V02, originally defined as the V02 at which exercise of increasing intensity fails to increase V02 by at least 150 mL/min despite increasing work rates, was rarely seen in our patients.
The possible reasons for a missing plateau of the V02-work rate relationship are numerous. Muscular deconditioning, a failing increase of pulmonary blood flow during exercise, a rising systemic shunt volume, and increasing hypoxemia contribute to a limited respiratory gas exchange, maximal V02, and exercise capacity.- Considering these limitations, determination of the highest V02 attainable for the given form of exercise— defined as peak V02— appears as the appropriate measure. In our patients, this parameter indicated a severely impaired functional capacity with a reduction in peak V02 of > 50% when compared to control subjects. This limitation in exercise capacity cannot be explained by impaired ventilatory capacity since the breathing reserve, calculated at peak exercise, was even larger in patients than in control subjects. Reading here
Determination of AT by Gas Exchange Kinetics in Cyanosis
A markedly lowered V02AT confirmed a cardiac and muscular limitation and reduced exercise capacity. However, the V02AT could not accurately be determined by the V-slope method despite additional inspection of gas exchange kinetics in almost one third of the patients.
The V-slope method is based on ventilatory adaptations to acid-base changes during the transition from aerobic to anaerobic metabolism. This requires a strictly carbon dioxide-controlled ventilatory drive. Considering the possible role of a hypoxic contribution to ventilatory control in severe sustained cyanosis, a reliable determination of the AT by the V-slope method appears questionable. In addition, the alveolar hyperventilation necessary to maintain a stable PaC02 makes a determination of the AT based on gas exchange kinetics more difficult.