This document discusses water balance and fluid compartments in the human body. It notes that water makes up 60% of total body weight and is divided between intracellular fluid (2/3 of total body water) and extracellular fluid (1/3 of total body water), with the extracellular fluid further divided into intravascular, interstitial, and transcellular compartments. Daily fluid intake and losses are also summarized.

1. By: Muhammad Izudin bin Ismail

3. • Water is the major constituent of tha body (60%).
• 2/3 of total body water is concentrated in the intracellular
fluid compartment.
• 1/3 of total body water is in the extracellular compartment
which can be divided into:
i. extravascular/interstitial (25%) compartment.
ii. intravascular (8%) compartment.
iii. transcellular (2%) compartment eg : CSF, peritoneal
fluid

4. Water Gain = Water Loss
Fluid Intake :
Food intake : 1200 mL
Oxidation of nutrients : 300
mL
Sensible :
• Urine : 500 mL
• Stools : 100 mL
Insensible :
• Skin (evaporation) :
400mL
• Lungs : 500 mL

5. 1. Water intoxication
Causes:
• Iatrogenic
• Secondary to underlying CHF, renal insufficiency and cirrhosis.
Reflected by:
• Peripheral edema
• Raised JVP
• Pulmonary edema
Treatment:
• Depends on degree of overhydration.
• Gross pulmonary edema and life threatening : dialysis is indicated.
• Less severe causes and previous normal renal function : water
restriction + diuretics.
• if cardiac failure present, digitalisation may be indicated.

6. 2. Water depletion
• Associated with hypernatremia : increase plasma
osmolality, concentrated urine and low urine sodium
concentration despite hypernatremia.
• Most common causes are GI loses , bleeding, fistula
drainage, soft tissue injuries, infections, third spaces,
poor oral intake and burns and aggravated by general
anaesthesia.
• Clinical manifestations as hypernatremia.
• Treatment consist of administration IV D5%W

7. Indications:
1. Oral intake is not possible.
2. Severe vomiting, diarrhea, dehydration and shock.
3. Hypoglycemia.
4. For administration of some medications.
5. Nutrition.

8. Crystalloid Colloid
What Aqueous solution of LMW ions Solution containing HMW
substances (protein)
Example Normal Saline and Ringer’s lactate Albumin, dextran and starch
Usages Fluids losses Fluid replacement needs
exceeds 3-4L prior to
transfusion
Advantages Inexpensive
No allergic
No risk of infection
Not depend on organ for
metabolism and excretion
Smaller amount required
Prolonged increase
intravascular volume (6-24H)
Maintain or increased plasma
oncotic pressure
Disadvantage
s
Short lived (rapidly distributed
throughout extravascular space)
Require large amount
Expensive
Interference with coagulation
Allergic

9. Fluid Glucos
e
Na K Cl Hco3 Osmolarit
y
calories
D5W 50 0 0 0 0 252 200
D10W 100 0 0 0 0 505 400
D50W 500 0 0 0 0 2525 2000
0.45% NS 0 77 0 77 0 154 0
0.9% NS 0 154 0 154 0 308 0
D5/0.22NS 50 38 0 38 0 329 200
D5/NS 50 154 0 154 0 406 200
LR 0 130 4 110 27 272 <10
D5/LR 50 130 4 11O 27 524 210
ALBUMIN
5%
0 145 4 145 0 330 200
ALBUMIN
25%
0 145 0 145 0 330 1000
PLASMA 135-
146
3.5-5.0 98-102 22-30 275-299

10. • Aqueous solutions of mineral salts or other water-soluble
molecules.
• Have a balanced electrolyte composition and expand
total extracellular volume.
• Types:
1. Balanced salt solution: electrolyte composition and
osmolality similar to plasma; example: lactated Ringer’s
2. Hypotonic salt solution: electrolyte composition lower
than that of plasma; example: D5W.
3. Hypertonic salt solution: 3% NaCl.

