PubMed Health⌕ Search

Biomedical subjects

M Lopata

Publications and source records attributed to M Lopata.

At least 37 records · Page 2Linked to original sources
PubMed1989

Effects of loading and unloading the respiratory system on respiratory control and muscle function.

To determine the effects of internal respiratory loading and unloading on respiratory neuromuscular function, ventilatory (Vi), occlusion pressure (P0.15), transdiaphragmatic pressure (Pdi) and diaphragmatic electromyogram (EMGdi) responses to CO2 rebreathing were assessed in 6 normal volunteers rebreathing gas mixtures denser (63% SF6, 30% O2, 7% CO2) and less dense (63% He, 30% O2, 7% CO2) than air (63% N2, 30% O2, 7% CO2). Loading with SF6 decreased the Vi response to CO2 rebreathing and increased P0.15 and Pdi for a given EMGdi, while the greater the increase in pressure response the less was the decrease in Vi. Unloading with He had the opposite effect. The pattern of breathing was altered with SF6, with Ti and Te increasing and frequency decreasing, while there was no change in timing with He. Internal loading of inspiration and expiration with SF6 elicits compensatory responses that depend on changes of respiratory timing and enhanced diaphragm efficiency. Adjustments to unloading are generally opposite to that observed with loading.

Adult↗
PubMed1987

Effects of continuous positive airway pressure on upper airway and respiratory muscle activity.

To study the effects of continuous positive airway pressure (CPAP) on lung volume, and upper airway and respiratory muscle activity, we quantitated the CPAP-induced changes in diaphragmatic and genioglossal electromyograms, esophageal and transdiaphragmatic pressures (Pes and Pdi), and functional residual capacity (FRC) in six normal awake subjects in the supine position. CPAP resulted in increased FRC, increased peak and rate of rise of diaphragmatic activity (EMGdi and EMGdi/TI), decreased peak genioglossal activity (EMGge), decreased inspiratory time and inspiratory duty cycle (P less than 0.001 for all comparisons). Inspiratory changes in Pes and Pdi, as well as Pes/EMGdi and Pdi/EMGdi also decreased (P less than 0.001 for all comparisons), but mean inspiratory airflow for a given Pes increased (P less than 0.001) on CPAP. The increase in mean inspiratory airflow for a given Pes despite the decrease in upper airway muscle activity suggests that CPAP mechanically splints the upper airway. The changes in EMGge and EMGdi after CPAP application most likely reflect the effects of CPAP and the associated changes in respiratory system mechanics on the afferent input from receptors distributed throughout the intact respiratory system.

Adult↗
PubMed1987

Changes in end-expiratory lung volume during sleep in patients with occlusive apnea.

Eight patients with occlusive sleep apnea were monitored during non-rapid-eye-movement (NREM) sleep to study the factors that contribute to negative inspiratory pressure generation and thus upper airway occlusion. End-expiratory lung volume assessed by respiratory inductive plethysmography [sum of end-expiratory levels (SUM EEL)] increased early and decreased late during the ventilatory phases (P less than 0.0001, one-way analysis of variance). Inspiratory change in esophageal pressure (Pes) and peak inspiratory diaphragmatic and genioglossal electromyograms (EMGdi and EMGge) decreased while the inspiratory pressure generated for a given diaphragmatic activity (Pes/EMGdi) increased during the preapneic phase (P less than 0.0001, for all). Multiple regression analysis with Pes/EMGdi as the dependent variable (R2 = 0.90) indicated that both the changes in SUM EEL and EMGge significantly contributed to the model (P less than 0.008 and 0.004, respectively). These results indicate that end-expiratory lung volume fluctuates during NREM sleep in patients with occlusive apnea and suggest that these changes along with the changes in upper airway muscle activity contribute to the generation of negative inspiratory pressure, leading to the passive collapse of the upper airways.

Adult↗
PubMed1987

Determinants of hypercapnia in occlusive sleep apnea syndrome.

