PubMed Health⌕ Search

Biomedical subjects

R D McEvoy

Publications and source records attributed to R D McEvoy.

At least 19 recordsLinked to original sources

Sleep hypoventilation in hypercapnic chronic obstructive pulmonary disease: prevalence and associated factors.

Sleep hypoventilation (SH) may be important in the development of hypercapnic respiratory failure in chronic obstructive pulmonary disease (COPD). The prevalence of SH, associated factors, and overnight changes in waking arterial blood gases (ABG), were assessed in 54 stable hypercapnic COPD patients without concomitant sleep apnoea or morbid obesity. Lung function assessment, anthropomorphic measurements, and polysomnography with ABG measurement before and after sleep were conducted in all patients. Transcutaneous carbon dioxide tension (Pt,CO2) was measured in sleep, using simultaneous arterial carbon dioxide tension (Pa,CO2) for in vivo calibration and to correct for drift in the sensor. Of the patients, 43% spent > or = 20% of sleep time with Pt,CO2 > 1.33 kPa (10 mmHg) above waking baseline. Severity of SH was best predicted by a combination of baseline Pa,CO2, body mass index and per cent rapid-eye movement (REM) sleep. REM-related hypoventilation correlated significantly with severity of inspiratory flow limitation in REM, and with apnoea/hypopnoea index. Pa,CO2 increased mean+/-SD 0.70+/-0.65 kPa (5.29+/-4.92 mmHg) from night to morning, and this change was highly significant. The change in Pa,CO2 was strongly correlated with severity of SH. Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease, and related to baseline arterial carbon dioxide tension, body mass index and indices of upper airway obstruction. Sleep hypoventilation is associated with significant increases in arterial carbon dioxide tension night-to-morning, and may contribute to long-term elevations in arterial carbon dioxide tension.

Aged↗

Long-term facilitation of ventilation is not present during wakefulness in healthy men or women.

Obstructive sleep apnea (OSA) is more common in men than in women for reasons that are unclear. The stability of the respiratory controller has been proposed to be important in OSA pathogenesis and may be involved in the gender difference in prevalence. Repetitive hypoxia elicits a progressive rise in ventilation in animals [long-term facilitation (LTF)]. There is uncertainty whether LTF occurs in humans, but if present it may stabilize respiration and possibly also the upper airway. This study was conducted to determine 1) whether LTF exists during wakefulness in healthy human subjects and, if so, whether it is more pronounced in women than men and 2) whether inspiratory pump and upper airway dilator muscle activities are affected differently by repetitive hypoxia. Twelve healthy young men and ten women in the luteal menstrual phase were fitted with a nasal mask and intramuscular genioglossal EMG (EMGgg) recording electrodes. After 5 min of rest, subjects were exposed to ten 2-min isocapnic hypoxic periods (approximately 9% O(2) in N(2), arterial O(2) saturation approximately 80%) separated by 2 min of room air. Inspired minute ventilation (Vi) and peak inspiratory EMGgg activity were averaged over 30-s intervals, and respiratory data were compared between genders during and after repetitive hypoxia by using ANOVA for repeated measures. Vi during recovery from repetitive hypoxia was not different from the resting level and not different between genders. There was no facilitation of EMGgg activity during or after repetitive hypoxia. EMGgg activity was reduced below baseline during recovery from repetitive hypoxia in women. In conclusion, we have found no evidence of LTF of ventilation or upper airway dilator muscle activity in healthy subjects during wakefulness.

Adult↗

Effect of CPAP on intrinsic PEEP, inspiratory effort, and lung volume in severe stable COPD.

BACKGROUND: Intrinsic positive end expiratory pressure (PEEPi) constitutes an inspiratory threshold load on the respiratory muscles, increasing work of breathing. The role of continuous positive airway pressure (CPAP) in alleviating PEEPi in patients with severe stable chronic obstructive pulmonary disease is uncertain. This study examined the effect of CPAP on the inspiratory threshold load, muscle effort, and lung volume in this patient group. METHODS: Nine patients were studied at baseline and with CPAP increasing in increments of 1 cm H(2)O to a maximum of 10 cm H(2)O. Breathing pattern and minute ventilation (I), dynamic PEEPi, expiratory muscle activity, diaphragmatic (PTPdi/min) and oesophageal (PTPoes/min) pressure-time product per minute, integrated diaphragmatic (EMGdi) and intercostal EMG (EMGic) and end expiratory lung volume (EELV) were measured. RESULTS: Expiratory muscle activity was present at baseline in one subject. In the remaining eight, PEEPi was reduced from a mean (SE) of 2.9 (0.6) cm H(2)O to 0.9 (0.1) cm H(2)O (p<0.05). In two subjects expiratory muscle activity contributed to PEEPi at higher pressures. There were no changes in respiratory pattern but I increased from 9.2 (0.6) l/min to 10.7 (1.1) l/min (p<0.05). EMGdi remained stable while EMGic increased significantly. PTPoes/min decreased, although this did not reach statistical significance. PTPdi/min decreased significantly from 242.1 (32.1) cm H(2)O.s/min to 112.9 (21.7) cm H(2)O.s/min). EELV increased by 1.1 (0.3) l (p<0.01). CONCLUSION: High levels of CPAP reduce PEEPi and indices of muscle effort in patients with severe stable COPD, but only at the expense of substantial increases in lung volume.

