Search PubMed⌕ Search

Biomedical subjects

J W Shepard

Publications and source records attributed to J W Shepard.

At least 37 records · Page 2Linked to original sources
PubMed1990

Cardiopulmonary consequences of obstructive sleep apnea.

During sleep, oxygen consumption and systemic blood pressure decrease in normal subjects; during rapid eye movement sleep, irregular ventilation can be accompanied by brief periods of apnea. In patients with obstructive sleep apnea, alveolar ventilation during an apneic episode is immediately reduced to zero, and the metabolic demands for oxygen must be met from oxygen stores within the body. As the stores of oxygen within the lung are diminished, the rate of arterial oxyhemoglobin desaturation increases. The development of alveolar hypoventilation during wakefulness seems to be based on a balance between central ventilatory drives to breathe and mechanical loads placed on the respiratory system. Coexistent cardiopulmonary or neuromuscular disease in patients with obstructive sleep apnea contributes to the development of alveolar hypoventilation. During apneic episodes, the systemic blood pressure increases while the heart rate and cardiac output decrease. Both bradycardias and increased ventricular ectopic activity have been associated with these disordered breathing episodes. Because of the possibility of apnea-associated arrhythmias, patients with obstructive sleep apnea may be at increased risk for cardiovascular mortality. The influence of these recurrent nocturnal episodes of asphyxia on cardiovascular longevity needs further investigation.

Arrhythmias, Cardiac↗
PubMed1990

Uvulopalatopharyngoplasty for treatment of obstructive sleep apnea.

Currently, uvulopalatopharyngoplasty (UPPP) is the most common surgical procedure used for the treatment of obstructive sleep apnea. Patients with clinically significant obstructive sleep apnea in whom medical treatment has failed or who are unwilling to comply with medical therapy are considered candidates for UPPP. The initial surgical results obtained in nonselected patients with obstructive sleep apnea were highly variable, approximately half of the patients experiencing more than a 50% reduction in the frequency of disordered breathing events postoperatively. Although differences in surgical technique likely account for some of the variability, preoperative differences in the site (or sites) of upper airway collapse are also thought to influence the surgical results. Because UPPP involves resection of the uvula, distal margin of the soft palate, palatine tonsils, and any excessive lateral pharyngeal tissue, patients with anatomic narrowing and collapse confined to the velopharyngeal or retropalatal region of the upper airway are considered optimal surgical candidates. Fiberoptic pharyngoscopy, cephalometric roentgenography, computed tomography, and somnofluoroscopy are procedures that can be used preoperatively to help select optimal candidates for UPPP. The results suggest that the success rate of UPPP can approach 66% with careful preoperative selection of patients.

Evaluation Studies as Topic↗
PubMed1990

Localization of upper airway collapse during sleep in patients with obstructive sleep apnea.

The present study was conducted to determine the effects of body position and sleep state, as well as the effect of uvulopalatopharyngoplasty (UPPP) on the regions over which the upper airway (UA) collapses during sleep. To accomplish this goal, 18 male patients with obstructive sleep apnea (OSA) underwent overnight polysomnography with simultaneous monitoring of pressures in the posterior nasopharynx, oropharynx, hypopharynx, and esophagus. From the profile of pressures recorded in the UA and esophagus, the regions over which the UA collapses during apneas could be determined. The patients were 54 +/- 14 y of age and were grossly obese with a body mass index of 37 +/- 2 kg/m2. They had moderately severe OSA with a mean apnea plus hypopnea index of 62 +/- 8 per hour. During NREM sleep, 10 of the 18 (56%) patients had collapse confined to the velopharyngeal or retropalatal segment of the upper airway. The remaining 44% of the patients demonstrated collapse of the retroglossal segment of the oropharynx located caudal to the inferior margin of the soft palate. Upper airway collapse at the level of the hyoid bone was not observed during NREM sleep. Observations made during REM sleep in nine patients demonstrated that collapse occurred in a more caudal segment of the UA in seven patients during REM than during NREM sleep. The effect of sleep position was evaluated in 10 patients and found to have little affect on the extent over which the UA collapsed during sleep independent of sleep state. The effects of UPPP on regional UA collapse were evaluated in a small group of six patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Nasal and oral flow-volume loops in normal subjects and patients with obstructive sleep apnea.

