How I manage differential gas exchange in peripheral venoarterial extracorporeal membrane oxygenation.

Dual circulation is a common but underrecognized physiological occurrence associated with peripheral venoarterial extracorporeal membrane oxygenation (ECMO). Competitive flow will develop between blood ejected from the heart and blood travelling retrograde within the aorta from the ECMO reinfusion cannula. The intersection of these two competitive flows is referred to as the "mixing point".

Polyuria due to Pressure Natriuresis in Venoarterial Extracorporeal Membrane Oxygenation.

We report a case of a 40-year-old woman who developed profound polyuria (>25 L urine output) immediately after initiation of venoarterial (VA) extracorporeal membrane oxygenation (ECMO). Investigations into the cause determined the polyuria was due to marked natriuresis (>85 g of sodium excreted in 1 day). This natriuresis persisted despite low cardiac filling pressures and high-negative ECMO venous pressures, suggesting clinical hypovolemia due to pressure natriuresis from locally high pressures at the renal artery due to arterial ECMO inflow.

Capillary leak syndrome: etiologies, pathophysiology, and management.

In various human diseases, an increase in capillary permeability to proteins leads to the loss of protein-rich fluid from the intravascular to the interstitial space. Although sepsis is the disease most commonly associated with this phenomenon, many other diseases can lead to a "sepsis-like" syndrome with manifestations of diffuse pitting edema, exudative serous cavity effusions, noncardiogenic pulmonary edema, hypotension, and, in some cases, hypovolemic shock with multiple-organ failure. The term capillary leak syndrome has been used to describe this constellation of disease manifestations associated with an increased capillary permeability to proteins.

The pathophysiology of edema formation in the nephrotic syndrome.

The mechanism of edema formation in the nephrotic syndrome has long been a source of controversy. In this review, through the construct of Starling's forces, we examine the roles of albumin, intravascular volume, and neurohormones on edema formation and highlight the evolving literature on the role of primary sodium absorption in edema formation. We propose that a unifying mechanism of sodium retention is present in the nephrotic syndrome regardless of intravascular volume status and is due to the activation of epithelial sodium channel by serine proteases in the glomerular filtrate of nephrotic patients.