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Biomedical subjects

R B Berry

Publications and source records attributed to R B Berry.

At least 37 records · Page 2Linked to original sources
PubMed1997

Upper airway anesthesia reduces phasic genioglossus activity during sleep apnea.

We hypothesize that stimulation of upper-airway mechanoreceptors during obstructive apnea augments upper airway muscle activity. If so, upper-airway anesthesia (UAA) should reduce mechanoreceptor output and therefore upper-airway muscle activity. To test this hypothesis, we studied the effect of UAA on the relationship between the phasic activity of the moving-time average (MTA) of the genioglossus electromyogram (EMG-GG) and the esophageal pressure deflection (DP) during obstructive apneas in non-rapid-eye-movement (NREM) sleep in a group of six men with severe sleep apnea. Before UAA, the phasic EMG-GG was linearly related to the deflections in esophageal pressure (DP) during the last three occluded breaths (both progressively increased). After UAA, the mean ratio of EMG-GG to DP decreased to 23% of the control value, from 0.17 +/- 0.04 to 0.04 +/- 0.01 (mean +/- SEM) arbitrary units/cm H2O (p < 0.05). The mean slope of the EMG-GG-versus-DP regression lines also decreased to 23% of the control value, from 0.22 +/- 0.03 to 0.05 +/- 0.01 arbitrary units/ cm H2O (p < 0.01). These findings suggest that stimulation of upper-airway mechanoreceptors during obstructive apnea in NREM sleep augments phasic genioglossus activity.

Anesthesia, Local↗
PubMed1996

Modeling the interaction between arousal and chemical drive in sleep-disordered breathing.

We have measured the ventilatory response to acoustically induced arousal in normal subjects and patients with obstructive sleep apnea syndrome (OSAS). The arousal responses are similar in magnitude and time-course over the first 3 breaths, but in OSAS the subsequent response declines much more rapidly. Incorporation of these empirical findings into an existing model of sleep-disordered breathing allows an improved characterization of state-chemoreflex interactions. The shorter time-course of the arousal response in OSAS promotes greater ventilatory and state instability at low-to-intermediate levels of CO2 gain.

Adolescent↗
PubMed1996

Ventilatory dynamics during transient arousal from NREM sleep: implications for respiratory control stability.

The polysomnographic and ventilatory patterns of nine normal adults were measured during non-rapid-eye-movement (NREM) stage 2 sleep before and after repeated administrations of a tone (40-72 dB) lasting 5 s. The ventilatory response to arousal (VRA) was determined in data sections showing electrocortical arousal following the start of the tone. Mean inspiratory flow and tidal volume increased significantly above control levels in the first seven breaths after the start of arousal, with peak increases (64.2% > control) occurring on the second breath. Breath-to-breath occlusion pressure 100 ms after the start of inspiration showed significant increases only on the second and third postarousal breaths, whereas upper airway resistance declined immediately and remained below control for > or = 7 consecutive breaths. These results suggest that the first breath and latter portion of the VRA are determined more by upper airway dynamics than by changes in the neural drive to breathe. Computer model simulations comparing different VRA time courses show that sustained periodic apnea is more likely to occur when the fall in the postarousal increase in ventilation is more abrupt.

Adult↗
PubMed1996

Sleep apnea impairs the arousal response to airway occlusion.

