Approach to hypokalemia Brief evaluation and treatment Ecg changes

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