11. Pharmacological basis Indications Contraindications
Provide major ECF
electrolytes
Water and salt depletion
eg: vomiting, diarrhea
Hypovolemic shock
Alkalosis with
dehydration
Avoid in CHF, renal
diseases and cirrhosis
Correct both water and
electrolyte deficit.
Severe salt depletion
and hyponatremia
Initial fluid therapy in
DKA
Hypercalcemia
Dehydration with severe
hypokalemia – deficit in
IC potassium
Increase iv volume
subtantially
Fluid challenge in
prerenal ARF
Large volume may lead
to hyperchloremic

12. Pharmacological basis Indications contraindications
Correct dehydration Prevention and treatment
of dehydration
Neurosurgical
procedures, cerebral
edema
Supply energy (170
Kcal/L)
Pre-post op fluid
replacement
Prevention of ketosis in
starvation, vomiting,
diarrhea
Hypovolemic shock
Not for volume
expansion
Correct hypernatremia
IV administration of
various drugs
Blood transfusion –
clumping, hemolysis if
used same iv line
Adequate glucose infusion
protects liver against toxic
Hyponatremia, water
intoxication

13. Pharmacological basis Indications contraindications
Most physiological fluid Severe hypovolemia Severe CHF
Rapid expand iv volume Replacing fluids in post
op pt, burns
Addison’s disease
Provide buffering
capacity
DKA by provide water,
correct metabolic
acidosis and supplies
potassium
Liver disease, severe
hypoxia and shock
Maintaining normal ECF
and electrolyte balance
Vomiting or NG tube
induced alkalosis

14. • It is LMW substances that remain in the intravascular
compartment to generate oncotic pressure.
• 3 times more potent.
• 1 mL blood loss = 1 mL colloids = 3 mL crystalloids

16. Pharmacological basis Indications contraindications
Maintain plasma oncotic
pressure (80%)
Plasma volume
expansion in acute
hypovolemic shock,
burns, severe
hypoalbuminemia.
Cardiac failure
Hypersensitivity reaction

17. Indications Advantages Adverse effects
Rapid plasma volume
expansion in
hypovolemic shock
Don’t interfere with
coagulation, blood
grouping
Shouldn’t mixed with
citrated blood
Volume pre-loading in GA Remain in blood 4-5
hours
Hypersensitive reaction
Priming of heart lung
machines
Infusion of 1L expands
plasma volume by 300-
350 mL
• Sterile, pyogen free 3.5% solution.
• Polymer of degraded gelatin with electrolytes.
• 2 types
 Succinylated gelatin (modified fluid gelatin)
 Urea cross linked gelatin (polygeline)

18. • Crystalloids is recommended as the initial fluid of choice
in resuscitating patients from hemodynamic shock.
(Svensen et al 1999)
• No evidence that resuscitation with colloids reduces the
risk of death, compared with crystalloids in patients with
trauma or burns or post-surgical.
(Robert et al 2004)

19. 1. Urine Output: at least 0.5 ml/kg/hr
2. Vital Signs: BP and HR normal
3. Physical Assessment: Skin and mucous
membranes not dry, no thirst in an awake
patient
4. Laboratory tests: periodic monitoring of
hemoglobin and hematocrit, electrolytes and
ABG.

21. • Cations
Sodium
Potassium
Calcium
Magnesium
• Anions
Chloride
Bicarbonate
Phosphate
• Concentration
 135-145 mEq/L
 3.5-5.0 mEq/L
 8.0-10.5 mEq/L
 1.5-2.5 mEq/L
 95-105 mEq/L
 24-30 mEq/L
 3.0-4.5 mEq/L

22. • Maintain body fluid volume and osmolarity
• Distribute body water between fluid compartments
• Regulate acid-base balance.

23. • Sodium is predominant extracellular cation.
• Controls and regulates volume of body fluids.
• For generation and transmission of nerve.
• Eliminated primarily by kidneys, smaller in stools and
perspiration.
• Normal serum level is 135-145 mmol/L
• Daily requirement is 1-2 mmol/L.
• Disorder of sodium concentration usually results from
relative excesses or deficits of water.