To assess the relative contributions of age, gender, obesity, pulmonary function, and the severity of sleep-induced respiratory abnormalities to the development of alveolar hypoventilation in patients with occlusive sleep apnea syndrome, prospective data from III patients with occlusive sleep apnea were analyzed by stepwise logistic and multiple regression techniques. The significant variables in a logistic regression model predicting the presence of hypercapnia were daytime arterial oxygen pressure (PaO2; p less than 0.0001) and gender (p less than 0.04), the latter reflecting the higher number of hypercapnic women in our patient population. Multiple regression analysis performed in the hypercapnic group to study the determinants of the severity of elevation of arterial carbon dioxide tension (PaCO2) revealed significant contribution from the PaO2, the apnea-plus-hypopnea index (AHI), and the percent predicted forced vital capacity (r2 = 0.56; p less than 0.0001), whereas in the normocapnic patients, PaCO2 related to PaO2 only. These results suggest that daytime hypoxemia, mechanical impairment of the respiratory system due to obesity or obstructive airway disease (or both), and the severity of sleep-induced respiratory abnormalities as assessed by AHI contribute to the severity of carbon dioxide retention in patients with occlusive sleep apnea in a multifactorial fashion.

Carbon Dioxide↗
PubMed1986

Induction of periodic breathing during sleep causes upper airway obstruction in humans.

To test the hypothesis that occlusive apneas result from sleep-induced periodic breathing in association with some degree of upper airway compromise, periodic breathing was induced during non-rapid-eye-movement (NREM) sleep by administering hypoxic gas mixtures with and without applied external inspiratory resistance (9 cmH2O X l-1 X s) in five normal male volunteers. In addition to standard polysomnography for sleep staging and respiratory pattern monitoring, esophageal pressure, tidal volume (VT), and airflow were measured via an esophageal catheter and pneumotachograph, respectively, with the latter attached to a tight-fitting face mask, allowing calculation of total pulmonary system resistance (Rp). During stage I/II NREM sleep minimal period breathing was evident in two of the subjects; however, in four subjects during hypoxia and/or relief from hypoxia, with and without added resistance, pronounced periodic breathing developed with waxing and waning of VT, sometimes with apneic phases. Resistive loading without hypoxia did not cause periodicity. At the nadir of periodic changes in VT, Rp was usually at its highest and there was a significant linear relationship between Rp and 1/VT, indicating the development of obstructive hypopneas. In one subject without added resistance and in the same subject and in another during resistive loading, upper airway obstruction at the nadir of the periodic fluctuations in VT was observed. We conclude that periodic breathing resulting in periodic diminution of upper airway muscle activity is associated with increased upper airway resistance that predisposes upper airways to collapse.

Adult↗
PubMed1986

Respiratory timing during NREM sleep in patients with occlusive sleep apnea.

To study respiratory timing mechanisms in patients with occlusive apnea, inspiratory and expiratory times (TI and TE) were calculated from the diaphragmatic electromyogram obtained in seven patients during non-rapid-eye-movement (NREM) sleep. Peak diaphragmatic activity (EMGdi) had a curvilinear relationship with TI during the ventilatory and occlusive phases such that TI shortened as EMGdi decreased during the ventilatory phase (r = 0.87, P less than 0.05) and it prolonged as EMGdi increased during the occlusive phase (r = 0.89, P less than 0.02). However, EMGdi vs. TI for the occlusive phase was shifted to the right of that for the ventilatory phase, reflecting the relatively longer TI during upper airway occlusion. TI also had a linear relationship with pleural pressure (r = 0.94, P less than 0.001) that remained unchanged during the ventilatory and occlusive phases such that it prolonged as negative inspiratory pressure increased. These results indicate that respiratory timing is continuously modified in patients with occlusive apnea as inspiratory neural drive fluctuates during NREM sleep and suggest that this modification is due to the net effects of changing inspiratory neural drive and afferent input predominantly from upper airway mechanoreceptors.

Diaphragm↗
PubMed1986

Respiratory muscle interaction during NREM sleep in patients with occlusive apnea.

To study respiratory muscle interaction in patients with occlusive apnea, diaphragmatic electromyogram (EMGdi) and gastric, pleural, and transdiaphragmatic pressures (Pga, Ppl, and Pdi, respectively) were studied in seven patients during non-rapid-eye-movement (NREM) sleep. Diaphragmatic force output, as assessed by Pdi, followed the periodic changes in EMGdi but during the occlusive phase the increase in Pdi was more than the increase in EMGdi. This increase in Pdi was essentially due to an increase in Ppl, since Pga and EMGdi had a linear relationship (r = 0.98, P less than 0.001) that did not change during the occlusive and ventilatory phases. Abdominal muscle recruitment evident in Pga and abdominal motion tracings during the occlusive phase when paradoxical rib cage motion was observed suggested that this increase in diaphragmatic efficiency was likely due to a change in diaphragmatic length-tension characteristics. These results demonstrate that, in patients with occlusive apneas, the diaphragm is the predominant respiratory muscle during NREM sleep and that its function is supported by abdominal muscle recruitment.

