Name: laxmi thapa &

ravisha
pokhrel
Help maintain
body temperature
and cell shape
Helps

transport
nutrients gases
and wastes
 The desirable amount of fluid intake and loss in adults ranges from
1500 to 3500 mL each 24 hours. Ave= 2500 mL
 Normally INTAKE = OUTPUT
FLUID IMBALANCE
• Changes in ECF volume = alterations in sodium balance
• Change in sodium/water ratio = either hypoosmolarity or hyperosmolarity
• Fluid excess or deficit = loss of fluid balance
• As with all clinical problems, the same pathophysiologic change is not of
equal significance to all people
• For example, consider two persons who have the same viral syndrome
with associated nausea and vomiting
 It is an abnormally decreased or
increased fluid volume or rapid shift
from one compartment of body
fluid to another
Hypovolemia

Hypervolemia
• May occur as a result of:
• Reduced fluid intake
• Loss of body fluids
• Sequestration (compartmentalizing) of body fluids
Pathophysiology

DECREASED FLUID VOLUME

Stimulation of ↑ ADH Secretion Renin-Angiotensin-

thirst center Aldosterone
System Activation
in ↑ Water resorption
Person complains of
hypothalamus
thirst ↓ Urine Output
↑ Sodium and
Water Resorption

↑ Urine specific gravity except

with osmotic diuresis
acute weight loss
Oliguria

Low bp

Sunken eyes

Dizziness

 Weakness

Decreased skin turgor

Concentrated urine
• Fluid Management
• Oral rehydration therapy – Solutions
containing glucose and electrolytes.
E.g., Pedialyte, Rehydralyte.

• IV therapy – Type of fluid ordered depends on

the type of dehydration and the clients
cardiovascular status.

• Diet therapy – Mild to moderate dehydration.

Correct with oral fluid replacement.
Monitor & measures fluids at least
every 8 hours and sometimes hourly
Monitor daily body weight

Monitor vital signs

Observe for weak, rapid pulse and
orthostatic hypotension
Monitor urine concentration by
measuring urine specific gravity
Assess degree of oral and mucous
membrane moisture
 Toprevent hypovolemia, the nurse
identifies patient at risk and takes
measures to minimize fluid loss. For
ex: the patient has diarrhoea,
measures should be implemented to
control diarrhoea and replacement
fluid administered. This includes
antidiarrheal medication and small
volume of oral fluids at frequent
intervals
It refers to an isotonic expansion of
the ECF caused by abnormal
retention of water and sodium in
approximately the same proportion
in which they normally exist in the
ECF.
It is most often secondary to
an increase in total body
water.
 Common Causes:
Congestive Heart Failure
Early renal failure
IV therapy
Excessive sodium ingestion
SIADH

Corticosteroid
 Signs/Symptoms

Increased BP
Weight gain
Bounding pulse
Venous
distention
Pulmonary
edema
 Dyspnea

 Orthopnea (diff. breathing when

 Pharmacological therapy
Diuretics such as thiazide diuretics and loop
diuretics
Thiazide diuretics: hydrochlorothiazide
Loop diuretics: furosemide, torsemide
 Potassium supplement
 I/O chart at regular intervals to identify
excessive fluid retention
 Breath sound are assessed at regular
intervals in at risk patient particularly if
parenteral fluid are being administered
 Monitor the degree of edema in most
dependent parts of body such as feet &
ankles
 Ifrenal function is so severely impaired
that pharmacologic agents cannot act
efficiently, other modalities are
considered to remove sodium and fluid
from the body. Haemodialysis or
peritoneal dialysis may be used to remove
nitrogenous wastes and control potassium
and acid base balance and to remove
sodium and fluid. Continuous renal
replacement therapy may also be
required
 IF it is important to detect FVE before the
condition become severe. Intervention
include promoting rest, restricting sodium
intake , monitoring parenteral fluid therapy
and administering appropriate medications
 Regular rest periods may be beneficial
because bed rest favours diuresis of fluid
 Sodium and fluid limitation should be
instituted as indicated
 Fowlers position should be maintain to
promote lung expansion
• Controls and regulates volume of body fluids
• Its concentration is the major determinant of ECF volume
•Participates in the generation and transmission of nerve
impulses
• Eliminated primarily by the kidneys, smaller in feces
• Salt intake affects sodium concentrations
•Sodium is conserved through reabsorption in the kidneys, a
process stimulated by aldosterone
• Normal value: 135-145 mEq/L
 Refers to the serum sodium concentration less than 135 mEq/L
 Common with thiazide diuretic use, but may also be seen
with loop and potassium-sparing diuretics as well
 Occurs with marked sodium restriction, vomiting and
diarrhea, SIADH, etc. The etiology may be multifactorial
 May also occur postop due to temporary alteration in
hypothalamic function, loss of GI fluids by vomiting or
suction, or hydration with nonelectrolyte solutions
 Postoperative hyponatremia is a more serious complication
in premenopausal women. The reasons behind this is
 unknown
Therefore monitoring serum levels is critical and careful
assessment for symptoms of hyponatremia is important for
all postoperative patients
 Sodium loss from the intravascular compartment

