Key result
Acute hyperoxia is linked to an early ~5% SVR decrease in HF, unlike healthy controls.
Why the study?
Little is known about the tonic influence of peripheral chemoreceptors on cardio-respiratory parameters in heart failure.
Does acute hyperoxia alter systemic vascular resistance differently in HFrEF patients compared to healthy controls?
Observational (n=60)
Single-blind
No
Does acute hyperoxia alter systemic vascular resistance differently in HFrEF patients compared to healthy controls?
Absolute Event Rate: 1174% vs 1242%
p-value: p=<0.01
Acute hyperoxia causes an initial drop in systemic vascular resistance in HFrEF patients, unlike the vasoconstriction seen in healthy controls, suggesting it unmasks augmented tonic activity of peripheral chemoreceptors.
Hyperoxia may initially lower SVR in HFrEF; hypothesis-generating and should not yet alter oxygen use.
Peripheral chemoreceptors' (PCh) hyperactivity increases sympathetic tone. An augmented acute ventilatory response to hypoxia, being a marker of PCh oversensitivity, was also identified as a marker of poor prognosis in HF. However, not much is known about the tonic (chronic) influence of PCh on cardio-respiratory parameters. In our study 30 HF patients and 30 healthy individuals were exposed to 100% oxygen for 1 min during which minute ventilation and hemodynamic parameters were non-invasively recorded. Systemic vascular resistance (SVR) and mean arterial pressure (MAP) responses to acute hyperoxia differed substantially between HF and control. In HF hyperoxia caused a significant drop in SVR in early stages with subsequent normalization, while increase in SVR was observed in controls. MAP increased in controls, but remained unchanged in HF. Bilateral carotid bodies excision performed in two HF subjects changed the response to hyperoxia towards the course seen in healthy individuals. These differences may be explained by the domination of early vascular reaction to hyperoxia in HF by vasodilation due to the inhibition of augmented tonic activity of PCh. Otherwise, in healthy subjects the vasoconstrictive action of oxygen remains unopposed. The magnitude of SVR change during acute hyperoxia may be used as a novel method for tonic PCh activity assessment.
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Tubek et al. (2021) conducted an observational in Heart failure with reduced ejection fraction (HFrEF) (n=60). Acute hyperoxia vs. Healthy controls was evaluated on Systemic vascular resistance (SVR) during 20-40 seconds of hyperoxia (H1) in dyn s cm-5 (p=<0.01). Acute exposure to 100% oxygen caused a significant early decrease in systemic vascular resistance in heart failure patients, contrasting with the vasoconstriction observed in healthy controls.
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