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Biomedical subjects

D W Hudgel

Publications and source records attributed to D W Hudgel.

At least 19 recordsLinked to original sources
PubMed1992

Mechanisms of obstructive sleep apnea.

This article has reviewed the anatomic, compliance, reflex, and respiratory muscle variables that affect upper airway caliber and abnormalities which may precipitate upper airway collapse during sleep. One or more of these variables may be important in the mechanism of OSA in any given patient. First, anyone with anatomic narrowing of the upper airway is susceptible to OSA. However, we do know if anatomic narrowing of the upper airway is necessary for the development of OSA. Surely, heavy snoring produces pharyngeal trauma and possibly edema or inflammation, which in turn may narrow the upper airway. Submucosal adipose tissue or cervical adipose tissue may compress the airway when the tonic electrical activity of the pharyngeal muscles decreases with sleep onset. Data reviewed support the idea that the upper airway of OSA patients may be more collapsible than the upper airway of nonapneic subjects. Intrinsic tissue abnormalities have not been demonstrated that might be responsible for this collapsibility. Changes in collapsibility found are consistent with, and may be due to, changes in tonic and phasic contraction of upper airway muscles. Abnormalities in reflexes affecting upper airway size surely might exist in OSA. Edema or inflammation of pharyngeal tissues might not only narrow the upper airway but might also impair normal function of the receptors responsible for initiating protective reflexes. We propose the fluctuation between a low- and a high-drive state contributes to upper airway collapse in OSA. With this fluctuation the balance of forces and critical pressure concepts discussed above come into play (Fig 6). By stimulating upper airway inspiratory muscles, CO2 eliminates the hypoapneic, low-drive, high-resistance periods and thereby reduces the number of apneas. In addition, preferential stimulation of upper airway muscle activity dilates the upper airway per se. If the relative value of each of these factors can be determined diagnostically, perhaps therapy can be made more specific. By being more specific, therapy should be more successful than the present practice of prescribing a particular therapy, regardless of the specific mechanism responsible for the OSA in a given patient.

Humans↗
PubMed1992

The role of upper airway anatomy and physiology in obstructive sleep apnea.

Research efforts to date have determined that both anatomic and physiologic variables may contribute to the pathophysiology of OSA. Whether specific factors within either of these two categories will be shown to predominate remains to be seen. Surely, experience with sleep apnea patients teaches us that different variables are important in different OSA patients. However, even those patients who initially appear to have predominantly an anatomic or physiologic cause of their OSA often fail to respond to specific treatment. Treatment failure implies the following: (1) The initial impression of the importance of a given variable was wrong. This may happen in the patient who has a narrow transpalatal airway and fails to respond to uvulopalatopharyngoplasty. In this individual, physiologic variables such as pharyngeal collapsibility or periodic breathing may need to be addressed. Of course, the reverse may occur; patients may be treated pharmacologically for an assumed physiologic mechanism and important anatomic factors may have been overlooked. Our ability to differentiate the importance of these different variables is poor. Therefore, our diagnostic acumen needs further refinement. (2) Of course, it is likely that the proper diagnosis was made, but the therapy chosen was imperfect. In the area of anatomy, investigators are just beginning to try surgical approaches designed specifically for the pharyngeal site of obstruction. In other words, uvulopalatopharyngoplasty is not the best approach for everyone. In physiology, treatments beyond continuous positive airway pressure will be needed. It is hoped that advances in the pharmacology of sleep disorders will establish more convenient and successful therapies. It is likely that OSA is a heterogenous disease process. We must realize that a treatment that helps one patient may not be applicable to the next individual. Through a better understanding of the pathophysiology of OSA, better treatment modalities should be developed, resulting in improved quality of life for OSA patients.

Humans↗
PubMed1991

Evaluation of the upper airway in patients with obstructive sleep apnea.

Multiple methods have been used to study the structure and physiological behavior of the upper airway (UA) in patients with obstructive sleep apnea (OSA). Valuable information may be obtained from the physiologic measurement of pressure and resistance along the UA, as well as from imaging techniques that include: direct or fiberoptic visualization, cephalometric roentgenograms, fluoroscopy, acoustic reflection, computerized tomography, and magnetic resonance imaging. This review summarizes the information that each of these methods has contributed to our understanding of the UA. The results obtained with these different methodologies have generally been complementary with structural narrowing being identified in the majority of patients with OSA. This narrowing is usually focal and located in the velopharyngeal or retropalatal segment of the UA. This is also the predominant site of initial UA collapse. Although obesity with enlargement of soft tissue structures is considered the predominant mechanism leading to UA narrowing, abnormal craniofacial development on a genetic or developmental basis plays an important contributory role.

