Effects of almitrine bismesylate on arterial blood gases in patients with chronic obstructive pulmonary disease and moderate hypoxaemia: a multicentre, randomised, double-blind, placebo-controlled study.

BACKGROUND: Advanced chronic obstructive pulmonary disease (COPD) generates high costs, especially when patients require domiciliary long-term oxygen therapy (LTOT). Almitrine bismesylate has been shown to improve gas exchange in the lungs. Our hypothesis was that long-term treatment with almitrine might postpone the prescription of LTOT. OBJECTIVE: To evaluate the effects of almitrine sequential treatment on arterial blood gases in COPD patients with moderate hypoxaemia. METHODS: COPD patients with moderate hypoxaemia [partial oxygen tension in arterialised blood (PaO(2)) between 7.33 and 8.66 kPa (56-65 mm Hg)] were investigated. After a 1-month run-in period, patients were given either almitrine 100 mg per day or placebo for sequential treatment for a total of 12 months. RESULTS: 115 patients in a steady state (57 in the almitrine and 58 in the placebo group) were included. Mean age was 60 years, mean forced expiratory volume in 1 s was 34 +/- 13% of predicted and mean PaO(2) was 8.04 +/- 0.5 kPa (60.5 +/- 3.8 mm Hg). 38 patients were lost to follow-up, 23 in the almitrine and 15 in the placebo group. The majority of drop-outs were due to adverse events (AE; 16 in the almitrine and 9 in the placebo group). Almitrine treatment resulted in PaO(2) improvement of 0.43 +/- 0.88 kPa (3.2 +/- 6.6 mm Hg) (p = 0.003). The treatment effect between almitrine and placebo was 0.45 kPa (3.4 mm Hg) (p = 0.003). In the almitrine group, two distinct subgroups were observed: responders (n = 19) and non-responders (n = 38). Almitrine treatment in responders resulted in a clinically significant improvement in PaO(2) of 1.36 +/- 0.7 kPa (10.2 +/- 5.3 mm Hg) (p < 0.0001) and a reduction of partial carbon dioxide tension in arterialised blood. 31 patients experienced serious AE: 17 in the almitrine and 14 in the placebo group. Five patients died during the study (3 in the almitrine and 2 in the placebo group). Most AE occurring during the study were related to underlying disease. Clinical diagnosis of polyneuropathy resulted in the withdrawal of 5 patients in the almitrine group and 3 patients in the placebo group. Four patients in the almitrine group experienced weight loss. CONCLUSIONS: Almitrine treatment of patients with severe COPD and moderate hypoxaemia resulted in a small but significant improvement in PaO(2) over 12 months. A clinically important improvement in gas exchange was observed in 33% of treated patients. These patients may be candidates for long-term treatment.

[Effect of nocturnal hypoxia on pulmonary hemodynamics in patients with obstructive sleep apnea]. / Wplyw nocnego niedotlenienienia krwi na krazenie plucne chorych na obturacyjny bezdech senny (OBS).

