Lecture By: By: Dr. Muhammad Asim Fazal ICU Doctor.Meeqat Hospital,Madina, KSA

1. By: Dr. Muhammad Asim Fazal

2. Definition
 An electrolyte disorder is an imbalance of certain
ionized salts
(i.e., bicarbonate, calcium, chloride, magnesium, phos
phate, potassium, and sodium) in the blood.

3. Electrolytes
 Electrolytes are ionized molecules found throughout
the blood, tissues, and cells of the body.
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Cations
Anions
+ ve
- ve

4. General Functions of Electrolytes
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Help to balance pH and acid-base levels in the body.
Facilitate the passage of fluid between and within
cells through osmosis
• Play a part in regulating the function of the
neuromuscular, endocrine, and excretory systems.

5. Specific Electrolytes – Functions
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Sodium (Na)
• Helps to balance fluid levels in the body and
• Facilitates neuromuscular functioning.
• Potassium (K)
• Main component of cellular fluid
• Helps to regulate neuromuscular function and
osmotic pressure.

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Calcium (Ca)
Affects neuromuscular performance and
Contributes to skeletal growth
Blood coagulation.
Magnesium (Mg)
Influences muscle contractions and
Intracellular activity

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Chloride (CI-)
Regulates blood pressure.
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Phosphate (HPO4)
Impacts metabolism and
regulates acid-base balance and
calcium levels.
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Bicarbonate (HCO3)
Assists in the regulation of blood pH levels

8. Normal levels of electrolytes
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Sodium.
135-145 mEq/L (serum)
Potassium.
3.5-5.5 mEq/L (serum)
Calcium(Serum)
8.8-10.4 mg/dL (total Ca)
Magnesium (Plasma)
1.4-2.1 mEq/L
Chloride(Serum)
100-108 mEq/L
Phosphate (Plasma)
2.5-4.5 mg/dL (adults)

9. Sodium
•
Normal : 135-145 mEq/L
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Sodium helps the kidneys to regulate the amount
of water the body retains or excretes.

10. HYPERNATREMIA
(Serum sodium > 145 mEq/L)
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Inadequate water intake
Increased sodium intake
Excessive free water loss:
Extra-renal
Burns
Sweating
Tachypnoea

11. •
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Renal
Central diabetes insipidus
Nephrogenic diabetes insipidus
Craniophariangioma
Post-operative

12. Symptoms of hypernatremia
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Non-specific,
Restlessness,
Irritability,
Muscular twitching,
Hyperreflexia,
Spasticity, and
Seizures
With hypotonic losses - signs of volume loss
Tachycardia,
Hypotension,
Decreased JVP,
Dry mucosa,
Reduced skin turgor and
Thick doughy skin

13. Treatment of Hypernatremia
 Acute Hypernatremia can be corrected rapidly
 Chronic Hypernatremia (more than 48 hours) should
be corrected slowly.
 If hypernatremia is rapidly corrected, the osmotic
imbalance may cause cerebral edema and potentially
severe neurologic impairment.
 Aim for serum sodium correction of approximately 12
mol/L/24h (0.5 mmol/L/h)

14. Volume in (L) to be replaced = Current TBW × [Na] – 140
/ 140
where TBW is typically 50% of total mass in women and
55% of total mass in men.

15. Hypernatremia with hypovolemia
 Patients should receive isotonic 0.9% normal saline to
restore euvolemia and to treat hyperosmolality
 After adequate volume resuscitation with normal
saline, 0.45% saline or 5% dextrose (or both) can be
used to replace any remaining free water deficit.

16. Hypernatremia with euvolemia
 Water ingestion or intravenous 5% dextrose will result
in the excretion of excess sodium in the urine.

17. Hypernatremia with hypervolemia
 Furosemide (1mg/kg) to get rid of sodium + Free water
replacement as 5% D/W
 • (* furosemide alone will aggravate the
hypernatremia
 • Dialysis may be required for patients with oliguric
renal failure

18. HYPONATREMIA
(Serum sodium less than 135
mEq/L)of all hospitalized patients develop
 Up to 1%
hyponatremia, making it one of the most common
electrolyte disorders.
 Hyponatremia usually reflects excess water retention
relative to sodium rather than sodium deficiency.
 The clinician should be wary about hyponatremia
since mismanagement can result in neurologic
catastrophes from cerebral osmotic demyelination.

20. Symptoms andis Signs depends on its
 Whether hyponatremia symptomatic
severity and acuity.
 Chronic disease can be severe (sodium concentration <
110 mEq/L), yet remarkably asymptomatic because the
brain has adapted by decreasing its tonicity over weeks
to months.
 Acute disease that has developed over hours to days
can be severely symptomatic with relatively modest
hyponatremia.

