Disease Facts Manifestations Treatment Nursing Interventions

1. Hyperosmolar Imbalance  It is caused by shifting fluids V/S:  Mild Dehydration: increase

from ICF to ECF causing the  increased in body temp fluid intake
cells to shrink.  Increased.PR (tachycardia)
inc in RR (tachypnea)  Moderate to Severe
 Na excess or water deficit.  dry mouth, & throat Dehydration: IVF Therapy
 warm, flushed skin
 Initial manifestation of  soft, sunken eyeballs  Administer hypotonic solution
dehydration: THIRST  concentrated urine with great care
 increased Hct, BUN,
 The most objective indicator of  increased serum Na electrolyte  Oral care for dry mouth &
dehydration is decreased in throat
body weight, next is decreased
in urine output.  Safety measures for altered
SENSORIUM

 Identify underlying cause to

focus treatment on the
cause of imbalance.
 Disease Facts Manifestations Treatment Nursing Interventions
2. Hypoosmolar Imbalance  It is caused by shifting of fluids  Sudden weight gain  Fluids restriction
from the ECF to swelling of the  Peripheral edema
cells.  Increased in BP, bounding  Administration of diuretics as
prescribed
pulse, increased in RR
 There is sodium deficit or
water excess  Change in mental status:  Administration of hypertonic
confusion, incoordination, saline solution per IV as
convulsions/seizure ordered.
 The most dangerous effect of
water intoxication is increased  Promote safety
in ICP
 Assess neurologic status
 Identify & treat underlying
cause ex: SIADH; Na deficit

