The document discusses fluid and electrolyte imbalances, emphasizing their importance for physiologic homeostasis and health outcomes. It covers body fluid compartments, mechanisms controlling fluid movement, fluid imbalances, clinical manifestations, and management strategies for both fluid volume deficit and excess. Additionally, it highlights the role of hormones and kidneys in regulating fluid balance, and the potential consequences of imbalances for various patient populations.

1. FLUID AND
ELECTROLYTE
IMBALANCES
Presented By-
Haranjan kaur
Msc (N) 1st YEAR
Presented To-
Mrs. Prabhjot Saini
HOD, MSN
CON, DMC& Hospital

3. INTRODUCTION
 Physiologic homeostasis depends upon the normal fluid
and electrolyte balance.
 Electrolyte imbalance is needed to be studied to promote
the positive health outcomes.
 Positives outcomes are achieved through health
promotion, health maintainance and health restoration
strategies.
 Clearly water is not only responsible for body’s structure
and function , it is also necessary for the maintainance of
equilibrium and of life itself.

4. INTRODUCTION
 Fluid and electrolyte imbalance commonly accompany
illnesses.
 Severe imbalances may results in death. Such imbalances
affect not only the acutely and chronically ill patients but
also clients with faulty diets and those who take selected
medications such as diuretics and gluccocorticoids
preparations.
 So, every nurse must understand the process of fluid and
electrolyte balance, identify clients at risk of imbalances ,
intervene as appropriate and evaluate the outcomes.

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

6. BODY FLUID COMPOSITION AND
COMPARTMENTS
The 60-40-20 Rule:
 60% of body weight is water.
 40% of body weight is intracellular fluids.
 20% of body weight is extracellular fluids.
interstitial intravascular
CELL
Intracellular
Extracellular

7. FLUIDS
 Body fluid compartments
1. Intracellular fluid- 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 30% of the total body weight. The
extracellular fluid consist of interstitial fluid,
intravascular fluid, cerebrospinal fluid , intraocular fluid,
synovial fluid , lymphatic fluid and secretions of
gastrointestinal tract.

8. DISTRIBUTION OF BODY FLUIDS
Pediatrics
◦ 75%-80% of body weight
◦ More symptomatic with dehydration
Aging- Prone to dehydration
◦ Decreased % of TBW
◦ Increased adipose and decreased muscle
mass
◦ Decreased Renal function
◦ Diminished thirst perception

10. 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 .

11. 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.

13. 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.

14. Decreased Volume
of ECF
Increased
Osmolality of ECF
Stimulates osmoreceptors
in hypothalmic thirst
centre
Decreased saliva
secretion
Dry mouth
Sensation of thirst
Water abosrbed
from GIT
Increased amount
of ECF
Deccreased
Osmolality of ECF
Fig. Factors stimulating water intake through the thirst mechanism
HYPOTHALAMIC
REGULATION / THIRST

15. RAAS

17. Mechanical ventilation,
drugs, anesthesia, pain

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

19. 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.

20. ADRENAL CORTICAL REGULATION
STRESS SIGNALS TO
HYPOTHALAMUS
ANTERIOR PITUITARY
INCREASES
SECRETION OF ACTH
ADRENAL CORTEX
INCREASES
ALDOSTERONE
INCREASES
CORTISOL
POSTERIOR PITUITARY
IN CREASES SECRETION
OF AN TIDIURETIC
HORM ON E
- KIDNEYS
INCREASES
WATER
REABSORPTION

21. INCREASES SODIUM
REABSORPTION
INCREASES
POTASSIUM
EXCRETION

22. RENAL REGULATION KIDNEYS
 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.

23. RENAL REGULATION KIDNEYS
 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.

24. ATRIAL NATRIURETIC PEPTIDE
CARDIAC ATRIA
RELEASE ATRIAL
NATRIURETIC FACTOR
[ANF]
INHIBITS RENIN
SECRETION
INCREASES
URINARY
EXCRETION OF
SODIUM AND
WATER
DECREASES BLOOD
VOLUM E AND
CAUSES
VASODILATION

25. 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.

