Fluid & electrolytes balance
and disturbances
Dr.HELEN SHAJI, Ph.D (N)
WHY IS IT IMPORTANT FOR NURSES
TO KNOW ABOUT FLUID &
ELECTROLYTE BALANCE
INTRODUCTION:
Water is found everywhere on earth
including human body
 In an adult 60% of the weight is water
 Two third of the body’s water is found in
the cell

DISTRIBUTION OF BODY
FLUIDS:
Body fluids are distributed in two
distinct compartments:
1.Extracellular fluids[ECF] Which includes
interstitial fluid & intravascular fluid
2.Intracellular fluids[ICF]
COMPOSITION OF BODY
FLUIDS:
The fluids circulating throughout the body
in extracellular and intracellular fluid
spaces contain
1.Electrolytes
2.Minerals
3.Cells
Fluid Volume Deficit
(Hypovolemia, Isotonic Dehydration)

Common Causes
– Hemorrhage
– Vomiting
– Diarrhea
– Burns
– Diuretic therapy
– Fever
– Impaired thirst
THREE TYPES OF ECFVD
Hyperosmolar fluid volume deficit water loss is greater than the electrolyte
loss
 Isosmolar fluid volume deficit – equal
proportion of fluid and electrolyte loss
 Hypotonic fluid volume deficit –
electrolyte loss is greater than fluid loss

Clinical Manifestations

Signs/Symptoms
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Weight loss
Thirst
Orthostatic changes in pulse rate and BP
Weak, rapid pulse
Decreased urine output
Dry mucous membranes
Poor skin turgor
Treatment/Interventions (FVD)

Fluid Management
– Diet therapy – Mild to moderate dehydration.
Correct with oral fluid replacement.
– 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.
Nursing Implications
 Monitor
postural heart rate and B.P
when getting patients out of bed
Fluid Volume Excess

Common Causes:
– Congestive Heart Failure
– Early renal failure
– IV therapy
– Excessive sodium ingestion
– SIADH (Syndrome of Inappropriate secretion
of Anti Diuretic Hormone)
– Corticosteroid
Clinical Manifestations

Signs/Symptoms
– Increased BP
– Bounding pulse
– Venous distention
– Pulmonary edema
 Dyspnea
 Orthopnea (diff. breathing when supine)
 crackles
Treatment/Interventions (FVE)

Drug therapy
– Diuretics may be ordered if renal failure is not
the cause.

Restriction of sodium and saline intake
 I/O
 Weight
More to consider?

Age
– Infants
– Older adults

Prior medical history
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Acute illness
Chronic illness
Environmental factors
Diet
Lifestyle
Medications

Physical Assessment
– Body systems
– I/O
– Weight
– Labs
Electrolyte Imbalance
NORMAL VALUE

Serum Sodium - 135 to 145 mEq/L
 Serum Potassium – 3.5 to 5.0 mEq/L
 Serum Calcium – 9 to 10.5 mEq/L
 Serum Phosphate – 2.5 to 4.5 mEq/L
 Serum Magnesium – 1.4 to 2 mEq/L
Hypokalemia (<3.5mEq/L)

Pathophysiology –
– Decrease in K+ causes decreased excitability of
cells, therefore cells are less responsive to
normal stimuli
Hypokalemia (<3.5mEq/L)

Contributing factors:
–
–
–
–
–
–
–
Diuretics
Shift into cells
Digitalis
Water intoxication
Corticosteroids
Diarrhea
Vomiting
Hypokalemia (<3.5mEq/L)

Interventions
– Assess and identify those at risk
– Encourage potassium-rich foods
– K+ replacement (IV or PO)
– Monitor lab values
– Stop potassium-wasting diuretics
– Treat underlying cause
Potassium- Rich Foods
Vegetables
 Avocado
 Raw carrot
 Baked potato
 Raw tomato
 Spinach
 Meat and Fish
 Beef
 Cod
 pork
Fruits
 Dried fruits
 Banana
 Apricot
 Orange
 Beverages
 Milk
 Orange juice
 Apricot nectar
Hyperkalemia (>5.0mEq/L)

Pathophysiology – An increase in K+
causes increased excitability of cells.
Hyperkalemia (>5.0mEq/L)

Contributing factors:
– Increase in K+ intake
– Renal failure
– K+ sparing diuretics (eg: Tab. Aldactone)
– Shift of K+ out of the cells
Hyperkalemia (>5.0mEq/L)

Interventions
– Need to restore normal K+ balance:
– Eliminate K+ administration
– Inc. K+ excretion
 Lasix
 Kayexalate (Polystyrene sulfonate)
– Infuse glucose and insulin
– Cardiac Monitoring
Hyponatremia (<135mEq/L)
 Contributing Factors
– Excessive diaphoresis
– Wound Drainage
– NPO
– CHF
– Low salt diet
– Renal Disease
– Diuretics
Hyponatremia (<135mEq/L)

