The seminar on fluid and electrolyte imbalance covers essential aspects of body fluid distribution, regulation, and the effects of imbalances such as dehydration and overhydration. Key hormones like aldosterone and antidiuretic hormone are discussed, along with conditions like hyponatremia and hypernatremia, detailing their causes, symptoms, and management strategies. Furthermore, critical management techniques for electrolyte imbalances, including nursing interventions and dietary recommendations, are essential for maintaining homeostasis.

1. Seminar On Fluid and
Electrolyte Imbalance
Raksha Yadav
1st Year M.Sc. Nursing
AIIMS Rishikesh

2. INTRODUCTION

3. HOMEOSTASIS

4. Water content of the body

5.  Body fluids are
distributed in two
distinct area:
intracellular fluid
(ICF)
40% body weight
Extracellular fluid
(ECF)
20% body weight
Interstitial fluid -
15% body weight
Plasma -5% body
weight

6. ELECTROLYTES

8. Mechanisms controlling fluid & electrolyte
movement
 Diffusion
 Facilitated diffusion
 Active transport
 Osmosis
 Hydrostatic pressure
 Oncotic pressure

9. Regulation of water balance

10.  Hypothalamic regulation
 Pituitary regulation
 Adrenal cortical regulation
 Renal regulation
 Cardiac regulation
 Gastro-intestinal regulation

12. Aldosterone
 Hormone secreted from the
zona glomerulosa cells of
adrenal cortex
 Stimulates kidneys
Retain sodium
Retain water
Secrete potassium

13. Antidiuretic hormone
 Also called arginine vasopressin (AVP).
 ADH is produced in neuron cell bodies
in supraoptic and paraventricular nuclei
of the Hypothalamus, and stored in
posterior pituitary.
 Physiological function
 Promote the reabsorption of water in
the collecting duct.

14. The natriuretic peptide family
 Four peptides of this family have been identified, including:
Atrial natriuretic peptide (ANP)
Brain natriuretic peptide (BNP)
C-type natriuretic peptide (CNP)
Urodilatin
 Function:
Diuretic and natriuretic actions

15. Atrial Natriuretic Peptide: Function

16. The sensation of thirst
 Conscious desire for water
 Major factor that determines fluid intake
 Initiated by the osmoreceptors in
hypothalamus that are stimulated by
increase in osmotic pressure of body fluids
 Also stimulated by a decrease in the blood
pressure through the baroreceptors.

17. The regulation of thirsty reaction
 The stimulus sensed by osmoreceptor:
• Not a change in the extracellular fluid osmolality
• But a change in osmoreceptor neuron size or in the some intracellular substance.

21. Abnormalities in the Regulation of Body Fluid.
 Fluid Volume Deficit (ECFVD)- Dehydration
 Fluid Volume Excess- Over hydration

22. Extra Cellular Fluid Volume
Deficit (ECFVD)
 A decrease in intravascular and interstitial fluids.
 It is a common and serious fluid imbalance that results
in vascular fluid volume loss (hypovolemia).

23.  Risk Factors:
 Diarrhea, vomiting
 Fistula drainage
 Diabetic ketoacidosis
 Hemorrhage
 Difficulty to swallowing
 Aged
 Severe mentally ill patient

24.  Degrees of dehydration:
o Mild
o Moderate
o Severe
 Types of dehydration:
o Hyper-osmolar
o Iso-osmolar
o Hypo-osmolar

26.  Laboratory findings:
 Increased Osmolality
 Increased or normal serum sodium level
 BUN (> 25 mg/d1)
 Hyperglycaemia (>120 mg / dl)
 Increased specific gravity of urine
 Elevated hematocrit (>55%)

27. Management of Dehydration
 Oral rehydration
 IV fluids
 Correction of the underlying problem
 Dietary management
 Nursing management

29. Falls Precautions:
 Assess for orthostatic hypotension
 Assess muscle strength in legs
 Orient the client to the environment
 Remind the client to call for help before getting out of bed or
a chair
 Help the client get out of bed or a chair
 Provide, or remind the client to use, a walker or cane for
ambulating

30.  Provide adequate lighting at all times, especially at night
 Keep the call light within reach, and ensure that the client can
use it
 Place the bed in the lowest position with the brakes locked
 Place objects that the client needs within reach
 Ensure that adequate handrails are present in the client's room,
bathroom, and hall
 Encourage family members or significant other to stay with the
client

31. Extra Cellular Fluid Volume Excess/
Overhydration
 ECFVE is increased fluid retention in the intravascular
& interstitial spaces (third spacing)

