The document discusses fluid and electrolyte imbalances in the body, highlighting the essential roles of intracellular and extracellular fluids in maintaining homeostasis. It covers mechanisms of fluid movement, hormonal regulation, and the clinical manifestations and management of fluid volume excess and deficit. Various factors influencing these imbalances, such as kidney function and gastrointestinal losses, are reviewed along with specific treatments for different fluid imbalance conditions.

1. FLUID AND
ELECTROLYTE
IMBALANCE
Mr. Aby Thankachan, M.Sc(N), PGDSH
Senior Tutor
Dept. of Medical Surgical Nursing
KMCH Con, Coimbatore

2. INTRODUCTION
Fluid And Electrolyte Plays Vital Role In Maintaining
Homeostasis With In The Body.
Our Body Consists Of Two Type Of Fluid Intracellular
And Extracellular Fluid.
Fluid Is A Major Component Of Our Body It Serves A Vital
Role In Our Health, And In Normal Cellular Function By
Serving As A Medium For Metabolic Reactions With In The
Cell.
It Also Is The Transporter And Waste Products , A
Lubricant , An Insulator And A Shock Absorber

3. FLUIDS
BODY FLUID
COMPARTMENTS
Intracellular fluid
(ICF)
Extracellular fluid
(ECF)

4. BODY FLUID COMPOSITION AND
COMPARTMENTS
The60-40-20 Rule:
 60% of body weight iswater.
 40% of body weight is intracellularfluids.
 20% of body weight is extracellularfluids.
interstitial intravascular
CELL
Intracellular
Extracellular

5. FLUIDS
Body fluid compartments
1. Intracellularfluid- It is located within the cell ,
constitutes about 40% of the body weight and 70% of the total water.
The intracellular fluid provides the cell within the internal aqueous
medium necessary for its chemical functions .
2. Extracellular fluid- It constitutes about 20% of the body
weight and
extracellular
30% of
fluid
the
consist
total body weight. The of
interstitial fluid,
intravascular fluid, cerebrospinal fluid , intraocular fluid,
synovial fluid , lymphatic fluid and secretions of
gastrointestinal tract.

7. FUNCTIONS OF
EXTRACELLULAR FLUID
Transport nutrients , electrolytes , oxygen to
cells and waste products for excretion.
Hydrolyzes food for digestive process.
Regulates heat.
Lubricates and cushions joints and membranes .

8. MECHANISM CONTROLLING FLUID
AND ELECTROLYTE MOVEMENT
DIFFUSION: Diffusion is the movement of molecules from
an area of higher concentration to an area of lower
concentration .
FACILITATED DIFFUSION: In facilitated diffusion , one
molecule moves from an area of higher concentration
to an area of lower concentration with the help of some
carrier. E.g., glucose is transported into the cell with the
help of insulin as a carrier molecule.

10. MECHANISM CONTROLLING FLUID
AND ELECTROLYTE MOVEMENT
ACTIVE TRANSPORT: Active transport is a process in which
molecules are moved from an area of lower concentration to an
area of higher concentration and they require external energy
for movement against the concentration gradient.
OSMOSIS: Osmosis is the flow of water between two
compartments separated by a membrane permeable to water but
not to solute. Osmosis requires no outside energy for movement.
Water moves from an area of low solute concentration to an
area of higher concentration from the compartment that is more
diluted to side that is more concentrated.

11. OSMOSIS

12. DecreasedVolume of ECF Increased Osmolality
ofECF
Stimulates osmoreceptors in
hypothalmic thirst centre
Decreased saliva
secretion
Dry mouth
Sensation ofthirst
Waterabosrbed from
GIT
Increased amount of ECF Deccreased
Osmolality ofECF
Fig. Factors stimulating water intake through the thirst mechanism
HYPOTHALAMIC
REGULATION / THIRST

13. RAAS

15. Mechanical ventilation,
drugs, anesthesia, pain

16. Two disorders of antidiuretic hormone [ADH] production illustrates the
effect of ADHon water balance and urine output .
1.Diabetes Inspidus - due to deficient of ADH production
of inappropriate antidiuretic hormone
due to excess release of antidiuretic
2.Syndrome
[SIADH]-
hormone .

17. ADRENAL CORTICAL REGULATION
Extracellular fluid volume is maintained by a combination of hormonal
influences . Hormones released by the adrenal cortex help regulate
both water and electrolytes . Two groups of hormones secreted by the
adrenal cortex are :
i. Glucocorticoids [Cortisol]- Inflammatory action and increase serum
glucose level.
ii. Mineralocorticoids [Aldosterone] Enhances sodium and potassium
excretion. When sodium is reabsorbed, water follows as a result of
osmotic changes.

18. ADRENAL CORTICAL REGULATION
STRESS SIGNALS TO
HYPOTHALAMUS
ANTERIOR PITUITARY
INCREASES
SECRETION OF ACTH
ADRENAL CORTEX
INCREASES
ALDOSTERONE
INCREASES
CORTISOL
POSTERIOR PITUITARY
INCREASES SECRETION
OF ANTIDIURETIC
HORMONE
- KIDNEYS
INCREASES
WATER
REABSORPTION

19. INCREASES SODIUM
REABSORPTION
INCREASES
POTASSIUM
EXCRETION

20. RENAL REGULATION
The primary organs for regulating fluid and
electrolyte balance are the kidneys.
They regulate the volume and osmolality of body fluids
by controlling the excretion of water and electrolytes.
The renal tubules are the main site of action for ADH
and aldosterone.

