Effects of supplemental O2 inhalation on cerebral oxygenation during exercise in patients with left ventricular dysfunction.

BACKGROUND: It has been recently reported that cerebral oxyhemoglobin (O(2)Hb) decreases during exercise in nearly 50% of patients with dilated cardiomyopathy. The present study evaluated whether the inhalation of supplemental O(2) diminishes the decrease in cerebral O(2)Hb during exercise. METHODS AND RESULTS: Ten patients with a left ventricular ejection fraction <50% and a clearly observable decrease in cerebral O(2)Hb during preliminary exercise testing underwent 2 additional symptom-limited incremental exercise tests: 1 while breathing room air (control) and the other while breathing 50% O(2). In the latter test, the switch from room air to 50% O(2) was performed, on average, at 43.0+/-14.2 W. Cerebral O(2)Hb was continuously monitored during exercise using near-infrared spectroscopy. In the control exercise test, cerebral O(2)Hb gradually decreased as the work rate increased in all the subjects. When the subjects breathed 50% O(2), this decrease in cerebral O(2)Hb was diminished. The change in cerebral O(2)Hb from rest to peak exercise during the test under 50% O(2) was significantly higher than that during the control test (-0.23 +/-1.89 vs -2.47+/-1.57 micromol/L, p=0.002). Similarly, the change in the cerebral tissue oxygenation index was significantly higher in the test under 50% O(2) (0.45 +/-4.46 vs -3.33+/-3.06%, p=0.023). CONCLUSIONS: Impaired cerebral oxygenation during moderate to heavy intensity exercise in patients with left ventricular dysfunction can be offset by breathing supplemental O(2).

Influence of cerebrovascular arteriosclerosis on cerebral oxygenation during exercise.

BACKGROUND: Although it is assumed that cerebral oxygenation during exercise is influenced by both cardiopulmonary function and cerebrovascular arteriosclerosis, the latter factor has not been fully clarified. In the present study the relationship between the degree of cerebrovascular arteriosclerosis and cerebral oxygenation during exercise was investigated. METHODS AND RESULTS: A total of 109 patients (69 patients with coronary artery disease, 40 patients with hypertensive heart disease) (61.7+/-9.7 years) performed a symptom-limited exercise test with respiratory gas measurements (CPX). From the respiratory gas analysis, peak O(2) uptake (VO(2)), the slope of the increase in VO(2) to the increase in work rate (DeltaVO (2)/DeltaWR), and the slope of the increase in ventilation to the increase in CO(2) output (VE/VCO(2) slope) were calculated. Oxyhemoglobin (O(2)Hb) at the forehead was monitored using near-infrared spectroscopy. The brain ischemic score was counted based upon fluid-attenuated inversion recovery images of magnetic resonance imaging and expressed from 0 to 4. When compared with patients with a lower ischemic score (<2, n=67), those with a higher ischemic score (> or =2, n=42) had a lower increase in brain O(2)Hb during exercise (-1.08 +/-2.7 vs 0.77+/-4.1 micromol/L, p=0.011). Of brain ischemic score, left ventricular ejection fraction, peak VO(2), DeltaVO(2)/DeltaWR, and the VE/VCO(2) slope, DeltaVO(2)/ DeltaWR was found to be the sole independent index determining cerebral O(2)Hb during exercise. The CPX parameters were also significantly related to the degree of cerebrovascular arteriosclerosis. CONCLUSIONS: Although cerebral oxygenation during exercise is mainly related to cardiopulmonary function, the degree of cerebrovascular arteriosclerosis partly influences cerebral oxygenation in patients with risk factors for atherosclerosis.

Critical level of cerebral oxygenation during exercise in patients with left ventricular dysfunction.

BACKGROUND: In a recent study the indexes of cerebral oxygenation decreased during maximal exercise in nearly half of all patients with left ventricular dysfunction. Whether these levels decrease severely enough to influence mental status or level of consciousness was evaluated in the present study. METHODS AND RESULTS: Forty-two patients with idiopathic dilated cardiomyopathy (IDC) and 29 healthy subjects underwent a symptom-limited maximal exercise test. The cerebral oxyhemoglobin (O(2)Hb) and tissue oxygenation index (TOI) were continuously monitored using near-infrared spectroscopy. The changes in O(2)Hb and TOI were also measured in 7 subjects: 2 who experienced episodes of reduced consciousness caused by sudden decreases in blood pressure during exercise recovery and 5 who exhibited sustained ventricular tachycardia during an electrophysiological study. The change in cerebral O(2)Hb during exercise in patients with IDC averaged 0.38+/-3.39 micromol/L, significantly lower than in the normal subjects (4.30+/-4.47 micromol/L, p<0.0001). The cerebral O(2)Hb decreased during exercise in 18 of 42 patients with IDC. The change in cerebral TOI in the IDC patients during exercise was significantly less than that in the normal subjects (-2.0+/-4.7 vs 2.1+/-5.8%, p=0.002). The mean decreases in cerebral O(2)Hb and TOI were -5.34 micromol/L and -9.7%, respectively, in the patients with reduced consciousness during exercise recovery, and -2.52 micromol/L and -16.5%, respectively, in those with ventricular tachycardia. CONCLUSION: The indexes of cerebral oxygenation may drop severely enough during maximal exercise in some patients with severe IDC that consciousness is affected.

Cerebral oxygenation during exercise and exercise recovery in patients with idiopathic dilated cardiomyopathy.

We compared cerebral oxygenation during exercise and during exercise recovery between 22 healthy subjects and 35 patients with idiopathic dilated cardiomyopathy (IDC). Although cerebral oxyhemoglobin increased during exercise in most of the healthy subjects, oxyhemoglobin decreased during exercise in 15 of 35 patients with IDC. Cerebral oxygenation during exercise and exercise recovery was related to left ventricular function in the patients with IDC.

Cerebral oxygenation during exercise in cardiac patients.

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 (DeltaO(2)Hb) at the forehead was negatively correlated with the slope of the increase in minute ventilation to the increase in carbon dioxide output (DeltaE/DeltaCO(2)), and positively correlated with the peak oxygen uptake (O(2)), gas exchange threshold (GET), and slope of the increase in O(2) to the increase in the work rate (DeltaO(2)/DeltaWR). 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 DeltaE/DeltaCO(2) and a lower peak O(2), GET, and DeltaO(2)/DeltaWR. 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.