26. INSENSIBLE WATER LOSS
 INSENSIBLE WATER LOSS: which is invisible
vaporization from the lungs and skin, assists in
regulating body temperature. Normally about
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.

27.  ONCOTIC PRESSURE- Colloid osmotic pressure,
is a form of osmotic pressure exerted by
proteins, notably albumin, in blood vessel’s
plasma (blood/ liquid) that usually tends to pull
water into the circulatory system.
 HYDROSTATIC PRESSURE- Pressure that is
exerted by a fluid at equilibrium at a given point
within the fluid, due to the force of gravity.
 It increases in proportion to depth measured
from the surface because of the increasing
weight of fluid exerting downward force from
above.

28. FLUID PRESSURE
 Body fluids shifts between interstitial
compartment and intravascular compartment
due to difference H.P. / O.P.
 In abnormal condition,
because of dec. plasma/ serum protein
which will decrease O.P. in blood vessels
fluid may remain into tissue spaces

29. Fluid in tissue spaces
Increased H.P.
cause pressure gradient
opposes fluid reabsorption into venous end of
capillaries
FLUID OVERLOAD

31. TONICITY

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

34. HYPERTONIC SOLUTIONS
 Higher solute concentration than RBC
 If injected into vein, Fluid moves from
interstitial space INTO veins.

35. Affects of Hypertonic Solution on
Cell
Cell
Shrunken
Cell
• The (solute) outside the
cell is higher than inside.
• Water moves from low
(solute) to high (solute).
• The cell shrinks.

36. Hypotonic Solutions
 Lower solute concentration than blood
 If injected into vein, fluid moves OUT of
veins into tissues.

37. Affects of Hypotonic Solution on
Cell
 The (solute) outside
the cell is lower than
inside
 Water moves from low
(solute) to high
(solute)
 The cell swells and
eventually bursts
Cell
Swelling
Cell
Ruptured Cell

40.  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)
INTRODUCTION

41.  Serum sodium does not signify amount of
sodium in ECF, but indicates relationship of
amount of water to dissolved sodium
Low salt High salt
Hyposmolar Hyperosmolar
 Serum Osmolality=
275-295mOsm/kgH2O
 Iso osmolar- F:E Same
 Hypo osmolar- F:E
 Hyper osmolar- F:E

42. Types of fluid imbalances
TYPES
Fluid Volume
Excess
Extracellular
Fluid Volume
Excess (ECFVE)
Intracellular
Fluid Volume
Excess
Fluid Volume
Deficit
Extracellular
Fluid Volume
Deficit
Intracellular
Fluid Volume
DeficitThird Space Fluid
Shift

43. 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.

44. ETIOLOGY
 Severe vomiting
 Severe diarrhea
 Traumatic injuries
 Excessive blood loss
 Third space fluid shifts&
 Insufficient water or fluid intake.
 Lack of fluid intake due to impaired thirst
mechanism.

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

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

47. 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.

48. 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

49. 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 .

50. 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

51. 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.

52. 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.

53. 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.

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

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

56. NURSING MANAGEMENT
1.Deficit fluid volume:
 Restore oral fluid intake.
 Restore fluid by intravenous.
 Reduce risk of deficit fluid volume.
 Control of underlying problems.
 Monitor for complications.

57. NURSING MANAGEMENT
2.Impaired oral mucous membrane:
• Oral care regularly 2-4 hourly.
• Apply lip moisturizer.
• Rinse client’s mouth every 1-2 hourly.
• Examine client’s mouth with penlight for debris.

58. NURSING MANAGEMENT
3.Risk for injury:
• Provide safety through step progression position
change.
• Place alarm monitors on client’s bedside.
• Restraints sometimes may be needed.

59. EXTRACELLULAR FLUID VOLUME EXCESS
(ECFVE)
 Definition: ECFVE is increased fluid volume
retention in the intravascular & interstitial spaces.
 It is a fluid overload or over hydration.
 The expansion of fluid compartment due to
increase in total sodium content.
 Sodium & water retention is same to as iso-
osmolar Fluid volume excess.

