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Biomedical subjects

A Ganassini

Publications and source records attributed to A Ganassini.

9 recordsLinked to original sources
PubMed1997

Maximal inspiratory pressure and inspiratory muscle endurance time in asthmatic children: reproducibility and relationship with pulmonary function tests.

Respiratory muscle strength, assessed by maximal inspiratory mouth pressure (PImax), and endurance, assessed as the length of time a subject could breathe against inspiratory resistance with a target mouth pressure > or = 70% of PI,max (Tlim), were measured in 20 symptomless asthmatic children, in order to assess the reproducibility of such measurements and their relationship to traditional pulmonary function tests or tests of bronchial hyperresponsiveness. After recording lung volumes and bronchial response to methacholine, PI,max and Tlim were measured twice in the same morning, with a 30-minute interval between each experimental trial. Mean (+/-SD) values of PI,max were 72.2 +/- 20.6 cmH2O in the first and 75.8 +/- 22.9 cmH2O in the second trial. Tlim was 154 +/- 65 and 164 +/- 66 seconds in the first and in the second trial respectively. A lack of agreement between different measurements was seen for both PI,max and Tlim. The coefficient of repeatability was 24.8 for PI,max and 92.3 for Tlim. A significant correlation between age and PI,max as well as between body mass index and PI,max were shown; no similar correlation was found for Tlim. No correlation was found between PI,max and Tlim in either of the two successive runs or between either PI,max or Tlim and lung volumes or bronchial response to methacholine. Our study shows that at this time the reproducibility of PI,max or Tlim in children with asthma in remission seems to be poor, although PI,max has a better reproducibility than Tlim. A standardized procedure to measure PI,max, should be obtainable in the near future. This would improve its clinical usefulness since PI,max is the only noninvasive test to assess respiratory muscle strength that can identify subjects at risk to develop respiratory muscle fatigue during an acute asthmatic attack.

Adolescent↗
PubMed1997

Pulmonary hyperinflation and ventilator-dependent patients.

Pulmonary hyperinflation is a major medical problem in patients with advanced chronic obstructive pulmonary disease (COPD) or acute asthma. The apparent beneficial effects of pulmonary hyperinflation on lung mechanics, such as an increased airway patency and lung elastic recoil, are by far overwhelmed by the deleterious effects on the pressure generating capacity of the respiratory muscles. Moreover, the ventilatory workload can be remarkably increased: 1) by the displacement of the respiratory system toward the upper, flat portion of the pressure-volume curve; 2) by the need to expand the chest wall and not only the lungs; and 3) by the intrinsic positive end-expiratory pressure (PEEPi) systematically associated with dynamic hyperinflation. In mechanically ventilated patients, the mechanisms underlying pulmonary hyperinflation as well as its pathophysiological consequences do not differ from those described in spontaneously breathing patients. However, there are some specific issues that should be taken into account, namely the effect of the endotracheal tube and the mode and setting of the ventilator. In mechanically ventilated patients, pulmonary hyperinflation increases the risk of barotrauma and may hamper weaning due to the excessive burden of PEEPi, which can even lead to ineffective inspiratory efforts. Because of its harmful consequences, pulmonary hyperinflation must be treated aggressively by pharmacological therapy and, when needed, by ventilatory treatment. The setting of the ventilator must be predetermined to ensure the longest possible time for expiration, and positive end-expiratory pressure can be applied to prevent an excessive workload for the patient and ineffective inspiratory efforts.

Airway Resistance↗
PubMed1997

Short-term regular beta 2-adrenergic agonists treatment is safe in mild asthmatics taking low doses of inhaled steroids.