Aged↗

Genioglossus muscle activity at rest and in response to brief hypoxia in healthy men and women.

Obstructive sleep apnea (OSA) is more common in men than in women for reasons that are not clearly understood. An underlying difference between men and women in the respiratory-related neural control of upper airway dilator muscles has been suggested as a possible reason for the gender difference. We have compared three aspects of upper airway dilator muscle function in healthy men and women: 1) resting inspiratory genioglossus electromyogram (EMGgg) activity, 2) the respiratory EMGgg "afterdischarge" after a brief hypoxic stimulus, and 3) the relationship between the EMGgg and pharyngeal airway pressure. Inspired minute ventilation (VI), epiglottic pressure (P(epi)), and EMGgg and diaphragm EMG (EMGdi) activity were measured in 24 subjects (12 men, 12 women in the luteal menstrual phase) and were compared between genders while lying supine awake. Every 7-8 min over 2 h, subjects were exposed to 45-s periods of isocapnic hypoxia (9% O(2) in N(2)) that were abruptly terminated with one breath of 100% O(2). The relationship between P(epi) and EMGgg activity was also compared between genders. The results of 117 trials with satisfactory end-tidal PCO(2) control and no sighs or swallows are reported. There was no gender difference in the resting level of peak inspiratory EMGgg [3.7 +/- 0.8 (women) vs. 3.2 +/- 0.6% maximal activity (men)]. Repeated-measures ANOVA showed no gender or gender-by-time interaction effect between men and women in VI or EMGgg or EMGdi activity during or after the hypoxic stimulus. The relationship between P(epi) and EMGgg was not different between men (slope -0.63 +/- 0.20) and women (slope -0.69 +/- 0.33). These results do not support the hypothesis that the higher prevalence of OSA in men is related to an underlying gender difference in respiratory neural control of upper airway dilator muscles.

Adult↗

Acute cardiovascular responses to arousal from non-REM sleep during normoxia and hypoxia.

STUDY OBJECTIVES: There is uncertainty concerning the relative contribution of arousal, chemoreceptor stimulation, and their potentially interactive effects, to the acute cardiovascular changes observed during sleep in patients with sleep-disordered breathing. The purpose of this study was to compare cardiovascular responses (heart rate, skin blood flow, and pulse transit time, a non-invasive measure of arterial wall stiffness) to auditory induced arousal from stage 2 sleep under conditions of normoxia and overnight mild hypoxia. DESIGN: Randomised crossover. SETTING: Sleep Disorders Unit in a 270-bed teaching hospital. PARTICIPANTS: Eleven healthy male subjects. INTERVENTIONS: Subjects slept wearing a facemask and breathed room air (one night; SaO2 approximately 98%) or an hypoxic gas mixture (two nights; SaO2 approximately 92%). Once in stage 2 sleep, subjects were administered one of 10 auditory tones (500 Hz, range 54-90 dB, 5-sec duration) via earphones or a sham tone (recording with no tone). MEASUREMENTS AND RESULTS: Cardiovascular responses were examined beat-by-beat for 20 seconds before and 30 seconds after auditory tones associated with arousals (3-10 second EEG changes) and after sham tones. Sleep efficiency and the percentage of sleep spent in each stage were not different between hypoxia and normoxia nights. Baseline heart rate was elevated on hypoxia nights compared with normoxia nights (59.5+/-1.7 vs. 54.4+/-1.6 b x min(-1), p=0.007). Heart rate, pulse transit time, and skin blood flow showed significant changes after arousal consistent with rapid parasympathetic withdrawal and sympathetic nervous system activation. No changes were observed after sham tones. There were no differences in time course or magnitude of cardiovascular responses between hypoxia and normoxia nights. CONCLUSIONS: We conclude that while mild hypoxia stimulates autonomic activity it does not augment the cardiovascular response to arousal from stage 2 sleep in normal subjects.