60.  Fluid excess in intravascular space-
Hypervolemia.
 Fluid excess in interstitial space- edema.
 Serum Na level – mostly within normal level
or
Inc. Because of excess water retention

61. Compromised regulation of fluid movement
and excretion, example- Hypothyroidism,
Renal disorder, Decreased plasma protein.
Excessive ingestion of fluids or foods
containing sodium, example- Excessive amount
of I/V saline, Ingestion of high sodium food,
Excessive use of enema with sodium.
 Increased ADH and aldosterone, example-
Certain barbiturates, narcotics, Cushing
syndrome, Glucocortiods, SIADH.
ETIOLOGY

62. ETIOLOGY
Increased
total body
sodium
content
Heart Failure
Renal
Disorders
Liver
Disorders
Increased
ingestion of
foods
containing
high amounts
of sodium

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

64. 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

65. 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

66. [B] With Renal Disease
Dec. Sodium & Water retention
Fluid volume excess in Blood vessels
Inc. H.P. in B/V
Pulmonary Edema Generalised Edema

67. [C] Liver Disease
Dec. production of Plasma Proteins
Dec. O.P. Of vascular Fluids
Less fluid reabsorption from tissue space
Fluid volume excess in ECF
Peripheral Edema Ascitis

68. [D] Lymphatic Obstruction
Decreases Absorption of interstitial fluid
Dec. transportation of capillary filtered protein
Dec. O.P. which pulls fluid towards it
Edema

69. [E] Inc. Capillary Permiability
Movement of plasma proteins into tissues
Inc. Tissue O.P.
Edema

70. 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 extremeties
• Weight gain
• Sacral edema
• In. B.P.
• Peripheral vein filling time greater than 5
seconds.
• Bounding pulse.
• Increased right atrial CVP and PCWP.

71. CLINICAL MANIFESTATIONS
 NEUROLOGICAL: Change in Level of
consciousness

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

73. 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.

74. MEDICAL MANAGEMENT
PHARMACOLOGY MANAGEMENT-
 Loop & Potassium sparing Diuretics- to
excrete potassium along with sodium and
water.
 Digoxin, a digitalis preparation- to increase
Myocardial Contraction or to slow the heart
rate if heart failure is cause of ECFVE.

75. 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.
 When reading food labels, low sodium is defined as
140 mg of sodium per serving.

77. NURSING MANAGEMENT
1. NSG. ASSESSMENT-
a. Assess history of symptoms i.e. Respiratory, Cardiac &
Neurogenic. (Onset, Duration, Location& Description).
b. Assess for related factors- Protein, Caloric & Alcohol Intake.
c. Assess for-
 Signs of fluid overload, pulse, B.P.,
Respiration.
 Edema and weight gain.
 Neck & hand vein engorgement
 Check Digitalis toxicity if infused with digitalis .

78. 2. NSG. INTERVENTIONS-
 Nsg. Diagnosis- Fluid volume excess r/t Heart failure, Renal
Failure Or Hypervolemia
 Implementation-
 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.
 Mobilize fluid electrolyte imbalances.
 Reduce complications like digitalis toxic effects.

79. INTRACELLULAR FLUID
VOLUME DEFICIT

80. DEFINITION
Intracellular fluid volume deficit is
decrease in fluid within the cells.

81. CAUSES
Excessive fluid loss. Insufficient fluid intake.
Failure of regulatory
mechanism.
Loss of GI fluid from
vomiting, diarrohea, GI
suctioning, intestinal
fistula and intestinal
drainage.
Haemorrhage.
Chronic abuse of
laxatives and enemas.
Water and sodium losses
during sweating from
exercise or increased
environmental
temperature.
Excessive renal losses of
water and sodium from
diuretic therapy.

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

83. CLINICAL MANIFESTATIONS
Dry , pale and cool extremities.
Orthostatic hypotension.
Decrease in capillary refill.
Increase body temperature.
Weight loss.
Thirst.

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

85. 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.

86. MANGEMENT
2. Intravenous therapy:
 When fluid deficit is severe or client is
unable to ingest fluid, the I/V route is used
to administer replacement fluid.

87. 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

88. 3. Fluid challenge:
 A fluid challenge, the rapid administration
of a designated amount of I/V fluid may
be performed to evaluate fluid volume
when urine output is low and cardiac or
renal functioning is questionable.

