Abstract
Cerebral tissue oxygen saturation (SctO2) reflects cerebral perfusion and tissue oxygen consumption, which decline in some patients with heart failure with reduced ejection fraction (HFrEF) or stroke, especially during exercise. Its physiologic basis and clinical significance remain unclear. We aimed to investigate the association of SctO2 with oxygen transport physiology and known prognostic factors during both rest and exercise in patients with HFrEF or stroke. Thirty-four HFrEF patients, 26 stroke patients, and 17 healthy controls performed an incremental cardiopulmonary exercise test using a bicycle ergometer. Integrated near-infrared spectroscopy and automatic gas analysis were used to measure cerebral tissue oxygenation and cardiac and ventilatory parameters. We found that SctO2 (rest; peak) were significantly lower in the HFrEF (66.3±13.3%; 63.4±13.8%,) than in the stroke (72.1±4.2%; 72.7±4.5%) and control (73.1±2.8%; 72±3.2%) groups. In the HFrEF group, SctO2 at rest (SctO2rest) and peak SctO2 (SctO2peak) were linearly correlated with brain natriuretic peptide (BNP), peak oxygen consumption (), and oxygen uptake efficiency slope (r between -0.561 and 0.677, p < 0.001). Stepwise linear regression showed that SctO2rest was determined by partial pressure of end-tidal carbon dioxide at rest (PETCO2rest), hemoglobin, and mean arterial pressure at rest (MAPrest) (adjusted R = 0.681, p < 0.05), while SctO2peak was mainly affected by peak carbon dioxide production () (adjusted R = 0.653, p < 0.05) in patients with HFrEF. In conclusion, the study delineates the relationship of cerebral saturation and parameters associated with oxygen delivery. Moreover, SctO2peak and SctO2rest are correlated with some well-recognized prognostic factors in HFrEF, suggesting its potential prognostic value.
Highlights
Cerebral desaturation may occur in patients with heart failure with reduced ejection fraction (HFrEF) or stroke [1, 2]
Oxygen saturation of cerebral tissue were significantly lower in the HFrEF (66.3 ±13.3%; 63.4±13.8%) than that in the stroke (72.1±4.2%; 72.7±4.5%) and control (73.1±2.8%; 72±3.2%) groups as revealed by two-way repeated measure ANOVA, while those in the stroke group were close to the healthy control
In the HFrEF group, SctO2 decreased significantly at peak exercise, a phenomenon not observed in the stroke or healthy control groups (Fig 1, Table 3)
Summary
Cerebral desaturation may occur in patients with heart failure with reduced ejection fraction (HFrEF) or stroke [1, 2]. The former is due to insufficient cardiac output and dead space ventilation. The latter could be due to disruption of cerebral blood flow (CBF) from vascular abnormalities and neurologic deficit-related respiratory muscle weakness [3,4,5]. Cerebral oxygenation is determined by arterial oxygen concentration, CBF, and cerebral tissue oxygen consumption, which represent oxygen supply and demand [7]. Insufficient hemoglobin (Hb) concentration, oxygen desaturation, and disruption of cerebral perfusion may result in decreased oxygen supply and cerebral desaturation
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