Biomedical subjects

Alan R Schwartz

Publications and source records attributed to Alan R Schwartz.

22 records · Page 2Linked to original sources

PubMed2002

Sleep-disordered breathing and insulin resistance in middle-aged and overweight men.

Sleep-disordered breathing is a prevalent condition associated with impairment of daytime function and may predispose individuals to metabolic abnormalities independent of obesity. The primary objective of this study was to determine the metabolic consequences and community prevalence of sleep-disordered breathing in mildly obese, but otherwise healthy, individuals. One hundred and fifty healthy men, without diabetes or cardiopulmonary disease, were recruited from the community. Measurements included polysomnography, a multiple sleep latency test, an oral glucose tolerance test, determination of body fat by hydrodensitometry, and fasting insulin and lipids. The prevalence of sleep-disordered breathing, depending on the apnea-hypopnea index (AHI) cutoff, ranged from 40 to 60%. After adjusting for body mass index (BMI) and percent body fat, an AHI gt-or-equal, slanted 5 events/h was associated with an increased risk of having impaired or diabetic glucose tolerance (odds ratio, 2.15; 95% CI, 1.05-4.38). The impairment in glucose tolerance was related to the severity of oxygen desaturation (DeltaSa(O(2))) associated with sleep-disordered breathing. For a 4% decrease in oxygen saturation, the associated odds ratio for worsening glucose tolerance was 1.99 (95% CI, 1.11 to 3.56) after adjusting for percent body fat, BMI, and AHI. Multivariable linear regression analyses revealed that increasing AHI was associated with worsening insulin resistance independent of obesity. Thus, sleep-disordered breathing is a prevalent condition in mildly obese men and is independently associated with glucose intolerance and insulin resistance.

Adult↗

PubMed2002

Use of dynamic negative airway pressure (DNAP) to assess sedative-induced upper airway obstruction.

BACKGROUND: Traditional methods of assessing ventilatory effects of sedative agents do not measure their propensity to cause upper airway obstruction (UAO). The primary objective of this study was to develop a method, using dynamic negative airway pressure (DNAP), for replicating UAO during deep sedation. METHODS: A state of deep sedation (defined as an Observer Assessment of Alertness and Sedation score of 3 and a bispectral index < 80) was attained in 10 healthy volunteers, aged 19-41, using midazolam. Volunteers breathed through a chamber connected to a regulated source of negative pressure that was gradually adjusted downward to produce UAO based on maximal inspiratory flow. The study consisted of three phases: A control phase while awake, a study phase during midazolam deep sedation, and a recovery phase after flumazenil administration. RESULTS: During the control phase no subject demonstrated airway obstruction at negative pressures to -30-cm H2O. All subjects exhibited complete UAO during DNAP episodes while sedated. Negative pressures required to cause complete UAO (Pcrit) ranged from -2 to -14 cm H2O. After administration of flumazenil, all subjects attained full consciousness within 5 min and did not demonstrate UAO at negative pressures to -30-cm H2O. CONCLUSIONS: Dynamic Negative Airway Pressure is a useful method for provoking midazolam-induced UAO, and may potentially be used to compare the potential for different sedatives and patient factors to cause UAO. Flumazenil was completely effective in reversing the potential for midazolam to cause UAO.

Adult↗

PubMed2002

Modulation of upper airway collapsibility during sleep: influence of respiratory phase and flow regimen.

We hypothesized that upper airway collapsibility is modulated dynamically throughout the respiratory cycle in sleeping humans by alterations in respiratory phase and/or airflow regimen. To test this hypothesis, critical pressures were derived from upper airway pressure-flow relationships in six tracheostomized patients with obstructive sleep apnea. Pressure-flow relationships were generated by varying the pressure at the trachea and nose during tracheostomy (inspiration and expiration) (comparison A) and nasal (inspiration only) breathing (comparison B), respectively. When a constant airflow regimen was maintained throughout the respiratory cycle (tracheostomy breathing), a small yet significant decrease in critical pressure was found at the inspiratory vs. end- and peak-expiratory time point [7.1 +/- 1.6 (SE) to 6.6 +/- 1.9 to 6.1 +/- 1.9 cmH(2)O, respectively; P < 0.05], indicating that phasic factors exerted only a modest influence on upper airway collapsibility. In contrast, we found that the inspiratory critical pressure fell markedly during nasal vs. tracheostomy breathing [1.1 +/- 1.5 (SE) vs. 6.1 +/- 1.9 cmH(2)O; P < 0.01], indicating that upper airway collapsibility is markedly influenced by differences in airflow regimen. Tracheostomy breathing was also associated with a reduction in both phasic and tonic genioglossal muscle activity during sleep. Our findings indicate that both phasic factors and airflow regimen modulate upper airway collapsibility dynamically and suggest that neuromuscular responses to alterations in airflow regimen can markedly lower upper airway collapsibility during inspiration.

Adult↗

PubMed2002

Ventilating with tracheal gas insufflation and periodic tracheal occlusion during sleep and wakefulness.

INTRODUCTION: The current invasive and noninvasive methods for delivering long-term ventilatory support rely on cumbersome patient interfaces that may interfere with upper airway function. To overcome these limitations, a novel system was developed to ventilate conscious, spontaneously breathing dogs through a self-contained cuffed cannula that was used for tracheal gas insufflation (TGI) and periodic tracheal occlusion (PTO). We hypothesized that TGI + PTO would provide greater ventilatory support than would TGI alone and that its effect would be more pronounced during sleep than wakefulness. METHODS: Chronically tracheostomized dogs were monitored for sleep (ie, EEG, electro- oculogram, and nuchal electromyogram) and breathing (ie, tracheal pressure [Ptr] and upper airway flow via snout mask). A thin transtracheal cannula housed within a cuffed tracheostomy tube was used for TGI and PTO monitoring. E, gas exchange, and breathing patterns were examined during sleep and wakefulness at baseline (ie, no TGI) and during the application of TGI alone (at 5, 10, and 15 L/min) and the application of TGI + PTO. RESULTS: Compared to baseline breathing without TGI, TGI at 5, 10, and 15 L/min decreased minute ventilation without influencing PaCO(2). In contrast, TGI + PTO led to progressive increases in ventilation, positive Ptr swings, and decreases in PaCO(2) as the flow rate was increased during sleep and wakefulness. Moreover, spontaneous breathing efforts ceased during TGI + PTO at flow rates of 10 and 15 L/min during wakefulness, and at all flow rates during sleep. CONCLUSIONS: The findings indicate that TGI + PTO can fully support ventilation in a spontaneously breathing canine model during sleep and wakefulness. Its streamlined interface could ultimately prove to be clinically significant, once technical concerns are addressed.

Animals↗