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Biomedical subjects

P M Suratt

Publications and source records attributed to P M Suratt.

At least 19 recordsLinked to original sources

Enlargement of the lateral pharyngeal fat pad space in pigs increases upper airway resistance.

Because the upper airway is partially enclosed in a rigid boundary, enlargement of soft tissue structures within this boundary could narrow the airway. The purpose of this study was to determine whether enlargement of the soft tissue space in the region of the lateral pharyngeal fat pad would increase pharyngeal resistance and narrow the retropalateal upper airway. In five young male anesthetized pigs, we inserted balloon occlusion catheters in the lateral pharyngeal fat pad under computerized tomographic scan guidance. We measured pharyngeal resistance with a pharyngeal catheter and a tightly fitting face mask before and after inflation of the balloons. We also measured pharyngeal airway cross-sectional area before and after inflation of the balloons. In all pigs, balloon inflation significantly increased pharyngeal resistance and significantly decreased the area of the retropalateal airway. We conclude that enlargement of the soft tissue space in the region of the lateral pharyngeal fat pad increases pharyngeal resistance and narrows the retropalateal airway in anesthetized pigs.

Adipose Tissue

Breath-holding capability of adults. Implications for spiral computed tomography, fast-acquisition magnetic resonance imaging, and angiography.

PURPOSE: The breath-holding capabilities of various groups of individuals were evaluated to develop protocols so that patients undergoing spiral computed tomography (CT), digital angiography, and breath-hold magnetic resonance imaging (MRI) can be studied successfully. METHODS: Twenty-five outpatients and 25 inpatients (all adults) were studied before undergoing body CT. Each subject was asked to hold his or her breath for as long as possible. Then each patient was asked to perform as many repetitive 12-second breath holds as possible. These data were correlated with demographic and historical information. RESULTS: The maximum breath-hold time for inpatients and those outpatients who were heavy smokers or had chronic obstructive pulmonary disease (COPD) or congestive heart failure (CHF) was 18 to 32 seconds (95% confidence interval) with a mean of 25 seconds. For all other outpatients, breath-hold time was 38 to 56 seconds (mean = 45 seconds). The 95% confidence interval for the number of 12-second breath holds for these two groups was 4 to 6 breath holds (mean = 4.9) and 6 to 7 breath holds (mean = 6.6), respectively. One inpatient could not hold his breath at all and three others were only able to hold their breath once for short periods. The sex and age of the patient had no significant effect on breath-holding performance. CONCLUSIONS: Breath-holding protocols must account for the diminished capabilities of most inpatients, and outpatients who are heavy smokers or have COPD or CHF. Most outpatients who are not heavy smokers or without COPD or CHF can achieve a single breath hold of 38 seconds, or up to six 12-second breath holds.

Angiography, Digital Subtraction

Mandible enclosure of upper airway and weight in obstructive sleep apnea.

Although anatomic lesions and obesity can produce obstructive sleep apnea (OSA), most subjects with OSA have no recognizable anatomic lesion. We hypothesized that the occurrence of OSA is related to the size of the region enclosed by the mandible and the degree of obesity. We studied 30 subjects with a range of OSA and obesity with magnetic resonance imaging (MRI). MRI was performed with T-1 weighted sequences. Nocturnal polysomnography was performed in all subjects. Univariate regression analysis indicated there was a significant correlation between the number of apneas and hypopneas per hour of sleep (AH/h) and (1) the area enclosed by the mandible ramus (AMR1) (r = 0.48, p < 0.01) and (2) the distance from the teeth to the posterior mandible ramus (r = 0.39, p < 0.05). Stepwise multiple regression analysis indicated that weight, AMR1, and height explained 69% of the variance of AH/h (r2 = 0.69). We conclude that the occurrence of OSA in these subjects is related to the size of the region enclosed by the mandible as well as to their weight.

Adult

Pharyngeal fat in obstructive sleep apnea.

Although most patients with obstructive sleep apnea (OSA) are obese, it is not known how obesity contributes to airway collapse during sleep. The purpose of this study was to determine whether the volume of adipose tissue adjacent to the pharyngeal airway in humans is related to the degree of OSA. We studied 30 subjects, nine without OSA and 21 with OSA; two subjects were studied before and after weight loss. Adipose tissue was detected with magnetic resonance imaging using T1-weighted spin echo sequences. The volume of adipose tissue adjacent to the upper airway was determined by measuring the volume of all pixels in the intensity range of adipose tissue within the region bounded by the ramus of the mandible, the spine, the anterior border of the soft palate, and the hard palate. Polysomnography was performed with conventional techniques. All subjects had a collection of adipose tissue adjacent to the upper airway; the volume of this adipose tissue correlated with the number of apneas plus hypopneas per hour of sleep (r = 0.59, p < 0.001). Both patients who lost weight and had fewer apneas and hypopneas had a marked decrease in the pharyngeal adipose tissue volume. We conclude that adipose tissue is deposited adjacent to the pharyngeal airway in patients with OSA and that the volume of this tissue is related to the presence and degree of OSA.