24. • Indicates absolute or relative water deficits
• Associated with hyperosmolarity.
• Causes:
1. Water deficiency:
 Inadequate intake
 Excessive loss :
 Renal : DI, osmotic diuresis (mannitol)
 Extrarenal : sweat, fever, diarrhea
2. Excess Na :
 Increase intake : hypertonic saline infusion
 Inadequate excretion : renal failure, primary hyperaldosteronism

25. • Hypernatremia results in contraction of brain cells as
water shifts to attenuate the rising ECF osmolality.
• The major symptom is thirst.
• The most severe symptoms of hypernatremia are
neurologic, including altered mental status, weakness,
neuromuscular irritability, focal neurologic deficits and,
occasionally, coma or seizures.
• The presence of encephalopathy is a poor prognostic
sign in hypernatremia, and carries a mortality rate as high
as 50%
Clinical presentations

26. • Target fall in serum Na concentration of 10 mmol/L per day,
except those whom hypernatraemia developed over a period
of hours.
• If patient with long-standing hypernatraemia is infused with
hypotonic fluids, there is danger of cerebral oedema.
• It is essential to lower extracellular hypertonicity slowly in
hypertonically-dehydrated patients, e.g. 0.5 mmol/hr
• If patient is able to tolerate orally, give water orally.
• If not, set up an IV infusion of D5% or 0.45% NaCl.
• Volume and rate of infusion may be calculated as follows:-
• Change in serum Na = Infusate Na – serum Na
Total body water + 1

27. • 1st we need to know how much Na there is in IV fluids.
• 1L of 0.9% NaCl will provide 150 mmol of Na.
• 1g of table salt = 17 mmol Na
Fluids Amount of sodium
3% NaCl (hypertonic
saline)
513 mmol per litre
0.9% NaCl (normal saline) 150 mmol per litre
0.45% (half saline) 77 mmol per litre

28. 1. Total body water (TBW) = body weight X
fraction
Fraction of body water:
0.6 in men, 0.5 in elderly men
0.5 in women, 0.45 in elderly women
2. Change in serum Na = Infusate Na – serum Na
Total body water + 1
If you use 3% saline to correct the
hypernatraemia, that means that infusate Na
value is 513 mmol.

29. • 60 kg female hypovolemic pt presented with Na level of
165 mmol/L
Change in serum Na = Infusate Na – serum Na
Total body water + 1
• Desired correction : 10 mmol/L over 24H
• 1L 0.45% NaCl reduce Na concentration by:
(77-165) ÷ (30 + 1) = 2.8 mmol/L
• Aim to decrease 10 mmol/L = (10 ÷ 2.8) = 3.6 L / 24H

30. • Most common due to excess water retention due to
inability to excrete ingested water. (dilutional
hyponatremia)
• Requirements for water excretion:
1. Adequate GFR
2. Functional tubules
3. Hypertonic medulla
4. Presence or absence of ADH

31. • Acute hyponatraemia
• Features related to osmotic water shift that leads to increased ICF
volume and brain cell swelling.
• Mild hyponatraemia – usually asymptomatic
• Serum Na+ 120 mmol/L may be associated with
disturbed mental status, restlessness, confusion and
irritability
• As Na approaches 110 mmol/l, seizures and coma may
occur.

32. • Cerebral Changes
• Depressed/ excitable
• Cerebral edema
• Increased intracranial
pressure
• Confusion/ mental status
change
• Intestinal Changes
• Increased motility
(hyperactive bowel sounds)
• Nausea
• Diarrhea (frequent and
watery)
• Neuromuscular changes
• Muscle weakness
• Reduced tendon reflexes
• Depressed respirations
• Cardiovascular changes
• Usually due to volume
depletion
• Weak, rapid pulse
• Orthostatic hypotension
• Low BP (light-headedness,
dizziness)

33. 1) Hypovolaemic hyponatremia
Low blood volume due to fluid loss
Occurs in patients taking thiazide diuretics, and
after severe vomiting or diarrhoea.

