Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Mar 2013
ReviewMechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading.
Patients with chronic heart failure (CHF) suffer increased alveolar VD/VT (dead-space-to-tidal-volume ratio), yet they demonstrate augmented pulmonary ventilation such that arterial [Formula: see text] ( [Formula: see text] ) remains remarkably normal from rest to moderate exercise. This paradoxical effect suggests that the control law governing exercise hyperpnea is not merely determined by metabolic CO2 production ( [Formula: see text] ) per se but is responsive to an apparent (real-feel) metabolic CO2 load ( [Formula: see text] ) that also incorporates the adverse effect of physiological VD/VT on pulmonary CO2 elimination. By contrast, healthy individuals subjected to dead space loading also experience augmented ventilation at rest and during exercise as with increased alveolar VD/VT in CHF, but the resultant response is hypercapnic instead of eucapnic, as with CO2 breathing. ⋯ These observations are consistent with the hypothesis that the increased series VD/VT in dead space loading adds to [Formula: see text] as with increased alveolar VD/VT in CHF, but this is through rebreathing of CO2 in dead space gas thus creating a virtual (illusory) airway CO2 load within each inspiration, as opposed to a true airway CO2 load during CO2 breathing that clogs the mechanism for CO2 elimination through pulmonary ventilation. Thus, the chemosensing mechanism at the respiratory controller may be responsive to putative drive signals mediated by within-breath [Formula: see text] oscillations independent of breath-to-breath fluctuations of the mean [Formula: see text] level. Skeletal muscle afferents feedback, while important for early-phase exercise cardioventilatory dynamics, appears inconsequential for late-phase exercise hyperpnea.
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Respir Physiol Neurobiol · Jan 2013
ReviewPeripheral chemoreceptors in congenital central hypoventilation syndrome.
Congenital central hypoventilation syndrome is a rare disorder caused by a mutation in the PHOX2B gene resulting in hypoventilation that is worse during sleep. Human physiologic studies show that patients with CCHS have absent or decreased rebreathing ventilatory responses to hypercapnia and hypoxemia during sleep as well as during wakefulness. Some ventilatory responses to hypoxia and hyperoxia can be demonstrated using a step change in inspired oxygen. ⋯ Human physiological studies predicted that the defect in CCHS lies in central integration of the central and peripheral chemoreceptor signals. New evidence suggests the RTN may be the respiratory controller where chemoreceptor inputs are integrated. In this review we present the clinical presentation of CCHS, revisit results of human physiologic studies, and discuss the findings in light of new knowledge about the role of PHOX2B and RTN in CCHS.
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The use of mechanical ventilation has become widespread in the management of hypoxic respiratory failure. Investigations of pulmonary mechanics in this clinical scenario have demonstrated that there are significant differences in compliance, resistance and gas flow when compared with normal subjects. This paper will review the mechanisms by which pulmonary mechanics are assessed in mechanically ventilated patients and will review how the data can be used for investigative research purposes as well as to inform rational ventilator management.
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Respir Physiol Neurobiol · Sep 2011
ReviewInflammatory pathways in children with insufficient or disordered sleep.
Sleep is not only an essential physiological function, but also serves important roles in promoting growth, maturation, and overall health of children and adolescents. There is increasing interest regarding the impact of sleep and its disorders on the regulation of inflammatory processes and end-organ morbidities, particularly in the context of metabolic and cardiovascular diseases (CVD) and their complications. Obstructive sleep apnea syndrome (OSAS) is an increasingly common health problem in children, and in the last decade, the emergence of increasing obesity rates has further led to remarkable increases in the prevalence of OSAS, along with more prominent neurocognitive, behavioral, cardiovascular and metabolic morbidities. ⋯ To this effect, it would appear that OSAS could be viewed as a chronic, low-grade inflammatory disorder. Furthermore, the concurrent presence of obesity and OSAS poses a theoretically increased risk of OSAS-related complications. In this review, we will critically review the current state of research regarding the impact of insufficient and disrupted sleep and OSAS on the immune processes and inflammatory pathways that underlie childhood OSAS as a distinctive systemic inflammatory condition in children, and will explore potential interactions between OSAS and obesity.
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Respir Physiol Neurobiol · Sep 2011
ReviewCongenital central hypoventilation syndrome and desogestrel: a call for caution: addendum to "C. Straus, H. Trang, M.H. Becquemin, P. Touraine, T. Similowski, Chemosensitivity recovery in Ondine's curse syndrome under treatment with desogestrel" [Respir. Physiol. Neurobiol. 171 (2010) 171-174].
Patients suffering from congenital central hypoventilation syndrome (CCHS) depend on mechanical ventilation during sleep, from birth and throughout life. They lack CO₂-chemosensitivity. ⋯ Desogestrel should not be prescribed to CCHS patients with a respiratory purpose until the results of a pending clinical trial (clinicaltrials.gov. NCT01243697) are available.