Airway Obstruction↗
PubMed1991

Uvulopalatopharyngoplasty in obstructive apnea. Value of preoperative localization of site of upper airway narrowing during sleep.

We hypothesized that those obstructive sleep apnea (OSA) patients with upper airway collapse during sleep within the transpalatal airway would have a more favorable response to uvulopalatopharyngoplasty (UPP) than those patients with obstruction within the hypopharyngeal airway. We tested this hypothesis in seven OSA patients with transpalatal and seven with hypopharyngeal obstruction undergoing UPP. Preoperatively the apnea/hypopnea index (AHI) was different between palatal and hypopharyngeal obstructors, 37.8 +/- 6.0 (+/- SEM) and 63.9 +/- 6.3, respectively (p less than 0.05), but the apnea-associated arterial oxygen desaturation and the lowest sleep saturation level were not different between the two groups. Postoperatively the AHI was 17.6 +/- 7.2 in the palatal obstructors and 40.3 +/- 15.6 in the hypopharyngeal obstructors (both p less than 0.05 from preoperative AHI). The palatal obstructors had a significant decrease in the percentage of sleep time spent apneic and the hypopharyngeal obstructors had a significant decrease in the hypopnea, but not apnea, time following surgery. The palatal obstructors had a significantly higher postoperative arterial oxygen saturation than the hypopharyngeal obstructors. Two hypopharyngeal obstructors worsened postoperatively. In addition we found that regardless of the site of the obstruction preoperatively, all obstructions occurred at the level of the palate postoperatively. We conclude that patients with preoperative transpalatal obstruction had diminution in obstructive apneas and those with hypopharyngeal obstruction had diminution in hypopneas but not apneas. Oxygenation was better postoperatively in the palatal obstructors, and none worsened postoperatively. These results suggest that identification of the site of upper airway obstruction in OSA may be beneficial.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Response of obstructive sleep apnea to fluoxetine and protriptyline.

Protripyline is the pharmacologic agent most commonly used to treat obstructive sleep apnea (OSA); however, its anticholinergic side effects make it intolerable to many patients. Because serotonin may be a central respiratory stimulant and because the serotonin-uptake inhibitor, fluoxetine, is usually well tolerated, we wanted to try fluoxetine in the treatment of OSA. Therefore, we compared the effect of fluoxetine to that of protriptyline in 12 patients with OSA. Both drugs significantly decreased the proportion of REM sleep time and decreased the number of apneas or hypopneas in NREM sleep. The response to fluoxetine was equivalent to that of protriptyline; however, for the group as a whole, there was no significant improvement in the number of arterial oxygen desaturation events, the level of arterial oxygen desaturation, or the number of arousals with either agent. Although there was wide variability in the response to each medication, six of the 12 patients had good responses, including improvement in oxygenation, to either fluoxetine or protriptyline. Three patients could not complete the trial of protriptyline. We conclude that fluoxetine is beneficial to some, but not all, patients with OSA. Fluoxetine was better tolerated than protriptyline.

Adult↗
PubMed1990

Fluctuation in timing of upper airway and chest wall inspiratory muscle activity in obstructive sleep apnea.

An imbalance in the amplitude of electrical activity of the upper airway and chest wall inspiratory muscles is associated with both collapse and reopening of the upper airway in obstructive sleep apnea (OSA). The purpose of this study was to examine whether timing of the phasic activity of these inspiratory muscles also was associated with changes in upper airway caliber in OSA. We hypothesized that activation of upper airway muscle phasic electrical activity before activation of the chest wall pump muscles would help preserve upper airway patency. In contrast, we anticipated that the reversal of this pattern with delayed activation of upper airway inspiratory muscles would be associated with upper airway narrowing or collapse. Therefore the timing and amplitude of midline transmandibular and costal margin moving time average (MTA) electromyogram (EMG) signals were analyzed from 58 apnea cycles in stage 2 sleep in six OSA patients. In 86% of the postapnea breaths analyzed the upper airway MTA peak activity preceded the chest wall peak activity. In 86% of the obstructed respiratory efforts the upper airway MTA peak activity followed the chest wall peak activity. The onset of phasic electrical activity followed this same pattern. During inspiratory efforts when phasic inspiratory EMG amplitude did not change from preapnea to apnea, the timing changes noted above occurred. Even within breaths the relative timing of the upper airway and chest wall electrical activities was closely associated with changes in the pressure-flow relationship. We conclude that the relative timing of inspiratory activity of the upper airway and chest wall inspiratory muscles fluctuates during sleep in OSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Differential activation of respiratory muscles during wakefulness and sleep.