34. 2) Hypervolaemic hyponatremia
 High blood volume due to fluid retention
 Occurs in people with liver cirrhosis, heart disease, or nephrotic
syndrome.
 Edema often develops with fluid retention.
3) Euvolaemic hyponatremia
 Increase in total body water
 Occurs in people with hypothyroidism, adrenal gland disorder, and
disorders that increase the release of the antidiuretic hormone
(ADH), such as tuberculosis, pneumonia, and brain trauma.

35. • Assess the following:-
1. Fluid status
2. Osmolality
3. Sodium correction (if hyperglycaemia)
4. Urinary sodium

36. • Patient’s fluid status
• Skin turgor
• Tongue moisture
• BP
• JVP
• Presence/ absence pulmonary odema
• Fluid chart (I/O chart)

37. • Measure serum osmolality
• Estimated osmolality :
2(Na + K) + BU + Glucose
Normal = 270 – 295 mosm/kg

38. • Measured serum Na in pts with hyperglycaemia
can be corrected by:
Adding approximately 1.6 mmol/l for every 5.5
mmol/l rise in glucose over 5.5 mmol/l.
In marked hyperglycemia, ECF osmolality rises and
exceeds that of ICF, since glucose not absorbed in the
absence of insulin, resulting in movement of water out
of cells into the ECF.
This condition has been called translational
hyponatremia because no net change in total body
water (TBW) has occurred.
Na concentration will return to normal once the plasma
glucose concentration is lowered.

39. • Urine Na combined with clinical assessment
of fluid status may help determine
underlying cause:
 Volume depletion from extra-renal cause with intact renal Na-
conserving mechanism – have low urinary Na concentration (<
10 mmol/L)
 Pts with isovolaemic hyponatraemia generally have urinary Na
> 20 mmol/L. Eg: SIADH.
 Dehydration with high urinary Na (> 20 mmol/L) suggests
inappropriate renal-salt wasting.
 Fluid overload with low urine Na (< 10 mmol/L) is seen in
conditions such as CCF or cirrhosis

40.  Confirm the patient truly has a hypo-osmolar state by checking serum osmolality
 Assess for serious signs or symptoms suggesting cerebral edema
 Determine the duration of development of hyponatremia (less or more than 48 hours)
 Assess the patient’s extracellular fluid volume status using clinical examination and
laboratory testing (spot urine sodium)
 Check the urine osmolality to see if the urine is appropriately dilute (< 100 mOsm/kg)
or inappropriately concentrated (≥ 100 mOsm/kg)
 Assess for underlying causes of hyponatremia that may correct rapidly with treatment
(e.g. hyponatremia induced by thiazide diuretics)
 Assess the patient’s medications (intravenous antibiotics, infusions) and nutritional
intake (total parenteral nutrition, tube-feeding) for sources of water
 Look for drugs the patient is taking that potentiate antidiuretic hormone action (ie,
selective serotonin uptake inhibitors)

41. • Acute drop in the serum osmolality 
neuronal cell swelling occurs due to the water
shift from the extracellular space to the
intracellular space .
• Swelling of the brain cells elicits the following
2 osmoregulatory responses:
• It inhibits both arginine vasopressin secretion from
neurons in the hypothalamus and hypothalamic
thirst center. This leads to excess water elimination
as dilute urine.
• There is an immediate cellular adaptation with loss
of electrolytes, and over the next few days, there is
a more gradual loss of organic intracellular
osmolytes.