89. 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.

90. 2. Ineffective tissue perfusion:
 Monitor changes in level of consciousness.
 Monitor serum creatinine, BUN, cardiac
enzymes.
 Change position 2 hourly.
NURSING MANAGEMENT

91. 3. Risk for injury:
 Keep side rails of bed up.
 Slowly raise the client from supine to sitting
then to standing position.
NURSING MANAGEMENT

92. INTRACELLULAR FLUID
VOLUME EXCESS
(ICFVE)

93. INTRACELLULAR FLUID VOLUME
EXCESS (ICFVE)
 Definition- ICFVE is a hypo-osmolar
disorder resulting from either water excess
or solute deficit and are mainly due to
sodium loss.
 The cells become engorged or swollen.

94. INTRACELLULAR FLUID VOLUME
EXCESS (ICFVE)
 In water excess- No. of solutes is normal but excess water
dilution.
 In solute deficit- Amount of water is normal but few
electrolyte(solute) per litre of water.
 In both cases, Hypo-osmolality of vascular fluid
Cellular Swelling

95. CAUSES
 Administration of Excessive amounts of hypo-
osmolar fluids- 0.45% Saline/ 5% Dextrose in
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.

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

97. 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.

98. 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)

99. 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.

100. CLINICAL MANIFESTATIONS
3. Others-
 Nausea
 Projectile vomiting
 Irritability
 Disorientation
 Confusion
 Drowsiness
 Decreased co-ordination
 Increase in TBW causes weight gain
 Convulsions.

101.  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
CLINICAL MANIFESTATIONS

102. LAB FINDINGS
 Serum sodium level <125meq/Lt.
 Decrease hematocrit value.

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

104. 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.

105. 3. Dietary management:
Because sodium retention is a primary cause
of fluid volume excess, so sodium restriction
diet is often prescribed.

106. 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.

107. 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.

108. NURSING MANAGEMENT
1. NSG. ASSESSMENT-
 Assess early signs of cerebral edema and
Inc. ICP.
 Assess absence of thirst, Dec. hematocrit, &
Serum Sodium less than 125 mEq./dL.

109. NURSING DIAGNOSIS
1. Excess fluid volume:
 Assess vital 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.

110. NURSING DIAGNOSIS
2. Risk for impaired skin integrity :
 Assess skin 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.

111. NURSING DIAGNOSIS
3. Risk for impaired gas exchange:
 Auscultate lungs for presence of 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 .

112. 4. Altered thought process r/t Cerebral
Edema:
 Restriction of oral/ I/V intake.
 Avoid tap water enema.
 Monitor I/O, Daily Weight & V/S.
 Irrigate N.G. tube with NS.
 Notify reflexes and change in V/S &
behaviour.
 Assess polyuria as indication that fluid has
shifted from cell to vascular spaces.

113. EXTRACELLULAR FLUID
VOLUME SHIFT:
THIRD SPACE FLUID

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

115.  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 space and
remains there is known as third spacing.
 Common sites for third spacing are :
Pleural cavity
Peritoneal cavity
Pericardial sac

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

117.  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

118.  Decreased protein intake production,
storage or increased loss in PEM and liver
or kidneys
 Altered lymphatic function/ Venous
thrombosis impairs fluid return to right
atrium, thus producing fluid shifting
 Peritoneal cavity- Impaired protein
synthesis, decreased colloidal osmotic
pressure.
ETIOLOGY

119. RISK FACTORS
 Major trauma
 Major surgery

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

121. PATHOPHYSIOLOGY
Fluid shift from interstitial space to
vascular space
Hypervolemia
Second
Phase

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

123. Diagnostic Assessment
 Inc. hematocrit
 Inc. BUN
 Inc. Serum sodium
 Inc. Urine specific gravity
When fluid returns to blood stream;
 Dec. Hematocrit
 Dec. BUN

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

125.  Burns/ crush injuries- result in
hypovolemia- give large volume of
ISOTONIC SOLUIONS.
 Amount of fluid- 3 times greater than
URINE OUTPUT.
 2nd Phase:- Fluid administration and intake
is limited because of fluid influx from tissue
spaces into vessels.
 Third space due to pericarditis and bowel
obstruction- remove fluid from the body- to
retain its function.

