1. Potassium Homeostasis & Its disordersBy
Dr. Mohammad El-Tahlawi

2. Objectives Potassium homeostasis Hypokalamia Definition Causes Effects
Diagnosis
Treatment

3. Potassium play an important role in:
1-Electerophysiology of cell membrane
for all cells in which polarization-
depolaization cycles are functionally
relevant(cardiac and neuromuscular cells).
2-Carbohydrates and protien synthesis

4. POTASIUM DISTRIBUTION
Extracellular 2%
70 meq
Intracellular 98%
3430 meq
Plasma
20%
15 meq
Na-K ATPase
K content = 50 meq/kg
In 70 kg
Total body K = 3500 meq

5. K level in meq / L K=140 meq/L Extra cellular K=4 meq/L (3.5-4.5meq)
Intracellular
K=140 meq/L
Extra cellular
K=4 meq/L
( meq)

6. intracellular K deficit
Decrease in plasma K from meq/L
intracellular K deficit BY
meq

7. intracellular K deficit
Decrease in plasma K from meq/L
intracellular K deficit BY
meq

8. Plasma K concentration Correlates poorly with the total body k deficit

9. Plasma potassium concentration
Intake
Intercompartmental
distribution
Potassium
Excretion

10. Dietary K intake = 80 meq/day Excretion = 70 meq/day (urine).
= 10 meq/day (GIT).

11. Regulation of K excretion
The major determinant of urinary K excretion
Extra cellular K
Aldesterone level
Tubular flow rate

12. Intercompartmental shift of Potassium
1- Extracellular pH.
2- Circulating insulin level.
3- Circulating catecholamine activity.
4- Plasma osmolality.
5- Hypothermia.
6- Exercise.

13. pH Insulin Hypothermia Rewarming Sympathetic activity
K 0.6 meq/L every.01
Change in pH
Insulin
Na-K ATPase
Acidosis
Alkalosis
Hypothermia
Rewarming
CELL
B2-agonist
B2-blokade
Sympathetic activity
(Na-K ATPase)
Plasma osmolality
increase K 0.6meq/L per
increase10mosm/L

14. HYPOKALEMIA

15. HYPOKALAEMIA Causes: (K ion less than 3.5 meq/L)
1-Intercompartmental shift of K.
2-Increase k loss.
3-Inadequate k intake.

16. Intercompartmental shift of K:
Causes of hypokalamia
Intercompartmental shift of K:
Alkalosis
Insulin administration
B2 adrenergic agonist
Hypothermia
Treatment of megaloplastic anaemia
Periodic paralasis
Transfusion of frozen blood

17. Increase K losses (Renal or extrarenal) Renal:
Causes of hypokalamia
Increase K losses (Renal or extrarenal)
Renal:
Diuretics
Increase mineralocorticiod activity
Renal tubular acidosis
Ketoacidosis
Hypomagesaemia
Urinary diversion with long ileal loop
Carbinecillin and Amphotericin B
Prim and Sec hyper alderostenism

18. Extrarenal: Decrease K intake GIT : Diarrhea,Vomiting,Fistula,
Causes of hypokalamia
Extrarenal:
GIT : Diarrhea,Vomiting,Fistula,
Laxative abuse,Urinary diversion.
Sweet
Dialysis
Decrease K intake

19. Effects of hypokalemia
Most of the patients are asymptomatic until
K level below 3 meq/L.
Cariovascular effects are most prominent

20. Effects of hypokalamia
Cardiovascular
ECG changes
Dysrhythmia
Myocardial dysfunction
Myocardial fibrosis
Orthostatic hypotension
Increase digitalis toxicity

21. Effects of hypokalamia
Prominent U -
wave
Flat T
Depressed ST
segment
Normal
Decreasing Serum K +
Cardiovascular
ECG changes
T wave flattening
Prominent U wave
ST segment depresion
Increase P wave amplitude
Prolongation of PR interval

22. Effects of hypokalamia
Neuromuscular
Skletal ms. Weakness up to respiratory failure.
Tetany
Rhabdomyolysis
Ileus , Urine retention
Renal
Polyuria
Increase amonium production
Increase HCO3 reabsorption
Increase Na retension
Increased renin secretion→ increase AngII→ thirst

23. Effects of hypokalamia
Metabolic
Decrease insulin secretion
Decrease growth hormone secretion
Decrease aldesterone secretion
Hormonal
Negative nitrogen balance
Encephalopathy in liver disease

24. Approach to diagnosis

25. Hypokalemia Urine K Urine Chloride Less than 30 meq/L
More than 30meq/L
Urine Chloride
Diarrhea
Less than 15meq/L
More than 15meq/L
NG Drainage
Diuretics
Alkalosis
Mg depletion

26. Treatment of hypokalemia
The goal of therapy:
Is to remove the patient from immediate
danger and not necessarily to correct the
entire K deficit.
Firstly concern :
Any condition that promotes transcellular
K shift.

27. Potassium replacement
Oral replacement with KcL solution is generally safe(60-80 meq/d)
IV replacement :(Remember )
Serious cardiac manifestation.
Peripheral line not exceed 8 meq/h.
More than 8meq/h, centeral line is indicated.
Dextrose containing solution should be avoided.
ECG monitoring is mandatory in high rate infusion.