We hypothesized that the increased arousal threshold to upper airway occlusion exhibited by patients with obstructive sleep apnea (OSA) is in part secondary to the disease process itself. To test this hypothesis, we studied the effects of withdrawal of three nights of nasal continuous positive airway pressure (CPAP) treatment on arousal in six male patients with severe OSA who were using nasal CPAP on a long-term basis. During the control week, patients slept with nasal CPAP at home and on the first of 2 nights in the sleep laboratory (night C1, CPAP; night C2, no CPAP). During the apnea week, patients slept without nasal CPAP for 2 nights at home and 2 nights in the sleep laboratory (AP1, AP2). The control and apnea weeks were consecutive and in random order. The mean (+/-SEM) apnea+hypopnea index was 76.9 +/- 7.1 on AP1 vs 3.1 +/- 1.0 events per hour on C1 (p<0.05). Thus, the laboratory night (and presumably the 2 nights at home) preceding AP2 had dramatic increases in apnea compared with the nights preceding C2. The apnea duration during nonrapid eye movement sleep on nights following apnea was greater (AP2: 28.7 +/- 1.5 vs C2: 25.5 +/- 1. 7 s; p<0/05) and the arousal threshold as reflected by the maximum esophageal pressure deflection preceding arousal was higher (DPmax) (AP2: 55.1 +/- 5.7 vs C2: 45.3 +/- 6.4 cm H2O; p<0.005). We conclude that prior sleep apnea increases the arousal threshold to upper airway occlusion on subsequent nights and prolongs the apneic events.

Adult↗
PubMed1996

Arterial blood gas changes during breath-holding from functional residual capacity.

Breath-holding serves as a model for studying gas exchange during clinical situations in which cessation of ventilation occurs. We chose to examine the arterial blood gas changes that occurred during breath-holding, when breath-holding was initiated from functional residual capacity (FRC) while breathing room air. Eight normal subjects who had a radial artery catheter placed for another study were taught to breath-hold on command from FRC. FRC was determined using respiratory inductance plethysmography. Arterial blood gas specimens were obtained at 5-s intervals until the termination of breath-holding. The average breath-holding time (+/-SD) was 35 (+/-10 s). The PaO2, PaCO2, and pH values were plotted against time and individually fit to logistic equations for each subject. The arterial PaO2 fell by a mean of 50 mm Hg during the first 35 s of breath-holding under these conditions, while the arterial PCO2 rose by a mean of 10.2 mm Hg during the first 35 s and the pH fell by a mean of 0.07 in the first 35 s. The rapid decline in PaO2 is greater than that previously reported using different methods and should be considered in clinical situations in which there is an interruption of oxygenation and ventilation at FRC while breathing room air. The changes in PaCO2 and pH are similar to those previously reported in paralyzed apneic patients.

Adolescent↗
PubMed1995

Triazolam in patients with obstructive sleep apnea.

The purpose of this study was to assess the effect of triazolam (0.25 mg) on apnea duration and the arousal response to airway occlusion during sleep in patients with severe obstructive sleep apnea (OSA). Twelve male subjects with a mean (+/- SD) age of 46.6 +/- 14.1 yr and body weight of 260.8 +/- 55.9 lb were studied on two nights separated by a nonstudy night. They ingested triazolam (0.25 mg) or placebo 0.5 h before bedtime in a randomized double-blind crossover manner. In non-rapid-eye-movement (NREM) sleep, the mean (+/- SEM) duration of apnea/hypopnea was slightly increased (26.8 +/- 1.7 versus 23.8 +/- 1.2 s, p < 0.02) and the mean nadir in arterial oxygen saturation lower (80.1 +/- 1.9 versus 84.2 +/- 1.4%, p < 0.001) on triazolam nights. In NREM sleep, the deflections in esophageal pressure prior to apnea termination were higher on triazolam nights (53.3 +/- 5.4 versus 44.5 +/- 4.8 cm H2O, p < 0.001). However, the rate of increase in inspiratory effort (esophageal pressure deflections) during obstructive events was not decreased by triazolam. We conclude that triazolam increases the arousal threshold to airway occlusion, but that this results in only modest prolongation of event duration and increased desaturation at a dose of 0.25 mg in a group of large sleep apnea patients.

Adult↗
PubMed1995

Effect of upper airway anesthesia on obstructive sleep apnea.

