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Biomedical subjects

I Hawryłkiewicz

Publications and source records attributed to I Hawryłkiewicz.

At least 19 recordsLinked to original sources
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↗
PubMed1999

[Functional disturbances in patients with interstitial lung diseases without signs of restriction].

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.

Adrenal Cortex Hormones↗
PubMed1999

[Usefulness of CD1 expression on surfaces of cells in bronchoalveolar fluid for diagnosis of histiocytosis X--our experience].

Histiocytosis X (HX), also referred as Langerhans cell granulomatosis is a disorder characterized by the presence of destructive granulomas containing Langerhans cells, lymphocytes, eosinophils and fibroblastes in the involved organs. Three presentations are commonly observed: 1) nonproductive cough or effort dyspnea, 2) spontaneous pneumothorax 3) incidental pulmonary infiltrates on chest X-ray in asymptomatic patients. HRCT may be helpful in the initial diagnosis of pulmonary HX. HRCT scans show nodules, cysts and estimate the extent of disease. But the final diagnosis of histiocytosis X requires the histologic demonstration of specific histiocytosis X cell in biopsy specimens of the lung. The aim of this study was to define the importance of the detection of Langerhans cells in bronchoalveolar lavage fluid (BALF) for the diagnosis of HX. The searched cells express a specific CD1 antigen, recognized by the monoclonal antibody OKT-6. In our study the demonstration of more than 5% of CD1 positive cells was defined to confirm HX. We have studied the BALF in 21 patients with suspected histiocytosis X. In BALF of 4 patients more than 5% of CD1 positive cells were found. In 1 of them HX was confirmed with open lung biopsy. Two patients displayed 5% of CD1 positive cells. The final diagnosis of the first patient was hypersensitivity pneumonitis and of the second one was bronchitis chronica. In 5 patients out of 15 patients in whom less than 5% of CD1 positive cells were found histiocytosis X was histologically proven. In other 10 patients the following disorders were histologically recognised: pulmonary emphysema 3 cases, pneumoconiosis-3, LMA-BOOP-1, sarcoidosis-1 and pleuritis eosinophilica-1. The estimation of Langerhans cells in BALF can be a useful method among the diagnostic procedures for histiocytosis X. It is necessary to remember that demonstration of less than 5% of CD1 positive cells do not exclude histiocytosis X.

Adult↗
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

[Intralobar pulmonary sequestration treated surgically in a patient with sarcoidosis].

Pulmonary sequestration is an uncommon but clinically significant congenital malformation characterised by the presence of nonfunctioning lung tissue that receives its blood supply from anomalous systemic arteries and has no communication with the normal bronchial tree. We describe a patient with an intralobar pulmonary sequestration of the left lower lobe associated with sarcoidosis. The patient was treated successfully by resection of the lesion. The postoperative period was uneventful. We found no report where a pulmonary sequestration was associated with sarcoidosis.

Adrenal Cortex Hormones↗
PubMed1996

[Prognostic value of pulmonary hypertension in patients with severe COPD].

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.

Female↗
PubMed1996

[Pulmonary circulation at rest and during exercise in patients with obstructive sleep apnea before and after one year of treatment with 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.

Exercise↗
PubMed1995

[Use of nasal intermittent positive pressure ventilation in treatment of exacerbation of chronic respiratory insufficiency].

A case of a 45 year old male with COPD is presented. In the past the patient required twice mechanical ventilation. During a current hospitalization Nasal Intermittent Positive Pressure Ventilation (NIPPV) was successfully applied. The treatment was carried out continuously for 8 days, during the next 7 days for 15 hours per day, during the next 8 days only at night time. A clinical improvement was seen. NIPPV was used for a shorter period of time than the classical mechanical ventilation. It was also less expensive.

Humans↗
PubMed1994

[Pulmonary hemodynamics in obstructive sleep apnea or overlap syndrome].

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.

Adult↗
PubMed1992

[Effect of short-term home oxygen therapy on pulmonary artery pressure does not predict the survival of patients with chronic obstructive lung disease].