 Free oral fluid intake, repeated

tap water enema, excess intake
of sodium
 Disease Facts Manifestations Treatment Nursing Interventions
3. Isotonic Imbalance A condition where water &  Acute weight loss esp.if more  Identify underlying cause & treat 1. Assess for FVD.
electrolytes are loss in the ECF in than 5% of total body weight the cause. 2. Monitor I & O every hour
excess the intake of fluids.  Administer isotonic solution as 3. Monitor v/s closely. Observe for
 Cardiovascular changes: dec prescribed. weak, rapid pulse & postural
BP, inc HR, postural hypotension.
Contributory Factors to ECF
 Hypotension  Once pt is normotensive, 4. Monitor daily BW( acute loss of
Volume Deficit: hypotonic elect solution is o.5kg represents fluid loss
 Hemorrhage  Decreased skin turgor
prescribed to provide both approximately to 500 mL;
 Profuse Sweating  Dry tongue, sticky mucous electrolytes & water for renal 5. Replace blood losses if the cause is
 Severe Diarrhea and membrane in the oral cavity excretion of metabolic wastes. hemorrhage
Vomiting  Decreased volume of urine - Whole blood is administered
 Draining Fistula  If fluid deficit is severe & pt is not within 4-6 hrs.
output & concentrated urine .
 Patients with Colostomies excreting enough urine 6. Provide oral care.
 Sunken eyeballs determine if the cause of 7. Skin & oral mucous membrane is
 Third-Space Fluid Shift (e.g.
edema, pleural effusion,  Cool clammy skin R/T depressed renal function is due monitored on a regular basis.
peripheral vasoconstriction. to reduced renal blood flow - Skin turgor is best measured by
ascites)
secondary to FVD or due to acute pinching the skin over
 Thirst
tubular necrosis from prolonged sternum, inner aspect of the
FVD. thighs, or forehead.
- Evaluating the tongue turgor is
 FLUID CHALLENGE TEST is done – a more valid assessment for
involves administration of 100-200 sign of dehydration than
ml of PNSS for 15 mins to provide evaluating the skin turgor.
fluids rapidly enough to attain
adequate tissue perfusion w/o Preventing FVD:
compromising the cardiovascular 1. Identify patients at risk &
system. minimize fluid losses.
2. Correcting FVDL: Oral fluids
 Expected response would be are given to correct FVD, w/
increased urine output & BP, CVP consideration given to like &
reading deslikes .
3. Provide oral mouth care
 SHOCK can occur if volume of fluid frequently & provide non-
loss exceeds 25% in the irritating fluids
intravascular volume or when fluid 4. If patient cannot eat & drink:
loss is rapid. the nurse may need to
 administer fluid by alternative
route(enteral or parenteral),
as prescribed to prevent renal
damage R/T prolonged FVD.
 Disease Facts Manifestations Treatment Nursing Interventions
4. Isotonic Volume Excess  It is a condition in which fluid intake  Circulatory overload  Identify & treat underlying 1. Assess & monitor neurologic status
excess fluid. cause to identify signs of
 It is an increased in water volume &
- sudden inc in BP, HR,
ICF deficit
solute concentration bounding pulse
in the ECF  Restrict water intake to a
 Interstitial edema 2. Monitor I & O every hour, daily
 It results to isotonic expansion of the volume that is less
ECF.  Rapid weight gain than urine output.
body weight monitoring
 It may be related to fluid overload or  Prolonged hypervolemia may
diminished function of the 3. Monitor v/s every hour, note for
homeostatic mechanisms responsible result to CHF  Administration of diuretics progression in
for regulating fluid balance.  Neck vein engorgement elevation of BP
 Crackles, wheezing, shortness  Symptomatic treatment &
CONTRIBUTORY FACTORS: 4. Provide patient teaching regarding
of breath restrict sodium.
 Increased intake of sodium & water, dietary modifications, avoidance of
either orally or IV.  Excretion of diluted urine high salt intake & signs of edema.
 Iso-osmolar fluid retention secondary
to impaired regulatory mechanism
 Labs: dec BUN & Hct, dec
Ex. renal, inappropriate ADH serum osmolality & Na, 5. Provide meticulous skin care, oral
secretion, cardiac disease care
 Chest x-ray result may reveal
 Use of cortecosteroids 6. To patients with signs of
 Common conditions: Chronic liver pulmonary congestion neurologic deficits, provide
disease, HF, RF safety &,comfort.
7. Monitor for progression of
NOTE: neurologic deficits.
 OVERHYDRATION RESULTS TO 8. High CHON diet ( except in RF &
EDEMA FORMATION
Liver Cirrhosis)
- the accumulation of fluids in the
9. Elevate edematous part of the
interstitial spaces.
body to promote venous
EDEMA OCCURS DUE TO: return.( except in CHF)
 Increased capillary hydrostatic 10. Protect edematous body parts
pressure from prolonged pressure or injury,
e.g. administration of large volume of IVFs extreme heat/cold.
 Decreased colloid osmotic 11. Keep skin dry & well-lubricated to
pressure maintain skin integrity
Hypoalbuminemia 12. dminister diuretics as ordered –
 Increased capillary permeability
promote excretion of sodium &
e.g.cellular injury; vasodilation due to
inflammation & histamine release
water.
 Lymphatic obstruction 13. Regulate flow rate of IVF at
e.g. removal of lymphnodes in mastectomy prescribed rate.
 Water & sodium excess
e.g. CHF, RF, inc secretion of aldosterone
 Disease Facts Manifestations Treatment Nursing Interventions
5. Hyponatremia Functions of Sodium: 1. Neurologic manifestations: due Identify cause of hyponatremia &
 Facilitate transmission of to shift of fluid from ECF to ICF, high risk patients for
nerve and muscle fibers cells swell hyponatremia.
through the Na-K pump  Twitchings, muscle cramps
 Determine and maintain  Headache  Restrict fluid intake to allow Na
volume of body fluid and ECF  Dizziness, confusion & H20 to balance. To a total of
osmolality  Convulsion/seizure 800 ml/day.
 Assist in maintaining acid-base  Patient may manifest
balance vomiting & diarrhea as the  Administer hypertonic
main cause of solution with caution- as
Serum sodium level below 135 hyponatremia hypertonic solution is
mEq/L administered, shift of fluid from
3. GIT – anorexia, nausea & the cell to ICF may occur, resulting
CONTRIBUTORY FACTORS: vomiting, abdominal to expansion of ECF leading to
 Prolonged use of diuretics. cramps CHF.
Impairs Na reabsorption in 4. Postural hypotension
the Loop of Henle. 5. Weight loss  Measure I & O, daily weights,
 Excessive burns – loss of 6. Poor skin turgor , dry - Note for fluid retention,
excess sodium in the mucous membrane, dec monitor v/s
burned areas of the skin. saliva production
 Excessive diaphoresis 7. Serum Na level below 135 Provide safety & comfort.
 Prolonged vomiting, mEq/L
diarrhea, laxative use,
suctioning.
 Renal disease – inability of
the kidneys to excrete large
amount of fluids from the
body
 Water is gained from adm
of large amount of dextrose
in water, compulsive
drinking, disease state
associated w/ SIADH,
adrenal insufficiency(dec
aldosterone)
 Disease Facts Manifestations Treatment Nursing Interventions
6. Hypernatremia Na excess with serum Na level of  Thirst  Monitor I & O. Monitor body
>145 mEq/L  Tachycardia, restlessness weight.
 Dry mucous membrane
CONTRIBUTORY FACTORS:  Oliguria  Restrict Na in the diet
 Administration of  Disorientation
hypertonic solution & tube  Increase oral fluids or
feedings administration of dextrose in
 Excessive intake of sodium water as prescribed.
in the diet.
 Fluids shift from ICF to ECF  Promote safety, monitor
to balance the excess Na changes in level of
which cause cell to shrink. consciousness
 Water is loss in excess of
sodium  Administer diuretics as
- watery stool prescribed.
- severe diaphoresis
- hyperventilation HIGH IMPACT CONCEPTS:
- Burns  HYPONATREMIA – Increase
- use of osmotic diuretics ICF – CELL SWELL
- diabetes insipidus  Hypernatremia – Decreased
- hyperaldosteronism ICF volume – cells shrink
 Disease Facts Manifestations Treatment Nursing Interventions
7. Hypokalemia Functions of Potassium:  Muscle weakness & cramps  Identify high risk patients to  Replace k+ by parenteral
 Major cation in the ICF  Hyporeflexia, paresthesia, hypokalemia & provide route- incorporate to IVF
 Maintain cellular integrity diminished deep tendon reflex proper education to solution
 It is necessary in the  Decreased bowel motility prevent k+ loss.  Never give k+ by IV bolus
conduction of nerve impulses  Hypotension  Be sure that flow rate is
 Promotes skeletal and cardiac
 Cardiac dysrhythmias  Encourage patient receiving adjusted to prescribed rate
muscle activity
 Lethargy, confusion, diuretic therapy to eat to prevent quick
 Assist in maintaining acid-base
balance depression foods rich in k+ administration of k+.
 Lab.results of potassium level  Monitor site for signs of
A decreased in serum potassium level below 3.5 mEq/L  To eat foods rich in k+ skin irritation.
of <3.5 meq/L  Replace k+ more rapidly by
 Monitor I & O, keeping in mind adding 10 mEq of kcl to
CONTRIBUTORY FACTORS: that the kidneys excrete 100mL PNSS to infuse in one
 Decreased intake of potassium potassium. hour using infusion pump.
rich foods like in starvation  Monitor v/s, serum k+
 Use of potassium wasting
 Administer oral k+ electrolytes
diuretics.
 Increased aldosterone
replacement with water to
secretion. prevent gastric irritation.
 GIT losses like in severe
vomiting & diarrhea.
 Shifting of potassium into cells
in the cells.
 Treatment of DKA
 Magnesium depletion causes
renal k+ loss & must be
corrected first, otherwise
urine loss of k+ will continue

