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Biomedical subjects

D Patakas

Publications and source records attributed to D Patakas.

At least 37 records · Page 2Linked to original sources
PubMed1993

Effects of extrinsic positive end-expiratory pressure on mechanically ventilated patients with chronic obstructive pulmonary disease and dynamic hyperinflation.

OBJECTIVE: To examine the circulatory and respiratory effects of extrinsic positive end-expiratory pressure (PEEPe) in patients with chronic obstructive pulmonary disease (COPD) and dynamic hyperinflation during controlled mechanical ventilation. DESIGN: Different levels of PEEPe were applied randomly in mechanically ventilated patients with COPD and dynamic hyperinflation. SETTING: Respiratory Intensive Care Unit of a University Hospital. PATIENTS: 9 patients with acute respiratory failure and dynamic hyperinflation due to acute exacerbation of COPD. INTERVENTIONS: PEEPe 35%, 58% and 86% of intrinsic PEEP (PEEPi) were applied. MEASUREMENTS AND RESULTS: Using flow-directed pulmonary artery catheters hemodynamic measurements were obtained, while simultaneously lung volumes, airflows and airway pressures were recorded. In order to estimate alveolar pressures (Palv), rapid airway occlusions during passive expiration were also performed. At no level of PEEPe were significant changes in cardiac output, gas exchange variables, dead space, airways inflation resistances and respiratory system static end-inspiratory compliance observed. At high level of PEEPe central venous, mean pulmonary arterial and pulmonary capillary wedge pressures were increased significantly. All but one patient were flow-limited during passive expiration. PEEPe 86% of PEEPi caused a significant increase in end-expiratory lung volume and total PEEP. Iso-volume pressure-flow curves showed volume-dependence expiratory flow limitation in 2 patients, while in 8 patients volume-dependence of critical driving pressure (Palv-mouth pressure) that decreased flows was also observed. CONCLUSIONS: The effects of PEEPe on iso-volume flow and hence on lung mechanics and hemodynamics, depend on many factors, such as airways resistances, lung volumes and airway characteristics, making the patient response to PEEPe unpredictable.

Aged↗
PubMed1993

Buspirone effect on breathlessness and exercise performance in patients with chronic obstructive pulmonary disease.

Buspirone is an anxiolytic agent that appears to have no sedative effects. The aim of this study was to assess the effects of buspirone on breathlessness and exercise tolerance in patients with chronic airway obstruction. Sixteen patients, age 56.9 +/- 17.0; forced expiratory volume in 1 s (FEV1) 1.15 +/- 0.42 l; FEV1/forced vital capacity (FVC) 50.7 +/- 15.0%; PaCO2 42.2 +/- 5.5 mm Hg; and PaO2 57.6 +/- 10 mm Hg, underwent a 6-min walking test, an incremental cycle ergometer test, an incremental treadmill walking test with self-assessment of dyspnea on Borg's scale during exercise and an assessment of respiratory drive (P 0.1), timing [inspiration time (TI)/total breathing time (Ttot)], PaO2, PaCO2, FVC, FEV1, following oral administration for 14 days of placebo or buspirone (20 mg daily) in a double-blind, cross-over randomized way. We also used the symptom check list-90-R for the assessment of subjective complaints and symptomatic behavior. A significant improvement in anxiety, depression and obsessive symptoms and complaints was noted after buspirone treatment. The P 0.1, TI/Ttot, arterial blood gases and respiratory mechanics did not change after drug treatment. There was an improvement in exercise tolerance and in the sensation of dyspnea during the buspirone period. Thus, as given in this study, oral buspirone has therapeutic potential in the treatment of dyspnea in patients with chronic lung disease.

Adult↗
PubMed1992

Respiratory short-term poststimulus potentiation (after-discharge) in patients with obstructive sleep apnea.

