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Biomedical subjects

J Milic-Emili

Publications and source records attributed to J Milic-Emili.

At least 199 records · Page 11Linked to original sources
PubMed1982

Reassessment of body plethysmographic technique for the measurement of thoracic gas volume in asthmatics.

We measured thoracic gas volume (Vtg) by the body plethysmographic technique in 4 normal subjects and in 9 asthmatics during remission and after bronchoconstriction induced with inhaled aerosolized histamine. Changes in both mouth (Pm) and esophageal pressure (Pes) were used to approximate changes in alveolar pressure (Palv), and both Vtg(m) and Vtg)(es) were computed. Because small changes in lung recoil occur during panting, delta Pes exceeds delta Pm, leading to a value of Vtg(m) that is slightly greater than Vtg(es). Indeed, in the normal subjects, Vtg(m) was significantly greater than Vtg(es), and the observed percentage error (E) between them (2.8%) corresponded with the expected value. In the asthmatics, during marked bronchoconstriction, there was an increased tendency for Vtg(m) to exceed Vtg(es), E averaging 12.2% and being greater than the predicted error. In some asthmatics, changes in volume led changes in Pm; the phase angle between volume and Pm averaged 6.3 degrees and was significantly greater than that between volume and Pes (1.7 degrees). In 3 asthmatics, increases in TLC(m) were not accompanied by similar changes in TLC(es). Our data are consistent with the hypothesis that when a compliant upper airway is coupled with a high airway resistance during panting against an occluded airway, transmission of changes in alveolar pressure to the mouth is incomplete. The resulting underestimation of delta Palv by delta Pm leads to artifactual increases in TLC.

Adult↗
PubMed1982

A simple method for assessing the validity of the esophageal balloon technique.

The validity of the conventional esophageal balloon technique as a measure of pleural pressure was tested in 10 subjects in sitting, supine, and lateral positions by occluding the airways at end-expiration and measuring the ratio of changes in esophageal (delta Pes) and mouth pressure (delta Pm) during the ensuing spontaneous occluded inspiratory efforts. Similar measurements were also made during static Mueller maneuvers. In both tests, delta Pes/delta Pm values were close to unity in sitting and lateral positions, whereas in the supine position, substantial deviations from unity were found in some instances. However, by repositioning the balloon to different levels in the esophagus, even in these instances a locus could be found where the delta Pes/delta Pm ratio was close to unity. No appreciable phase difference between delta Pes and delta Pm was found. We conclude that by positioning the balloon according to the "occlusion test" procedure, valid measurements of pleural pressure can be obtained in all the tested body positions.

Adult↗
PubMed1982

Comparison of esophageal, tracheal, and mouth occlusion pressure in patients with chronic obstructive pulmonary disease during acute respiratory failure.

In 14 acutely ill patients with chronic obstructive pulmonary disease who were either intubated or breathed via a tracheostomy, we measured the pressures generated in the esophagus and trachea during the first 0.1 s of spontaneous inspiratory efforts against closed airway (P0.1). No significant difference was found between P0.1 in the trachea and esophagus, where it was measured at 2 balloon levels (distance from balloon tip to nares: 35 and 45 cm). In 4 of the patients we also compared esophageal and mouth occlusion pressures during mouth breathing, the orifice of tracheostomy being temporarily obstructed. Mouth P0.1 in the 4 patients averaged approximately 47% of the esophageal occlusion pressure (4.4 +/- 1.7 versus 8.9 +/- 3.1 cm H2O, respectively). Because in patients with COPD with upper airways bypassed (tracheostomized or intubated) the changes in esophageal and tracheal pressure during occluded respiratory efforts were similar, it is concluded that the difference between esophageal and mouth occlusion pressure is due to the tissue compliance of the oropharynx.

Aged↗
PubMed1982

Hypoxemia, hypercapnia, and breathing pattern in patients with chronic obstructive pulmonary disease.

The results of lung function tests (total and functional residual capacities, residual volume/total lung capacity ratio, forced expiratory volume in one second) breathing patterns and arterial PO2 and PCO2 were studied in 651 ambulatory male patients with chronic obstructive pulmonary disease, functionally and clinically stable. Function tests were only loosely correlated with gas tensions: abnormalities in mechanics and in gas exchange are not necessarily related. In patients matched for the degree of obstruction, the breathing pattern depended upon both PaO2 and PaCO2. Isolated hypoxemia was accompanied by increased respiratory frequency without any variation in tidal volume: this suggests that the chemoreceptive systems still responded to changes in PaO2. Isolated hypercapnia was accompanied by a decrease in tidal volume and an increase in respiratory frequency. Consequently, the dead space/tidal volume ratio increased, leading to a drop in alveolar ventilation and to CO2 retention.