21. As the filtrate [plasma] moves through renal tubules ,
selective reabsorption of water and electrolytes and
secretion of electrolytes result in the production of urine
that is generally different in composition and
concentration than plasma [filtrate]. This helps to
maintain normal plasma osmolality, electrolyte balance,
blood volume and acid-base balance.
Impaired kidney function may leads to edema , potassium
and phosphorous retention , acidosis and other
electrolyte imbalances.

22. GASTROINTESTINAL REGULATION
Most of the body’s water is excreted by
kidneys.
A small amount of fluid is normally eliminated
by the GI tract in faeces , but sometimes or
usually diarrhoea and vomiting leads to fluid
and electrolyte imbalances.

23. INSENSIBLE WATER LOSS
INSENSIBLE WATER LOSS: which is invisible
vaporization from the lungs and skin, assists in
Normally aboutregulating body temperature. 900ml
per day is lost.
SENSIBLE WATER LOSS: excess sweating/ sensible perspiration
caused by fever or high temperature environmental may lead to
large loss of water and electrolyte.

25. TONICITY

27. ISOTONIC SOLUTIONS
Same solute concentration as blood.
If injected into vein, no net movement of
fluid.
Example: 0.9% NS Solution

28. HYPERTONIC SOLUTIONS
Higher solute concentration than RBC
If injected into vein, Fluid moves from
interstitial space INTO veins.
Eg: 5% Dextrose

29. AFFECTS OF HYPERTONIC SOLUTIONON
CELL
Cell
Shrunken
Cell
• The(solute) outside the cell is
higher thaninside.
• Water moves from low (solute)
to high(solute).
• Thecell shrinks.
Cell
Shrunken
Cell

30. HYPOTONIC
SOLUTIONS
Lower solute concentration than
blood
If injected into vein, fluid moves
OUT of veins into tissues.

31. AFFECTS OF
HYPOTONIC
SOLUTIONON
CELL
Cell
Cell
Ruptured Cell

33. Osmolarity- is concentration of all solutes per litre of
solution. (to pull water to it)
Osmolality- controls water movement & distribution
between and within body fluid compartments by
regulating concentration of fluid in each compartment. It
is determined by no. of dissolved particles per kg water.
(Na is main electrolyte)
Inc. Na(Hyperosmolality)
Dec. Na (Hypoosmolality)

35. TYPES OF FLUID IMBALANCES
TYPES
FluidVolume
Excess
Extracellular
Fluid Volume
Excess (ECFVE)
Intracellular
FluidVolume
Excess
FluidVolume
Deficit
Extracellular
FluidVolume
Deficit
Intracellular
FluidVolume
DeficitThird SpaceFluid Shift

36. EXTRA CELLULAR FLUID VOLUME
DEFICIT (ECFVD)
Commonly called dehydration or Decrease in
intravascular and interstitial fluids.
Common and serious fluid imbalance that results
in vascular fluid volume loss (hypovolemia).
Can lead to cellular fluid loss owing to fluid
shifting from the cells to the vascular fluid to
restore fluid balance.

37. ETIOLOGY
Severe vomiting
Severe diarrhea
Traumatic injuries
Excessive blood loss
Third space fluid shifts
Insufficient water or fluid intake.
Lackof fluid intake due to impaired thirst mechanism.

38. ETIOLOGY
• Excessive fluid output through diaphoresis,GI
suction, burns, deceased antidiuretic hormone.
• Alteration in any of the regulators of fluid balances.
• Increased Renin-Angiotensin Aldosterone response
that causes sodium retention.

39. RISK FACTORS
In DKA
Experiencing severe vomiting or diarrhea
Having difficulty swallowing
Elderly, confused persons

40. CLINICAL MANIFESTATIONS
Mild ECFVD- 1-2 liter of water & 2% of
body weight is lost.
Moderate ECFVD- 3-5 liter of water & 5%
of body weight is lost.
Severe ECFVD- 5-10 liter of water & 8%
of body weight is lost.

41. CLINICAL MANIFESTATIONS
Changes in intake and output i.e., thirst and urine
output decreases.
Changes in vital signs: systolic blood pressure
decreases, weak pulse, CVP decreases, pulmonary
capillary wedge pressure decreases, heart rate
increases, elevated temperature
Flat jugular vein.
Decreased skin turgor
Dry mucous membrane

42. CLINICAL MANIFESTATIONS
Dry cracked lips or tongue
Furrows on tongue
Eye balls sunken & soft
Restlessness, coma in severe deficit
Orthostatic hypotension
Muscle weakness.
Decreased and hard faeces .
Hallucinations and confusion .

43. LAB FINDINGS
Increased Osmolality: > 295 mOsm/kg
Hypernatremia: > 145 mEq/L
BUN (>25 mg/dl)
Hyperglycemia (>120 mg/dl)
Elevated hematocrit (>55%), value
Increased Specific gravity

44. MEDICAL MANAGEMENT
1.ORAL REHYDRATION- Oral glucose replacement
solution are palatable, a good source of fluid,
glucose and electrolytes and even they are absorbed
quickly.
2.INTRAVENOUS REHYDRATION- Intravenous fluids are
used for replacement. The volume of fluid is calculated
on basis of client’s weight and other factors.
Isotonic ECFVD is treated with isotonic solution.
Hypertonic ECFVD is treated with hypotonic solution.
Hypotonic ECFVD is treated with hypertonic solution.

45. MEDICAL MANAGEMENT
I/V- D5% in water (D5W) or D5% in 0.2% Saline
(D5/0.2%NaCl)
If hemorrhage,
Blood loss less than 1L- NS/RL.
Blood loss more than 1L- blood replacement.