126. Stabilize other problems:
 I/V antibiotics are given to prevent sepsis.
 Vasodilators are given to maintain blood
pressure.
 Steroids are given for inflammatory
disorders.

127.  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.

128. NURSING MANAGEMENT
 Assess V/S: 1-8 hourly.
 Monitor I/V fluid replacement: If fluids are
administered rapidly, hypervolemia(fluid
overload) may occur.
 Asses chest crackles, difficulty in breathing,
neck vein engorgement to prevent pulmonary
edema with fluid volume excess.
 Measure abdominal girth 8 hourly in case of
ascitis.

129. NURSING MANAGEMENT
 If extremities are involved, circumference of
extremities and peripheral pulses should be
measured 1 hourly.
 Monitor LOC.
 Take seizure prevention strategies.
 Skin care for edematous areas to prevent skin
breakdown.
 I/V fluid replacement is decreased when fluid shift
back with repair of tissue damage.

130. 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.

131. ELECTROLYTE
IMBALANCES

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

133. 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)

134. DEFINITIONS
 NON-ELECTROLYTE: Substances that do not
dissociate into ions in solution. E.g. Glucose
and urea .
 OSMOLALITY: A measure of the total
substance [solute] concentration per
kilogram of solvent.
 OSMOLARITY: A measure of the total
substance [solute] concentration per litre
of the solvent.

135. DEFINITIONS
 SOLUTE: Substance that is dissolved in
solvent.
 SOLUTION: Homogenous mixture of solutes
dissolved in a solvent.
 SOLVENT: Substances that is capable of
dissolving a solute.

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

137. 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].
 Milliequivalents equals weight [in milligrams ]
divided by atomic weight and multiplied by
the valence.

138. SODIUM
IMBALANCES

139.  Sodium is the most plentiful electrolyte in
extracellular fluid [ECF].
 Sodium is the primary regulator of volume,
osmolality and distribution of ECF.
 Normal serum sodium: 135- 145 mEq/L.

140. SODIUM
IMBALANCES
HYPONATREMIA HYPERNATREMIA

141.  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.

142. REGULATION OF SODIUM
BALANCE IN THE BODY
• 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.

143. HYPONATREMIA

144. HYPONATREMIA
 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 .

146.  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.

147.  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

148. 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.

149.  Hyponatremia occurs when total body
water (TBW) is reduced. It is of four types:
S.NO. TYPES TBW BODY
SODIUM
1. Hypovolemic
hyponatremia
Dec. Dec.
2. Euvolemic
hyponatremia
Inc. Normal
3. Hypervolemic
Hyponatremia
Inc. Inc./ Normal
4. Redistributive
Hyponatremia
Normal Normal

150. RISK FACTORS
 More in elderly and children
 Vomitting & Diarrhea
 Cardiac & Renal Disorders
 Addison’s Disease
 NPO+IV infusion
 Client on Diuretics

151. 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

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

154. CLINICAL MANIFESTATIONS
1. Gastro
Intestinal
2. Cardiovascular 3. Pulmonary 4. Neurologic
• Nausea
• Vomitting
• Diarrhea
• Hyperactive
Bowel Sounds
• Abdominal
Cramps
• Anorexia
• Weight loss
• Dry mucous
membrane
• Dec. Diastolic B.P.
• Tachycardia
• Weak Pulse
• Orthostatic
Hypotension
• Elevated B.P.
• Full Rapid Pulse
• Decreased CVP and
jugular venous filling
• Change in rate
of Respiration
• Adventitious
Lung Sounds
• Headache
• Apprehension
• Lethargy
• Weakness
• Cellular edema
• Irritability
• Confusion
• Personality
changes
• Tremors
• Seizures
• Coma
• Hyperrflexia
• Muscle spasm
• Depression
• Dulled
sensorium
5. Muscular
• Muscle
cramps
• Weakness
• Fatigue

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

156. DIAGNOSTIC ASSESSMENT
3. Diagnostic assessment are based on
clinical manifestations and serum lab
values.
 Serum Sodium- less than 135mEq/L.
 Urine Sodium- less than 40mEq/L.
 Serum Osmolality- less than 275mOs/kg
H2O.
 24 hour urine specimen to evaluate sodium
excretion.

