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Posted On Jun 23, 2025

Updated On Jul 01, 2025

Treating Bradycardia In Addisonian Dogs

Emergency & Critical Care

This question was submitted in relation to a past webinar titled Canine Addison's Disease:

Question:
In an atypical Addison's case, how long would it take to resolve the bradycardia from time of diagnosis to effect of steroid treatment? Would this require a specific dose of steroids or should the physiological dose be enough for resolution of bradycardia?

Answer by Elisa Mazzaferro, MS, DVM, PhD, DACVECC:
In Atypical Addisons, with glucocorticoid (cortisol) deficiency alone, I would not expect to necessarily have bradycardia unless the patient is in end-stage decompensatory hypovolemic or septic shock. In those cases, intravascular volume replacement should improve the bradycardia even without glucocorticoid administration. If the animal is bradycardic, it should be a sinus bradycardia or periods of sinus arrest and not atrial standstill / idioatrial rhythm that is observed with true hypoadrenocorticism with hyperkalemia. 

Atypical Addisons cases are more challenging to diagnose as they do not have the classic electrolyte abnormalities of hyponatremia and hyperkalemia. As such, I do not administer glucocorticoids until I have the results of a resting cortisol < 2 mcg/dL and if that occurs, the results of a full ACTH stimulation test before I administer glucocorticoids. If I have a suspected typical Addisonian with hypernatremia and hyperkalemia with subsequent bradycardia and atrial standstill, I may administer both glucocorticoid in the form of dexamethasone and either Florinef or DOCP. 

 The bradycardia observed with Typical Addisons is due to the cardiotoxic effects of hyperkalemia, and the treatment is IV regular insulin with dextrose, terbutaline, sodium bicarbonate or calcium chloride / gluconate to either drive potassium intracellularly (regular insulin/dextrose, terbutaline, sodium bicarbonate) or protect the heart from the cardiotoxic effects of the hyperkalemia (calcium solutions), so the improvement in heart rate is not due to the glucocorticoid, but rather due to intravascular volume replacement and the medications administered to treat the effects of hyperkalemia. Ultimately the mineralocorticoid (either florinef or DOCP) treats the hyperkalemia.