This document discusses electrolyte disturbances, focusing on sodium, potassium, and calcium. It provides normal levels, causes of hypo- and hyper- conditions, signs and symptoms, diagnostic tests, and treatment approaches for each electrolyte. For sodium, it describes hyponatremia and hypernatremia in detail. For potassium, it addresses hypokalemia and hyperkalemia. For calcium, it discusses hypocalcemia and the key roles of calcium in the body. The document is intended as an educational reference for electrolyte abnormalities.

1. Electrolytes disturbances
Radhwan Hazem Alkhashab
Consultant anaesthesia & ICU
2022

2. Sodium
Normal Na level in the blood is 135-145 meq/l.
Hyponatremia :
serum sodium is < 135 meq/l consider hyponatremia.
Results from excess Na loss or water gain
GI losses, diuretic therapy, severe renal dysfunction, severe
diaphoresis, DKA, unregulated production of ADH associated
with cerebral trauma, narcotic use, lung cancer, some drugs
Clinical manifestations
↓ BP, confusion, headache, lethargy, seizures, decreased
muscle tone, muscle twitching and tremors, vomiting, diarrhea,
and cramps
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3. Diagnosis of hyponatremia
Clinically which depend on underlying causes & serum levels:
Cerebral edema < 120 meq/l
Cardiac symptoms < 100 meq/l
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4. Labratory tests
we have 3 tests
1.plasma osmolality.
2.urinary osmolality.
3.urinary sodium excretion,(low Na and Cl concentration).
4.The cell is going to swell as water is pulled in from the ECF,
resulting in the increased Hct, and sometimes the increased K.
Decreased Na, Cl, Bicarbonate.
5. Urine specific gravity ↓ 1.010.
6. Generally, urine sodium is decreased EXCEPT in cases of
SIADH. In those cases, the urine Na is greater than 20 mEq/ L,
and the urine specific gravity is high.
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5. Treatment
Treatment should start when patient have symptoms or whem serum
Sodium < 120 meq/l.
Mild
 Water restriction if water retention problem (Euvolemic &
Hypervolemic).
 Increase Na in foods if loss of Na
Moderate
 IV 0.9% NS, LR (Hypovolemic)
Severe
 3% NS – short-term therapy in ICU setting (Hypovolemic)
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6. Calculation of Na deficit can be obtain from this equation .
Sodium deficit=total body water X (desired Na - present Na)
TBW = body wt x 0.6 males
TBW = body wt x 0.5 females
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7. Rate of correction depends on absence or presence of neurologic
dysfunction.
 In mild to moderate symptomatic patients :
(0.5 to 1 meq/l/hr or 10 to 12 meq/l over first 24 hours).
 In Severe symptomatic hyponatremia (<110 meq/l), hypertonic saline
in 1-2meq/l/h in the ist 3-4h.(total not exceed 12meq/l/24h)
Rapid correction can lead to…
1. osmotic demyelination syndrome(central Pontine myelinolysis).
2. chronic hyponatremia.
3. flaccid paralysis,dysarthria,dysphagia.
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8. Hypernatremia
S.sodium > 145 meq/l
Gain of Na in excess of water or loss of water in excess of Na
The symptoms are generally neuro in origin, and thought to be
related to the cellular shrinking as water goes to the ECF(contracted
ICF volume). Permanent brain damage can occur with prolonged or
severe hypernatremia
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9. Causes of hypernatremia
Deprivation of water; hypertonic tube feedings without water
supplements, watery diarrhea, greatly increased insensible
water loss, renal failure, use of large doses of adrenal
corticoids, excess sodium intake
 Impaired thirst coma.
 Diabetic ketoacidosis
 Non-ketotic hyperosmolar coma
 Excessive water loss diabetes insipidus
 Following administration of large quantities of hypertonic
saline solutions
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10. Signs/Symptoms
Early: Generalized muscle weakness, faintness, muscle
fatigue, desire for water .
Moderate: Confusion, thirst.