32. Etiology:
 Administering fluids rapidly or in a large amount
 Failure to excrete fluids:
o Heart failure
o Renal disorders
o Venous obstructions
o Decreased plasma proteins
o Excessive fluid ingestion
o Increased ADH & Aldosterone
Decreased Excretion
Increased absorption

35.  Laboratory findings:
 Decreased Osmolality
 Decreased or normal serum sodium level
 BUN (<8 mg/dl)
 Decreased specific gravity of urine
 Decreased hematocrit (<45%)

36. Management of over hydration
 ICFVE is treated by the addition of solutes to IV fluids.
 Use of D5%, 0.45% Nacl will help to correct ICFVE
when the cause is water excess.
 Oral fluids such as water and soft drinks should be
given in addition to water and ice chips.
 IV therapy should be monitored every hour.

37.  Monitor vital signs and intake- output
 Weight should be checked daily to measure fluid gain or
loss.
 Administer prescribed antiemetic as needed to allow
food and fluids to be ingested.
 Safety measures are necessary when the client displays
behavioral changes.

38. NURSING INTERVENTIONS
 Monitor cardiovascular, respiratory, neuromuscular,
renal, integumentary, and gastrointestinal status.
 Prevent further fluid overload and restore normal fluid
balance.
 Administer diuretics; osmotic diuretics typically are
prescribed first to prevent severe electrolyte imbalances.

39.  Restrict fluid and sodium intake as prescribed.
 Monitor intake and output; monitor weight.
 Monitor electrolyte values, and prepare to administer
medication to treat an imbalance if present.

41. Electrolyte Balance and Imbalance
 Sodium:
Hyponatremia
Hypernatremia

42. Hyponatremia
• Definition:
– Commonly defined as a serum sodium
concentration <135 mEq/L
– Hyponatremia represents a relative excess of
water in relation to sodium.

43. Hyponatremia is the most common electrolyte disorder
Acute hyponatremia (developing over 48hr or less) are
subject to more severe degrees of cerebral edema
sodium level is less than 105 mEq/L, the mortality is
over 50%
Chronic hyponatremia (developing over more than 48hr)
experience milder degrees of cerebral edema

44. Types of hyponatremia
Hypovolemic hyponatremia
Euvolemic hyponatremia
Hypervolemic hyponatremia
Redistributive hyponatremia

45. Hypovolemic hyponatremia
 Develops as sodium and free water are lost and/or
replaced by inappropriately hypotonic fluids
 Sodium can be lost through renal or non-renal routes

46.  Nonrenal loss:
 GI losses
Vomiting, Diarrhea, fistulas, pancreatitis
 Excessive sweating
 Third spacing of fluids
ascites, peritonitis, pancreatitis, and burns
 Cerebral salt-wasting syndrome
traumatic brain injury, aneurysmal subarachnoid
hemorrhage, and intracranial surgery
Must distinguish from SIADH

47.  Renal Loss:
Acute or chronic renal insufficiency
Diuretics

48. Euvolemic hyponatremia
 Sodium deficit is more and the volume remains same.
 Etiology:
Psychogenic polydipsia, often in psychiatric patients
Administration of hypotonic intravenous (5% DW) or
irrigation fluids ( sorbitol, glycerin) in the immediate
postoperative period

49. administration of hypotonic maintenance intravenous
fluids
Infants who may have been given inappropriate
amounts of free water
bowel preparation before colonoscopy or colorectal
surgery

50. Hypervolemic hyponatremia
 Total body sodium increases, and TBW increases to a greater
extent.
 Can be renal or non-renal
acute or chronic renal failure
dysfunctional kidneys are unable to excrete the ingested
sodium load
cirrhosis, congestive heart failure, or nephrotic syndrome

51. Redistributive hyponatremia
Water shifts from the intracellular to the extracellular
compartment, with a resultant dilution of sodium. The TBW
and total body sodium are unchanged.
This condition occurs with hyperglycemia
Administration of mannitol

52. MEDICAL MANAGEMENT
 Determine cause of hyponatremia and to correct it.
 If client has hyponatremia due to fluid volume excess,
intake of fluids will be restricted to allow the sodium to
regain balance.
 If the serum sodium level falls below 125 mEq/L,
sodium replacement is needed.

53. PHARMACOLOGIC MANAGEMENT
 For client with moderate hyponatremia 125 meq/ L I/V
saline solution (0.9% Nacl) or lactated Ringer solution
may be ordered.
 When the serum sodium level is 115 meq / L or less, a
concentrated saline solution such as 3 % Nacl is
indicated.