Adult↗
PubMed1981

Configuration of the chest wall and occlusion pressures in awake humans.

During CO2 rebreathing in sitting position seven of nine conscious men showed a progressive fall in expiratory reserve volume, most of it due to a decrease in abdominal volume. Diaphragm length at end expiration was thus increased, and some elastic recoil pressure became available to drive inspiration. In four out of six subjects, when CO2 tension was greater than 55 Torr, there was a dip in abdominal pressure at the beginning of inspiration, and the change in transdiaphragmatic pressure during the first 100 ms of an occluded inspiration was smaller than the simultaneous change in mouth pressure (P0.1). In the subjects who showed the smallest diaphragmatic pressure in this 100 ms, electromyogram recordings showed that abdominal activity ceased before the onset of inspiration, and diaphragm activity did not appear until later than 100 ms into inspiration. We conclude that, in four our of our six subjects in the sitting posture, P0.1 can be generated in whole or in part by release of chest wall elastic recoil or in intercostal muscle contraction. In the supine posture, there was no change by end-expiratory chest wall configuration, and onset of diaphragm contraction coincided with beginning of inspiration in the two subjects in whom diaphragm electromyogram was recorded.

Abdomen↗
PubMed1981

Phrenic activity, respiratory pressures, and volume changes in cats.

In eight anesthetized cats we measured the integrated ("moving time average") phrenic activity [using phrenic electroneurogram (EPHR)] and the active transdiaphragmatic pressure [Pdi(mus)] during room air breathing, hypoxia, and hypercapnia. The relationship between Pdi(mus) and EPHR was unaffected by either hypoxic or hypercapnic stimulation of breathing, suggesting that in spontaneously breathing cats the pressure losses are negligible. In all cats, however, there was a substantial volume-related decrease in Pdi(mus), indicating that with increasing lung volume the effectiveness of the diaphragm as a pressure generator decreases. In addition, we have developed a model that allows prediction of the time course changes in lung volume for different morphology of inspiratory driving pressure. This model explains many of the features of control of breathing found experimentally in our cats.

Animals↗
PubMed1981

Time course of phrenic activity and respiratory pressures during airway occlusion in cats.

The morphology of integrated ("moving time average") phrenic electroneurograms (EPHR) and of tracheal (Ptr) and transdiaphragmatic (Pdi) pressure waves during occluded inspirations was studied in eight anesthetized cats breathing air and various hypercapnic and hypoxic mixtures. The shape of the rising part of EPR-, Ptr-, and Pdi-time profiles varied between animals (from convex to concave), but in each animal it remained virtually unchanged by hypoxia and hypercapnia. The shape of the Ptr and Pdi occlusion waves reflected the shape of EPHR. The relationship of EPHR to Pdi and Ptr did not change with chemical drive. It is concluded that central inspiratory activity (CIA) (as reflected by EPHR and its mechanical transforms Pdi and Ptr) increases in amplitude with stimulation of breathing but that the profile of CIA remains essentially unchanged. However, substantial differences in the time course development of phrenic activity, Pdi, and Ptr exist between cats. The fixed interrelationships among EPHR, Pdi, and Ptr indicate a proportional increase in activity among all inspiratory muscles with increased chemical drive.

Airway Obstruction↗
PubMed1981

Ventilatory responses to muscular vibrations in healthy humans.

In healthy humans, we studied the effect of high-frequency mechanical vibrations applied unilaterally to the tendon of the biceps or triceps brachialis on ventilation and the breathing pattern. This stimulus preferentially activates the muscle spindle afferents. Increase of respiratory frequency and changes in the ventilatory timing started at the first or second inspiration during tendon stimulation, and no adaptation occurred as long as the vibrations continued. The tidal volume and mean inspiratory flow rate were only enhanced in individuals having high-frequency breathing during eupnea. The changes in ventilatory variables were observed when the motor response to vibrations was tested under isometric or isotonic conditions. Various experimental procedures enabled us to induce a tonic reflex contraction in either the vibrated muscle or the antagonist of no reflex contraction in either group of muscles. In all cases the increase in minute ventilation was identical. These changes in breathing pattern was not associated with a significant decrease in alveolar CO2 pressure and did not seem to be responsible for important variations in respiratory gas exchanges. The response to high-frequency vibrations was also studied after ventilation was increased with added dead space. The magnitude of hyperventilation an the pattern of ventilatory response produced by tendon stimulation did not change with increased ventilation. In conclusion, the stimulation of muscle spindles in human induces changes in ventilation and pattern of breathing , and the occurrence of a reflex muscular contraction does not seem necessary in order to obtain such effects.

