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Chemical control of breathing in obstructive sleep apnoea (OSA) patients has been studied by many authors. The results of previous studies, especially those dealing with hypoxic drive, are discordant. Respiratory responses were studied during hypercapnic and hypoxic stimulation in a group of 37 normocapnic patients with OSA during wakefulness. The diagnosis of OSA was established by standard polysomnography. These patients had increased apnoea/hypopnoea index (AHI; 51 +/- 22 (mean +/- SD)), obesity (body mass index (BMI) 32.4 +/- 5.6 kg.m-2) and normal lung function tests. The control group consisted of 14 healthy obese subjects (BMI 31.2 +/- 3.3 kg.m-2). Respiratory responses (ventilatory and mouth occlusion pressure (P0.1)) during hypercapnic and hypoxic rebreathing tests were measured with the use of computerized equipment. Respiratory responses during hypercapnic stimulation were similar to those in the control group (change in (delta) minute ventilation (V'E)/delta carbon dioxide tension (PCO2) 23.5 +/- 14.8 versus 22.3 +/- 10.0 L.min-1.kPa-1, delta P0.1/delta PCO2 4.6 +/- 3.6 versus 4.2 +/- 2.6 cmH2O.kPa-1). During isocapnic hypoxic stimulation in OSA patients the mean ventilatory response was higher than in the control group (delta V'E/delta arterial oxygen saturation (Sa,O2) 2.6 +/- 1.7 versus 1.7 +/- 0.7 L.min-1.%-1) but this difference was not statistically significant. Nevertheless, it was found that 13 (35%) OSA patients had increased ventilatory responses. The mean P0.1 response in OSA patients was higher but did not differ significantly from those in the control group (delta P0.1/delta Sa,O2) 0.43 +/- 0.38 versus 0.35 +/- 0.12 cmH2O.%-1). The results demonstrated that respiratory responses to chemical stimulation in awake normocapnic patients with obstructive sleep apnoea were in the normal range, similar to those in control obese subjects. During hypoxic stimulation some of them had increased ventilatory (35%) and mouth occlusion pressure (16%) responses.

Patients with OSA have many episodes of increased airway resistance because of repeated collapses of upper airways during night. The aim of this work was to evaluate respiratory response during chemical stimulation without and with added inspiratory resistive load (10 cmH2O/L/sec). The studies were performed during quiet breathing with air and during hypercapnic and hypoxic rebreathing tests without and with inspiratory resistive loading in 23 obese (BMI = 34.4 +/- 4.3 kg/m2) patients with OSA and in 10 healthy subjects with similar weight (BMI = 32.4 +/- 4.3 kg/m2). The measurements of respiratory responses (ventilation, mouth occlusion pressure) were performed with the use of computerized equipment. During quiet breathing in response to added load an increase of P0.1 in controls and in OSA patients was observed. During hypercapnic stimulation the ventilatory response with additional load decreased in patients as well as in controls. The slope of mouth occlusion pressure response increased significantly in controls (from 4.40 to 6.83 cmH2O/kPa, p < 0.001) and slightly weaker in OSA patients (from 4.21 to 5.43 cmH2O/kPa, p < 0.05). Although the difference between the slopes was not significant, we found that the absolute increase of P0.1 measured at point 8 kPa of PEtCO2 during loaded breathing was significantly smaller in OSA patients in comparison to controls. (2.1 vs. 10.3 cm H2O; p < 0.001). During hypoxic stimulation occlusion pressure responses were similar in both examined groups. In conclusion we postulate that OSA patients have impaired respiratory compensation of additional inspiratory load, what was demonstrated during hypercapnic rebreathing test.