Diffusion of water into the interstitial spaces

Sodium in the interstitial space is diluted

Decreased osmolarity of ECF

Water moves into the cell as a result of sodium loss

Water moves into the cell and cell swells

Extracellular compartment is depleted of water

CLINICAL SYMPTOMS
 Muscle APATHY
Weakness

Postural Nausea and

hypotensi Abdominal Weight
on Cramps Loss
In severe hyponatremia: mental confusion, delirium, shock and coma
  Contributing Factors
Excessive diaphoresis
Wound Drainage (esp. GI)
NPO
CHF
Low salt diet
Renal Disease
Diuretics
Vomiting
Diarrhea
Decreased secretion of aldosterone
Fresh water drowning; SIADH; Hyperglycemia
  Assessment findings:
 Neuro - Generalized skeletal muscle weakness.
Headache / personality changes/ confusion/ seizure/ coma;
Diminished DTR
 Resp.- Shallow respirations; ineffective respiration is a late
manifestation
 CV - Cardiac changes depend on fluid volume

 GI – Increased GI motility; Nausea, Hyperactive bowel

sounds; abdominal cramping; Diarrhea (explosive)
 GU - Increased urine output
 Integumentary: Dry mucous membranes
Plasma osmolality:
2Na + glucose/18 + BUN/2.8
 Interventions/Treatment
Restore Na levels to normal and prevent further
decreases in Na.
Drug Therapy –
 (FVD) - IV therapy to restore both fluid and

Na.
If severe may see 2-3% saline.
 (FVE) – Administer osmotic diuretic (Mannitol)

to excrete the water rather than the sodium.

Increase oral sodium intake and limit oral fluid
intake.
Watch for lithium toxicity in clients taking
lithium as hyponatremia precipitates it.
• A serum sodium level above 145 mEq/L is termed
hypernatremia
• May occur as a result of fluid deficit or sodium
excess
• Frequently occurs with fluid imbalance
• Develops when an excess of sodium occurs without a
proportional increase in body fluid or when water
loss occurs without proportional loss of sodium
• Risk Factors: excess dietary or parenteral sodium
intake, watery diarrhea, diabetes insipidus, damage
to thirst center, too young, too old, those with
physical or mental status compromise, and people
with hypothalamic dysfunction
 Increased Sodium concentration in ECF

Osmolarity rises

Water leaves the cell by osmosis and enters

the the extracellular compartments

Dilution of fluids in ECF Cells are water depleted

CLINICAL SYMPTOMS

Suppression of aldosterone Sodium is exreted in the

secretion urine
 Dry, sticky mucous Firm, rubbery
membranes tissue
turgor

DEATH
Tachycardia
Manic excitement
  Assessment findings:
Neuro – early: Spontaneous muscle twitches.
Late: Irregular muscle contractions. Skeletal muscle
weakness. Diminished or absent deep tendon reflexes
CNS: altered cerebral function; hypo & normovolemia:
agitation; confusion; seizures
Hypervolemia: lethargy; stupor; coma
 Resp. – Pulmonary edema if with hypovolemia
 CV – Diminished CO. HR and BP depend on vascular
volume.
 GU – Dec. urine output; Inc. specific gravity
 Skin – Dry, flaky/ flushed skin. Dry
sticky tongue and mucous membrane;
Edema r/t fluid volume changes.
 Interventions/Treatment