In conscious normal humans after a brief hypoxic ventilatory stimulus, ventilation slowly decays to baseline and does not undershoot though the subjects are hyperoxic and hypocapnic. This phenomenon is attributed to short-term poststimulus potentiation (STP), which may be an important factor promoting ventilatory stability by preventing periodic breathing. It has been proposed that obstructive sleep apnea (OSA) is a variant of periodic breathing, with obstruction occurring when ventilatory drive is low. If this were the case, patients with OSA might have reduced STP. To test this, seven normal adults and 12 patients with OSA (mean apnea index, 52.4 +/- 6.9 SE events/h) were studied. Ventilation (VI) was measured in awake seated subjects during 30 to 45 s of exposure to hypoxia (end-tidal O2: 50 mm Hg) followed by hyperoxia. A total of 57 hypoxic-hyperoxic runs were analyzed (36 in the patients and 21 in the normal subjects). During hypoxia VI increased and end-tidal CO2 decreased by similar amounts in both groups. In normal subjects after hypoxia there was a gradual decay in VI to prehypoxic levels without an undershoot. In patients, there was on average a ventilatory undershoot at 35 s of hyperoxia, with a mean VI of 83% of baseline. The undershoot was due mainly to a decrease in tidal volume, which was significantly lower than that of the normal subjects for several seconds. These changes were particularly prominent in seven patients who were not different from the others in terms of baseline characteristics, hypoxic responses, and OSA severity.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1991

Nocturnal hypoxia in unilateral diaphragmatic paralysis.

Pulmonary function has been studied extensively in patients with unilateral diaphragmatic paralysis (UDP), but there is scarce information regarding the respiratory function during sleep in this condition. We therefore studied pulmonary function in 12 patients with UDP when awake and when asleep. Diaphragmatic dysfunction was confirmed by the demonstration of low maximal transdiaphragmatic pressures in most of our patients; paradoxical gastric pressure swing was observed in 6 patients. There was a restrictive pattern in pulmonary function tests and resting arterial blood gases were rather well preserved (range SaO2 90-95%). Overnight sleep monitoring showed that the time spent in REM sleep and stage 3 and 4 sleep was reduced. The mean maximum decrease in SaO2 was 15.2 +/- 6.2% and the time with an SaO2 drop of more than 5% of the awake SaO2 was 25.4 +/- 22.8 min. None of our patients was in respiratory failure or had clinical evidence of cor pulmonale. We conclude that UDP leads to significant nocturnal hypoxemia but, in the absence of systemic lung disease, does not lead to chronic respiratory failure and cor pulmonale.

Adult↗
PubMed1990

Comparison of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep in patients with chronic obstructive lung disease.

The effects of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep were compared in six patients with chronic obstructive lung disease and carbon dioxide retention. Patients received 1.5 mg/kg almitrine (a peripheral chemoreceptor stimulant), 100 mg of medroxyprogesterone (a central respiratory stimulant), or matched placebo daily for 15 days in random order in a crossover trial. When subjects were awake almitrine increased the ventilatory response to hypoxia and increased arterial oxygen tension (PaO2) to a greater extent than medroxyprogesterone, whereas medroxyprogesterone augmented the ventilatory response to hypercapnia and decreased arterial carbon dioxide tension (PaCO2) to a greater extent than almitrine. Neither drug influenced sleep architecture significantly, except that medroxyprogesterone increased the number of arousals. Almitrine had a more favourable effect than placebo on oxygenation as estimated from arterial oxygen saturation (SaO2) during the different stages of sleep, the number of episodes of hypoxaemia, and the amount of time that SaO2 was below 80%. The only change with medroxyprogesterone by comparison with placebo was a decrease in the number of hypoxaemic episodes. It is concluded that both active drugs improved blood gases during wakefulness, but that 1.5 mg/kg of almitrine is superior to 100 mg of medroxyprogesterone in improving SaO2 during sleep.

Almitrine↗
PubMed1988

Effects of captopril in patients with chronic obstructive pulmonary disease and secondary pulmonary hypertension.

Ten patients with chronic obstructive pulmonary disease (COPD) with normal left ventricular function were given a single dose of captopril (0.25 mg/kg). Mean systemic arterial pressure, heart rate and coronary flow to the right ventricle were reduced significantly after captopril. In contrast captopril did not cause a significant fall in pulmonary arterial pressure or pulmonary vascular resistance. We conclude that captopril fails to produce haemodynamic benefits in such hypoxic patients and that angiotensin II is not playing a significant role in maintaining pulmonary vasoconstriction.