Restriction is a typical functional abnormality in interstitial lung diseases (ILD) patients but not all of them represent this pattern. The aim of this study was to evaluate 164 patients with ILD in whom normal lung volumes (FVC and TLC > 80% predicted) were found. There were 111 patients with sarcoidosis (phase I--9, II--77, III--25 patients), 25 patients with pulmonary fibrosis, 12 patients with allergic alveolitis and 16 patients with disseminated radiological changes in the lungs of different etiology. Some patients (40%), mostly with fibrosis and allergic alveolitis, were treated with corticosteroids. Measured parameters included static compliance (Cst), transfer factor for CO (TLco and Kco) and maxima expiratory flow-volume curves (MEF50). 33% of patients had all examined functional parameters in normal range, 50% had decreased maximal expiratory flows (particularly in the sarcoidosis group), 46% decreased Cst and 24% decreased transfer factor. Decreased Cst was found in 31% of patients with sarcoidosis, in 67% of patients with allergic alveolitis and in 96% of patients with lung fibrosis. Decreased TLco or Kco was found only in 11% of patients with sarcoidosis, in 42% of patients with allergic alveolitis and in 60% of patients with pulmonary fibrosis. It seems that, these discussed tests are very helpful in detecting functional abnormalities in patients with ILD without signs of restriction. Increased lung elasticity and decreased transfer factor for CO indicate the existence of early or presisting functional disturbances (despite treatment) in patients with ILD and normal lung volumes.

The authors have studied chemical control of breathing in 37 normocapnic patients with OSA. These patients had increased apnea-hypopnea index (AHI = 51 +/- 22), obesity (BMI = 32.4 +/- 5.6 kg/m2) and normal lung function tests. Control group consisted of 20 healthy subjects with normal weight (BMI = 23.1 +/- 2.4 kg/m2). Respiratory responses (ventilatory and P0.1) to hypercapnic and hypoxic stimulation during rebreathing tests were measured with computerized methods. The obtained results in OSA patients were compared with the data of the control group. The results exceeding mean values of the control group above 1.64 SD were recognized as hyperreactive responses. The majority e.g. 26 patients (OSA-N) had normal respiratory responses during hypercapnic stimulation. delta V/delta PCO2 = 16.8 +/- 4.5 L/min/kPa, P0.1/delta PCO2 = 3.5 +/- 2.4 cm H2O/kPa/. In remaining 11 patients (OSA-H) respiratory responses were significantly increased delta V/delta PCO2 = 39.1 +/- 18.8 L/min/kPa, P0.1/delta PCO2 = 8.6 +/- 3.9 cm H20/kPa). During isocapnic hypoxic stimulation majority e.g. 25 patients (OSA-H) had significantly increased respiratory responses delta V/delta SaO2 = 3.28 +/- 1.63 L/min/%, delta P0.1/delta SaO2 = 0.54 +/- 0.43 cm H2O/%/. In remaining 12 patients (OSA-N) respiratory responses were within normal limits delta V/SaO2 = 1.2 +/- 0.28 L/min/%, delta P0.1/ delta SaO2 = 0.21 +/- 0.07 cm H2O/%/. The above results indicated, that majority OSA patients (67.5%) had increased ventilatory and P0.1 responses to hypoxic stimulation. Among them also 11 patients had increased respiratory responses to hypercapnia. It seems, that increased respiratory responses to hypoxic stimulus in OSA patients are symptoms of protective reaction to hypoxaemia occurring during repetitive sleep apnoea and reveals increased neuro-muscular output.

The neuromuscular drive is increased in patients with an airway obstruction. The aim of the study was to estimate an influence of beta-agonist on breathing pattern and mouth occlusion pressure (P0.1) in patients with reversible and nonreversible airway obstruction. Ventilatory function tests, pattern of breathing analysis, mouth occlusion pressure (P0.1) and inspiratory impedance (P0.1/Vt/Ti) were measured in 23 obstructive patients and 20 healthy subjects. In all patients these measurements were repeated 20 minutes after bronchodilator inhalation (0.2 mg fenoterol). During quiet room-air breathing in patients we observed increased Vt, Vt/Ti comparing with healthy persons. The time of inspiration (Ti) and total time (Ttot) were shortened in comparison to our control group. P0.1 and inspiratory impedance were significantly increased (P0.1 3.6 +/- 1.6 vs 1.6 +/- 0.3 cm H2O, p < 0.01 and P0.1/Vt/Ti 6.6 +/- 2.3 vs 3.8 +/- 1.0 cm H2O/L/s). Measurements performed after bronchodilator inhalation revealed decrease of P0.1 and P0.1/Vt/ Ti in patients responsive to beta-agonist (delta FEVI > 15%). In unresponsive patients (delta FEVI < or = 15%) such decrease in neuromuscular respiratory drive was not observed. We conclude that diminishing of increased neuromuscular respiratory drive in patients with reversible obstruction is a consequence of airway resistance decreasing. It seems to be an additional, advantageous for a patient, effect of bronchodilator inhalation.

