1

Fluids in Human Body

I. Fluid Status of Human Body

A. Homeostasis: state of the body when maintaining a state of
balance in the presence of constantly changing conditions
B. Includes balance of fluid, electrolytes, and acid-base
balance
C. Body water intake and output approximately equal (2500
mL/24 hr.)

II. Body Fluid Composition

A. Water: 60% of body weight
B. Electrolytes: substances that become charged particles in
solution
1. Cations: positively charged (e.g. Na+, K+)
2. Anions: negatively charged (e.g. Cl-)
3. Both are measured in milliequivalents per liter
(mEq/L)
C. Osmolality: concentration of a solution measured in
milliosmoles per liter
D. Balance of hydrostatic pressure and osmotic pressure
regulates movement of water between intravascular and
interstitial spaces

III. Body Fluid Distribution:

A. 2 body compartments:
1. Intracellular fluids (ICF): fluids within cells of body
[major intracellular electrolytes: Potassium (K+),
Magnesium (Mg +2)]
2. Extracellular fluids (ECF): fluid outside cells; [major
extracellular electrolytes: Sodium (Na+),
Chloride(Cl-)]; this is where transportation of
nutrients, oxygen, and waste products occurs
B. Locations of ECF:
1. Interstitial: fluid between most cells
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2. Intravascular: fluid within blood vessels; also called

plasma
3. Transcellular: fluids of body including urine,
digestive secretion, cerebrospinal, pleural, synovial,
intraocular, gonadal, pericardial

IV. Mechanisms of Body Fluid Movement (i.e. movement of

solutes, solvents across different extracellular locations)
A. Osmosis: water is mover; water moves from lower
concentration to higher concentration
1. Normal Osmolality of ICF and ECF: 275 – 295
mOsm/kg
2. Types of solutions according to osmolality
a. Isotonic: all solutions with osmolality same as
that of plasma
Body cells placed in isotonic fluid: neither
shrink nor swell
b. Hypertonic: fluid with greater concentration of
solutes than plasma
Cells in hypertonic solution: water in cells
moves to outside to equalize concentrations:
cells will shrink
c. Hypotonic: fluid with lower concentration of
solutes than plasma
Cells in hypotonic solution: water outside cells
moves to inside of cells: cells will swell and
eventually burst (hemolyze)
3. Different intravenous solutions, used to correct some
abnormal conditions, categorized according to
osmolality:
a. Hypertonic: 5%glucose ,45% NaCl solution
b. Isotonic: 9% NaCl, Lactated Ringers solution
c. Hypotonic: 45% NaCl
B. Diffusion: solute molecules move from higher
concentration to lower concentration
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1. Solute, such as electrolytes, is the mover; not the

water
2. Types: simple and facilitated (movement of large
water-soluble molecules)
C. Filtration: water and solutes move from area of higher
hydrostatic pressure to lower hydrostatic pressure
1. Hydrostatic pressure is created by pumping action of
heart and gravity against capillary wall
2. Usually occurs across capillary membranes
D. Active Transport: molecules move across cell
membranes against concentration gradient; requires
energy, e.g. Na – K pump

V. Mechanisms that Regulate Homeostasis: How the body adapts

to fluid and electrolyte changes
A. Thirst: primary regulator of water intake (thirst center in
brain)
B. Kidneys: regulator of volume and osmolality by
controlling excretion of water and electrolytes
C. Renin-angiotension-aldosterone mechanism: response
to a drop in blood pressure; results from vasoconstriction
and sodium regulation by aldosterone
D. Antidiuretic hormone: hormone to regulate water
excretion; responds to osmolality and blood volume
E. Atrial natriuretic factor: hormone from atrial heart
muscle in response to fluid excess; causes increased urine
output by blocking aldosterone

