Fifty Shades of Central Venous Pressure in the Cardiorenal Syndrome

摘要

Cardio renal syndrome is the result of many hemodynamic, physiological, hormonal, biochemical or structural interactions. The interactions are bidirectional: acute or chronic cardiac failure may induce acute or chronic renal failure. The renal blood flow is kept constant for mean arterial pressure (MAP) between 70 and 130 mmHg. This self-regulation is made possible by two mechanisms. The first is myogenic by the contraction/relaxation of the afferent vessels in reaction to pressure, and the second is the tubule-glomerular feedback, which also regulates the diameter of the afferent arteriole as a function of NaCl concentration in the filtration liquid arriving at the macula densa. The sodium concentration is a function of the quantity of blood, which arrives in the afferent arteriole and the glomerulus. In pathological situations such as septic shock, the MAP is reduced below 65 mmHg. The collapse of MAP spectacularly reduces the afterload with a cardiac output capable of increasing due to sepsis to values ranging from 10 to 15 L/min. At the same time, fall in MAP decreases renal blood flow following the loss of self-regulation leading to renal failure and so-called “kidney shock”.