Atrial wall tension changes and the release of atrial natriuretic factor on relief of cardiac tamponade

Abstract

Cardiac tamponade causes elevation and equalization of cardiac filling pressures, sodium and water retention, and a paradoxically low plasma atrial natriuretic factor (ANF) concentration despite increased intraatrial pressures. Recent reports suggested that plasma ANF concentrations rise after relief of tamponade. The purposes of the present study were (1) to determine the time course and extent of ANF release on relief of cardiac tamponade; (2) to measure the atrial transmural wall pressures, atrial sizes, and atrial wall tension changes associated with relief of tamponade; and (3) to determine the biologic activity of elevated plasma ANF during and after relief of tamponade. We sampled blood for ANF and cyclic guanosine monophosphate (cGMP) immediately before and up to 24 hours after relief of cardiac tamponade in 10 patients. Atrial and pericardial pressures were measured immediately before and shortly after pericardiocentesis, and atrial dimensions were determined by two-dimensional echocardiography before and within 1 hour after the tap. Urine volumes were measured in 8-hour increments before and after the procedure. Relief of cardiac tamponade was associated with a prompt and massive increase in plasma ANF concentrations, reaching pharmacologically active levels. The rise in ANF was negatively correlated with atrial pressures but positively correlated with atrial transmural pressures, atrial size, and calculated wall tension. Plasma ANF levels peaked at 515 ± 95 pg/ml 40 minutes after relief of tamponade and leveled off at 140% to 180% of the pretap concentrations. Plasma cGMP exhibited a slightly delayed but similar time course to the rise in ANF levels, and urine flow rate increased fourfold in the 8 hours after relief of tamponade. We conclude that (1) the relief of cardiac tamponade stimulates the release of atrial natriuretic factor by increasing atrial transmural wall pressures, atrial size, and calculated wall tensions; (2) evidence for the biologic activity of the increased plasma ANF concentrations is provided by the temporal association of increased cGMP levels and increased urine flow rate; and (3) that the release of ANF is governed by changes in atrial transmural wall, pressures and calculated atrial wall tensions.