For electrolytes

1. Electrolyte disturbances

2. Disorders of sodium balance
Normal plasmas sodium’s 135 to 145 meq /l

3. Hyponatremia
Plasma sodium < 135 meq/l
( Hypoosmolal hyponatremia)

4. Types
• Hypovolemic
• Euvolemic
• Hypervolemic

5. • Renal
• Diuretics
• mineralocorticoid deficiency
• salt wasting nephropathies
• osmotic diuresis
• renal tubular acidosis
• Gastrointestinal
• vomiting
• Diarrhea
• Fistula
• integumentary
• sweating
Hypovolemic

6. Euvolemic
• Primary polydipsia
• SIADH
• Arginine vasopressin release due to pain, nausea
• Glucocorticoid deficiency
• Hypothyroidism
• Chronic renal insufficiency

7. Hypervolemic
• Congestive cardiac failure
• Cirrhosis
• Nephrotic syndrome

8. Pseudohyponatremia
• Hyponatremia with normal plasma Osmolality
marked hyperlipidemia
marked hyperproteinemia
TURP syndrome
Hyponatremia with elevated plasma osmolality
hyperglycemia

9. Clinical features
• Primarily neurological
• Increased ICF volume
• Severity : depends on rapidity of onset and absolute
increase In plasma sodium concentration
• Asymtomatic or nausea, vomiting
• Depressed level of consciousness, confusion,
agitation
• Stupor , seizures and coma.

10. • Cerebral edema < 120meq/I
• Cardiac symptoms < 100meq/l

11. Diagnosis
• history &physical examination
• 3 tests
plasma osmolality
urinary osmolality
urinary sodium excretion
•Plasma osmolality= 2 Na+ glucose+ BUN
18 2.8

12. Treatment
Goals of therapy
• To raise plasma sodium concentration by restricting
water intake and promoting water loss
• To correct underlying disorder

13. principles
• 0.9% & 3% saline: Hypovolemic
• Water restriction: Euvolemic
&
Hypervolemic

14. • When to treat...?
•Symptomatic
•Plasma sodium < 120meq/l

15. • Cont....
•Rate of correction depends on absence or presence
of neurologic dysfunction.
•In a symptomatic patients :
0.5 to 1meq/I/hr or 10 to 12meq/l
over First 24 hours
• Severe symptomatic hyponatremia(<110meq/I)
hypertonic saline
1 to 2 meq /l/hr for the first 3 to 4 hrs
total not exceeding more than 12meq/l/24 hr

16. To calculate Na deficit
•Sodium deficit =total body water X
(desired Na – present Na)
•TBW= body wt x 0.6 males
0.5 females
Change in plasma sodium
infusate Na/1 – serum Na
TBW + 1

17. Case history
• A 45year male,50 kg by wt presented with altered sensorium and agitation
.a diagnosis of hypoosmolar hyponatremia is made .plasma sodium is 110
meq /1.
• Sodium requirement =desired Na – serum Na X TBW
= 130-110 Х 0.6 Х 50 =600meq
Change in Na= infusate Na – serum Na
TBW + 1
=513-110 = 403 = 13 meq /1
30+ 1 31
100ml 1.3meq/1
800 ml over 24hrs app 34ml/ hr

18. Rapid correction can lead to
• osmotic demyelination syndrome(central Pontine
myelinolysis)
• chronic hyponatremia
• flaccid paralysis, dysarthria, dysphagia.
• No specific treatment.

19. Anesthetic implications
•Plasma Na > 130meq/l for patients undergoing
elective surgery & is considered safe
• Lower level scan result in significant cerebral
edema
Decrease in MAC :intraoperatively
Agitation & confusion: postoperatively

20. Hypernatremia
Plasma sodium >145meq/l

21. causes
 Impaired thirst
• Coma
• essential hypernatremia
Solute diuresis
• Diabetic ketoacidosis
• non- ketotic hyperosmolar coma
excessive water loss
• diabetes insipidus
• sweating

22. Types
 Hypernatremia with low body sodium content
 Hypernatremia with normal body sodium content
 Hypernatremia and increased body sodium content

23. Hypernatremia with low body sodium content
 Water loss in excess of sodium loss
• Eg :
₋Osmotic diuresis
₋Diarrhea
₋sweating

24. Hypernatremia with normal total body
sodium content
 Due to water loss
 Diabetes insipidus
• central diabetes insipidus
•nephrogenic diabetes insipidus

25. Hypernatremia and increased total body
sodium content
• Following administration of large quantities of hypertonic
saline solutions

26. Clinical features
• Mainly due to contracted ICF volume
• Mainly neurological
₋ alerted mental status
₋ irritability
₋ weakness
₋ focal neurological deficits
₋ coma & death
• Prone for intracerebral or subarachnoid hemorrhage

27. Treatment
•Goals of therapy
• To correct water deficit
• To stop ongoing water loss

28. principles
• Correction should be done over 48 to 72 hours.
• Hypotonic solution like 5%dextrose.
• Plasma Na should be lowered by 0.5meq/1/ hr or not
more than 12 meq /l/24hrs.

