American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Jun 2001
Randomized Controlled Trial Clinical TrialPhysiologic effects of negative pressure ventilation in acute exacerbation of chronic obstructive pulmonary disease.
To assess the physiologic effects of continuous negative extrathoracic pressure (CNEP), negative pressure ventilation (NPV), and negative extrathoracic end-expiratory pressure (NEEP) added to NPV in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD), we measured in seven patients ventilatory pattern, arterial blood gases, respiratory mechanics, and pressure- time product of the diaphragm (PTPdi) under four conditions: (1) spontaneous breathing (SB); (2) CNEP (-5 cm H(2)O); (3) NPV; (4) NPV plus NEEP. CNEP and NPV were provided by a microprocessor-based iron lung capable of thermistor-triggering. ⋯ NEEP added to NPV further slightly decreased PTPdi and improved patient-ventilator interaction by reducing dynamic PEEPi and nontriggering inspiratory efforts. We conclude that CNEP and NPV, provided by microprocessor-based iron lung, are able to improve ventilatory pattern and arterial blood gases, and to unload inspiratory muscles in patients with acute exacerbation of COPD.
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Am. J. Respir. Crit. Care Med. · Jun 2001
Local inflammatory responses following bronchial endotoxin instillation in humans.
To study local lung inflammation, 34 subjects had endotoxin (1-4 ng/kg) instilled into a lung segment and saline instilled into a contralateral segment followed by bronchoalveolar lavage (BAL) at 2 h, 6 h, 24 h, or 48 h. Endotoxin instillation resulted in a focal inflammatory response with a distinct time course. An early phase (2 h to 6 h) revealed an increase in neutrophils (p = 0.0001) with elevated cytokines (tumor necrosis factor [TNF]-alpha, TNF receptors [TNFR], interleukin [IL]-1beta, IL-1 receptor antagonist, IL-6, granulocyte-colony-stimulating factor [G-CSF], all p < or = 0.002, but no change in IL-10) and chemokines (IL-8, epithelial neutrophil activating protein-78, monocyte chemotactic protein-1, macrophage inflammatory protein [MIP]-1alpha, MIP-1beta, all p < or = 0.001, but no change in growth-regulated peptide-alpha). ⋯ Blood C-reactive protein, serum amyloid A, IL-6, IL-1ra, G-CSF, but not TNF-alpha increased by 8 h (all p < or = 0.008). The local pulmonary inflammatory response to endotoxin has a unique qualitative and temporal profile of inflammation compared with previous reports of intravenous endotoxin challenges. This model provides a means to investigate factors that initiate, amplify, and resolve local lung inflammation.
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Am. J. Respir. Crit. Care Med. · Jun 2001
Influence of tidal volume on alveolar recruitment. Respective role of PEEP and a recruitment maneuver.
Both reduction in tidal volume (VT) and alveolar recruitment may be important to limit ventilator-associated lung injury during mechanical ventilation of patients with the acute respiratory distress syndrome (ARDS). The aim of this study was to assess the risk of alveolar derecruitment associated with VT reduction from 10 to 6 ml/kg. Whether this VT-related derecruitment could be reversed, either by a recruitment maneuver or by an increase in positive end-expiratory pressure (PEEP) level, was also investigated. ⋯ In 10 patients, Vrec was also measured before and after a recruitment maneuver (two sustained inflations at 45 cm H(2)O), and after an increase in PEEP (by 4 cm H(2)O). Low VT-induced derecruitment was reversed by a recruitment maneuver and by increasing PEEP. We conclude that a reduction in VT could be responsible for alveolar derecruitment, which may be transiently reversed by a reexpansion maneuver or prevented by a PEEP increase above Plip.