We wanted to verify if the acute effect of oxygen on pulmonary arterial pressure (PPA) is related to survival on LTOT as was suggested recently in the literature. We studied 46 COPD patients qualified for LTOT. The acute effects of O2 on pulmonary haemodynamics were assessed by pressure and flow measurements before and after 30 mins of O2 breathing via 28% Ventimask. Thirty nine patients reacted with a fall of the mean PPA of less than 5 mm Hg. These were termed nonresponders (NR). In seven patients mean PPA fell > 5 mm Hg. They were called responders (R). After the initial investigations patients were followed up on LTOT for 2 years or until death. During two years of LTOT 15 patients died (12 from NR and 3 from R groups). The first two years survival rate was 69% in NR and 57% in R groups respectively. We conclude that survival on LTOT is not related to the acute effect of oxygen on the pulmonary arterial pressure in COPD patients investigated in the steady-state period of the disease.

Adult↗
PubMed1991

[Unusual health improvement in a patient with pulmonary heart disease in kyphosis and scoliosis after home treatment with oxygen].

Male obese patient, aged 35 years with kyphoscoliosis due to poliomyelitis was admitted in respiratory and cardiac failure. Severe desaturations during sleep were found. After successful hospital treatment patient was submitted to the long-term oxygen therapy. Reduction of weight and smoking cessation was suggested. Patient stopped smoking, lost 14 kg in 12 months and breathed oxygen for 12 hours per day (mainly at night). Treatment resulted in a significant improvement in ventilatory reserves, blood gases and normalization of pulmonary arterial pressure.

Adult↗
PubMed1989

[Effect of steroid therapy on pulmonary circulation in pulmonary sarcoidosis].

Effect of 12 month steroid therapy on pulmonary circulation at rest and during exercise was assessed in 24 patients with histologically confirmed stage II and III pulmonary sarcoidosis. Pulmonary hypertension was found in 3 patients before starting therapy. In the remaining 21 pulmonary artery pressure was within normal limits. In 18 of these an abnormal increase of pulmonary arterial pressure during exercise was found. After 12 months of steroid therapy in all except 2 patients radiological regression was observed. In most patients pulmonary function improved. Normal pulmonary arterial pressure was found in 22 patients. An abnormal increase of pulmonary arterial pressure during exercise was seen in 12 patients. No correlation could be demonstrated between radiological evaluation, respiratory function and effect of steroids on pulmonary circulation.

Adrenal Cortex Hormones↗
PubMed1989

[Assessment of pulmonary hemodynamics in patients with idiopathic pulmonary fibrosis].

Pulmonary hemodynamics were assessed in 52 patients with idiopathic pulmonary fibrosis of which 25 were confirmed histopathologically. The study group consisted of 26 males and 26 females, of a mean age of 41 +/- 15 years. Pulmonary function studies revealed restrictive changes and increased elastic recoil. Mean vital capacity was 2.6 +/- 1.2 L, compliance - static 97 +/- 59 ml/cm H2O, dynamic 71 +/- 50 ml/cm H2O. Esophageal pressure was - 8.0 +/- 5.3 mm Hg. Mean pulmonary artery pressure was slightly elevated - 22.6 +/- 8.3 mm Hg. Transmural pulmonary pressure was 31.3 +/- 9.8 mm Hg, cardiac output was 7.6 +/- 3.8 L/min, pulmonary resistance 206 +/- 119 dyn sec cm-5. A mild hypoxemia was observed--PaO2 71.8 +/- 13.3 mm Hg. In part of the study group (27 subjects) the response to exercise was assessed. A mean increase of pulmonary artery pressure from 20.4 +/- 7.2 to 38.0 +/- 14.7 mm Hg and a decrease of PaO2 from 74.2 +/- 11.7 mm Hg to 62.5 +/- 15.3 mm Hg were found. Negative correlation was found between mean artery pulmonary pressure and arterial oxygen partial pressure, vital capacity and one-second forced expiratory volume, and a higher correlation between mean transmural pulmonary pressure and PaO2, VC, FEV1 and Cdyn.

Adolescent↗