46. 3.MONITORING FOR COMPLICATIONS OF
FLUID RESTORATION-
• A client with severe ECFVD is accompanied by severe heart ,
pulmonary, liver or kidney disease can not tolerate large
volume of fluid or sodium without the risk for development of
heart failure.
• For unstable client , monitors are used to detect increasing
pressure from fluid.
• If deficit has existed for more than 24hrs , it is dangerous to
correct this deficit too rapidly.
• Urine output , body weight and laboratory volumes of sodium ,
osmolality , BUN and potassium are monitored closely.

47. 4. Correction of underlying problem:
• Antiemetics
• Antidiarrhoeals
• Antibiotics
• Antipyretics

48. DIETARY MANAGEMENT
Avoid fatty or fried foods and milk products

49. NURSING MANAGEMENT
Deficit fluid volume:
Restoreoral fluid intake.
Restorefluid byintravenous.
Reducerisk of deficit fluidvolume.
Control of underlyingproblems.
Monitor for complications.

50. NURSING MANAGEMENT
Impaired oral mucousmembrane:
• Oral care regularly 2-4hourly.
• Apply lip moisturizer.
• Rinseclient’s mouth every 1-2hourly.
• Examineclient’s mouth with penlight fordebris.

51. EXTRACELLULAR FLUID VOLUME EXCESS
(ECFVE)
Definition:ECFVE is increased fluid volume
retention in the intravascular & interstitial spaces.
It is afluid overload orover hydration.
The expansion of fluid compartment due to
increase in total sodiumcontent.
Sodium & water retention is same to as iso- osmolar
Fluid volume excess.

54. ETIOLOGY
Increased
total body
sodium
content
HeartFailure
Renal
Disorders
Liver
Disorders
Increased
ingestion of
foods
containing high
amounts of
sodium

55. ETIOLOGY
Excessive
amounts of IV
fluids
containing
Sodium
Varicose veins,
thrombus,
immobility,
chronic phlebitis.
IncreasedH.P. in
B/V.
Decreased
colloid
osmotic
pressure

56. RISK FACTORS
Clients with heart, renal or
liver disorders
Hyperaldosteronism
Cushing Syndrome
Patients uing glucocorticoids
Use of hypotonic solutions to
irrigate N.G. tubes & enemas
Lymphatic and venous
obstruction
SIADH, Sepsis

57. PATHOPHYSIOLOGY
[A] Causes/ [Risk Factors]
Increased H.P. in arterial end of capillary
Inc. peripheral vascular resistance Fluid movement into tissues
Inc. L.V. pressure Edema
Inc. left atrial pressure
Pulmonary Edema

58. [B] With RenalDisease
Dec.Sodium & Waterretention
Fluid volume excessin Bloodvessels
Inc. H.P.
Pulmonary Edema Generalised Edema

59. [C] LiverDisease
Dec.production of PlasmaProteins
Dec.O.P.Of vascularFluids
Lessfluid reabsorption from tissuespace
Fluid volume excessin ECF
Peripheral Edema Ascitis

60. CLINICAL MANIFESTATIONS
RESPIRATORY CARDIOVASCULAR
• Constant irritating
cough
• Dyspnea
• Crackles in lungs
• Pallor
• Cyanosis
• Deceased tissue
perfusion
• Increased CO2 in
ABG
• Neck vein engorgement in semi fowler position
• Hand vein engorgement
• Systematic venous engorgement
• Pitting edema of lower extremities
• Weight gain
• Sacral edema
• Inc. B.P.
• Peripheral vein filling time greater than 5 sec
• Bounding pulse.
• Increased right atrial CVP and Pulmonary
Capillary wedge Pressure / LA pressure
Neurological : Loss
of Consciousness

61. LAB FINDINGS
Serum osmolality: <275mosm/kg
Serum sodium: <135meq/L
Decreased hematocrit value: <45%
Specific gravity: <1.010
BUN: < 8 mg/dl

62. MANAGEMENT
Restriction of sodium and fluids: Because
sodium retains water, sodium intake is
commonly restricted especially in renal or heart
failure patients.
Promoting urine output: Mild diuretics and
digitalis promote fluid loss and diuretics also
causes excretion of magnesium and potassium
loss in urine.

63. MEDICAL MANAGEMENT
PHARMACOLOGY MANAGEMENT-
Loop & Potassium sparing Diuretics- to excrete
potassium along with sodium and water.
Eg: Furosemide (Lasix), Hydrochlorothiazide
Digoxin, a digitalis preparation- to increase
Myocardial Contraction or to slow the heart rate if
heart failure is cause of ECFVE.

64. DIETARY MANAGEMENT
A low sodium diet is prescribed in order to reduce fluid
retention.
Eat less than 2,000 milligrams of sodium per day.
Eliminate salty foods from your diet and reduce the
amount of salt used in cooking.
Choose low sodium foods.

66. 2.NSG. INTERVENTIONS- Fluid volume excess Or Hypervolemia
V/S to be checked with bounding pulse and elevated B.P.
Assess/ Auscultate breath sounds for crackles
Assess neck& hand vein engorgement
Monitor daily weight, I/O 4-8 Hourly
Check edema & LOC.
Fluid volume restriction may be necessary.
Provide skin care for general edema.
Reduce sodium and fluid intake.
Reduce complications like digitalis toxic effects.

67. INTRACELLULAR
FLUID VOLUME
DEFICIT

68. DEFINITION
Intracellular fluid volume deficit is decrease in
fluid within thecells.

69. CAUSES
Excessive fluid loss. Insufficient fluid intake.
Failure of regulatory
mechanism.
Lossof GIfluid from
vomiting, diarrohea,GI
suctioning, intestinal
fistula and intestinal
drainage.
Haemorrhage.
Chronic abuse of
laxatives andenemas.
Water and sodiumlosses
during sweating from
exerciseor increased
environmental
temperature.
Excessive renal lossesof
water and sodium from
diuretic therapy.