REGULATION OF K+: REGULATED BY

RENAL

KEY POINTS:
 Hypokalemia, due to decreased
muscular irritability,
EVERYTHING IS LOW & SLOW.
 Severe Hypokalemia can cause
death due to cardiac or
respiratory arrest
 Disease Facts Manifestations Treatment Nursing Interventions
8. Hyperkalemia Serum Potassium Level >5.0 mEq/L Due to neuromuscular irritability:  Identify high risk patients &
 GIT : Nausea, vomiting, monitor condition for signs
CONTRIBUTORY FACTORS: diarrhea, colic of hyperkalemia
 Increased intake of potassium  CNS: numbness, tingling,
rich foods. confusion, paresthesia  Check patient’s urine output
 Excessive potassium  Muscular: weakness, flaccid before administering k+
replacement paralysis, replacement
 Renal failure  Cardio: ventricular
 Metabolic acidosis fibrillation, may lead to  Correct acidosis to shift
 Excretion of sodium which cardiac arrest potassium into cells.
increase potassium  ECG: Tall T-wave, prolonged
 reabsorption P-R interval  Administer glucose with
 Cellular injury like in burns,  Kidneys: oliguria, anuria in insulin by IV as ordered.
where k+ moves out of the RF
cells.  To patients with RF,
 Administration of FWB which hemodialysis is done to
have been stored in the correct hyperkalemia.
blood bank for a long period of
times  Monitor I & O, Monitor v/s.

 Provide safety to patients

with muscular weakness.

 Patients with hyperkalemia

should be attached to
cardiac monitor.

