Key result
Acute hypoxia increases carotid blood flow ~16% in HF patients, but not in healthy controls.
Why the study?
Does acute hypoxia differentially affect cerebral blood flow and hemodynamics in patients with chronic heart failure compared to matched controls?
Case-Control (n=31)
Open-label
No
Does acute hypoxia differentially affect cerebral blood flow and hemodynamics in patients with chronic heart failure compared to matched controls?
Acute hypoxia induces compensatory increases in carotid blood flow and diameter in heart failure patients to preserve cerebral perfusion, despite a blunted sympathetic amine response compared to healthy controls.
Answers are grounded in this paper and cite their sources.
Hypoxia may augment carotid flow via reduced resistance in heart failure; case-control data leave open relevance to clinical hypoxic exposures.
Objective Heart failure (HF) is associated with intermittent hypoxia, and the effects of this hypoxia on the cardiovascular system are not well understood. This study was performed to compare the effects of acute hypoxia (10% oxygen) between patients with and without HF. Methods Fourteen patients with chronic HF and 17 matched control subjects were enrolled. Carotid artery changes were examined during the first period of hypoxia, and brachial artery changes were examined during the second period of hypoxia. Data were collected at baseline and after 2 and 4 minutes of hypoxia. Norepinephrine, epinephrine, dopamine, and renin were measured at baseline and after 4 minutes hypoxia. Results The carotid blood flow, carotid systolic diameter, and carotid diastolic diameter increased and the carotid resistance decreased in patients with HF. Hypoxia did not change the carotid compliance, distensibility, brachial artery blood flow and diameter, or concentrations of sympathomimetic amines in patients with HF, but hypoxia increased the norepinephrine level in the control group. Hypoxia increased minute ventilation and decreased the oxygen saturation and end-tidal carbon dioxide concentration in both groups. Conclusion Hypoxia-induced changes in the carotid artery suggest an intensification of compensatory mechanisms for preservation of cerebral blood flow in patients with HF.
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Mansur et al. (2018) conducted a case-control in Chronic heart failure (n=31). Acute hypoxia (10% oxygen in nitrogen with titrated CO2 for isocapnia) in chronic heart failure vs. Matched healthy control subjects breathing 10% oxygen (and baseline room air) was evaluated on Carotid artery blood flow (CBF, L/min/m2) at 4 minutes of acute hypoxia vs baseline in heart failure patients (p=0.002). Acute hypoxia (10% O2) significantly increased carotid blood flow from 0.58 to 0.67 L/min/m2 (P=0.002) and decreased carotid resistance (P=0.005) in heart failure patients, but not in healthy controls.
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