70. CLINICAL MANIFESTATIONS
Dry and sticky mucous membrane.
Decreased urine output.
Anxiety
Confusion.
Diminished skin turgor.

71. Dry , pale and coolextremities.
Orthostatic hypotension.
Decreasein capillary refill.
Increase body temperature.
Weight loss.
Thirst.

72. DIAGNOSTIC EVALUATION
Serum electrolyte:sodium
increases and potassium
decreases.
Serum osmolality: osmolality is
high.
Hematocrit: high.
Urine specific gravity:high.
Central venous pressure:low.

73. MANGEMENT
1. Oral rehydration:
Safest and most effective treatment for fluid
volume deficit in alert clients who are able to take
oral fluids.
Adults requires minimum of approximately 30ml
per kg body weight for maintenance.
2. Intravenous therapy:
When fluid deficit is severe or client is unable to
ingest fluid, the I/V route is used to administer
replacementfluid.

74. MANGEMENT
• 5% dextrose in water D5W
• 0.9% sodium chloride
• 5% dextrose and 0.45% sodium chloride
• Ringer’s solution
Isotonic
• 10% dextrose in water
• 20% dextrose in water
• 50% dextrose in water
• 3% sodium chloride
Hypertonic
• 0.45% sodium
chloride
Hypotonic

75. NURSING MANAGEMENT
1. Deficit fluid volume:
Assess intake and output regularly.
Monitor fluid balances regularly.
Assess vital signs, CVP, peripheral pulses.
Check weight daily.
Administer I/V fluids.
Monitor laboratory values: electrolytes, serum
osmolality, BUN and hematocrit.

76. 2. Ineffective tissue perfusion:
Monitor changesin level ofconsciousness.
Monitor serum creatinine, BUN,cardiac enzymes.
Changeposition 2 hourly.
NURSING MANAGEMENT

77. INTRACELLULAR FLUID
VOLUME EXCESS
(ICFVE)

78. INTRACELLULAR FLUIDVOLUME EXCESS
(ICFVE)
Definition- ICFVE resulting from either water excess
or solute deficit and are mainly due to sodium loss.
The cells become engorged or swollen.

79. INTRACELLULAR FLUIDVOLUMEEXCESS(ICFVE)
In water excess- No. of solutes is normal but excesswater dilution.
In solute deficit- Amount of water is normal but few
electrolyte(solute) per litre ofwater.
In both cases,Hypo-osmolality of vascularfluid
Cellular Swelling

80. CAUSES
of Excessive amounts of hypo-
0.45% Saline/ 5% Dextrose in
Administration
osmolar fluids-
water.
May occur in clients who receive continuous D5%
IV fluids, in those with brain injury.
Stress condition causes increase in release of ADH and
aldosterone which increases water reabsorption from renal
tubules.
Psychiatric disorders like schizophrenia.

81. CAUSES
Water Excess-
Excessive intake of fluid
Inability to excrete excess water(Renal)
Administration of tap water enema(hypotonic)
Dilutes ECF Dec. serum Osm

82. Solute Deficit-
Poor sodium intake
Use of diuretics
Loss of sodium and water & replaced only by water
Fluid overload i.e., water and sodium retention.

83. PATHOPHYSIOOGY
With water and sodium imbalance
Water more than solute, solute less than water
Water excess in cells due to Hypo-osmolality
Osmosis occur to maintain fluid equilibrium
Force fluids to move from less concentration(B/V) to high conc.(cells)
Cellular Swelling
Edema (Cerebral Edema)

84. CLINICAL MANIFESTATIONS
1. Cerebral Edema- Behavioral changes, headache Inc. ICP, &
pupillary changes
2. Vital Signs alterations-
Bradycardia
Increased systolic B.P.
Widened Pulse Pressure
Increased respiration
Full, bounding pulse.

85. CLINICAL MANIFESTATIONS
3. Others-
Nausea
Projectile vomiting
Irritability
Disorientation
Confusion
Drowsiness
Decreasedco-ordination
Increase in TBWcausesweight gain
Convulsions.

86. Peripheral or generalized oedema
Circulatory overload causes
Full , bounding pulse
Distended neck and peripheral vein
Increased CVP
Cough , dyspnoea , orthopenea
Moist crackles in lungs
Pulmonary edema if severe ICFVE
Increased urine output
Ascites
Altered mental status and anxiety
Unknown fear

87. Serumsodium level <125meq/Lt.
Decreasehematocrit value.

88. MANAGEMENT
1. Medication: Diuretics- commonly used to treat fluid
volumeexcess.
• They inhibit sodium and water reabsorption,
increasing urine output.
LOOP DIURETICS: Furosemide[Lasix].
THIAZIDE LIKE DIURETICS: Chlorothiazide [Diuril].
POTASSIUM SPARINGDIURETICS:
Spironolactone [Aldactone]

89. 2. Fluid Management:
Fluid intake may be restricted to client having
fluid volume excess.
The amount of fluid allowed per day is
prescribed by primary care provider.
All fluid must be calculated, including meals and that
is used to administer medication orally or I/V.

90. 3. DIETARY MANAGEMENT:
Because sodium retention is a primary cause of fluid
volume excess, so sodium restriction diet is often
prescribed.

91. MANAGEMENT
Addition of solutes to IV fluids.
Use of D5% or 0.45% NaCl will help to correct ICFVE
when the cause is water excess.
Oral fluids- juices, soft drinks, water & ice chips.
Check- Reflexes and pupillary response.
Monitor I/V therapy hourly.