157. MEDICAL MANAGEMENT
• GOAL- to correct water osmolality and therfore
restore cell volume by raising the ratio of
sodium to water in ECF.
• If client is in hyponatremia due to fluid volume
excess, fluids will be restricted to allow Na
regain balance.
• Is Na is less than 125mEq/L, Na replacement
needed.
• Rapid correction of serum sodium levels should
not be done as this may inc. Fluid- Volume level
and damage CNS.

158. PHARMACOLOGICAL
MANAGEMENT
 Moderate hyponatremia 125mEq/L- IV Normal Saline
(0.9% NaCl)/ RL.
 High hyponatremia mEq/L- concentrated Saline Solution
(3% NaCl).
 If hyponatermia is 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.

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

161. 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.

162. 1. Hyponatremia r/t vomitting, diarrhea, gastric
suctioning.
 IMPLEMENTATATION-
 Check V/S every 4-8 Hours.
 Monitor serum sodium, monitor the I/O &
daily weight.
 Sodium level less than 125mEq/L indicate the
need for prompt medical care.

163.  Irrigate N.G. Tube & wound sites with NS. Plan
for fluid restriction if hyponatremia is due to
fluid volume excess.
 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 the diet.
 If the client is taking lithium, monitor the
lithium level, because hyponatremia can cause
diminished lithium excretion, resulting in
toxicity.

164. 2. Risk for imbalanced fluid volume:
 Implementation:
Monitor intake and output.
Weight daily.
Use IV flow control devices.
Explain and clear doubts of client and his
family.

165. 3. Risk for ineffective cerebral tissue perfusion
 Implementation:
Monitor serum electrolytes and serum
osmolality.
Assess neurological changes.
Monitor mental status and orientation.
Assess muscle strength and tone and deep
tendon reflexes.

166. HYPERNATREMIA

168. 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

169. ETIOLOGY
 Altered thirst
 Inability to respond to thirst sensation or obtain
water
 Decreased synthesis 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].

172. Thirst mechanism is
stimulated
Increase the intake of
water

173. PATHOPHYSIOLOGY
Causes
Inc. Na levels
Osmotic shift of water from cells to ECF to maintain
balance& dilute the hyperosmolar state.
Cellular Dehydration.

174. IN BRAIN
If Hypernatremia slow/ chronic,
brain develops its own osmotic particles,
IDIOGENIC OSMOLES,
to prevent fluid shifts into and out of brain cells.
Cerebral Edema

176. Causes
Inc. Na levels
Heart is sensitive to increasing Na levels.
Na molecules compete with Ca in slow Ca channels
of heart
Dec. Myocardial Contractility
Myocardial Depolarisation- Arrhythmia

177. Causes
Inc. Na levels
Dec. secretion of ADH & Aldosterone
Sodium is excreted in urine

178. 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

179. SIGN & SYMPTOMS

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

181. 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.

182. MANAGEMENT
 Monitor the clients cardiovascular, respiratory,
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.

183. TREATMENT

185. HYPERNATREMIA

186. 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.
Prevent osmotic diuresis from D5W by
maintaining the prescribed rate.

187. NSG. MANAGEMENT
 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.

188. NURSING MANAGEMENT
 NSG. DIAGNOSIS- Risk for injury.
 NSG. INTERVENTIONS-
Maintain fluid replacement.
Monitor serum sodium and osmolality.
Monitor neurologic functioning.
Institute safety precautions as necessary.
Make client oriented to time, place and
person.

189. POTASSIUM
IMBALANCES

190. POTASSIUM
IMBALANCES
HYPOKALEMIA HYPERKALEMIA

191. HYPOKALEMIA
 DEFINITION:
Hypokalemia is serum potassium level
lower than 3.5mEq/L. It is a life threatening
condition because every body system is
affected.

195. 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.