Effects of apnoea induced nocturnal hypoxia on pulmonary haemodynamics (PH) in pts with OSA are still under debate. We studied PH in 67 pts (64 M and 3 F) mean +/- SD: age 45 +/- 8 years, with severe OSA, AHI 62 +/- 22. Patients had normal spirometry: FVC 98 +/- 15% N, FEV1 97 +/- 16% N and arterial blood gases--PaO2 72 +/- 10 mmHg, PaCO2 40 +/- 4 mmHg. PH were studied using Swan-Ganz thermodilution catheter. PH were within normal range: right atrial pressure 4.2 +/- 2.7 mmHg, right ventricular systolic/enddiastolic pressure 28.1 +/- 7.1/5.0 +/- 3.3 mmHg, mean pulmonary artery pressure (PAP) 15.8 +/- 4.6 mmHg, mean pulmonary wedge pressure (PW) 6.8 +/- 3.1 mmHg, cardiac output (CO) 5.6 +/- 2.2 L/min. and pulmonary vascular resistance (PVR) 150 +/- 83 dyn.sec.cm-5. During exercise (44 pts) PAP rose from 15.8 +/- 4.3 to 29.8 +/- 9.4 mmHg, PW rose from 6.8 +/- 3.2 to 12.6 +/- 6.8 mmHg and CO from 4.9 +/- 1.9 to 9.2 +/- 4.2 L/min. All patients presented with nocturnal desaturations. Mean oxygen saturation (SaO2 mean) was: 87.4 +/- 5.4%, minimal saturation (SaO2 min) was 57.4 +/- 15.9%. Time spent in desaturation SaO2 < 90% (T90) was 50.7 +/- 26.5%. Results of PH investigations were related to results of pulse oximetry. Linear regression analysis showed week negative correlations between SaO2 mean and: PAP (r = -0.37 p = 0.003), PVR (r = -0.37 p = 0.007), and positive correlation between T90 and PAP (r = 0.37 p = 0.008). We conclude that there is no diurnal pulmonary hypertension at rest in patients with severe OSA and normal lung function even in the presence of severe overnight nocturnal desaturations. In half of studied patients we observed pulmonary hypertension during exercise.

[Effects of nocturnal desaturation on pulmonary hemodynamics in patients with overlap syndrome (chronic obstructive pulmonary disease and obstructive sleep apnea)]. / Wplyw nocnego niedotlenienia na cisnienie w tetnicy plucnej u chorych z zespolem nakladania (przewlekla obturacyjna choroba pluc i obturacyjny bezdech senny).

We studied pulmonary haemodynamics and nocturnal desaturation in 17 patients with an overlap syndrome (OS), all males, mean age 51.4 +/- 8.3 years, mean BMI 37 +/- 4.2 kg/m2. Diagnosis of COPD was based on pts history, clinical examination, lung function tests and chest radiography. Spirometry showed: FVC 2.7 +/- 0.7 L (59 +/- 16% N), FEV1 1.5 +/- 0.7 L (43 +/- 16% N), FEV1% FVC 54 +/- 13%, Raw 0.58 +/- 0.4 kP.s/L, RV 3.3 +/- 1.2 L (144 +/- 51% N), TLC 6.6 +/- 1.3 L (100 +/- 14% N) and RV% TLC (49.5 +/- 12.1%. Arterial blood gas values were: PaO2 56.9 +/- 9.5 mmHg, PaCO2 46.9 +/- 9.8 mmHg, pH 7.37 +/- 0.05. Mean apnoea/hypopnoea index (AHI) was 63.9 +/- 18.9. Pulmonary haemodynamics at rest (Swan Ganz thermodilution catheter) were: mean pulmonary artery pressure (PAP-SP) 24.2 +/- 7.4 mmHg, mean pulmonary wedge pressure (PW-SP) was 9.1 +/- 7.3 mmHg, cardiac output (CO-SP) was 5.6 +/- 2.3 L/min. and pulmonary vascular resistance (PVR) was 229 +/- 97 dyn.sec.cm-5. During exercise (40 Watts, 7 mins, in 8 pts) PAP rose from 19 +/- 6 mmHg to 41.2 +/- 15.1 mmHg, PW rose from 7.4 +/- 7.2 mmHg to 11 +/- 10.2 mmHg, CO rose from 5.8 +/- 2.7 L/min to 12.7 +/- 2.4 L/min. Overnight pulse oximetry showed: mean oxygen saturation (SaO2 mean) 80.2 +/- 8.5%, minimal saturation (SaO2 min) was 50.7 +/- 19.7%. Time spent in desaturation SaO2 < 90% (T 90) was 76.9 +/- 25.7%. We conclude that pts with OS have resting pulmonary hypertension and elevated PVR. During low grade exercise the rise in PAP was highly abnormal. Statistical analysis showed no correlations between nocturnal SaO2 and diurnal pulmonary haemodynamics data.