29. • To calculate water deficit
• Water deficit = plasma Na - 140 X TBW
140
Rapid correction can lead to ......
 Seizures or permanent neurologic damage

30. Disorders o f potassium balance
•Normal plasma potassium is 3 . 5 to 5 meq/l

31. Hypokalemia
Plasma potassium < 3 . 5 meq/l

32. causes
1. Redistribution into cells
2. Increased loss
3. Decreased intake

33. Redistribution into cells :
Metabolic alkalosis
 Hormonal
insulin
beta2 agonist
alpha antagonist
 Anabolic state
vit B 12/folic acid
total parentral nutrition
 others
Hypokalemic periodic paralysis
hypothermia
barium toxicity.

34. Increased-loss :
• Renal
primary hyperaldosteronism
secondary hyperaldosteronism
congenital adrenal hyperplasia
cushings syndrome
bartters syndrome
liddles syndrome
renal tubular acidosis
diabetic keto acidosis
diuretics, aminoglycosides, penicillin amphotericin-B
• Gastrointestinal

35. Decreased intake :
• Starvation
•Clay ingestion

36. Clinical features
• Manifestations vary between patient
• Asymptomatic
• < 3mq/l
• Fatigue , myalgias & lower extremity
• Weakness

37. Neuromuscular
• Fatigue , myalgia , muscular weakness
• Progressive weakness and hypoventilation as severity
increases
• Rhabdomyolysis
• Paralytic ileus

38. cardiovascular
• Abnormal electrocardiogram
• Arrhythmias
• Orthostatic hypotension
• Decreased cardiac contractility
• Potentiates arrhythmogenic potential of digoxin
• Myocardial fibrosis

39. Therapeutic goals
• To correct potassium deficit
• To minimize ongoing losses
• To prevent life threatening complications

40. principles
• Safer to correct potassium via oral route
• A decrement of 1mmol/l in plasma potassium may
represent a total body k+ deficit of 200 to 400meq
• Dextrose containing solutions avoided

41. When to treat...?
₋ 3.5 to 4 mq/l
Increased intake of potassium containing food.
₋ 3 to 3.5mq/l
 Only in high risk patients.
₋ < 3 mq/l
needs definitive treatment.

42. Oral potassium
• Safer
• Potassium chloride preparation of choice
• Potassium bicarbonate and citrate
• Mild to moderate hyperkalemia kcl 60 to 80meq/day in 3 to 4 divided
doses
• Severe or symptomatic - kcl 40 mq 6 th hourly under ECG
monitoring
• 15 ml solution=20 meq

43. Iv potassium
• Severe symptomatic hypokalemia
• Continuous ECG monitoring &frequent k+ estimation
• Never give KCI directly IV
• Rapid IV correction can caused dangerous hyperkalemia.
• Use isotonic saline
• Do Not mix with dextrose containing

44. • Cont.....
 15% KCI solution in 10 ml ampoule.
 10m l= 20meq of potassium=1.5 g KCI.
 How long to give?
 As cardiac rhythm returns to normal KC drip is tapered and oral k
+ initiated.
 Should not exceed 8meq/ hr via peripheral vein
centrals Venous catheter in case of faster replacements & should
not exceed more than 20meq/hour

45. Hyperkalemia
•Plasma potassium > 5 meq/l

46. •Causes
• Decreased renal excretion of potassium
renal failure
primary hypoaldosteronism
secondary hypoaldosteronism
• Drugs
Spironolactone
Nsaids
ace inhibitors
trimethoprim

47. Cont...
• Due to extracellular movement of k +
Acidosis
hyperkalemic periodic paralysis
Succinylcholine
Rhabdomyolysis
cell lysis following chemotherapy digitalis overdose
• Enhanced chloride reabsorption
Cyclosporine
Gordons syndrome
• Increased potassium intake

48. Clinical features
Skeletal
• Weakness , flaccid paralysis
• Hypoventilation

49. cardiac
• Increased T-wave amplitude 6t o7meq/1
Prolonged PR interval
• QRS widening 7 to 8meq/1
• Loss of P wave
• Sine wave pattern 8 to 9 meq/1
• Ventricullar fibrillation or asystole > 9meq/1

50. Treatment
Principles
• >6meq/I should be treated
• To minimize membrane excitability
• To shift potassium into cells
• Promote potassium loss