42. Effects of hyponatremia on
the brain.
Minutes after the development
of hyponatremia, the
decreased osmolality causes
swelling of the brain. Rapid
adaption occurs within hours
as a result of the cellular loss
of electrolytes. Slow adaption
occurs over several days
through the loss of organic
osmolytes from brain cells to
normalize brain volume.
Aggressive correction of
hyponatremia may lead to
irreversible brain damage
(osmotic demyelination);
however, proper correction of
hyponatremia reestablishes
normal osmolality without the
risk of brain damage.
From Adrogue HJ, Madias NE:
Hyponatremia. N Engl J Med
342:1581–
1589, 2000; reprinted with
permission.

43. • IMPORTANT! Correction of hyponatremia must
take into account the chronicity of the condition.
• Correction of serum sodium that is too rapid can
precipitate severe neurologic complications –
osmotic demyelination.

44. • Degree of brain edema and consequent neurologic
symptoms depends on the rate and duration of
hypotonicity.
• Clinical manifestations are typically delayed for 2 to 6
days after the correction of plasma sodium
concentration.
• Symptoms: headache, nausea, vomiting, muscle
cramps, restlessness, disorientation, depressed reflexes,
dysarthria, dysphagia, paraparesis or quadreparesis,
lethargy and coma.
• Seizures may also be seen but less common.
• Some symptoms may be irreversible or partially
reversible.

46. • In general, serum Na should not be increased:
• By > 10 mmol/l in asymptomatic patient
• By > 12 mmol/l in symptomatic patient
• In a 24-hour period.
• If plasma Na is > 120 mmol/l, aggressive treatment is not
necessary.
• Gradually correct with either water restriction or administration of
normal saline.
• If plasma Na < 110 mmol/l, or patient is severely
symptomatic, urgent treatment is required with a more
rapid rate of increase of 1-2 mmol/L/hr for the 1st 3 – 4
hours.

47. • 60 kg isovolemic 40 years old male pt presented with
grand mal seizure with level of Na of 111 mmol/L
• TBW: 60 x 0.6 = 36 L
• Desired correction : 3 mmol/L in first 3H
• Based on formula:
Change in serum Na = Infusate Na – serum Na
Total body water + 1
• 1L of 3% NaCl increase Na = (513 – 111) ÷ (36 + 1)
=10.9 mmol/L
• Aim for 3 mmol elevation = 3 ÷10.9 = 0.275 L over 3H

48. • Potassium is predominant intracellular cation with
concentration 150 mmol/L (90%).
• The more K, the less Na and vice versa.
• Vital role in transmission of impulses, cellular building
and maintainance of cellular metabolism and excitation.
• Excreted primarily by the kidneys.
• Extracellularly, potassium concentration is 3.5-5.0
mmol/L
• Daily requirement : 1-2 mmol/kg/d

49. • Severe hyperkalemia is considered if serum K > 7
mmol/L and/or presence of ECG changes.
• Causes :
1. Increase intake :
 Use of K supplement, potassium containing medications
 Stored or irradiated blood tranfusion
2. Decrease excretion :
 Mineralocorticosteroid deficiency
 Drugs : Potassium sparing diuretic

50. 3. Increased release from
cells
• Shift of K out of cells –
Acidosis
– Insulin deficiency e.g.
DKA
– Aldosterone deficiency
• Tissue breakdown
– Severe intravascular
haemolysis e.g. severe
malaria
– Rhabdomyolysis
– Tumour lysis syndrome
– Tissue necrosis/ crush
injury
– Vigorous exercise
4. Pseudohyperkalaemia
• Increased in vitro release
from abnormal cells
– Thrombocytosis
– Leucocytosis
• Haemolysis of sample
(commonly encountered)

51. • Neuromuscular : weakness, parasthesia, areflexia
• Cardiac : bradycardia, prolonged AV conduction,
complete heart block, wide complex tachycardia,
ventricular fibrillation, asystole
• Diarrhea
• Oliguria
• Drowsiness

52. • 1st ECG sign of hyperkalemia is peaked T waves (K ≥ 6
mmol/l)
• 2nd sign: prolonged PR interval (K ≥ 7 mmol/l)
• 3rd sign: absent P waves and widen QRS – a VERY
DANGEROUS SIGN! (K between 8 – 9 mmol/l) *Atrial
activity is lost and the stage is set for ventricular
tachycardia/ fibrillation
• If continue to ignore the changes above, ventricular
tachycardia/ fibrillation will ensue.

