Case Studies

Case 6: Atrial fibrillation and congestive heart failure

A man aged 72 years is found to have atrial fibrillation. He is prescribed digoxin to control the ventricular response rate. Blood test results at the time included: Na⁺ 135 mmol/L (133–148), K⁺ 4.0 mmol/L (3.4–5.3), creatinine 145 µmol/L (45–120), urea 15 mmol/L (2.5–7.0). Three years later, he has gained weight and has swollen ankles. He is also short of breath on minimal exertion and is waking up at night severely breathless. Congestive heart failure is diagnosed and the patient is prescribed bendroflumethazide and enalapril. His symptoms improve but within a year he is brought to hospital where he is found to be in complete heart block. Blood tests reveal: Na⁺ 140 mmol/L, K⁺ 2.2 mmol/L, creatinine 370 µmol/L, urea 45 mmol/L.

• (a) How does digoxin control the ventricular rate?

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  In addition to its direct effects on the heart, digoxin acts centrally and stimulates vagal activity, increasing ACh release from parasympathetic nerve endings in the heart. This slows atrioventricular conductance and prolongs the refractory period of the atrioventricular node. The atrial arrthythmia is unaffected but the ventricular rate is slowed, allowing improved ventricular filling and pumping efficiency.

• (b) What did the first blood tests indicate?

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  Renal impairment

• (c) What did the second blood tests indicate? What might have caused the changes in blood chemistry?

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  The blood tests show a deterioration in renal function. This could be due to an adverse effect of the enalapril. ACE inhibitors may impair renal function by reducing glomerular filling pressure or causing glomerulonephritis. This patient’s plasma creatine levels should have been measured after initiation and regularly during his treatment.

• (d) Can any of the changes in blood chemistry be responsible for the heart block and if so describe the mechanisms involved.

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  Correct answer:

  Digoxin is cleared mainly by the kidneys. In this patient raised creatine and urea plasma levels indicate renal impairment. This may have reduced the clearance of digoxin to such an extent that the plasma concentration of drug reached toxic levels. The patient also has hypokalaemia, probably caused by the diuretic (Chapter 14). Potassium competes for digoxin at the site of action of the drug on the cardiac muscle Na⁺/K⁺–ATPase. Thus, a low plasma concentration of K⁺ increases the action of digoxin, causing adverse effects such as the heart block that occurred in this patient.