Acid-base state in patients after cardiac transplantation

Abstract

Patients with advanced heart failure commonly develop simple or mixed acid-base disturbances. The altered acid-base homeostasis can occur as a consequence of the heart failure itself, the therapeutic interventions, or associated conditions. The present study examined acid-base disorders in patients with heart failure who received successful heart transplantation. The information collected should provide light on the determinants of acid-base disorders in this patient population. Seventy status 2 UNOS (United Network Organ Sharing) patients listed for heart transplantation were enrolled in this study. All patients received loop diuretics, spironolactone, ACE inhibitors, carvedilol and digitalis as needed. Patients were studied again at discharge after transplantation, under cyclosporine, azathioprine, steroids, loop diuretics and ACE inhibitors. After heart transplantation, a significant increase of ejection fraction from 19.7 +/- 0.63 to 53.6 +/- 0.9% (p < 0.0001) occurred along with a concomitant reduction of central venous pressure (p < 0.0001) from 12.6 +/- 0.20 to 6.9 +/- 0.21 mm Hg. Before heart transplantation there was high-normal pH (7.43 +/- 0.009), slight loss of hydrogen ions (35.4 +/- 0.4 nmol/l), slightly reduced pCO(2 )(37.6 +/- 1.1 mm Hg). After heart transplantation a stability of blood pH and hydrogen ion concentrations was found but bicarbonate increased significantly (p < 0.02) from 24.2 +/- 0.61 to 26.2 +/- 0.51 mmol/l and pCO(2) from 37.6 +/- 1.1 to 39.3 +/- 0.7 mm Hg (p < 0.05). Plasma renin activity averaged 3.80 +/- 0.6 pg/ml before heart transplantation and 2.82 +/- 0.4 pg/ml after (p < 0.01). Aldosterone concentration averaged 380 +/-15 pg/ml before heart transplantation and 280 +/- 10 pg/ml after (p < 0.01). These data suggest that in patients before heart transplantation there is a mixed acid-base imbalance that includes respiratory alkalosis and metabolic alkalosis. After transplantation the recovery of the abnormal circulatory status erased the initial respiratory alkalosis but metabolic alkalosis persisted and accounted for a further rise in plasma bicarbonate.