We hypothesized that upper airway mechanoreceptors contribute to the arousal stimulus that occurs with upper airway occlusion in obstructive sleep apnea (OSA). If so, upper airway anesthesia (UAA) should reduce the arousal stimulus and impair the arousal response. To test this hypothesis, we studied the effects of UAA on apnea duration and the esophageal pressure deflection before arousal in a group of patients with severe OSA. On two study nights separated by one week, subjects were monitored for 2 h after lights out. They were then awakened and either 5 cc of 4% lidocaine or saline (random order) was dripped into the upper airway via the nose over 10 min. Another 2 h of monitoring was then performed. Variables on the first and second parts of the control (C1 and C2) and lidocaine nights (L1 and L2) were compared during non-rapid eye movement sleep using the analysis of variance. With lidocaine, the mean (+/- SEM) apnea duration increased from 24.2 +/- 2.6 (L1) to 30.7 +/- 2.3 (L2) s but with saline the apnea length was unchanged from 23.3 +/- 1.5 (C1) to 23.4 +/- 1.6 (C2) (L2 > [L1, C1, C2], p < 0.01). In addition, the maximum esophageal pressure deflection (cm H2O) before arousal increased after lidocaine from 63.6 +/- 14.5 (L1) to 84.1 +/- 14.7 (L2) but after saline was unchanged from 62.1 +/- 15.4 (C1) to 60.0 +/- 15.2 (C2), (L2 > [L1, C1, C2], p < 0.05). We conclude that UAA impairs the arousal response to airway occlusion. This suggests that input from upper airway mechanoreceptors during obstructive events contributes to the total arousal stimulus in patients with OSA.

Anesthesia, Local↗
PubMed1994

Effects of sleep on the antidepressant response to sleep deprivation.

The effect of a 90-min nap period on mood was studied in 22 sleep-deprived patients with a diagnosis of major depression. All patients remained awake from 7 AM until 12 noon the following day at which time they were permitted to nap while being monitored by sleep encephalography. Fifteen subjects showed a significant response to sleep deprivation as defined by a 35% improvement on the Hamilton Rating Scale for Depression. After the nap a relapse of depressive symptoms occurred which was significantly related to the amount of non-rapid eye movement sleep time.

Adult↗
PubMed1994

Rapid eye movement sleep periodic leg movements in patients with spinal cord injury.

We describe three spinal cord injury cases exhibiting periodic leg movements (PLMs) in both rapid eye movement (REM) and nonrapid eye movement (NREM) sleep. The difference in the average periodicity in REM and NREM sleep was modest, but was generally shorter in REM than in NREM sleep. However, the variability associated with the PLMs was nearly three to six times smaller in REM than in NREM sleep, suggesting that the periodicity of the PLMs in REM sleep was more precise than in NREM sleep. The finding of PLMs in these patients suggests that a spinal cord injury may permit the expression of a spinal PLM generator, which may be an unusual presentation of a spinal locomotor generator. The PLM generator would be displayed when the descending inhibitory spinal pathways are interrupted by a spinal injury. The rapid periodicity of the PLM generator in REM sleep, compared with NREM sleep, may result from an increase in sympathetic activity normally accompanying this sleep state. Alternative explanations for the occurrence of PLMs in spinal injury are the influence of adverse sleeping position, age, an increase in circulating catecholamines and peripheral perfusion. We conclude that the presence of PLMs may be an important, but neglected, sleep disorder in spinal cord patients. Therefore, health care professionals should be aware of the possibility of sleep-related PLMs when these patients have sleep and/or waking complaints.

Adult↗
PubMed1994

Variability of cardiac output over time in medical intensive care unit patients.