Acoustic Stimulation↗

Ventilatory decline after hypoxia and hypercapnia is not different between healthy young men and women.

The gradual decay in ventilation after removal of a respiratory stimulus has been proposed to protect against cyclic breathing disorders such as obstructive sleep apnea (OSA). The male predominance of OSA, and the increased incidence of OSA in women after menopause, indicates that the respiratory-stimulating effect of progesterone may provide protection against OSA by altering the rate of poststimulus ventilatory decline (PSVD). It was therefore hypothesized that PSVD is longer in premenopausal women than in men and is longer in the luteal menstrual phase compared with the follicular phase. PSVD was measured in 12 men and in 11 women at both their luteal and follicular phases, after cessation of isocapnic hypoxia and normoxic hypercapnia. PSVD was compared between genders and between women in the luteal and follicular phases by repeated-measures ANOVA. There were no significant differences in PSVD between any of the groups after either respiratory stimulus. This suggests that the higher occurrence of OSA in men does not reflect an underlying gender difference in PSVD and implies the increased prevalence of OSA in women after menopause is not representative of an effect of progesterone on PSVD.

Adult↗

Sustained isocapnic hypoxia suppresses the perception of the magnitude of inspiratory resistive loads.

The sensation of increased respiratory resistance or effort is likely to be important for the initiation of alerting or arousal responses, particularly in sleep. Hypoxia, through its central nervous system-depressant effects, may decrease the perceived magnitude of respiratory loads. To examine this, we measured the effect of isocapnic hypoxia on the ability of 10 normal, awake males (mean age = 24.0 +/- 1.8 yr) to magnitude-scale five externally applied inspiratory resistive loads (mean values from 7.5 to 54.4 cmH(2)O. l(-1). s). Each subject scaled the loads during 37 min of isocapnic hypoxia (inspired O(2) fraction = 0.09, arterial O(2) saturation of approximately 80%) and during 37 min of normoxia, using the method of open magnitude numerical scaling. Results were normalized by modulus equalization to allow between-subject comparisons. With the use of peak inspiratory pressure (PIP) as the measure of load stimulus magnitude, the perception of load magnitude (Psi) increased linearly with load and, averaged for all loaded breaths, was significantly lower during hypoxia than during normoxia (20.1 +/- 0.9 and 23.9 +/- 1.3 arbitrary units, respectively; P = 0. 048). Psi declined with time during hypoxia (P = 0.007) but not during normoxia (P = 0.361). Our result is remarkable because PIP was higher at all times during hypoxia than during normoxia, and previous studies have shown that an elevation in PIP results in increased Psi. We conclude that sustained isocapnic hypoxia causes a progressive suppression of the perception of the magnitude of inspiratory resistive loads in normal subjects and could, therefore, impair alerting or arousal responses to respiratory loading.

Adult↗

Portable computerized polysomnography in attended and unattended settings.

STUDY OBJECTIVE: We compared the validity of a new portable polysomnographic recorder against a laboratory-based polysomnographic system from the same manufacturer. DESIGN AND PATIENTS: Simultaneous, full polysomnographic recordings from the portable device (PSGP) and the laboratory-based system (PSGL) were obtained using separate sets of sensors on 20 patients referred for investigation of sleep apnea. SETTING: After initial optimization of signals, the portable device was left unattended in 10 of the patients (to simulate home studies), while in the other 10 the signals were reviewed on a laptop computer screen and adjustments to electrode or sensor placement made as needed during the studies. Recordings were manually scored by a technologist blinded to the origin of the data. MEASUREMENTS AND RESULTS: The quality of signals was comparable between the PSGP and PSGL studies, apart from a slight decrease in respiratory signal quality during PSGP studies that led to reduced confidence in respiratory event scoring. SaO2 signal loss was also greater in unattended PSGP. There was good agreement between PSGP and PSGL for sleep variables and the apnea-hypopnea index (r=0.99). The periodic limb movement index was slightly lower during unattended PSGP. Blinded physician assessment of the records led to a recommendation for repeat studies due to poor signal quality in one (10%) attended and one (10%) unattended portable recording. There was no significant discordance between PSGP and PSGL in the final diagnostic formulations. CONCLUSION: Portable polysomnography is a viable alternative to laboratory-based polysomnography and may be improved further by better sensor attachment.

Adult↗

Sleep apnoea related hypoxia is associated with cognitive disturbances in patients with tetraplegia.