54. NURSING INTERVENTIONS
 Monitor cardiovascular, respiratory, neuromuscular,
cerebral, renal, and gastrointestinal status of the client.
 If hyponatremia is accompanied by a fluid volume
deficit (hypovolemia), IV sodium chloride infusions are
administered to restore sodium content and fluid
volume.

55.  If hyponatremia is accompanied by fluid volume
excess (hypervolemia), osmotic diuretics are
administered to promote the excretion of water rather
than sodium.
 Instruct the client to increase oral sodium intake and
inform the client about the foods to include in the diet.
 If the client is taking lithium (Lithobid), monitor the
lithium level, because hyponatremia can cause
diminished lithium excretion, resulting in toxicity.

56. Hypernatremia
 Hypernatremia is usually due to water deficit
 Etiology:
 Excess water loss : eg- heat exposure
diabetes insipidus
 Impaired thirst: eg - primary hypodypsia,
comatose
 Excessive Na+ retention

57. Clinical features of hypernatremia
 Excessive thirst, polyuria, nausea
 Muscular weakness, neuromuscular
irritability
 Altered mental status,focal
neurological deficit occasionally coma
or seizures

58. Treatment
 correct water deficit
 Rate of correction :
-Acute hypernatremia- 1mEq/L/hr
-Chronic hypernatremia-1mEq/L/hr or 10mEq/L over 24hr
-rapid correction may lead to cerebral edema

59. Dietary management

61. HYPOKALEMIA
Hypokalemia is a serum potassium level of less
than 3.5 mEq /L

62. Etiological factors of hypokalemia

63. Clinical manifestations

65. Medical management
 Determining & correcting the cause of the imbalance.
 Extreme hypokalemia requires cardiac monitoring.

66. Pharmacological Management
 Oral potassium replacement therapy is usually prescribed for
mild hypokalemia.
 Potassium is extremely irritating to gastric mucosa; therefore
the drug must be taken with Glass of water or juice or during
meals.
 Potassium chloride can be administered intravenously for
moderate or severe hypokalemia & must be diluted in IV
fluids.

67.  Administration of potassium by IV push may result in
cardiac arrests. Potassium can be given in doses of 10 to
20 mEq/ hour diluted in IV fluid if the client is on heart
monitor.
 High concentration of potassium is irritating to heart
muscle. Thus correcting a potassium deficit may take
several days.

68. Dietary management
 The administration of foods
that are high in potassium
help to correct the problem
as well as prevent further
potassium losses.

69. HYPERKALEMIA
Hyperkalemia is an Elevated potassium level over 5.0 mEq/L.

70. ETIOLOGY
 Retention of Potassium- Renal insufficiency, renal failure,
decreased urine output, potassium sparing diuretics.
 Excessive release of Cellular Potassium - severe traumatic
injuries. Severe burns, severe infection, metabolic
acidosis.
 Excessive IV infusions or Oral administration of
potassium.

71. CLINICAL MANIFESTATIONS

73. LABORATORY FINDINGS

74. MEDICAL MANAGEMENT
 When serum potassium level is 5.0 to 5.5 mEq/L restrict
potassium intake.
 If potassium Excess is due to metabolic acidosis,
correcting the acidosis with sodium bicarbonate
promotes potassium uptake into the cells.
 Improving urine output decreases elevated serum
potassium level.

75. DIETARY MANAGEMENT
 When hyperkalemia is severe, immediate actions are
needed to be taken to avoid severe Cardiac disturbances.
 The administration of foods that are low in potassium help
to correct the problem as well as prevent further
potassium excess.

77. NURSING INTERVENTIONS
 Monitor cardiovascular, respiratory, neuromuscular,
renal, and gastrointestinal status; place the client on a
cardiac monitor.
 Discontinue IV potassium and hold oral potassium
supplements.
 Prepare to administer potassium-excreting diuretics if
renal function is not impaired.

78.  Initiate a potassium-restricted diet.
 If renal function is impaired, prepare to administer
sodium polystyrene sulfonate (Kayexalate).
 Prepare the client for dialysis if potassium levels are
critically high.
 Prepare for the IV administration of hypertonic glucose
with regular insulin to move excess potassium into the
cells.

79.  Monitor renal function.
 Teach the client to avoid foods high in potassium.
 Instruct the client to avoid the use of salt substitutes or
other potassium-containing substances.