Fluid and Electrolyte Imbalances

I. Fluid Volume Deficit (too little fluid in body)
A. Common Stimuli:
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1. Excessive fluid loss, e.g. hemorrhage, excess

loss of GI fluids (vomiting, diarrhea, or wound
drainage)
2. Insufficient fluid intake, e.g. no access to fluid,
unable to drink
3. Failure of regulatory mechanisms, fluid shifts
B. Terminology:
1. Dehydration: technically loss of water alone
(but usually any state of low fluid)
2. Hypovolemia: decreased circulating blood
volume
3. Third Spacing: shift of fluid from vascular
space (inside blood vessels) to another area
such as abdomen/bowels, soft tissues (like
swelling that occurs with a severe injury –like
a twisted ankle)
C. Signs/Symptoms
More rapid fluid loss, equals more rapid
development of symptoms
1. Weight loss (liter fluid = 2.2 lb or 1 kg.)
2. Diminished skin turgor, tongue turgor (more
reliable in elderly)
3. Postural (orthostatic) hypotension: drop of
15mm Hg of systolic BP with position change
from lying to standing
4. Flat neck veins when recumbent
5. Diagnostic test findings (usual, not absolute):
a. Electrolytes: isotonic fluid loss: Na is
within normal limits; if loss of water only,
Na is elevated
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b. Serum Osmolality: isotonic fluid loss:

osmolality is within normal limits; loss of
water alone, osmolality is elevated
c. Urine specific gravity, urine osmolality:
both elevated as urine becomes more
concentrated as kidneys conserve water
d. Increased hematocrit due to
hemoconcentration
e. Possible elevated blood urea nitrogen
(BUN)
f. CVP (mean pressure in right atrium of
heart) sub normal
D. Compensatory Mechanisms (how the body
responds to restore homeostasis)
Goal: to conserve water and Na; to maintain
circulation
1. Tachycardia (may lead to hypotension)
2. Vasoconstriction as evidenced by pale, cool
skin
3. Decrease in urinary output with rise in urine
specific gravity
E. Collaborative Care
1. Prevent deficits in clients at risk: especially
aged; anyone with increased fluid loss, such as
persons with prolonged vomiting and diarrhea;
during hot weather, those under physical
exertion without adequate fluid replacement
2. Correct the deficits and treat the underlying
cause
a. Replacement of fluids and electrolytes by
oral, IV, or enteral route; Isotonic
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electrolyte IV solutions for hypotensive

clients and those with abnormal losses
b. Fluid challenge: Physician orders a
specific amount of IV fluid over short
period of time (e.g. 300 mL of isotonic
solution over 10 minutes). Obtain baseline
assessment of vital signs, breath sounds,
output, mental status before initiation;
compare results after fluid challenge
completed; physician re-evaluates
response and orders fluids accordingly
c. Assess parameters pertinent to the signs
and symptoms, vital signs, and level of
consciousness; reassess lab results
d. Notify physician if urine output < 30
mL/hr (client has a foley catheter with
hourly output as monitoring)
3. Pertinent nursing diagnoses
a. Deficit Fluid Volume
b. Ineffective Tissue Perfusion
c. Risk for Injury

II.Fluid Volume Excess (too much fluid in body)

Water and sodium are proportionately excessive and in
extracellular compartment
A.Common Stimuli (one or combinations of
conditions)
1. Pathophysiology: mechanisms that should
maintain homeostasis are impaired:
a. Heart failure
b. Kidney failure
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c. Cirrhosis of liver
d. Adrenal disorders or corticosteroid
administration
e. Stress conditions causing release of ADH
and aldosterone
2. Excessive intake of sodium and fluid
a. Excessive intake of foods high in sodium
(salt)
b. Excessive intake of IV fluids containing
sodium (0.09% NaCl)

B.Terminology
1. Hypervolemia: excess intravascular fluid
2. Edema: excess interstitial fluid
C.Signs/Symptoms
1. Weight gain: > 5% of body weight over short
time
2. Circulatory overload: bounding pulse; S3 heart
sound; neck and peripheral vein distention;
increased CVP, i.e. mean pressure in right
atrium of heart; cough; dyspnea; orthopnea;
breath sounds, moist crackles; pulmonary
edema; polyuria; ascites
3. Peripheral edema worse in most dependent
body part: pedal, sacral for bed-bound client;
anasarca (severe generalized over all body
edema); possibly cerebral edema, i.e. altered
mental status
4. Diagnostic test findings:
a. Chest xray: variable degrees of
pulmonary edema
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b. Serum sodium and osmolality: usually