53. 1. To protect the heart from effects of potassium by
antagonizing its effects on cardiac conduction (calcium)
2. To shift potassium from ECF to ICF (Na bicarb, insulin
and glucose)
3. To reduce total body potassium (resins, dialysis)
*Urgent treatment if K > 6.5 mmol/l or ECG shows changes
of hyperkalemia

54. Mild-moderate hyperkalaemia (K 5.5 – 6.5 mmol/l) with no
ECG changes
• Low potassium diet
• Stop drugs which may cause hyperkalemia
• Cation - exchange resins
• Correction of acidosis in patients with metabolic acidosis
• +/- glucose and insulin infusion

55. Lytic cocktail with continuous ECG monitoring
• 10 ml 10% IV calcium gluconate slow infusion for cardiac
protection, second dose may be given if no ECG changes
after 5 minutes.
*Effect within minutes, lasts for 1 hour
• Rapid acting insulin 10 U with 50 ml of dextrose 50% infused
slowly for 30-60 minutes. In patient with renal failure, need
higher dose of glucose (100-150 ml).
*Onset within 30 – 60 minutes, lasts for several hours
*Can be repeated 6 – 8 hrly.
• Arrange for urgent dialysis

56. Beta agonist therapy
• IV salbutamol 0.5 mg IV in 15 mins or 10 mg nebulization
(with or without glucose and insulin infusion) has been
shown to be effective in reducing K level (IV preferred in
patient with ESRD)
• If effective, plasma K will fall by 0.5 – 1.5 mmol/l in 15-30
mins and effect will last for several hours.
*However, beware of tachycardia.

57. Cation-exchange resins (Kalimate)
• Binds potassium in exchange for another cation in GI
tract, thereby removing K from body
• Usually given orally Kalimate (calcium polystyrene
sulphonate) 5-10g TDS
• Can be given as enemas (Kalimate 30g in 100 mls 3-4
times/d)

58. Sodium bicarbonate infusion :
• IV infusion of bicarbonate 100 – 200 mmol/l over 30 mins
produces metabolic alkalosis which lowers K in ECF.
• Onset of action occurs within 30 mins and lasts for 1-2
hours.
• Less effective in patients with renal failure and may
worsen sodium overload leading to pulmonary edema.
• Don’t give in the same line with IV Calcium gluconate
(can precipitate calcium)

59. • Can result from:
– Poor potassium intake
– Increased translocation into cells
– Increased losses in urine or GI tract (most common)
• Kidney can lower excretion to a minimum of 5 mmol per
day to 10 mmol per day in the presence of decreased
potassium intake.
– Poor intake without excessive potassium loss is a rare
cause of hypokalaemia.

60. • Excessive loss of potassium – common cause.
• Most common mechanisms:
– Increased urinary losses due to increased sodium
delivery to the distal nephron (e.g. with diuretics)
– Mineralocorticoid excess (e.g. Conn’s syndrome)
– Increased urine flow (e.g. osmotic diuresis)

61. • Rare hereditary defects of renal salt transporters
• Hypomagnasemia
– direct effect of low cytosolic magnesium on potassium
channels and enhanced potassium secretion
• Diabetic ketoacidosis
– Obligate loss of potassium from kidney as a cationic
partner to the negatively charged ketone and β-
hydroxybutyrate

62. • Neuromuscular disorders
- Weakness, flaccid paralysis, respiratory arrest,
constipation
• Dysrhythmias, appearance of U wave
• Postural hypotension
• Cardiac arrest

63. Symptoms usually appear when K < 2.5 mmol/l
– Malaise, fatigue
– Neuromuscular disturbance: weakness, hyporeflexia,
paraesthesias, cramps, restless leg syndrome,
rhabdomyolysis, paralysis
– GI: constipation, ileus
– Polyuria, polydipsia, metabolic alkalosis