[Comparison of pulmonary hemodynamics in patients with COPD and patients with overlap syndrome with similar severity of airway obstruction and gas exchange]. / Porównanie hemodynamiki plucnej u chorych na p.o.ch.p. i u chorych z zespolem nakladania z podobnego stopnia uposledzeniem rezerw wentylacyjnych pluc oraz z zaburzeniami wymiany gazowej.

It may be assumed that pulmonary hypertension due to apnea related desaturations during sleep develops earlier in the natural course of the overlap syndrome (OS) than in patients with COPD only. We aimed to verify this hypothesis by comparing pulmonary haemodynamics in COPD patients and patients with OS with similar severity of airway limitation and of pulmonary gas exchange. We studied pulmonary haemodynamics in 17 males with OS--group I (mean AHI 63.9 +/- 18.9), and in 20 males with COPD--group II. Both groups were age (I = 51.4 +/- 8.3 years, II = 53.7 +/- 7.7 years), FVC (I = 2.7 +/- 0.7 L, II = 2.9 +/- 0.6 L), FEV1 (I = 1.5 +/- 0.7 L, II = 1.3 +/- 0.3 L), PaO2 (I = 56.9 +/- 9.5 mm Hg, II = = 61.7 +/- 14.6 mm Hg) and PaCO2 (I = 46.9 +/- 9.8 mm Hg, II = 48.3 +/- 6.6 mm Hg) matched. Haemodynamic measurements were performed at rest and in 7th minute of exercise if 40 Watts using Swan-Ganz thermodilution catheter. Both groups presented with similar severity of pulmonary hypertension at rest (mean PPA = 24.2 +/- 7.4 mm Hg in OS and 24.3 +/- 9.2 mm Hg in COPD) and on exercise (mean PPA 41.2 +/- 15.1 mm Hg in OS and 44.5 +/- 11.5 mm Hg in COPD). COPD patients had higher PVR than OS (335 +/- 138 d.s.cm-5 versus 229 +/- 97 d.s.cm-5, p < 0.005). We concluded that pulmonary hypertension in OS patients is not more advanced than in COPD patients with matched ventilatory and gas exchange impairment.

[Quality of sleep and periodic breathing in healthy individuals working at an altitude of 3700 meters]. / Jakosc snu i oddychanie okresowe u ludzi zdrowych pracujacych na wysokosci 3700 metrów.

We performed full polysomnography (PSG) in 7 healthy miners of Kyrghyz origin (mean age 25 +/- 6 years) working in 2 weeks shifts at Kumtor gold mines at the elevation of 4200 m. They slept in comfortable dormitories situated at 3700 m. To avoid acute mountain sickness all subjects received acetazolamide 3 x 0.25 daily during 2 days preceding ascent and during 2 days at altitude: PSG was performed three times: at 760 m (1) and on the 1st (2) and 7th night (3) after rapid ascent (aircraft) to high altitude using SomnoTrac 4250 sleep laboratory. We found that sleep efficiency was good at lowland and in the mountains averaging 81.79% and 84% respectively. Although there were no significant differences in percentage of sleep stages and of total sleep time between lowland and both nights at high altitude, arousals and awakenings were more frequent in the mountains. Episodes of periodic breathing (PB) appeared at high altitude. There was a large individual variability in PB on both nights at altitude. The time spent in PB ranged from 4 to 30 minutes during the first night at altitude and from 3 to 17 minutes during the second one. PB appeared mainly during non-REM sleep and aggravated arterial blood desaturation.

Effects of long-term oxygen therapy on pulmonary hemodynamics in COPD patients: a 6-year prospective study.