Abdominal Muscles↗
PubMed1986

Upper airway occlusion during sleep in patients with Cheyne-Stokes respiration.

Sleep-induced periodic breathing has been suggested to lead to the development of occlusive apneas in patients with sleep apnea syndrome. If this were true, patients with Cheyne-Stokes respiration should also develop upper airway occlusion during sleep. To study this hypothesis, 6 nonobese patients with Cheyne-Stokes respiration lacking evidence for sleep apnea syndrome and anatomic upper airway abnormalities underwent polysomnography during daytime naps. A total of 463 apneas were analyzed in the 6 patients studied. In 1 patient, no evidence of upper airway occlusion was observed. In the remaining 5 patients, a varying frequency of upper airway occlusion resembling the pattern of mixed apnea was seen in 3 to 97% of the total apneas analyzed. The mean number (+/- 1 SD) of occluded inspiratory efforts per mixed apnea in these 5 patients was 1.69 +/- 0.59. These results show that patients with Cheyne-Stokes respiration may develop upper airway occlusion during sleep and are consistent with the contention that sleep-induced periodic breathing in patients with sleep apnea syndrome is primary to the development of occlusive apneas.

Carbon Dioxide↗
PubMed1985

Dynamics of respiratory drive and pressure during NREM sleep in patients with occlusive apneas.

To study the dynamics of respiratory drive and pressure in patients with occlusive apneas, diaphragmatic electromyogram (EMGdi), esophageal pressure (Pes), and genioglossal electromyogram (EMGge) were monitored during nocturnal sleep in five patients. Both EMGs were analyzed as peak moving time average, and Pes was quantitated as the peak inspiratory change from base line. During the ventilatory phase both EMGs decreased proportionally. The decrease in Pes was less than the decrease observed in EMGdi, and Pes generated for a given EMGdi increased during the preapneic phase in spite of the proportional decrease in EMGdi and EMGge during this period. We conclude that negative inspiratory pressures which lead to the passive collapse of oropharyngeal walls are dependent on both respiratory and upper airway muscle activity and that occlusive apneas of non-rapid-eye-movement (NREM) sleep do occur in spite of proportional changes observed in the activity of both muscle groups. The preapneic increase in negative inspiratory pressures generated for a given respiratory muscle activity is most likely due to the decrease in upper airway muscle activity that is associated with an increase in oropharyngeal resistance.

Adult↗
PubMed1985

Respiratory load compensation in chronic airway obstruction.

To assess respiratory neuromuscular function and load compensating ability in patients with chronic airway obstruction (CAO), we studied eight stable patients with irreversible airway obstruction during hyperoxic CO2 rebreathing with and without a 17 cmH2O X l-1 X s flow-resistive inspiratory load (IRL). Minute ventilation (VE), transdiaphragmatic pressure (Pdi), and diaphragmatic electromyogram (EMGdi) were monitored. Pdi and EMGdi were obtained via a single gastroesophageal catheter with EMGdi being quantitated as the average rate of rise of inspiratory (moving average) activity. Based on the effects of IRL on the Pdi response to CO2 [delta Pdi/delta arterial CO2 tension (PaCO2)] and the change in Pdi for a given change in EMGdi (delta Pdi/delta EMGdi) during rebreathing, two groups could be clearly identified. Four patients (group A) were able to increase delta Pdi/delta PaCO2 and delta Pdi/delta EMGdi, whereas in the other four (group B) the IRL responses decreased. All group B patients were hyperinflated having significantly greater functional residual capacity (FRC) and residual volume than group A. In addition the IRL induced percent change in delta Pdi/delta PaCO2, and delta VE/delta PaCO2 was negatively correlated with lung volume so that in the hyperinflated group B the higher the FRC the greater was the decrease in Pdi response due to IRL. In both groups the greater the FRC the greater was the decrease in the ventilatory response to loading. Patients with CAO, even with severe airways obstruction, can effect load compensation by increasing diaphragmatic force output, but the presence of increased lung volume with the associated shortened diaphragm prevents such load compensation.

