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Biomedical subjects

P Sliwinski

Publications and source records attributed to P Sliwinski.

At least 19 recordsLinked to original sources
PubMed2001

Diaphragm activation during exercise in chronic obstructive pulmonary disease.

Although it has been postulated that central inhibition of respiratory drive may prevent development of diaphragm fatigue in patients with chronic obstructive pulmonary disease (COPD) during exercise, this premise has not been validated. We evaluated diaphragm electrical activation (EAdi) relative to maximum in 10 patients with moderately severe COPD at rest and during incremental exhaustive bicycle exercise. Flow was measured with a pneumotachograph and volume by integration of flow. EAdi and transdiaphragmatic pressures (Pdi) were measured using an esophageal catheter. End-expiratory lung volume (EELV) was assessed by inspiratory capacity (IC) maneuvers, and maximal voluntary EAdi was obtained during these maneuvers. Minute ventilation (V E) was 12.2 +/- 1.9 L/min (mean +/- SD) at rest, and increased progressively (p < 0.001) to 31.0 +/- 7.8 L/min at end-exercise. EELV increased during exercise (p < 0.001) causing end-inspiratory lung volume to attain 97 +/- 3% of TLC at end-exercise. Pdi at rest was 9.4 +/- 3.2 cm H(2)O and increased during the first two thirds of exercise (p < 0.001) to plateau at about 13 cm H(2)O. EAdi was 24 +/- 6% of voluntary maximal at rest and increased progressively during exercise (p < 0.001) to reach 81 +/- 7% at end-exercise. In conclusion, dynamic hyperinflation during exhaustive exercise in patients with COPD reduces diaphragm pressure-generating capacity, promoting high levels of diaphragm activation.

Diaphragm↗
PubMed2000

Respiratory parameters during professional flute playing.

We studied three professional flautists while playing to determine: (1) what respiratory muscles and percent vital capacity (%VC) were used; (2) how mouth pressure (Pm), embouchure resistance (Rem), embouchure aperture (Aem), flow (V) and velocity (Vel) affect sound loudness (I) and frequency (F). We measured Pm, esophageal, gastric, transdiaphragmatic, transpulmonary (PL) pressures, diaphragmatic EMG, sound and chest wall displacements directly. Lung volume (VL) was estimated from PL during playing and the static deflation PL-VL curve measured separately; V from Delta VL/Delta t; Rem from Pm/(Delta VL/Delta t). Staccati and sustained notes at different F and I were performed. I increased mainly with V and F with Vel. V and Vel are independently controlled by Pm and Aem. The variation of mean Pm was small (6-11 cm H(2)O) and large for VC (72-83%) suggesting braking inspiratory muscle activity while playing. However, rib cage (RC) and abdominal (Ab) motion were different for each subject. One displaced Ab>RC at high VL and RC>Ab at low VL, another the opposite pattern; the third was in between. We conclude that while different flautists use different strategies to control Pm, the results are similar. Independent control of V and Vel by Pm and Aem allow flautists to control I and F regardless of how Pm is generated.

Adult↗
PubMed2000

Expiratory muscle pressure and breathing mechanics in chronic obstructive pulmonary disease.

Expiratory muscle recruitment is common in stable chronic obstructive pulmonary disease (COPD) patients. Due to airway obstruction, there is little reason to believe that active expiration in COPD would be mechanically effective in lowering operating lung volume. The physiological significance of expiratory muscle recruitment in COPD, therefore, remains unknown. The purpose of this study was to assess, in COPD patients breathing at rest, the effect of expiratory muscle contraction on force generating ability of the diaphragm. The force generating ability of the diaphragm was evaluated from its pressure swing (Pdi) for a given diaphragm electrical activity (Edi), where Edi was normalized as % of its maximal value (Pdi/Edi/Edi,max). Phasic expiratory muscle contraction was measured as the total expiratory rise in gastric pressure (Pga,exp.rise). Nineteen seated patients with moderate to severe COPD, participated in the study and 10 exhibited phasic rise in Pga during expiration with a mean Pga,exp.rise of 1.91+/-0.89 cmH2O. The patients were thus divided into passive expiration (PE) and active expiration (AE) groups. There was no significant difference in various lung function and breathing pattern parameters between the two groups. Pdi/Edi/Edi,max was 0.63+/-0.07 and 0.54+/-0.07 cmH2O/% in PE and AE groups, respectively, and was not significantly different between each other. Compared with PE group, AE group not only recruited expiratory muscles, but also preferentially recruited inspiratory rib cage muscles and derecruited the diaphragm. The results do not support a significant improvement of the force-generating ability of the diaphragm by phasic contraction of expiratory muscles at rest in chronic obstructive pulmonary disease patients.