Aged↗
PubMed1988

Intermittent and continuous salbutamol rotacaps inhalation in asthmatic patients.

We studied 18 asthmatic patients over an 8-week period. Each patient received for 4 weeks continuous and for 4 weeks intermittent salbutamol rotacaps (400 micrograms) using a double-crossover technique. No significant differences were found between the two treatment regimens as judged by daily card scores and daily PEFR (both a.m and p.m.). Lung Function tests performed monthly in the hospital showed no significant differences between two treatments or the development of bronchial beta-adrenoreceptor resistance.

Administration, Inhalation↗
PubMed1987

Nifedipine treatment of patients with bronchial asthma.

Nifedipine, 30 mg/day for 4 weeks, was compared to placebo in a double-blind, randomized, crossover study, as an additional drug added to the usual treatment of 14 patients with bronchial asthma. Nifedipine did not significantly change peak expiratory flow rates or subjective symptoms like cough, sputum, wheezing, shortness of breath, or disturbed sleep. Nifedipine did not decrease the number of salbutamol rotacaps inhaled per day. Arterial blood pressure significantly decreased (p less than 0.01) after nifedipine treatment, and side effects (headache and flushing) were not uncommon. In this study, long-term treatment with nifedipine had essentially no effect on subjective symptoms at peak expiratory flow rates.

Adult↗
PubMed1987

Almitrine effect on nocturnal hypoxaemia in patients with chronic obstructive pulmonary disease (COPD).

Almitrine bismesylate (A) is a peripheral chemoreceptor agonist that increases ventilation, improves V/Q matching, increases PaO2 and decreases PaCO2 in patients with COPD. We have used a placebo-controlled double-blind cross-over study to compare the effect of 1.5 mg.kg-1 A and placebo (P) (given orally twice a day for 14 days with a 2 wk wash-out period between) on sleep quality, blood oxygenation during sleep and the ventilatory response to hypoxia and hypercapnia when awake. We have measured ear oxygen saturation (SaO2) and EEG sleep stages during nocturnal sleep in 13 patients with COPD (FEV1 0.94 +/- 0.31 1). When awake and during P period PaO2 was 51.4 +/- 10.7 mmHg (SD), PaCO2 53.1 +/- 7.1 mmHg and SaO2: 83.1 +/- 8.0%: during A treatment PaO2 increased to 55.8 +/- 7.8 mmHg (p less than 0.01 paired Wilcoxon test), PaCO2 decreased to 48.5 +/- 6.4 mmHg (p less than 0.05) and SaO2 increased to 86.9 +/- 2.6 (p less than 0.01). A reduced nocturnal hypoxaemia: 1) during P treatment mean stage I SaO2 was 73.2 +/- 13.2%, stage II 70.5 +/- 15.7%, stage III 66.5 +/- 18.5%, stage IV 73.3 +/- 12.7% and rapid eye movement (REM) sleep 59.2 +/- 14.8%; the corresponding SaO2 values during A treatment were higher: stage I SaO2 80.6 +/- 5.2% (p less than 0.05), II 78.6 +/- 6.2% (p less than 0.01), III 77.3 +/- 7.4% (p less than 0.01), IV 80.4 +/- 3.8% (p less than 0.05), REM 69.9 +/- 7.9% (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1984

Cerebral blood flow, oxygen, carbon dioxide tensions, and blood bicarbonate in controlling drive and timing in patients with chronic obstructive pulmonary diseases.

In patients with chronic obstructive pulmonary disease, respiratory drive as estimated from occlusion pressures (PO.1 and PO.1/PCO2, cm H2O/mm Hg) and respiratory timing (T1, T1/TTOT) were predicted accurately by multiple regression analysis from the respiratory parameters PO2, PCO2, and blood HCO3 in conjunction with estimates of cerebral blood flow. We used four linear models to obtain essentially the same multiple correlation coefficient, indicating that these independent variables are all important factors in controlling both the drive and timing of respiration.