Adipose Tissue

Adipose tissue deposition in sleep apnea.

To determine whether adipose tissue is deposited in the neck adjacent to the upper airway in patients with obstructive sleep apnea (OSA), we studied 21 subjects with OSA and nine without OSA using magnetic resonance imaging with a T-1 weighted spin echo sequence and polysomnography. We observed that patients with OSA had a larger volume of adipose tissue adjacent to their upper airway than did subjects without OSA.

Adipose Tissue

Effect of very-low-calorie diets with weight loss on obstructive sleep apnea.

To determine the effect of very-low-calorie diets (VLCDs) with weight loss on obstructive sleep apnea (OSA), we studied eight obese subjects with OSA, five males and three females. Subjects consumed a VLCD of 1760 kJ (420 kcal) (67% protein, 4% fat, 29% carbohydrate) or 3350 kJ (800 cal) (20% protein, 30% fat, 50% carbohydrate) with 100% of the recommended daily allowance of vitamins and minerals. Mean (+/- SD) values of weight and respiration before and after weight loss were, for weight, 153 +/- 37 and 132 +/- 29 kg (P less than 0.05); for BMI (kg/m2), 54 +/- 13 and 46 +/- 10 (P less than 0.05); for desaturations/h sleep, 106 +/- 50 and 52 +/- 45 (P less than 0.05); for apneas + hypopneas/h sleep, 90 +/- 32 and 62 +/- 49; for Pco2, 48 +/- 10 and 42 +/- 4 torr (P less than 0.05). Desaturation episodes/h and apnea + hypopneas/h improved in six patients. The most obese subject (female, BMI 81) who lost the most weight (47 kg) did not improve, nor did the subject who lost the least weight, 7 kg. The number of movements + arousals from sleep decreased in all patients (P less than 0.05). We conclude that VLCD with weight loss can produce improvement in OSA; subjects who lose a small amount of weight or subjects who are extraordinarily obese before and after weight loss may not improve.

Adult

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

Respiratory-related recruitment of the masseter: response to hypercapnia and loading.

To test the hypothesis that a muscle that closes the jaw, the masseter, can be recruited by ventilatory stimuli, we studied the electromyographic activation of the masseter and genioglossus in seven normal awake males who were exposed in random order to progressive hyperoxic hypercapnia, inspiratory threshold loading (-40 cmH2O), and combined hypercapnia and loading. With hypercapnia, the masseter was generally recruited after the genioglossus had been activated. Once recruited, activation of both muscles increased linearly with increasing CO2. Combined hypercapnia and loading produced more activation than either stimulus alone. These data indicate that the masseter is activated by ventilatory stimuli that activate the genioglossus. Earlier recruitment of the genioglossus suggests that activation of the masseter serves to stabilize the mandible and allow the genioglossus to function as a more efficient dilator of the upper airway.

Adult

Mandible position and activation of submental and masseter muscles during sleep.

Movement of the mandible could influence pharyngeal airway caliber because the mandible is attached to the tongue and to muscles that insert on the hyoid bone. In normal subjects and patients with obstructive sleep apnea (OSA) we measured jaw position during sleep with strain gauges, as well as masseter and submental electromyograms, airflow, esophageal pressure, oximetry, electroencephalograms, and electrooculograms. Jaws of patients with OSA were open more than those of normal subjects at end expiration and opened further at end inspiration, particularly at the termination of apneas when the masseter and submental muscles contracted. Masseter activation occurred only in patients with OSA and in a pattern similar to that of submental muscles. Jaw opening at end expiration could narrow the upper airway, whereas opening at end inspiration could reflect efforts to expand the airway with tracheal tug and with submental muscle activation and efforts to open the mouth to allow mouth breathing. Masseter contraction does not close the jaw but may serve to stabilize it.

Adult

Activation of masseter muscles with inspiratory resistance loading.

Closure of the jaw exerts traction on muscles that insert on the hyoid bone and that may stabilize or expand the pharyngeal airway. We postulated that the masseter muscles, which close the jaw, would be activated when the patency of the pharyngeal airway is threatened. We therefore measured electromyographic activation of the masseters during inspiratory resistance loading and compared it with activation of chin muscles and alae nasi in 10 normal subjects. We observed no masseter activation during quiet unloaded breathing, but as pharyngeal pressure became lower there was a significant increase in masseter activation in all subjects. The change in masseter activation relative to pharyngeal pressure was similar to that of chin muscles and alae nasi. Activation of the masseter preceded the fall in pharyngeal pressure as also occurred in the chin muscles and alae nasi. We conclude that the masseters are activated by inspiratory resistance loading and have respiratory activity similar to pharyngeal airway muscles.

Adult

Driving simulator performance in patients with sleep apnea.

