1. Potassium Disorders
N Ganesh Yadlapalli, MD Professor of Medicine University of Cincinnati College of Medicine

2. K+ Balance Intake: dietary and parenteral Urinary excretion (90%)
Regulated mainly by aldosterone
GI loss (10%)
Inc’d with CKD

3. Potassium Distribution
ECF
mEq
ICF
About 4000 mEq
Saltwater extracellular is not K

4. Body Weight of 90 Kg
Intra Cellular Fluid Liters
K mEq/L
Extra Cellular Fluid Liters
K mEq/L
Total K + = 100 mEq
Plasma
K mEq/L

5. Intra cellular Fluid 40 Liters
K mEq/L
Extra Cellular Fluid Liters
( 100 mEq of K)
PO intake
40 mEq of
of K +
Total K + =
K + Na
K + increases from
4.5 to mEq/L
Plasma
K mEq/L

6. Potassium Balance Insulin Catecholamine pH
Intra cellular Fluid Liters
K mEq/L
Extra Cellular Fluid Liters
PO intake of
40 mEq K+
Total K + = 100
Inc in intracellular Potassium
K +
K + Na
K + dec’s from
6.5 to mEq/L
Plasma
K mEq/L
Potassium Balance

7. Potassium Balance Insulin Catecholamine pH
Intra cellular Fluid Liters
K mEq/L
Extra Cellular Fluid Liters
PO intake of
40 mEq K+
Total K + = 100
K +
K +
Increase in intracellular Potassium
Na +
K + decreases from
6.5 to mEq/L
Plasma
Potassium Balance
K mEq/L
Urinary Excretion
GI excretion

8. Potassium levels back to normal
Intra cellular Fluid Liters
K mEq/L
Extra Cellular Fluid Liters
Potassium levels back to normal
Total K + = 100
K +
Na +
K mEq/L
Normalization of intracellular Potassium
Plasma
K mEq/L
Urinary Excretion
GI excretion

9. Intra cellular Fluid 40 Liters
K mEq/L
Extra Cellular Fluid Liters
Total K + = 100
K +
Na +
K mEq/L
Normalization of intracellular Potassium
Plasma
K mEq/L

10. Causes of Hyperkalemia
Inc’d Dietary Intake
Dec’d Urinary Excretion
Dec’d GFR
Aldosterone deficiency
Adrenal insufficiency
ACE inhibitors ( dec aldosterone)
Hyporeninemic hypoaldosteronism
Diabetic nephropathy
Aldosterone resistance
Potassium sparing diuretics
Internal Redistribution
IC to EC shift
Acidosis
Exercise
Cell Lysis
Rhabdomyolysis
Tumor lysis syndrome

11. Question 1
50yoM PMHx uncontrolled DM, had routine blood tests. His laboratory tests revealed serum creatinine 1.3 mg/dl, glucose 130 mg/dl, potassium 5.8 mEq/l, and a non-anion gap metabolic acidosis with serum HCO3 of 19 mEq/l. His BP control is chlorthalidone, lisinopril and amlodipine.

12. Question 1 Which of the following is the likely dx of his hyperkalemia and metabolic acidosis?
CKD
Lisinopril
Type 4 RTA
Increased intake
D – Inc’d intake

13. Hyperkalemia
Clinical Features Muscle weakness Cardiac effects- No clear correlation between serum potassium level and EKG changes Presence of hemodynamic instability indicates medical emergency

14. TTKG
Gradient of K between tubular lumen at collecting tubule level and interstitial space TTKG < 3 indicate kidney is not wasting K+ > 7 indicate renal wasting
U[K+]
UOsm
TTKG = 
P[K+]
POsm
U[K+]  POsm =
P[K+]  UOsm

15. Tx of Hyperkalemia Intra cellular Fluid 40 Liters K + 150 mEq/L
Extra Cellular Fluid Liters
PO intake
or IV
Potassium
Hyperkalemia
K +
Na +
To shift K from
EC to IC compartment
with
Plasma
Insulin
Catecholamine
Bicarbonate
Hyperkalemia
Urinary Excretion
GI excretion

16. Question 2 Give oral or rectal sodium polystyrene sulfonate
45yoF cc significant weakness. His potassium level is 6.5 mEq/L. ECG showed peaked T waves, but BP is stable. Which of the following statement is true regarding the mgmt ?
Give oral or rectal sodium polystyrene sulfonate
Sodium bicarbonate, 50-mL IV push and repeat K
Patient is stable and tx can safely wait for repeat labs
In addition to K depleting measures, give calcium gluconate
D – lower K and give calcium gluconate

17. Question 3
All of the following drugs cause shift in potassium from extracellular to intracellular space except ?
Inhaled albuterol
IV Sodium bicarbonate
Sodium polystyrene sulfonate
IV Insulin with Dextrose
C – sodium polystyrne sulfonate does not shift K ECF to ICF.