64. – Flat or inverted T waves – Prominent U waves –
Depressed ST segments
– Arrhythmias: 1st and 2nd degree heart blocks, atrial
fibrillaIon, ventricular tachycardia, ventricular fibrillaIon

65. • Oral therapy: method of choice for mild-to-moderate
hypokalaemia (K > 2.5 mmol/l)
• Can also be given as slow release K (slow K, 1
tablet 600 mg = 8 mmol) or liquid forms (mist KCL 10
ml = 1g = 14 mmol)
• Slow K less efficacious in correcting more severe
degrees of hypokalemia (slow release), also shown
to be associated with gastric erosions
• 40 – 200 mmol daily of KCl may be required over
periods of days or weeks e.g. 20 – 40 mmol for 2 – 4
x daily depending on severity of depletion (as
frequent as 2 – 4 hrly may be required)

66. • 1g of KCL contains 14 mmol of potassium
• If K level is < 3 mmol/l, potassium supplements should be
given.
• In patient with hypokalemia with low urinary K excretion
(< 20 mmol/l), hypokalemia of extra- renal origin should
be suspected (i.e. GI loss).
• In asymptomatic patient with K between 3 -4 mmol/l,
who are vulnerable to cardiac arrhythmias e.g. CCF,
digoxin, history of MI/ IHD, potassium supplements are
recommended.

67. • IV therapy is method of choice in:
– Severe hypokalaemia (K < 2.5 mmol/l)
– With ECG changes
– Patient not able to take orally
– Symptomatic e.g. cardiac arrhythmias with rapid
ventricular response, familial periodic paralysis, severe
myopathy

68. • In asymptomatic patients without ECG changes, K should
be given as follows :
– At a concentration of < 40 mmol/l (< 3g KCL per liter) in
normal saline (avoid dextrose fluid)
– Given at a rate of < 20 mmol/hr (10 mmol/hr
recommended) e.g. 2 g KCL in 1 pint over 3 hour.
– Monitor plasma K regularly, ECG monitoring advised.

69. • In emergency e.g cardiac arrhythmias, severe myopathy,
K can be given:
1. At rates up to 40 mmol/l per hour (i.e. KCL 3g/hr)
2. In concentrations of 200 – 400 mmol/l (by mixing 20 –
40 mmol/l or 1.5 – 3.0g KCl in 100 mls NS)
3. IV administration of K at a rate of > 10 mmol/hr
requires continuous ECG monitoring.
As soon as ECG changes normalize, cardiac rhythm
returns to normal or respiratory muscle strength is restored,
gradually taper IV infusion and discontinued. Then, initiate
oral KCL.

70. • Most important potential risk of IV K administration =
acute hyperkalaemia (most likely in pts with renal
insufficiency)
• Use large central vein: femoral venous infusion is
preferable than upper body central vein to avoid
deleterious effects on cardiac conduction.
• Concentration of > 60 mmol/l should not be given through
peripheral vein.

71. • 99% in bone and teeth.
• High Ca, low Po4
• For nerve impulses transmission, blood clotting, for vitamin B12 absorption. Most
in ECF
• Regulated by:
1. Parathyroid hormone
 ↑Blood Ca by stimulating osteoclasts
 ↑GI absorption and renal retention
2. Calcitonin from the thyroid gland
 Promotes bone formation
 ↑ renal excretion
• Albumin bound = 40-60%
• Excreted in urine, faeces, bile, digestive secretions and perspiration.
• Normal value: 8.5-10.5 mmol/L
Corrected Ca = 4 - serum albumin x 0.8 + serum Ca

74. 1. Correct underlying causes
2. Monitor serum Ca and correction of deficit
3. Check albumin
4. Acute symptomatic:
• IV Calcium gluconate 2-3 g
• Continuous cardiac monitoring.
5. Chronic hypocalcemia: high calcium diet or oral calcium
salts
6. Mild symptoms : give calcium 5 mmol/6H with daily
plasma Ca level
7. In severe symptoms : give IV 10% calcium gluconate
over 30 mins, repeat as necessary.
8. In CKD : may require alfacalcidol
9. Encourage careful ambulation to min bone resorption.