within normal range
c. Hematocrit and hemoglobin: usually
slightly decreased
d. Decreased blood urea nitrogen (BUN), in
some cases
D.Compensatory Mechanisms
Heart failure results when heart is unable to increase
workload to handle excess blood volume
1. Left-side heart failure: pulmonary edema
2. Right-side heart failure: peripheral edema
E. Collaborative Care
1. Prevent fluid volume excess in at risk
populations (those receiving IV fluids,
significant at risk health histories, elderly)
2. Effective fluid management:
a. Assessment of signs/symptoms of fluid
overload, lab results
b. Fluid restrictions as ordered
c. Dietary management: sodium-restricted
diets
d. Monitor intake and output, daily weights
3. Treatment with diuretic medications
a. Loop diuretics (e.g. Furosemide (Lasix))
b. Thiazide-type diuretics (e.g.
Hydrochlorothiazide (HCTZ))
c. Potassium-sparing diuretics (e.g.
Bumetanide (Bumex))
F. Nursing Diagnoses
1. Excess Fluid Volume
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2. Risk for Impaired Skin Integrity (related to

peripheral edema)
3. Risk for Impaired Gas Exchange (related to
pulmonary congestion and/or edema)
4. Activity Intolerance

III. Electrolyte Imbalances

One electrolyte or several; often treat underlying cause;
careful observation as over treatment may cause
additional imbalances
A. Sodium
1. Characteristics:
a. Mainly in ECF
b. Blood normal values: 135 – 145 mEq/L
c. Actions:
1. Regulates volume
2. Regulates osmolality
3. Maintains neuromuscular activity
d. Sources: dietary intake, prescription drugs
and self-remedies
e. Compensatory mechanisms: kidney
excretes or conserves sodium in response
to changes in vascular volume, e.g. drop
in blood pressure
1. Stimulates renin-angiotension-
aldosterone system
2. Regulates ADH secretion
3. Modulates glomerular filtration rate
4. Controls Atrial natriuretic peptide
release (sodium excretion)
2. Hyponatremia
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Serum sodium is lower than normal (Serum Na

< 135 mEq/L)
a. Common Stimuli
1. Water shifts to ECF; osmolality
changes and cells swell
2. Loss of sodium (without water)
a. Excessive through urine
(e.g.diuretics, kidney disease)
b. GI (e.g. vomiting, diarrhea, GI
suction)
c. Skin (e.g. sweating, burns)
d. Water gain to dilute ECF
3. Diseases: heart or renal failure;
cirrhosis; Syndrome of Inappropriate
secretion of Anti-Diuretic Hormone
(SIADH); excessive hypotonic IV
fluids
b. Signs and Symptoms (depend on rapidity
and severity of onset)
1. Early: (Na at 125)
a. Muscle cramps, weakness,
fatigue
b. GI: anorexia, vomiting,
diarrhea, nausea, abdominal
cramping
2. Later (Na<120)
a. Cerebral edema symptoms
(brain cells swell)
b. Headache, depression,
personality changes
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c. Lethargy, muscle twitching,

tremors
d. Further progress to convulsions
and coma with severely low
levels
3. Diagnostic test findings
a. Decreased serum Na (<135
mEq/L)
b. Serum Osmolality (<275
mOsm/kg)
c. 24-hour urine collection for Na
used to differentiate cause
c. Collaborative Care
Restoration of blood volume and sodium
levels
1. Medications
a. Isotonic IV solution (Ringer’s,
0.9% NaCl)

b. Hypertonic IV Na solution (3%

NaCl) is used to treat the client
with severe hyponatremia (Na :
110 – 115 mEq/L)
c. Loop diuretics (e.g.
Furosemide) to promote
isotonic diuresis
2. Fluid and Dietary Management
a. Increase foods high in sodium
b. Restrict fluid in volume
3. Assessment of signs/symptoms of
hyponatremia, especially
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a. Continual mental status

assessment
b. Seizure precautions
c. Strict intake and output and
monitoring weight daily
d. Reassess lab results
d. Nursing Diagnoses
1. Risk for Impaired Fluid Volume
2. Risk for Decreased Intracranial
Adaptive Capacity
3. Hypernatremia
Serum sodium is higher than normal (Serum
sodium>145 mEq/L)
Hyperosmolality of ECF; may occur with fluid
volume deficit or excess
a. Common Stimuli
1. Sodium gained in excess of water,
e.g. excessive salt intake or
hypertonic IV solutions, clients with
heat stroke, near drowning in
seawater
2. Water lost in excess of sodium, e.g.
clients unable to respond to thirst as
with altered mental status or physical
disability; diabetes insipidus
b. Signs and Symptoms (depend on rapidity
and severity of onset)
1. Initially: thirst
2. If not responded to: altered
neurologic function; lethargy;
irritability; seizures; coma; death
 13