Late: Edema, restlessness, thirst, hyperreflexia, muscle
twitching, irritability, seizures, possible coma
Severe: Permanent brain damage, hypertension, tachycardia,
N & V
Patient may prone for intracerebral or subarachnoid
haemorrhage
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11. Labs:
Increased serum Na above normal level .
 Increased serum osmolality
 Increased urine specific gravity
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12. Treatment
Free water to replace ECF volume
Gradual lowering with hypotonic saline
Decrease by no more than 2 mEq/L/hr
Supplement tube feedings with free water
Correction should be done over 48 to 72 hours.
 Hypotonic solution like 5% dextrose.
Plasma Na should be lowered by 0.5 meq/l/hr or not more than
12meq/l/ 24 hrs.

13. To calculate water deficit
 Water deficit = plasma Na - 140 X TBW
140
Rapid correction can lead to…
 Seizures or permanent neurologic damage
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14. Anaesthetic implications
 Enhance uptake of inhalation anaesthtics by decreasing
cardiac output.
Predisposes to hypotension & hypoperfusion of tissues.
Decreases volume of distribution and reduction in dose of
intravenous agents
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15. Potassium
 Normal 3.5-5.5 mEq/L
 Major ICF cation.
Potassium is Vital in maintaining:
1. Normal cardiac and neuromuscular function,
2. Influences nerve impulse conduction,
3. Important in CHO metabolism,
4. Helps maintain acid-base balance,
5. Control fluid movement in and out of cells by osmosis
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16. Hypokalemia
Serum potassium level below 3.5 mEq/L
Causes
1) Loss of GI secretions.
2) Movement of K into the cells (DKA)
3) Prolonged fluid administration without K supplementation
4) Diuretics (some)
5) Metabolic alkalosis.
6) Hormonal( insulin).
7) Drugs : Beta 2 agonist, alpha antagonist.
8) Anabolic state , total parentral nutrition.
9) Renal :Hyperaldosteronism ,Congenital adrenal hyperplasia
10) Cushings syndrome
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17. Signs/Symptoms
1. Neuromuscular
Fatigue,
Myalgia,
Muscular weakness
Progressive weakness and hypoventilation
As severity increases
 Rhabdomyolysis
Paralytic ileus
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18. 2. Cardiovascular
Abormal electrocardiogram
Arrhythmias
 Orthostatic hypotension
 Decreased cardiac contractility
Potentiates arrhythmogenic potential of digoxin
 Myocardial fibrosis
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19. ECG Changes of hypokalemia
Appearance of U wave
 Flattening or inversion of T wave
ST segment depression
 Prolonged QT interval
 Prominent U wave
Prolonged PR interval
 Widening of QRS complex
 Ventricular arrhythmias
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20. Treatment
Hydrate if low UOP.
Oral replacement through high K diet.
IV supplementation :
No more than 10 mEq/hr; for child 2-4 mEq/kg/24 h.
No more than 40 mEq/L.
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21. Treatment of hypokalemia
If s.potassium < 3 mq/l needs definitive treatment
Management of severe symptomatic hypokalemia in patient with nil by
mouth:
1)Potassium deficit in mmol is calculated as given below:
Kdeficit (mmol) = (Knormal lower limit - Kmeasured) x kg body weight x 0.4
2) Daily potassium requirement is around 1 mmol/Kg body weight.
3) 13.4 mmol of potassium found in 1 g KCl.
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22. Example of K replacement
Suppose we get an asymptomatic patient of 70 Kg with a
serum potassium level of 3.0 mmol/L and he is on nil by
mouth but having an adequate diuresis, we proceed this way.
1) Deficit of potassium in mmol = (3.5 - 3.0) x 70 x 0.4 = 14
mmol
2) Daily potassium requirement = 1 x 70 = 70 mmol
3) Total requirement = 14+70 = 84 mmol = (84/13.4) = 6.3 g
KCl
Therefore we can give the patient 1.0 g KCl (around 13 mmol
of K+) in 500 mL Normal Saline (N/S) solution to run 4 hourly
and reassess the serum potassium level after 1 day. So, in
around 24 hours, we have given the patient around (24/4 = 6
pints of N/S solution, total KCl administered = 6.0 g i.e. around
80 mmol K+).