A 32-year-old, hypertensive, morbidly obese (BMI 49 kg/m2) woman was referred to us suspected of sleep-disordered breathing. Polycythaemia, right heart and respiratory failure, restrictive ventilatory impairment, decreased hypercapnic respiratory drive, high number of very short apneas mostly of central origin (698 vs 530 obstructive), and overnight hypoxaemia were found. The diagnosis of obesity-hypoventilation syndrome was established and the treatment with almitrine, aminophylline and low-calorie diet was started. After 6 months body weight decreased significantly (BMI 38 kg/m2). RBC, spirometry, blood gas analysis, overnight oximetry, hypercapnic respiratory drive and polysomnography showed results within normal limits. Causes, pathophysiology and possible treatment of obesity-hypoventilation syndrome are discussed.

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)

The foundations for a computer program allowing to monitor "on line" physiological data to clinically evaluate ventilatory control were set up. The new equipment demonstrates important innovations--lowered flow resistance, and decreased dead space, modernization of the blocking steering the computer valve. The new program allowed to decrease the time for analysis from couple of minutes to seconds. The results of ventilatory control studies in 11 healthy volunteers were found in ranges of normal values calculated earlier using an analogue method and are similar to those from literature.

20 obese men with OSAS were examined. Polysomnography confirmed this diagnosis. In the daytime pattern of breathing, mouth occlusion pressure (P0.2) and ventilatory responses during CO2 rebreathing test were evaluated. Lung function indices were within normal limits except decreased value of MEF 25 and slight hypoxaemia (Pa0.2 -67 +/- 6 mm Hg). In comparison to control subjects the patients with OSAS when awake had increased ventilation, Vt/Ti ratio and P0.2. This suggests increased inspiratory neuromuscular output in daytime. During CO2 rebreathing test the whole ventilatory and P0.2 response lines were shifted to the left but the slopes of these lines were within normal limits. We conclude that the control of breathing in OSAS patients is changed in comparison to healthy subjects with normal weight.

Twenty eight COPD patients with respiratory insufficiency were studied. These included: 12 hypoxemic and normocapnic patients, 16 hypoxemic and hypercapnic patients, and 22 healthy volunteers. During at rest respiration both COPD groups differed from the control group--demonstrating a higher respiratory incidence, VT/Ti and PO2 values. During hypercapnic stimulation using the rebreathing method the ventilatory response to CO2 in the COPD patients was lowered in comparison with the control. Increase of occlusion pressure as a response to the increasing hypercapnia was lowered in both groups, significantly in patients with hypercapnia.

22 normal volunteers, 57 patients with obstructive changes and 34 with restrictive type changes were studied. The following parameters were analyzed: maximal inspiratory and expiratory pressures, occlusion pressure and components of the breathing pattern. The patients were divided according to the degree of airway resistance and fall of vital capacity. All patients compared with the healthy volunteers demonstrated higher minute ventilation, and a higher neuro-muscular respiratory drive as shown by the VT/Ti index and occlusion pressure. The breathing pattern did not correlate significantly with the different abnormalities of respiratory function in the studied groups. In the patients with obstructive changes a weak correlation was found between the occlusion pressure and airway resistance. In patients with restrictive type changes a weak correlation between occlusion pressure, static and specific compliance was found. The occlusion pressure was a more specific parameter characterizing respiratory drive compared with the VT/Ti index. Disturbances of pulmonary mechanics have a small but significant effect on respiratory control.