21. 
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Nausea
• Abdominal cramping, and/or vomiting
• Headache
• Edema (swelling)
• Muscle weakness and/or tremor
• Paralysis
• Disorientation
• Slowed breathing
• Seizures
• Coma

22. Complications
 The most serious complication of hyponatremia is
iatrogenic cerebral osmotic demyelination from overly
rapid sodium correction.
 Also called central pontine myelinolysis.
 Demyelination may occur days after sodium
correction or initial neurologic recovery from
hyponatremia.
 The neurologic effects are generally catastrophic and
irreversible.

23. Correction of Hyponatremia
 Treatment depends on:
 Etiology and types of hyponatremia
 Clinical Condition
 Serum Na level
 Ongoing loss

24.  Regardless of the patient’s volume status, another
common feature is to restrict free water and hypotonic
fluid intake, since these solutions will exacerbate
hyponatremia.
 Free water intake from oral intake and intravenous
fluids should generally be < 1–1.5 L/d.

25. Hypovolemic patients
 Require adequate fluid resuscitation from isotonic
fluids (either normal saline or lactated Ringer
solution) to suppress the hypovolemic stimulus for
ADH release.
 Patients with cerebral salt wasting may require
hypertonic saline to prevent circulatory collapse; some
may respond to fludrocortisone.

26. Hypervolemic patients
 May require loop diuretics or dialysis, or both, to
correct increased total body water and sodium.
 To treat the basic CAUSE.

27. Euvolemic patients
 May respond to free water restriction alone.

28. Formula for Correction

29. For Example
 a non edematous, severely symptomatic 70 kg woman
with a serum sodium of 122 mEq/L should have her
serum sodium corrected to approximately 132 mEq/L
in the first 24 hours. Her sodium deficit is calculated
as:

31.  3% hypertonic saline has a sodium concentration of
514 mEq/1000 mL. The delivery rate for hypertonic
saline can be calculated as:

33.  Hypertonic saline in hyper-volemic patients can be
hazardous, resulting in worsening volume
overload, pulmonary edema, and ascites.

34. Potassium
• Normal : 3.5-5.5 mEq/L
 Main component of cellular fluid
•
Helps to regulate neuromuscular function and
osmotic pressure

35. Hyperkalemia
S. Potassium > 5.5 m Eq/L
 Signs and Symptoms
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Fatigue
Weakness
Tingling, numbness, or other unusual sensations
Paralysis
Palpitations
Difficulty breathing

36. ECG Changes
 ECG changes in hyperkalemia include bradycardia, PR
interval prolongation, peaked T waves, QRS
widening, and biphasic QRS–T complexes.
 Conduction disturbances, such as bundle branch block
and atrioventricular block, may occur.
 Ventricular fibrillation and cardiac arrest are terminal
events.

37. Hyperkalemia - Etiology
 What Causes It?
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Inadequate Excretion :
• Renal failure
• Addison’s disease
• Excessive intake
• Diet high in potassium
(bananas, oranges, tomatoes, dates, high protein
diets, salt substitutes, potassium supplements)

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Shifting of potassium from tissues
• Trauma, especially crush injuries or burns
• Hemolysis
• Acidosis
• Insulin deficiency
• Drugs
• Digoxin, scuuinyl choline, beta agonists, potassium
sparing diuretics

39. Treatment of Hyperkalemia
 Mild: (Serum K+ = 5.5 to 6.0 m Eq/L)
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Stop intake of potassium
 • Stop offending drugs
 Restrict potassium rich diet

40.  Moderate to Severe: (in addition to above..)
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(Serum K+ = 6.0 to 8.0 m Eq/L or peaked T
waves)
 • Glucose Insulin Infusion : (0.5g/kg with 0.3 U
regular insulin / g of glucose)
 • Sodabicarb infusion (2 mEq/kg of NaHCO3 over 5
– 10 min)

41.  IV Calcium gluconate 0.5 mEq/kg – to reverse cardiac
effects
 • Dialysis in cases of resistant hyperkalemia
 • Nebulized salbutamol
 • Sodium polyesterene sulphate - ion exchange resin
for long term management

42. Hypokalemia
(Serum K+ < 3.5 mEq/L)
 Increased Potassium Loss:
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Extrarenal – Diarrhoea
Renal – RTA, polycystic kidneys, Drugs
Endocrine – Cushing’s disease, hyperaldosteronism
Decreased Stores
Malnutrition
Shift into intracellular compartment
Alkalosis
hyperinsulinemia

43. Symptoms and Signs
 Muscular weakness, fatigue, and muscle cramps are
frequent complaints in mild to moderate hypokalemia.
 Gastrointestinal smooth muscle involvement may
result in constipation or ileus.
 Flaccid
paralysis, hyporeflexia, hypercapnia, tetany, and
rhabdomyolysis may be seen with severe hypokalemia
(< 2.5 mEq/L).