 Monitor serum potassium

level – report for any
abnormality in results to
physician.
 Disease Facts Manifestations Treatment Nursing Interventions
9. Hypocalcemia Functions of Calcium: 
 Contributes to bone rigidity
and teeth rigidity and strength
 Required for nerve. Muscle,
and cardiac contraction
 Required for hormonal
secretions

REGULATION:
1. GI REGULATION
 Absorbed in the GIT &
excreted I the urine.
 Vit.D, activated by the kidneys
to 1,25
dihydroxycholecalceferol
 Required for Vit D absorption.
2. RENAL REGULATION
 Filtered in the glomerulus &
reabsorbed in the kidney
tubules
 Excess of calcium can
precipitate in the kidneys.
3. ENDOCRINE
 Parathyroid gland – responds
to low serum calcium level by
releasing PTH which
stimulates release of calcium
from the bones & may result
to bone resorption.
 Calcium & phosphorous has
inverse relationship- if serum
calcium is elevated,
phosphorous level is
decreased, & if serum calcium
is decreased, phosphorous
level is increased.
 Calcitonin – a thyroid
hormone, moves calcium from
plasma to bone decreasing
serum calcium level
Disease Facts Manifestations Treatment Nursing Interventions
Serum Calcium Level of below 8.5 Due to increased cell  Identify patients at risk for
mg/dL membrane permeability, it results hypocalcemia
to increased neuromuscular rigidity.
CONTRIBUTORY FACTORS: Causing:  Increased high calcium in
1. Inadequate intake or  CNS: tingling sensations, the diet
absorption of calcium due to: spasm, tetany, convulsion/
 Anorexia seizure  Administer of Vit D & PTH
 Renal Failure ( vit D is not  GIT: increased peristalsis, supplements as ordered
activated ) nausea, vomiting, diarrhea
 Vit D deficiency  CARDIO: decreased cardiac  Promote safety as seizure
 Alkalosis or excessive output, dysrhythmias, may occur.
administration of HCO3 cardiac arrest
 Administration of citrated  + TROSSEAUS SIGN &  Protect from injury/trauma
blood CHEVOSTEK’S SIGN
 Alcohol abuse  Easy bruising & petechiae
 Prolonged prothrombin  Monitor respiratory
2. Excessive elimination or time function because
excretion of calcium due to  ECG prolonged Q-T hypocalcemia may cause
large doses of loop diuretics. intervals laryngospasm.

3. Some drugs may contribute to  Encourage mobilization

hypocalcemia like:  REMEMBER:
 Dilantin & phenobarbital – HYPOCALCEMIA . >  In severe hypocalcemia,
inhibits GI calcium INCREASED CELL administration of calcium
absorption MEMBRANE PERMEABILITY gluconate with caution as
 PO4 binds to calcium > INCREASED MUSCULAR ordered.
 Calcitonin - enhances IRRITABILITY > SPASM,
mobilization of calcium to TETANY, CONVULSION  Monitor laboratory serum
the bones calcium level.
 Disease Facts Manifestations Treatment Nursing Interventions
10. Hypercalcemia Serum Calcium Level Of above 10.5  Diminished Deep Tendon  Institute measures to
mg/dl Reflex prevent hypercalcemia
 GIT:
CONTRIBUTORY FACTORS:  Decreased Peristalsis May  Identify patients at risk
 Calcium loss from the Result To Constipation Or
bones like in bone Paralytic Ileus
tumor/metastasis,  Limit intake of foods rich in
immobility.  Fatigue, Muscle Weakness, calcium
 Excessive intake of foods Flaccid Paralysis
rich in calcium, vit D or  Encourage mobility,
antacids/  Decreased cardiac electrical exercise
drugs containing calcium activity causing dysrhythmia
 Hyperparathyroidism then cardiac arrest
 Encourage fluid intake at
REMEMBER: HYPERCALCEMIA > Other signs & symptoms: least 3-4 liters/day as
DECREASED CELLULAR  Osteoporosis tolerated
PERMEABILITY > RESULTS TO >  Fracture
DECREASED NEUROMUSCULAR  Excess calcium maybe  Administer sodium chloride
IRRITABILITY deposited to the kidneys solution to enhance calcium
causing renal stone formation Excretion

 Administration of calcitonin
as prescribed

 Provide acid – ash fruit

juices ( to acidify urine &
prevent stone formation)
e.g. cranberry juice, vit C,
PRUNES