Aged↗
PubMed2000

Incidence of nocturnal desaturation while breathing oxygen in COPD patients undergoing long-term oxygen therapy.

STUDY OBJECTIVE: It is suggested that oxygen flow be increased by 1 L/min during sleep in COPD patients undergoing long-term oxygen therapy (LTOT) in order to avoid nocturnal desaturations. The purpose of this study was to investigate the occurrence of nocturnal desaturations while breathing oxygen in COPD patients receiving LTOT. SETTING: Inpatient/university hospital. PATIENTS: We studied 82 consecutive COPD patients. Their functional characteristics were as follows (mean +/- SD): FVC, 2.15 +/- 0.69 L; FEV(1), 0.87 +/- 0.33 L; PaO(2), 51.6 +/- 5 mm Hg; and PaCO(2), 47 +/- 8 mm Hg. MEASUREMENTS: Overnight pulse oximetry (PO) was performed twice: (1) while breathing air and (2) while breathing supplemental oxygen assuring satisfactory diurnal resting oxygenation (mean PaO(2) during oxygen breathing, 67 +/- 6 mm Hg; mean arterial oxygen saturation [SaO(2)] during oxygen breathing, 93%). RESULTS: PO performed while patients were breathing air showed a mean overnight SaO(2) of 82.7 +/- 6.7%. Patients spent 90% of the recording time with an SaO(2) of < 90%. While breathing oxygen, 43 patients (52.4%) remained well oxygenated. Their mean overnight SaO(2) while breathing oxygen was 94.4 +/- 2.1%, and time spent with saturation < 90% was 6.9 +/- 8.6%. Thirty-nine patients (47.6%) spent > 30% of the night with an SaO(2) of < 90% while breathing supplemental oxygen. Their mean overnight SaO(2) while breathing oxygen was 87.1 +/- 4.5%, and time spent with an SaO(2) of < 90% was 66.1 +/- 24.7% of the recording time. Comparison of ventilatory variables and daytime blood gases between both groups revealed statistically significantly higher PaCO(2) on air (p < 0.001) and on oxygen (p < 0. 05), and lower PaO(2) on oxygen (p < 0.05) in the group of patients demonstrating significant nocturnal desaturation. CONCLUSIONS: We conclude that about half of COPD patients undergoing LTOT need increased oxygen flow during sleep. Patients with both hypercapnia (PaCO(2) > or = 45 mm Hg) and PaO(2) < 65 mm Hg while breathing oxygen are most likely to desaturate during sleep.

Circadian Rhythm↗
PubMed1999

Modified Campbell diagram to assess respiratory muscle action in speech.

Ten normal and four moderate to severe stutterers participated in the study. Pleural (Ppl) and abdominal (Pab) pressure was studied using oesophageal and gastric balloon catheter systems and VL (VL) was studied using magnetometry. The classical Campbell diagram was modified by plotting Pab versus VL. In a preliminary study we determined whether a surrogate curve could be substituted for the true curve in the Campbell diagram. We obtained true relaxation curves in six subjects. We obtained surrogate chest wall relaxation curves by joining the Pab value at functional residual capacity (FRC) to a point on the dynamic expiratory Pab, VL curve where Pab had decreased to half its maximum inspiratory excursion. In order to obtain the mirror image of the elastic recoil curve of the lung subjects breathed slowly from FRC to total lung capacity. Dynamic Pab, VL and Ppl, VL measurements during quiet breathing and speech were superimposed on static lung and chest wall curves. The simultaneous plot of Ppl and Pab provided a continuous measure of transdiaphragmatic pressure as a function of VL. We inferred non-diaphragmatic muscle recruitment vis-à-vis the diaphragm by the relationship of Pab to Ppl and Pab to the relaxation curve. We compared dynamic Ppl during phonation with that during breath-holding with the glottis open at the same VL, as an estimate of subglottic pressure (Psg). Analysis of variance testing showed that the true, surrogate and predicted relaxation slopes were not significantly different. The strategies that stutterers used to speak were either higher or lower VL than normal subjects and they had a different pattern of respiratory muscle recruitment. Stutterers were unable to achieve the appropriate degree of recruitment to develop and maintain a normal Psg for conversational speech and this contributed to dysfluency. We conclude that the quiet breathing loops can provide a reasonable approximation to the relaxation curve in normal healthy subjects and that modifications to the Campbell diagram provide useful means of measuring Psg and assessing respiratory muscle recruitment patterns.

