ST LOUIS REVIEW CENTER

Iligan City

MS: Fluid and Electrolytes

Compiled by: Roquee Hospicio H. Paragoso, BSN, RN

ANATOMY AND PHYSIOLOGY

A. Fluid
a. Accounts for about 60% of adult’s total body weight
b. ICF is 2/3 of this amount while ECF is 1/3 of this amount
c. ECF – intravascular space (fluid within blood vessels), interstitial
space (fluid that surrounds the cell) and transcellular fluid
(digestive juices, water and solutes in the renal tubules and
bladder, pleural fluid
d. 3rd space fluid shift – loss of ECF into a space that does not
contribute to equilibrium between the ICF and ECF
e. Body water distribution according to age:
i. Infant – 80% of body weight
ii. Male – 60% of body weight
iii. Female – 50% of body weight

B. Electrolytes
a. Substance that dissociates and forms ions when mixed with
water
b. ICF – K and PO4 are major electrolytes
c. ECF – Na and Cl are major electrolytes; Na level is the primary
determinant of ECF concentration
d. Normal Values:
i. Na – 135-145 mEq/L
ii. K – 3.5-5.5 mEq/L
iii. Ca – 4.5-5.5 mEq/L
iv. HPO4 – 1.7-2.6 mEq?L
v. Cl – 98-108 mEq/L
vi. Mg – 1.5-2.5 mEq/L

C. Acid-Base Balance
a. Acid – substance that ionizes water and forms H+ ions and
anions; hydrogen donor
b. Base – substance that can bind to hydrogen ions; hydrogen
acceptor
c. pH – hydrogen ion concentration in the blood; the more the
hydrogen, the more acidic is the medium, the lower its pH.
Normal pH: 7.35-7.45

D. Regulatory Mechanisms
a. Osmosis – fluid shifting from an area of low solute concentration
to an area of higher solute concentration
b. Diffusion – fluid movement from an area of high solute
concentration to one of lower solute concentrations
c. Filtration – removal of particles from a solution through the
movement of fluid across a membrane or other partial barrier
d. Active transport – energy-requiring process that transport ions
across the cell membrane against a concentration gradient

↓ Na

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 ↓ Blood volume
↓ Blood pressure
↓
Angiotensinogen
↓
Angiotensin I
↓
Angiotensin II
↓
Vasoconstriction ↑ Aldosterone
↓ ↓
↑ Peripheral Resistance ↑ Na and water retention
(kidneys)
↓
↑ Blood Pressure
↑ Blood Volume

E. Sources of normal fluid loss

a. Kidneys – output of 1-2 L daily
b. Sensible losses – 0-1 L daily depending on the temperature
c. Insensible losses – 600 ml daily; increase during fever
d. Lungs – 300-400 ml daily; increase with fever
e. GI – 100-200 ml daily

F. Homeostatic mechanisms
a. Kidneys
i. Filters 170 L of plasma daily
ii. Reabsorbs HCO3 and secrete H+ and produce NH3
iii. Slower than the lungs; takes days to achieve homeostasis
b. Cardiovascular system
i. Normal ABG values:
1. pH – 7.35-7.45
2. PO2 – 80-100 mmHg
3. PCO2 – 35-45 mmHg
4. HCO2 – 22-26 mEq/L
c. Lungs
i. Controls CO2 and H2CO3 excretion
ii. PCO2 – most powerful respiratory stimulant
d. Buffer systems
i. Chemical systems that maintain body pH by releasing H
ions
ii. HCO3 and H2CO3 – primary buffer system; 20:1 ratio
iii. HCO3 – regulated by kidneys
iv. H2CO3 – regulated by lungs
v. Phosphate and protein buffers – less important
e. Endocrine
i. ADH – secreted by pituitary gland
ii. Aldosterone – adrenal cortex; causes sodium retention and
potassium loss
iii. Parathormone – regulates calcium and phosphate balance

ABNORMALITIES

A. Fluid Volume Deficit – hypovolemia; excessive loss of water and

electrolytes in equal proportion; vascular, cellular or intracellular
dehydration