3. Diagnostic test findings:

a. Serum Na is greater than 145
mEq/L
b. Serum Osmolality > 295
mOsm/kg
c. Collaborative Care
1. Treatment according to cause with
slow correction of Na to avoid
development of cerebral edema
2. Medications
a. Oral or intravenous water
replacement (hypotonic IV
solutions such as 5%dextrose or
0.45% NaCl)
b. Diuretics for Na excretion
3. Assessment
a. Nursing history for precipitating
factors as stimuli
b. Vital signs, including
temperature
c. Mental status
d. Signs/symptoms consistent with
fluid volume deficit or excess
e. Reassess lab results
d. Nursing Diagnoses: Risk for Injury

B. Potassium
1. Characteristics
a. Primary intracellular cation
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b. Normal serum potassium level 3.5 – 5.0

mEq/L
c. Actions: vital role in cellular metabolism,
heart function, and neuromuscular
function
d. Need daily intake of potassium, usually
through food
e. Kidneys eliminate potassium from body
under regulation by aldosterone
f. Shifts in and out of cells in response to
concentration of hydrogen ion (pH) in the
blood
2. Hypokalemia
Serum potassium is lower than normal (< 3.5
mEq/L)
a. Common Stimuli
1. Excessive loss of potassium
a. Through kidneys: secondary to
drugs, hyperaldosteronism,
diabetes mellitus
b. Through GI tract: severe
vomiting, gastric suction,
diarrhea or ileostomy drainage
2. Inadequate intake
a. Unable or unwilling to eat,
anorexia nervosa
b. Alcoholism
3. Shift from extracellular to
intracellular space
b. Signs and Symptoms
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1. Abnormal heart rhythms including

atrial and ventricular
Potentiates digitalis toxicity
(medication to treat heart failure)
2. Muscle weakness, including leg
cramps
3. Slowed abdominal peristalsis
4. Diagnostic test findings:
a. Serum K: if K+=2.5 – 3.0,
moderate; if < 2.5, severe and
probably symptomatic
b. Arterial blood gases
(hypokalemia associated with
alkalosis, elevated pH)
c. Electrocardiogram changes:
flattened or inverted T, U waves
c. Collaborative Care
1. Medications
a. Potassium supplements, oral or
parenteral
b. Never give potassium IV push,
only as IV infusion
2. Dietary management
Potassium rich foods (fruits and
vegetables)
3. Health promotion: Prevention of
hypokalemia
a. Using balanced electrolyte
fluids with GI loss
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b. Diet teaching and/or potassium

supplements with meds that
predispose to hypokalemia
c. Regular monitoring of serum
potassium levels
4. Assessment
a. Nursing history for precipitating
factors as stimuli
b. Mental status
c. Vital signs
d. Reassess lab results
d. Nursing Diagnoses
1. Activity Intolerance
2. Decreased Cardiac Output
3. Risk for Imbalance Fluid Volume
4. Acute Pain (Potassium can be
irritating to veins even when diluted;
never give IV push)
3. Hyperkalemia
Serum potassium is higher than normal (>5.0
mEq/L)
a. Common Stimuli
1. Inadequate excretion of potassium
a. Impaired renal excretion of
potassium (untreated renal
failure, adrenal insufficiency)
b. Medications that impair K+
excretion by kidneys (e.g. K+
sparing diuretics)
2. Excessively high intake of potassium
 17

a. Excess oral potassium by

supplement, salt-substitute
b. Rapid IV administration of
potassium, transfusion of aged
blood
3. Shift from intracellular to
extracellular space
May occur with acidosis, severe
tissue trauma
b. Signs and Symptoms
1. Abnormal heart function: slowing of
heart rate and conduction; ventricular
dysrhythmias progress to cardiac
arrest
2. Skeletal muscle irritability, tremors
progress to weakness, and paralysis
3. GI disturbances: initially, diarrhea
and colic
4. Diagnostic test findings
a. Serum K: > 5.0 mEq/L
b. Electrocardiogram: peaked T
waves, prolonged conduction P-
R, QRS
c. Arterial blood gases to
determine presence of acidosis
c. Collaborative Care
1. Medications
a. Stop all potassium supplements
orally and IV, if receiving
b. Medications to lower serum
potassium and stabilize
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conduction system of heart,