Diaphragm↗
PubMed1985

Effects of position on respiratory muscle function during CO2 rebreathing.

The effects of changing from the sitting to supine position on respiratory muscle function was assessed during CO2 rebreathing. Gastric (Pg), pleural (Ppl) and transdiaphragmatic (Pdi) pressures and thoracoabdominal motion were monitored. Diaphragmatic EMG was measured by a bipolar esophageal electrode and quantitated as a moving time average (EMGdi). From sitting to supine, in only 2 of 7 subjects (group A) the diaphragm gained a mechanical advantage as evident by an increased slope of the Pdi versus EMGdi relationship not present in the other 5 subjects (group B). At high levels of ventilation while sitting, only group B increased expiratory abdominal muscle activity leading to a more favorable diaphragm length and a passive descent of the abdomen-diaphragm on inspiration. In the supine position functional residual capacity progressively increased in all subjects and the above abdominal pattern was not seen. We conclude that during upright CO2 rebreathing the recruitment of the expiratory abdominal muscles assists diaphragmatic function by placing the diaphragm in an advantageous pressure generating configuration.

Abdominal Muscles↗
PubMed1985

Relationship between pulmonary function and sleep-induced respiratory abnormalities.

The relationships between pulmonary function and sleep-induced respiratory events were studied in 34 consecutive male patients with suspected sleep apnea syndrome. In view of the effects of obstructive airway disease on pulmonary volume and airway resistance (Raw), patients were divided into two groups, those with and those without obstructive airway disease. Percent predicted functional residual capacity (FRC) correlated significantly with the apnea-plus-hypopnea index (AHI) in patients with and without obstructive airway disease (r = -0.62 and p less than 0.01; and r = -0.57 and p less than 0.01, respectively) whereas percent predicted total lung capacity had a significant relationship with AHI only in patients with obstructive airway disease (r = -0.80; p less than 0.001). In patients without such disease, a significant correlation between inspiratory airway conductance (Gaw) and AHI (r = -0.47; p less than 0.05) was also present, while percent predicted FRC and Gaw did not correlate with normalized weight. These findings suggest that decreased pulmonary volume and increased Raw contribute to the severity of sleep-induced respiratory abnormalities in patients with sleep apnea syndrome regardless of the degree of obesity.

Adolescent↗
PubMed1985

Cardiorespiratory disease associated with Hallermann-Streiff syndrome: analysis of craniofacial morphology by cephalometric roentgenograms.

This paper analyzes the craniofacial morphology in a patient with typical Hallermann-Streiff syndrome (HSS) who developed symptomatic cardiorespiratory deficiency at the age of 48 years. The patient had obstructive sleep apnea (OSA), hypoxia, hypercarbia, pulmonary hypertension, tricuspid insufficiency, and right ventricular failure. Analysis of cephalometric roentgenograms, done 15 years earlier, revealed severe mandibular hypoplasia with marked underdevelopment of the ramus and body. The gonial angle was abnormally obtuse. The condylar and coronoid processes were reduced in size. The anteroposterior dimension of the upper airway was markedly narrowed. Cephalometric roentgenograms of six other HSS patients from our clinic were compared to those of the reference patient. Considerable variation in the features of the syndrome were noted. None of the other patients showed definitive airway obstruction. Comparison was also made with cephalometric roentgenograms of a patient with Treacher Collins syndrome and of a patient with progeria. The former showed airway obstruction associated with a deformed hypoplastic mandible; the latter had an unobstructed airway despite a small mandible because of associated hypoplasia of the maxilla and tongue. The HSS reference patient improved after oxygen therapy, diuretics, antibiotics, and relief of OSA. Patients with HSS, as well as those with Treacher Collins syndrome, appear to be at risk for the development of cardiopulmonary disease if they have obstructed airways. OSA has been shown to have developed in two patients with HSS. The resultant cardiopulmonary insufficiency of such patients may be preventable if airway obstruction can be relieved relatively early in life.

Adolescent↗
PubMed1983

Respiratory muscle function during CO2 rebreathing with inspiratory flow-resistive loading.