OBJECTIVE: To investigate effects of 6 years of domiciliary oxygen therapy on pulmonary hemodynamics in a large group of COPD patients. DESIGN: Prospective longitudinal study with serial measurements. SETTING: Research institute of pulmonary diseases. PATIENTS: Ninety-five patients (72 men, 23 women), mean age 58+/-9 years, had COPD but were free of any other serious disease. Functional characteristics at entry, mean+/-SD, were as follows: FVC=2.24+/-0.51 L; FEV1=0.84+/-0.31 L; PaO2=55+/-6 mm Hg; PaCO2=48+/-9 mm Hg; mean pulmonary arterial pressure (PAP)=28+/-11 mm Hg; and pulmonary vascular resistance (PVR)=353+/-172 dynexsxcm(-5). METHODS: Pulmonary hemodynamics were investigated using Swan-Ganz thermodilution catheters. After initial assessment, all patients were started on a regimen of long-term oxygen therapy (LTOT). Follow-up consisted of medical examination, spirometry, and arterial blood gas analysis every 3 months. Pulmonary artery catheterization was repeated every 2 years. RESULTS: Seventy-three subjects survived 2 years of LTOT. In 39 subjects catheterized after 2 years, PAP fell from 25+/-8 to 23+/-6 mm Hg (not significant [NS]). From 31 patients who completed 4 years of LTOT, hemodynamic data were obtained in 20. In these 20 patients, PAP averaged 24+/-7 mm Hg at entry, and 23+/-5 and 26+/-6 mm Hg after 2 and 4 years, respectively (NS). In 12 patients who completed 6 years of LTOT, PAP was 25+/-7 at entry, and 21+/-4, 26+/-7, and 26+/-6 mm Hg at 2, 4, and 6 years, respectively (p < 0.01 for 2 vs 6 years). PVR was 313+/-159 dynexsxcm(-5) at entry, and 268+/-110, 344+/-82, and 332+/-205 dynexsxcm(-5) at 2, 4, and 6 years, respectively (NS). During 6 years of follow-up, PaO2 decreased from 61+/-3 to 46+/-9 mm Hg (p < 0.001) and PaCO2 increased from 44+/-13 to 49+/-9 mm Hg (p < 0.01). CONCLUSION: LTOT for 14 to 15 h/d resulted in a small reduction in pulmonary hypertension after the first 2 years followed by a return to initial values and subsequent stabilization of PAP over 6 years. The long-term stabilization of pulmonary hypertension occurred despite progression of the airflow limitation and of hypoxemia.

[Three week stay at a height of 3700-4200 m. causes mild pulmonary hypertension in healthy men]. / Trzytygodniowy pobyt na wysokosci 3700-4200 m. wywoluje lagodne nadcisnienie plucne u zdrowych mezczyzn.

High altitude hypoxia leads to development of hypoxic pulmonary hypertension. We studied 27 healthy caucasian subjects aged 24 to 59 years, mean 41.6 +/- 9 y, working on 4 week shifts at the Kumtor gold mines at the altitude of 3700-4200 m. Pulmonary circulation was studied twice by Echo-Doppler using Toshiba SSD-160. The first investigation was performed at the level of 730 m at the end of 4 week holiday spent in the lowland, the second investigation on the 23rd day at altitude. Pulmonary artery acceleration time decreased from 131 +/- 14 ms to 105 +/- 14 ms (p < 0.001). Calculated pulmonary arterial mean pressure increased from 15.1 +/- 2 to 25.4 +/- 8 mmHg (p < 0.001). Right ventricular preejection period increased from 93 +/- 14 to 102 +/- 19 ms (p < 0.05). Other echo variable did not change. We conclude that healthy subjects submitted to 3 week exposure to high altitude hypoxia (oxygen pressure in the inspired air 82-88 mmHg), developed mild pulmonary hypertension, regressing after recovery at the lowland.

[Behavior of arterial blood oxygen saturation at night in patients with obstructive lung diseases qualifying for home oxygen therapy]. / Zachowanie sie wysycenia krwi tetniczej tlenem w nocy u chorych no POCP kwalifikowanych do DLT.