51. Calcium gluconate
• 10% solution in 10 ml ampoules
• 10 ml 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

52. Insulin & glucose
• 10 to 20 units of regular insulin in 50 ml of 25 to 50%
dextrose
• Initial bolus should be followed by continuous infusion of 5%
dextrose
• effect begins in 15 min & peak in 60 min

53. cont.....
• Sodium bicarbonate
7.5% of 50 to 100 ml is given as IV slowly over 10 to 20 min
• Beta agonist
Salbutamol 20 mg in 4 ml saline by nebulization
• Loop & thiazide diuretics
• Cation exchange resins
sodium polystyren sulphonate promote exchange of Na for K in GIT
25 to 50 g with 100 ml of 20% sorbitol 3 to 4 times a day
• Haemodialysis

54. Anesthetic implications
• ECG monitoring
• Succinylcholine avoided
• Potassium free solutions
• Avoid acidosis
• Potentiates neuromuscular blockers
• Mild hyperventilation

55. Disorders of calcium balance
Normal plasma calcium 8.5 to 10.5mg/dI.
1. 50% in ionized form
2. 40% protein bound
3. 10% complexed with anions

56. Hypocalcemia
Plasma calcium < 8.5mg dl

57. Causes
• Hypoparathyroidism
• Vitamin D deficiency
Nutritional
malabsorption
• Hyperphosphatemia
• Precipitation of calcium
Pancreatitis
rhabdomyolysis
• Chelation o f calcium
rapid blood transfusion
rapid infusion of large amount of albumins

58. • Hallmark of hypocalcemia is TETANY
• Paresthesia in circumoral region & extremities
• Laryngospasm, bronchospasm
• Abdominal cramps, urinary frequency
• Hypotension &arrhythmias
• Latent hypocalcemia
Chvosteks sign
Trousseaus sign
ECG prolongation of QT interval

59. Treatment
• Symptomatic hypocalcemia- emergency
10ml of 10% calcium
gluconate IV over 10 minutes
• Iv calcium should not be given with bicarbonate or phosphate
containing solution
• Serial calcium measurements
• Correction of co-existing alkalosis

60. Hypercalcemia
Plasma calcium > 10.5 mg/dl

61. causes
• Hyperparathyroidism
• Malignancy
• Paget's disease of bone
• Excessive vitamin D intake
• Granulomatous disorders
• Milk-alkali syndrome
• Drugs
Thiazides
lithium

62. Clinical features
• Anorexia
• Nausea , vomiting
• Weakness
• Polyuria
• Ataxia
• Irritability
• Lethargy
• confusion

63. ECG changes
• Pronged PR interval
• Widened QRS complex
• Shortened QT

64. Treatment
• Hydration with normal saline
• Loop diuretics like frusemide
• hemodialysis
• Urine output > 3 liters /day
• k+ and Mg+
• Severe cases bisphosphonates
Pamidronate 60 to 80 mg iv over 4 hrs.
calcitonin 2 to 8 U subcutes
• 90% due to malignancy

65. Anesthetic implications
• Saline diuresis
• K+ & Mg+
• Decreased dose of neuromuscular blockers
• Cup & pulmonary pressure monitoring
• Hyperventilation avoided

66. Disorders o f magnesium balance
Hypomagnesemia
Plasma mg+ < 1 . 7meq/l

67. causes
• Inadequate intake
• Reduced gastrointestinal absorption
Malabsorption
small bowel /biliary fistula
severe diarrhea
prolonged nasogastric suctioning
• Renal losses
Diuresis
hyperparathyroidism
• Drugs
Theophylline
diuretics, ethyl alcohol
Aminoglycoside , amphotericin B

68. Clinical features
• Asymptomatic
• Associated with hypocalcemia & hypokalemia
• Anorexia , weakness , paresthesia
• Confusion , seizures & coma
• Atrial fibrillation
• Potentiates digitalis toxicity
• Prolongation o f PR &QT interval

69. Treatment
• Asymptomatic
2goralmagnesiumsulfate
• Symptomatic
magnesium sulfate 1 TO 2 g IV over 10 min
1ml of 50% solution contains 4meq

70. Things to be monitored
• Tendon reflexes
• Respiratory rate
• Urine output

71. Anesthetic implications
• No specific anesthetic interactions
• Coexistent electrolyte imbalances should be corrected

72. Hypermagnesemia
Plasma mg > 2 . 5meq /l

73. causes
• Antacids or laxatives
• Iatrogenic
• Hypothyroidism
• Adrenal insufficiency
• Lithium administration

74. Clinical features
• Hyporeflexia drowsiness & skeletal muscle weakness
• Hypotension
• Prolonged PR interval &widening of QRS complex
• Respiratory arrest

75. Treatment
• 10 ml of 10% calcium gluconate IV over 10min
• Loop diuretic with 0.5 normal saline in 5%dextrose
• Peritoneal/ hemodialysis