Sigh in supine and prone position during acute respiratory distress syndrome

Interventions aimed at recruiting the lung of patients with acute respiratory distress syndrome (ARDS) are not uniformly effective. Because the prone position increases homogeneity of inflation of the lung, we reasoned that it might enhance its potential for recruitment. We ventilated 10 patients with early ARDS (PaO2/FIO2, 121 +/- 46 mm Hg; positive end-expiratory pressure, 14 +/- 3 cm H2O) in supine and prone, with and without the addition of three consecutive "sighs" per minute to recruit the lung. Inspired oxygen fraction, positive end-expiratory pressure, and minute ventilation were kept constant. Sighs increased PaO2 in both supine and prone (p < 0.01). The highest values of PaO2 (192 +/- 41 mm Hg) and end-expiratory lung volume (1840 +/- 790 ml) occurred with the addition of sighs in prone and remained significantly elevated 1 hour after discontinuation of the sighs. The increase in PaO2 associated with the sighs, both in supine and prone, correlated linearly with the respective increase of end-expiratory lung volume (r = 0.82, p < 0.001). We conclude that adding a recruitment maneuver such as cyclical sighs during ventilation in the prone position may provide optimal lung recruitment in the early stage of ARDS

‘No Time to be Lost!’: Ethical Considerations on Consent for Inclusion in Emergency Pharmacological Research in Severe Traumatic Brain Injury in the European Union

Severe Traumatic Brain Injury (TBI) remains a major cause of death and disability afflicting mostly young adult males and elderly people, resulting in high economic costs to society. Therapeutic approaches focus on reducing the risk on secondary brain injury. Specific ethical issues pertaining in clinical testing of pharmacological neuroprotective agents in TBI include the emergency nature of the research, the incapacity of the patients to informed consent before inclusion, short therapeutic time windows, and a risk-benefit ratio based on concept that in relation to the severity of the trauma, significant adverse side effects may be acceptable for possible beneficial treatments. Randomized controlled phase III trials investigating the safety and efficacy of agents in TBI with promising benefit, conducted in acute emergency situations with short therapeutic time windows, should allow randomization under deferred consent or waiver of consent. Making progress in knowledge of treatment in acute neurological and other intensive care conditions is only possible if national regulations and legislations allow waiver of consent or deferred consent for clinical trials

Sildenafil attenuates pulmonary arterial pressure but does not improve oxygenation during ARDS

OBJECTIVE: Pulmonary hypertension is a characteristic feature of acute respiratory distress syndrome (ARDS) and contributes to mortality. Administration of sildenafil in ambulatory patients with pulmonary hypertension improves oxygenation and ameliorates pulmonary hypertension. Our aim was to determine whether sildenafil is beneficial for patients with ARDS. DESIGN: Prospective, open-label, multicenter, interventional cohort study. SETTING: Medical-surgical ICU of two university hospitals. PATIENTS: Ten consecutive patients meeting the NAECC criteria for ARDS. INTERVENTIONS: A single dose of 50 mg sildenafil citrate administered via a nasogastric tube. MAIN RESULTS: Administration of sildenafil in patients with ARDS decreased mean pulmonary arterial pressure from 25 to 22 mmHg (P = 0.022) and pulmonary artery occlusion pressure from 16 to 13 mmHg (P = 0.049). Systemic mean arterial pressures were markedly decreased from 81 to 75 mmHg (P = 0.005). Sildenafil did not improve pulmonary arterial oxygen tension, but resulted in a further increase in the shunt fraction. CONCLUSION: Although sildenafil reduced pulmonary arterial pressures during ARDS, the increased shunt fraction and decreased arterial oxygenation render it unsuitable for the treatment of patients with ARD

The effects of pressurization rate on breathing pattern, work of breathing, gas exchange and patient comfort in pressure support ventilation.

BACKGROUND: Although placing patients with acute respiratory failure in a prone (face down) position improves their oxygenation 60 to 70 percent of the time, the effect on survival is not known. METHODS: In a multicenter, randomized trial, we compared conventional treatment (in the supine position) of patients with acute lung injury or the acute respiratory distress syndrome with a predefined strategy of placing patients in a prone position for six or more hours daily for 10 days. We enrolled 304 patients, 152 in each group. RESULTS: The mortality rate was 23.0 percent during the 10-day study period, 49.3 percent at the time of discharge from the intensive care unit, and 60.5 percent at 6 months. The relative risk of death in the prone group as compared with the supine group was 0.84 at the end of the study period (95 percent confidence interval, 0.56 to 1.27), 1.05 at the time of discharge from the intensive care unit (95 percent confidence interval, 0.84 to 1.32), and 1.06 at six months (95 percent confidence interval, 0.88 to 1.28). During the study period the mean (+/-SD) increase in the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen, measured each morning while patients were supine, was greater in the prone than the supine group (63.0+/-66.8 vs. 44.6+/-68.2, P=0.02). The incidence of complications related to positioning (such as pressure sores and accidental extubation) was similar in the two groups. CONCLUSIONS: Although placing patients with acute respiratory failure in a prone position improves their oxygenation, it does not improve surviva

Sigh in supine and prone position during acute respiratory distress syndrome.