In COPD patients undergoing LTOT recent ATS and ERS guidelines suggest increase of oxygen flow by I L/min. to avoid severe desaturations during sleep. The aim of this study was to investigate frequency of overnight desaturations in COPD patients qualified for LTOT. We studied 101 consecutive COPD patients qualified for LTOT. Their functional characteristics were as follows: FVC = 2.24 +/- 0.78 L, FEVI = 0.88 +/- 0.39 L, PaO2 = 50 +/- 5 mmHg, PaCO2 = 48 +/- 8 mmHg. Overnight pulse oximetry was performed twice, while breathing air and on supplemental oxygen assuring satisfactory oxygenation (PaO2/O2 at rest when awake = 65 +/- 7 mmHg). We distinguished three groups of patients according to mean overnight arterial blood saturation breathing supplemental oxygen (mean SaO2/O2). First group - 40 patients (39.6%) had mean SaO2/O2 > 93% and time spent in saturation below 90% (T90/O2) = 4.5 +/- 6.7% of the recording time. Second group - 30 patients (29.7%) had mean SaO2/O2 between 90% and 92% and T90/O2 = 32.7 +/- 15.3%. Third group - 31 patients (30.6%) had mean SaO2/O2 < 90% and T90/O2 = 81.8 +/- 16.2% of the recording time. Comparison of ventilatory variables and daytime blood gases in these groups revealed statistically significant elevation of PaCO2 in group 3 (54 +/- 9 mmHg) compared to group 1 and 2 (45 +/- 6 mmHg and 47 +/- 7 mmHg respectively). FVCI, PaO2 and age were similar in all groups. We conclude that around 1/3 of COPD patients qualified for LTOT need increased oxygen flow during sleep. Such need should to be confirmed by the overnight pulse oximetry.

[Twenty year observation of pulmonary hypertension in a patient with COPD]. / Dwudziestoletnia obserwacja rozwoju nadcisnienia plucnego u chorego na POChP.

Evolution of pulmonary hypertension over 20 years of observation in a patient with COPD is presented. Originally patient presented with normal pulmonary arterial pressure. First bout of pulmonary hypertension was observed during severe pulmonary infection resulting in respiratory failure. Smoking cessation, regular use of bronchodilators and antibiotics during bacterial exacerbations produced long-term stabilisation of FEV1, blood gases and pulmonary arterial pressure.

Acute effects of CPAP and BiPAP breathing on pulmonary haemodynamics in patients with obstructive sleep apnoea.

Continuous positive airway pressure (CPAP) breathing increases alveolar and intrathoracic pressures, hampering venous return and pulmonary capillary flow. Bilevel positive airway pressure (BiPAP) breathing assuring lower expiratory pressure should impede less the pulmonary circulation. We aimed to compare the effects of CPAP and BiPAP breathing on pulmonary haemodynamics in patients with obstructive sleep apnoea (OSA). Nine male OSA patients (mean ( +/- SD) apnoea-hypopnoea index (AHD = 46 +/- 22) were studied. In each patient, intravascular and oesophageal pressures were measured and mean transmural pulmonary artery and transmural wedge pressures were calculated. After baseline recordings, patients were submitted to 25 min of CPAP and BiPAP breathing delivered in random order. The pressure of 10 cmH2O for CPAP and 10/4 cmH2O for BiPAP was used. At baseline, subjects presented with normal pulmonary arterial pressures and cardiac output (Q'). CPAP breathing resulted in a slow increase in mean pulmonary intravascular pressure from 13.8 +/- 2.0 mmHg reaching 14.8 +/- 1.8 mmHg at the 25th minute of investigation (p < 0.05). Transmural pressure did not change. There was also no change in the Q' and in the pulmonary vascular resistance. BiPAP breathing had no effect on intravascular and transmural pressures, Q' and pulmonary vascular resistance. We conclude that continuous positive airway pressure breathing increases pulmonary intravascular but not transmural, true, pressure. Bilevel positive airway pressure breathing does not affect central pulmonary haemodynamics.