Adult↗
PubMed1981

Previous volume history of the lung and regional distribution of residual volume.

By use of 133Xe, the regional distribution of residual volume (RV) was measured in six seated healthy men, following a fast vital capacity (VC) expiration a) without and b) with a breath hold at residual volume of approximately 30 s and c) following a slow (greater than 30 s) VC expiration from total lung capacity (TLC) without a breath hold at RV. After the breath hold at RV, regional RV/TLC in the lower lung zones decreased significantly compared wih results obtained with fast expiratory VC and no breath hold at RV. At lung top the opposite was true. The distribution of regional RV/TLC was the same following the slow VC expiration with no breath hold at RV as with the fast expiration with the breath hold at RV. The different regional distribution of RV in b and c relative to a was probably due mainly to collateral ventilation, i.e., during the breath hold at RV and the slow expiration some of the gas that was trapped in the dependent lung zones behind closed airways escaped into the upper regions of the lung where the small airways had remained patent, leading to increased expansion of upper alveoli.

Adult↗
PubMed1981

Ventilation, respiratory center output, and contribution of the rib cage and abdominal components to ventilation during CO2 rebreathing in children with cystic fibrosis.

Although there has been extensive research into the control of breathing in adults with chronic obstructive lung diseases, there is little information in this area in children with cystic fibrosis (CF). The purpose of this study was to investigate the respiratory response of children with CF to CO2 under hyperoxic conditions. Using a standard CO2 rebreathing technique, we studied 14 children with CF. We evaluated their response to CO2 in terms of ventilation (VE), mean inspiratory flow rate (VT/TI), and the pressure generated at the mouth after 0.1 s of an inspiratory effort against an occlusion (P0.1). In order to understand the contributions of the rib cage and abdominal components to ventilation, we assessed the volume change in each compartment by attaching magnetometers to the chest and abdomen. Overall changes in lung volume were assessed in a volume displacement plethysmograph. We found that, when corrected for the height of the child, the slope of VE versus end tidal CO2 (PETCO2), as well as the slope of VT/TI versus PETCO2 correlated significantly with the degree of airway obstruction as expressed by the forced expiratory flow between 25 and 75% of vital capacity. The values for P0.1 were all within the normal range and showed no correlation with the degree of airway obstruction. The contribution of the rib cage and abdomen to ventilation during rebreathing was similar to that previously reported for adults. No changes were observed in functional residual capacity during rebreathing. We showed that tests involving a mechanical response to CO2 correlated with the degree of airway obstruction, but there was no evidence that the neuromuscular drive was abnormal.

Adolescent↗
PubMed1980

Respiratory changes induced by the large glucose loads of total parenteral nutrition.

Total parenteral nutrition (TPN) using glucose as nonprotein calories was associated with increases in O2 consumption (VO2) and CO2 production (VCO2). The magnitude of the changes was a function of the patient's clinical state and glucose load. Depleted patients showed a minimal increase in VO2, while VCO2 increased 23%. Minute ventilation (VE) increased 32%. Hypermetabolic patients (major trauma, sepsis) had a 30% increase in VO2 and a 57% increase in VCO2, while VE increased 71%. Patients with mild to moderate injuries (energy expenditure +/- 15% of normal) showed a 21% increase in VO2 and a 53% increase in VCO2, while VE increased 121%. Large carbohydrate intakes were associated with increases in CO2 production in all patients, while increases in O2 consumption were seen primarily in hypermetabolic patients. These changes suggest that the high glucose loads of TPN may be a physiologic stress.

Adult↗
PubMed1980

Pattern of breathing and mouth occlusion pressure during acclimatization to high altitude.

Pattern of breathing and mouth occlusion pressure have been investigated during a 6-day sojourn at an altitude of 3457 m in six resting subjects breathing ambient air or an hyperoxic mixture. It has been shown that ventilation increases and alveolar PCO2 decreases, both variables reaching a steady-state after about 4 days at altitude. Changes in ventilation are caused by modifications, at first, in the timing component of the respiratory cycle and later on, in the mean inspiratory airflow. This suggests that the output of the respiratory center is qualitatively modified during the acclimatization period. Mouth occlusion pressure, an index of neuromuscular inspiratory drive, increased on the first day at altitude, remaining constant thereafter. The mean inspiratory flow did not change on the first day, but progressively increased in the subsequent 3 days. The observation that flow increased in the face of a constant neuromuscular inspiratory drive suggests that during acclimatization to altitudes, the progressive increase in ventilation is due to changes in mechanics of the ventilatory pump rather than changes in central neural drive.