Evidence exists that strongly suggests that an imbalance in both the magnitude and timing of electrical activity between the upper airway and chest wall inspiratory muscles can exist during sleep. Too little or delayed activity of upper airway inspiratory muscles is associated with upper airway narrowing or collapse in patients with obstructive apnea. Preferential activation of upper airway muscles is associated with a decrease in upper airway resistance or in reopening of the airway following an apnea. These interrelationships between the upper and lower respiratory muscles may be exacerbated during the periodic breathing in sleep, thereby contributing to airway closure. This concept, in conjunction with those related to airway collapsibility and reflex control of upper airway caliber, should lead us closer to understanding the pathophysiology of obstructive sleep apnea.

Airway Resistance↗
PubMed1989

Neuropsychiatric manifestations of obstructive sleep apnea: a review.

Obstructive sleep apnea (OSA) may result in neuropsychiatric complications. Psychiatrists need to be alert to the possibility that patients who present to them with cognitive and/or affective disorders, who also have sleep related complaints such as snoring and significant daytime hypersomnolence, may have OSA. Clinical suspicion needs to be reinforced by obtaining a history from the bed partner. A polysomnogram will establish the diagnosis. Once the diagnosis is made, several treatment options are available. Treatment of sleep apnea usually leads to a resolution, or at least improved control, of the complicating neuropsychiatric disorder. Physicians must be aware that sedating neuroleptic or antipsychotic agents may worsen sleep apnea and, thereby, aggravate the neuropsychiatric disturbance.

Humans↗
PubMed1988

Characteristics of the upper airway pressure-flow relationship during sleep.

In examining the mechanical properties of the respiratory system during sleep in healthy humans, we observed that the inspiratory pressure-flow relationship of the upper airway was often flow limited and too curvilinear to be predicted by the Rohrer equation. The purposes of this study were 1) to describe a mathematical model that would better define the inspiratory pressure-flow relationship of the upper airway during sleep and 2) to identify the segment of airway responsible for the sleep-related flow limitation. We measured nasal and total supralaryngeal pressure and flow during wakefulness and stage 2 sleep in five healthy male subjects lying supine. A right rectangular hyperbolic equation, V = (alpha P)/(beta + P), where V is flow, P is pressure, alpha is an asymptote for peak flow, and beta is pressure at a flow of alpha/2, was used in its linear form, P/V = (beta/alpha) + (P/alpha). The goodness of fit of the new equation was compared with that for the linearized Rohrer equation P/V = K1 + K2V. During wakefulness the fit of the hyperbolic equation to the actual pressure-flow data was equivalent to or significantly better than that for the Rohrer equation. During sleep the fit of the hyperbolic equation was superior to that for the Rohrer equation. For the whole supralaryngeal airway during sleep, the correlation coefficient for the hyperbolic equation was 0.90 +/- 0.50, and for the Rohrer equation it was 0.49 +/- 0.25. The flow-limiting segment was located within the pharyngeal airway, not in the nose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Alteration in obstructive apnea pattern induced by changes in oxygen- and carbon-dioxide-inspired concentrations.

In patients with obstructive apnea, it was hypothesized that stimulation of the ventilatory system by hypercapnia during sleep would increase pharyngeal inspiratory muscle activity and thereby increase upper airway caliber. We predicted that this increase in caliber would decrease the number of apneas and sleep time spent apneic. In contrast, suppression of the ventilatory system activity with hyperoxia was predicted to decrease both inspiratory muscle activity and pharyngeal caliber and thereby increase the number of apneas and apnea time. In all 7 patients with symptomatic obstructive sleep apnea studied, 3 with upper airway narrowing obvious during wakefulness, inhalation of 3 to 6% CO2 preferentially stimulated upper airway inspiratory muscle tonic electrical activity relative to the activity of chest wall inspiratory muscles and diminished periodic breathing. Apnea time decreased from 60 +/- 2% (mean +/- SEM) of sleep time during ambient air inhalation to 12 +/- 3% during CO2 inhalation; 50% O2 had the reverse effect on inspiratory muscle tonic electrical activity and increased apnea time to 75 +/- 5% of sleep time. We conclude that manipulation of inspiratory muscle tonic activity and alteration of the pattern of breathing by CO2 and O2 inhalation lead to significant changes in the pattern of upper airway inspiratory collapse during sleep. We speculate that physiologic variables related to the control of upper airway inspiratory muscle function are instrumental in the pathophysiology of obstructive sleep apnea.