44. Laboratory Findings
 Urinary potassium concentration is low (< 20 mEq/L)
as a result of extrarenal loss (eg, diarrhea, vomiting)
and inappropriately high (> 40 mEq/L) with renal
loss (eg, mineralocorticoid excess, Bartter
syndrome, Liddle syndrome)

45. Electrocardiogram
 The electrocardiogram (ECG) shows decreased
amplitude and broadening of T waves, prominent U
waves, premature ventricular contractions, and
depressed ST segments.

46. Treatment of Hypokalemia
 Oral potassium supplementation is the safest and
easiest treatment for mild to moderate deficiency.
 Intravenous potassium is indicated for patients with
severe hypokalemia and for those who cannot take oral
supplementation.
 For severe deficiency, potassium may be given through
a peripheral intravenous line in a concentration up to
40 mEq/L and at rates up to 10 mEq/h.

47.  Concentrations of up to 20 mEq/h may be given
through a central venous catheter.
 Continuous ECG monitoring is indicated, and the
serum potassium level should be checked every 3–6
hours.
 Magnesium deficiency should be
corrected, particularly in refractory hypokalemia.

48. Formula for correction of
Potassium
 Required K+ in mmol = 0.3 × Weight × [ Desired K+
level – Measured K+ level]
 Deficit corrected over 24 hour period.

49. HYPERCALCEMIA
(Serum Ca++ > 12 mg/dL)
 Parathyroid excess
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Multiple myeloma,
Vitamin D excess
Sarcoidosis
Subcutaneous fat necrosis
William’s syndrome
Thyrotoxicosis
Prolonged immobilization

50.  Metastatic cancer,
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Multiple bone fractures,
• Milk-alkali syndrome, and
• Paget's disease.
• Drugs
• Excessive use of calcium-containing supplements
• Certain over-the-counter medications
(i.e., Antacids) may also cause hypercalcemia.

51. HYPERCALCEMIA - Symptoms
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Nonspecific
• fatigue
• constipation
• depression
• confusion
• muscle pain
• nausea and vomiting
• dehydration
• increased urination
• irregular heartbeat (arrhythmia)
• Urinary stones
• Nephrocalcinosis
• Stupor & coma – S.Ca > 15 mg/dL)

52. HYPERCALCEMIA - Management
 Forced saline diuresis with fruesemide
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Treat primary cause
 Bisphosphonates are the treatment of choice for
hypercalcemia of malignancy. Although they are safe,
effective, and normalize calcium in > 70% of patients,
bisphosphonates may require up to 48–72 hours before
reaching full therapeutic effect.
 Calcitonin may be helpful in the short-term until
bisphosphonates reach therapeutic levels.

53.  In emergency cases, dialysis with low calcium dialysate
may be needed.

54. HYPOCALCEMIA
(Serum Calcium < 8 mg/dL)
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Vitamin D deficiency
• Malabsorption
• Abnormal metabolism
• Prolonged phynetoin medication
• Increased Losses
• Idiopathic hypercalcuria
• Renal tubular necrosis
• Frusemide therapy
• Hypomagnesemia
• Hyperphosphatemia

55. •
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Metabolic causes
Hypoparathyroidism
Pseudohyperthyroidism
Hypoprotenemia
Acute pancreatitis

56. HYPOCALCEMIA - Symptoms
 Muscle cramps and spasms
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Tetany and/or convulsions
Mood changes (depression, irritability)
Dry skin
Brittle nails
Facial twitching
Latent Tetany
Trousseu’s sign
Chvostek’s sign

57. HYPOCALCEMIA - Management
 Tetany, laryngospasm, seizures
•
2 ml/kg of 10 5 Calcium gluconate slow IV under
cardiac monitoring
 • Later
 • Oral calcium supplementation – 40 to 80 mg/kg/d
 • Treat Vit. D def.

58. HYPERMAGNESEMIA
 End-stage renal disease,
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Addison's disease, or
An overdose of magnesium salts.

59.  Lethargy
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Hypotension
Decreased heart and respiratory rate
Muscle weakness
Diminished tendon reflexes

60. Treatment
 Exogenous sources of magnesium should be
discontinued.
 Calcium antagonizes Mg2+ and may be given
intravenously as calcium chloride, 500 mg or more at a
rate of 100 mg (4.1 mmol) per minute.
 Hemodialysis or peritoneal dialysis may be necessary
to remove magnesium, particularly with severe kidney
disease.

61. HYPOMAGNESEMIA
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Inadequate dietary intake
• Chronic alcoholism
• Malnutrition
• Malabsorption syndromes,
• Pancreatitis,
• Aldosteronism,
• Burns,
• Hyperparathyroidism,
• Digestive system disorders, and
• Diuretic use.

62. Signs and symptoms
 Leg and foot cramps
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Weight loss
Vomiting
Muscle spasms, twitching, and tremors
Seizures
Muscle weakness
Arrthymia

63. Treatment
 Symptomatic hypomagnesemia requires intravenous
magnesium sulfate 1–2 g over 5–60 minutes mixed in
either dextrose 5% or 0.9% normal saline.

64. THANKYOU