Acclimatization↗
PubMed1980

Caffeine effect on breathing pattern and vagal reflexes in newborn rabbits.

Ventilation, breathing pattern and vagal reflexes were studied in anaesthetized (pentobarbital) newborn rabbits aged 2-7 days before and after injection of 10 mg/kg of caffeine. With caffeine, tidal volume decreased and respiratory frequency increased but minute ventilation remained unchanged. Mean inspiratory flow increased only in the older rabbits. The breath-to-breath variability in tidal volume, mean inspiratory flow, inspiratory and expiratory times observed under control conditions was diminished in several animals following caffeine injection. Vagal pulmonary afferentation was not affected by caffeine. A facilitatory effect of caffeine on the central mechanisms controlling the breathing pattern was indicated by: (1) an enhanced Hering-Breuer expiratory-promoting reflex; (2) lack of effect on the Hering-Breuer deflation reflex; and (3) qualitatively similar effects of caffeine postvagotomy as prevagotomy.

Animals↗
PubMed1980

Effects of respiratory apparatus on breathing pattern.

The effects of ventilatory apparatus on breathing pattern and gas exchange were studied in normal supine subjects. Using a canopy system, measurements of O2 consumption, CO2 production, tidal volume (VT), frequency (f), minute ventilation, mean inspiratory flow, and inspiratory, and expiratory time (TI and TE) were made and compared to data obtained with the use of a mask (m) and mouthpiece plus noseclip (mp + nc). Use of the m or mp + nc caused a 32.5 and 15.5% increase in VT, respectively, whereas f, TI, and TE remained unchanged. As TI did not change the increase in VT was caused entirely by increased inspiratory flow.

Adult↗
PubMed1980

Central respiratory drive in acute respiratory failure of patients with chronic obstructive pulmonary disease.

Control of breathing was studied in patients with chronic obstructive pulmonary disease, both in the chronic state and during acute respiratory failure. The results were compared to those in a group of age-matched normal subjects. In patients breathing air, minute ventilation was not different during acute and chronic states, and was similar to that in normal subjects. The pattern of breathing, however, was different: acutely ill patients took shorter and smaller breaths, with a breathing frequency higher than that of normal subjects. The pattern of the chronic group was intermediate between that of acutely ill patients and that of normal subjects. Mouth occlusion pressure, an index of neuromuscular respiratory drive, was 5 times greater in acutely ill patients than in normal subjects. Administration of O2 at a flow of 5 L/min caused a small (14%), bus significant, decrease in minute ventilation due to decreased respiratory frequency. The tidal volume did not change, so the decrease in minute ventilation was the result of decreased inspiratory flow. This was associated with a decreased mouth occlusion pressure that was still 3 times greater than that of normal subjects. The increase in arterial PCO2, observed after administration of O2 was not correlated with the decrease in ventilation, indicating that other factors must be responsible for the increase in arterial PCO2. We concluded that (1) despite the poor mechanical advantage of the respiratory muscles in acute respiratory failure, the increased drive to breathe results in high mouth occlusion pressure and inspiratory flow, and (2) the increase in arterial PCO2, observed during administration of O2 is not related solely to changes in respiratory drive.

Aged↗
PubMed1980

Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure.

The effects of the administration of 100% oxygen on minute ventilation (VE) and arterial blood gases were studied in patients with chronic obstructive pulmonary disease during acute respiratory failure. The administration of O2 resulted in an early decrease in VE, which averaged 18% +/- 2 SE of the control VE, and was due to a decrease in both tidal volume (VT) and respiratory frequency (f). This was followed by a slow increase in VE, such that after 15 min of breathing O2, VE rose to 93 +/- 6% of the control room air value, with both VT and f similar to control values. Despite the small difference between VE while breathing room air and that at the fifteenth minute of O2 inhalation, PaCO2 increased by 23 +/- 5 mmHg, and no significant correlation was found between the changes in VE and PaCO2. By the fifteenth minute of O2 inhalation the PaO2 averaged 225 +/- 23 mmHg, and it was concluded that despite the removal of the hypoxic stimulus of O2 inhalation, the activity of the respiratory muscles remained great enough to maintain VE at nearly the same degree as that while breathing room air. Consequently, the changes in PaCO2 after the administration of O2 were mainly due to increased inhomogeneity of VA/Q distribution within the lungs.

Aged↗