Do inhaled vasodilators in ARDS make a difference?

Inhaled vasodilators have a compelling physiologic rationale in the management of critically ill patients with acute respiratory distress syndrome (ARDS). Accordingly, early preclinical and clinical observational studies suggested that inhaled nitric oxide (NO) could substantially improve arterial oxygenation. Other laboratory investigations reported additional benefits of NO on platelet and leukocyte function. These collective findings inspired several randomized clinical trials and systematic reviews. These trials, however, do not support a role for inhaled NO in the routine management of patients with acute lung injury and ARDS. In fact, meta-analyses suggest this approach to patient care is more likely to cause harm through increased renal failure and possibly mortality. For intensive care clinicians, there are now sufficient data-in quantity and quality-to suggest that inhaled NO should not be used in the routine management of patients with ARDS. Using the same physiologic rationale as for inhaled NO in ARDS, investigators have also tested the role for inhaled prostaglandins, reporting improved oxygenation in some studies. Direct comparisons of nebulized epoprostenol and inhaled NO have generally reported similar clinical effects between the two agents. Whether or not inhaled vasodilator therapy can make a difference in the setting of severe, life-threatening refractory hypoxemia is uncertain but any potential benefit should be weighed against the risk for extrapulmonary side effects such as renal failure, and its high cost.