Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo
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Monaldi Arch Chest Dis · Oct 1997
Randomized Controlled Trial Clinical TrialAcute 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). ⋯ 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.
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Monaldi Arch Chest Dis · Oct 1997
Case ReportsTreatment of acute respiratory failure secondary to pulmonary oedema with bi-level positive airway pressure by nasal mask.
We report the successful outcome of first-line intervention of noninvasive positive pressure ventilation (NPPV) in four patients, three of whom had hypercapnic acute respiratory failure (ARF) and one hypoxaemic ARF, secondary to pulmonary oedema. The clinical condition showed rapid improvement and the NPPV, performed together with aggressive medical treatment, was effective in decreasing the respiratory frequency, and in correcting gas exchange abnormalities within the first 3 h. ⋯ NPPV was applied, by nasal mask, using a bi-level positive airway pressure (BiPAP) delivering pressure support ventilation (PSV). We conclude that application of noninvasive positive pressure ventilation may be effective in correcting gas exchange abnormalities, in relieving respiratory distress and, perhaps, in avoiding endotracheal intubation in selected patients with acute respiratory failure secondary to reversible medical condition such as pulmonary oedema.
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Monaldi Arch Chest Dis · Oct 1997
Haemodynamic effects of ketanserin either alone or with oxygen in COPD patients with secondary pulmonary hypertension.
To indirectly test the hypothesis whether serotonin (5-HT) might have a role in the increase in pulmonary vascular resistance, we evaluated the haemodynamic and gas exchange response of intravenous ketanserin (K), a 5-HT receptor inhibitor, in eight severe but stable patients with chronic obstructive pulmonary disease with secondary pulmonary hypertension (mean pulmonary artery pressure (Ppa) 30.3 +/- 7.3 mmHg). Measurements were done at baseline, after oxygen breathing (2 L.min-1), K bolus (6-15 mg) and finally during oxygen breathing (2 L.min-1) added to K infusion (3-6 mg.h-1). K bolus induced a significant reduction of mean Ppa (p < 0.05), mean systemic arterial pressure (p < 0.01) and total systemic resistance (p < 0.01). ⋯ When we individually analysed the changes of pulmonary vascular resistances by plotting the driving pressure through the pulmonary circulation against the cardiac output, we observed that an active vasodilating effect on the pulmonary circulation occurred with K in only one patient, while in three other patients there was rather a recruitment effect of the pulmonary vessels due to the systemic effects of the drug. In conclusion, this study of a small number of patients with severe chronic obstructive pulmonary disease associated with pulmonary hypertension shows that the parenterally given serotonin antagonist ketanserin predominantly affects the systemic circulation. Our results do not support the hypothesis that in stable chronic obstructive pulmonary disease patients with pulmonary hypertension, serotonin might have a role in the increase of pulmonary vascular tone.
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Monaldi Arch Chest Dis · Aug 1997
ReviewPharmacological treatment of exertional dyspnoea in stable COPD patients.
Exertional dyspnoea is one of the most common and disabling symptoms in patients with stable chronic obstructive pulmonary disease (COPD). Because little can be done for its resolution, the idea of its symptomatic treatment is attractive. There is no gold standard for the pharmacological management of exertional dyspnoea in stable COPD. A reassessment of the available literature shows the current perspectives and limits.
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During spontaneous breathing, respiratory muscle pressure (Pmus) waveform is determined by a complex system consisting of a motor arm, a control centre and various feedback mechanisms that convey information to the control centre. In mechanically ventilated patients, the pressure delivered by the ventilator (Paw) is incorporated into the system that controls breathing and may alter Pmus, which in turn modifies the Paw waveform. Thus, the response of the patient's respiratory effort to Paw and the response of Paw to patient effort constitute the two components of the control of breathing during mechanical ventilation. ⋯ On the other hand, the response of patient effort to Paw is mediated through four feedback systems: 1) mechanical; 2) chemical; 3) reflex; and 4) behavioural. It follows that in mechanically ventilated patients the ventilatory output is determined by the interaction between the function of the ventilator and the patient's breathing control system. This interaction should be taken into account in the management of mechanically ventilated patients.