Adult↗
PubMed1984

Pulmonary hypertension and respiratory failure in the development of right ventricular hypertrophy in patients with chronic obstructive airway disease.

The high incidence of right ventricular hypertrophy in patients with chronic obstructive pulmonary disease is a well-known fact. In clinical medicine according to our present status of thinking, severe impairment of ventilatory function and pulmonary hypertension are the two essential prerequisites for right ventricular involvement. To investigate this accepted assumption we studied 51 patients with chronic obstructive pulmonary disease, while they were in a remission period. The patients were subjected to clinical examination, chest roentgenography, spirometry, blood gas examination, electrocardiography, vectorcardiography, echocardiography, and right heart catheterization. The majority of the patients with significantly compromised ventilatory function and abnormal blood gases had right ventricular hypertrophy with elevation of the pulmonary artery pressure. Two subgroups of patients could be distinguished: One included 15 patients (29.4% of all patients) with normal pulmonary artery pressure and evidence of right ventricular hypertrophy. In this subgroup are included 10 patients (19.6% of all patients) showing mild ventilatory impairment and mild hypoxaemia. The second subgroup consisted of 5 patients (9.8% of all patients) with elevated mean pulmonary artery pressure at rest and right ventricular hypertrophy showing relatively mild ventilatory impairment and moderate hypoxaemia. Two conclusions could be drawn: (1) the pulmonary artery pressure at rest could be normal despite the evidence of right ventricular hypertrophy, and (2) a mild ventilatory impairment does not exclude an elevated pulmonary artery pressure or the development of right ventricular hypertrophy in patients with chronic obstructive pulmonary disease.

Aged↗
PubMed1983

Nifedipine in bronchial asthma.

In 11 patients with bronchial asthma and regular overnight falls in PEFR of greater than 15%, we demonstrated significant bronchodilation restricted only to large airways after the administration of a single dose of 10 mg of nifedipine. A statistically significant increase in PEFR, SGaw, and FEV1 was noticed at 1 and especially 2 hr after nifedipine administration. During 4 days of nifedipine treatment (10 mg t.i.d.), the overnight fall in mean PEFR was statistically significant (p less than 0.02) and less than the mean fall of PEFR during the 4 days of placebo treatment. Thus nifedipine does modify the basal bronchial tone of patients with asthma and diminishes the circadian swing of airway resistance.

Adult↗
PubMed1983

Beta-blockers in bronchial asthma: effect of propranolol and pindolol on large and small airways.

In 11 asthmatic subjects the relative magnitude and the site of airway bronchoconstriction were compared after the oral administration of 40 mg of propranolol and 2.5 mg of pindolol and the magnitude and site of bronchodilation produced by 0.5 mg subcutaneous terbutaline were tested after pretreatment with propranolol and pindolol. Specific airway conductance (sGaw) and peak expiratory flow rate (PEFR), both believed to reflect changes in large airways, and capacity isoflow (Ciso-v) and delta Vmax50, both believed to reflect changes in small airways, were determined before and after administration of placebo, pindolol, and propranolol. Treatments were given double blind and in random order. After the administration of propranolol we noted a significant bronchoconstrictive effect in the large airways (mean values of PEFR and sGaw, expressed as percentages of control values, decreased by 87.4% +/- 13.2% and 43.3% +/- 8.9%) and in the small airways (mean value of Ciso-v increased by 20.6% +/- 4.7% and that of delta Vmax50 decreased by 50% +/- 11.9% of control). By contrast, pindolol produced no significant effect on sGaw or PEFR but the tests of small airway function showed significant bronchoconstriction (mean values of Ciso-v increased by 12.9% +/- 2.6% and those of delta Vmax50 decreased by 47.2% +/- 9.2%). This action makes pindolol potentially dangerous in asthmatic patients. The bronchodilator action of terbutaline on large airways is diminished after the use of both propranolol and pindolol.

