Hemodynamics and Therapy in Ards

Abstract

ARDS patients suffer from diffuse injury of the pulmonary microvasculature with increased permeability to plasma proteins. A definitive diagnosis of ARDS requires evidence of the following:

• a) increased venous admixture $({\rm{e}}{\rm{.g}}{\rm{.,\dot QS/\dot QT > 30}}\% {\rm{ or P}}_a {\rm{O}}_2 /{\rm{F}}_{{\rm{I }}} {\rm{O}}_2 < 250);$

• b) acute bilateral diffuse radiographic infiltrates;

• c) an appropriate cause (see Table 1, not pulmonary embolism, atelectasis or congestive heart failure). Many clinicians lump diffuse pneumonia (bacterial, viral etc.) in the ARDS group. Sepsis syndrome and post-traumatic ARDS account for over half the ARDS patients in our ICU;

• d) a pulmonary capillary wedge pressure of less than 18 mmHg. Thus a Swan-Ganz catheter is necessary to make a definitive diagnosis (unless an LA line is present). Congestive heart failure and ARDS may be coincident. The precise causes for the development of ARDS in man are poorly understood and despite advanced supportive treatment with mechanical ventilation, diuretics and other pharmacological therapies to improve organ function, more than half of all ARDS patients will die (1).