92. MANAGEMENT
Monitor V/S and intake, output every 4-8 hrs.
Check weight daily.
Administer prescribed antiemetic as needed to allow
food and fluids to be ingested.
Safety measures- if client shows behavioral
changes.

93. NURSING DIAGNOSIS
1. Excess fluid volume:
Assessvital signs, heart sounds,CVP, and
volume of peripheral arteries.
Assess for the presence of edema.
Obtain weight daily at same time of day.
Provide oral hygiene 2hourly.
Teach client about sodium restricted diet.
Report significant changes in serum electrolytes.
Administer oral fluids cautiously, adhering to any
prescribed fluid retention.
Administer diuretics as prescribed.

94. 2. Risk for impaired skin integrity :
Assessskin in pressure area and over bony
prominences.
Change position of client 2 hourly.
Provide alternating pressure mattress, foot cradle, heel
protectors, to reduce pressure on tissues.

95. 3. Risk for impaired gas exchange:
Auscultate lungs for presenceof wheezes and
crackles.
Place in fowler’s position if having dyspnea or
orthopenea.
Monitor oxygen saturation level and ABG’s.
Administer oxygen as indicated.
Ausculcate heart for extra heart sounds .

97. EXTRACELLULAR FLUID VOLUME
SHIFT: THIRD SPACE FLUID
DEFINITION: A change in the location of extracellular
fluid between the intravascular and the interstitial
spaces.

98. Fluids shifts are of 2 types:
1. Vascular fluid shifts to interstitial space.
2. Interstitial fluid shift to vascular space.
Fluid that shifts into interstitial spaceand remains
there is known as third spacing.
Common sites for third spacing are :
Pleural cavity
Peritoneal cavity
Pericardial sac

99. ETIOLOGY
Blister
Sprain
Crush injuries
Extensive Burns
Perforated Peptic Ulcer
Intestinal Obstruction
Lymphatic Obstruction

100. Increased hydrostatic pressure
Increased capillary permeability
Decreased serum protein level
Obstruction of venous portion of capillary or non
functional lymphatic drainage system
Pathologic process that triggers the
inflammatory process
ETIOLOGY

101. Decreased protein intake production, storage or
increased loss in PEM and liver or kidneys
ETIOLOGY

102. RISK FACTORS
Major trauma
Major surgery

103. PATHOPHYSIOLOGY
Tissue Injury
causes
Release of Histamine, Bradykinin
Inc. Capillary Permeability
Fluid, Protein, other Solutes shift into
interstitial spaces
HYPOVOLEMIA
First
Phase

104. PATHOPHYSIOLOGY
Fluid shift from interstitial spaceto vascular
space
Hypervolemia
Second
Phase

105. CLINICAL MANIFESTATIONS
Skin pallor
Cold extremities
Weak & rapid pulse
Hypotension
Oliguria
Decreased level of consciousness
Bounding pulse
Engorgement of peripheral and jugular vein

106. DIAGNOSTIC ASSESSMENT
Inc. hematocrit
Inc. BUN
Inc. Serum sodium
Inc. Urine specific gravity
When fluid returns to blood stream;
Dec. Hematocrit
Dec. BUN

107. Replace fluid:
I/V fluid administration to replace
intravascular volume.
Albumin given to replace protein loss from
trauma.
Fluidsare titrated to maintain adequate blood
pressure, CVP, PCWP, urine output.
MEDICAL MANAGEMENT

108. Stabilize other problems:
I/V antibiotics are given to preventsepsis.
Vasodilators are given to maintain blood pressure.
Steroids are given for inflammatory disorders.

109.  Monitor the followings regularly:
Abdominal girth 8 hourly.
Limb circumference.
Skin integrity to prevent skin breakdown of edematous
area.
Urine output 8 hourly.
Plasma sodium, BUN and creatinine level.

111. NURSING MANAGEMENT
Monitor urine output 1 hourly. Maintain urine output
at least 25ml/hr. urine output is usually decreased in
case of tissue injury, because of decreased renal
circulation and the fluid shift into the injured tissue
spaces.
Monitor BUN and Ammonia levels in case of patients
with ascitis.

112. ELECTROLYTE
IMBALANCES

113. INTRODUCTION
Electrolytes are the substances found in
ECF and ICF whose molecules dissociate
into electrically charged particles known as
ions when placed in water.

114. DEFINITIONS
IONS: Ions are electrically charged particles .
CATIONS: Cations are positively charged particles.
E.g.- Na , K+, Ca2+ etc.
ANIONS: Anions are negatively charged particles.
E.g.- Cl-, PO4, HCO3-
ICF- K, Mg, PO4-, (K as a main ion)
ECF- Na, Ca, Cl (Na as a main ion)

115. Electrolytes has major influence on-
1. Body water regulation
2. Acid Base Regulation
3. Enzyme Reaction
4. Neuromuscular activity

116. MEASUREMENT OF ELECTROLYTES
Electrolytes can be measured by weight or combining
power.
The unit of weight is milligram per deciliter [mg/dl] and
combining power is miliequivalents per litre [mEq/L].

118. SODIUM
IMBALANCES
HYPONATREMIA HYPERNATREMIA

119. HYPONATRENMIA: When sodium levels are low, water
is drawn into the cells of the body, causing them to
swell.
HYPERNATREMIA: High levels of sodium in
extracellular fluid, draw water out of body cells,
causing them to shrink.

120. REGULATION OFSODIUM
BALANCE IN THEBODY
• Kidneys are the primary regulator of sodium balance
in the body.
• Mechanisms are:
RAAS: Promotes the renal tubules to reabsorb
sodium.
Antidiuretic hormone: released from posterior
pituitary ADH promotes sodium and water
reabsorption in the distal tubules of kidney.

