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
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 · 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
Efficacy of noninvasive positive pressure ventilation by facial and nasal mask in hypercapnic acute respiratory failure: experience in a respiratory ward under usual care.
Noninvasive intermittent positive pressure ventilation (NIPPV) via a nasal or facial mask is an effective treatment of hypercapnic acute respiratory failure (ARF) caused by various diseases preventing endotracheal intubation (ETI) in 60-90% of patients. The technique can even be effective for routine care, using simplified ventilators, after adequate personnel training. In this study, the effectiveness, in a general respiratory ward under usual care, of NIPPV delivered by simplified ventilators via facial or nasal mask was evaluated in 40 patients with hypercapnic ARF (NIPPV group) and compared to 30 matched historical patients under conventional treatment (Conv group). ⋯ In the NIPPV group no differences were found in the admission characteristics between patients successfully and unsuccessfully ventilated, although a significant improvement was observed after 1 h, for pH from 7.31 +/- 0.058 to 7.36 +/- 0.57 and Pa,CO2 from 9.2 +/- 1.3 to 8.3 +/- 1.3 kPa in successfully ventilated patients. In patients who failed to be ventilated with NIPPV pH worsened, from 7.26 +/- 0.069 to 7.24 +/- 0.078 and Pa,CO2 from 10.0 +/- 2.1 to 11.3 +/- 2.5 kPa. In conclusion, addition of noninvasive positive pressure ventilation delivered by nasal or face mask to conventional therapy, reducing the need for endotracheal intubation, may improve the management of patients with hypercapnic acute respiratory failure as compared to conventional therapy alone, even when instituted in a respiratory ward under usual care with simplified ventilators.
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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.