Adolescent↗
PubMed1998

Partitioning of the elastic work of inspiration in patients with COPD during exercise.

During exercise, dynamic hyperinflation-induced intrinsic positive end-expiratory pressure (PEEPi) and decreased dynamic lung compliance (CL,dyn) of patients with chronic obstructive pulmonary disease (COPD) increase the elastic work of inspiration (Wi) more than would be predicted from the increase in tidal volume (VT). This contributes significantly to their exertional breathlessness. In 10 stable patients with COPD, the dynamic Wi was measured during incremental bicycle exercise to exhaustion. The total Wi was then partitioned into the portion required to overcome PEEPi (Wi,PEEPi) and nonPEEPi elastic load (Wi,nonPEEPi). The latter is used to overcome the increase in the total respiratory system elastance during inflation. From resting breathing to peak exercise, Wi more than doubled (p<0.001). This increase was largely due to Wi,PEEPi, which significantly rose from 1.7+/-0.3 to 5.3+/-0.8 L x cm H2O(-1) (p<0.001). In comparison, Wi,nonPEEPi increased from only 3.0+/-0.4 to 5.1+/-0.5 L x cm H2O(-1) (p<0.01). Consequently, Wi,PEEPi as a fraction of total Wi increased from 35.5+/-5.6 to 51.0+/-3.3% (p<0.02). In addition, the measured Wi,nonPEEPi at peak exercise, when expressed as a percentage of its value during resting breathing, was 25% more than that predicted from the increase in VT alone. Assuming a constant chest wall compliance, this can be attributed to the exercise-induced decrease in CL,dyn, which was 0.27+/-0.04 and 0.17+/-0.02 L x cm H2O(-1) (p<0.01), respectively, during resting breathing and peak exercise. In conclusion, the dynamic hyperinflation-induced intrinsic positive end-expiratory pressure is more important than the increase in tidal volume in raising the work of inspiration during exercise in patients with chronic obstructive pulmonary disease; the decrease in dynamic lung compliance plays a definite but less important role.

Adult↗
PubMed1997

Respiratory effort sensation during exercise with induced expiratory-flow limitation in healthy humans.

Nine healthy subjects (age 31 +/- 4 yr) exercised with and without expiratory-flow limitation (maximal flow approximately 1 l/s). We monitored flow, end-tidal PCO2, esophageal (Pes) and gastric pressures, changes in end-expiratory lung volume, and perception (sensation) of difficulty in breathing. Subjects cycled at increasing intensity (+25 W/30 s) until symptom limitation. During the flow-limited run, exercise performance was limited in all subjects by maximum sensation. Sensation was equally determined by inspiratory and expiratory pressure changes. In both runs, 90% of the variance in sensation could be explained by the Pes swings (difference between peak inspiratory and peak expiratory Pes). End-tidal PCO2 did not explain any variance in sensation in the control run and added only 3% to the explained variance in the flow-limited run. We conclude that in healthy subjects, during normal as well as expiratory flow-limited exercise, the pleural pressure generation of the expiratory muscles is equally related to the perception of difficulty in breathing as that of the inspiratory muscles.

Adult↗
PubMed1997

Human respiratory muscle actions and control during exercise.