Drug therapy
Lowering of serum sodium level by infusion of
hypotonic electrolyte solution
Diuretics also may be prescribed to
treat sodium gain
Desmopressin acetate to treat diabetes
insipidus if it is cause of
hypernatremia
Diet therapy
 Mild – Ensure water intake
 The nurse should assess for abnormal loss of
water or low water intake and for large gains of
sodium as might occur with ingestion of OTC
medication that have high sodium content
 The nurse should obtain a medication history,
because some prescription medications have a
high sodium content
 The nurse also notes the patients thirst or
elevated body temperature and evaluates it in
relation to other clinical sign and symptoms
The more K, the less Na. The less K, the more Na
•Plays a vital role in such processes such as transmission of
electrical impulses, particularly in nerve, heart, skeletal,
intestinal and lung tissue; CHON and CHO metabolism; and
cellular building; and maintenance of cellular metabolism and
excitation
•Assists in regulation of acid-base balance by cellular
exchange with H
•Sources: bananas, peaches, kiwi, figs, dates, apricots,
oranges, prunes, melons, raisins, broccoli, and potatoes, meat,
dairy products
•Normal value: 3.5 – 5 mEq/L
 Serumlevel is below 3.5 mEq/l (3.5
mmol/L) usually indicates a deficit in
potassium store
 = Action Potential

Nerve and Muscle Activity

Increase in The cell

Low
resting becomes less
Extracellular
membrane excitable
K+
potential
 Aldosterone is secreted

Sodium is retained in the body through resorption by the

kidney tubules

Potassium is excreted

Use of certain diuretics such as thiazides and furosemide, and corticosteroids

Increased urinary output

Loss of potassium in urine

 Administration of 40- 80 mEq/day of
potassium is adequate in adult if there
are no abnormal losses of potassium
 Dietary intake of potassium in average
adult is 50-100 mEq/day
 When dietary intake is inadequate for any
reason, oral or IV potassium supplements
may be prescribed
 The nurse needs to monitor for its early
presence in patients at risk
 Fatigue, anorexia, muscle weakness,
decreased bowel motility, paraesthesia
and dysrhythmias are signal that warrant
assessing the serum potasium
concentration
 Interventions
Assess and identify those at risk
Encourage potassium-rich foods
K+ replacement (IV or PO)
Monitor lab values
D/c potassium-wasting diuretics
Treat underlying cause
 Serum potassium level greater than
5 mEq/L
 Less common than hypokalaemia, but it
is usually dangerous
 Contributing factors:
Increase in K+ intake
Renal failure
K+ sparing diuretics
Shift of K+ out of the cells
 In non acute situations, restriction of dietary
potassium and potassium containing
medications may correct the imbalance
 Administration either orally or by retention
enema of cation exchange resins (e.g.
Kayexalate)
 EMERGENCY PHARMACOLOGIC THERAPY
 If serum potassium level are dangerously
elevated, it may be necessary to adm.
IV calcium gluconate
 Monitor blood pressure
 Patients at risk for potassium excess need
to be identified and closely monitored
for signs of hyperkalemia
 Nurse should monitor I/O and observe for
signs of muscle weakness and dysrythmias
 Serum potassium level as well as BUN,
creatinine, glucose & arterial blood gas
values are monitored for patient at
risk for developing hyperkalemia
 Interventions
Need to restore normal K+ balance:
Eliminate K+ administration
Inc. K+ excretion
 Lasix

 Kayexalate (Polystyrene sulfonate)