OBJECTIVES: To determine the amount of spontaneous variability of cardiac output over time in critically ill patients, and to determine the effect of mechanical ventilation on cardiac output variability over time. DESIGN: Case series. SETTING: Medical intensive care unit in a Veterans Affairs Medical Center. PATIENTS: Twenty-two patients with indwelling pulmonary artery flotation catheters were studied. Two patients were studied twice. INTERVENTIONS: During a 1-hr time period in which no interventions were required or made, thermodilution cardiac output was determined at baseline and then every 15 mins for 1 hr. At each time point, five individual cardiac output measurements were made and a mean was computed. The covariables of heart rate, respiration rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary artery occlusion pressure, and temperature were also recorded at each time point. MEASUREMENTS AND MAIN RESULTS: The variability of the five cardiac output measurements made at each time point was expressed by calculating for each patient a coefficient of variation of the measurements. The overall mean coefficient of variation of the measurements was 5.8%. The variability of the cardiac output measurements over time was expressed by calculating for each patient a coefficient of variation over time. The overall mean coefficient of variation over time was 7.7%. A subgroup of 15 "covariable stable" patients (defined as those patients with covariables within +/- 5% of the mean covariable values during the hour) had a mean coefficient of variation over time of 6.4%, whereas "covariable unstable" patients (with > +/- 5% changes in any covariable) had a mean coefficient of variation over time of 9.9% (p < .05). Patients breathing spontaneously had a mean coefficient of variation over time of 10.1%, whereas mechanically ventilated patients had a mean coefficient of variation over time of 6.3% (p < .05). CONCLUSIONS: The spontaneous variability of cardiac output should be considered when interpreting two cardiac output determinations made at separate times. Due to spontaneous variability alone, a patient with a baseline cardiac output of 10.0 L/min would be expected (95% confidence interval) to have a cardiac output range of 9.2 to 10.8 L/min if covariables were stable, and a range of at least 8.8 to 11.2 L/min if covariables were unstable. Patients who were mechanically ventilated displayed less variability than patients who were breathing spontaneously.

Adult↗
PubMed1994

Effects of abstinence from smoking on sleep and daytime sleepiness.

This study examined the effect of smoking abstinence on sleep quality, daytime sleepiness, and mood in 18 subjects (10 men and 8 women) aged 35 to 49 years who had smoked at least 20 cigarettes per day for more than 2 years. Subjects were studied on two consecutive weeks following an adaptation night. During week 1 (study nights 1, 2, and 3), the subjects smoked as usual. Smoking abstinence was mandatory during week 2 beginning 3 h prior to night 4 and ending after the final tests on night 6. Complete sleep monitoring each night was followed by multiple sleep latency tests (MSLTs) throughout the day. Psychomotor tests and mood observations were performed throughout the day between the MSLTs. The results of testing when the subjects smoked were compared with those during nonsmoking days and nights. Nights 1 and 4 were considered adaptation nights and not included in the analysis. Overnight studies showed a significant increase in the number of relative arousals (a change in sleep stage to wake, stage 1 sleep, or movement), stage changes, and awakenings during smoking cessation. The MSLT latency to stage 1 sleep decreased during smoking cessation. Also during abstinence, the subjects reported that they felt more irritable, had increased feelings of anxiety, felt greater tension, and had more cravings for cigarettes. We conclude that smoking cessation is associated with increased daytime sleepiness and impaired mood. The daytime sleepiness may be due to the combination of sleep disturbance and withdrawal of the nicotine normally provided through smoking.

Adult↗
PubMed1994

Oral-nasal continuous positive airway pressure as a treatment for obstructive sleep apnea.

The effect of continuous positive airway pressure (CPAP) applied via a mask covering the nose and mouth (oral-nasal CPAP = ONCPAP) on obstructive sleep apnea (OSA) was studied in ten male patients with a mean (+/- SD) age of 48.1 +/- 11.1 years who could not tolerate nasal CPAP (NCPAP) due to nasal congestion. Using ONCPAP at pressures of 11.0 +/- 4.5 cm H2O, the apnea+hypopnea index was reduced from 58.3 +/- 22.3 (baseline night) to 5.2 +/- 1.6 events per hour (ONCPAP night) (p < 0.001). Five of these patients were studied on a subsequent night with a dual chamber mask allowing separate measurement of nasal and oral flow. All patients had combined oral and nasal flow at times during the night, but the fraction of time spent with this breathing pattern was lower during sleep than wakefulness. In a separate study, we compared the effects of a therapeutic level of CPAP pressure (12.8 +/- 2.5 cm H2O) applied through a nasal mask (NCPAP) and ONCPAP in a different group of patients (mean age 60 +/- 14.6 years) with moderate to severe OSA using NCPAP on a long-term basis. The apnea-hypopnea indexes on NCPAP nights (7.2 +/- 3.5) and ONCPAP nights (7.6 +/- 4.9 events per hour of sleep) were very similar. We conclude that ONCPAP may be a reasonable treatment alternative in patients who cannot tolerate NCPAP due to nasal congestion and that the pressure required to maintain upper airway patency may be similar to the level required using NCPAP.