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 a. Causes: ↓ fluid intake, ↑ output (diarrhea, vomiting,
hemorrhage), massive third-space fluid shifting
b. Manifestations: dry mucous membranes, poor skin turgor,
hypotension, tachycardia, severe thirst, weight loss, weakness
and mental status changes, renal shutdown and coma
c. Laboratory: urine specific gravity - >1.020; BUN>creatinine; ↑
Hct
d. Management:
i. Monitor I/O, urine specific gravity and weight (same time,
same clothes)
ii. Adequate hydration through oral or IV supplementation
iii. Ongoing assessment
iv. Maintain skin integrity
v. Tell patient to change positions slowly
B. Fluid Volume Excess – hypervolemia; excessive retention of water and
electrolytes in equal proportion; increased local or total body fluid
volume
a. Causes: ↑ fluid intake, ↓ ability to excrete fluid (renal disease),
abnormal fluid retention (CHF), ↑ Na intake
b. Manifestations: Weight gain, dependent edema, dyspnea and
crackles, mental status changes, bounding pulse, jugular vein
distention
c. Laboratory: ↓ BUN and Hct
d. Management:
i. Monitor I/O, weigh the client daily (same time, same
clothes), assess V/S, presence of sacral and peripheral
edema
ii. Monitor IV rate regularly.
iii. Assess lung sounds; if pulmonary edema occurs, elevate
head of bed, have the client turn and cough and deep
breathe q 2 hours
iv. Turn the client q 2 hours; edematous tissue is prone to skin
breakdown.
v. Administer diuretics
vi. DIET: sodium and water restriction
vii. Check medications if they contain Na.
C. Hyponatremia – serum Na level below 135 mEq/L resulting from
excessive Na loss or excessive water gain
a. Causes: fluid loss (vomiting, diarrhea, fistulas, diaphoresis,
diuretic therapy, NG suctioning), adrenal insufficiency (↓
aldosterone), SIADH, ↑ water gain from intake of Na-deficient
parenteral fluids, compulsive water drinking
b. Manifestations: Anorexia, nausea and vomiting, muscle cramps,
altered LOC (lethargy, disorientation, headache, confusion),
convulsions (Na <115 mEq/L)
c. Laboratory: Na <135 mEq/L, urinalysis – (+) urine Na, ↑ specific
gravity (SIADH) or ↓ specific gravity (Na loss)
d. Management:
i. Monitor I/O, weigh daily, assess for signs of FVD
ii. Na supplementation (oral, IV, parenteral)
iii. Infuse hypotonic solutions cautiously
iv. Assess neurologic (lethargy, confusion, muscle twitching,
seizures) and GI status (anorexia, nausea, vomiting,
abdominal cramping)
v. Maintain SEIZURE PRECAUTIONS
vi. Monitor serum Na levels

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 vii. Strict water restriction
D. Hypernatremia - serum Na level above 145 mEq/L caused by a gain of
sodium in excess of water or loss of water in excess of Na
a. Cause: water loss (diarrhea, fever, hyperventilation, diabetes
insipidus), ↓ water replacement (↓ intake of water by the
elderly, cognitively impaired, comatose), inability to swallow,
seawater ingestion, ↑ sodium intake
b. Manifestations: Thirst, poor skin turgor, edematous dry tongue
and sticky mucous membranes, ↑ body temperature, lethargy
and restlessness, peripheral and pulmonary edema
c. Laboratory: Na >145 mEq/L, serum osmolality >295 mOs/kg,
urinalysis - ↑ specific gravity and urine osmolality
d. Management:
i. Monitor I/O, weigh daily
ii. ↑ fluid intake as appropriate
iii. Infuse hypertonic solution cautiously
iv. Monitor serum Na levels
v. Assess V/S, skin turgor, neurologic status and thirst
vi. Reposition the client frequently
vii. Raise side rails
E. Hypokalemia – serum K level below 3.5 mEq/L
a. Cause: ↓ K intake, excessive K loss (diuretic therapy, gastric
suctioning, colostomy, ileostomy, GI disorders, diaphoresis and
renal disorders), metabolic alkalosis, hyperaldosteronism
b. Manifestations: anorexia, nausea and vomiting, fatigue, muscle
weakness, leg cramps or paresthesia, cardiac arrhythmias, ↓
bowel motility, ileus or abdominal distention
c. Laboratory: K < 3.5 mEq/l, ECG – flattened T wave, prominent U
wave, depressed ST segment and prolong PR interval
d. Management:
i. Oral K replacements daily
ii. Assess for abdominal pain or GI bleeding – may indicate
bowel lesions that require intervention
iii. Infuse parenteral K supplement; dilute in at least 100 ml of
solution, administer on an IV pump and monitor ECG during
therapy
iv. Never administer K by IV push or IM!
v. DIET: ↑ K-rich foods: Apricots, Bananas, Cantaloupe, Dates,
Orange juice, Potatoes, Peach
vi. Assess the clients on digitalis therapy (toxicity: GI distress)
F. Hyperkalemia – K level above 5.5 mEq/L
a. Causes: ↓ renal excretion due to renal failure,
hypoaldosteronism, acidosis, severe tissue trauma, ↑ K
supplementation
b. Manifestations: cardiac arrhythmias, muscle weakness,
paresthesias and possibly paralysis, irritability and anxiety,
abdominal cramps with diarrhea
c. Laboratory: K >5.5 mEq/L, ECG – tall T waves, prolong PR interval
and QRS duration, absent P waves and ST depression
d. Management:
i. Kayexalate (cation-exchange resins) – oral or by retention
enema; draws K into the bowel so that it may be excreted
in the feces
ii. Ca gluconate administration – counters abnormal cardiac
conditions
iii. NaHCO3 – causes a temporary shift of K into cells

