Digoxin [Antiarrhythmic (Class III)] competes with Potassium for binding to cellular Na+/K+ ATPase pumps. Hypokalemia predisposes the patient to Digoxin toxicity. Most common arrhythmia associated with Digoxin toxicity is paroxysmal atrial tachycardia with 2:1 block. However, Bradycardia can occur and presence of a bidirectional ventricular tachycardia is practically pathognomonic for Digoxin toxicity!

HOW?? When potassium levels are low, it allows increased Digoxin binding to ATPase pumps to exert its inhibitory effects.

NOTE: Digoxin toxicity can cause Hyperkalemia (Digoxin inhibits Na+/K+ ATPase, so K+ remains in the plasma). In theory, if you give IV Calcium it can cause an influx of Calcium into the cardiac myocytes resulting in a non-contractile state (the so called “Stone Heart“).

REFERENCES

  1. Levine M et al. The Effects of Intravenous Calcium in Patients wit h Digoxin Toxicity. J Emerg Med. 2011;40(1):41–46.
  2. CHAPTER 124: Toxicology in Adults. Patrick McCafferty Lank; Thomas Corbridge; Patrick T. Murray. Principles of Critical Care, 4e
  3. Chapter 95. Adverse Cardiovascular Drug Interactions and Complications. Ileana L. Piña; Gerard Oghlakian. Hurst’s The Heart, 13e

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