Assessment findings:
– Neuro - Generalized skeletal muscle weakness.
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–
–
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Headache / personality changes.
Resp.- Shallow respirations
CV - Cardiac changes depend on fluid volume
GI – Increased GI motility, Nausea, Diarrhea
(explosive)
GU - Increased urine output
Hyponatremia (<135mEq/L)

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 restrict oral
fluid intake.
Hypernatremia (>145mEq/L)

Contributing Factors
– Hyperaldosteronism
– Renal failure
– Corticosteroids
– Increase in oral Na intake
– Na containing IV fluids
– Decreased urine output with increased urine
concentration
Hypernatremia (>145mEq/L)

Contributing factors (cont’d):
– Diarrhea
– Dehydration
– Fever
– Hyperventilation
Hypernatremia (>145mEq/L)

Assessment findings:
– Neuro - Spontaneous muscle twitches.
Irregular contractions. Skeletal muscle
weakness. Diminished deep tendon reflexes
– Resp. – Pulmonary edema
– CV – Diminished CO. HR and BP depend
on vascular volume.
Hypernatremia (>145mEq/L)
GU – Dec. urine output. Inc. specific
gravity
Skin – Dry, flaky skin. Edema r/t fluid
volume changes.
Hypernatremia (>145mEq/L)

Interventions/Treatment
– Drug therapy
 (FVD) .45% NSS. If caused by both Na and fluid
loss, will administer NaCL. If inadequate renal
excretion of sodium, will administer diuretics.
– Diet therapy
 Mild – Ensure water intake
Hypocalcemia (<9.0mEq/L)

Contributing factors:
– Dec. oral intake
– Lactose intolerance
– Dec. Vitamin D intake
– End stage renal disease
– Diarrhea
Hypocalcemia (<9.0mEq/L)

Contributing factors (cont’d):
Acute pancreatitis
Hyperphosphatemia
Immobility
Removal or destruction of parathyroid gland
Hypocalcemia (<9.0mEq/L)

Assessment findings:
– Neuro –Irritable muscle twitches.
 Positive Trousseau’s sign.
 Positive Chvostek’s sign.
– Resp. – Resp. failure d/t muscle tetany.
– CV –
Dec. HR., dec. BP, diminished
peripheral pulses
– GI – Increased motility. Increased Bowel
Sounds, Diarrhea
Positive Trousseau’s Sign
TROUSSEAU’S SIGN

Elicitation: Inflating a sphygmomanometer
cuff above systolic blood pressure for
several minutes
 Postitive response: Muscular contraction
including flexion of the wrist and metacarpo
phalangeal joints, hyperextension of the
fingers, and flexion of the thumb on the
palm, suggestive of neuromuscular
excitability caused by hypocalcemia
Positive Chvostek’s Sign
CHVOSTEK’S SIGN

Elicitation: Tapping on the face at a point
just anterior to the ear and just below the
zygomatic bone
 Postitive response: Twitching of the
ipsilateral facial muscles, suggestive of
neuromuscular excitability caused by
hypocalcemia
Hypocalcemia (<9.0mEq/L)

Interventions/Treatment
– Drug Therapy
 Calcium supplements
 Vitamin D
– Diet Therapy
 High calcium diet
– Prevention of Injury
 Seizure precautions
Hypercalcemia

Contributing factors:
– Excessive calcium intake
– Excessive vitamin D intake
– Renal failure
– Hyperparathyroidism
– Malignancy
– Hyperthyroidism
Hypercalcemia (>10.5mg/dL)

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. BS. Constipation
– GU – Inc. urine output. Formation of renal calculi
Hypercalcemia (>10.5mg/dL)

Interventions/Treatment
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Eliminate calcium administration
Drug Therapy
Isotonic NaCL (Inc. the excretion of Ca)
Diuretics
Calcium reabsorption inhibitors (Phosphorus)
Cardiac Monitoring
Hypophosphatemia (<2.5mg/L)

Contributing Factors:
– Malnutrition
– Starvation
– Hypercalcemia
– Renal failure
– Uncontrolled DM
Hypophosphatemia (<2.5mg/L)

Assessment findings:
Neuro – Irritability, confusion
CV – Dec. contractility
Resp. – Shallow respirations
Hematologic – Inc. bleeding
Dec. platelet aggregation
Hypophosphatemia (<2.5mg/L)

Interventions
– Treat underlying cause
– Oral replacement with vit. D
– IV phosphorus (Severe)
– Diet therapy
 Foods high in oral phosphate
Hyperphosphatemia (>4.5mg/L)
 Causes
few direct problems with body
function. Care is directed to
hypocalcemia.
 Rarely occurs
Hypomagnesemia (<1.4mEq/L)

