CLINICAL CASE SCENARIO OF DIGOXIN TOXICITY FOR MEDICAL STUDENTS

  Mrs X is a 67-year-old woman brought into the opd complaining of loss of appetite and nausea for the preceding 2 days. She also reports hazy vision with "halos" but thinks that is due to her tiredness. 

PastMedicalHistory : CHF, HTN. 

Medications: Digoxin. 

She recently started taking an angiotensin-converting enzyme Inhibitor (Ace-I) . 

Case Conclusion :

Mrs X's presentation was consistent with digoxin toxicity. Labs returned with a normal potassium value (3.9 mEq/L) and a supratherapeutic digoxin level (2.6 microg/l). Her digoxin and ACE-I were immediately discontinued. Within 2 days. X was starting to feel like herself again. The ACE-I and oral digoxin were restarted (at lower doses)


Digoxin increases contractility of the heart muscle by inhibiting the Na+/K+ ATPase pump. In a normally functioning heart. intracellular calcium stored in the sarcoplasmic reticulum is released and activates the contractility of the muscle. The Na+/Ca2+ exchanger located in the cell membrane controls normal intracellular calcium levels. Exchangers use the Na+ ion gradient, maintained by the Na+/K+ ATPase, to move calcium ions out of the cell. when digoxin inhibits the Na '/K+ ATPase, intracellular sodium levels increase. This increase in sodium shifts the balance of the Na+/Ca2+ exchanger, leading to increased stores of intracellular calcium available in the sarcoplasmic reticulum and stronger contraction of the heart muscle.

When starting digoxin therapy, it is important to obtain baseline electrolyte levels and renal function. Electrolyte imbalances (hypokalemia, hypomagnesemia, or hypercalcemia) predispose patients to digoxin toxicity. When serum potassium is low, digoxin uptake increases because digoxin and potassium compete for the same site on the Na+/K+ ATPase. Increases in serum calcium can facilitate digitalis toxicity by causing overloading of intracellular calcium stores that can induce arrhythmias. Low magnesium also can contribute to toxicity. In addition, digoxin is cleared by the kidney; therefore. it is important to obtain baseline renal function values to determine if dose adjustments are necessary.

Because of digoxin's narrow therapeutic range, toxicity can often occur. especially in those who have predisposing factors, such as hypokalemia, concurrent therapy with potassium wasting diuretics, age (elderly and pediatrics), small body size. and drug interactions. Common signs of toxicity include GI complaints (nausea, vomiting, and anorexia). arrhythmias, and CNS effects (I.e., confusion, hallucinations. and visual disturbances).

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