Pulmonary edema due to increased microvascular permeability to fluid and protein.

Abstract

THE USUAL clinical designation of pulmonary edema as either cardiogenic or noncardiogenic implies a pathophysiology that is not necessarily true and, in the case of noncardiogenic edema, is singularly uninformative. A better classification would be one based upon the two major variables in the equation for transvascular fluid flow (Starling's equation), namely, Net fluid flow = conductance x driving pressure or, in symbols,where Qf is the net transvascular fluid flow, K is the fluid filtration coefficient, P is the hydrostatic pressure in the microvascular* lumen (mv) and perimicrovascular* interstitial fluid (pmv), respectively; a is a weighted plasma protein reflection coefficient which determines the "effective" transvascular protein osmotic pressure difference; and II is the protein osmotic pressure in the plasma (mv) and perimicrovascular (pmv) compartments, respectively.According to Equation 1, the two major types of edema are that due to increased driving pressure (high pressure edema) and that due to altered integrity of the microvascular membrane (permeability edema).High pressure edema may be of cardiac origin (increased microvascular hydrostatic pressure due to left atrial hypertension), but it also may occur when cardiac function is normal as in overexpansion of extracellular volume by crystalloid fluid infusions' (increased pulmo-

A Model for Interstitial Drainage Through a Sliding Lymphatic Valve

“…Clinical studies show that in obesity [16], pregnancy [1,35] and in the elderly [17,29] vascular permeability increases. Furthermore that cases of oedema are common in patients who have a high vascular permeability [3,51]. This might appear to be at odds with the results of our model.…”

Adenosine receptor A2b on hematopoietic cells mediates LPS-induced migration of PMNs into the lung interstitium

“…In the early phase, inflammatory cells migrate into the lungs, release inflammatory cytokines, perpetuating inflammatory response, and ultimately resulting in tissue damage. The lung vascular permeability increases and results in the accumulation of pulmonary edema fluid (48): as a long-term consequence, fibrotic remodeling can occur and considerably deteriorates pulmonary gas exchange.…”

Does the administration of the calcium-antagonist verapamil in tocolysis with beta-sympathicomimetics still make sense?

“…The reason for this is the rapid biotransformation of the active substance Verapamil into ineffective or only weakly effective metabolites [34], Our own studies [38] have revealed that the average serum concentration of the mother after administration of Verapamil at a dosage rate of 2 Mg/kg/min was 19.3 ± 3 ng/ml. Since fluid displacements in the lungs up to the severity of manifest pulmonary edema after administration of adrenergics is due at least in part to hemodynamic factors [3,10,36], it comes äs no surprise that the administration of Verapamil has no influence on the fluid displacement from the intravascular to the extravascular space induced by Fenoterol.…”