Because flow-volume loops (FVLs) are clinically useful in evaluating upper airway (UA) obstruction and the fact that patency of the nasopharyngeal ventilatory pathway is important to the prevention of obstructive sleep apnea (OSA), the present study examined the role of nasal compared with oral FVLs in evaluating patients with OSA. Fourteen obese male patients 56 +/- 3 yr of age with a mean apnea plus hypopnea index (AHI) of 51 +/- 9/h were studied along with 14 nonobese, healthy, age- and sex-matched control subjects whose mean AHI was 6 +/- 1/h. Nasal and oral FVLs obtained in the normal subjects indicated the nose behaved like a variable resistor, with flow limitation during inspiration but not during expiration. In the patient group, flow limitation was observed during expiration as well as inspiration indicating nondistensibility of the nasopharyngeal ventilatory pathway in the patients compared to the control subjects. A change in body position from upright to supine in the OSA group was associated with small reductions in expiratory but not inspiratory flow rates. The area under the nasal supine flow-volume loop (FVLANaSup) was found to be highly correlated with awake resting PaO2 (r = 0.80) and PaCO2 (r = -0.83) in the patient group. In addition, multiple linear regression analysis revealed that PaO2 and the area under the nasal FVLs independently contributed to the prediction of AHI with a multiple R of 0.89. These results suggest that limitations to ventilation via the nasopharynx may significantly influence both gas exchange and the frequency of sleep-disordered breathing in patients with OSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1990

Cardiovascular effects of sleep disorders.

Normal sleep provides a period of physiologically reduced workload for the cardiovascular system for almost one third of the human life span. Snoring, the most common disorder of sleep, heralds the presence of an unstable upper airway and alerts perceptive clinicians to the possibility of OSA. Epidemiologic evidence has implicated snoring as an independent risk factor for the development of hypertension, ischemic heart disease, and cerebral infarction. However, many investigators would attribute these adverse cardiovascular effects to the substantial prevalence of OSA in habitual snorers. The detrimental effects of OSA on hemodynamics and cardiac rhythm have been well documented, and recent data have linked OSA with increased cardiovascular mortality. Worsening hypoxemia during sleep likely contributes to the nocturnal mortality observed in patients with severe COPD. Effective treatment to prevent nocturnal hypoxemia is available for OSA and COPD, with current evidence supporting beneficial effects on survival.

Cardiovascular Diseases↗
PubMed1990

Upper airway distensibility and collapsibility in patients with obstructive sleep apnea.

The present study was performed to evaluate the distensibility and collapsibility characteristics of regional segments of the UA in patients with OSA and in normal subjects in response to changes in airway pressure. Seventeen male patients with moderately severe OSA and 13 normal subjects underwent CT of the UA in the supine position while awake. Axial views were obtained from the level of the hard palate to the hypopharynx under conditions of -5, 0, and +10 cm H2O of CAP. The results indicated that the Amin occurred within 20 mm of the hard palate in the retropalatal region of the UA in 16 (94 percent) of the 17 patients and in 12 (92 percent) of the 13 normal subjects. Continuous negative airway pressure of -5 cm H2O failed to significantly decrease either Amin or Amean in either the patients or normal subjects, suggesting good UA load compensation during wakefulness. Continuous positive airway pressure of 10 cm H2O significantly increased Amin and Amean to a similar extent in both groups. The Amin was significantly smaller by 40 percent, 33 percent, and 37 percent in the patients with OSA, compared to the normal subjects, at -5, 0, and +10 cm H2O of CAP, respectively. In contrast, Amean did not differ between the groups. The CT scan criterion of Amin less than or greater than 1.0 cm2 during tidal ventilation of atmospheric pressure correctly categorized patients with OSA and normal subjects with an accuracy of 70 percent. While the behavior of the UA in response to nasal CPAP and CNAP failed to increase the accuracy of CT scan criteria to a level sufficient for clinical use in the diagnosis of OSA, the results clearly indicate that structural changes in the UA contribute to the development of OSA.

