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Hypocapnia in women with fibromyalgia.

Scand J Pain

January 2024

Department of Public Health and Caring Sciences, Section of Family Medicine, Uppsala University, Box 564, SE-751 22, Uppsala, Sweden.

Objectives: The purpose of this study was to investigate whether people with fibromyalgia (FM) have dysfunctional breathing by examining acid-base balance and comparing it with healthy controls.

Methods: Thirty-six women diagnosed with FM and 36 healthy controls matched for age and gender participated in this cross-sectional study. To evaluate acid-base balance, arterial blood was sampled from the radial artery.

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Dynamics of the cerebral autoregulatory response to paced hyperventilation assessed using subcomponent and time-varying analyses.

J Appl Physiol (1985)

August 2022

Department of Cardiovascular Sciences, Cerebral Haemodynamics in Ageing and Stroke Medicine (CHiASM) Research Group, University of Leicester, Leicester, United Kingdom.

Cerebral blood flow (CBF) can be altered by a change in partial pressure of arterial CO (Pco), being reduced during hyperventilation (HPV). Critical closing pressure (CrCP) and resistance area product (RAP) are parameters that can be studied to understand this change, but their dynamic response has not been investigated during paced HPV (PHPV). Seventy-five participants had recordings at rest and during PHPV.

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Background: Mechanical ventilation interferes with cerebral perfusion via changes in intrathoracic pressure and/or as a consequence of alterations in CO2. Cerebral vascular vasoreactivity is dependent on CO2, and hypocapnia can potentially lead to vasoconstriction and subsequent decrease in cerebral blood flow. Thus, we aimed at characterizing whether protective ventilation with mild permissive hypercapnia improves cerebral perfusion in infants.

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Non-pulsatile blood flow is associated with enhanced cerebrovascular carbon dioxide reactivity and an attenuated relationship between cerebral blood flow and regional brain oxygenation.

Crit Care

December 2019

Division of Cardiothoracic and Vascular Anaesthesia and Intensive Care Medicine, Department of Anaesthesia, Intensive Care Medicine, and Pain Medicine, Vienna General Hospital, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria.

Background: Systemic blood flow in patients on extracorporeal assist devices is frequently not or only minimally pulsatile. Loss of pulsatile brain perfusion, however, has been implicated in neurological complications. Furthermore, the adverse effects of absent pulsatility on the cerebral microcirculation are modulated similarly as CO vasoreactivity in resistance vessels.

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Slow V˙O kinetics in acute hypoxia are not related to a hyperventilation-induced hypocapnia.

Respir Physiol Neurobiol

May 2018

Canadian Centre for Activity and Aging, The University of Western Ontario, London, ON, Canada; School of Kinesiology, The University of Western Ontario, London, ON, Canada; Department of Physiology and Pharmacology, The University of Western Ontario, London, ON, Canada. Electronic address:

We examined whether slower pulmonary O uptake (V˙O) kinetics in hypoxia is a consequence of: a) hypoxia alone (lowered arterial O pressure), b) hyperventilation-induced hypocapnia (lowered arterial CO pressure), or c) a combination of both. Eleven participants performed 3-5 repetitions of step-changes in cycle ergometer power output from 20W to 80% lactate threshold in the following conditions: i) normoxia (CON; room air); ii) hypoxia (HX, inspired O = 12%; lowered end-tidal O pressure [PO] and end-tidal CO pressure [PCO]); iii) hyperventilation (HV; increased PO and lowered PCO); and iv) normocapnic hypoxia (NC-HX; lowered PO and PCO matched to CON). Ventilation was increased (relative to CON) and matched between HX, HV, and NC-HX conditions.

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