Total Body Potassium: a 70 kg person has about 7500 mEq of total body K, but the extracellular fluid has only about 48 mEq! Of course the difficulty with K replenishment is that the total body stores may be depleted by far more than can possibly be quickly repleted. The estimated deficit associated with a serum decrease from 4.0 to 3.0 mEq/L is 100-200 mEq of total body K, and from 3.0 to 2.0, the associated loss is double, at 200-400 mEq.* [

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But 100 mEq given all at once would raise the serum K by 30 mEq/L (and be immediately fatal)!!





*The NEJM review referenced below (and ACLS, for what that is worth), states that, on average, in a "typical" 70 kg person , the serum K falls by 0.3 mEq/L for every 100 mEq total body deficit. However, this review references the Sterns article above, which by my reading does not state this.





Here are some calculations for a safe rapid dose:

A 70 kg person has about 5 liters of blood, and 3 liters are serum (2 liters are RBCs). If 10 mEq is given very rapidly, leaving no time for intracellular shift, then it will raise serum K by about 3.3 mEq/L. If the patient is at 1.8, that will raise it to 5.1 mEq/L. One need only get the K above 3.0 to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5 mEq/L). 5 mEq rapid bolus would raise this patient's K from by 1.6, from 1.8 to 3.4 mEq/L. The difficulty is in estimating the ongoing shift. As you infuse K, it will start to shift into depleted cells and the serum K will fall again rapidly. Thus, it is critical in patients like this to repeatedly and rapidly, after each bolus, measure the K, and supplement as needed.





In the case presented, it is not clear to me that the 10 mEq of K was given rapidly. I suspect it was set to go over 1 hours on a pump, which is the usual practice. It would be difficult to get a nurse to give it faster! However, in this case, it would be appropriate to give it over 5-10 minutes, with monitoring, then immediately measure the K again and be ready to give more.





Further complicating the issue is that severe hypokalemia can result in rhabdomyolysis and subsequent K release, with resulting hyperkalemia!





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Here is another post on hypoK:





In this post, I discussed another patient I took care of :

Prehospital Cardiac Arrest due to Hypokalemia



I recently had a case of prehospital cardiac arrest that turned out to be due to hypokalemia.

We could not resuscitate her, but we did have excellent perfusion with LUCAS CPR, such that pulse oximetry had excellent waveform and 100% saturations, end tidal CO2 was 35, and cerebral perfusion monitoring was near normal throughout the attempted resuscitation. This was before we started doing ECMO for refractory V Fib.



During the resuscitation, I ordered 10 mEq KCl push, but the patient received 40 mEq of KCl, push (far more than recommended) The resident had ordered 40 mEq and that is what the nurses heard.



Is 40 mEq too much? Or the right amount?



Contrary to my expectations, after pushing 40 mEq, the K only went up to 4.2 mEq/L.



What is the right amount of K to push in life-threatening hypoK? In a 70 kg person, there are 5 liters of blood and 3 liters of serum. Since it takes some time (how long?) for K to shift out of the intravascular space into the interstitial space and then into the intracellular space, 3.0 mEq of K pushed fast and circulated theoretically would raise serum K immediately by 1.0 mEq/L, and 10 mEq would increase it by 3.3 mEq/L, from 1.9 to 5.2. Thus, 40 mEq should raise it by 13 mEq/L!!



But this is before redistribution to the interstitial space.

As I indicated above, in our cardiac arrest case, after pushing 40 mEq, the K only went up to 4.2 mEq/L. There are about 13 liters of extracellular fluid in a 70 kg person (10 liters interstitial fluid + 3 liters serum). So if K redistributes very quickly to this extracellular space, then 40 mEq is appropriate.



The difficulty is in estimating the ongoing shift. As you infuse K, it will start to shift into depleted cells and the serum K will fall again rapidly. Thus, it is critical in patients like this to repeatedly and rapidly, after each bolus, measure the K, and supplement as needed. I recently had a case of prehospital cardiac arrest that turned out to be due to hypokalemia.We could not resuscitate her, but we did have excellent perfusion with LUCAS CPR, such that pulse oximetry had excellent waveform and 100% saturations, end tidal CO2 was 35, and cerebral perfusion monitoring was near normal throughout the attempted resuscitation. This was before we started doing ECMO for refractory V Fib.During the resuscitation, I ordered 10 mEq KCl push, but the patient receivedThe resident had ordered 40 mEq and that is what the nurses heard.Is 40 mEq too much? Or the right amount?Contrary to my expectations, after pushing 40 mEq, the K only went up to 4.2 mEq/L.







Here is review of hypokalemia from the NEJM , but it is mostly about etiology, and says little about rapid replacement in life-threatening hypokalemia EXCEPT to emphasize how dangerous rapid replacement is.





I have read articles that say that patients without ischemia are at low risk of complications from hypokalemia, But it is not entirely without risk. I saw this 30 year old woman with no cardiac disease who was resuscitated from ventricular fibrillation

:

Classic Hypokalemia, with large U-waves. K was 1.3 mEq/L.







Learning Points:



1. Severe hypokalemia in the setting of STEMI or dysrhythmias is life-threatening and needs very rapid treatment. 5-10 mEq over 5-10 minutes is appropriate for a K of 1.8 mEq/L.



2. Be certain that your laboratory value is accurate and that it corresponds with the ECG findings! If the ECG shows no evidence of hypokalemia, it may be an artifactual value. If the ECG shows no evidence, it is unlikely to be life-threatening!



3. In a 70 kg person, a 10 mEq bolus will raise serum K by 3.3 mEq/L in the absence of any intracellular shift



4. It is optimal to give such a bolus through a central line, but this may not always be possible.



5. It is difficult to correct K without also correcting low magnesium. In this case, the Mg was 1.9 mEq/L (within normal limits)



6. Learn the management of Polymorphic VT, including Torsades.









Literature





Two Articles on Rapid Replacement of Potassium





Objective: To evaluate the efficacy and safety of potassium replacement infusions in critically ill patients.

Design: Prospective cohort study.

Setting: Multidisciplinary critical care unit.

Intervention: Potassium chloride infusions (20,30, or 40 mmol in 100 mL normal saline over 1 hr) were administered to patients for serum potassium levels of <3 .5="" but="" style="font-family: times, 'times new roman', serif;">3.2 mmol/L (n = 26), 3.0 to 3.2 mmol/L (n = 11), and3>

Measurements and Results: All patients tolerated the infusions without evidence of hemodynamic compromise, ECG change, or new dysrhythmia requiring treatment. The mean maximum potassium increase was 0.5 +/- 0.3 mmol/L, 0.9 +/- 0.4 mmol/L, and 1.1 +/- 0.4 mmol/L in the 20-, 30-, and 40-mmol groups, respectively. The increase in serum potassium was maximal at the completion of the infusion and was significant (p < .05) compared with baseline in all groups. Peak potassium levels were the same in patients with normal renal function (n = 33) compared with those with renal insufficiency (n = 15).

Urinary excretion of potassium increased in all groups during the infusion and was significant (p < .05) in the 30- and 40-mmol groups, but was no greater in those patients who had received diuretics (n = 8) compared with those patients who had not (n = 40).

Conclusions: In the select group of hypokalemic patients studied, potassium infusions of 20 to 40 mmol delivered over 1 hr were safe to administer and effectively increased serum potassium levels in a dosedependent and predictable fashion. Furthermore, these results were independent of the patient's underlying renal function or associated diuretic administration. (Crit Care Med 1991; 19:694)





Sterns RH, et al. Internal potassium balance and the control of the plasma potassium concentration. Medicine (Baltimore) 1981;60:339-54]