Airway Resistance↗
PubMed1990

Primary pulmonary artery sarcoma. A method of resection.

Primary pulmonary artery sarcoma classically presents with symptoms and findings suggestive of acute pulmonary artery occlusion. An angiocentric mass or the finding of spindling neoplasm on needle biopsy should suggest this neoplasm. The rare unilateral location in the present case permitted resection by pneumonectomy. An endarterectomy technique was used to extract loosely adherent tumor-thrombus from the more proximal portions of the left pulmonary artery.

Female↗
PubMed1990

Fast-CT evaluation of the upper airway during wakefulness in patients with obstructive sleep apnea.

Fast-CT scanning was used to study the dynamic changes in the upper airway (UA) during quiet tidal ventilation (VT) in 25 patients with obstructive sleep apnea (OSA). Ten fast-CT scans were sequentially obtained over one respiratory cycle from the level of the hard palate to the hypopharynx with the patients awake in the supine position. The patients were 44 +/- 2 years old, weighed 104 +/- 5 kg, and had moderately severe OSA with an apnea plus hypopnea index (AHI) of 59 +/- 7 per hour. Maximum and minimum UA cross-sectional areas (Amax -Amin) were determined for each UA level and percent reductions in UA size or collapsibility index (CI) were computed as (Amax -Amin)*100/Amax. The lower velo-pharynx was the narrowest (Amin = 80 +/- 12 mm2) and most collapsible segment of the UA (Cl = 55 +/- 5%). Amin was less than 25, 50, or 75 mm2 in 64%, 76%, and 88% of the patients, respectively. Significant narrowing was confined to the proximal segment (levels 1 to 4) in the majority, with the remaining patients having narrowing in both the proximal and distal segments. None of the patients had major narrowing confined to the distal segment alone. Mean UA cross-sectional area (Amean) was generally largest at end-inspiration and smallest at end-expiration. In conclusion, fast-CT has documented substantial changes in UA cross-sectional area during quiet VT in awake supine patients with OSA. The velopharyngeal (retropalatal) segment was the narrowest and most collapsible region. Maximal narrowing was greatest at end-expiration, consistent with relaxation of UA dilator muscle activity.

Adult↗
PubMed1989

Evaluation of the upper airway by computerized tomography in patients undergoing uvulopalatopharyngoplasty for obstructive sleep apnea.

This study utilized computerized tomography (CT) to evaluate the effects of uvulopalatopharyngoplasty (UPPP) on upper airway (UA) dimensions. The objectives were to determine whether CT scan results would be useful in identifying UA characteristics predictive of a good surgical result as well as elucidating reasons for failure of this operative procedure. Twenty-three male patients with obstructive sleep apnea (OSA) had CT scans and polysomnography performed before and after UPPP. Preoperatively, the apnea plus hypopnea index (AHI) was 64 +/- 6 per hour and the minimal UA cross-sectional area (Amin) was located at 10 and 20 mm below the level of the hard palate in 87% (20 of 23) of the patients. Uvulopalatopharyngoplasty more than doubled UA cross-sectional areas at these two proximal levels. In contrast, the hypopharyngeal segment located 50 to 70 mm below the hard palate decreased in cross-sectional area by 23 to 25% after surgery. Eight patients (35%) had a good response to UPPP based on a greater than 50% decrease in AHI. Preoperatively, seven of these eight patients had Amin located 20 mm below the hard palate. Uvulopalatopharyngoplasty increased Amin and oropharyngeal cross-sectional areas to a greater extent in the good than in the poor responders. A poor response to UPPP was associated with preoperative Amin greater than 1 cm2, location at site other than 20 mm below the hard palate, and postoperative narrowing at the level of the hard palate. Patients with Amin less than 1.0 cm2 located 20 mm below the hard palate (lower velopharynx) were most likely to obtain a favorable result with surgery.

Carbon Dioxide↗
PubMed1987

Effects of hydralazine on mouth occlusion pressure and ventilatory response to hypercapnia in patients with chronic obstructive pulmonary disease and pulmonary hypertension.

