Effects of heart failure on cerebral blood flow in COPD: Rest and exercise

Oliveira, Mayron F.; Alencar, Maria Clara; Arbex, Flávio; Souza, Aline; Sperandio, Priscila A.; Medina, Luiz Antonio Rodrigues; Medeiros, Wladimir Musetti; Hirai, Daniel M.; O’Donnell, Denis E.; Neder, J. Alberto

doi:10.1016/j.resp.2015.10.005

Cited by 26 publications

(27 citation statements)

References 38 publications

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“…Full pulmonary function tests (spirometry, lung volume components including IC, diffusing capacity of the lung and resting arterial O 2 saturation) are also a prerequisite. Documentation of comorbidities potentially associated with exertional dyspnoea (obesity [73][74][75][76], cardio-circulatory disorders [77][78][79], anaemia, etc.) is also essential for proper CPET interpretation.…”

Section: Measuring Dyspnoea During Cpetmentioning

confidence: 99%

Exertional dyspnoea in COPD: the clinical utility of cardiopulmonary exercise testing

et al. 2016

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Activity-related dyspnoea is often the most distressing symptom experienced by patients with chronic obstructive pulmonary disease (COPD) and can persist despite comprehensive medical management. It is now clear that dyspnoea during physical activity occurs across the spectrum of disease severity, even in those with mild airway obstruction. Our understanding of the nature and source of dyspnoea is incomplete, but current aetiological concepts emphasise the importance of increased central neural drive to breathe in the setting of a reduced ability of the respiratory system to appropriately respond. Since dyspnoea is provoked or aggravated by physical activity, its concurrent measurement during standardised laboratory exercise testing is clearly important. Combining measurement of perceptual and physiological responses during exercise can provide valuable insights into symptom severity and its pathophysiological underpinnings. This review summarises the abnormal physiological responses to exercise in COPD, as these form the basis for modern constructs of the neurobiology of exertional dyspnoea. The main objectives are: 1) to examine the role of cardiopulmonary exercise testing (CPET) in uncovering the physiological mechanisms of exertional dyspnoea in patients with mild-to-moderate COPD; 2) to examine the escalating negative sensory consequences of progressive respiratory impairment with disease advancement; and 3) to build a physiological rationale for individualised treatment optimisation based on CPET. @ERSpublications Measurement of symptom intensity, ventilatory control and mechanics during exercise exposes mechanisms of dyspnoea

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Section: Measuring Dyspnoea During Cpetmentioning

confidence: 99%

Exertional dyspnoea in COPD: the clinical utility of cardiopulmonary exercise testing

et al. 2016

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“…Nonetheless, MAP was not correlated with SctO 2peak . Previous investigations confirmed that CBF does not increase or even decline at peak exercise even though MAP rises in patients with HFrEF [ 9 , 51 ]. In other words, MAP does not reflect CBF during exercise in patients with HFrEF.…”

Section: Discussionmentioning

confidence: 87%

Cerebral desaturation in heart failure: Potential prognostic value and physiologic basis

et al. 2018

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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.

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“…Eine zerebrale Dysfunktion wurde bei COPD und Herzinsuffizienz ebenfalls häufiger beobachtet [145,146]. Wenn COPD-Patienten ohne Herzinsuffizienz körperlich belastet wurden, stieg ihr zerebraler Blutfluss wie bei gesunden Personen steil an [147]. Bestand gleichzeitig eine Herzinsuffizienz, stieg der Blutfluss unter Belastung langsamer an und erreichte ein weniger hohes Niveau.…”

Section: Kardiovaskuläre Erkrankungenunclassified

Expertentreffen COPD: Exazerbation der COPD

et al. 2017

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Acute worsenings of chronic obstructive pulmonary disease (COPD) were for a long time regarded as transient deteriorations, although occasionally life-threatening. No connection to disease progression was recognized. Data emerging during the last decade showed that patients had a considerably worse survival outcome after severe exacerbations. This insight was consolidated in 2012 by a large population-based cohort analysis. At present, severe exacerbations are regarded as key risk factors for COPD disease progression. The present article summarises the current knowledge on exacerbations of COPD, as delineated during an expert workshop in February 2017. It comprises pathogenic mechanisms, exacerbation triggers, the characteristics of frequent exacerbators, and the predictors of worse survival outcome. The role of comorbidities is considered more closely. The presentation of the pharmacotherapy of acute exacerbation is supplemented by an overview of ventilatory support. Finally, pharmacological and nonpharmacological preventive measures are summarised.

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Effects of heart failure on cerebral blood flow in COPD: Rest and exercise

Cited by 26 publications

References 38 publications

Exertional dyspnoea in COPD: the clinical utility of cardiopulmonary exercise testing

Exertional dyspnoea in COPD: the clinical utility of cardiopulmonary exercise testing

Cerebral desaturation in heart failure: Potential prognostic value and physiologic basis

Expertentreffen COPD: Exazerbation der COPD

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