Infuse glucose and insulin

Cardiac Monitoring
 HYPOCHLOREMIA is a serum chloride level
below 97meq/L (97mmol/L)
 Irritability
 Tremors
 Muscle cramps
 Hyperactive deep tendon reflexes
 Slow shallow respiration
 Seizures
 Coma
 Correcting the cause of hypochloremia
and contributing electrolytes and
acid- base imbalances
 Normal saline (0.9% sodium chloride) or
half strength saline(0.45% sodium
chloride) solution is administered by IV to
replace the chloride
 Monitor the patient I/O, arterial blood gas
values and serum electrolyte levels
 Changes in pts level of consciousness,
muscle strength and movement
should be reported to the physician
promptly
 Vital signs are monitored and respiratory
assessment is carried out frequently
 Educate the pt. about food with high
chloride content which include tomato
juice, banana, eggs, cheese, etc.
 Serum level of chloride exceeds 107
meq/L
 Hypernatremia, bicarbonate loss and
metabolic acidosis can occur with high
chloride levels
 Tachypnea
 Weakness
 Lethargy
 Deep and rapid respiration
 Hypertension
 Dimnished cognitive ability
 If untreated it leads to:
 Decrease in cardiac output, dysrhythmias

and coma
 Correcting the cause of underlying cause of
hyperchloremia and restoring electrolyte
fluid and acid base balance are essential
 Hypotonic IV solution may be administered to
restore balance
 Lactated Ringers solution may be
prescribed to convert lactate to
bicarbonate in liver
 Diuretics may be administered to eliminate
chloride as well
 Sodium chloride and fluid are limited
 Monitoring vital sign , arterial blood gas
values and I/O is important to assess the
patients status and the effectiveness
of treatment
 Assessment findings related to
respiratory, neurologic and cardiac
systems are documented and changes are
discussed with physician
 Educate about the diet
 More than 90% of body’s calcium is located in
the skeletal system
 The normal total serum calcium level is 8.6-
10.5 mg/dl (2.2 to 2.6 mmol/L)
 The serum calcium value lower than
8.6 mg/dl
 Occurs in variety of clinical
situation
 Older people and those with disabilities, who
spend on increased amount of time in bed
have an increased risk of hypocalcemia
because bed rest increases bone resorption
 Contributing factors:
Dec. oral intake
Lactose intolerance
Dec. Vitamin D intake
End stage renal disease
Diarrhea
 Contributingfactors (cont’d):
Acute pancreatitis
Hyperphosphatemia
Immobility
Removal or destruction of parathyroid gland
 Numbness
 Tingling of finger, toes and circumoral region
 Anxiety
 Hyperactive deep tendon reflex
 Bronchospasm
 diarrhea
 Assessment findings:
Neuro –Irritable muscle twitches.
 Positive Trousseau’s sign.
 Positive Chvostek’s sign.

Resp. – Resp. failure r/t muscle tetany.

CV – Dec. HR., dec. BP,
diminished peripheral pulses
GI – Inc. motility; Inc. Bowel Sound;
Diarrhea
 Interventions/Treatment
Drug Therapy
 Calcium supplements
 Vitamin D