122. DEFINITION- Hyponatremia is a serum sodium
level is below 135mEq/L.
Hyponatremia may result from a loss of sodium
from the body , but it may also be caused by water
gain than dilute ECF .

124. CAUSES- CAUSES ARE ASSOCIATED
WITH FLUID VOLUME STATUS.
1. Increased sodium excretion:
a) Excessive diaphoresis
b) Diuretics
c) Vomiting
d) Diarrhea
f) Renal disease
g) Wound drainage specially G.I.

125. 2. INADEQUATE SODIUM
INTAKE
a) Nothing by mouth
b) Low salt diet
3. Dilution of serum sodium
a) Excessive ingestion of hypotonic fluids
b) Renal failure
c) Freshwater drowning
d) Hyperglycemia
e) Congestive heart failure

126. OTHERS
Inappropriate use of sodium free or hypotonic IV fluids
after surgery or trauma.
Administration of fluids in patients with renal failure or
psychiatric disorders.
SIADH will result in dilutional hyponatremia.
Loss of sodium rich body fluid from GIT, kidneys or skin
directly.
Excessive hypotonic solutions.

127. RISKFACTORS
More in elderly and children
Vomitting & Diarrhea
Cardiac & Renal Disorders
Addison’s Disease
NPO+IV infusion
Client on Diuretics

128. PATHOPHYSIOLOGY
Etiological Factors
As ECF concentration of Na Dec.
Na conc. Gradient (diff.) b/w ECF& ICF Dec.
Osmolality (Hypo- osmolality)
Osmosis (Water shift from ECF to ICF)
Intracellular Edema (Cellular Swelling)
Less Na. present to move across excitable membrane

129. Decreased Serum Osmolality
Delayed membrane depolarisation
Hyponatremia
Further Electrolyte imbalances(K, Ca, Cl)
Uncorrected Hypovolemic
Hyponatremia
Uncorrected Hypervolemic
Hyponatremia
Shock ECF volume excess
Convulsions & Coma Edema

131. CLINICAL MANIFESTATIONS

132. DIAGNOSTIC EVALUATION
1. Health history:
• Current manifestations
• Precipitating factors
• Chief complaints
2. Physical assessment:
• Head to toe examination for detecting the clinical
features or any abnormality in body functioning .

133. DIAGNOSTIC ASSESSMENT
3. Diagnostic assessment are based on
clinical manifestations and serum lab
values.
Serum Sodium- lessthan135mEq/L.
Urine Sodium- lessthan40mEq/L.
Serum Osmolality- less than 275mOs/kg H2O.
24hour urine specimen to evaluate sodium excretion.

134. IV Normal SalineModerate hyponatremia 125mEq/L-
(0.9% NaCl)/ RL.
High hyponatremiamEq/L-concentratedSalineSolution
(3% NaCl).
If hyponatermiais accompanied by fluid volume excess
osmotic diuretics and Loop diuretics are asdministered.
If caused by inappropriate or excessive secretion of antidiuretic
hormone, medications that antagonize antidiuretic hormone may be
administered. Vasopressin receptor antagonist- Tab. Tolvapton- 15mg.

135. DIETARY MANAGEMENT
diet in MildIncreaseintake of sodium rich
Hyponatremia.
Sodium Replacement- in Severe Hyponatremia.
Fluid Restricted Diet- hyponatremia due to excess fluid
(800- 1000ml/day)

136. NURSING MANAGEMENT
A. ASSESSMENT-
Assess history and clinical manifestation.
Do physical examination.
Assess lab values for serum sodium.
Urine output and daily weight should be
observed.
Asess I/O, V/S, LOC, body weight, bounding
pulse, neck vein enlargement etc.

137. 1. Hyponatremia r/t vomitting, diarrhea,gastric suctioning.
IMPLEMENTATATION-
 CheckV/Severy 4-8 Hours.
 Monitorserum sodium, monitor the I/O & daily weight.
 Sodium level lessthan 125mEq/Lindicatethe need for
prompt medicalcare.

138.  Irrigate N.G. Tube & wound sites with NS. Plan for fluid
restriction if hyponatremia is due to fluid volumeexcess.
 If client is disoriented, reorient the client and provide safety
measures.
 Instruct the client to increase oral sodium intake and inform
client about the foods to include in thediet.
 If the client is taking lithium, monitor the lithium level, because
hyponatremia can cause diminished lithium excretion, resulting
in toxicity.

139. 2. Risk for imbalanced fluidvolume:
Implementation:
Monitor intake andoutput.
Weight daily.
UseIV flow control devices.
Explain and clear doubts of client andhis family.

141. HYPERNATREMIA
DEFINITION:- Hypernatremia is a serum sodium
level that exceeds 145mEq/l.
CAUSES:
Decreased sodium excretion:
Corticosteroids
Renal failure
Cushings syndrome
Increased sodium intake
Decreased water intake

142. ETIOLOGY
Altered thirst
Inability to respond to thirst sensation or obtain water
Decreasedsynthesis of ADH from posterior pituitary
gland
Excessive sweating
Diarrhea
Oral electrolyte solutions or hyperosmolar tube- feeding
formulas
Excessive IV fluid such as normal saline, 3% or 5% sodium
chloride , or sodium bicarbonate
Primary hyperaldosteronism [hypersecretion of
aldosterone].

144. Thirst mechanismis
stimulated
Increase the intakeof
water

145. CLINICAL MANIFESTATIONS
NEUROLOGICAL MANIFESTATIONS:
Lethargy, weakness
Irritability
Seizures, coma and death
Altered mental status
Decreased level of consciousness
Muscle twitching
Dry and sticky mucous membrane

147. SIGNS & SYMPTOMS

148. ASSESSMENT
Heart rate and blood pressure.
Pulmonary edema.
Extreme thirst.
Decreased urine output.
Dry and flushed skin.
Dry and sticky tongue.
Skeletal muscle weakness.