197. SIGN & SYMPTOMS
CARDIOVASCU
LAR SYSTEM
RESPIRATORY
SYSTEM
NEUROLOGICSY
STEM
GI SYSTEM 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

198. LAB FINDINGS
 Serum Potassium: <3.5 meq/ L.

199. MANAGEMENT
• Determining & correcting the cause of the
imbalance.
• Extreme hypokalemia requires cardiac
monitoring.

200. 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.

201. 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.

202. 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.

203. MANAGEMENT

206. 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.

207. Foods
Cabbage
Carrot
Cucumber
Mushrooms
Spinach

208. Foods
Tomato
Banana
Gauva
orange

209. COMPARISON OF HYPO AND
HYPERKALEMIA

211. NURSING MANAGEMENT
Hypokalewmia r/t vomiting, diarrhea, cushing
syndrome or decreased intake.
Risk for injury r/t muscle weakeness &
hypotension.
Imbalanced nutrition less than body
requirement r/t insufficient intake of foods rich
in potassium.

212. HYPERKALEMIA

213. HYPERKALEMIA
DEFINITION:
 Hyperkalemia is a serum potassium level
that exceeds 5.0 mEq/L.

214. CAUSES

215. CAUSES:
 Excessive potassium intake:
Over ingestion of potassium containing food or
medications.
Rapid infusion of potassium containing I/V
infusions.
 Decreased potassium excretion
Potassium sparing diuretics
Renal failure
Renal insufficiency
Decreased urine output

216. 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

217. CLINICAL MANIFESTATIONS

219.  CARDIOVASCULAR SYSTEM:
 Slow, weak, irregular heart rate
 Decreased blood pressure
 RESPIRATORY SYSTEM:
 Profound weakness of the skeletal muscles leading to
respiratory failure
 NEUROMUSCULAR SYSTEM:
 Numbness in the hands and feet
 Ascending flaccid paralysis
CLINICAL MANIFESTATIONS
CARDIOVASCUL
AR SYSTEM
RESPIRATORY
SYSTEM
GI SYSTEM NEUROMUSCUL
AR SYSTEM
R
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
Numbness in
the hands and
feet
Parasthesia
Ascending
flaccid paralysis
Muscle
weakness
Muscle
cramps



220. CLINICAL MANIFESTATIONS
CARDIOVASCULAR
SYSTEM
RESPIRATORY
SYSTEM
GI SYSTEM NEUROMUSCULAR
SYSTEM
RENAL
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
Numbness in the
hands and feet
Parasthesia
Ascending flaccid
paralysis
Muscle weakness
Muscle cramps
Oliguria,
Later
anuria

221. LAB FINDINGS
Serum
Potassium
>5.0 meq/L.
Serum
Osmolality
295Mosm/Kg
Serum
creatinine >
1.5 mg/dl
BUN
>25mg/dl

222. 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.

223. MEDICAL MANAGEMENT
 Severe hyperkalemia- take immediate
actions- to avoid severe 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.

224. 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.

225. NURSING MANAGEMENT
Hyperkalemia r/t
renal dysfunction,
shock from traumatic
injuries or burns.
Potential for
dysrhythmias r/t
hyperkalemia.

226. CALCIUM
IMBALANCES

227. CAlCIUM
IMBALANCES
HYPOCALCEMIA HYPERCALCEMIA

228. HYPOCALCEMIA

229. HYPOCALCEMIA
 Serum calcium below 4.5 meq/L or
8.5mg/dL.

230. 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)

231. 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

232. 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.

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

234. 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.

235. NURSING MANAGEMENT
Hypocalcemia r/t diarrhea,
pancreatitis, renal failure or
decreased intake.
Risk for injury r/t increased
neuromuscular irritability
resulting from hypocalcemia.
Altered health maintenance
r/t knowledge deficit
regarding foods high in
calcium.

236. HYPERCALCEMIA

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

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

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

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

241. 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.

242. 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.

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

244. NURSING MANAGEMENT
Hypercalcemia r/t
metastatic lesions,
hyperparathyroidism,
thiazide therapy or
increased intake of
calcium.
Altered health
maintenance r/t
excessive ingestion of
calcium supplements
and calcium
containing antacids.
Risk for injury r/t
potential pathologic
fractures, mental
confusion and
immobility.