Interventions aimed at recruiting the lung of patients with acute respiratory distress syndrome (ARDS) are not uniformly effective. Because the prone position increases homogeneity of inflation of the lung, we reasoned that it might enhance its potential for recruitment. We ventilated 10 patients with early ARDS (PaO2/FIO2, 121 +/- 46 mm Hg; positive end-expiratory pressure, 14 +/- 3 cm H2O) in supine and prone, with and without the addition of three consecutive "sighs" per minute to recruit the lung. Inspired oxygen fraction, positive end-expiratory pressure, and minute ventilation were kept constant. Sighs increased PaO2 in both supine and prone (p < 0.01). The highest values of PaO2 (192 +/- 41 mm Hg) and end-expiratory lung volume (1840 +/- 790 ml) occurred with the addition of sighs in prone and remained significantly elevated 1 hour after discontinuation of the sighs. The increase in PaO2 associated with the sighs, both in supine and prone, correlated linearly with the respective increase of end-expiratory lung volume (r = 0.82, p < 0.001). We conclude that adding a recruitment maneuver such as cyclical sighs during ventilation in the prone position may provide optimal lung recruitment in the early stage of ARDS

I CASE REPORTS Sildenafil Can Increase the Response to Inhaled Nitric Oxide

INHALED nitric oxide (NO) reduces pulmonary artery pressure and increases arterial oxygen tension (Pao2) in many patients with pulmonary hypertension&apos;,* and acute respiratory failure.&apos; Not all patients, however, manifest an equally effective r e~p o n s e ,~ and investigators have sought to enhance the physiologic effects of inhaled NO.5 One possible strategy is to increase the availability of cyclic guanosine monophosphate (cGMP), an intracellular messenger of NO, by blocking its degradation by cGMP-specific phosphodiesterase (PDE-5). Dipyridamole, a PDE-5 inhibitor, has been used in combination with inhaled NO to decrease pulmonary artery pressure in patients with pulmonary hypertension of various etiologies.&quot;~&apos; However, the results of these small series have been inconsistent, possibly because of the multiple pharmacologic actions of this drug. &apos; Sildenafil is a newer PDE-5 inhibitor used in the management of erectile dysfunction&quot; that acts by increasing the local availability of endogenous NO. Sildenafil has a higher PDE-5 selectivity than dipyridamole and a predict- [email protected] able gastrointestinal absorption,9 which make it an attractive complement to inhaled NO for the management of acute pulmonary hypertension in critically ill patients. Rather than simply adding the effect of a second vasodilator, sildenafil may enhance the selective pulmonary vasodilator effect of inhaled NO by making more messenger cGMP available locally. For example, the administration of sildenafil was recently reported to attenuate the acute pullnonary hypertension associated with the withdrawal of inhaled NO in two infants treated for pulmonary hypertension. lo We report the case of a patient with severe hypoxemia caused by pulmonary hypertension and venous blood shunting through a patent foramen ovale (PFO) that was reversed using inhaled NO in association with systemic sildenafil administration. Case Report A 52-yr-old woman with severe interstitial piilmonary fibrosis, Crohn disease, and previous pulmonary thromboembolism developed acute respiratory failure while being evaluated for a living related-donor lung transplant. The likely cause of her exacerbation was infectious. Chest radiograms showed her chronic diffuse pattern of pulmonary infiltrates and a new parenchymal consolidation iit the right lung base. Gram stains of bronchial secretions showed abundant neutrophils without predominant organisms. She was administered broad-spectrum antibiotics, her trachea was intubated, and mechanical ventilation was begun. A norepinephrine infusion (1-3 pg/min) was used to treat hypotension. Pulmonaiy artery (PA) catheterization revealed a niran PA pressure of 50 mmHg, a cardiac output of 4.8 I/min with a stroke volume of 47 ml, a pulmonary artery occlusion pressure of 14 nimHg, and a central venous pressure of 9 mmHg. An echocardiogram showed normal left ventricular function, mild right ventricular (RV) dilation, mild tricuspid regurgitation, and a PFO. The latter was not present in a study performed a year earlier, when the systolic RV pressure had been estimated at 41 mmHg. To confirm the presence of a hemodynamically significant shunt, an indocyanine dilution study was performed, which showed a pattern of early dye recirculation compatible with a right-to-left intracardiac shunt