Contributing factors:
– Malnutrition
– Starvation
– Diuretics
– Aminoglcoside antibiotics
– Hyperglycemia
– Insulin administration
Hypomagnesemia (<1.4mEq/L)

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
Hypomagnesemia (<1.4mEq/L)

Interventions:
– Eliminate contributing drugs
– IV MgSO4
– Assess DTR’s hourly with MgSO4
– Diet Therapy
Hypermagnesemia (>2.0mEq/L)

Contributing factors:
– Increased Mg + intake
– Decreased renal excretion
Hypermagnesemia (>2.0mEq/L)

Assessment findings:
Neuro – Reduced or weak DTR’s. Weak
voluntary muscle contractions. Drowsy to
the point of lethargy
CV – Bradycardia, peripheral
vasodilatation, hypotension. ECG changes.
Hypermagnesemia (>2.0mg/dL)

Interventions
– Eliminate contributing drugs
– Administer diuretic
– Calcium gluconate reverses cardiac effects
– Diet restrictions
Acid- Base Balance
– Acid: is a hydrogen (H+) donor.
– Base: is an H+ acceptor (bind to hydrogen ions).
– The pH is a measure of acid-base balance (hydrogen
ion concentration in the blood). The more hydrogen
ions, the more acidic is the medium and <7.4. The less
hydrogen ions, the more base and > 7.4. Normal pH
for humans is approximately 7.4.




Normal values of acid-base balance
components:
♦ PH: 7.35 - 7.45
♦ PaC02: Normal = 35 to 45 mmHg
♦ HC03: Normal =22 to 26mEq/L
♦ PaO2: 80-100.
Types of Acid Base
Imbalances

Metabolic Acidosis
 Metabolic Alkalosis
 Respiratory acidosis
 Respiratory alkalosis
Types of Acid – base
imbalance

Metabolic Acidosis:
Definition: Excessive absorption or retention of acid or
excessive excretion of HC03.
Cause:
 Ketoacidosis (DM) and prolonged fasting.
 renal disease
 Abnormal HCO3 losses( surgery, drains, or severe
diarrhea.)
Clinical manifestations:
 Headache, drowsiness, confusion, and weakness.
 Increased respiratory rate and depth
 hypotension, cold and sweaty skin

pH below 7.35 and HCO3 below 22 mEq/L
Nursing management:
1.
2.
3.
Monitor ABG value,
Administer sodium bicarbonate.
Monitor cardiovascular status closely,
noting blood pressure, pulse rate and
rhythm, capillary refill, and warmth and
color of extremities.
Metabolic alkalosis
Definition: Excessive loss of acid or excessive gain of
HCO3
Causes:
1.
2.
3.
4.
prolonged vomiting or gastric suctioning.
Excessive intake of alkali e.g. antacids.
Respiratory insufficiency.
Massive blood transfusion
Clinical manifestations:
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–
–
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Tingling of the fingers and toes and tetany.
Slow, shallow respirations; possibly apnea.
Cardiac arrhythmias and death.
ABG studies: pH > 7.45 and HCO3 above 26 mEq/L
Nursing management:
1.
2.
3.
4.
Monitor ABG values,
I&O, and for cardiac arrhythmias.
Correct electrolyte deficits, especially of potassium and
sodium.
Monitor respiratory rate and pattern and auscultate lung
sounds.
Respiratory acidosis:
Increased arterial PaCo2 and decreased blood pH.
Causes:
1. Chronic obstructive respiratory disorders, such
as bronchial asthma
2. Acute disorders such as chest wall trauma,
pulmonary edema, pneumothorax, pneumonia
Clinical manifestations:
1. Increased pulse, BP, and respiratory rate
2. Mental cloudiness, and headache
3. ABG studies: pH below 7.35 and PaCo2 above
45 mmHg.
Nursing management
Monitor ABG, respiratory & cardiovascular
status, & LOC.
2. Improve ventilation with
1.
1.
2.
3.
4.
5.
6.
7.
bronchodilators;
postural drainage;
antibiotic therapy;
regular coughing,
positioning,
turning,
deep breathing.
Maintain a quiet, relaxed environment & provide
periods of complete rest.
4. Maintain fluid and electrolyte balance.
3.
Respiratory Alkalosis
decreased arterial Pco2 and increased blood pH.
Causes:
1.
2.
Hyperventilation (most common) due to
anxiety, hypoxia, improper mechanical
ventilation
Fever
Clinical manifestations:
1. Light headache, deep rapid breathing,
2. Muscle twitching, convulsions, and cardiac
dysarrhythmias.
3. ABG: pH above 7.45 and Pco2 below 35 mmHg.
Nursing management
1. Monitor ABG values and respiratory status.
2. Treat the cause, e.g. ↓ pain, fever, and anxiety.
3. Encourage slow, deep breathing; instruct the
client to breathe into air of a paper bag, if
necessary, to reverse hyperventilation.
Thank you