Abstract
Since its first description in 1967 (1), acute respiratory distress syndrome (ARDS) represents a well known major clinical problem in intensive care units (ICUs), carrying a high morbidity and mortality. Differentiating between hydrostatic or cardiogenic pulmonary edema (CPE) and ARDS is challenging, especially in the early stages of illness (2). This diagnostic task becomes more difficult in older patients, where a higher number of morbidities often coexists. Moreover, in septic patients with ARDS, the myocardium is dysfunctional due to systemic inflammatory activation and mitochondrial impairment, and sepsis related cardiomyopathy (3) is a recognized cause of left ventricular failure and of an increase in hydrostatic extravascular lung water and CPE.
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