Hypokalemia & Potassium Repletion: 5 Pearls Segment

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Pearl 1:  How much of a deficit is hypokalemia and what is the evidence behind repletion?

1. Hypokalemia
   1. Defined as K < 3.5 mEq/L
      1. Can be from total body deficit or intracellular K shifts
      2. Variation on exact amount deficit: 
         1. Some quote 1 mEq below 4 = 100-200 mEq deficit vs. every 0.3mmol is 100 mEq of K+ deficit
         2. Note: Does not account for ongoing K losses
2. Where does the data for potassium repletion come from?
   1. These is observational data that low K levels are associated with higher rates of ventricular arrhythmias in patients who were
      1. Post-myocardial patients
      2. Post-cardiac surgery patients
      3. Active diuresis in heart failure
   2. However, most of this evidence comes from observational studies decades ago before beta-blockers were widely used
   3. In a 2012 study,  patient with acute myocardial infarction had mortality rates lowest in those with a post-admission potassium level between 3.5 and <4.5 mEq/L 
   4. Despite these observations, we do not have evidence that repleting serum K leads to better outcomes!

Pearl 2:  Causes of Hypokalemia

1. Four MAIN buckets!
   1. Poor oral intake:
      1.  Less common
      2. <1 g intake/day
   2. Excretion in the urine:
      1. Diuretics
         1. Secondary to chloride depletion and alkalosis
         2. Torsemide tends to lead to less hypokalemia than furosemide
      2. Type 1 & Type 2 Renal Tubular Acidosis (RTA)
         1. Think for hypokalemia + non-anion gap acidosis
      3. Increased distal delivery of Na + Cl
         1. Normal saline (does not contain K)
            1. Increased Na delivery to distal nephron → K loss in urine
         2. Excretion with non-absorbable anions. Example:
            1. Antibiotics: IV Penicillin in large doses, aminoglycoside
            2. Excess [bicarbonate] with vomiting or NG suction
               1. Excess [bicarb] will be urinated out and takes K+ along with it!
            3. B-hydroxybutyrate in DKA
         3. Osmotic diuresis Ex:
            1. Hyperglycemia
            2. Urea excretion after relief of chronic urinary obstruction
   3. GI loss:
      1. ABOVE: Vomiting/NG Tube losses
         1. Loss of Cl rich fluid → Increased [bicarbonate] → excess bicarb will be urinated and takes K+ along with it
            1. So technically a urinary loss
      2. BELOW: Diarrhea/Laxatives/Enemas
         1. Anything that increase stool volume can lead to K loss through the GI tract
   4. Intracellular shifts:
      1. ↑ B-adrenergic activity (Catecholamines)
         1. Increased epinephrine → K into cells
            1. Activate Na/K pumps
         2. Examples of highly adrenergic states:
            1. Acute MI
            2. Alcohol withdrawal
            3. Panic attacks (anxiety & hyperventilation)
      2. Insulin
         1. “Insulin also pushes potassium in to cells”
         2. Promotes Na/K-ATPase activity and pulls K+ into cells
      3. Alkalemia
         1. Favors K+ into cells and H+ out of cells
      4. ↑ Hematopoietic cell production
         1. ↑ K+ uptake by new cells
         2. Ex. GM-CSF, vitamin B, folic acid
      5. Rare: periodic paralysis, hypothermia

Pearl 3:  What is the goal for K+ repletion?

1. Normal range:  3.5 - 4 mEq/L
   1. Goal is WITHIN this range
      1. Depending on the patient:
         1. Examples:
            1. Patient on diuretic
               1. Continuous loss of K → more aggressive repletion
            2. Patient with uncomplicated pneumonia
               1. Low risk for ventricular arrhythmia → less aggressive repletion
      2. Urgency of K repletion is patient dependent
         1. More urgent (patients who may have a more sensitive myocardium)
            1. Post acute MI
            2. Active diuresis (heart failure)
         2. Less urgent (avoid repleting to 4.0 exactly)
            1. No cardiac risk factors
            2. Good PO intake
2. 2. What about long-term, chronic low K?
      1. May cause metabolism issues and linked to other adverse outcomes
         1. High K diet →  Decreased incidence of stroke, cardiovascular events, and mortality

Pearl 4:  How to replete potassium?

1. IV vs. PO
   1. If they have a gut, try to use it!
      1. If the patient has GI distress, divide into multiple doses over the course of the day
   2. IV can be limited in that small mEq are given an hour infusion.
2. Multiple K+ supplements are available
   1. Consider what ELSE the patient might need
      1. Potassium chloride
         1.  If patient has metabolic alkalosis
      2. Potassium phosphate
         1. If patient  has phosphate deficit
      3. Potassium citrate (especially for outpatients!)
         1. If patient has kidney stones
            1. Citrate is a natural stone inhibitor that chelates calcium
         2. If patient has hypocitraturia
      4. Note: Potassium phosphate & citrate are also on K rich foods like figs, dried fruits, and avocados!
3. What are other options?
   1. Check the patient’s medications!
   2. Is there something causing kaliuresis? (urinary potassium excretion)
      1. Furosemide
         1. Consider switching to torsemide
            1. Less kaliuresis
            2. Good oral absorption
      2. PPIs
         1. Can lead to hypomagnesemia which can lead to hypokalemia
      3. Fluids

Pearl 5:  When to order potassium labs?

1. Do we over check labs?
   1. Often we check twice a day for patients who are undergoing diuresis
      1. Decide based on the clinical scenario:
         1. Ex: patient is not urinating much (low diuresis)
            1. Don’t need to check labs!
   2. Think if routine morning labs are needed for you patient
      1. Harms of checking labs that are not needed
         1. Time (of everyone involved)
         2. Patient comfort
         3. Money
2. Changing practices around labs and repletion
   1. Requires interdisciplinary education
   2. Requires a range of physicians (interns to attendings) to change the framework of when to replete K!

Contributors

Shreya Trivedi, MD, ACP Member – Host / Editor
Benjamin Osher, MD - Author
Mahathi Komaragiri, MD - Author
Santiago Callegari, MD - Author
Melanie Koenig, MD - Expert
Anthony Breu, MD, ACP Member - Expert

Reviewers

Jeff William, MD
Larissa Kruger-Gomes, MD

Those named above, unless otherwise indicated, have no relevant financial relationships to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.  All relevant relationships have been mitigated.

Release Date:  October 18, 2023

Expiration Date: October 17, 2026

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