Cerebral blood flow and cerebral oxygen consumption in patients with COPD on mechanical ventilation

Sari, Atsuo; Oshiata, S.; Toriumi, Takashi; Yamashita, Shigeki; Kojima, Shinya; Kakumoto, Shinichi; Yonei, Akitomo

doi:10.1007/bf01708580

Cited by 7 publications

(7 citation statements)

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“…This component includes items such as 'I dread having to do things' and 'I don't feel like doing anything'. Low oxygen levels may be associated with changes in cognitive function [ 33 , 34 ] and stimulate affective areas of the brain, mainly in the frontal lobe, which is associated with motivational process [ 35 , 36 ]. Feasibly, the administration of oxygen during exertion may be associated with lower fatigue levels and enhanced motivation.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of psychological and physiological predictors of fatigue in patients with COPD

2009

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BackgroundFatigue in COPD impairs functional status; however there are few studies examining mechanistic pathways of this symptom. The aims of this study are to compare fatigue between COPD patients and healthy age-matched subjects, and to identify predictors of fatigue in COPD.MethodsSeventy four COPD patients, mean age 69.9 (49-87) yrs, mean (SD) % predicted FEV1 46.5 (20.0) % and FEV1/FVC ratio 0.45 (0.13) and 35 healthy subjects, mean age 67.1 (50-84) yrs completed the Multidimensional Fatigue Inventory (MFI 20). Patients' assessment included Depression (HADS), lung function, BMI, muscle strength, incremental shuttle walk test (ISWT), exercise oxygen saturation (SpO2), Borg breathlessness (CR-10) and exertion (RPE). Serum level of Interleukin 6 (IL-6) was recorded. Differences in MFI 20 between groups were examined and predictors of fatigue identified using logistic regression.ResultsSignificant differences (p < 0.01) were found between the COPD and healthy subjects for all MFI 20 dimensions. There were significant differences when classified according to GOLD and dyspnoea stages for selected dimensions only. Predictors of General Fatigue were depression, muscle strength and end SpO2 (R2 = .62); of Physical Fatigue: depression, % predicted FEV1, ISWT and age (R2 = .57); Reduced Activity: % predicted FEV1, BMI and depression (R2 = .36); Reduced Motivation: RPE, depression and end SpO2 (R2 = .37) and Mental Fatigue: depression and end SpO2 (R2 = .38).ConclusionAll dimensions of fatigue were higher in COPD than healthy aged subjects. Predictive factors differ according to the dimension of fatigue under investigation. COPD-RF is a multi component symptom requiring further consideration.

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Section: Discussionmentioning

confidence: 99%

Evaluation of psychological and physiological predictors of fatigue in patients with COPD

2009

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“…In three studies, cerebral reactivity to CO 2 was maintained (Cannizzaro et al 1997; Van de Ven et al 2001, 2002), whereas it was impaired in another study (Clivati et al 1992). At high altitude, cerebral metabolic rate of oxygen appears maintained (Moller et al 2002), yet this important variable was found to be reduced markedly in patients with COPD on mechanical ventilation (Sari et al 1992). The disparities between studies are probably explained by the following factors: (1) different tools to assess CBF; (2) experimental considerations that may influence CBF and cerebral metabolism (e.g.…”

Section: Regulation Of Cbf – Influence Of Chronic Lung Diseasementioning

confidence: 99%

Regulation of cerebral blood flow in mammals during chronic hypoxia: a matter of balance