80. Calcium

83. HYPOCALCEMIA
 Hypocalcemia is serum calcium below 4.5 meq/L or 8.5 mg/dl.

84. Etiology
 Malabsorption of fat in intestine.
 Metabolic alkalosis
 Renal failure with hyperphsophatemia, acute
pancreatitis, Burns, Cushing’s disease,
hypoparathyrodism.
 Medications – Magnesium sulfate.

85. CLINICAL MANIFESTATIONS
 Neuromuscular: Tetany symptoms: Twitching around
mouth, tingling and numbness of fingers, facial spasm,
convulsions.
 Respiratory: Dyspnea, laryngeal spasm.
 Gastrointestinal: increased peristalsis, diarrhea.
 Cardiovascular: Dysrhythmias, palpitations

89. MEDICAL MANAGEMENT
 Determining & correcting the cause of hypocalcemia.
 Asymptomatic hypocalcemia is usually corrected with oral
calcium gluconate, calcium lactate or calcium chloride.
 Administer calcium supplements 30 minutes before meals
for better absorption and with glass of milk because vitamin
D is necessary for absorption of calcium from the intestine.

90.  Intravenous calcium chloride or calcium gluconate
(10%) is given slowly to avoid hypertension,
bradycardia & other arrhythmias.
 Chronic or mild hypocalcemia can be treated in part by
having the client consume a diet high in calcium.

92. NURSING INTERVENTIONS
 Monitor cardiovascular, respiratory, neuromuscular, and
gastrointestinal status; place the client on a cardiac monitor.
 Administer calcium supplements orally or calcium
intravenously.
 When administering calcium intravenously, warm the injection
solution to body temperature before administration and
administer slowly, monitor for electrocardiographic changes,
and monitor for hypercalcemia.

93.  Administer medications that increase calcium
absorption. i.e. Vitamin D aids in the absorption of
calcium from the intestinal tract.
 Initiate seizure precautions.
 Keep 10% calcium gluconate available for treatment of
acute calcium deficit.
 Instruct the client to consume foods high in calcium.

94. HYPERCALCEMIA
 Hypercalcemia is a serum level over 5.5 meq/L or 11 mg/L

95. ETIOLOGY
 Metastatic malignancy-lung, breast, Ovarian, Prostatic,
bladder, leukemia, Kidney.
 Hyperparathyroidism.
 Thiazide diuretic therapy.
 Prolong immobilization.
 Excessive intake of calcium supplements and vitamin D.

96. CLINICAL MANIFESTATIONS
 Gastrointestinal: Anorexia, Vomiting, Constipation
 Neuromuscular:
Mild to moderate hypercalcemia state –weakness
Severe hypercalcemic state-Extreme lethargy
 Cardiovascular: Dysrhythmias
 Electro-cardiographic Changes: Shortened ST Segment and
lengthened QT interval.
 Musculoskeletal: Bone pain, fracture.

97. LABORATORY FINDINGS

98. MEDICAL MANAGEMENT
 Treatment consists of correcting the underlying cause.
 Intravenous normal saline (0.9% Nacl) given rapidly
with furosemide to prevent fluid overload, Promote
urinary calcium excretion.
 Corticosteroid drugs decrease calcium levels by
competing with vitamin D thus resulting in decreased
intestinal absorption of calcium.

99.  If the cause is excessive use of calcium or vitamin D
supplements or calcium containing antacids these agents
should be either avoided or used in reduced dosage.
 A newer form of drug therapy is etidronate di-sodium.
This drug reduces serum calcium by reducing normal
and abnormal bone reabsorption of calcium and
secondarily by reducing bone formation.

100. NURSING INTERVENTIONS
 Monitor cardiovascular, respiratory, neuromuscular, renal,
and gastrointestinal status; place the client on a cardiac
monitor.
 Discontinue IV infusions of solutions containing calcium and
oral medications containing calcium or vitamin D.
 Discontinue thiazide diuretics and replace with diuretics that
enhance the excretion of calcium.

101.  Administer medications as prescribed that inhibit calcium
resorption from the bone, such as phosphorus, calcitonin,
bisphosphonates, and prostaglandin synthesis inhibitors
(aspirin, nonsteroidal anti-inflammatory drugs).
 Prepare the client with severe hypercalcemia for dialysis if
medications fail to reduce the serum calcium level.
 Instruct the client to avoid foods high in calcium.