Regular treatment with beta 2-adrenergic agonists is controversial in bronchial asthma. To investigate whether beta 2-adrenergic agonists can be used safely if associated with low doses of inhaled steroids, for a short period, without a deterioration of asthma control, we have examined 24 mild asthmatics. In a parallel, double-blind, placebo-controlled study, 1 week of run-in and run-out period framed 3 weeks of treatment. All patients received inhaled beclomethasone dipropionate (BDP 250 micrograms t.i.d.); after 1 week, 12 patients inhaled 400 micrograms of broxaterol and 12 patients received placebo t.i.d. FVC, FEV1, PD20-FEV1 methacholine, morning and evening PEF, and PEF amplitude % mean were measured before, during, and after treatment. No significant changes were noted in patients receiving inhaled broxaterol. There were no differences in symptoms and the use of rescue medication (salbutamol spray). We conclude that short-term regular treatment with beta 2-adrenergic agonists is not associated with a deterioration in asthma control in mild asthmatics inhaling low doses of steroids.

Administration, Inhalation↗
PubMed1997

Physiological and clinical consequences of positive end-expiratory pressure.

The aims of positive end-expiratory pressure (PEEP) are: 1) in acute lung failure, to increase lung volume and to improve oxygenation; 2) in acute exacerbation of chronic obstructive pulmonary disease (COPD), to unload inspiratory muscles. Excessive levels of PEEP may increase the risk of barotrauma. Application of low levels of PEEP may replace intrinsic PEEP in acute exacerbation of COPD, without increasing lung volume; however, the haemodynamic consequences of PEEP must be taken into account.

Acute Disease↗
PubMed1996

Aging and the respiratory system.

All the components of the respiratory system are affected by aging, though at different rates: i) the lung elastic recoil decreases; ii) PaO2 decreases and the D(A-a)O2 increases; iii) the chest wall becomes stiffer; iv) the inspiratory muscles loose strength; and v) the respiratory centres are less sensitive. Residual volume, closing volume and function residual capacity increase, whereas vital capacity and FEV1 progressively decrease. The flow volume curve becomes more convex to the volume axis at low lung volume. Whether these changes are due to aging or associated with aging is a matter of debate. However, the aging lung is more fragile in the face of respiratory and systemic diseases than the respiratory system of young adults. Nutrition, smoking habits and sleep-related disorders also affect the respiratory system. Although bronchial asthma may also appear in the elderly, chronic obstructive pulmonary disease is one of the most common respiratory diseases in advanced life and is a major cause of respiratory failure and ICU admission. Age in itself is not a risk factor of respiratory failure, but elderly patients have an increased risk of mortality for both acute respiratory failure (the failing lung), and exacerbated chronic ventilatory failure (the failing pump). Although advanced age can influence the final outcome of elderly patients from the intensive care unit (ICU), admission to the ICU as well as the institution of mechanical ventilation should not be denied on the basis of age alone, since the severity of illness, prior health status and admitting diagnosis have more weight than age in the final outcome.

Adult↗
PubMed1995

Invasive pulmonary aspergillosis complicating allergic bronchopulmonary aspergillosis.

Invasive pulmonary aspergillosis is a frequent complication in immunocompromised patients. The role of the prolonged use of steroids in predisposing to invasive aspergillosis has been recognized, but exceptionally described in asthmatic patients. We report the case of a 59-year-old woman with bronchial asthma treated with steroid therapy for a long time, who developed an invasive pulmonary aspergillosis with an unusual combination of invasive and allergic disease. It seems reasonable to think that allergic disease due to allergic bronchopulmonary aspergillosis (ABPA) preceded the terminal invasive process. Adjunctive therapy with antifungal agents in patients with ABPA is considered, since there is the risk of an invasive pulmonary aspergillosis.

Aspergillosis↗
PubMed1986

Amiodarone-induced pulmonary toxicity.

A patient with atrial premature depolarizations developed pulmonary toxicity during long-term treatment with amiodarone. The clinical features were cough and dyspnea. Pulmonary function tests showed a restrictive defect and severe impairment of gas transfer. Diffuse interstitial and intra-alveolar shadows were noted on chest X-ray. Lung specimens obtained by transbronchial biopsy showed hyperplasia of pneumocytes and widening of the alveolar septa. After discontinuation of amiodarone and institution of steroid therapy the patient improved symptomatically, and after 3 weeks the chest X-ray showed clearing of the bilateral infiltrates. The patient was never given any other antiarrhythmic drugs, had no important heart disease, and received the lowest daily dose of amiodarone reported in the literature of cases of pulmonary injury.

Amiodarone↗