As alluded to in the first post, don’t be fooled by a “normal” potassium in the setting of DKA because osmotic diuresis and H+/K+ exchange means that total body potassium is actually LOW. You all know this, but don’t forget to check the potassium before starting insulin. But what about the acidemia? How does that affect physiology? (reminder: […]

the first symptom of hyperkalemia is death Earlier post covered temporizing measures to counter hyperkalemia — namely, intracellular shift, increasing cardiac myocyte threshold potential. Give furosemide if the patient still urinates and consider dialysis, but then ask yourself: how did the patient get hyper K in the first place? Often, it’s b/c of missed HD. But don’t […]

Previous post reviewed the safety of balanced crystalloids in hyper K. But what was up with serum bicarbonate decreasing with saline administration? This post introduces a new way of looking at the anion gap to possibly answer this phenomenon. This is the way we normally think of the anion gap (composed of anions like phosphate, albumin, […]

Is it safe to give LR or plasmalyte to a hyperkalemic patient (these balanced crystalloids have 4-5 mEq/L K as opposed to 0 mEq/L K in normal saline)? Postponing the discussion of renal handling of potassium to review the physiology of fluid resuscitation in the setting of hyper K (per request by Dr Hickey). This has been debunked […]

You’ll likely encounter hyperkalemia on your next Resus / Cardiac shift, and you’ll instinctively treat it. But take a moment to review the fascinating physiology behind the “cocktail”! First, consider how K+ is buffered by cells:How do our treatments shift K+ intracellularly? … Key: Na-K-ATPase! 3Na+ out, 2K+ IN! And stimulated by the β2 and insulin […]