75. • If Ca >3.5 and symptomatic:
1. Correct hydration with NS
2. Bisophosphonates prevent bone resorption by inhibiting
osteolast
3. Furosemide- used once fully hydrated. It promoted
renal excretion of Ca.

76. • If Ca >3.5 and symptomatic:
1. Correct hydration with NS
2. Bisophosphonates prevent bone resorption by inhibiting
osteolast
3. Furosemide- used once fully hydrated. It promoted
renal excretion of Ca.

77. • Mostly found within body cells: heart, bone, nerve and
muscles.
• Second most important cation ICF.
• For protein and DNA synthesis, transcription and
translation.
• Absorbed in intestines and excreted by kidneys
• Normal value : 1.5-2.5 mmol/L

79. 1. Recognition risk factors, signs and symptoms.
2. If hypokalemia doesn’t respond to potassium
replacement, hypomagnesemia should be suspected.
3. Continuous cardiac monitoring.
4. Mild or chronic (1-1.5 mmol/L, asymptomatic)
• Magnesium oxide 240 mg od-bd
5. Severe <1mmol/L
• Iv magnesium sulfate comes in 49.3% 5ml solution.
• IV magnesium sulfate 1-2g over 15 min – 2H
6. Frequent mg level

81. 1. Mild symptoms and normal renal function
• Observe
• Withold any magnesium-containing meds
2. Moderate symptoms
• Iv NS and Frusemide
• Watch K
3. Severe symptoms
• Iv 10% calcium gluconate 10-20mL bolus over 10 mins
(antagonizes membrane effects of Mg and reverses respiratory
depression)

82. • Hypophosphatemia causes include Vit D deficiency,
alcohol withdrawal. S & S include muscle weakness or
rhabdomyolysis, red cell and white cell and platelet
dysfunction and cardiac arrest or arrthymias. Tx by oral
or parenteral phosphate supplementation.
• Hyperphosphatemia most commonly due to CKD, when
it is treated with phosphate binder. Also catabolic state
such as tumor lysis syndrome. Tx treatment in patients
with renal failure is reduction of intake of PO4 and PO4-
binding drugs taken with meals

83. Perioperative fluid therapy includes:
• Compensatory intravascular volume expansion
• Pre-existing deficits
• Normal maintainance requirements
• Surgical fluid loses.

84. A. Compensatory intravascular volume expansion:
Compensate for the vasodilatation and cardiac
depression caused by anesthetic drugs
B. Pre-existing deficits:
Due to fasting or pre-operative loses
Should be replaced properly

85. C. Normal maintainance requirements:
• If patients need IV fluids for routine maintenance alone, restrict
the initial prescription to:
 25–30 ml/kg/day of water
 ~ 1 mmol/kg/day of potassium, sodium and chloride
 ~ 50–100 g/day of glucose to limit starvation ketosis.
• For patients who are obese, adjust the IV fluid prescription to
their ideal body weight. Use lower range volumes per kg
(patients rarely need more than a total of 3 litres of fluid per
day)
• Do not exceed 30 ml/kg/day for routine fluid maintenance
• Consider prescribing less fluid (25 ml/kg/day fluid) for patients
who:
 older or frail
 have renal impairment or cardiac failure.
• When prescribing for routine maintenance alone, consider
using 25–30 ml/kg/day sodium chloride 0.9% alternate with
5% dextrose.

86. • Fluid therapy is critically important during the
perioperative period.
• The most important goal is to maintain hemodynamic
stability and protect vital organs from hypoperfusion
(heart, liver, brain, kidneys).
• All sources of fluid losses must be accounted for.
• Good fluid management goes a long way toward
preventing problems.