 Provide safety to patient

always.
 Disease Facts Manifestations Treatment Nursing Interventions
11. Hypomagnesemia Functions of Magnesium:  Tremors  Prevention is the best 1. Assess the pt’s mental status &
 Inhibits acetylcholine release  Paresthesia treatment. report changes.
 2nd most abundant cation in the  Convulsion
cells  Tachycardia  Watch patients who are high 2. Reorient him as needed.
 Assist in the contraction of  Increased BP risk for magnesium
3. Evaluate the patient’s
cardiac and skeletal muscle cells  Dysrhythmia( due to imbalance. neuromuscular status regularly by
 Causes vasodilation which can myocardial irritability)
change BP and cardiac output  - cardiac arrest if not 4. Checking for hyperactive DTRs ,
 Facilitate Na K pump corrected.  Treat underlying cause to tremors, & tetany.
prevent further imbalance.
5. Check patient for dysphagia before
 REGULATION:  In mild cases, giving food,
- Regulated by the kidneys hypomagnesemia maybe
6. Oral fluids, or giving oral meds.
excretion & absorption corrected with diet
modifications.
7. Monitor & record patient’s v/s.
 ABSORPTION: Report any abnormalities if any
- In the jejunum & ileum  Patient maybe given oral to physician.
supplements such as
Serum Magnesium Level <1.5mEq/L magnesium chloride.
8. Monitor I & O and record. Report
CONTRIBUTORY FACTORS:  Administration of for any imbalance in the intake &
 GI losses from the bowel magnesium supplement output.
 Fluids losses from the oral/parenteral
9. If patient is receiving digoxin,
bowel
monitor for signs of digoxin
 Administration of loop  Check for the following
toxicity.
diuretics before Mg administration:
 Inadequate intake due to  Deep tendon reflex 10. If seizures occur, ensure patient’s
starvation  BP safety at all times.
 Excessive alcohol intake  Respiratory rate 11. Reorient patient after seizure.
results to decreased  Urine output 12. When injecting magnesium I.M.,
 Absorption  inject into the deep
gluteal muscle; if giving more than
one injections, alternate injection
PATHOPHYSIOLOGY:
sites
Hypomagnesemia  inhibits
acetylcholine release increased
neuromuscular irritability
 Disease Facts Manifestations Treatment Nursing Interventions
12. Hypermagnesemia CONTRIBUTORY FACTORS:  Vasodilation which may cause  Prevent hypermagnesemia to
 Inadequate excretion due hypotension, flushing & warm high risk patients
to decreased urine output sensation.
like in RF  Administer calcium gluconate as
 Bradycardia
ordered with caution to
 Excess intake of meds  Hypoactive deep tendon antagonize cardiac effects of
containing Mg or excess reflexes magnesium.
parenteral administration  Depressed respiration &
of magnesium. Magnesium neuromuscular activity  Monitor v/s and cardiac rhythm
is use for treatment of  Generalized weakness which
toxemia in pregnancy. may progress to flaccid  Be alert for signs of
hypotension & respiratory
paralysis.
 TPN that contains too much depression which are indicative
of magnesium.  Drowsy & lethargic due to for signs of hypermagnesemia.
depression of the CNS.
 Continuous infusion of  Serum magnesium level above  Check urine output to ensure
magnesium sulfate to treat 2.5 mEq/L. excretion of magnesium
conditions such as seizures,
gestational hypertension,  Restrict dietary magnesium
or preterm labor. intake.
- An abnormally high
magnesium level depress  Encourage fluid intake to ensure
the neuromuscular system. proper elimination of
It blocks neuromuscular magnesium from the kidneys.
transmission, reducing
cell excitability.
-
 Disease Facts Manifestations Treatment Nursing Interventions
13. Respiratory Acidosis - is a condition resulting from  Headache GOAL: 1. Maintain patent airway.
inadequate excretion of CO2 - because CO2 dilates the IMPROVE RESPIRATORY FUNCTION
due to inadequate ventilation & LOWER the CO2 level. 2. Monitor vital signs, assess
resulting in cerebral blood vessels
cardiac rhythm.
elevation of PaCO2 to above
 Bronchodilators to open
45 mmHg, with pH  Altered LOC, ranging from constricted airways. 3. Monitor patient’s neurologic
of below 7.35. restlessness, confusion,  Supplemental oxygen as status & report
CONTRIBUTORY FACTORS: apprehension, to somnolence needed significant changes
- Neuromuscular Disease – and coma.  Antibiotic to treat infection
Guillain Barre syndrome, - If remain untreated, flapping  Correct hyperkalemia 4. Report variations in ABG.
myasthenia gravis,
tremor and depressed  Chest physiotherapy.
poliomyelitis,. The respiratory 5. Administer oxygen as ordered.
muscles fail to respond to the reflexes may develop.
respiratory drive. 6. Perform suctioning as indicated.
- CNSTrauma Or Brain Lesions DIAGNOSTICS:
- causing hypoventilation
• ABG-pH: 7. Make sure that patient takes
- Sedatives, Anesthetic Agents
- causing respiratory depression - below 7.35, PaCO2 ABOVE enough fluids, both oral & IV, &
at the 45 mmHg, HCO3 – Normal if MAINTAIN ACCURATE I & O
- respiratory center of the brain not compensated; above 26 records.

