Help maintain

body temperature
and cell shape
Helps
transport
nutrients
gases and
 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: fluid intake
• Reduced
• Loss of body fluids
• Sequestration (compartmentalizing) of
body fluids
Pathophysiology

DECREASED FLUID VOLUME

Stimulation of ↑ ADH Secretion Renin-Angiotensin-
thirst center in Aldosterone System
Activation
hypothalamus ↑ Water resorption
Person complains of
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
To prevent 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
o Dyspnea

o Orthopnea (diff. breathing

when supine)
o crackles
❑ Pharmacological therapy
Diuretics such as thiazide diuretics and
loop diuretics
Thiazide diuretics:
hydrochlorothiazide Loop diuretics:
furosemide, torsemide
❑ Potassium supplement
❖ I/Ochart 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
If renal 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 restriction
should be instituted as indicated
▪ Fowlers position should be
maintain to promote lung
• 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 mulfactorial
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 as a result of sodium loss

Extracellular compartment is depleted of water

CLINICAL SYMPTOMS
 Muscle APATH
Weakne Y
ss

Postura Nausea
and
l Abdomi Weig
hypote nal ht
nsi on Cramp Loss
In severe hyponatremia: mental confusion, delirium, shock and coma
s
Contributing
Factors
■ Excessive
diaphoresis
■ Wound Drainage
■ NPO
■ CHF
■ Low salt diet
■ Renal Disease
■ Diuretics
 Assessment
findings:
■ Neuro - Generalized skeletal muscle
weakness. Headache / personality
changes.
■ Resp.- Shallow respirations
■ CV - Cardiac changes depend on fluid
volume
■ GI – Increased GI motility, Nausea,
Diarrhea (explosive)
■ GU - Increased urine output

Plasma osmolality:
2Na + glucose/18 + BUN/2.8
Interventions/
Treatment
■Restore Na levels to normal and prevent
further decreases in Na.
■Drug Therapy –
o (FVD) - IV therapy to restore both fluid

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

(Mannitol) to excrete the water rather

than the sodium.
■Increase oral sodium intake and restrict oral
fluid intake.
• 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 Firm,
mucous rubbery
membranes tissue
turgor

DEAT
H
Tachycard
Manic ia
excitement
Assessment findings:
■Neuro - Spontaneous muscle
twitches. Irregular contractions.
Skeletal muscle wkness.
Diminished deep tendon reflexes
■Resp. – Pulmonary edema
■CV – Diminished CO. HR and BP depend
on vascular volume.
■ GU – Dec. urine output. Inc. specific
gravity

■ Skin – Dry, flaky skin. 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
o Mild – Ensure water intake
❑ The nurse should assess for abnormal
looses 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
Serum level 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 od 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 50-100meq/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
Interventio
ns
■ 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 5meq/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
❑ EMERGENCY PHARMACOLOGIC
THERAPY
▪ If serum potassium level are
dangerously elevated, it may be
necessary to adm. IV calcium
gluconate
❖ 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
Interventio
ns
■ Need to restore normal K+
balance:
■Eliminate K+ administration
■Inc. K+ excretion
o Lasix

o 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
➢ Coma
➢ seizures
❖ 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 and 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
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
❖ 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-
10.2 mg/dl (2.2 to 2.6 mmol/L)
The serum calcium value lower
than 8.6mg/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
hypocalcaemia because bed rest
increases bone resorption
Contributing
factors:
■ Dec. oral intake
■ Lactose intolerance
■ Dec. Vitamin D
intake
■ End stage renal
disease
■ Diarrhea
Contributing factors (cont’d):
Acute
pancreatitis
Hyperphosphate
mia
Immobility
Removal or
destruction of
parathyroid gland
Numbness
Tingling of finger, toes and circumoral
region Anxiety
Hyperactive deep tendon
reflex Bronchospasm
diarrhoea
Assessment
findings:
■ Neuro –Irritable muscle twitches.
o Positive Trousseau’s sign.
o Positive Chvostek’s sign.
■ Resp. – Resp. failure d/t muscle
tetany.
■ CV – Dec. HR., dec. BP,
diminished peripheral pulses
■ GI – Inc. motility. Inc. BS. Diarrhea
Interventions/
Treatment
■ Drug Therapy
o Calcium
supplements
o Vitamin D
■ Diet Therapy
o High calcium diet
■ Prevention of
Injury
o 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
10.2 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
■ Malignancy
■ Hyperthyroidism
Muscular
weakness
Constipation
Anorexia
Nausea &
vomiting
Dehydration
Hypoactive deep tendon
reflexes Calcium stones
Assessment
■ Neuro – Disorientation, lethargy, coma, profound
findings:
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. BS. 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
■ Renalfailure
■ Uncontrolled
DM
Paresthesia
Muscle
weakness
Bone pain &
tenderness Chest
pain
Confusion
Cardiomyopat
hy 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
MANAGEME
NT
■ Treat underlying cause
■ Oral replacement with vit. D
■ IV phosphorus (Severe)
■ Serum phosphate level should be closely
monitored
■ Diet therapy
o 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
Serum phosphorus level that exceeds
4.5mg/dl (1.45 mmol/L)
Tetany
Tachycardi
a 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 chnages 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 gluonate 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 institued
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:
■ Increased Mag 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 3.0ml/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