Hydralazine has been shown to increase minute ventilation (VE) in patients with chronic obstructive pulmonary disease and pulmonary hypertension. The mechanism by which hydralazine produces this effect has not been defined. We investigated the effects of orally administered hydralazine on hypercapnic ventilatory response (delta VE/delta PaCO2) and central respiratory drive (delta P0.1/delta PaCO2) as well as the effects on hemodynamics, ventilation, and gas exchange in 10 male patients (mean age, 59 +/- 2 yr). The patients had a severe degree of chronic air-flow obstruction (FEV1, 1.07 +/- 0.08 L) and mild pulmonary hypertension (mean pulmonary artery pressure, 25 +/- 4 mm Hg). After hydralazine, the slope of delta VE/delta PaCO2 increased by 177% (p less than 0.005), and the slope of delta P0.1/delta PaCO2 increased by 145% (p less than 0.05). Resting ventilation increased from 14.8 +/- 1.0 to 17.1 +/- 1.4 L/min (p less than 0.02), primarily as a result of increased respiratory frequency. After hydralazine, PaO2 increased from 66 +/- 4 to 70 +/- 3 mm Hg (p less than 0.05) at rest and from 54 +/- 3 to 59 +/- 3 mm Hg (p less than 0.02) during exercise. PaCO2 decreased from 46 +/- 3 to 42 +/- 3 mm Hg (p less than 0.001) at rest and from 50 +/- 3 to 45 +/- 3 mm Hg (p less than 0.001) during exercise. No change was seen in the dead space to tidal volume ratio or the degree of venous admixture. Mean pulmonary artery pressure and total pulmonary resistance both at rest and during exercise were unchanged after hydralazine.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

Cardiopulmonary disorders during sleep: diagnosis and management.

Sleep-related breathing disorders may contribute to the nocturnal peak in human mortality. Nocturnal hypoxia has been associated with serious ventricular tachyarrhythmias as well as life-threatening bradyarrhythmias. Obesity and snoring, both of which increase with age, have been identified as risk factors for sleep-related breathing disorders, as have hypertension and heart disease.

Aged↗
PubMed1986

Pulmonary hypertension in chronic obstructive pulmonary disease. Multivariate analysis.

The severity of pulmonary hypertension was evaluated by right cardiac catheterization in 89 patients with stable chronic obstructive pulmonary disease, both at rest and during maximum treadmill exercise. Thirty-one patients were found to have pulmonary hypertension at rest, defined as a mean pulmonary arterial pressure of 20 mm Hg or more. Although the remaining 58 patients had normal mean pulmonary arterial pressure at rest, three developed pulmonary hypertension during exercise (mean pulmonary arterial pressure greater than or equal to 35 mm Hg). Multiple anthropometric, spirometric, radiographic, and gas-exchange variables were analyzed and correlated with the hemodynamic data to define their value in predicting mean pulmonary arterial pressure. While arterial oxygen pressure (PaO2) at maximum exercise was the variable most highly correlated with resting mean pulmonary arterial pressure (r = -0.67), stepwise multiple linear regression analysis indicated that measurement of the diameter of the right descending pulmonary artery and arterial carbon dioxide tension (PaCO2) also contributed to the prediction of mean pulmonary arterial pressure. Spirometric indices of airflow obstruction, hyperinflation, and the diffusing capacity of the lung for carbon monoxide correlated poorly with the severity of pulmonary hypertension and consequently were not useful predictors of mean pulmonary arterial pressure. The threshold criteria of a PaO2 less than 60 mm Hg or a PaCO2 more than 40 mm Hg were reasonably accurate for a diagnosis of pulmonary hypertension. These arterial blood gas criteria were superior to the spirometric and radiographic variables examined in predicting pulmonary hypertension prior to the development of clinically overt cor pulmonale.

Aged↗
PubMed1985

Relationship of ventricular ectopy to nocturnal oxygen desaturation in patients with chronic obstructive pulmonary disease.

