I recently had a Chronic kidney diesease patient on low dose Ramipril with a stable potassium level for many months, got admitted to the hospital for an hypertensive urgency.Her renal function & K were stable on admission. She was started on a Labetalol infusion overnight.Next day her potassium level was 6.9mEq/L, and she needed two Insulin dextrose treatment( couple of hours apart) to get that back to normal. Her TTKG(transtubular potassium gradient) was 4. This is hyperkalemia due to Labetalol.
Lets see how........ There are 2 mechanisms by which betablockers can cause hyperkalemia.
1. Beta blockers suppress catecholamine-stimulated renin release, thereby decreasing aldosterone synthesis.
2. More importantly nonselective beta blockers decrease cellular uptake of potassium.(NEJM )
The primary mechanism for handling an acute potassium load is by redistribution into the cells.Normally, agonist binding to the beta2-adrenergic receptor stimulates the formation of cyclic AMP, which acts through protein kinase A to phosphorylate and activate the Na-K-ATPase pump, leading to the influx of potassium into cells. Competitive inhibition of the beta2 receptor by beta blockers decreases Na-K-ATPase function and reduces potassium uptake by cells.
So..this seems to happen only with non-selective beta blockers(Labetalol, Propranolol, Carvedilol, Nadolol).
Based on some retrospective studies, nonselective beta blockers have caused or contributed to hyperkalemia in 4% to 17% of hospitalized patients studied.
Have a look at this study on renal transplant patients receiving Labetalol, ended up having hyperkalemia more frequently than patients treated with agents other than labetalol.(AJNephrology 2002). The fact that hyperkalemia developed immediately after Labetalol infusion strengthens the hypothesis of blocking cellular intake of potassium than catecholamine suppression as the primary cause of Hyperkalemia with non selective betablockers.
So...just add nonselective betablockers to your differential for Hyperkalemia ......especially in patients who cannot excrete potassium properly (renal failure, on ace-i or ARD, spironolactone etc)
Sorry guys...I could not get full text of articles...will update once I get access to them!
Dear Blogger,
ReplyDeleteThank you for emphasizing the addition of non-selective beta blocker to the list of hyperkalemia. Same effect has been observed with Carvedilol (indicated for CHF).
Keep up the good work.
Regards
Sabahat Husain Zaidi
Sheffield
Thank you very much.
ReplyDeletei was search for the relationship between hyperkalemia and beta-blockers.
Ahmad Basheer
Medical student
i guess this is for residents and not for medical students who are preparing for step 1 although usmleworld explained it. I was under the impression that beta blocker suppression of renin was the more important one but as my senior friend has underlined, potassium uptake block seems to be more important. Nice article sir
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Honestly, very good article pertinent to me. I am not a doctor but I have found that I suffer from a potassium ratio level to sodium that is too low. I started supplementing with potassium, managing my sodium intake, drinking coconut water, eating bananas and becoming familiar with other foods that are high in potassium to incorporate into my diet. My goal was to minimize potassium supplementation and I was successful. My potassium deficiency symptoms abated.
ReplyDeleteFor about a month now for another condition I was put on the beta blocker proprananolol. I have noticed my potassium deficiency symptoms returning and I could not understand why. realizing that only proprananolol was the newest thing that changed I decided to Google for potassium deficiency and proprananolol. this explains everything about my condition and I'll talk to my doctor about this.
By the way your blog desperately needs a moderator. The spam in this blog is just way too much and discredits your work.
Honestly, very good article pertinent to me. I am not a doctor but I have found that I suffer from a potassium ratio level to sodium that is too low. I started supplementing with potassium, managing my sodium intake, drinking coconut water, eating bananas and becoming familiar with other foods that are high in potassium to incorporate into my diet. My goal was to minimize potassium supplementation and I was successful. My potassium deficiency symptoms abated.
ReplyDeleteFor about a month now for another condition I was put on the beta blocker proprananolol. I have noticed my potassium deficiency symptoms returning and I could not understand why. realizing that only proprananolol was the newest thing that changed I decided to Google for potassium deficiency and proprananolol. this explains everything about my condition and I'll talk to my doctor about this.
By the way your blog desperately needs a moderator. The spam in this blog is just way too much and discredits your work.
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ReplyDeleteSir I wanted to ask if beta blockers increase aldosterone release as written in Harrison's ( table 406-4 , page 2320, 19th ed ) ,,,, and if so , how ????
ReplyDeleteSir I wanted to ask if beta blockers increase aldosterone release as written in Harrison's ( table 406-4 , page 2320, 19th ed ) ,,,, and if so , how ????
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