We measured pressures and power of diaphragm, rib cage, and abdominal muscles during quiet breathing (QB) and exercise at 0, 30, 50, and 70% maximum workload (Wmax) in five men. By three-dimensional tracking of 86 chest wall markers, we calculated the volumes of lung- and diaphragm-apposed rib cage compartments (Vrc,p and Vrc,a, respectively) and the abdomen (Vab). End-inspiratory lung volume increased with percentage of Wmax as a result of an increase in Vrc,p and Vrc,a. End-expiratory lung volume decreased as a result of a decrease in Vab. DeltaVrc,a/DeltaVab was constant and independent of Wmax. Thus we used DeltaVab/time as an index of diaphragm velocity of shortening. From QB to 70% Wmax, diaphragmatic pressure (Pdi) increased approximately 2-fold, diaphragm velocity of shortening 6.5-fold, and diaphragm workload 13-fold. Abdominal muscle pressure was approximately 0 during QB but was equal to and 180 degrees out of phase with rib cage muscle pressure at all percent Wmax. Rib cage muscle pressure and abdominal muscle pressure were greater than Pdi, but the ratios of these pressures were constant. There was a gradual inspiratory relaxation of abdominal muscles, causing abdominal pressure to fall, which minimized Pdi and decreased the expiratory action of the abdominal muscles on Vrc,a gradually, minimizing rib cage distortions. We conclude that from QB to 0% Wmax there is a switch in respiratory muscle control, with immediate recruitment of rib cage and abdominal muscles. Thereafter, a simple mechanism that increases drive equally to all three muscle groups, with drive to abdominal and rib cage muscles 180 degrees out of phase, allows the diaphragm to contract quasi-isotonically and act as a flow generator, while rib cage and abdominal muscles develop the pressures to displace the rib cage and abdomen, respectively. This acts to equalize the pressures acting on both rib cage compartments, minimizing rib cage distortion.

Abdominal Muscles↗
PubMed1997

Reliability of inspiratory capacity for estimating end-expiratory lung volume changes during exercise in patients with chronic obstructive pulmonary disease.

The inspiratory capacity (IC) maneuver is increasingly used to monitor exercise-induced dynamic hyperinflation in patients with COPD. However, the reliability of this method in patients with COPD exercising to symptom limitation has not been systematically studied and presented. The purpose of the present study was therefore to evaluate the reliability of the IC maneuver in assessing changes in end-expiratory lung volume (EELV) by assessing the pressure developed during IC maneuvers, in patients with COPD during incremental bicycle exercise to exhaustion. Fifteen patients with stable COPD performed bicycle exercise to symptom limitation. During the experiment, the patients performed IC efforts during resting breathing and at the end of each exercise work load. Esophageal pressure (Pes) measured at peak inspired volume plateau (zero flow) was -13.5 +/- 1.9 and -13.4 +/- 1.9 cm H2O (p = 0.79) during IC maneuvers at resting breathing and during the final exercise work load, respectively. When the Pes values at the peak inspired volume plateau during IC efforts at each exercise level were expressed as a percentage of those during resting breathing, the great majority of the ratios were above 90% with the lowest at 84%, and these ratios were independent of exercise intensity. Despite a constant Pes during IC, there was a progressive decrease in IC with increasing exercise work load in most patients, suggesting an increase in EELV. At the highest exercise work load achieved, delta EELV calculated as the decrease in IC was 0.26 +/- 0.06 L (p < 0.001). We conclude that repeated IC maneuver is a simple and reliable method for estimating EELV changes during exercise to exhaustion in patients with COPD.

Exercise↗
PubMed1997

Inspiratory muscle mechanics of patients with chronic obstructive pulmonary disease during incremental exercise.

