PubMed Health⌕ Search

Biomedical subjects

D Górecka

Publications and source records attributed to D Górecka.

At least 55 records · Page 3Linked to original sources
PubMed1991

[Evaluation of the effectiveness of medical consultation regarding smoking cessation].

Smoking habits were assessed by a questionnaire in workers of a small factory during their prophylactic medical check-up. In all subjects spirometry and CO levels in expired air were determined. In the studied group 43.8% were smokers. Respiratory indices were decreased in smokers in comparison to ex- and non-smokers. In all smokers higher (3x) levels of CO were found. After a year 5 subjects ceased to smoke (15.6% of the smokers).

Adult↗
PubMed1989

The effects of mexiletine on cardiac arrhythmias in patients with cor pulmonale.

Cardiac arrhythmias (CA) are a frequent and dangerous complication of respiratory and cardiac failure in patients with chronic obstructive pulmonary disease (COPD). The aim of the study was to investigate the effects of mexiletine on CA in patients with cor pulmonale in a state of cardio-respiratory decompensation. We studied 32 COPD patients with severe airways obstruction; mean VC 2.35 +/- 0.53 litres; FEV1, 0.92 +/- 0.3 litres and respiratory failure, PaO2 = 56 +/- 5 mm Hg, PaCO2 = 47 +/- 9 mm Hg allocated by random numbers to 20 treated and 12 controls. Continuous 24-hour Holter monitoring was performed for 3 consecutive days after admission to the department following routine treatment which consisted of low-flow oxygen, antibiotic, bronchodilators and diuretics. On the first day, the type and frequency of CA were analysed. Then the treated patients were given mexiletine 250 mg i.v. + 200 mg orally followed by 200 mg every 8 h for the next 48 h. Controls continued the routine treatment only. Mexiletine treatment resulted in a highly significant reduction in the mean number of premature ventricular beats from 163 to 28 and 30/24 h, respectively (p less than 0.01). Episodes of ventricular tachycardia were abolished. The mean number of premature supraventricular beats also fell from 85 to 67 and 48/24 h (p less than 0.01). Number of episodes of sinus tachycardia fell from 17 during the first day to 13 and 10 on the 2nd and 3rd days, respectively. In the controls, the frequency and type of CA remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1989

[Pulmonary arterial pressure and the effect of short term oxygen therapy on it in patients qualified for home oxygen treatment].

Forty patients with chronic bronchitis and emphysema qualified for domiciliary oxygen treatment according to widely accepted criteria were assessed. Only two patients had normal pulmonary artery pressure. Pulmonary arterial pressure correlated well with oxygen arterial partial pressure. It seems that pulmonary hemodynamic studies are not necessary in patient qualification for domiciliary oxygen therapy. Short oxygen therapy (30 min.) produced only a small decrease of pulmonary artery pressure from 31 +/- 10 to 29 +/- 8 mm Hg. Only in 7 patients was the fall greater than 5 mm Hg. Fall of pressure in pulmonary artery produced by oxygen correlated only with initial pulmonary artery pressure and rose proportionally with increase of pressure.

Adult↗
PubMed1986

Captopril effects on pulmonary and systemic hemodynamics in chronic cor pulmonale.

A placebo-controlled single-blind study on acute effects of captopril on hypoxic pulmonary hypertension was performed in 15 patients with severe chronic obstructive lung disease recovering from right heart failure. Ten patients received active drug (25 mg captopril orally), five patients received placebo and served as control subjects. Before drug administration, there was no difference in lung function data and pulmonary hemodynamics between patients in both groups. Captopril produced highly significant fall in systemic arterial pressure. No change in breathing frequency, minute ventilation, and pulmonary gas exchange was observed. There was no significant change in studied variables after placebo. The presented data suggest that captopril does not decrease pulmonary vascular resistance in patients with hypoxic pulmonary hypertension. A fall in pulmonary wedge pressure reflects a decrease in left ventricular afterload.

Captopril↗
PubMed1983

Effects of almitrine and oxygen on ventilation and gas exchange in patients with chronic respiratory insufficiency.

Effects of a new respiratory stimulant almitrine on lung ventilation and gas exchange were studied in 15 patients suffering from chronic respiratory insufficiency. The variables examined were measured during 4 consecutive periods lasting 30 min each. During the first period initial data were collected. From the second period to the end of the investigation, oxygen, 1.5 1/min, was administered. During the third phase, almitrine was infused at a dose of 0.33 mg/kg. Administration of oxygen increased arterial oxygen tension without change in lung ventilation. Infusion of almitrine increased minute ventilation by 27%. The increase in VE was entirely due to increase in tidal volume. There was a significant rise in arterial oxygen tension and decrease in carbon dioxide tension. Hyperventilation and improvement in blood gases were still observed 30 min after the infusion was completed. It is suggested that almitrine increases minute ventilation in patients with respiratory failure receiving oxygen.

Adult↗
PubMedDate not supplied

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.

Aged↗
PubMedDate not supplied

Pulmonary haemodynamics in patients with OSAS or an overlap syndrome.

BACKGROUND: Alveolar hypoxia is the most important mechanism leading to pulmonary arterial vasoconstriction, remodelling and pulmonary hypertension. Patients with Obstructive Sleep Apnoea Syndrome (OSAS) experience multiple short periods of alveolar hypoxia during apnoeic episodes. However, the question as to whether these hypoxic episodes are responsible for the development of permanent pulmonary hypertension is still debatable. We aimed to investigate the relationship between the episodes of nocturnal desaturation and pulmonary haemodynamics in two distinct group patients: with pure OSAS or an overlap syndrome. METHODS: We studied 67 patients with severe OSAS (means: age 45+/-8 years, AHI 62+/-22, FEV1 3.6+/-0.8 L = 97+/-16% of predicted PaO2 72+/-10 mmHg, PaCO2 40+/-4 mmHg) and 17 patients with an overlap syndrome (OS), means: age 51+/-5 years, AHI 64+/-19, FEV1 1.5+/-0.7 = 43+/-16% of predicted PaO2 57+/-9 mmHg). All subjects underwent pulmonary artery catheterisation with pressure and flow recordings and an overnight full sleep study. RESULTS: On average patients with OSAS had nocturnal desaturation (mean overnight SaO2 = 87+/-5%) and normal PPA (15.8+/-4.6 mmHg). Only 11 out of 67 subjects (16%) presented with pulmonary hypertension. Patients with OS had nocturnal desaturation (mean overnight SaO2 = 80.2+/-8.5%) and mild pulmonary hypertension (PPA 24.2+/-7.4 mmHg). Only three out of 17 patients had normal pulmonary arterial pressure. CONCLUSIONS: In patients with severe OSAS, pulmonary hypertension is rare (16%) and is related best to the severity of the disease and to obesity. In OS patients diurnal pulmonary hypertension is frequent but does not correlate with the severity of nocturnal desaturation.

Adult↗