Sudden death and oxyhemoglobin desaturation are known to occur during sleep in patients with chronic obstructive pulmonary disease. The present study was undertaken to determine the frequency with which nocturnal oxygen desaturation promotes an increase in ventricular ectopic activity, since such a relationship could represent a potential pathophysiologic mechanism for sudden death during sleep. Forty-two clinically stable subjects with moderately severe obstructive airways disease, mean ratio of one-second forced expiratory volume to forced vital capacity = 51 +/- 12 percent, underwent overnight polygraphic sleep study. Oxyhemoglobin saturation was monitored by ear oximetry, and electrocardiographic leads CC5 and CM5 were employed for arrhythmia detection. Premature ventricular complexes were detected in 27 (64 percent) of the subjects and were complex (multifocal, repetitive, or both) in 17. No significant relationship between premature ventricular complex frequency and arterial oxygen saturation was detected for the group as a whole. In part, this result can be attributed to the relatively mild hypoxemic stress experienced by the 22 subjects in whom arterial oxygen saturation remained greater than 80 percent. In contrast, six (30 percent) of the 20 patients who had desaturation to less than 80 percent showed a greater than 150 percent increase in premature ventricular complex frequency with oxygen desaturation. These results suggest that nocturnal hypoxemia, if of sufficient magnitude, is capable of increasing ventricular ectopy during sleep in a substantial number of patients with chronic obstructive pulmonary disease.

Adult↗
PubMed1985

Gas exchange and hemodynamics during sleep.

Sleep in normal individuals is associated with mild alveolar hypoventilation, which results in 2 to 8 mm Hg increases in PaCO2 and 3 to 11 mm Hg reductions in PaO2, which decreases mean arterial oxyhemoglobin saturation by less than 2 per cent. Arterial blood pressure and heart rate consistently decrease during sleep, and cardiac output either decreases or remains unchanged. Greater variability in these hemodynamic variables occurs during REM than during NREM sleep. Cyclical fluctuations in ventilation, blood pressure, and heart rate have been observed in normal subjects, and fewer than five apneas per hour sleep is considered to be normal. In patients with obstructive sleep apnea, reductions in SaO2 that occur with apneas and hypopneas are highly variable within and between individuals. Multiple variables interact to determine the severity of the episodes of oxyhemoglobin desaturation that are associated with cyclical changes in heart rate and systemic blood pressure. The magnitude of the increase in systemic pressure is related to the severity of the oxyhemoglobin desaturation, with mean elevations in systolic and diastolic pressures being on the order of 25 per cent. However, the magnitude of the systemic pressor response to oxygen desaturation varies widely between individuals. Pulmonary artery pressure often increases with sequential apneas to substantially elevated values, and this increase in combination with the large negative intrathoracic pressures generated during obstructive apneas increases ventricular afterload. Alterations in stroke volume and cardiac output in response to the dynamic events that occur with apneas have not been adequately investigated. Reductions in heart rate that occur during apneas are related to the severity of the oxyhemoglobin desaturation and the arterial chemoreceptor-mediated increase in vagal efferent activity. Marked sinus bradycardia, sinus pauses of 2 to 13 seconds' duration, second-degree heart block, and ventricular tachyarrhythmias have all been associated with severe arterial hypoxemia. Sudden death during sleep in obstructive sleep apnea presumably results from a lethal cardiac arrhythmia, but the relative contributions of severe bradyarrhythmias and ventricular tachyarrhythmias are unknown.

Adult↗
PubMed1985

Relationship of ventricular ectopy to oxyhemoglobin desaturation in patients with obstructive sleep apnea.