18. Hyperkalemia
Protect heart from high EC potassium levels, if EKG abNMLities present
CaCl or Ca gluconate (10 ml of 10% solution)
Protects the conduction system from the effects of high K
No effect on potassium levels

19. Potassium Shift From EC to IC
Insulin with Glucose
Rapid or slow infusion of Insulin with dextrose
Action starts within 10 to 20 minutes
2 agonist
Inhaled or IV albuterol
Less predictable compared to Insulin
IV Bicarbonate
Alkalosis causes K shift into cells

20. Reducing Total Body K+ Loop diuretics Mineralocorticoid
Inc’s renal potassium loss
It can be combined with thiazide diuretics
For acute cases, use IV doses of furosemide or bumetanide
Mineralocorticoid
Fludrocortisone 0.1 – 0.3 mg PO once a day
For mgmt of chronic hyperkalemia
ex. type IV RTA

21. Reducing Total Body K+ To inc GI excretion
Sodium polystyrene sulfonate (Kayexalate)
Exchanges K+ for Na+ in the colon
Is given with sorbitol (by mouth)
15-30 g and repeat the dose as needed
Use of sorbitol is associated with bowel necrosis.
If the patient is NPO, give just kayexalate without sorbitol rectally
Patiromer (Veltassa)
Exchanges K+ for Ca+ in the colon
Sodium free
No reports of bowel necrosis
Avoid taking medication for 3 hours after taking medication
Dialysis
Most effective, but limited to patients with renal failure

22. Question 4
45yoF cc kidney stone, PMHx generalized weakness, muscle pain, vomiting, joint pains. Dx of SLE was entertained, not confirmed, because of MSK symptoms and positive ANA. Physical examination was unremarkable except in pain secondary to kidney stone. . Laboratory test showed potassium of 2.6 mEq/l, non-anion gap metabolic acidosis with HCO3 of 15 mEq/l, and random urine pH of 7.0. CT scan of the abdomen revealed bilateral nephrocalcinosis.

23. Question 4
Which of the following is the likely cause of her clinical & laboratory presentation?
Type 4 RTA
Type 1 RTA
Type 2 RTA
Vomiting
B – type 1 RTA

24. Hypokalemia Serum Potassium < 3.5 mEq/l Causes: Poor PO intake
Redistribution into cells
Inc’d loss
Renal
Non-renal

25. Laboratory Renal potassium wasting: if Non-renal potassium wasting
Urine potassium loss > 20 mmol/ 24-hour
a spot urine K+ > 15 mmol per liter
Non-renal potassium wasting
Urine K+ < 20 mmol / 24-hour period
a spot urine <15 mmol per liter

26. Pseudohypokalemia
Inc’d uptake of potassium by metabolically active cells in a blood sample
laboratory artifact that may occur when blood samples remain in warm conditions for several hours before processing

27. Potassium Re-distribution
Hypokalemic periodic paralysis
Alkalosis
Catecholamines, insulin, B2 agonist
Barium

29. Hypokalemia with HTN High aldosterone and high renin:
Malignant HTN, renal artery stenosis and
renin secreting tumor.
b. High aldosterone and low renin:
Primary hyperaldosteronism, adenoma
Idiopathic hyperaldosteronism
Glucocorticoid remediable dz <1% and
Carcinoma <1%
c. Low aldosterone and low renin:
Cushing's syndrome (high cortisone levels),
Liddle Syndrome,
Apparent Mineralocorticoid Excess,
licorice ingestion (low cortisone levels)

30. HypoK Tx
Degree of K + deficit depends on size of intracellular compartment
~ mEq/L of K+ deficit in pts with serum K
~ mEq of K+ deficit in pts w/ plasma K+ from mEq/L.

31. Pearls >95% of total body potassium is present intracellularly
Potassium balance is maintained mainly by urinary excretion (90%) which is primarily regulated by aldosterone
In patients with CKD, GI excretion plays an important role in K+ excretion
Symptoms of hyperkalemia are usually nonspecific
Presence of ECG changes in hyperkalemia is an emergency, and requires tx with IV calcium gluconate
Goals are: to shift K from EC to IC compartment and deplete body K+ by inc’ing GI and renal excretion
Barium toxicity causes acute hypokalemia
Renal potassium wasting: if urine potassium loss > 20 mmol/ 24-hour, > 15 mmol/l on a spot urine sample in a hypokalemic person.
Highlight Points:
Do not wait for laboratory values to initiate treatment for patient with suspected Hyperkalemia based on ECG or PE