Adult↗
PubMed1994

Acquired laryngomalacia as a cause of obstructive sleep apnea.

We describe a patient who, 4 years after a radical neck dissection and radiotherapy, presented with obstructive sleep apnea; upon bronchoscopy, he was found to have acquired laryngomalacia. Inspiration induced upper airway obstruction due to a large flaccid epiglottis, large aryepiglottic folds, and edema of the supraglottic area. We suggest that acquired laryngomalacia can lead to obstructive sleep apnea. Patients with obstructive sleep apnea after radical neck dissection need to be evaluated for laryngomalacia with fiberoptic laryngobronchoscopy. Examination of the upper airway is useful to determine the nature and extent of any upper airway collapse.

Adult↗
PubMed1993

Effect of hypercapnia on the arousal response to airway occlusion during sleep in normal subjects.

The effect of an acute increase in PCO2 on the arousal response to occlusion of a mask covering the nose with the mouth sealed during non-rapid-eye-movement sleep was studied in six normal males aged 28.3 +/- 8.3 (SD) yr. Baseline occlusions, while subjects breathed a room air-O2 mixture adjusted to produce an arterial O2 saturation of 98%, were alternated with hypercapnic occlusions in which a small amount of 100% CO2 was added to increase the preocclusion end-tidal PCO2 by 3.5 +/- 0.59 Torr above the baseline value. The maximum deflections in supraglottic airway pressure (Pmax) were measured on the initial occluded breath (PmaxI) and the final breath preceding arousal (PmaxF). In the hypercapnic occlusions, the time to arousal was shorter (23.7 +/- 13.9 vs. 35.2 +/- 15.9 s, P < 0.03) and PmaxI and rate of change in Pmax were higher. However, the PmaxF in the baseline (20.2 +/- 4.1 cmH2O) and hypercapnic occlusions (20.4 +/- 4.4 cmH2O) did not differ. We conclude that an increase in PCO2 before airway occlusion shortens the time to arousal by increasing the initial occluded inspiratory effort (suction pressure) and the rate of increase in effort but does not change the arousal threshold.

Adolescent↗
PubMed1993

Does the hypoxic ventilatory response predict the oxygen-induced falls in ventilation in COPD?

The purpose of this study was to determine whether supplemental oxygen-induced decreases in ventilation (VE) and mouth occlusion pressure (P0.1) in patients with COPD are related to the ventilatory or P0.1 responses to hypoxia (delta VE/delta SaO2, delta P0.1/delta SaO2). We measured these responses in 14 patients with a (mean +/- SD) FEV1 of 0.95 +/- .41 L. The VE and P0.1 were also measured while the patients sequentially breathed either room air or supplemental oxygen (1-2 L/min) for 10 min in a randomized single blind fashion. The mean (+/- SEM) SaO2 increased from 90.8 +/- 0.99 percent to 95.2 +/- 0.46 percent and the VE decreased during oxygen breathing from 12.3 +/- 0.46 to 11.6 +/- 0.47 L/min (p < 0.03). However, the individual changes in VE were not significantly related to the corresponding changes in SaO2 (CHG SaO2), (delta VE/delta SaO2), or (delta VE/SaO2) (CHG SaO2). Similarly, the P0.1 decreased from 2.50 +/- 0.27 to 2.26 +/- 0.20 cm H2O (p < 0.05), but the individual changes in P0.1 were not significantly related to (CHG SaO2), (delta P0.1/delta SaO2), or (delta PO.1/delta SaO2) (CHG SaO2).