Sleep disordered breathing is common in patients with tetraplegia. Nocturnal arterial hypoxemia and sleep fragmentation due to sleep apnoea may be associated with cognitive dysfunction. We therefore studied the influence of sleep disordered breathing on neuropsychological function in 37 representative tetraplegic patients (mean age 34 +/- 9.7 years). Thirty percent (11 of 37 patients) had clinically significant sleep disordered breathing, defined as apnoea plus hypopnoea index (AHI) greater than 15 per hour of sleep. Most apnoeas were obstructive in type. Seven patients (19%) desaturated to < 80% during the night. Neuropsychological variables were significantly correlated with measures of sleep hypoxia, but not with the AHI and the frequency of sleep arousals. The neuropsychological functions most affected by nocturnal desaturation were: verbal attention and concentration, immediate and short-term memory, cognitive flexibility, internal scanning and working memory. There appeared to be a weak association between the presence of severe sleep hypoxia and visual perception, attention and concentration but no association was found between sleep variables and depression scores. We concluded that sleep disordered breathing is common in patients with tetraplegia and may be accompanied with significant oxygen desaturation. The latter impairs daytime cognitive function in these patients, particularly attention, concentration, memory and learning skills. Cognitive disturbances resulting from sleep apnoea might adversely affect rehabilitation in patients with tetraplegia.

Adolescent↗

Ventilatory responses to sustained eucapnic hypoxia in healthy males during wakefulness and NREM sleep.

The effects of sustained eucapnic hypoxia (SEH, 20 minutes SaO2, approximately 80%) on ventilation and supraglottic airflow resistance (Rua) plus genioglossal (gg) and diaphragmatic (di) electromyograms (EMGs) were compared during wakefulness and nonrapid eye movement (NREM) sleep in six healthy normal male subjects. Early augmentation of ventilation was followed by decline or roll-off in both states. The augmentation of ventilation was less in sleep than wakefulness (e.g., after 5 minutes hypoxia, 140% and 167% of baseline, respectively, p < 0.05). This appeared to be due to three factors: 1) sleep-related increases in Rua [the ventilatory responses to SEH (sleep vs. awake) were inversely related to changes in Rua (sleep vs. awake) (p < 0.05)], 2. reduced central neural drive (inspiratory phasic EMG di after 5 minutes SEH, 111% and 121% of baseline, p < 0.05), and 3) failure to increase respiratory frequency during SEH sleep. There was also a nonsignificant trend to a biphasic response in EMG gg and a small increase in Rua during SEH.

Adult↗

Comparison of effects of sustained isocapnic hypoxia on ventilation in men and women.

Sleep-related respiratory disturbances are more common in men than in premenopausal women. This might, in part, be due to different susceptibilities to the respiratory depressant effects of hypoxia. Therefore, we compared ventilation during 10 min of baseline room-air breathing and 20-min sustained isocapnic hypoxia (fractional inspired O2 = 11%, arterial saturation of O2 approximately 80%) followed by 10 min of breathing 100% O2 in 10 normal men and in 10 women in the follicular phase of the menstrual cycle. Control measurements were made during two transitions from room air (10 min) to 100% O2 (10 min) and averaged. Inspired minute ventilation (VI) after 2 min of hypoxia was the same in men and women [131 +/- 6.1% baseline for men, 136 +/- 7.7% baseline for women; not significant (NS)] and declined to the same level after 20 min (115 +/- 5.0% baseline for men, 116 +/- 6.6% baseline for women; NS) associated with a similar decline in inspiratory time and tidal volume. Breathing frequency did not change. VI decreased transiently during subsequent 100% O2 breathing in both men and women, associated with reduced frequency and duty cycle and increased expiratory time. The fall in VI was significantly greater than that observed during control hyperoxia experiments in men but not in women. We conclude that ventilatory responses to sustained isocapnic hypoxia do not differ between awake healthy men and women in the follicular phase of their menstrual cycle. However, after termination of isocapnic hypoxia, men appear to depress their ventilation to a greater degree than women.

Adult↗

Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea.