28. Potassium replacement
Solutions
Potassium chloride and potassium phosphate
Kcl: is available in 2meq/mL (5ml)
is of choice with metabolic alkalosis as it corrects chloride shifts.
Osmolality = 4000 mosm/kgH2O
K phosphate: is of choice with coexisting hypophatemia (e.g DKA)

29. Potassium replacement
Deficit =(3.5 - acutal serum K ) x 0.4 BW
Maintenence = 1 meq / kg BW / day

30. Potassium replacement
Infusion rate (pripheral line)
Not exceed 8 meq / h
Infusion rate (centeral line)
Standard method = 20 meq KcL in 100 ml saline/h
Maximum rate (serum k less than 1.5 meq/L)
We need peripheral line
= 40 meq kcL / h
= ( ½ BW meq/h)

31. Practical approach
If K level <2 mEq/L, deficit= 0.4 x wt(normal – measured K) we can give up to 0.5 mEq/kg/hr.
If K level reaches 2.5 mEq/L, slowly corrects K by giving 10 mEq/hr.
Add the daily intake (1 mEq/kg)

32. It is advisable to give K salts into large but not central vein.
Potassium products:
IV preparations
Oral: 15ml= 40 mEq (if conc. Of KCl in sol. is 10%)
Natural sources:
-Orange: one orange=300mg K
one litre juice=2.8gm K
-Bananas: one piece= 750mg K
K therapy in pediatrics: 1-3mEq/kg/every 1mEq decrease in K level with max. 3mEq/kg/day

33. Response to the treatment
At first The serum K may be slow to rise particularly if K losses are ongoing
Full replacement usually takes few days.
If there is refractory hypokalemia check magnessium level

34. ?

35. CONCLUSION Potassium has important role to vital body function .
Plasma K concentration is a function of relationship between entry, the intercompartemental distribution and excretion of K.
Hypokalemia : serum K less thd 3.5meq/L
Cause : Decrease intake, Losses and Intercompartemental
shift.
Effects : Cardiovascular,Neuromuscular,renal,Hormonal
and metabolic.
Diagnosis .
Treatment :Goals, replacement and response

36. Hyperkalemia

37. Hyperkalemia Plasma [K+] > 5.0
Hyperkalemia may be the result of disturbances in external balance (total body K+ excess) or in internal balance (shift of K+ from intracellular to extracellular compartments)

38. Hyperkalemia: Disorders of External Balance
Excessive
K+ intake
Acute & chronic
renal failure
Pseudo
hyperkalemia
 Distal tubular
flow
Distal tubular
dysfunction
Mineralocorticoid
deficiency

39. Fist clenching (local exercise effect)
Pseudohyperkalemia
Movement of K+ out of cells during or after blood drawing
Hemolysis
Fist clenching (local exercise effect)
Marked leukocytosis

40. Hyperkalemia: Disorders of External Balance
Excessive Potassium Intake
Oral or Parenteral Intake
K pencillin in high doses
Stored blood

41. Hyperkalemia: Disorders of External Balance
Decreased Renal Excretion
Acute and Chronic Renal Failure
Decreased Distal Tubular Flow
Volume depletion
Decreased effective arterial blood volume (CHF, cirrhosis)
Drugs altering glomerular hemodynamics with a decrease in GFR (NSAIDs, ACE inhibitors, ARBs)
Mineralocorticoid Deficiency
Combined glucocorticoid and mineralocorticoid (adrenal insufficiency)
Hyporeninemic hypoaldosteronism (diabetes mellitus)
Drug-induced (ACE inhibitors, ARBs)
Distal Tubular Dysfunction
Disorders causing impaired renal tubular function with hyporesponsiveness to aldosterone (interstitial nephritis)
Potassium-sparing diuretics (amiloride, triamterene, spironolactone)

42. Hyperkalemia: Disorders of Internal Balance
Insulin deficiency
2-Adrenergic blockade
Hypertonicity
Acidemia
Cell lysis

43. Clinical Manifestations of Hyperkalemia
Clinical manifestations result primarily from the depolarization of resting cell membrane potential in myocytes and neurons
Prolonged depolarization decreases membrane Na+ permeability through the inactivation of voltage-sensitive Na+ channels producing a reduction in membrane excitability
Cardiac toxicity
EKG changes
Cardiac conduction defects
Arrhythmias
Neuromuscular changes
Ascending weakness, ileus

44. EKG Manifestations of Hyperkalemia
Wide QRS
Complex
Shortened QT Interval
Prolonged PR Interval
Further Widening of
QRS Complex
Absent P -
Wave
Sine
Wave Morphology
(e.g. Ventricular Tachycardia)
Peaked T
wave
Normal
Increasing Serum K +

45. Medical Treatment of Hyperkalemia
Membrane Stabilization
IV calcium
Internal Redistribution
IV insulin (+ glucose)
-adrenergic agonist (albuterol inhaled)
Enhanced Elimination
Kayexalate (sodium polystyrene sulfonate) ion exchange resin
Loop diuretic
Hemodialysis

46. Practical approach Mild cases: K<6.5mEq/L→causal management
Moderate cases: K=6.5-8mEq/L:
-glucose infusion.
-glucose insulin infusion.
-NaHCO3
Severe cases: K>8mEq/L→calcium injection

47. Emergency measures:
-Dextrose 10%:
ml over 30min.
ml over the next few hours.
-Dextrose/insulin infusion
Insulin: 0.1U/kg then 1U/kg/hr (add minimum 2-3 glucose/U insulin). Onset of effect is 1-5 min.
-NaHCO3: 150mEq over several minutes
?increased pH causes K shift into cells.

48. Definitive measures:
Key oxalate (Na polysterene)
-Oral: 15-30g 2-4 times/day + sorbitol 20-25% (50ml/15gm resin)
The resin induces diarrhea and leads to K loss.
-Retention enema: 50gm in 200ml sorbitol 25%.
Every gm resin combines with 1mEq K in GIT.
Dialysis : in cases of RF.

49. ?

50. Potassium Disorders Normal homeostasis Hypokalemia Hyperkalemia
Etiologic factors
Algorithm for diagnosis
Hyperkalemia
Potassium Disorders