Spectral analysis of ventilation in elderly subjects awake and asleep

Pack, Allan I.; Silage, Dennis; Millman, Richard P.; Knight, Herbert; Shore, Eric; Chung, David C.

doi:10.1152/jappl.1988.64.3.1257

Cited by 68 publications

(36 citation statements)

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“…Arousal from sleep leads to hyperventilation and the resulting hypocapnia (and reduced central respiratory drive) could promote a CSA following sleep resumption. The correlation between fluctuations in EEG frequency and changes in tidal volume in elderly people support this idea [44]. In the present study, sleep onset did not produce significant periodic or unstable breathing in elderly or young people.…”

Section: Mechanisms Of Csa In the Elderlysupporting

confidence: 82%

Ageing does not influence the sleep-related decrease in the hypercapnic ventilatory response

Browne¹,

Adams²,

Simonds³

et al. 2003

Eur Respir J

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In young people, a sleep-related reduction in the gain of the ventilatory chemoreflex feedback loop occurs; in the elderly, it has been reported that no sleeprelated reduction occurs. A relatively high loop gain could contribute to periodic breathing and central sleep apnoea in the elderly. This study tested the hypothesis that ageing is associated with a reduction in the magnitude of the sleep-related decrease in the hypercapnic ventilatory response (HCVR).The HCVR was measured using a steady state method, awake and asleep, in groups (n=10) of elderly (66-81 yrs) and young (23-35 yrs) nonapnoeics. Upper airway resistance was maintained close to wakefulness levels using continuous positive airway pressure (mean sleep-related increase in resistance: elderly 1.6¡1.

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Section: Mechanisms Of Csa In the Elderlysupporting

confidence: 82%

Ageing does not influence the sleep-related decrease in the hypercapnic ventilatory response

Browne¹,

Adams²,

Simonds³

et al. 2003

Eur Respir J

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“…21 In an elderly population, periodical breathing with subsequent hypoxemia is more common. 22 It has been suggested that an underlying defect of chemoreceptor sensitivity can lead to an unstable feedback control of respiration 23 and contribute to abnormal blood pressure regulation.…”

Section: Discussionmentioning

confidence: 99%

Altered cardiorespiratory transfer in hypertension.

et al. 1994

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The effect of continuously slowing respiration (from 0.46 to 0.05 Hz, eg, from 30 to 3 breaths per minute) on cardiovascular variables was studied in 14 hypertensive patients and 16 normotensive subjects. Beat-to-beat time-frequency (Wigner) distributions were used for dynamic analysis of RR interval and systolic and diastolic pressures. Dominant breathing frequency at rest did not differ in hypertensive patients from the control group (0.21 versus 0.19 Hz). However, in the hypertensive group it was disturbed 34.4% of the time by slow breathing and apneas, which evoked transient blood pressure instability and increased spectral powers at low frequencies (range, 0.01 to 0.1 Hz). The nonrespiratory fluctuations (NONRFs) and respiratory fluctuations (RFs) in RR interval and NONRFs in systolic pressure were smaller in hypertensive patients (/ > <.001). In both groups, slowing of respiratory frequency from 0.46 to 0.05 Hz entrained RFs in the RR interval and systolic and diastolic pressures. RFs in the RR interval remained diminished in hypertensive patients (P<.001), but RFs in systolic pressure increased higher at maximum, corresponding to breathing frequencies from 0.07 to 0.09 Hz (P< .001). A dynamic cardiorespiratory index (ratio of RFs in RR interval and systolic pressure) was smaller (P<.01) in hypertensive patients than in normotensive subjects. Irregular breathing at rest was found in hypertensive patients. The transfer from respiration into RR interval was diminished, suggesting an impaired parasympathetic responsiveness in mild hypertension. (Hypertension. 1994^3:104-113.) Key Words • spectrum analysis • cardiovascular system • respiration • hypertension, essential T he problem of hyperreactivity of the sympathetic nervous system in essential hypertension has been studied frequently in the last two decades. An exaggerated sympathetic tone in mild hypertension can result from an increased intrinsic activity of the brain stem vasomotor neurons or can be secondary to a reduction of the inhibitory potency of baroreceptors 12 and pulmonary volume receptors. An augmentation of sympathetic tone was considered a primary mechanism of hypertension in a subgroup of patients in which elevated levels of plasma norepinephrine and epineph-rine 34 were found. High RR interval fluctuations from 0.05 to 0.1 Hz were reported and attributed to the augmentation of sympathetic efferent activity. 5 ' 6 However , these oscillations are under combined parasympa-thetic and sympathetic influences. Only the parasympa-thetic muscarinic blockade consistently suppresses RR interval fluctuations over the range of 0.01 to 0.4 Hz, and the effect of sympathetic blockade is ambiguous. 7 ' 8 Moreover, direct recordings of sympathetic efferent activity did not show exaggerated resting levels of sympathetic tone. 9 Heart rate fluctuations at respiratory frequencies are recognized as a noninvasive measure of cardiovagal activity 7 ' 8 and reflect more modulation of the firing of barore-ceptors and of cardiac and pulmonary volume receptors than a...

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“…The aetiology of the disease probably changes due to changes in parapharyngeal fat pad deposition [30], serotonergic dysregulation of brainstem respiratory control (due to ''wear and tear'') [31] and age-related changes in bony structures, such as edentulism [32]. Variations in neuromuscular control of the upper airway become more important in the elderly [33], and increased background prevalences of cardiac and cerebrovascular disease increase the likelihood of periodic breathing. The clinical phenotype of OSAHS also changes.…”

Section: The Phenotypic Complexity Of Osahs Heterogeneity Of Osahsmentioning

confidence: 99%

The phenotype and genotype of adult obstructive sleep apnoea/hypopnoea syndrome

Riha¹,

Gislasson²,

Diefenbach³

2009

European Respiratory Journal

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Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is a common condition affecting ,2-4% of the middle-aged population. A hereditary component to the condition has long been recognised but its genetic basis has been difficult to elucidate. Progress in determining the genotype of OSAHS is hampered by the lack of a consistent definition of phenotype and the large environmental influences on its expression. ''Intermediate phenotypes'', such as craniofacial structure, obesity and upper airway control, have been utilised. Multiple gene polymorphisms have been explored in association with the latter, as well as with the sequelae of OSAHS, such as hypertension and increased insulin resistance. To date, two genome-wide scans have identified potential regions that may be of interest in further defining the intermediate phenotypes. The present paper focuses on human studies with an update of the most recent work in the area, including a short discussion on methods of genetic studies.

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Spectral analysis of ventilation in elderly subjects awake and asleep

Cited by 68 publications

References 0 publications

Ageing does not influence the sleep-related decrease in the hypercapnic ventilatory response

Ageing does not influence the sleep-related decrease in the hypercapnic ventilatory response

Altered cardiorespiratory transfer in hypertension.

The phenotype and genotype of adult obstructive sleep apnoea/hypopnoea syndrome

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