In those patients with profound hypokalemia causing unstable dysrhythmias or cardiac arrest, obviously the potassium needs replacing much faster. What is the best way (how much and how fast) to replace potassium in a patient with cardiac arrest?
I have huge respect for Dr. Slovis, but what he says about not relying on magnesium levels to determine therapy contradicts what I was taught in med school and residency. I’m wondering if he could provide any references, specifically as regards the statement that serum magnesium levels are not reliable and that magnesium should be given whenever potassium is being repleted. Thanks!
Here's a reply from Corey: Magnesium deficiency is a state of decreased total body magnesium content. The human body contains 21-28 g of magnesium, the majority of which is localized in bone (>53%) and nonmuscular tissue (approximately 19%). Hypomagnesemia (low serum magnesium concentration) is generally defined as serum magnesium <1.8 mEq/L. However, only 1% of magnesium is found in the extracellular fluid, so the serum magnesium level is a poor indicator of the total magnesium content and availability in the body. There is no simple, rapid, and accurate laboratory test to determine total body magnesium status in humans. [1] Franz KB. A functional biological marker is needed for diagnosing magnesium deficiency. J Am Coll Nutr. 2004;23:738S-741S. This summarizes best and follows with Magnesium deficiency is usually detected because of the resultant hypomagnesemia. However, it may also be revealed by the development of clinical symptoms or associated hypokalemia or hypocalcemia. If you want to know the serum magnesium level, then draw a serum potassium
Wow a great segment! Thank you! I don't recall there being a mention of how soon to check a serum level after repletion? Does it change if it was po or iv? Thanks for any advice.
From Corey: The most important thing in K replacement is lots over time along with magnesium For a quick check, other than QT interval shortening: wait at least four hours post Oral replacement and 30-60 minutes post IV to allow for cellular redistribution to stabilize Giddy UP
Hi Corey. Yosef here from Israel. About 14 years ago I lectured at Vanderbilt. I have a question on the segment. Perhaps I misunderstood. The kidney works completely on the rules of osmosis. So if there is a profound total body deficit of potassium, how can it be that you would pee most of the supplemented potassium out? Best to Keith
Yosef, The kidney does not work only via osmosis there are active transport mechanisms and different electrolytes are transported in or out of the kidneys in different locations potassium is predominantly transported from urinary excretion back into the body via the distal exchange site governed by aldosterone. How much is reabsorbed is finite and is dependent on multiple variables including acid-base balance hope you are well and hope you can re-visit us at Essentials in Vegas…..
Hi! Great segment! Any guidance on how to approach asthma/COPD patients with hypokalemia potentially secondary to being slammed with albuterol? Take it at face value? Any reliable estimation for how much K+ will decrease with albuterol? And yes, I also probably would have preferred triage not to order labs on my 25yo asthmatic, but they did...
Henry, check the audio around 15:30. Corey leads into this segment discussing that emergency treatment isn't needed with things like peaked T waves but once you get to a widened QRS (or bradydysrhythmia or blocks due to hyperK) you'll need to give calcium. Corey specifically mentions the use of CaCl2 though it would be okay to use gluconate as well.
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Andrew R. - August 10, 2018 6:41 PM
In those patients with profound hypokalemia causing unstable dysrhythmias or cardiac arrest, obviously the potassium needs replacing much faster. What is the best way (how much and how fast) to replace potassium in a patient with cardiac arrest?
Dylan N. - August 12, 2018 5:28 PM
I have huge respect for Dr. Slovis, but what he says about not relying on magnesium levels to determine therapy contradicts what I was taught in med school and residency. I’m wondering if he could provide any references, specifically as regards the statement that serum magnesium levels are not reliable and that magnesium should be given whenever potassium is being repleted. Thanks!
Anand S. - August 13, 2018 5:46 AM
Here's a reply from Corey:
Magnesium deficiency is a state of decreased total body magnesium content. The human body contains 21-28 g of magnesium, the majority of which is localized in bone (>53%) and nonmuscular tissue (approximately 19%). Hypomagnesemia (low serum magnesium concentration) is generally defined as serum magnesium <1.8 mEq/L. However, only 1% of magnesium is found in the extracellular fluid, so the serum magnesium level is a poor indicator of the total magnesium content and availability in the body. There is no simple, rapid, and accurate laboratory test to determine total body magnesium status in humans. [1]
Franz KB. A functional biological marker is needed for diagnosing magnesium deficiency. J Am Coll Nutr. 2004;23:738S-741S.
This summarizes best and follows with
Magnesium deficiency is usually detected because of the resultant hypomagnesemia. However, it may also be revealed by the development of clinical symptoms or associated hypokalemia or hypocalcemia.
If you want to know the serum magnesium level, then draw a serum potassium
Katherine B. - August 18, 2018 11:35 AM
Wow a great segment! Thank you! I don't recall there being a mention of how soon to check a serum level after repletion? Does it change if it was po or iv? Thanks for any advice.
Anand S. - August 19, 2018 10:23 AM
From Corey:
The most important thing in K replacement is lots over time along with magnesium
For a quick check, other than QT interval shortening: wait at least four hours post Oral replacement and 30-60 minutes post IV to allow for cellular redistribution to stabilize
Giddy UP
J. B. L. - August 22, 2018 8:31 AM
Hi Corey. Yosef here from Israel. About 14 years ago I lectured at Vanderbilt.
I have a question on the segment. Perhaps I misunderstood. The kidney works completely on the rules of osmosis. So if there is a profound total body deficit of potassium, how can it be that you would pee most of the supplemented potassium out?
Best to Keith
Anand S. - August 22, 2018 3:00 PM
Yosef, The kidney does not work only via osmosis there are active transport mechanisms and different electrolytes are transported in or out of the kidneys in different locations potassium is predominantly transported from urinary excretion back into the body via the distal exchange site governed by aldosterone. How much is reabsorbed is finite and is dependent on multiple variables including acid-base balance
hope you are well and hope you can re-visit us at Essentials in Vegas…..
Corey
Ryan E. - August 30, 2018 10:05 AM
Hi! Great segment! Any guidance on how to approach asthma/COPD patients with hypokalemia potentially secondary to being slammed with albuterol? Take it at face value? Any reliable estimation for how much K+ will decrease with albuterol? And yes, I also probably would have preferred triage not to order labs on my 25yo asthmatic, but they did...
Anand S. - September 16, 2018 2:07 PM
Ryan - here's Corey's reply:
albuterol usually lowers serum potassium by about 0.5 meq/L in normal pts in Hyper K it can lower it by up to 1.0
Henry A. - October 31, 2018 12:19 PM
I was taught to give Calcium IV first for Hyperkalemia to stabilize the heart. This was not mentioned in the lecture. Can you comment.
Henry Amon, MD
Anand S. - October 31, 2018 4:55 PM
Henry, check the audio around 15:30. Corey leads into this segment discussing that emergency treatment isn't needed with things like peaked T waves but once you get to a widened QRS (or bradydysrhythmia or blocks due to hyperK) you'll need to give calcium. Corey specifically mentions the use of CaCl2 though it would be okay to use gluconate as well.