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23. Anaesthetic implications
oChronic hypokalemia more succeptible for arrhythmias.
oECG monitoring.
oGlucose free solutions.
oPotentiates neuromuscular blockers.
oAvoid alkalosis.
oHyperventilation avoided
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24. Hyperkalemia
Serum potassium level above 5.3 mEq/L
Causes:
1. Decreased renal excreation of potassium.
2. Renal failure.
3. Hypoaldosteronism.
4. Drugs: Spironolactone, ACE inhibitors.
5. Excessive K intake (IV or PO) especially in renal failure.
6. Tissue trauma.
7. Acidosis.
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25. 8. Due to extracellular movement of k+
 Acidosis.
 Hyperkalemic periodic paralysis.
 Succinylcholine.
 Rhabdomyolysis.
 Cell lysis following chemotherapy.
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26. Signs/Symptoms
ECG changes – tachycardia to bradycardia to possible
cardiac arrest.
 On EKG, tall tented T waves are noted. This is because
changes in cardiac conduction are occuring. Ventricular
dysrhythmias are common. Generally, cardiac changes begin
with a K around (6 – 7meq/l), but are always present with a K
level around 8.
 Muscle weakness, paralysis, paresthesia of tongue, face,
hands, and feet, N/V, cramping, diarrhea, metabolic acidosis
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27. Treatment
1. Calcium gluconate
10ml of 10% calcium gluconate IV over 5 to 10 min. Repeated
if no change in ECG is seen after 5 to 10 min
How it helps……?
 protects the myocardium
from toxicity to potassium
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28. 2. Insulin & glucose:
10 to 20 units of regular insulin in 50 ml of 25 to 50 % dextrose
Initial bolus should be followed by continous infusion of 5%
dextrose , the effect begins in 15 min & peak in 60 Min
3. Sodium bicarbonate:
 7.5 % of 50 to 100 ml is given as IV slowly over 10 to 20 min.
4. Beta agonist:
Salbutamol 20 mg in 4 ml saline by nebulisation
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29. 5. Loop & thiazide diuretics.
6. Cation exchange resins:
Sodium polystyren sulphonate, promote exchange of Na for K
in GIT , 25 to 50g with 100ml of 20% sorbitol 3 to 4 times a
day.
7. Haemodialysis
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30. Calcium
Ionized calcium is generally accepted as between 4.5 – 5.5.
Ionized calcium is the only form of calcium that is
physiologically relevant. Serum calcium is frequently
reported and must be adjusted for albumin levels and serum
proteins.
Normal plasma calcium 8.5 to 10.5 mg/dl.
 50% in ionized form ,40% protein bound,10% complexed
with anions
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31. Calcium
Required for :
Blood coagulation.
Neuromuscular contraction.
Enzymatic activity.
Strength and durability of bones and teeth
Ca absorption and concentration influenced by Vit D,
calcitriol (active form of Vitamin D), PTH, calcitonin, serum
concentration of Ca and Phosphate.
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32. Causes of Hypocalcemia
1. Hypoparathyroidism.
2. Vitamin D deficiency.
3. Nutritional malabsorption .
4. Hyperphosphatemia .
5. Pancreatitis.
6. Rhabdomyolysis.
7. Chelation of calcium:(Rapid blood transfusion, rapid infusion
of large amount of albumins).
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33. Signs/Symptoms
Abdominal and/or extremity cramping
Tingling and numbness
Positive Chvostek (Chvostek sign – abnormal spasm of the facial
muscle elicited by light taps on the facial nerve ),or Trousseau signs
(carpal spasm induced by inflating BP cuff on upper arm to pressure
exceeding systolic BP for 3 minutes ).
Tetany(Tetany is the most common sign of decreased calcium),
hyperactive reflexes
Irritability, reduced cognitive ability, seizures
Prolonged QT on ECG, hypotension, decreased myocardial
contractility
Abnormal clotting
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34. Treatment
 Symptomatic hypocalcemia – emergency 10 ml of 10%
calcium gluconate IV over 10 minutes.