Although previous studies have shown that patients with obstructive sleep apnea have a higher automobile crash rate than normal subjects, objective measurements of driving performance in patients with sleep apnea have not been reported. Therefore, we compared the driving performance of subjects with untreated, severe sleep apnea to that of control subjects on two driving simulators. Using a simulator with road films, six subjects with untreated, severe apnea performed worse than did a control group of seven normal subjects on both highway and city/rural driving (p less than 0.05). Using a personal computer program simulating a monotonous highway drive, 12 subjects with untreated sleep apnea performed worse than 12 control subjects. The patients with apnea hit a greater number of road obstacles during their 30-minute simulated drive than did the control subjects (44 +/- 52 in patients with apnea versus 9 +/- 7 in control subjects, p less than 0.05). Six patients with apnea hit fewer road obstacles after treatment with nasal continuous positive airway pressure (CPAP) than before treatment (29 +/- 19 before CPAP versus 13 +/- 8 after CPAP, p less than 0.05). We conclude that: (1) driving simulator performance of untreated subjects with severe obstructive sleep apnea is worse than that of control subjects; (2) driving simulator performance of subjects treated with nasal CPAP improves.

Adult

Prolonged relaxation rate of inspiratory muscles in patients with sleep apnea.

To evaluate whether inspiratory muscle function is impaired in patients with sleep apnea, we measured inspiratory muscle strength and relaxation rate before and after sleep in 13 patients. The sleep apnea group was composed of eight patients with severe obstructive sleep apnea, and the non-apnea group was composed of five patients without significant sleep apnea. We chose the time constant of relaxation (TauR) as an index of impaired inspiratory muscle contractility, and in subsets of each group, we measured the inspiratory pressure-time index as an indicator of a fatiguing breathing pattern. In patients with sleep apnea, presleep TauR was 79 +/- 22 ms (SD), longer than that of normal subjects (normal, 59 +/- 7 ms) (p less than 0.05). TauR increased by 21 +/- 16 ms during sleep (p less than 0.01). In patients without apnea, presleep TauR was 67 +/- 7 ms and it did not change after sleep. Maximal inspiratory and expiratory pressures were unchanged after sleep. We conclude that patients with sleep apnea do not develop overt inspiratory muscle failure but do have impaired contractility. We speculate that hypoxemia as well as increased work load was responsible.

Adult

Evaluation of respiratory disorders during sleep.

A respiratory sleep study should be performed in subjects suspected of having sleep apnea or in subjects suspected of hypoventilating during sleep who have unexplained hypersomnolence, erythrocytosis, pulmonary hypertension, or cor pulmonale. Sleep studies should include sleep staging, measurement of airflow, respiratory effort, oxyhemoglobin saturation, and electrocardiogram. Screening and at-home studies may be valuable, but further studies are necessary before they can be generally recommended. Analysis should include the number of apneas and hypopneas and an index of respiratory effort to determine whether the subject has obstructive, central, or mixed apnea. Oxyhemoglobin saturation should be analyzed quantitatively to note the degree of hypoxemia during sleep and to determine whether the subject could benefit from treatment to correct the hypoxia.

Clinical Protocols

Upper airway muscle activation is augmented in patients with obstructive sleep apnea compared with that in normal subjects.

Although phasic electromyographic (EMG) activity of upper airway muscles in patients with obstructive sleep apnea (OSA) decreases at apnea onset, the presence of phasic activity in normal subjects has not been studied and compared with that in patients. We consequently compared the percentage of total sleep time in which phasic activity of the genioglossal EMG activity was present in 8 adult patients with OSA and 3 control groups without OSA, one consisting of 6 young, normal subjects, one matched for age, and one matched for age and obesity. From wakefulness to sleep, genioglossal EMG phasic activity time increased in patients but not in control subjects. Patients with OSA had more phasic genioglossal group EMG activity during non-REM sleep than did control subjects. At apnea onset, phasic EMG activity decreased in patients but remained greater than zero. In many control subjects, phasic activity was not detected, yet their pharyngeal airway remained patent. We conclude that phasic genioglossal group EMG activity occurs more frequently during sleep in patients with OSA than in control subjects, suggesting that it is a compensatory mechanism that occurs when patency of the pharyngeal airway is precarious.

Airway Resistance

Automobile accidents involving patients with obstructive sleep apnea.

Although patients with obstructive sleep apnea often report falling asleep while driving, the frequency of auto accidents involving these patients has not been rigorously studied. Therefore, we compared the driving records of 29 patients with obstructive sleep apnea with those of 35 subjects without sleep apnea. The patients with sleep apnea had a sevenfold greater rate of automobile accidents than did the subjects without apnea (p less than 0.01). The percentage of persons with one or more accidents was also greater in the patients with apnea than in the control subjects without apnea (31% versus 6%, p less than 0.01). The percentage of persons having one or more accidents in which they were at fault was also greater in the patients with apnea than in the control subjects (24% versus 3%, p less than 0.02). The automobile accident rate of the patients with sleep apnea was 2.6 times the accident rate of all licensed drivers in the state of Virginia (p less than 0.02). In addition, 24% of patients with sleep apnea reported falling asleep at least once per week while driving. We conclude that patients with obstructive sleep apnea have a significantly higher frequency of auto accidents than do subjects without apnea. Impaired drivers with sleep apnea may cause many preventable auto accidents.

Accidents, Traffic