Patients with obstructive sleep apnea are considered to be at increased risk of sudden, presumably arrhythmia-related death during sleep. The present study was undertaken to determine the relationship between ventricular ectopy and the severity of oxyhemoglobin desaturation in these patients. Thirty-one male patients with obstructive sleep apnea (mean age, 55 +/- 11 years) underwent overnight polysomnography. Arterial oxyhemoglobin saturation (SaO2) was monitored by ear oximetry, and premature ventricular complexes (PVC) were detected using electrocardiographic leads CC5 and CM5. The data were recorded on electromagnetic tape for subsequent computer-assisted analysis to obtain PVC frequency as a function of decile levels of SaO2. Total sleep time averaged 333 +/- 75 minutes, the apnea index was 44 +/- 26 per hour, and the hypopnea index was 18 +/- 24 per hour. Premature ventricular complexes were observed in 23 (74 percent) of the subjects. By analysis of variance, no significant relationship was found between PVC frequency and decile levels of SaO2 for saturations greater than 60 percent; however, in the 16 subjects with SaO2 below 60 percent, a significant increase in PVC frequency was detected with decreasing SaO2 (p less than 0.01). Ventricular bigeminy was observed with SaO2 below 60 percent in three of these 16 subjects. From these results, we conclude that patients with obstructive sleep apnea are at relatively low risk of developing ventricular arrhythmias provided SaO2 remains greater than 60 percent, while those with SaO2 below 60 percent are at increased risk and should be managed accordingly.

Adult↗
PubMed1984

Effects of hydralazine on hemodynamics, ventilation, and gas exchange in patients with chronic obstructive pulmonary disease and pulmonary hypertension.

Reports on hemodynamic effects of hydralazine on pulmonary hypertension (primary or secondary) usually include cases with severe disease or with mixed varieties of pulmonary vascular disease. Serious side effects and death have been reported. Effects of this drug on ventilation and gas exchange are unknown. We investigated the short-term effects of hydralazine treatment on hemodynamics, ventilation, and gas exchange in a relatively homogeneous group of patients with severe chronic obstructive pulmonary disease and moderate exertional pulmonary hypertension (mean pulmonary artery pressure, 43 +/- 3 mmHg). Hydralazine produced significant improvement in cardiac index, total pulmonary resistance, and oxygen transport. We also observed significant improvement in alveolar ventilation (mean PaCO2, decreased from 47 +/- 2 to 40 +/- 3 mmHg at rest and from 51 +/- 3 to 43 +/- 3 mmHg during exercise). The severe exertional hypoxemia of the group (mean PaO2, 48 +/- 2 mmHg) improved significantly (mean PaO2, 57 +/- 3 mmHg). Four of 11 patients showed increased exercise tolerance after hydralazine. This change is probably related to a combined improvement in hemodynamics plus a newly observed improvement in gas exchange and ventilation. Three of 14 patients could not tolerate hydralazine because of marked tachycardia. Serious side effects were not observed in the remaining group.

Drug Tolerance↗
PubMed1984

Myocardial stress. Exercise versus sleep in patients with COPD.

Epidemiologic investigation has revealed that patients with pulmonary disease are at increased risk of dying during the early morning hours. To provide a pathophysiologic explanation for these excessive nocturnal mortality statistics, we tested the hypothesis that episodes of arterial O2 desaturation during sleep can produce as severe a stress on the maintenance of myocardial O2 balance as maximal exercise in patients with chronic obstructive pulmonary disease (COPD). Thirty-one subjects with COPD underwent both overnight sleep and treadmill exercise study to their dyspnea-limited maximum. During both activities, systemic blood pressure was directly recorded and myocardial oxygen consumption (MVO2) estimated from the pulse rate (HR) - systolic blood pressure (SBP) product. Arterial O2 content (CaO2) was calculated from hemoglobin concentration and arterial O2 saturation (SaO2) measured by ear oximetry. Using these data and the Fick principle, myocardial blood flow (MBF) was continuously estimated during both exercise and sleep. During sleep, mean SaO2 was 88 +/- 7 percent while the average of the lowest SaO2 recorded for each subject was 71 +/- 14 percent. Episodes of nocturnal oxyhemoglobin desaturation produced consistent elevations in SBP frequently accompanied by an increase in HR. Because this hemodynamic response resulted in increased MVO2 at precisely the times when arterial O2 contents were low, high demands for MBF were generated. The average of the highest individual values for MBF during sleep was 244 +/- 144 (ml/100 g LV/min). This value was not significantly different from the value of MBF = 281 +/- 91 (ml/100 g LV/min) determined for maximal exercise. This finding suggests that the demand for coronary blood flow during episodes of nocturnal hypoxemia can be transiently as great as during maximal exercise in patients with COPD.

Adult↗