 Serial calcium measurements .
 Correction of co-existing alkalosis
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35. Anaesthetic implicatons
Potentiates negative inotropic effect of barbiturates and
volatile anaesthetics.
 Laryngospasm.
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36. Hypercalcemia
Plasma calcium > 10.5 mg/dl.
Severe hyperCa is a very dangerous imbalance, and has greater
than a 50% mortality rate if not treated promptly.
Causes:
Mobilization of Ca from bone
Malignancy
Hyperparathyroidism
Immobilization – causes bone loss
Thiazide diuretics
Thyrotoxicosis
Excessive ingestion of Ca or Vit D
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37. Signs/Symptoms
Anorexia, constipation
Generalized muscle weakness, lethargy, loss of muscle tone,
ataxia
Depression, fatigue, confusion, coma
Dysrhythmias and heart block
Deep bone pain and demineralization
Polyuria & predisposes to renal calculi
Pathologic bone fractures.
Cardiac standstill can and does occur when the serum Ca
level near 18 mg / dl.
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38. ECG changes of hypercalcemia
Shortened QT
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39. Magnesium
Normal Mg level: 1.5 to 2.5 mEq/L.
Mg share in :
K and Na transport across cell membrane
Important in CHO and protein metabolism
Plays significant role in nerve cell conduction
Important in transmitting CNS messages and maintaining
neuromuscular activity.
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40. Magnesium
As Mg plays a role in nerve conduction, Mg affects the
cardiovascular system peripherally by producing vasodilation.
Decreases peripheral vascular resistance
Balance - closely related to K and Ca balance
Intracellular compartment electrolyte
Hypomagnesemia - < 1.5 mEq/L
Hypermagnesemia - > 2.5 mEq/L
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41. Hypomagnesemia
Causes
1. Inadequate intake
2. Reduced gasroinestinal absorption
3. Malabsorption
4. Small bowel /biliary fistula
5. Severe diarrhea
6. Prolonged nasogastric suctionig
7. Renal losses
8. Diuresis
9. Hyperparathyroidism
10.Drugs: theophylline, diuretics,ethyl alcohol
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42. Signs/Symptoms
1. Asymptomatic .
2. Associated with hypocalcemia & hypokalemia Anorexia.
3. Weakness.
4. Parasthesia.
5. Confusion,seizures&coma .
6. Atrial fibrillation.
7. Potentiates digitalis toxicity.
8. Prolongation of PR &QT interval
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43. Treatment
Mild:
Diet – Best sources are unprocessed cereal grains, nuts,
legumes, green leafy vegetables, dairy products, dried fruits,
meat, fish. (Diarrhea is a common side effect of increased dietary
Mg.
Magnesium salts
Symptomatic magnesium sulfate 1 - 2 g IV over 10 min.(1 ml of
50% solution contains 4 meq ).
 Monitor Mg q 12 hr
 Monitor vital signs, knee reflexes
 Precautions for seizures/confusion
 Check swallow reflex .
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44. Hypermagnesemia
Plasma mg > 2.5 meq/
Most common cause is renal failure, especially if taking large
amounts of Mg-containing antacids; DKA with severe water loss
Signs and symptoms
Hypotension, drowsiness, respiratory depression, coma, cardiac
arrest
 ECG – Bradycardia, CHB, cardiac arrest, tall T waves
 Hyporeflexia ,drowsiness & skeletal muscle
 Weakness
 Hypotension
 Prolonged PR interval & widening of QRS complex
 Respiratory arrest.
NOTE: Can appear falsely elevated with hemolyzed specimens.
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45. Treatment
Withhold Mg-containing products
Calcium chloride or gluconate IV for acute symptoms
IV hydration and diuretics
Monitor VS, LOC
Check patellar reflexes.
Do not administer Mg to renal impaired clients.
Ventilatory support and IV Ca is indicated for emergencies.
Dialysis can reduce Mg levels within 2-4 hours.
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46. Anaesthetic considerations
Potentiates negative inotropic effects of anaesthetics.
Neuromuscular blockers decreased by 25 to 50%
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47. End of lecture
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