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P Sliwiński

Publications and source records attributed to P Sliwiński.

At least 19 recordsLinked to original sources
PubMed2004

Three-dimensional Ewald method with correction term for a system periodic in one direction.

A three-dimensional Ewald summation formula with a shape-dependent correction term for Coulomb interactions in systems with one-dimensional periodicity is derived. Test molecular dynamics simulations of acetone molecules in cylindrical silica pores show that the formula is efficient only when size of the system in a plane perpendicular to the periodicity direction is small in comparison with the periodicity length.

Journal Article↗
PubMed2001

[Ten years experience of the sleep laboratory at the Institute of Tuberculosis and Lung Disease in Warsaw].

Between 1991-2000 2052 patients (81% men and 19% women) were referred to our Sleep Laboratory because of OSA suspision. In 1194 (58%) subjects (88% men and 12% women) diagnosis of obstructive sleep apnoea (OSA, AHI > 10) was confirmed. In 430 of them (36%) mild OSA (AHI 11-25), in 243 (20%) moderate OSA (AHI 26-40), and in 521 (44%) severe OSA (AHI > 40) was diagnosed. Epworth sleepiness scale score in those groups was 10.4, 10.5 and 13.0 points respectively. 908 (76%) of patients with OSA were submitted to nCPAP treatment. Effective CPAP pressure ranged from 5 to 20 milibars, mean 8.4 mbars. In 21 patients upper airway resistance syndrome (UARS) was diagnosed. Central sleep apnoea, most frequently of Cheyne-Stokes respiration type was diagnosed in 13 patients. The most common diseases accompanying OSA were: systemic hypertension (46%), coronary heart disease (29%), diabetes (12%), and COPD (9%). Majority of OSA patients (61%) were obese (BMI > 30 kg/m2), 32% were over weight (BMI 25-30 kg/m2). Only 7% had normal body weight (BMI 20-25 kg/m2). Long-term (more than one year) compliance to treatment was found in 70% of patients prescribed CPAP.

Adolescent↗
PubMed2000

[Effect of nocturnal hypoxia on pulmonary hemodynamics in patients with obstructive sleep apnea].

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.

Adult↗
PubMed2000

[Effects of nocturnal desaturation on pulmonary hemodynamics in patients with overlap syndrome (chronic obstructive pulmonary disease and obstructive sleep apnea)].

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.

Circadian Rhythm↗
PubMed2000

[Respiratory failure during the course of congenital myopathy effectively treated with nocturnal noninvasive nasal positive pressure ventilation].

Respiratory muscle weakness in myopathy may result in respiratory failure. 41 year old male with congenital myopathy was successfully treated with nocturnal noninvasive nasal positive pressure ventilation. NPPV resulted in improvement of arterial blood gases and allowed to close tracheostomy. Patient was able to return to full time employment.

Adult↗
PubMed1999

[Noninvasive positive pressure ventilation in COPD patients with hypercapnic respiratory failure].

The effects of noninvasive positive pressure ventilation (NIPPV) in COPD patients (pts) with hypercapnic respiratory failure were evaluated. The study group consisted of 19 COPD pts (16M, 3F, mean age 60 +/- 8 years) on LTOT for at least 6 month before study. Patients were enrolled in random order to group I, which continued LTOT and to group II, which started nocturnal NIPPV and continued LTOT. There were 12 pts in group 1 and 7 pts in group II. Two pts from the group did not tolerate NIPPV and were transferred to group I. To ventilate the pts we used portable, volume ventilators. Mean time of follow-up in group I was 23 +/- 13 months and 16 +/- 10 months in group II. During that time died 5 pts from 1 and 4 pts from group II. Differences between functional variables (FEV1, FVC, FEV1/VC, PaO2, PaCO2, pH, PEmax, 6MWD), dyspnea, number of hospitalizations and mortality in both groups were not statistically significant. In both groups progression of the disease (decrease of FEV1, worsening of hypoxaemia and increase of hypercapnia) was observed. NIPPV did not slow down progression of the disease.

Aged↗
PubMed1999

[Noninvasive intermittent positive pressure ventilation in treatment of chronic respiratory disease exacerbation].

Noninvasive intermittent positive pressure ventilation (NIPPV) via nasal mask became a routine method of treatment of severe exacerbations of chronic respiratory failure. The aim of the study was to apply NIPPV in patients with COPD admitted to hospital due to exacerbation of the disease who on standard treatment developed progressing respiratory acidosis (pH < 7.30). Fourteen COPD patients were treated with NIPPV. Arterial blood gases at the beginning of treatment were: PaO2 41 +/- 9 mmHg, PaCO2 = 87 +/- 17 mmHg, pH = 7.30 +/- 0.05. In 10 patients NIPPV applied quasi continuously resulted in clinical improvement and an amelioration of arterial blood gases. PaO2 rose from 41 +/- 9 mmHg to 56 +/- 12 mmHg, PaCO2 fell from 85 +/- 17 to 57 +/- 9 mmHg and pH rose from 7.30 +/- 0.05 to 7.41 +/- 0.04. In 4 patients NIPPV did not prevent further progression of respiratory acidosis. They were intubated and mechanically ventilated. Three patients survived and were discharged home. One patient died from septic shock. We conclude that NIPPV is an effective method to treat respiratory acidosis developing during exacerbation of severe COPD.

Acidosis, Respiratory↗
PubMed1999

[Comparison of pulmonary hemodynamics in patients with COPD and patients with overlap syndrome with similar severity of airway obstruction and gas exchange].

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.

Airway Obstruction↗
PubMed1998

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.

Blood Gas Analysis↗
PubMed1997

Effect of long-term oxygen therapy on survival in patients with chronic obstructive pulmonary disease with moderate hypoxaemia.

BACKGROUND: To date only two controlled studies have been published on the effects of domiciliary oxygen treatment on survival in patients with chronic obstructive pulmonary disease (COPD) with advanced respiratory failure. The survival in such patients despite oxygen treatment remains poor. The prescription of long term oxygen therapy (LTOT) in less severe disease remains controversial. The aim of this study was to evaluate the rationale for prescribing oxygen to patients with COPD with moderate hypoxaemia. METHODS: One hundred and thirty five patients with COPD, with PaO2 7.4-8.7 kPa (56-65 mmHg) and advanced airflow limitation (mean (SD) forced expiratory volume in one second (FEV1) 0.83 (0.28) 1), were randomly allocated to a control (n = 67) and LTOT (n = 68) group. The patients were followed every three months for at least three years or until death. RESULTS: The cumulative survival rate was 88% at one year, 77% at two years, and 66% at three years. No significant differences were found in survival rates between patients treated with LTOT and controls, nor did longer oxygen use (over 15 hours per day) improve survival. Younger age, better spirometric values, and higher body mass index predicted better survival. CONCLUSIONS: Domiciliary oxygen treatment does not prolong survival in patients with COPD with moderate hypoxaemia. Airway limitation seems to determine survival in this group of patients.

Female↗
PubMed1997

[Behavior of arterial blood oxygen saturation at night in patients with obstructive lung diseases qualifying for home oxygen therapy].

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.

Adult↗
PubMed1997

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.

Humans↗
PubMed1996

Influence of global inspiratory muscle fatigue on breathing during exercise.

We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30, 60, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Esophageal and gastric pressures, anteroposterior displacement of the rib cage and abdomen, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. We conclude that the respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.

Adult↗
PubMed1996

[The influence of increased pressure in the pulmonary artery during exertion and evolution of pulmonary hypertension on survival of patients with COPD].

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).

Female↗