[Effect of positive pressure respiration on diurnal catecholamine excretion by patients with obstructive sleep apnea]. / Wplyw oddychania pod dodatnim cisnieniem na dobowe wydalanie katecholamin przez chorych na obturacyjny bezdech senny.

The aim of the study was to investigate effects of CPAP treatment on diurnal catecholamine excretion in urine in patients with obstructive sleep apnea (OSA). 12 males with severe OSA (mean AHI = 63) were measured in 3 separate 8 hour samples by fluorimetric method. NA levels were higher in OSA patients in all urine samples than in obese, mildly hypertensive males (control group = C). In C group patients NA levels were significantly lower at night than during the day contrary to OSA patients in whom NA levels dropped insignificantly during sleep. In OSA patients NA levels during sleep correlated with severity of apneas (r = 0.42) and night hypoxaemia (r = -0.46). CPAP treatment resulted in significant fall in NA levels during sleep (p < 0.01). A levels did not change after CPAP treatment. We conclude that abnormally high NA level during sleep in OSA patients may be related to sleep fragmentation and hypoxia. CPAP treatment restores normal circadian rhythm of NA excretion.

[The influence of increased pressure in the pulmonary artery during exertion and evolution of pulmonary hypertension on survival of patients with COPD]. / Wplyw wzrostu cisnienia w tetnicy plucnej podczas wysilku na ewolucje nadcisnienia plucnego i przezycie chorych na POChP.

We aimed to investigate relations between PAP increase on exercise and long-term evolution of pulmonary hypertension and survival. 43 COPD pts were investigated. Initially they with mild pulmonary hypertension and abnormally high increase in PAP on exercise (40 W, 5 min). All pts were followed-up for 3-5 years. During follow-up 21 pts. died (group I), mean survival time was 28 +/- 17 month, and 22 survived (group II), mean observation period was 59 +/- 22 month. Survivors were recatheterized after 3-7 yrs (mean 5 yrs). PAP increased by 3.4 +/- 4.9 mm Hg and correlated better with initial PAP (r = 0.91, p < 0.001) than with delta PAP on exercise (r = 0.61, p < 0.02). Survivors differed from dead in FEV1 (1.59 +/- 55 vs 1.17 +/- 0.33 L, p < 0.02), VC (3.54 +/- 1.0 vs 2.8 +/- 0.84 L, p < 0.02), resting PaO2 (39.1 +/- 9.0 vs 46.3 +/- 11.5 mm Hg, p < 0.05) resting heart rate (82.5 +/- 13.6 vs 93.8 +/- 16.1 beats/min p < 0.02) resting PAP (20.7 +/- 8.2 vs 32.3 +/- 13.2 mm Hg, p < 0.002), and resting PW (7.6 +/- 2.0 vs 11.6 +/- 7.4 mm Hg, p < 0.05).

[Prognostic value of pulmonary hypertension in patients with severe COPD]. / Prognostyczne znaczenie nadcisnienia plucnego w ciezkiej postaci POCHP.