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 iv. Regular insulin + glucose administration – temporary shift
of K into cells
v. Hemodialysis
vi. Assess for signs of muscular weakness, cardiac
arrhythmias, paresthesias, nausea and intestinal colic
vii. Monitor ECG, serum K levels
viii. Administer K IV cautiously
ix. DIET: ↓ K-rich foods
x. Use salt-substitutes sparingly: contains 60 mEq of K/
teaspoon
G. Hypocalcemia – serum calcium level < 8 mg/dl (Normal: 8.5-10.5
mg/dl)
a. Causes: hypoparathyroidism, pancreatitis, inadequate Vit D
intake or synthesis, renal failure, drug therapy, insufficient
calcium intake
b. Manifestations: tetany (tingling in fingers and circumoral area,
muscle spasms associated with pain in extremities and face),
Trousseau’s sign (carpopedal spasm) and Chvostek sign
(twitching of facial muscles when facial nerve is tapped),
hyperactive DTR and seizures due to neuromuscular irritability
c. Laboratory: Ca <8.5 mg/dL, ECG – prolonged QT interval
d. Management:
i. SEIZURE PRECAUTIONS
ii. Administer parenteral Ca; prevent infiltration – causes
tissue necrosis
iii. Administer parenteral Ca cautiously in patients with
digitalis therapy – may cause cardiac arrest
iv. Provide a relaxed, quiet environment and promote
adequate rest
v. Vitamin D - ↑ Ca absorption from the GI tract
vi. Diet: ↑ Ca intake to 1000-1500 mg/day
vii. Regular exercise; ↓ bone loss of calcium
H. Hypercalcemia – serum Ca level above 10.5 mg/dl
a. Causes: ↑ Ca intake, movement of Ca from bones to serum
(prolonged immobilization and malignant neoplastic disorders), ↓
renal excretion due to renal failure, drug therapy with thiazide
diuretics, hyperparathyroidism
b. Manifestations: Anorexia, nausea, vomiting, constipation,
muscular weakness, incoordination, altered LOC, polyuria,
polydipsia, cardiac arrhythmias, hypoactive DTR
c. Laboratory: Ca > 10.5 mg/dl, ECG – shortened QT interval,
bradycardia, heart blocks
d. Management:
i. PNSS – dilutes serum calcium and inhibit tubular
reabsorption of Ca
ii. PO4 – enhances deposition of calcium
iii. Furosemide - ↑ Ca excretion
iv. Treat the underlying cause
v. Assess for DHN, mental confusion and psychotic behavior
vi. 3-4 quarts of fluid daily to facilitate excretion, ↑ fiber diet
for constipation
vii. Bed side rails up; secure all invasive lines!
viii. Teach about early ambulation and daily weight-bearing
activities.
I. Metabolic Acidosis – excessive absorption or retention or acid or
excessive excretion of HCO3; Bicarbonate deficit

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 a. Causes: ketoacidosis, lactic acidosis,, prolonged fasting, salicylic
poisoning, oliguric renal disease, abnormal HCO3 losses, which
can occur in loss of fluid from the lower GI tract from surgery,
drains or severe diarrhea
b. Manifestations
i. Headache
ii. Mental dullness
iii. Kussmaul’s respiration
iv. K excess
c. Management
i. Treatment of underlying cause and restoration of
electrolyte balance
ii. Na bicarbonate IV
iii. Maintain good respiratory function
iv. Fluid replacement, measure I/O
v. Protect from injury

J. Metabolic Alkalosis – Results from loss of hydrogen ions or addition of

base to body fluids
a. Causes: excessive ingestion of NaCO3 or baking soda, vomiting,
gastric suctioning, intestinal fistulas
b. Manifestations: depressed breathing, mental confusion,
dizziness, numbness and tingling of fingers and toes, muscle
twitching, tetany convulsions, K deficit
c. Management:
i. NaCl or Ammonium chloride oral or IV
ii. Carbonic anhydrase inhibitor (Diamox) – increase excretion
of bicarbonate by kidneys
iii. Maintain good respiratory function
iv. Protect from injury
K. Respiratory Acidosis – caused by failure of the respiratory system to
remove CO2 from body fluids as fast as it is produced in the tissues
a. Causes: obstructive/restrictive lung disease, impaired movement
of thoracic cage, depressed respiratory centers, neuromuscular
disease
b. Manifestations: Hyperpnea, visual disturbances, headaches,
ventricular fibrillation, late: confusion, drowsiness, coma, K
excess
c. Management:
i. Bronchodilators
ii. Postural drainage
iii. Chest clapping
iv. Na bicarbonate for ventricular fibrillation or potassium
excess
L. Respiratory Alkalosis – caused by loss of CO2 from the lungs at a faster
rate than it is produced in the tissues
a. Causes: Anxiety, fever, meningitis, ASA poisoning, pneumonia
b. Manifestations: lightheadedness, numbness or tingling of fingers
or toes, tetany, convulsions, K deficit
c. Management:
i. Treat underlying conditions
ii. Encourage slow, deep breathing; instruct the client to
breathe into and out of a paper bag
iii. SEIZURE PRECAUTIONS

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