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Hemodynamic Monitoring

General Principles/Strategies

In most patients, ARDS is part of an early and generalized systemic inflammation that is responsible for hemodynamic dysfunction. While conservative fluid management in later ARDS is associated with improved outcomes, optimal fluid management in this early period remains unclear. Methods of hemodynamic optimization and fluid management which account for dynamic changes over time are most likely to have a positive impact on patient outcomes. The risks associated with excessive fluid administration have led to development of strategies to assess “fluid responsiveness” before performing volume expansion. In principle, the only reason to administer fluid is to increase stroke volume (SV); if SV does not increase, fluid administration serves no rational purpose and is likely to be harmful [43]. Studies in heterogeneous groups of critically ill and injured patients have consistently demonstrated that only about 50% of hemodynamically unstable patients are fluid responsive, that is, their SV will increase by greater than 10-15% following a fluid bolus [44, 45]. These considerations suggest that determining whether a patient is fluid responsive as well as determining the patient’s “position” on his or her Frank-Starling curve should occur prior to each fluid bolus. According to the Frank-Starling principle, as the preload increases, left ventricular SV increases until the optimal preload is achieved at which point the SV remains relatively constant [46]. A necessary requirement for this model is that both ventricles are operating on similar points of their Frank-Starling curve. In patients with RV dysfunction, SV may not increase with fluid loading (it may actually decrease) even though the LV is preload responsive. The adverse effects of fluid loading occur as the patient reaches the plateau of his or her Frank-Starling curve, when atrial pressures increase sharply, increasing venous and pulmonary hydrostatic pressures, which causes a shift of fluid into the interstitial space with an increase in pulmonary and peripheral tissue edema. Furthermore, increased cardiac filling pressures increase the release of natriuretic peptides which cleave membrane- bound proteoglycans and glycoproteins off the endothelial glycocalyx, thereby further increasing endothelial permeability [47, 48].

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