Hypokalemia is an electrolyte disorder characterized by serum potassium levels below 3.5 meq/l, which can lead to serious complications like arrhythmias and paralysis. The document discusses potassium's physiological functions, its distribution in the body, clinical manifestations of hypokalemia, causes, diagnostic approaches, and treatment options. Effective management involves potassium replacement and addressing the underlying causes, with oral treatment preferred unless severe cases necessitate intravenous administration.

1. HYPOKALEMIA
Dr. Adhiya.N.S.S
M.D GENERAL MEDICINE
First Year Post Graduate

2. POTASSIUM
• It is the most abundant cation in the Human
Body.
– Total Body stores are approximately 3000 to 4000
mEq.
• It is a major intracellular cation.
– Intracellular K concentration : 130 -140 mEq/L
– Extracellular K concentration : 4 – 5 mEq/L
• It is found primarily in the muscles (70%), and to
a lesser extent in bone, red blood cells, liver and
skin.

3. FUNCTIONS OF POTASSIUM
• The normal ratio between extracellular and
intracellular potassium concentration is
important for the maintenance of the resting
membrane potential and neuromuscular
functioning.
• Intracellular Potassium:
– Cell growth and maintenance of cell volume
– DNA and Protein synthesis
– Acid –Base balance

4. POTASSIUM HOMEOSTASIS

8. HYPOKALEMIA
• It is an electrolyte disorder characterized by
Serum Potassium concentrations less than 3.5
mEq/L. (Normal Range: 3.5 – 5.0 mEq/L).
• It is present in upto 20% of hospitalized
patients and is associated with a ten-fold
increase in in-hospital mortality.
• It may be asymptomatic or have dangerous
complications such as arrthymias or paralysis.

9. CLINICAL MANIFESTATIONS OF
HYPOKALEMIA
• CARDIOVASCULAR:
– Increased Blood Pressure.
– Increased sensitivity to Arrhythmias.
– Increased risk of Digitoxicity.
• SKELETAL MUSCLES:
– Weakness, Flaccid muscle paralysis, Rhabdomyolysis.
• SMOOTH MUSCLE:
– Constipation, Ileus and rarely bladder dysfunction.
• ENDOCRINE:
– Worsening of glucose control in diabetics.

10. • RENAL:
– Polyurea due to Nephrogenic Diabetes Insipidus.
– It may lead to formation of Renal cysts.
– It may precipitate or worsen hepatic
encephalopathy due to increased renal ammonia
production.
– Increased ammonia production might also
contribute to the development of metabolic
alkalosis. Conversely metabolic alkalosis may
increase renal potassium excretion and cause
hypokalemia
– It may also cause Renal Failure as potassium
depletion causes tubulointerstitial fibrosis which is
characterised by vacuolization of PCT.

11. ECG CHANGES IN HYPOKALEMIA
• Flattening of T waves
• Prominent U waves
• Biphasic T waves (Dip and Rise pattern)
• ST depression
• QT prolongation/ QU prolongation (T-U fusion wave)
• PR prolongation
• Wide QRS
• Ventricular arrhythmias if associated with
hypomagnesaemia

12. POTASSIUM
LEVELS
ECG CHANGES
3.5 – 4.0 NORMAL
< 3.5 FLATTENING OF T WAVES
PROMINENT U WAVES
PROLONGED QT/ QU INTERVAL
< 3 SAGGING/ DEPRESSION OF ST SEGMENT
< 2.5 QRS WIDENING
PR PROLONGATION

13. CAUSES OF HYPOKALEMIA
• PSEUDOHYPOKALEMIA:
– After phlebotomy, if the blood is stored for
prolonged periods at room temperature, if large
number of leucocytes are present, they might take
up the potassium present in the serum.
– The most common cause is acute leukemia.
– Rapid separation of plasma and storage at 4
degree celcius is used to confirm this diagnosis.

14. CAUSES (Cont...)
• DECREASED INTAKE:
– Starvation or Dietary Deficiency
– Clay ingestion
• REDISTRIBUTION INTO CELLS:
A. Acid-Base:
1. Metabolic Alkalosis
B. Hormonal:
1. Insulin
2. Increased Beta 2 adrenergic activity – Post MI or Head
Injury
3. Beta 2 adrenergic agonists – Bronchodilators and
Tocolytics
4. Alpha adrenergic agonists
5. Thyrotoxic Periodic Paralysis
6. Downstream stimulation of Na/K – ATPase: Theophylline,
Caffeine

15. CAUSES (Cont...)
C. Anabolic state:
1. Vitamin B12 or Folic Acid administration leading to
increased Red Blood Cell production.
2. Granulocyte-Macrophage colony stimulating factor
leading to White Blood Cell production.
3. Total Parenteral Nutrition.
D. Familial Hypokalemic Periodic Paralysis
E. Hypothermia
F. Barium Toxicity: Systemic inhibition of Potassium
leak channels.

