Chapter 036. Edema (Part 3)

EndothelinThis potent peptide vasoconstrictor is released by endothelial cells; its concentration is elevated in heart failure and contributes to renal vasoconstriction, Na+ retention, and edema in heart failure.Natriuretic Peptides Atrial distention and/or a Na+ load cause release into the circulation of atrial natriuretic peptide (ANP), a polypeptide; a high-molecular-weight precursor of ANP is stored in secretory granules within atrial myocytes. Release of ANP causes (1) excretion of sodium and water by augmenting glomerular filtration rate, inhibiting sodium reabsorption in the proximal tubule, and inhibiting release of renin and aldosterone; and (2) arteriolar and venous dilation by antagonizing thevasoconstrictor actions...
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Chapter 036. Edema (Part 3) Chapter 036. Edema (Part 3) Endothelin This potent peptide vasoconstrictor is released by endothelial cells; itsconcentration is elevated in heart failure and contributes to renal vasoconstriction,Na+ retention, and edema in heart failure. Natriuretic Peptides Atrial distention and/or a Na+ load cause release into the circulation ofatrial natriuretic peptide (ANP), a polypeptide; a high-molecular-weight precursorof ANP is stored in secretory granules within atrial myocytes. Release of ANPcauses (1) excretion of sodium and water by augmenting glomerular filtration rate,inhibiting sodium reabsorption in the proximal tubule, and inhibiting release ofrenin and aldosterone; and (2) arteriolar and venous dilation by antagonizing thevasoconstrictor actions of AII, AVP, and sympathetic stimulation. Thus, ANP hasthe capacity to oppose Na+ retention and arterial pressure elevation inhypervolemic states. The closely related brain natriuretic peptide (BNP) is stored primarily inventricular myocardium and is released when ventricular diastolic pressure rises.Its actions are similar to those of ANP. Circulating levels of ANP and BNP areelevated in congestive heart failure and in cirrhosis with ascites, but obviously notsufficiently to prevent edema formation. In addition, in edematous states there isabnormal resistance to the actions of natriuretic peptides. Clinical Causes of Edema Obstruction of Venous (and Lymphatic) Drainage of a Limb In this condition the hydrostatic pressure in the capillary bed upstream(proximal) to the obstruction increases so that an abnormal quantity of fluid istransferred from the vascular to the interstitial space. Since the alternative route(i.e., the lymphatic channels) may also be obstructed or maximally filled, anincreased volume of interstitial fluid in the limb develops, i.e., there is trapping offluid in the extremity. Tissue tension rises in the affected limb until itcounterbalances the primary alterations in the Starling forces, at which time nofurther fluid accumulates. The net effect is a local increase in the volume ofinterstitial fluid, causing local edema. The displacement of fluid into a limb mayoccur at the expense of the blood volume in the remainder of the body, therebyreducing effective arterial blood volume and leading to the retention of NaCl andH2O until the deficit in plasma volume has been corrected. This same sequenceoccurs in ascites and hydrothorax, in which fluid is trapped or accumulates in thecavitary space, depleting the intravascular volume and leading to secondary saltand fluid retention. Congestive Heart Failure (See also Chap. 227) In this disorder the impaired systolic emptying of theventricle(s) and/or the impairment of ventricular relaxation promotes anaccumulation of blood in the venous circulation at the expense of the effectivearterial volume, and the aforementioned sequence of events (Fig. 36-1) is initiated.In mild heart failure, a small increment of total blood volume may repair thedeficit of arterial volume and establish a new steady state. Through the operationof Starlings law of the heart, an increase in ventricular diastolic volume promotesa more forceful contraction and may thereby restore the cardiac output. However,if the cardiac disorder is more severe, fluid retention continues, and the incrementin blood volume accumulates in the venous circulation. With reduction in cardiacoutput, a decrease in baroreflex-mediated inhibition of the vasomotor centeractivates renal vasoconstrictor nerves and the RAA system, causing Na+ and H2Oretention. Figure 36-1