Impairment of Vascular Homeostasis in Acute Heart Failure: Enter the Monocyte?

Excerpt

The major function of the systemic circulation is the delivery of oxygen, nutrients, and circulating hormones such as nitric oxide (NO) to the tissues, together with reciprocal return of tissue metabolites, notably carbon dioxide, to the pulmonary vascular bed for clearance from the body. In 1896, Ernest Starling proposed an equation to summarise the interactions between hydrostatic and tissue oncotic forces which govern exchange of fluid within the peripheral microcirculation [1]. This equation of control of peripheral vascular homeostasis of fluid balance proposed high filtration rates outwards within the arteriolar side of the peripheral circulation, with similar return of fluid on the venular side. This equation has had a longstanding and profound effect on clinical interpretation of circulatory physiology, with the corollary that development of peripheral oedema reflects either increases in venular pressure and/or decreases in oncotic pressure of venous blood. Clinically, the concepts inherent in the original Starling equation are consonant with the gradual development both of peripheral oedema and of pulmonary congestion: for example, plasma albumin concentrations may decrease gradually, or pulmonary venous pressures may rise as a result of impairment of left ventricular relaxation and/or of mitral valve regurgitation. However, in many cases, pulmonary oedema develops suddenly, often in the face of chronic impairment of left ventricular systolic and diastolic function, and not necessarily in association with any acute decline in that function. This common clinical scenario is superficially at odds with the original version of the Starling equation and is most consistent with the occurrences of transient increases in microvascular permeability [2]. …