Insert Program or Hospital Logo Abstract Slow Junctional Rhythm due to Digoxin Toxicity in Hyperaldosteronism-Induced Hypokalemia secondary to Congestive Heart Failure Mehnaz Jabeen, MD PGYIII 1 ; Ashraf Aly, MD 2 ; Amyn Jiwani, MD 2 and Sunil Jain MD 3 Department of Pediatrics University of Texas Medical Branch, Galveston, Texas Discussion Case history A premature (31 weeks) male infant presented with a systolic murmur & cardiomegaly on CXR at birth. An echo revealed a moderate VSD, a large PDA & a normal left ventricular function. Genetic testing showed partial trisomy 8. At the 4 th week of life, he developed hypotension, oliguria, rapid weight gain, tachypnea & apnea requiring intubation. CXR revealed cardiomegaly & pulmonary edema (Fig. 1) consistent with CHF. NT-proBNP was elevated. Electrolytes revealed hypernatremia, hypokalemia (which required IV supplementation of KCL), ↑ BUN/creatinine, and urinary Na + /K + ratio >1. He was started on Furosemide, Captropril, Dopamine and Digoxin. Within two days, he developed bradycardia (heart rate 47/min). An EKG revealed a junctional rhythm (Fig. 2). Digoxin level was 2.2 ng/mL (toxic level) & hypokalemia further ↑ed digoxin toxicity. Digoxin was discontinued & digoxin antigen-binding fragments (DigiBind) were given. Within 48 hours, EKG reversed to sinus rhythm (Fig. 2). In figure 3, x-axis represents day 1 as start of digoxin; y-axis is in mmol/L. It demonstrates ↑ed K + excretion and ↓ed Na + excretion in the presence of elevated serum aldosterone. Spironolactone was started to block the effect of aldosterone on kidney. Subsequently, urinary K + excretion dropped & hypokalemia resolved. Serum aldosterone & NT- proBNP also ↓ed with clinical improvement for the next 3 weeks. At the 11 th week of life, he developed worsening respiratory distress, renal failure & seizures. An echo showed a significant pulmonary hypertension. The patient died despite being on maximum support. Conclusions 1.This case illustrates the role of RAAS activation in CHF, resulting hypokalemia which ↑ed digoxin toxicity. 2.It demonstrates the utility of obtaining aldosterone & urinary electrolyte levels in these patients. 3.Recognition of this pathophysiology is critical in treating CHF with aldosterone-antagonists (spironolactone) in addition to ACE inhibitors and diuretics. References Texas Pediatric Society Electronic Poster Contest Fig. 4. The Renin-Angiotensin-Aldosterone system 1 Fig. 2. Junctional rhythm reversed after DigiBind Fig. 3. Variations in urine and serum electrolytes in our patient Fig. 1. CXR showing cardiomegaly and pulmonary edema 1.In CHF, ↓ed renal perfusion activates renin- angiotensin-aldosterone system (RAAS) → ↑ed aldosterone levels (Fig. 4.). 2.Aldosterone ↑es urinary K + excretion →hypokalemia & Na + retention → hypernatremia. 3.Hypokalemia → ↑es digoxin toxicity. 4.Measurement of aldosterone levels should be done in setting of RAAS in CHF. 5.Aldosterone antagonists (spironolactone) and ACE inhibitor (Captopril) reduces aldosterone (Fig. 3) as seen in the index case presented. 6.Digoxin toxicity should be suspected & treated early with digoxin-specific antibodies. 7.Use of digoxin, especially in the setting of RAAS activation should be avoided. A premature male infant presented with a heart murmur that was found to be due to a VSD and a large PDA. At 4 weeks of age, he developed florid congestive heart failure (CHF) with elevated NT-proBNP. Serum electrolytes revealed hypernatremia and persistent hypokalemia despite IV potassium supplementation. Urine electrolytes showed hyperkaliuria and hyponatriuria. Serum aldosterone was very elevated. Two days after starting Furosemide, Captropril, Dopamine and Digoxin, he developed bradycardia with a slow junctional rhythm. Hypokalemia-potentiated Digoxin toxicity was suspected and Digoxin was discontinued. EKG was normalized after administering IV Digoxin antigen-binding fragments. Spironolactone was added with reduction in kaliuria, serum aldosterone and NT-proBNP. Patient was clinically stable for three weeks. At the 11 th week of life, he developed pulmonary hypertension and died despite being on nitric oxide, and maximum pressor support. Liver KidneyAdrenal 1.Weber K.T. Aldosterone in congestive heart failure. NEJM. Vol 345. No. 23 (2001) Tsutamoto T. et al. Effect of spironolactone on plasma brain natriuretic peptide and left ventricular remodeling in patients with congestive heart failure. Journal of American College of Cardiology. Vol 32. No. 5 (2001)