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...
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Chapter 036. Edema (Part 4) Chapter 036. Edema (Part 4) Sequence of events leading to the formation and retention of salt andwater and the development of edema. ANP, atrial natriuretic peptide; RPF, renalplasma flow; GFR, glomerular filtration rate; ADH, antidiuretic hormone.Inhibitory influences are shown by broken lines. Incomplete ventricular emptying (systolic heart failure) and/or inadequateventricular relaxation (diastolic heart failure) both lead to an elevation ofventricular diastolic pressure. If the impairment of cardiac function primarilyinvolves the right ventricle, pressures in the systemic veins and capillaries rise,augmenting the transudation of fluid into the interstitial space and enhancing thelikelihood of peripheral edema. The elevated systemic venous pressure istransmitted to the thoracic duct with consequent reduction of lymph drainage,further increasing the accumulation of edema. If the impairment of cardiac function (incomplete ventricular emptyingand/or inadequate relaxation) involves the left ventricle primarily, then pulmonaryvenous and capillary pressures rise. Pulmonary artery pressure rises and this, inturn, interferes with the emptying of the right ventricle, leading to an elevation ofright ventricular diastolic and of central and systemic venous pressures, therebyenhancing the likelihood of the formation of peripheral edema. The elevation ofpulmonary capillary pressure may cause pulmonary edema, which impairs gasexchange. 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 diminishedcolloid oncotic pressure due to losses of large quantities of protein into the urine.With severe hypoalbuminemia and the consequent reduced colloid osmoticpressure, the NaCl and H2O that are retained cannot be restrained within thevascular compartment, and total and effective arterial blood volumes decline. Thisprocess initiates the edema-forming sequence of events described above, includingactivation of the RAA system. Impaired renal function contributes further to theformation of edema. A similar sequence of events occurs in other conditions thatlead 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 hepaticvenous outflow blockade, which, in turn, expands the splanchnic blood volumeand increases hepatic lymph formation. Intrahepatic hypertension acts as a potentstimulus for renal Na+ retention and a reduction of effective arterial blood volume.These alterations are frequently complicated by hypoalbuminemia secondary toreduced hepatic synthesis, as well as systemic vasodilation, which reduce theeffective 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 livers failureto metabolize this hormone. Initially, the excess interstitial fluid is localizedpreferentially proximal (upstream) to the congested portal venous system andobstructed hepatic lymphatics, i.e., in the peritoneal cavity (ascites, Chap. 44). Inlater stages, particularly when there is severe hypoalbuminemia, peripheral edemamay develop. The excess production of prostaglandins (PGE 2 and PGI2) incirrhosis attenuates renal Na+ retention. When the synthesis of these substances isinhibited by nonsteroidal anti-inflammatory drugs (NSAIDs), renal functiondeteriorates 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), arteriolardilatation (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 antagonistsThiazolidinedionesSteroid hormonesGlucocorticoidsAnabolic steroidsEstrogensProgestinsCyclosporineGrowth hormoneImmunotherapiesInterleukin 2OKT3 monoclonal antibodySource: From Chertow.