Adult↗
PubMed1983

Bronchodilatory effect of inhaled versus oral salbutamol in bronchial asthma.

The bronchodilator effect of salbutamol inhalation was compared with the oral administration of the drug in 10 patients with bronchial asthma. The study consisted of treating each patient for 4 consecutive days with: (1) a combined regimen consisting of a 2-mg tablet of salbutamol and 10 puffs of salbutamol inhalation (100 micrograms in each puff) given in pairs of two puffs every 20 min (regimen 1); (2) salbutamol inhalation (regimen 2); (3) salbutamol tablet (regimen 3), and (4) placebo, tablet and inhalation (regimen 4). The bronchodilator effect was assessed measuring the forced expiratory volume in 1 s, the forced vital capacity and the peak expiratory flow rate. The bronchodilator response was significantly greater on the inhalation alone and the combined regimen than on the oral and placebo regimens. The combined regimen showed a better although not significant bronchodilatory response than the inhalation regimen. We conclude that the inhalation treatment with salbutamol is superior to the oral route of administration in treating bronchial asthma and that the oral treatment has an added effect.

Administration, Oral↗
PubMed1982

Reduced baroreceptor sensitivity in patients with chronic obstructive pulmonary disease.

Baroreceptor sensitivity, reflected by the slope of the linear regression of the electrocardiographic R-R interval on the rise of systolic blood pressure after injection of phenylephrine, was significantly lower in 27 patients with chronic obstructive pulmonary disease (4.67 +/- 2.67) than in 10 normal subjects (12.07 +/- 3.3) of comparable age (p less than 0.001). In 20 patients in whom right heart catheterisation was performed, pulmonary artery pressure was inversely related to baroreflex sensitivity (r = - 0.603, p less than 0.01). Independent variables such as arterial Po2, Pco2, and mean pulmonary artery pressure were examined in order to assess their ability to predict baroreflex sensitivity. The independent variable that made the most significant contribution was mean pulmonary artery pressure. It seems that the attenuation of baroreflex response in patients with chronic obstructive pulmonary disease is caused mainly by pulmonary hypertension and partly by the central effects of hypoxia and hypercapnia.

Aged↗
PubMed1982

Vectorcardiographic and hemodynamic correlation in chronic obstructive pulmonary disease.

Vectorcardiograms in 34 patients with chronic obstructive pulmonary disease and 30 normal people were analyzed with the aim of developing sensitive criteria for the detection of pulmonary artery hypertension. The pulmonary artery pressure was correlated with the known vectorcardiographic measurements of the area of the QRS loop and with two new linear measurements which reflect the QRS loop displacement of the right ventricular hypertrophy. The proposed linear vector-cardiographic and the QRS loop area criteria provided a sensitive means for the noninvasive approximate estimation of mean pulmonary artery pressure in patients with chronic obstructive pulmonary disease. Their sensitivity and specificity were proved to be considerable.

Adult↗
PubMed1981

Concomitant presence of left anterior hemiblock and inferior myocardial infarction: electrocardiographic recognition of each entity.

The ECGs of 72 patients with an unequivocal vectorcardiographic diagnosis of either left anterior hemiblock (LAH) or inferior myocardial infarction (IMI) or both were reviewed. Our intention was to identify definite electrocardiographic criteria for the diagnosis of the left anterior hemiblock and of inferior myocardial infarction when both were present vectorcardiographically. All patients with left anterior hemiblock, accompanied or not by IMI, had a left axis deviation, a negative terminal deflection (S wave) in leads II, III and a VF; the majority of them also had a terminal r wave in lead a VR (50 of 52, 96%). The diagnosis of LAH was therefore always possible in the concomitant presence of both entities. A negative initial deflection (Q wave) significant in size or not significant was present in a minority of patients with both LAH and IMI (9 of 24, 37.5% in lead II; 7 of 24, 25% in lead III; and 12 of 24, 50% in lead aVF). In the patients with insignificant Q waves, as well as in the rest of the patients with rS configuration, the electrocardiographic diagnosis of IMI was not possible due to the concomitant presence of LAH.

Adult↗