Background: Until recently, compensatory mechanisms have been believed to regulate adequately cerebral blood flow in humans. However, this has been called into question by a series of new investigations suggesting that patients with left ventricular dysfunction suffer from cerebral hypoperfusion. We compared cerebral oxygenation during incremental exercise between patients with valvular heart disease and normal subjects.
Methods: Thirty-three patients with valvular disease and 33 normal subjects performed a symptom-limited incremental exercise test using a cycle ergometer. Oxyhemoglobin at the forehead was continuously monitored during exercise using near-infrared spectroscopy. Respiratory gas measurements were performed on a breath-by-breath basis.
Results: The increase in oxyhemoglobin during exercise was significantly lower in the patients with valvular disease than in normal subjects. The change in oxyhemoglobin during exercise (ΔO2Hb) at the forehead was negatively correlated with the slope of the increase in minute ventilation to the increase in carbon dioxide output (ΔV̇e/ΔV̇co2), and positively correlated with the peak oxygen uptake (V̇o2), gas exchange threshold (GET), and slope of the increase in V̇o2 to the increase in the work rate (ΔV̇o2/ΔWR). Among the patients with valvular disease, 15 patients showed a decrease in oxyhemoglobin at the forehead during exercise. When compared with the patients with increased oxyhemoglobin, those with decreased levels exhibited a higher ΔV̇e/ΔV̇co2 and a lower peak V̇o2, GET, and ΔV̇o2/ΔWR.
Conclusions: The present findings strongly suggest that cerebral oxygenation during exercise is dependent on the cardiovascular and pulmonary systems. The study also indicated the presence of cerebral hypoperfusion during exercise in cardiac patients whose cardiac output fails to increase normally.