Inspiratory muscles are weak and contribute to exercise limitation in chronic obstructive pulmonary disease (COPD). Differential inspiratory pressure contributions from the diaphragm and inspiratory rib cage muscles (RCMs) during exercise in patients with COPD patients are insufficiently described. We measured, in 16 patients with COPD, the global inspiratory muscle pressure (delta Pmus) and transdiaphragmatic pressure (delta Pdi) during an incremental bicycle exercise to exhaustion. The pressures needed to overcome the elastic load were further partitioned into portions for overcoming the PEEPi-imposed inspiratory threshold load (before the beginning of inspiratory flow) and for inflating the respiratory system (between the beginning and end of inspiratory flow). The delta Pdi/delta Pmus ratio was used to quantify the pressure contribution from RCMs relative to that from the diaphragm for a given inspiratory effort. We observed that in patients with COPD during exercise (1) there is a progressive increase in total inspiratory pressure contribution from RCMs relative to that of the diaphragm, and the magnitude of this increase appears to depend on the RCMs reserves during resting breathing; (2) most of the diaphragmatic pressure contribution occurs before the beginning of inspiratory flow, to overcome the PEEPi-imposed inspiratory threshold load; (3) RCMs pressure contribution predominates during the period of inspiratory flow once PEEPi is neutralized, not only for overcoming the elastic load caused by increased tidal volume, but also for compensating for the diaphragmatic pressure contribution during this interval that was gradually lost with increasing exercise work load.

Exercise Test↗
PubMed1997

Inspiratory muscle dysfunction as a cause of death in COPD patients.

Although fatigue of the inspiratory muscles has been well documented, its prevalence in patients with chronic obstructive pulmonary disease (COPD) and its influence on mortality are unknown, because of the lack of a simple, clinically available diagnostic test. The hypothesis and experimental evidence relating inspiratory muscle dysfunction to the development of hypercapnia and hypercapnic ventilatory failure are reviewed. Since a poor prognosis in COPD is associated with carbon dioxide retention, inspiratory muscle weakness and/or fatigue may have an association with survival in these patients.

Cause of Death↗
PubMed1996

Association of chest wall motion and tidal volume responses during CO2 rebreathing.

The purpose of this study is to investigate the effect of chest wall configuration at end expiration on tidal volume (VT) response during CO2 rebreathing. In a group of 11 healthy male subjects, the changes in end-expiratory and end-inspiratory volume of the rib cage (delta Vrc,E and delta Vrc,I, respectively) and abdomen (delta Vab,E and delta Vab,I, respectively) measured by linearized magnetometers were expressed as a function of end-tidal PCO2 (PETCO2. The changes in end-expiratory and end-inspiratory volumes of the chest wall (delta Vcw,E and delta Vcw,I, respectively) were calculated as the sum of the respective rib cage and abdominal volumes. The magnetometer coils were placed at the level of the nipples and 1-2 cm above the umbilicus and calibrated during quiet breathing against the VT measured from a pneumotachograph. The delta Vrc,E/delta PETCO2 slope was quite variable among subjects. It was significantly positive (P < 0.05) in five subjects, significantly negative in four subjects (P < 0.05), and not different from zero in the remaining two subjects. The delta Vab,E/delta PETCO2 slope was significantly negative in all subjects (P < 0.05) with a much smaller intersubject variation, probably suggesting a relatively more uniform recruitment of abdominal expiratory muscles and a variable recruitment of rib cage muscles during CO2 rebreathing in different subjects. As a group, the mean delta Vrc,E/delta PETCO2, delta Vab,E/delta PETCO2, and delta Vcw,E/delta PETCO2, slopes were 0.010 +/- 0.034, -0.030 +/- 0.007, and -0.020 +/- 0.032 1/Torr, respectively; only the delta Vab,E/delta PETCO2, slope was significantly different from zero. More interestingly, the individual delta VT/delta PETCO2 slope was negatively associated with the delta Vcr,E/delta PETCO2 (r = 0.68, P = 0.021) and delta Vcw,E/delta PETCO2 slopes (r = 0.63, P = 0.037) but was not associated with the delta Vab,E/delta PETCO2 slope (r = 0.40, P = 0.223). There was no correlation of the delta Vrc,E/delta PETCO2 and delta Vcw,E/delta PETCO2 slopes with age, body size, forced expiratory volume in 1 s, or expiratory time. The group delta Vab,I/delta PETCO2 slope (0.004 +/- 0.014 1/Torr) was not significantly different from zero despite the VT nearly being tripled at the end of CO2 rebreathing. In conclusion, the individual VT response to CO2, although independent of delta Vab,E, is a function of delta Vrc,E to the extent that as the delta Vrc,E/delta PETCO2 slope increases (more positive) among subjects, the VT response to CO2 decreases. These results may be explained on the basis of the respiratory muscle actions and interactions on the rib cage.

