Based on the data we obtained, it remains difficult to differentiate whether these eight patients actually did not recruit anaerobic metabolism during exercise or the determination of AT was obscured by alterations in ventilatory pattern and control. Thus, VO2AT values should be carefully interpreted in patients with cyanotic heart disease.
An increased VE had been reported for different causes of hypoxemia, eg, for persons living at high altitude, and patients affected by cyanotic congenital heart disease. As previously described, the increase in ventilation correlates with the magnitude of the right-to-left shunt and therefore the severity of cyanosis. To our knowledge, no data were available describing the correlation between parameters of ventilatory efficiency and symptomatic state in this patient group. Our data show significantly elevated ventilatory requirements secondary to a marked reduction in ventilatory efficiency. The impaired ventilatory efficiency strongly correlates with the extent of cyanosis as determined by PaO2 values at rest and under exercise. In contrast, no correlation between Pa02 and ventilatory efficiency exists in healthy volunteers. add comment
Factors that contribute to the impairment of ventilatory efficiency are elevated ventilation of physiologic or anatomic dead space or alveolar hyperventilation. Similarly, a decrease in PetC02 and an increase in PeT02 can result from the elevated ventilation of physiologic dead space, as well as from alveolar hyperventilation. An increased ventilation of anatomic dead space should not influence PeT02 significantly.
The dependence of ventilatory efficiency on physiologic dead space has been described in patients with chronic heart failure and pulmonary hyper-tension. Changes were considered to be due to pulmonary vasoconstriction with alveolar hypoperfusion and ventilation/perfusion mismatching.A. Our study included patients with primary pulmonary hyperperfusion due to left-to-right shunt and consecutive pulmonary hypertension (eg, patients with Eisenmenger syndrome), or patients affected by pulmonary hypoperfusion (eg, patients with pulmonary stenosis due to Fallot tetralogy). In both conditions, alveolar hypoperfusion leads to an increase in physiologic dead space and, therefore, impaired ventilatory efficiency. For these reasons, altered ventilation of physiologic dead space appears to be more important for the observed changes in ventilatory efficiency than possible variations in anatomic dead space ventilation.