We investigated the respiratory muscle contribution to inspiratory load compensation by measuring diaphragmatic and intercostal electromyograms (EMGdi and EMGic), transdiaphragmatic pressure (Pdi), and thoracoabdominal motion during CO2 rebreathing with and without 15 cmH2O X l-1 X s inspiratory flow resistance (IRL) in normal sitting volunteers. During IRL compared with control, Pdi measured during airflow and during airway occlusion increased for a given change in CO2 partial pressure and EMGdi, and there was a greater decrease in abdominal (AB) end expiratory anteroposterior dimensions with increased expiratory gastric pressure (Pga), this leading to an inspiratory decline in Pga with outward AB movement, indicating a passive component to the descent of the abdomen-diaphragm. The response of EMGic to IRL was similar to that of EMGdi, though rib cage (RC)-Pga plots did infer intercostal muscle contribution. We conclude that during CO2 rebreathing with IRL there is improved diaphragmatic neuromuscular coupling, the prolongation of inspiration promoting a force-velocity advantage, and increased AB action serving to optimize diaphragm length and configuration, as well as to provide its own passive inspiratory action. Intercostal action provides increased assistance also. Therefore, compensation for inspiratory resistive loads results from the combined and integrated effort of all respiratory muscle groups.

Abdominal Muscles↗
PubMed1983

Effects of expiratory positive airway pressure on sleep-induced respiratory abnormalities in patients with hypersomnia-sleep apnea syndrome.

In order to explore the efficacy of expiratory positive airway pressure (EPAP) in the prevention of sleep-induced respiratory abnormalities, we studied 9 patients with typical presentation of hypersomnia-sleep apnea syndrome 1 wk apart, without and with 10 cm water of EPAP. We found that EPAP significantly reduced apnea index (p less than 0.01), maximal and mean duration of apneas (p less than 0.01) and desaturation index (p less than 0.001), and significantly improved mean and minimal oxygen saturation (p less than 0.01) and awake supine arterial oxygen saturation (p less than 0.01) in all 9 patients. We also found that EPAP significantly decreased the relative time spent in Stages 1 and 2 NREM sleep (p less than 0.01) and increased the relative time spent in Stages 3 and 4 NREM sleep (p less than 0.01). These results indicate that EPAP reduces frequency and duration of apneas and the degree of nocturnal oxygen desaturation and improves sleep quality in patients with hypersomnia-sleep apnea syndrome.

Adult↗
PubMed1982

Pathogenesis of apneas in hypersomnia-sleep apnea syndrome.

To define the pathogenesis of apneas, eight patients with hypersomnia-sleep apnea syndrome were studied during nocturnal sleep. Diaphragmatic and genioglossal electromyograms quantitated as moving time average activity showed parallel periodic fluctuations resembling the pattern of Cheyne-Stokes breathing. Hypopneas and occlusive apneas occurred at the nadir of these cyclic changes, and mixed apneas represented an extreme of this periodicity with no inspiratory activity at the nadir of the cycle. Tracings of central apneas were compatible with an extremely prolonged expiratory phase. Electromyogram activity of both muscles showed an inversely linear relationship with oxygen saturation but genioglossal activity at the resolution of upper airway occlusion was increased out of proportion to the increase in diaphragmatic activity and the degree of oxygen desaturation. These results indicated that occlusive and mixed apneas result from an instability of ventilatory control during sleep, which seems to be an exaggeration of periodic breathing observed at sleep onset.

Adult↗
PubMed1982

Mass loading, sleep apnea, and the pathogenesis of obesity hypoventilation.

To define the roles of mechanical loading, respiratory neuromuscular control, and sleep apnea in the pathogenesis of obesity hypoventilation, respiratory muscle drive and output, assessed by diaphragmatic electromyogram (EMGdi) and mouth occlusion pressure (P 0.15), respectively, were determined during CO2 chemostimulation in nonobese volunteers who were subjected to abdominal mass loading, and in three groups of markedly obese patients: eucapnic obese without sleep apnea (O), eucapnic obese with sleep apnea (OSA), and hypercapnic obese with sleep apnea (OH). The P0.15 responses were decreased in OSA and OH, but the EMGdi responses were not significantly different from those in control subjects. In O patients EMGdi responses were significantly greater than those in control subjects as well as those in OSA and OH patients. EMGdi and P0.15 responses increased in all nonobese subjects when they were subjected to mass loading. We conclude that both OSA and OH patients were equally unable to develop the expected increase in respiratory muscle drive and output. The presence of sleep apnea, possibly by causing nocturnal hypoxemia and/or sleep fragmentation, may result in impaired mass load compensation and predispose obese patients to develop hypercapnia.

Abdomen↗