UNLABELLED: There is a continuing debate on the role of pulmonary hypertension in the natural history of COPD. The aim of the study was to compare 2 groups of COPD pts, one investigated before domiciliary oxygen treatment era (Group I) with the other benefiting from LTOT (Group II). Both were followed-up for 5 years. INCLUSION CRITERIA: pure COPD, PaO2 < 60 mmHg, PAP > 20 mmHg. Group I consisted of 16 pts (13M, 3F), mean age 55 +/- 9y. On initial evaluation their FEV1 averaged 0.93 +/- 0.3L and PaO2 54 +/- 6 mmHg. Their mean pulmonary arterial pressure (PAP) was 37.9 +/- 9 mmHg. During five years 12 patients (75%) died. Mean survival time of pts who died was 18.9 +/- 14.7 months. Group II consisted of 34 pts (27M, 7F) mean age 56 +/- 8y (NS vs group I), FEVI 0.83 +/- 3L (NS). PaO2 53 +/- 6 mmHg (NS), PAP 30.9 +/- 8.5 mmHg (p < 0.02). During five years 26 pts (76.5%) died. Mean survival time was 25 +/- 16 months (NS). Mean oxygen breathing time was 14h/ day. The Cox's survival analysis did not show difference between patients group I and II. We conclude that high initial PAP in group I patients did not affect survival compared to patients with similar severity of respiratory failure and lower PAP. The finding that LTOT did not improve survival may depend on many other variables not included into analysis.

[Pulmonary circulation at rest and during exercise in patients with obstructive sleep apnea before and after one year of treatment with CPAP]. / Krazenie plucne w spoczynku i podczas wysilku u chorych na obturacyjny bezdech senny przed i po rocznym leczeniu za pomoca CPAP.

We studied pulmonary haemodynamics in 19 male patients, mean age 45 +/- 5 years, suffering from severe OSA, mean apnea/hypopnea index (AHI) 68 +/- 17. Pulmonary haemodynamisc were studied using Swan-Ganz thermodilution catheter in the supine position at rest, and at the end of the 7th minute of steady-state exercise (40 W). Investigations were repeated after one year of treatment with nasal CPAP. At rest mean pulmonary artery pressure (PPA), pulmonary wedge pressure (PW) and cardiac output (CO) were normal, PPA = 16.6 +/- 5.7 mmHg, PW = 5.2 +/- 1.8 l/min. Pulmonary vascular resistance (PVR) was slightly elevated = 155 +/- 65 d.sec.cm-5. On exercise only PVR remained unchanged. After a year of treatment PPA changed to 15.8 +/- 4.0 mmHg (NS), Pw-7.5 +/- 3.1 mmHg (NS), CO-4.9 +/- 1.6 L/min (NS), PVR - 145 +/- 35 d.sec.cm-5 (NS). In two patients with resting hypertension PPA dropped from 33 mmHg to 25 mmHg and 28 mmHg to 18 mmHg respectively. Statistical analysis showed no significant change in any of the studied variables after one year of the CPAP therapy.

[Evaluation of a Polish apparatus for creating continuous positive airway pressure (nCPAP)]. / Ocena Polskiego aparatu do wytwarzania stalego dodatniego cisnienia w drogach oddechowych (nCPAP).

The aim of the study was to evaluate technical features of polish CPAP machine and to compare its parameters with two commonly used models of foreign origin. Physical signs, noise, produced flows and pressures were compared. POL-CPAP was bulkier and noisier than foreign models. Flows and pressures were not completely satisfactory. We conclude that POL-CPAP fulfill the criteria required from such type of equipment. However the evaluated device requires further improvement of technical parameters.

[Effect of CPAP and BiPAP assisted breathing on pulmonary hemodynamics in patients with obstructive sleep apnea]. / Wplyw oddychania za pomoca CPAP lub BiPAP na hemodynamike plucna u chorych na obturacyjny bezdech senny.

CPAP breathing increases alveolar and intrathoracic pressures. We aimed to investigate the effects of CPAP and BiPAP breathing on pulmonary haemodynamics in patients with OSA. Ten male patients with OSA (AHI = 48 +/- 22) were studied. In each patient intravascular and esophageal pressures were measured and mean transmural pulmonary artery and transmural wedge (Pwtm) pressures were calculated. After baseline recordings patients were submitted to 25 min. of CPAP and BiPAP breathing in random order. The pressure of 10 cm H20 for CPAP and 10/4 cm H20 for BiPAP was used. At baseline pulmonary arterial pressures and flow were normal. CPAP breathing resulted in an increase in mean pulmonary intravascular pressure from 15.5 +/- 1.8 mmHg to 17.1 +/- 2.3 mmHg (p < 0.05). Transmural pressure did not change. There was also no change in the cardiac output (CO) and pulmonary vascular resistance (PVR). At some time points pulmonary arterial pressures were higher during CPAP breathing than during BiPAP breathing (p < 0.01). BiPAP breathing had no effect on intravascular and transmural pressures, CO and PVR. We conclude that CPAP breathing increase pulmonary intravascular but not transmural, true, pressure. BiPAP breathing does not change pulmonary haemodynamics what may be of importance as pulmonary circulation is concerned.