102. Phosphorus
 Hypophosphatemia
 Hyperphosphatemia

103. Hypophosphatemia
 Hypophosphatemia is defined as plasma phosphorus
<1.2mEq/L

104. Causes of hypophosphatemia
 Malabsorption syndrome
 TPN
 Alcohol withdrawal
 Phosphate binding anta-acids
 Respiratory alkalosis
 Recovery from DKA

105. Clinical manifestations
 Muscle weakness
 Osteomalacia
 Rhabdomyolysis
 Cadiac problems- Dysrhythmias, decreased stroke
volume
 CNS dysfunction

106. Management:
 Mild cases- treated with dietary restrictions
 Teach client about balanced diet
 Severe cases: phosphate supplementation

107. Hyperphosphatemia
 Hyperphosphatemia is defined as plasma
phosphorus >3mEq/L

108. Causes of hyperphosphatemia
 Excess intake of high phosphate foods
 Excess vitamine D supplementation especially in renal
insufficiency
 Impaired colonic motility
 Hypoparathyroidism
 Addison’s disease

109. Clinical manifestations
 Tachycardia, palpitations
 Restlessness
 Anorexia, nausea, vomiting
 Hyper-reflexia, tetany
 Dysrhythmias

110. Management:
 Mild cases- limit phosphate rich foods ( milk, ice-cream,
cheese, meat, fish)
 Giving calcium, aluminium products that promotes
binding & excretion of phosphate.
 Dialysis is the TOC in case of hyperphosphatemia with
renal failure.

111. Magnesium
Hypomagnesemia
Hypermagnesemia

112. Hypomagnesemia
 Hypomagnesemia is defined as plasma magnesium
<1.8mg/dl

113. Causes of hypomagnesemia
 Diarrhea, vomiting
 Chronic alcoholism
 Prolonged malnutrition
 Hyperaldosteronism
 Impaired GI absorption
 NG suction
 Poorly controlled DM

114. Clinical manifestations
 Myocardial irritability
 Anorexia, nausea
 Abdominal distention
 Severe cases: Chvostek’s & Trousseau’s sign, tetany,
convulsions, stroke

116. Management:
 Oral magnesium replacement (anta-acids)
 Parenteral magnesium sulphate
 Increase dietary intake of magnesium (chili, tofu, wheat
gram)
 Initiate safety & seizure precautions in severe cases and
monitor all electrolytes.
 Keep watch on rising magnesium levels.

117. Hypermagnesemia
 Hypermagnesemia is defined as plasma magnesium
>3mg/dl

118. Causes of hypermagnesemia
 Renal insufficiency
 Excessive anta-acid use
 Adrenal insufficiency
 Ketoacidosis

119. Clinical manifestations
Clinical amnifestations are related to blocked release of
Acetylcholine from myoneronal junction which affects muscle
cell activity.
 Hypotension
 Muscle weakness
 Loss of DTR
 Prolonged QT, PR interval
 Lethargy, drowiness
 Respiratory paralysis, loss of consiosness

120. Management:
 Low magnesium diet (eat chicken, eggs, green peas, white
bread, hamburger)
 Decrease magnesium sulphate use
 In severe cases saline infusion with diuretics is give to
promote magnesium excretion
 IV calcium (antagonistic action)
 Drugs: Albuterol
 If renal failure is also present than hemodialysis is done in
severe cases

124. Bibliography
 Priscilla Lemone, Karen Burke. “Medical surgical nursing, critical thinking in client care”.
4th edition (2008). Page no. 185-198
 Ignatavicius Workman. “Medical surgical nursing, Patient centred collaborative care”. 6th
edition (2010). Elsevier publication. Page no. 1022-1024
 Brunner and Suddharth. “Text book of medical surgical nursing”. Page no. 249-255
 Guyyton and Hall. “Text book of medical physiology”. 11th edition (2006). Elsevier
publications. Page no. 642-650
 Gerard.J.Tortora. “Principles of anatomy and physiology”. 11th edition (2006). Wiley
publication. Page no. 1122-1130

125.  K. Sembulingam, Prema Sembulingam. “Essentials of medical
physiology”. 5thedition (2010). Jaypee publications. Page no. 302-
309

132. 1. The type of fluid used to manipulate fluid shifts
among compartments states is:
A. Whole blood
B. TPN
C. Albumin
D. Normal saline

133. 2. The balance of anions and cations as it occurs
across cell membranes is known as:
A. osmotic activity
B. Electrical neutrality
C. Electrical stability
D. Sodium potassium pump

134. 3. A diet containing the minimum
daily sodium requirement for an adult would
be:
A. no-salt diet
B. diet including 2 gm sodium
C. diet including 4 gm sodium
D. 1500 calorie weight-loss diet

135. THANK YOU…………