Chapter 036. Edema (Part 4)

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Sequence of events leading to the formation and retention of salt and water and the development of edema. ANP, atrial natriuretic peptide; RPF, renal plasma flow; GFR, glomerular filtration rate; ADH, antidiuretic hormone. Inhibitory influences are shown by broken lines. Incomplete ventricular emptying (systolic heart failure) and/or inadequate ventricular relaxation (diastolic heart failure) both lead to an elevation of ventricular diastolic pressure. If the impairment of cardiac function primarily involves the right ventricle, pressures in the systemic veins and capillaries rise, augmenting the transudation of fluid into the interstitial space and enhancing the likelihood of peripheral edema. The elevated systemic...

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Chapter 036. Edema (Part 4) Sequence of events leading to the formation and retention of salt and water and the development of edema. ANP, atrial natriuretic peptide; RPF, renal plasma flow; GFR, glomerular filtration rate; ADH, antidiuretic hormone. Inhibitory influences are shown by broken lines. Incomplete ventricular emptying (systolic heart failure) and/or inadequate ventricular relaxation (diastolic heart failure) both lead to an elevation of ventricular diastolic pressure. If the impairment of cardiac function primarily involves the right ventricle, pressures in the systemic veins and capillaries rise, augmenting the transudation of fluid into the interstitial space and enhancing the likelihood of peripheral edema. The elevated systemic venous pressure is transmitted to the thoracic duct with consequent reduction of lymph drainage, further increasing the accumulation of edema.
If the impairment of cardiac function (incomplete ventricular emptying and/or inadequate relaxation) involves the left ventricle primarily, then pulmonary venous and capillary pressures rise. Pulmonary artery pressure rises and this, in turn, interferes with the emptying of the right ventricle, leading to an elevation of right ventricular diastolic and of central and systemic venous pressures, thereby enhancing the likelihood of the formation of peripheral edema. The elevation of pulmonary capillary pressure may cause pulmonary edema, which impairs gas exchange. The resultant hypoxemia may impair cardiac function further, sometimes causing a vicious circle. Nephrotic Syndrome and Other Hypoalbuminemic States (See also Chap. 277) The primary alteration in this disorder is a diminished colloid oncotic pressure due to losses of large quantities of protein into the urine. With severe hypoalbuminemia and the consequent reduced colloid osmotic pressure, the NaCl and H2O that are retained cannot be restrained within the vascular compartment, and total and effective arterial blood volumes decline. This process initiates the edema-forming sequence of events described above, including activation of the RAA system. Impaired renal function contributes further to the formation of edema. A similar sequence of events occurs in other conditions that lead to severe hypoalbuminemia, including (1) severe nutritional deficiency states; (2) severe, chronic liver disease (see below); and (3) protein-losing enteropathy.
Cirrhosis (See also Chaps. 44 and 302) This condition is characterized by hepatic venous outflow blockade, which, in turn, expands the splanchnic blood volume and increases hepatic lymph formation. Intrahepatic hypertension acts as a potent stimulus for renal Na+ retention and a reduction of effective arterial blood volume. These alterations are frequently complicated by hypoalbuminemia secondary to reduced hepatic synthesis, as well as systemic vasodilation, which reduce the effective arterial blood volume further, leading to activation of the RAA system, of renal sympathetic nerves, and of other NaCl- and H2O-retaining mechanisms. The concentration of circulating aldosterone is often elevated by the liver's failure to metabolize this hormone. Initially, the excess interstitial fluid is localized preferentially proximal (upstream) to the congested portal venous system and obstructed hepatic lymphatics, i.e., in the peritoneal cavity (ascites, Chap. 44). In later stages, particularly when there is severe hypoalbuminemia, peripheral edema may develop. The excess production of prostaglandins (PGE 2 and PGI2) in cirrhosis attenuates renal Na+ retention. When the synthesis of these substances is inhibited by nonsteroidal anti-inflammatory drugs (NSAIDs), renal function deteriorates and Na+ retention increases. Drug-Induced Edema
A large number of widely used drugs can cause edema (Table 36-1). Mechanisms include renal vasoconstriction (NSAIDs and cyclosporine), arteriolar dilatation (vasodilators), augmented renal Na+ reabsorption (steroid hormones), and capillary damage (interleukin 2). Table 36-1 Drugs Associated with Edema Formation Nonsteroidal anti-inflammatory drugs Antihypertensive agents Direct arterial/arteriolar vasodilators Hydralazine Clonidine Methyldopa Guanethidine Minoxidil Calcium channel antagonists α-Adrenergic antagonists
Thiazolidinediones Steroid hormones Glucocorticoids Anabolic steroids Estrogens Progestins Cyclosporine Growth hormone Immunotherapies Interleukin 2 OKT3 monoclonal antibody Source: From Chertow.