149. DIAGNOSIS
Serum Na- More than 145mEq/L.
Urine Sodium- More than 220mEq/L.
Serum Osmolality- More than 295mOs/kg H2O.
Water deprivation test is performed .
History- oral intake Current manifestations,
precipitating factors, chief complaints.
Physical exam- for detecting the clinical features or
any abnormality in body functioning. V/S,BUN,
creatinine, glucose, urine osmolality.

150. MANAGEMENT
respiratory,Monitor the clients cardiovascular, cerebral
and renal status.
Cause is fluid loss- administer isotonic IV infusions- 0.45% or
0.2% NS, 5%DW and TPN/tube feed.
Cause is inadequate renal excretion of sodium- administer
diuretics that promote sodium loss.
 Ex.- Thiazide Diuretics, Loop Diuretics.
 Ex.- indapamide, chlorothiazide, Furosemide, torsemide.
Restrict sodium and fluid intake.

151. NURSING MANAGEMENT
NSG. DIAGNOSIS- Hypernatremia r/t dec. thirst, excessive
administration of salt solutions, or impaired excretion of
sodium and water.
NSG. INTERVENTIONS-
Monitor the client for response to I/V fluid replacement of
hypo osmolar electrolyte solutions.
Absence of S/S of hypernatremia.
Return to normal Na levels.
D5W byPrevent osmotic diuresis from
maintaining the prescribed rate.

152. OFFER WATER AND FLUIDS TO PATIENTS WITH HYPO OR
EUVOLEMIC HYPERNATREMIA.
Restrict fluid and sodium in hyper osmolar hypernatremia
patients
Give gastric feeding to patient if he tolerates.
Consult with doctor if S/S indicates worsening
Hypernatremia or fluid overload, such as increasing weight
gain, or pulmonary, cardiovascular or neurological
manifestations.

154. POTASSIUM
IMBALANCES
HYPOKALEMIA HYPERKALEMIA

155. HYPOKALEMIA
DEFINITION:
Hypokalemia is serum potassium level lower than
3.5mEq/L.

156. CAUSES
Actual total body
potassium loss
Inadequate
potassium intake
Movement of
potassium from
extracellular fluid
into intracellular
fluid
Dilution of serum
potassium
• Excessive use of
medication such as
diuretics or
corticosteroids.
• Increased secretion
of aldosterone.
• Vomiting, Diarrhea.
• Wound drainage.
• Excessive
diaphoresis.
• NPO. • Alkalosis.
• Hyperinsulinism.
• Water intoxication.
• IV Therapy with
potassium- poor
solutions.

157. SIGN & SYMPTOMS
CARDIOVASCU
LAR SYSTEM
RESPIRATORY
SYSTEM
NEUROLOGICSY GI
SYSTEM STEM
MUSCULO-
SKELETAL
SYSTEM
• Thready ,
weak,
irregular
pulse.
• Weak
peripheral
pulses
• Orthostatic
hypotension
• Dysrhythmias
• Vertigo
• Flattened T
wave
• Shallow,
ineffective
respirations
• Diminished
breath
sounds
• SOB
• Anxiety,
confusion,
coma
• Loss of tactile
discrimination
• Paresthesias
• Deep tendon
hyporeflexia
• Fatigue
• Lethargy
• Absence of
bowel sounds
• Nausea,
vomiting,
diarrhea,
abdominal
distension
• Muscle
weakness
• Paralysis
• Leg cramps

160. MANAGEMENT
Monitor cardiovascular, respiratory,neuromuscular,
renal and gastric status.
Place client on a cardiac monitor.
Monitor electrolyte levels.
Administer potassium supplements orally and IV.
Institute safety measures for the client experiencing muscle
weakness.
Instruct the client about foods that are high in potassium
content.

161. PHARMACOLOGICAL
MANAGEMENT
1. Oral Potassium Replacement therapy- for mild
hypokalemia (Serum Potassium- 3.3-3.5 meq/L).
• Instruct client to take medicine with a glass of water because
potassium is extremely irritating to gastric mucosa.

162. PHARMACOLOGICAL
MANAGEMENT
2. I/V KCl: for moderate to severe hypokalemia.
Must be diluted in I/V fluids.
Potassium by I/V push may result in cardiac arrest.
Give potassium in doses of 10-20 meq/hour diluted in I/V
fluid if client is on cardiac monitor.
 High concentration of potassium is irritating to heart muscle.
Thus, correcting a potassium deficit may take several days.

163. DIETARY MANAGEMENT
Foods rich in potassium help to correct and further
prevent further potassium loss.
Adult recommended allowance- 1875- 5625mg.
Foods- cabbage, carrot, cucumber,
mushrooms, spinach, tomato, fruits- banana,
gauva, orange.

