Non-invasive mechanical ventilation has been increasingly used to avoid or serve as an alternative to intubation. Compared with medical therapy, and in some instances with invasive mechanical ventilation, it improves survival and reduces complications in selected patients with acute respiratory failure. The main indications are exacerbation of chronic obstructive pulmonary disease, cardiogenic pulmonary oedema, pulmonary infiltrates in immunocompromised patients, and weaning of previously intubated stable patients with chronic obstructive pulmonary disease. Furthermore, this technique can be used in postoperative patients or those with neurological diseases, to palliate symptoms in terminally ill patients, or to help with bronchoscopy; however further studies are needed in these situations before it can be regarded as first-line treatment. Non-invasive ventilation implemented as an alternative to intubation should be provided in an intensive care or high-dependency unit. When used to prevent intubation in otherwise stable patients it can be safely administered in an adequately staffed and monitored ward.
Continuous epoprostenol therapy improves exercise capacity and cardiopulmonary hemodynamics in patients with pulmonary hypertension due to the scleroderma spectrum of disease.
Noninvasive positive-pressure ventilation does not prevent the need for reintubation or reduce mortality in unselected patients who have respiratory failure after extubation.
Recent studies suggest that noninvasive positive pressure ventilation (NPPV) administered by nasal or oronasal mask avoids the need for endotracheal intubation, rapidly improves vital signs, gas exchange, and sense of dyspnea, and may reduce mortality in selected patients with acute respiratory failure, but few controlled trials have been done. The present study used a randomized prospective design to evaluate the possible benefits of NPPV plus standard therapy versus standard therapy alone in patients with acute respiratory failure. Patients to receive NPPV were comfortably fitted with a standard nasal mask connected to a BiPAP ventilatory assist device (Respironics, Inc., Murrysville, PA) in the patient flow-triggered/time-triggered (S/T) mode, and standard therapy consisted of all other treatments deemed necessary by the primary physician, including endotracheal intubation. The need for intubation was reduced from 73% in the standard therapy group (11 of 15 patients) to 31% in the NPPV group (5 of 16 patients, p < 0.05). Among chronic obstructive pulmonary disease (COPD) patients, the reduction was even more striking, with 8 of 12 (67%) control patients requiring intubation compared with 1 of 11 (9%) NPPV patients (p < 0.05). Heart and respiratory rates were significantly lower in the NPPV group than in control patients within 1 h, and PaO2 was significantly improved in the NPPV group for the first 6 h. Dyspnea scores and maximal inspiratory pressures were better in the NPPV than in control patients at 6 h, and nurses and therapists spent similar amounts of time at the bedside for both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Quetiapine added to as-needed haloperidol results in faster delirium resolution, less agitation, and a greater rate of transfer to home or rehabilitation. Future studies should evaluate the effect of quetiapine on mortality, resource utilization, post-intensive care unit cognition, and dependency after discharge in a broader group of patients.
Sitaxsentan may benefit patients with pulmonary arterial hypertension by blocking the vasoconstrictor effects of endothelin-A while maintaining the vasodilator/clearance functions of endothelin-B receptors. Patients with pulmonary arterial hypertension that was idiopathic, related to connective tissue disease or congenital heart disease, were randomized to receive placebo (n = 60), sitaxsentan 100 mg (n = 55), or sitaxsentan 300 mg (n = 63) orally once daily for 12 weeks. The primary endpoint was change in peak VO(2) at Week 12. Secondary endpoints included 6-minute walk, New York Heart Association class, VO(2) at anaerobic threshold, VE per carbon dioxide production at anaerobic threshold, hemodynamics, quality of life, and time to clinical worsening. Although the 300-mg group increased peak VO(2) compared with placebo (+3.1%, p < 0.01), none of the other endpoints derived from cardiopulmonary exercise testing were met. However, both the 100-mg dose and the 300-mg dose, compared with placebo, increased 6-minute walk distance (100 mg: +35 m, p < 0.01; 300 mg: +33 m, p < 0.01); functional class, cardiac index, and pulmonary vascular resistance also improved (p < 0.02 for each parameter at both doses). The incidence of elevated aminotransferase values (> three times normal) was 3% for the placebo group, 0% for the 100-mg group, and 10% for the 300-mg group.
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