Diet Therapy
 High calcium diet
Prevention of Injury
 Seizure precautions
 Status of airway is clearly monitored
 Safety precaution to be taken if confusion is
present
 Educate the patient about hypocalcemia,
and calcium containing foods like milk,
yogurt, cheese, sea fruit, legumes, fruits
 Avoid overuse of laxatives and antacids
 serum calcium value greater than 10.0
mg/dl
 It is a dangerous imbalance when severe
infact, hypercalcemic crisis has a mortality
rate as high as 50% if not treated promptly
 Contributing factors:
Excessive calcium intake
Excessive vitamin D intake
Renal failure
Hyperparathyroidism
Hyperthyroidism
Malignancy
 Muscular weakness
 Constipation
 Anorexia
 Nausea & vomiting
 Dehydration
 Hypoactive deep tendon reflexes
 Calcium stones
  Assessment findings:
Neuro – Disorientation, lethargy, coma, profound muscle
weakness
Resp. – Ineffective resp. movement
CV - Inc. HR, Inc. BP. , Bounding peripheral pulses,
Positive Homan’s sign.
Late Phase – Bradycardia, Cardiac arrest
GI – Dec. motility; Dec. Bowel Sound; Constipation
GU – Inc. urine output; Formation of renal calculi
 Interventions/Treatment
Eliminate calcium administration
Drug Therapy
Isotonic NaCL (Inc. the excretion of Ca)
Diuretics
Calcium reabsorption inhibitors (Phosphorus)
Cardiac Monitoring
 Increasing patient mobility and encouraging
fluids
 Encourage to drink 2.8 to 3.8L of fluid daily
 Adequate fiber in diet is encouraged
 Safety precaution are implemented
 It is indicated by value below 2.5 mg/dl
 Contributing Factors:
Malnutrition
Starvation
Hypercalcemia
Renal failure
Uncontrolled DM
Alcoholism
 Paresthesia
 Muscle weakness
 Bone pain & tenderness
 Chest pain
 Confusion
 Cardiomyopathy
 Seizures
 Tissue hypoxia
 Assessment findings:
on lab analysis, serum phosphate level is less
than 2.5 mg/L
Serum magnesium may be decreased due to
increased urinary excretion of
magnesium
X-ray may show skeletal changes of rickets
 MANAGEMENT
Treat underlying cause
Oral replacement with vit. D
IV phosphorus (Severe)
Serum phosphate level should be closely monitored
Diet therapy
 Foods high in oral phosphate
 Identify the patient at risk for
hypophosphatemia
 Close monitoring of patient
 Vital signs and monitor serum phosphorous
level
 Check the level of consciousness
 Health education
 Serumphosphorus level that exceeds
4.5mg/dl (1.45 mmol/L)
 Tetany
 Tachycardia
 Anorexia
 Nausea & vomiting
 Muscle weakness
 Hyperactive reflexes
 Administration of vit.D such as calcitriol which is
available both oral ( Rocaltrol) & parenteral
( Calajex, paricalcitol forms)
 Calcium binding antacids
 Administration of amphojel with meals
 Restriction of dietary phosphate, forced diuresis
with loop diuretics volume replacement with
saline
 Surgery may be indicated for removal of
large calcium and phosphorus deposits
 Dialysis may also lower phosphorus
 The nurse monitor patient at risk for
hyperphosphatemia
 If low phosphorus diet is prescribed, patient is
instructed to avoid phosphorus rich food such as
hard cheese, cream, nuts, meats, etc
 Nurse instruct patient to avoid phosphate
containing laxatives and enemas
 Monitoring for changes in urine output
 HYPOMAGNESEMIA
 Refers to below normal serum magnesium
concentration 1.3mg/dl (0.62 mmol/L)
 It is frequently associated with
hypokalemia
 Contributing factors:
Malnutrition
Starvation
Diuretics
Aminoglcoside antibiotics
Hyperglycemia
Insulin administration
 Neuromuscular irritability
 Mood changes
 Anorexia
 Vomiting
 Increased bp
 Increased deep tendon reflex
 insomnia
 Assessment findings:
*Neuro - Positive Trousseau’s sign.
Positive Chvostek’s sign. Hyperreflexia.
Seizures
*CV – ECG changes. Dysrhythmias. HTN
*Resp. – Shallow resp.
*GI – Dec. motility. Anorexia. Nausea
 Mild magnesium deficiency can be corrected by
diet alone
 Magnesium salt can be administered orally in an
oxide or gluconate form
 Vital signs must be assessed frequently
 Calcium gluconate must be readily available to
treat
 IV. MgSo4
 Observe for its sign and symptom
 Safety precaution are instituted
 Due to dysphagia, patient should be screened
 Health education
 Serum magnesium level higher than 2.3
mg/dl
 It is a rare electrolyte abnormality because
kidney efficiently excrete magnesium
 Contributing factors:
IncreasedMg intake
Decreased renal excretion
 Flushing
 Hypotension
 Muscle Weakness
 Drowsiness
 Depressed respiration
 Cardiac arrest
 Diaphoresis
Assessment
 findings:
Serum magnesium level is greater than 2.3mg/dl
creatinine clearance decreases to less than 3.0
ml/min
ECG finding: prolonged PR interval
: tall T waves
: widened QRS
 Administration of magnesium
 Ventilatory support
 IV calcium gluconate
 Administration of loop diuretics and sodium
chloride
 Administration of lactated Ringers IV solution
 Risk for hypermagnesemia are identified and
assessed
 Monitor vital signs, noting hypotension and
shallow respiration
 Observe for decreased deep tendon reflex and
changes in level of consciousness
 Caution is essential when preparing and
medicating magnesium containing fluid
parenterally