 Pulmonary lung disease that mEq/L if partially

8. Provide reassurance to the
decrease the amount of compensated family.
pulmonary surface area
available for gas exchange like • Serum potassium 9. Keep in mind that that any
in pulmonary infections, COPD,
- above 5 mEq/L sedative given to the patient can
acute asthma attacks, chronic
bronchitis, pulmonary edema decrease the respiratory rate.

 Chest-wall trauma, leading to 10. Institute safety measures as

pneumothorax needed to protect a confused
patient.
 Airway obstruction due to
retained secretions,
tumors, laryngeal spasm, or
lung disease that interfere
with alveolar ventilation.
 Mechanical ventilators that
under ventilates a patient.
 Disease Facts Manifestations Treatment Nursing Interventions
14. Respiratory Alkalosis - results from alveolar  Increase in rate & depth of FOCUSES ON CORRECTING 1. Allay anxiety to prevent
hyperventilation & respirations is a primary sign of UNDERLYING DISORDER. hyperventilation.
hypocapnea resulting in respiratory alkalosis.  If acute hypoxemia is the
decreased elimination of cause, oxygen is initiated. 2. Monitor v/s. report changes in
CO2, PH is greater than  Patient may appear anxious neurologic, neuromuscular, or
7.45, Pa CO2 is greater than & restless as well as complain  If anxiety is the cause, cardiovascular function.
45 mmHg. of weakness or difficulty patient maybe given
breathing. sedative or anxiolytic. 3. Monitor ABG, serum
CONTRIBUTORY FACTORS: electrolytes, immediately report
 Any clinical condition that  Hyperventilation may be any variations.
increase the respiratory counteracted by having the
rate or depth can cause the patient breathe into a 4. Check ventilator settings
lungs to eliminate or blow paper bag or into a cupped frequently
off CO2. hands.
 The common cause of acute 5. Provide undisturbed rest periods
respiratory alkalosis is  Mechanical ventilator
hyperventilation from settings may be adjusted by 6. Stay with the patient is periods
anxiety or panic attack. decreasing the tidal of extreme stress & anxiety.
 Hypermetabolic states such volume
as fever, liver failure, &
sepsis 7. - Offer reassurance, &
 Certain drugs that stimulate maintain calm, quiet
the respiratory center environment.
like ASA.
 Overventilation with the 8. Institute safety measures &
use of mechanical seizure precautions as needed.
ventilator causes the lungs
to blow off more CO2 9. Document all care.
 Acute hypoxia secondary to
high altitude, pulmonary
disease, severe anemia, or
hypotension.
 Such condition may
stimulate the respiratory
center causing
hyperventilation
Disease Facts Manifestations Treatment Nursing Interventions
15. Hypernatremia Na excess with serum Na level of  Thirst  Monitor I & O. Monitor body
>145 mEq/L  Tachycardia, restlessness weight.
 Dry mucous membrane
CONTRIBUTORY FACTORS:  Oliguria  Restrict Na in the diet
 Administration of  Disorientation
hypertonic solution & tube  Increase oral fluids or
feedings administration of dextrose in
 Excessive intake of sodium water as prescribed.
in the diet.
 Fluids shift from ICF to ECF  Promote safety, monitor
to balance the excess Na changes in level of
which cause cell to shrink. consciousness
 Water is loss in excess of
sodium  Administer diuretics as
- watery stool prescribed.
- severe diaphoresis
- hyperventilation HIGH IMPACT CONCEPTS:
- Burns  HYPONATREMIA – Increase
- use of osmotic diuretics ICF – CELL SWELL
- diabetes insipidus  Hypernatremia – Decreased
- hyperaldosteronism ICF volume – cells shrink