[Pulmonary hemodynamics in obstructive sleep apnea or overlap syndrome]. / Krazenie plucne u chorych na obturacyjny bezdech senny i u chorych z zespolem nakladania.

We studied pulmonary haemodynamics at rest and on exercise in 44 consecutive patients with moderate to severe obstructive sleep apnea (OSA), mean AHI > 40. The diagnosis was confirmed by standard polysomnography (PSG). According to history and results of spirometric measurements patients were divided to two groups, pure OSA and OSA complicating chronic obstructive pulmonary disease (overlap syndrome). In 34 pts with OSA (31 M, 3 F), means: age 45 +/- 8 years, body weight 108 +/- 22 kg, BMI49, VC 107 +/- 16% of N, FEV1 101 +/- 15% of N, PaO2 71 +/- 10 mmHg, PaCO2 39 +/- 3 mmHg, PSG showed AHI 66 +/- 15. Pulmonary haemodynamics at rest were within normal limits: PPA 16 +/- 5 mmHg, PW 7 +/- 3 mmHg, CO 4.5 +/- 1.5 l/min, PVR 184 +/- 92 dyne.s.cm-5. On low grade exercise (40 W) PPA increased to 31 +/- 10 mmHg, Pw to 12 +/- 6 mmHg and CO to 8.6 +/- 4.0 l/min, PVR remained unchanged. In eight pts abnormal rise in PPA on exercise resulted from the increase in driving pressure (PPA-Pw). In 2 pts it was due to abnormal increase in wedge pressure. In ten male pts presenting with COPD means: age 53 +/- 8 y, body weight 109 +/- 11 kg, BMI49, VC 53 +/- 14% of N, FEV1 36 +/- 16% of N, PaO2 57 +/- 10 mmHg, PaCO2 47 +/- 7 mmHg, PSG showed AHI 63 +/- 20. All pts presented with pulmonary hypertension (PH) at rest, PPA ranging from 21 to 37 mmHg, mean 26 +/- 5 mmHg. We conclude that patients with OSA have normal PPA at rest, 1/2 of them have PH on exercise due to restriction of pulmonary arterial bed and/or left ventricle dysfunction. Pts with overlap syndrome have moderate resting PH resulting from alveolar hypoxia.

[Effect of large doses of nifedipine on pulmonary hypertension in patients with recurrent pulmonary thromboembolism]. / Wplyw duzych dawek nifedypiny na nadcisnienie plucne u chorych z nawracajaca zatorowoscia plucna.

Thromboembolic pulmonary hypertension is an uncommon condition with poor prognosis. Vasodilators may be effective in some patients with that disease. The effect of nifedipine on hemodynamics was investigated in two patients with thromboembolic pulmonary hypertension treated with acenocoumarol. Nifedipine was administered in 20 mg doses hourly during right cardiac catheterization and was repeated after 1 hour until a decrease in systemic pressure occurred. Patients received 80 mg and 120 mg of nifedipine. Pulmonary artery pressures decreased in both cases. An increase of cardiac output and decrease of pulmonary vascular resistance were observed after 60-80 mg of nifedipine and continued to the end of the investigation. No effect on heart rate was observed. We suggest that high doses of nifedipine may be--in some patients--effective in reducing thromboembolic pulmonary hypertension.