16. CAUSES (Cont...)
• NON-RENAL LOSS:
– Gastrointestinal loss:
• Upper GI loss – Vomiting, Nasogastric aspiration:
Associated with metabolic alkalosis.
• Lower GI loss – Diarrhoea, Laxative abuse, Villous
adenoma, Bowel obstruction/ fistula,
Ureterosigmoidostomy
– Integumentary loss:
• Sweat – In extremes of physical exertion.

17. CAUSES (Cont...)
• RENAL LOSS:
– Increased Tubular Flow:
• Diuretics
• Osmotic diuresis
• Salt-wasting Nephropathies
– Increased secretion of Potassium:
• Mineralocorticoid excess:
– Primary hyperaldosteronism
– Secondary hyperaldosteronism
– Genetic hyperaldosteronism
– Cushing’s Syndrome
– Bartter’s Syndrome
– Gitelman’s Syndrome

18. RENAL LOSS: (Cont...)
• Apparent mineralocorticoid excess:
– Genetic deficiency of 11 Beta dehydrogenase 2
– Inhibition of 11 Beta hydrogenase 2 (Carbenoxolone,
licorice)
– Liddle’s syndrome
• Distal delivery of non reabsorbed anions:
– Renal Tubular Acidosis
– Diabetic Ketoacidosis
– Penicillin derivatives
– Toluene Abuse (Glue sniffing)
• Magnesium deficiency

19. APPROACH TO HYPOKALEMIA

21. TRANSTUBULAR POTASSIUM
GRADIENT
• TTKG is the ratio of potassium concentration in
the lumen of cortical collecting duct to that in the
peritubular capillaries.
• TTKG = Urine Potassium x Serum osmolality/
Serum Potassium x Urine osmolality
• During hypokalemia, TTKG should fall below 3
indicating an appropriately reduced urinary
excretion of potassium.
• TTKG greater than 4 indicates renal potassium
loss due to increased distal potassium secretion.

22. TREATMENT OF HYPOKALEMIA
• The goals of therapy are
– To prevent life-threatening or serious consequences
– To replace the potassium deficit
– To correct the underlying cause
• Urgency of therapy depends on severity of
hypokalemia, rate of decline and associated
clinical factors.
• Serum potassium drops by 0.27 mmol for every
100 mmol reduction in body stores.

23. REPLACEMENT OF POTASSIUM DEFICIT
• Oral correction is the preferred route of
treatment.
• Potassium Chloride is the mainstay of therapy
because increase in extracellular potassium is fast
compared with other salts.
• Potassium phosphate is appropriate in patients
with combined hypokalemia and
hypophosphatemia.
• Potassium citrate should be considered in
patients with concomitant metabolic acidosis.

24. REPLACEMENT OF POTASSIUM DEFICIT
(Continued..)
• IV administration should be limited to patients
unable to use enteral route or in the setting of
severe complications.
• IV KCl is preferred.
• It should be administered in saline solutions,
rather than dextrose , because the dextrose
induced increase in insulin can acutely
exacerbate hypokalemia.

25. REPLACEMENT OF POTASSIUM DEFICIT
(Continued..)
• The peripheral intravenous dose is 20-40 mEq/L.
Higher concentrations can cause chemical
phlebitis, irritation and sclerosis.
• If severe hypokalemia(<2.5 mEq/L) is present or if
the patient is critically symptoatic, IV KCl should
be administered through a central line at the
rates of 10-20 mEq/hr.
• 1 ampule of KCl is equal to 10ml.
1 ml is equal to 2 mEq.
So 1 ampule has 20 mEq. And 20 mEq increases
potassium by 0.25 mEq/L.

26. REFERENCES
• HARRISON’S PRINCIPLES OF INTERNAL
MEDICINE – 20TH EDITION
• Comprehensive Clinical Nephrology by Richard
J. Johnson
• Hypokalemia: a clinical update
Efstratios Kardalas, Stavroula A
Paschou, Panagiotis Anagnostis, Giovanna
Muscogiuri, Gerasimos
Siasos, and Andromachi Vryonidou

27. THANK YOU