Abdominal Muscles↗
PubMed1996

Effect of topical upper airway anesthesia on apnea duration through the night in obstructive sleep apnea.

It has previously been reported that the duration of obstructive apneas increases from the beginning to the end of the night (M. Charbonneau, J. M. Marin, A. Olha, R. J. Kimoff, R. D. Levy, and M. Cosio. Chest 106: 1695-1701, 1994). The purpose of this study was to test the hypothesis that stimulation of upper airway (UA) sensory receptors during obstructed inspiratory efforts contributes to arousal and apnea termination and that a progressive attenuation of this mechanism through the night contributes to apnea lengthening. We studied seven patients (six men, one woman) with severe obstructive sleep apnea (apnea-hypopnea index = 93 +/- 26 events/h) during two consecutive nights of polysomnographic monitoring. On one night (random order), we performed topical UA anesthesia with 0.2% tetracaine and on the control night, sham anesthesia. We measured apnea duration, esophageal pressure (Pes) during apneas, and apneic O2 desaturation. Consistent with previous findings, apnea duration, number of efforts per apnea, and peak Pes at end apnea increased from the beginning to the end of the control nights. UA anesthesia produced a significant increase in apnea duration at the beginning of the night but no change in apnea length at the end of the night. Peak Pes and the rate of increase in Pes during the anesthesia nights were greater than during control nights, but the rate of increase in Pes was similar for the beginning and end of the control and anesthesia nights. These findings suggest that UA sensory receptors play a role in mediating apnea termination at the beginning of the night but that the contribution of these receptors diminishes as the night progresses such that greater inspiratory efforts are required to trigger arousal, leading to apnea prolongation.

Adult↗
PubMed1996

Comparison of static and dynamic intrinsic positive end-expiratory pressure using the Campbell diagram.

Intrinsic positive end-expiratory pressure (PEEPi) due to dynamic hyperinflation has been measured as a plateau airway opening pressure during airway occlusion (PEEPi,stat). PEEPi has also been dynamically determined as a fall in esophageal pressure (Pes) before the inspiratory flow starts (PEEPi,dyn). The aims of the current study were to systematically compare PEEPi,stat and PEEPi,dyn and to explain the underlying mechanisms of their difference. The study was performed in healthy subjects with dynamic hyperinflation induced by expiration through a Starling resistor. The Campbell diagram was constructed for each subject by determining the static pressure-volume curves of the lung (Pst,[l]) and chest wall (Pst,[w]). For a given end-expiratory volume, PEEPi,stat was measured on the Campbell diagram as the pressure difference between Pst(w) and -Pst(l). PEEPi,dyn was measured as mentioned above. The effects of respiratory muscle recruitment on PEEPi,dyn were estimated by the Pes values when Pes started to fall relative to Pst(w). We found that: (1) there was a great variability of the PEEPi,dyn/PEEPi,stat ratio among and within subjects; (2) expiratory muscle recruitment was evident on most occasions; (3) persistent inspiratory muscle activity during expiration was present in some subjects; (4) the Pes values at the start of inspiratory flow were frequently on the left of -Pst(l), which contributed to the difference between PEEPi,stat and PEEPi,dyn and implied a greater dynamic than static elastance presumably due to viscoelastic properties; (5) chest wall distortions characterized by inflation of the abdomen with deflation of the rib cage during the initial inspiratory efforts were observed in three subjects. In conclusion, interpretation of PEEPi,dyn needs to be cautious because both expiratory and tonic inspiratory muscle activities that lead to significant over- or underestimation of PEEPi by PEEPi,dyn, respectively, are associated with acute dynamic hyperinflation. In addition, the effects of viscoelastic properties and chest wall distortions on PEEPi,dyn need to be further investigated.

Adult↗
PubMed1995

Effects of fatigue, fiber length, and aminophylline on human diaphragm contractility.

