Acute respiratory distress syndrome ("ARDS"): no more than a severe acute lung injury?

Continuous Dose Furosemide as a Therapeutic Approach to Acute Respiratory Distress Syndrome (ARDS)

“…ARDS continues to be a significant clinical challenge despite all the advances made in the areas of resuscitation and monitoring of shock states [2,3]. This is the result of our inability as clinicians to correct the pathophysiology of ARDS.…”

“…In the current literature there is very little information regarding corrective approaches for the treatment of ARDS. However, there are many papers on how further iatrogenic injury can be avoided while providing supportive care [2,3,[21][22][23][24]. The first major work on the nondiuretic capacity of furosemide was performed by Ali et al [4 -9].…”

“…These ef- 1 Financial support is from Iowa Health Systems. 2 To whom correspondence should be addressed. fects of furosemide have been attributed to a direct pulmonary vasodilatation which presumably redirects blood flow away from edematous, flooded alveolar regions to nonflooded alveolar regions, thus decreasing intrapulmonary shunt and improving gas exchange [1, 4 -10, 14, 15].…”

“…These processes result in decreased pulmonary compliance, compromised gas exchange, and extensive intrapulmonary shunting with concomitant ventilation-perfusion mismatching. The current working definition is one that classifies ARDS as a continuum of injury ranging from the milder form "acute lung injury (ALI)" to the more severe form "ARDS" [2,3]. In this continuum, ALI is defined by a PO 2 /FIO 2 ratio of less than 300 and greater than or equal to 200 without clinical signs of congestive heart failure and ARDS is defined similarly with a PO 2 /FIO 2 ratio of less than 200 and no signs of congestive heart failure (or if measured, a pulmonary capillary wedge pressure of less than 18 mm Hg) [3].…”

Acute respiratory distress syndrome

“…EDITOR, - In their review of the acute respiratory distress syndrome Richard Beale and colleagues maintain that a pulmonary artery occlusion pressure of less than 18 mm Hg is required to allow differentiation between the syndrome and pulmonary oedema secondary to acute heart failure and fluid overload 1. I would caution against using a specific pulmonary artery occlusion pressure to distinguish pulmonary oedema of cardiac origin from that due to increased permeability.…”