The role of vasopressin and atrial natriuretic factor in postoperative fluid retention after the Fontan procedure

Risk factors for persistent pleural effusions after the extracardiac Fontan procedure

“…The hormonal mechanism involves activation of the renin-angiotensin system, 31 and more recent evidence suggests involvement of the atrial natriuretic peptide and vasopressin. 32 Lower preoperative oxygen saturation was an independent risk factor for both prolonged duration and increased volume of pleural drainage after surgical intervention. The mechanism by which lower preoperative oxygen saturations increase the risk of persistent pleural effusions after the Fontan procedure remains speculative.…”

Vasopressin After the Fontan Operation

“…15 The hormonal theory is based on the idea that afferent arteriolar hypotension in the postoperative period stimulates release of renin and angiotensin II, which in turn triggers release of aldosterone which is associated with resorption of ions and water in the kidneys. 16,18,19 All three mechanisms mentioned ultimately act through a final common pathway by altering Starling's transcapillary forces, which govern the normal physiology of pleural fluid turnover and pathogenesis of pleural effusion. 20 Both surgical and medical strategies have been used in attempts to address the issue of prolonged pleural effusion.…”

Perioperative administration of angiotensin converting enzyme inhibitors decreases the severity and duration of pleural effusions following bidirectional cavopulmonary anastomosis

“…In addition to the hemodynamic factor of elevated systemic venous pressure, perturbation of hormonal axes involved in fluid and electrolyte homeostasis may have an effect on effusions after bidirectional cavopulmonary anastomosis and modified Fontan. Elevated plasma levels of renin, angiotensin, aldosterone, atrial natriuretic factor, and antidiuretic hormone, which have been documented after bidirectional cavopulmonary anastomosis and Fontan procedures, [10][11][12] are likely to promote fluid retention and thus to facilitate effusive complications.…”

“…monary anastomosis and modified Fontan procedures, and these factors are also likely to interfere with normal fluid homeostasis. [10][11][12] Angiotensin converting enzyme inhibitors, which block the conversion of angiotensin I to angiotensin II by the angiotensin converting enzyme, are commonly used in the treatment of hypertension in pediatric patients, and for afterload reduction in patients with certain forms of congenital heart disease, cardiomyopathy, or decreased ventricular function due to other causes. Although their primary therapeutic effect depends on the decrease in serum angiotensin II, which acts as a vasoconstrictor, they also lead to decreases in aldosterone, which is secreted from the adrenal glands in response to angiotensin II binding, and bradykinin, by blocking the enzyme that cleaves its precursor.…”