Aged↗
PubMed1993

Relationship of thermodilution cardiac output to metabolic measurements and mixed venous oxygen saturation.

To determine the individual contributions of variables in the Fick equation to cardiac output, we simultaneously measured oxygen uptake (VO2), carbon dioxide production (VCO2), venous oxygen saturation (SvO2) and thermodilution cardiac output (Qth) in 28 medical and surgical ICU patients. Patients were intubated and ventilated with the intermittent mandatory ventilation mode. VO2 and VCO2 (averaged over 3 min) were obtained from a metabolic cart. SvO2 was measured with fiberoptic reflectance oximetry (and COoximetry). Thirty-nine studies (average duration, 4.3 h) with 151 Qth measurements were performed. The relationships between Qth and VO2, Qth and VCO2, Qth and SvO2, and 1/Qth and SvO2, as well as between the sequential changes in these variables were analyzed by least squares linear regression. The ability of changes in the variables VO2, VCO2, and SvO2 to predict changes in Qth were analyzed by receiver operating characteristic (ROC) curves. Qth was weakly related to VO2 (r = 0.45), VCO2 (r = 0.45), or SvO2 (r = 0.36). Changes in Qth were weakly related to changes in VCO2 (r = 0.40), and even less to changes in VO2 (r = 0.18) and SvO2 (r = 0.13). The areas under the ROC curves for increases in Qth > 10 percent were as follows: 0.66 for VCO2, 0.50 for VO2, and 0.55 for SvO2. The areas for decreases in Qth < 10 percent were as follows: 0.78 for VCO2, 0.65 for VO2, and 0.49 for SvO2. None of the above oximetry relationships were substantially altered by use of COoximetry venous oxygen saturations. We conclude that Qth cannot be predicted well solely from VO2, VCO2, or SvO2 nor can changes in Qth be predicted well solely from changes in VO2, VCO2, or SvO2. Of the metabolic variables, changes in VCO2 best predicted changes in Qth.

Carbon Dioxide↗
PubMed1992

Effect of ethanol on the arousal response to airway occlusion during sleep in normal subjects.

The effect of ethanol on the arousal response to airway occlusion during non-rapid eye movement sleep was studied in normal male subjects by testing the response to the occlusion of a face mask covering the nose and mouth on a control (C) and an ethanol (E) ingestion (2 ml/kg of 50% vodka) night in random order. In part A, five subjects breathed room air while in part B another five subjects breathed a mixture of air and oxygen adjusted to maintain a baseline sleeping SaO2 of 98%. In both parts, the time to arousal (TTA) was significantly longer on E nights. The TTA (mean +/- SEM) in part A on C versus E nights was 14.6 +/- 1.9 versus 20.6 +/- 1.4 s in stage 2 and 19.9 +/- 1.9 versus 29.2 +/- 1.8 in stage 3/4 (p less than 0.01). The corresponding values in part B were 22.2 +/- 3.6 versus 39.9 +/- 8.4 in stage 2 and 32.1 +/- 4.1 versus 63.7 +/- 9.6 in stage 3/4 (p less than 0.01). In part B, the maximum deflections in airway pressure were measured at a supraglottic location during airway occlusion to reflect the degree of inspiratory effort. The maximum airway suction pressure preceding arousal was significantly higher on E nights. Conversely, the rate of increase in inspiratory effort (maximum pressure) during occlusion was decreased by E. We conclude that moderate ethanol ingestion prolongs the time to arousal following airway occlusion by increasing the threshold of inspiratory effort associated with arousal and by decreasing the rate of increase in the magnitude of inspiratory efforts.

Adult↗