Air↗
PubMed1988

Palate and hypopharynx--sites of inspiratory narrowing of the upper airway during sleep.

In order to determine the specific site of inspiratory narrowing within the upper airway during sleep, we measured supralaryngeal, oropharyngeal, and nasopharyngeal pressures and inspiratory flow in 11 healthy nonsnoring male subjects awake and in NREM sleep. Resistance was calculated at 0.01 L/s, a point along the linear portion of the pressure-flow relationship, and at peak inspiratory pressure, a point within the curvilinear section of the pressure-flow relationship. During sleep, nasal resistance increased minimally. At peak inspiratory pressure, both transpalatal and hypopharyngeal resistances increased more than 700% in NREM sleep. At 0.01 L/s inspiratory flow, transpalatal and hypopharyngeal resistances increased 200 and 400%, respectively. Six subjects had a greater increase in transpalatal than hypopharyngeal resistance, and five subjects had a greater increase in hypopharyngeal than transpalatal resistance. Three subjects in each of these two subgroups had an increase in resistance exclusively across the palate or the hypopharynx. The site of increased resistance during sleep was not predictable from awake resistance measurements. From these data, we conclude that the site of inspiratory narrowing within the upper airway during sleep occurs primarily at either the level of the palate or hypopharynx and is variable among subjects. The pattern of palatal or hypopharyngeal narrowing is the same as that observed in obstructive sleep apnea patients, but quantitatively different.

Adult↗
PubMed1988

Nonspecific airway hyperreactivity in nonsmoking bituminous coal miners demonstrated by quantitative methacholine inhalation challenge.

Because nonsmoking underground bituminous coal miners often have symptoms of chronic bronchitis and because a high proportion of patients with chronic bronchitis have nonspecific airway hyperreactivity, we hypothesized that coal miners would have a higher prevalence of nonspecific airway hyperreactivity than nonminer nonsmoking control subjects. By use of a quantitative methacholine provocative inhalation challenge test, we evaluated 22 underground bituminous coal miners and 41 nonminer age- and sex-matched control subjects from the same community. We found that a significantly higher proportion of miners had reactivity to inhalation of 100 mg/ml or less of methacholine, X2 = 6.19, p less than 0.02. The slope of phase III of the single-breath nitrogen washout test was higher in the reactive miners than in the nonreactive miners and reactive control subjects, even though the reactive miners had only been working underground 8 +/- 3 (SEM) years. Within the reactive miner subgroup, the higher the reactivity to methacholine, the more abnormal the slope of phase III of the single-breath nitrogen test, r = 0.79. Miners had more symptoms than controls; the presence of methacholine reactivity was not associated with increased symptoms. We conclude that the bituminous coal miners in our study had an increased prevalence of nonspecific airway hyperreactivity and that within the reactive miner subgroup there was evidence of early airways disease. We speculate that the nonspecific airway hyperreactivity may be related to, and also be an indicator of, lung injury in coal miners.

Adult↗
PubMed1987

Neuromuscular and mechanical responses to inspiratory resistive loading during sleep.

The purposes of this study were 1) to characterize the immediate inspiratory muscle and ventilation responses to inspiratory resistive loading during sleep in humans and 2) to determine whether upper airway caliber was compromised in the presence of a resistive load. Ventilation variables, chest wall, and upper airway inspiratory muscle electromyograms (EMG), and upper airway resistance were measured for two breaths immediately preceding and immediately following six applications of an inspiratory resistive load of 15 cmH2O.l-1 X s during wakefulness and stage 2 sleep. During wakefulness, chest wall inspiratory peak EMG activity increased 40 +/- 15% (SE), and inspiratory time increased 20 +/- 5%. Therefore, the rate of rise of chest wall EMG increased 14 +/- 10.9% (NS). Upper airway inspiratory muscle activity changed in an inconsistent fashion with application of the load. Tidal volume decreased 16 +/- 6%, and upper airway resistance increased 141 +/- 23% above pre-load levels. During sleep, there was no significant chest wall or upper airway inspiratory muscle or timing responses to loading. Tidal volume decreased 40 +/- 7% and upper airway resistance increased 188 +/- 52%, changes greater than those observed during wakefulness. We conclude that 1) the immediate inspiratory muscle and timing responses observed during inspiratory resistive loading in wakefulness were absent during sleep, 2) there was inadequate activation of upper airway inspiratory muscle activity to compensate for the increased upper airway inspiratory subatmospheric pressure present during loading, and 3) the alteration in upper airway mechanics during resistive loading was greater during sleep than wakefulness.