Changes in sleep posture have been shown to improve obstructive sleep apnea (OSA). To investigate the mechanisms by which this occurs we assessed upper airway stability in eight patients with severe OSA in three postures (supine, elevated to 30 degrees, and lateral). We used a specially adapted nasal continuous positive airway pressure (nCPAP) mask to measure upper airway closing pressure (UACP) and upper airway opening pressure (UAOP) during non-REM sleep. Statistical comparisons were made between postures using ANOVA for repeated measures. Elevation resulted in a less collapsible airway compared with both the supine and lateral positions (mean UACP: 30 degrees elevation -4.0 +/- 3.2 compared with supine 0.3 +/- 2.4 cm H2O, p < 0.05 and; lateral -1.1 +/- 2.2 cm H2O, p < 0.05). Supine UACP and lateral UACP were not significantly different. Elevation or lateral positioning produced a 50% reduction in mean UAOP (supine 10.4 +/- 3.5 cm H2O compared with 30 degrees elevation 5.3 +/- 2.1, p < 0.05; and lateral 5.5 +/- 2.1 cm H2O, p < 0.05). We conclude that in severely affected OSA patients upper body elevation, and to a lesser extent lateral positioning, significantly improve upper airway stability during sleep, and may allow therapeutic levels of nCPAP to be substantially reduced.

Adult↗

A comparison of two long-acting vasoselective calcium antagonists in pulmonary hypertension secondary to COPD.

UNLABELLED: STUDY OBJECTIVES AND PATIENTS: Pulmonary hypertension (PH) is common in COPD and may predict mortality in this disorder. We have compared the pulmonary vasodilator effects, dose-response characteristics, and tolerability of two calcium channel blockers, amlodipine and extended-release (ER) felodipine, in 10 patients (seven men, age 68+/-4.8 [SD] years) with clinically stable COPD and PH. DESIGN: Drugs were given in equal single daily oral doses (2.5, 5, and 10 mg), increasing weekly for 3 weeks, in a randomized investigator-blinded crossover manner with a 1-week wash-out period between the two treatments. MEASUREMENTS: Doppler measurements of pulmonary hemodynamics were made on the seventh day of treatment at each drug dose. Lung function, arterial blood gases, and adverse events were also monitored weekly. RESULTS: A dose-dependent decline of pulmonary artery pressure (PAP) was observed with each drug. A dose of 2.5 mg produced a significant decrease in PAP compared with baseline (20% amlodipine, 17% felodipine ER). Additional decreases in PAP were observed at 5 mg and 10 mg that were similar for both drugs, but did not reach statistical significance compared with 2.5 mg. There was a dose-related decrease in pulmonary vascular resistance and increase in oxygen delivery with amlodipine and felodipine ER. Lung function and blood gas values were stable throughout. Side effects (headache and ankle edema) were less frequent during amlodipine treatment (p<0.05). CONCLUSIONS: Both amlodipine and felodipine ER, given as a single daily oral dose of > or = 2.5 mg, are effective pulmonary vasodilators in COPD patients with PH. Their dose-response characteristics are similar, but amlodipine treatment was associated with fewer side effects.

Aged↗

Effects of sustained and repetitive isocapnic hypoxia on ventilation and genioglossal and diaphragmatic EMGs.

We compared the effects of sustained isocapnic hypoxia (SIH; 20 min) and repetitive isocapnic hypoxia (RIH; 10 2-min episodes) on ventilation (VI), genioglossal (EMGgg) and diaphragmatic electromyographic (EMGdi) activities, and supraglottic airway resistance in 11 normal supine male subjects (36.6 +/- 2.2 yr) during wakefulness. Seven of the subjects had control measurements on a separate day. Desaturation was similar (arterial O2 saturation 80-84%) in the SIH and RIH protocols. SIH and RIH caused a biphasic ventilatory response: early augmentation of VI (169.5 +/- 6.9 and 168.9 +/- 4.3% of baseline, respectively; not significant) followed by a significant roll-off (VI after 20 min of cumulative hypoxia 153 +/- 4.0 and 150.8 +/- 10.2% respectively; not significant). Moving-time-average EMGdi signals (peak inspiratory and phasic) demonstrated a similar biphasic response in the two protocols. Mean EMGgg responses, however, differed. During SIH, peak inspiratory EMGgg increased early and remained elevated. Phasic and tonic EMGgg signals showed a similar trend. During RIH, early augmentation of peak inspiratory and phasic EMGgg signals was followed by a marked roll-off in activity such that by the 10th hypoxic episode neither value increased above baseline. In the 2-min periods between hypoxic episodes, there was a progressive suppression of peak inspiratory and phasic EMGgg values below baseline. Supraglottic airway resistance did not change significantly during either SIH or RIH. VI and phasic EMGs did not change during control experiments. We conclude that in awake normal male subjects SIH and RIH cause similar biphasic responses in VI and EMGdi activity. Phasic EMGgg activity responses differ between SIH and RIH: EMGgg remains augmented during SIH, whereas during RIH early augmentation is followed by marked suppression.

Adult↗