The clinical relevance of methylxanthines as therapeutic agents for improving diaphragmatic contractility is controversial. In a double-blind, placebo-controlled trial, we investigated the effect of aminophylline on the contractility of fresh and fatigued human diaphragm at different lung volumes, and therefore as a function of fiber length. The diaphragmatic contractility of normal subjects was assessed by measurements of transdiaphragmatic pressure changes (Pdi,T) in response to single, bilateral, supramaximal phrenic-nerve shocks during relaxation from total lung capacity (TLC) to functional residual capacity (FRC). Fatigue was induced by resistive breathing. Therapeutic levels of theophylline were reached in all subjects. Under fresh (i.e., nonfatigue) conditions, aminophylline significantly increased Pdi,T at lung volumes above 75% of the inspiratory capacity (IC). Fatigue in the absence of aminophylline caused a disproportionately greater reduction of Pdi,T at high than at low lung volume (J. Appl. Physiol. 1992; 72:1064), which was rapidly reversible with rest. With aminophylline, the disproportionate decrease in diaphragmatic contractility at short fiber lengths was not observed. Aminophylline potentiates diaphragmatic contractility to a proportionately greater extent at short than at long fiber lengths, under both fresh and fatigued conditions. We explain these findings by known effects of muscle shortening, fatigue, and methylxanthines on excitation-contraction coupling mechanisms.

Adult↗
PubMed1995

Control of breathing in obstructive sleep apnoea and in patients with the overlap syndrome.

In some patients obstructive sleep apnoea (OSA) may co-exist with chronic obstructive pulmonary disease (COPD) and respiratory failure; the so-called "overlap syndrome". Obstructive, hypercapnic patients have both blunted ventilatory and mouth occlusion pressure responses during CO2 stimulation. The purpose of this study was to compare the pattern of breathing and CO2 response between OSA patients and those with the overlap syndrome. Twenty obese men with OSA and normal lung function (Group A), 11 obese men with overlap syndrome (Group B) and 13 healthy nonobese subjects (Group C) were examined. Lung function tests, breathing pattern, mouth occlusion pressure (P0.2) at rest, and respiratory responses during CO2 rebreathing were investigated. Diagnosis of OSA was established by standard polysomnography. There were no statistical differences between Groups A and B in apnoea & hypopnoea index (62 vs 54), mean arterial oxygen saturation (SaO2) during sleep (85 vs 84%) and in body mass index (BMI) 34.3 vs 36.3 kg.m-2. Minute ventilation, mean inspiratory flow and P0.2 at rest were increased in both groups of patients in comparison to controls. During CO2 rebreathing, group A had normal ventilatory and P0.2 responses, similar to controls, (2.7 +/- 1.1 vs 2.1 +/- 0.4 l.min-1.mmHg-1 and 0.7 +/- 0.3 vs 0.71 +/- 0.25 cmH2O.mmHg-1, respectively). However, Group B had significantly decreased ventilatory and P0.2 responses to CO2 (0.71 +/- 0.23 l.min-1.mmHg-1 and 0.34 +/- 0.17 cmH2O.mmHg-1, respectively). This comparison showed that patients with OSA had normal CO2 response when awake, whereas those with overlap syndrome had diminished CO2 response when awake.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effect of global inspiratory muscle fatigue on ventilatory and respiratory muscle responses to CO2.

We evaluated the effect of global inspiratory muscle fatigue on ventilation and respiratory muscle control during CO2 rebreathing in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. CO2 response curves were measured before and after fatigue. During CO2 rebreathing, global fatigue caused a decreased tidal volume (VT) and an increased breathing frequency but did not change minute ventilation, duty cycle, or mean inspiratory flow. Both esophageal and transdiaphragmatic pressure swings were significantly reduced after global fatigue, suggesting decreased contribution of both rib cage muscles and diaphragm to breathing. End-expiratory transpulmonary pressure for a given CO2 was lower after fatigue, indicating an additional decrease in end-expiratory lung volume due to expiratory muscle recruitment, which leads to a greater initial portion of inspiration being passive. This, combined with the reduction in VT, decreased the fraction of VT attributable to inspiratory muscle contribution; therefore the inspiratory muscle elastic work and power per breath were significantly reduced. We conclude that respiratory control mechanisms are plastic and that the respiratory centers alter their output in a manner appropriate to the contractile state of the respiratory muscles to conserve the ventilatory response to CO2.

Adult↗