Ainslie

Ogoh

2010

Experimental Physiology

138

148

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Respiratory-induced changes in the partial pressures of arterial carbon dioxide (P aCO 2 ) and oxygen (P aO 2 ) play a major role in cerebral blood flow (CBF) regulation. Elevations in P aCO 2 (hypercapnia) lead to vasodilatation and increases in CBF, whereas reductions in P aCO 2 (hypocapnia) lead to vasoconstriction and decreases in CBF. A fall in P aO 2 (hypoxia) below a certain threshold (<40-45 mmHg) also produces cerebral vasodilatation. Upon initial exposure to hypoxia, CBF is elevated via a greater relative degree of hypoxia compared with hypocapnia. At this point, hypoxia-induced elevations in blood pressure and loss of cerebral autoregulation, stimulation of neuronal pathways, angiogenesis, release of adenosine, endothelium-derived NO and a variety of autocoids and cytokines are additional factors acting to increase CBF. Following 2-3 days, however, the process of ventilatory acclimatization results in a progressive rise in ventilation, which increases P aO 2 and reduces P aCO 2 , collectively acting to attenuate the initial rise in CBF. Other factors acting to lower CBF include elevations in haematocrit, sympathetic nerve activity and local and endothelium-derived vasoconstrictors. Hypoxia-induced alterations of cerebrovascular reactivity, autoregulation and pulmonary vascular tone may also affect CBF. Thus, the extent of change in CBF during exposure to hypoxia is dependent on the balance between the myriad of vasodilators and constrictors derived from the endothelium, neuronal innervations and perfusion pressure. This review examines the extent and mechanisms by which hypoxia regulates CBF. Particular focus will be given to the marked influence of hypoxia associated with exposure to high altitude and chronic lung disease. The associated implications of these hypoxia-induced integrative alterations for the regulation of CBF are discussed, and future avenues for research are proposed. The partial pressures of arterial carbon dioxide (P aCO 2 ) and oxygen (P aO 2 ) play a major role in cerebral blood flow (CBF) regulation. Whilst the role of P aCO 2 in the regulation of CBF has been well described (Ainslie & Duffin, 2009), the influence of hypoxia in the regulation of the cerebral circulation has received little focus, especially in humans. This is somewhat surprising given the development of arterial hypoxaemia in both 'normal' physiological endeavours, such as exercise and ascent to high altitude (HA), and during pathology (e.g. chronic lung disease and heart failure). It has been well reported that hypoxia, reflected in a fall in P aO 2 below a certain threshold (<40-45 mmHg), produces cerebral vasodilatation. The mechanisms underling these responses of hypoxia upon CBF, appearing simple at first, are highly complex and involve interactions of many physiological, metabolic and biochemical processes. The major factors underlying the extent of change in CBF during exposure to reductions in P aO 2 are depicted in Fig. 1. These factors, with particular focus on the integrative mechanisms linking reducti...

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“…To achieve an acute respiratory acidosis to pH < 7.0, Pa CO 2 would have to exceed 100mmHg (Keele et al, 1982; Hare et al, 2003). High levels of Pa CO 2 are often observed in patients with chronic obstructive pulmonary disease (COPD) and chronic sleep apnea, and can also occur in breath-hold divers (Koo et al, 1975; Sari et al, 1992; Guardiola et al, 2004; Binks et al, 2007), but in such cases, Pa CO 2 typically only increases up to 50 – 70mmHg, leading to a concomitant decrease in pH to only 7.2–7.3 (Koo et al, 1975; Keele et al, 1982). It has been estimated that a person would need to hold their breath for 20 minutes to cause Pa CO 2 to rise to higher than 100 mm Hg (Frumin et al, 1959).…”

Section: Arguments Against a Role Of 5-ht Neurons As Chemoreceptorsmentioning

confidence: 99%

Medullary serotonin neurons and central CO2 chemoreception

Corcoran

Hodges

et al. 2009

Respiratory Physiology & Neurobiology

135

128

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Serotonergic (5-HT) neurons are putative central respiratory chemoreceptors, aiding in the brain's ability to detect arterial changes in P CO 2 and implement appropriate ventilatory responses to maintain blood homeostasis. These neurons are in close proximity to large medullary arteries and are intrinsically chemosensitive in vitro, characteristics expected for chemoreceptors. 5-HT neurons of the medullary raphé are stimulated by hypercapnia in vivo, and their disruption results in a blunted hypercapnic ventilatory response. More recently, data collected from transgenic and knock-out mice have provided further insight into the role of 5-HT in chemosensitivity. This review summarizes current evidence in support of the hypothesis that 5-HT neurons are central chemoreceptors, and addresses arguments made against this role. We also briefly explore the relationship between the medullary raphé and another chemoreceptive site, the retrotrapezoid nucleus, and discuss how they may interact during hypercapnia to produce a robust ventilatory response.

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Cerebral blood flow and cerebral oxygen consumption in patients with COPD on mechanical ventilation

Abstract: The sensitivity of CBF in CO2 remained but CMRO2 was reduced markedly in COPD patients.

Cited by 7 publications

References 15 publications

Evaluation of psychological and physiological predictors of fatigue in patients with COPD

Evaluation of psychological and physiological predictors of fatigue in patients with COPD

Regulation of cerebral blood flow in mammals during chronic hypoxia: a matter of balance

Medullary serotonin neurons and central CO2 chemoreception

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