Adult↗
PubMed1987

Changes in inspiratory muscle electrical activity and upper airway resistance during periodic breathing induced by hypoxia during sleep.

We hypothesized that: the balance of electrical activities between the upper airway and chest wall inspiratory muscles affects upper airway inspiratory caliber, and at low levels of central respiratory neural efferent activity, an imbalance between the electrical activities of these 2 inspiratory muscle groups exists that results in a decreased upper airway caliber. These hypotheses were tested during periodic breathing induced by mild hypoxemia in NREM sleep in 9 healthy male subjects. In 6 subjects during periodic breathing as central respiratory neural activity decreased, the tonic and phasic EMG activity of the upper airway inspiratory muscles decreased at a rate greater than that of the chest wall EMG activity. When the ratio of upper airway to chest wall EMG activity decreased below a critical level, which was reproducible across subjects, upper airway inspiratory resistance increased hyperbolically. Resistance at peak inspiratory flow increased from 4.10 +/- 0.97 (mean +/- SEM) to 48.70 +/- 21.00 cmH2O/L/s as tidal volume decreased from 0.79 +/- 0.12 to 0.20 +/- 0.02 L during periodic breathing in these subjects. In the 3 remaining subjects, the ratio of the upper airway to chest wall EMG activity did not decrease below the critical level as the activity of both muscle groups decreased during periodic breathing, and upper airway resistance did not increase. We conclude that within the confines of this study the nonlinear activation of upper airway and chest wall inspiratory muscles contributed to fluctuations in upper airway resistance observed during periodic breathing in sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Role of beta adrenergic receptors in carotid body function of the goat.

Previous studies in anesthetized or decerebrate cats and rabbits and awake man have shown conflicting results regarding a potential role for beta-adrenergic receptors in carotid body function. Therefore, we sought to clarify the role of beta-adrenergic receptor activity in carotid body function by assessing: the ventilatory response to intravenous isoproterenol infusion in awake and anesthetized carotid body intact and carotid body denervated goats, the effect of propranolol on the ventilatory response to isocapnic hypoxemia, and carotid sinus nerve chemoreceptor discharge rate response to isoproterenol and hypoxia. Isoproterenol increased ventilation to a similar degree in carotid body intact and denervated awake and anesthetized goats. This ventilatory increase was blocked by propranolol. Propranolol did not alter the hypoxic ventilatory response. Although ventilation increased, carotid sinus nerve chemoreceptor discharge rate was not altered by isoproterenol infusion or bolus IV injection in anesthetized goats. Hypoxia did increase carotid sinus nerve discharge rate. In this study, beta-adrenergic stimulation of ventilation did not occur via the carotid body, and beta-adrenergic blockade did not affect the carotid body hypoxic ventilatory response. Therefore, we found no evidence of functional beta-adrenergic activity within the carotid body of the goat.

Anesthesia↗
PubMed1986

Variable site of airway narrowing among obstructive sleep apnea patients.

The purpose of this was to determine whether the site of physiological narrowing within the upper airway was uniform or differed among patients with obstructive sleep apnea. Inspiratory pressures were measured with an esophageal balloon catheter and three catheters located at different sites along the upper airway: supralaryngeal airway, oropharynx, and nasopharynx. Peak inspiratory pressure differences between catheters allowed assessment of pressure gradients across three airway segments: lungs-larynx-retroepiglottal airway (esophageal-supralaryngeal pressure), hypopharynx (supralaryngeal-oropharynx pressure), and transpalatal airway (oropharynx-nasopharynx pressure). In five patients, hypopharyngeal obstruction was present, and in four patients no hypopharyngeal obstruction existed. In these four patients the site of obstruction was located at the level of the palate. In a given subject, the site of obstruction was the same during repeated measurements. The presence or absence of hypopharyngeal narrowing during sleep was not predictable from gradients measured across different segments of the upper airway during wakefulness. We conclude that the site of physiological upper airway obstruction varies among patients with obstructive sleep apnea and is not predictable from pressure measured during wakefulness. We speculate that uvulopalatopharyngoplasty may not relieve obstructive apneas in patients with hypopharyngeal obstruction.

Adult↗