164. FOODS
Cabbage
Carrot
Cucumber
Mushrooms
Spinach

165. FOODS
Tomato
Banana
Gauva
orange

166. HYPERKALEMIA

167. HYPERKALEMIA
DEFINITION:
Hyperkalemia is aserum potassium level that exceeds
5.0 mEq/L.

168. CAUSES

169. CAUSES
Excessive potassium intake:
Over ingestion of potassium containing food or
medications.
containing I/VRapid infusion of potassium
infusions.
Decreased potassium excretion
Potassium sparing diuretics
Renal failure
Renal insufficiency
Decreased urine output

170. CAUSES:
Movement of potassium from intracellular fluids into extracellular
fluids
Tissue damage
Acidosis
Excessive release of Cellular Potassium- severe traumatic injuries,
severe burns, severe infection, metabolic acidosis.
severe burns
severe infection
metabolic acidosis.
severe traumatic injuries

173. CLINICAL MANIFESTATIONS
CARDIOVASCULAR
SYSTEM
RESPIRATORY GI SYSTEM
SYSTEM
First tachycardia
then bradycardia
Slow, weak, irregular
heart rate
Decreased blood
pressure
ECG changes-
peaked narrow T-
waves, wide QRS
complex, Depressed
ST segment, widened
PR interval
Profound weakness
of the skeletal
muscles leading to
respiratory failure
Nausea
Diarrhea
Hyperactive
bowel sounds
Parasthesia
Ascending flaccid
paralysis
Muscle weakness
Muscle cramps
NEUROMUSCULAR RENAL
SYSTEM
Numbness in the Oliguria,
hands and feet
Later
anuria

174. MEDICAL MANAGEMENT
When serum Potassium level is 5.0-5.5 meq/L,
restriction of dietary potassium intake.
Cause is metabolic acidosis- correct acidosis with Na
Bicarbonate- promotes K intake into cells.
Improving urine output- decreases elevated serum
potassium level.

175. MEDICAL MANAGEMENT
Severe hyperkalemia-
actions- to avoid
take
severe
immediate
cardiac
disturbances.
I/V Calcium Gluconate- to decrease antagonist effect
of potassium excess on myocardium.
Anti hyperkalemia- IV insulin+ glucose+ sodium
bicarbonate.- to promote potassium uptake into cells.

176. MANAGEMENT
MONITOR RENAL
FUNCTION.
Monitor cardiovascular, respiratory, neuromuscular, renal and
G.I.system of the patient.
Prepare to administer potassium excreting diuretics.
Prepare the client for dialysis if potassium levels are critically
high.
Fresh blood should be administered when blood transfusion is
prescribed.

177. CALCIUM
IMBALANCES

178. CALCIUM
IMBALANCES
HYPOCALCEMIA HYPERCALCEMIA

179. HYPOCALCEMIA

180. HYPOCALCEMIA
4.5 meq/L orSerum calcium below
8.5mg/dL.

181. ETIOLOGY
Inadequate dietary intake of calcium
Vitamin D deficiency
Malabsorption of fat in intestine
Metabolic acidosis
Renal failure with hyperphosphatemia, acute pancreatitis, burns, Cushing’s Disease,
hypoparathyroidism.
Medications- Magnesium sulfate.
Malignancy (Multiple Myloma)

182. CLINICAL MANIFESTATIONS
NEURO-
MUSCULAR
RESPIRATORY GI CV HEMATOLOGIC
• Tetany
Symptoms-
 Twitching
around
mouth,
 Tingling and
numbness of
fingers
 Facial spasm
 Convulsions
• Dyspnea
• Laryngeal
Spasm
• Increased
peristalsis
• Diarrhea
• Dysrhythmias
• Palpitations
• Prolonged
bleeding time

183. MEDICAL MANAGEMENT
Determine and correct the cause of hypocalcemia.
Asymptomatic hypocalcemia- Oral calcium
gluconate, calcium lactate, 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.

184. MEDICAL MANAGEMENT
I/V Calcium Gluconate or Calcium
Chloride(10%) – slowly to avoid
hypertension, bradycardia and other
symptoms.

185. DIETARY MANAGEMENT
Chronic/Mild Hypocalcemia: diet high in Calcium.
E.g: cheese, milk, spinach.
Hypocalcemia due to parathyroid deficiency- Avoid
foods high in phosphates. E.g: milk products,
carbonated beverages.

189. HYPERCALCEMIA

190. HYPERCALCEMIA
Serum calcium level more than 5.5 meq/L Or
11mg/dL.

191. ETIOLOGY
Metastatic Malignancy of- lung,
ovaries, prostate, bladder,
leukemia, kidney.
Hyperparathyroidism
Thiazide diuretic therapy
Prolonged immobilization
Excessive intake of calcium
supplements and Vitamin D.

192. CLINICAL MANIFESTATIONS
GI NEURO- CV RENAL
MUSCULAR
MUSCULO-
SKELETAL
• Anorexia
• Vomitting
• Constipatio
n
• Deccreased
peristalsis
 Depression
 Difficulty to
concentrate
• Severe
Hypercalcemia-
 Extreme lethargy
 Confusion
 Coma
• Mild-Moderate •
Hypercalcemia-
 Weakness •
 Fatigue
Dysrhythmias
Heart Block
• Polyuria
• Kidney
Stones
• Renal
failure
• Bone pain
• Fracture

193. LAB FINDINGS
Serum Calcium- >5.5 meq/L (>11.5mg/dL)
ABG- pH <7.45, HCO3 >26meq/L

194. MEDICAL MANAGEMENT
Correct the underlying cause.
I/V NS (0.9%)+ Furosemide- is given rapidly to prevent fluid
overload, promote urinary calcium excretion.
Calcitonin- decreases- serum calcium- inhibit the effect of
PTH on osteoclasts and increasing urinary calcium excretion.
Corticosteroids- decrease calcium by competing with vitamin
D thus resulting in decreased intestinal absorption of calcium.

195. MEDICAL MANAGEMENT
Avoid or use in reduced dosage- calcium or vitamin D
supplements or calcium containing antacids if they are the
cause.
Etidronate disodium- reduces serum calcium by reducing
normal and abnormal bone reabsorption of calcium and
secondarily by reducing bone formation.

196. DIETARY MANAGEMENT
Oral fluids-
 Assisst in adequately hydrating the client
 Flushing excess calcium through the kidney.