This document summarizes hypokalemia, including its physiology, causes, diagnostic approach, and treatment. Key points include: - Hypokalemia is defined as a plasma potassium level below 3.5 mmol/L. It can be caused by reduced intake, redistribution into cells, or increased losses from the GI tract or kidneys. - Diagnosing the cause involves assessing urinary potassium excretion to distinguish renal vs extrarenal losses, and evaluating acid-base status. - Treatment involves oral potassium supplementation, with dosage based on the potassium deficit and serum level. Intravenous potassium may also be used. Addressing underlying causes like diuretic use or gastrointestinal losses is important.

1. HYPOKALEMIA
Dr.Vgks Vaishnavi
D.n.b gen med
aditya hospital, hyderabad

2. • PHYSIOLOGY in nephron
- most of k+ gets reabsorbed in PCT and loop of henle
- Secretion occurs in Distal tubule and collecting duct
Diuretics- hypokalemia-
Thiazides > loop diuretics
Thiazides also cause hypomagnesemia

3. • Hypokalemia – when plasma potassium falls below 3.5mmol
CAUSES
Reduced intake Redistribution Increased losses
• PSEUDOHYPOKALEMIA
• HYPOMAGNESEMIA
-Such patients can be refractory to potassium replacement alone.

4. INCREASED ENTRY INTO CELLS
• Increased availability of insulin (both exogenous and endogenous)
• Beta adrenergic activity
• Alkalemia
• FPP vs TPP

5. • Paradoxical hypokalemia in some individuals
-
Certain individuals with either periodic or nonperiodic hypokalemia ca
n develop worsening, "paradoxical" hypokalemia after
potassium repletion.
- These pts have higher thyroxine levels- require higher KCL repletion-
have exaggerated uptake of potassium – resulting in
further hypokalemia

6. • Barium/Cesium intoxication
• Chloroquine intoxication
• Antipsychotics
• Increased GI/Urinary losses
• Dialysis
• Plasmapheresis
• ANABOLIC STATES

7. • History
- diarrhea
- drug intake ( beta agonists, alpha antagonists, laxatives, diuretics,
antibiotics like penicillins, b12 and folate administration)
- Insulin
Insulin depletes potassium by 2 ways..
1. By stimulating Na+K+ATPase , thus drives K+ into the cell
2. Insulin induced Hypoglycemia causes release of epinephrine
---- Stimulation of a beta-adrenoceptor linked to membrane Na/K
ATPase causing potassium influx { beta2 > beta 1}

8. Hypokalemia is a major risk factor for both ventricular and
atrial arrhythmias.
Hypokalemia predisposes to digoxin toxicity

9. • Aminoglycosides like amikacin and gentamicin can cause
hypokalemia..
• Bartter like syndrome has been identified----hypokalemia, metabolic
alkalosis, hypomagnesemia with urinary magnesium wasting, and
hypercalciuria, which resolve two to six weeks after drug
termination
(type 5 bartter syndrome)

10. 2 major components to the diagnostic evaluation:
• Assessment of Urinary K+ excretion to distinguish renal potassium
losses from other causes of hypokalemia
• Assessment of acid-base status, since some causes of hypokalemia
are associated with metabolic alkalosis or metabolic acidosis.

11. Diagnostic Approach
- history
• Any drug intake, dietary habits,
• h/o periodic weakness – age of onset below 25years and improved
with potassium supplementation
• Severe diarrhea
- physical examination- for any weakness, thyrotoxicosis, cushings
-Assesment of Volume status, BP, metabolic alkalosis or acidosis
- Rule out HypoMg

12. Se. K <3.5 ?
?pseudohypokalemia
?Mg deficiency
Treat accordingly

13. Urine K+
< 15 mmol/day > 15 mmol/day
Extrarenal losses Renal losses
1. Met. Acidosis
2. normal
3. Met. alkalosis

14. If renal losses+
TTKG
< 2 - osmotic diuresis (tubular flow)
> 4 - Increased distal K+ secretion
BP & Volume status

15. LOW BP
Metabolic acidosis Metabolic alkalosis
1.RTA
2.DKA Urine Cl-
3.Amphoterecin B
4.Acetazolamide >20 <10
Urine Ca/Cr
>0.20 <0.15
1. Loop diuretic 1. Thiazides
2. Bartter 2. Gitelman's

16. HIGH BP
Measure Aldosterone levels
High Low
Measure Renin levels Measure Cortisol levels
1. High- RAS,RST,Mal.HTN 1. High- Cushing's
2. Low- PA, FH-1 2. Normal- Liddle's, SAME

17. ECG CHANGES IN HYPOKALEMIA-
1. Prominent U waves
2. Nonspecific ST depression and T-wave flattening as the U
wave becomes more prominent
3. Prolongation of the QU interval
4. Fusion of the T and U waves
5. Ventricular arrhythmias, especially torsade de pointes

21. TREATMENT
- oral potassium is the main stay of treatment
- the total deficit correlates with serum K+,
serum K+ drops by ~0.27 mM for every 100 mmol reduction in total-
body stores
loss of 400–800 mmol of total-body K+ results in a reduction in serum
K+ by ~2.0 mM
- The peripheral intravenous dose is usually 20–40 mmol/l
- Propranolol, MgSo4

22. THANK YOU