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 pCO₂(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 pCO₂ 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.

Acid–base and electrolyte abnormalities in heart failure: pathophysiology and implications

“…This justifies the occurrence of metabolic alkalosis, metabolic acidosis, respiratory alkalosis, as well as respiratory acidosis alone or in combination. Several studies have systematically evaluated the prevalence of acid–base disturbances in CHF [88–90]. About 37 % of CHF subjects show at least one acid–base abnormality, most commonly metabolic alkalosis, alone or associated with respiratory alkalosis.…”

“…Alkalemia is more common in subjects with more advanced CHF (36 % in subjects with class IV compared with 11 % of those with class III) [4]. Other studies confirm the trend toward alkalemia of mixed metabolic and respiratory origin in unselected advanced CHF subjects [88, 90]. In addition, diuretic therapy increases the prevalence of metabolic alkalosis, although the subjects who improve the circulatory status with diuretic therapy may improve their alkalosis [91].…”

Comparison of the patients with COVID-19 pre-diagnosis admitted to the emergency department in terms of acid-base imbalance

“…Metabolic alkalosis in addition to respiratory acidosis in these patients increases survival of the patient (18,27). Metabolic alkalosis, metabolic acidosis, respiratory alkalosis and respiratory acidosis may occur alone or in combination in the patients with heart failure (28). Renal tubular acidosis (hyperchloremic metabolic acidosis) is common in the patients with cancer (29).…”

Association between early central venous pressure measurement and all-cause mortality in critically ill patients with heart failure: A cohort of 11,241 patients

“…Our research has established that a heightened serum anion gap is an independent prognostic indicator of adverse outcomes in patients critically ill with heart failure [ 29 ]. Hemodynamic instability leading to peripheral tissue hypoperfusion and metabolic acidosis is closely linked with a negative prognosis in heart failure patients [ 8 , [30] , [31] , [32] ]. The serum anion gap is positively correlated with the levels of acidic metabolites, such as lactate, and indirectly reflects tissue hypoperfusion.…”