including
1. Intravenous Calcium
Gluconate
2. Intravenous 50 gm of
glucose and regular insulin
(Moves K+ intracellularly)
3. Sodium polystyrene
sulfonate (Kayexalate),
orally or rectally (binds K+
in GI tract)
c. Loop diuretics (e.g. Furosemide
(Lasix)), if adequate renal
function
2. Dialysis “artificial kidney” removes
excess potassium
3. Health promotion: Teach clients at
risk to read food and dietary
supplements for potassium
4. Assessment
a. Nursing history for precipitating
factors as stimuli
b. Cardiac status with continuous
cardiac monitoring
c. Vital signs
d. Reassess lab results.
e. Hemolyzed blood sample: if
serum K+ is very high and client
does not appear ill enough to
have a potassium that high,
blood should be redrawn and re-
 19

tested. First blood sample may

have been hemolyzed.
d. Nursing Diagnoses
1. Risk for Activity Intolerance
2. Risk for Decreased Cardiac Output
3. Risk for Imbalanced Fluid Volume

C. Calcium
1. Characteristics
a. Abundant in body
b. Normal serum calcium level 8.5 – 10.0
mEq/L
c. Body’s source is from diet; 20% of
calcium ingested is absorbed
d. 99% calcium is in bones and teeth and is
bound to phosphorus
e. Extracellular, and only ionized form is
active
f. Actions:
1. Regulates muscle contraction and
relaxation, including respiratory
muscles
2. Maintains cardiac function
3. Acts in blood clotting process
g. Calcium levels are affected by acid-base
balance
2. Hypocalcemia
Total serum calcium level < 8.5 mg/dL
Systemic effects caused by decreased levels of
ionized Ca in extracellular fluid
a. Common Stimuli
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1. Hypoparathyroidism (neck surgery

24 – 48 hr post op)
2. Acute pancreatitis
3. Electrolyte imbalances (low
magnesium, high phosphate),
alkalosis
4. Malabsorption disorders
5. Certain medications, e.g. loop
diuretics (Furosemide)
anticonvulsants (phenytoin
(Dilantin))
6. Massive transfusion of banked blood
b. Signs and Symptoms
1. Neuromuscular:
a. Most serious is tetany (tonic
muscle spasm) and convulsions
b. Earlier: numbness and tingling
around mouth, in hands and feet
advancing to muscle spasms of
face and extremities,
hyperactive deep tendon
reflexes (DTR’s)
c. Positive Chvostek’s sign: face
spasm with cheek tapping;
positive Trousseau’s sign:
carpal spasm with inflation of
BP cuff on arm
2. Respiratory status: muscle spasms
can lead to laryngeal spasms
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3. Cardiac: hypotension, bradycardia,

ventricular dysrhythmias and cardiac
arrest
4. Diagnostic test findings
a. Total serum Ca < 8.5 mg/dL
b. Serum albumin affects Ca
c. Serum magnesium: low, < 1.6
mg/dL is associated with low
Ca
d. Serum phosphate: elevated, >
4.5 mg/dL is inversely related to
Ca
e. Parathryoid hormone (PTH) to
detect hyperparathyroidism
f. Electrocardiogram: evaluate
cardiac conduction: such as
prolonged ST segment
c. Collaborative Care
1. Medications
a. Calcium supplements:
b. Severe hypocalcemia:
intravenous (CaChloride or
CaGluconate)
c. Chronic asymptomatic; oral
forms, sometimes with Vitamin
D
2. Dietary management includes
calcium in diet (milk, figs, salmon)
3. Health promotion: Teaching to
include prevention of osteoporosis
 22

(calcium moves from bones; not

measured by serum Ca)
4. Assessment:
a. Nursing history for precipitating
factors as stimuli
b. Neuro assessment, cardiac
status and vital signs
c. Continuous cardiac monitoring
and airway support, if indicated;
d. Reassess lab results
d. Nursing Diagnoses: Risk for Injury
3. Hypercalcemia
Total serum calcium level > 10.0 mg/dL.
Systemic effects caused by increased levels of
ionized Ca in extracellular fluid
a. Common Stimuli
1. Increased reabsorption of calcium
from bones
a. Hyperparathyroidism
b. Malignancies: cancers with
metastasis (bone destruction by
the tumor)
c. Result of immobility and lack
of weight-bearing
2. Diminished elimination of calcium
Occurs with medications (e.g.
thiazide diuretics, lithium)
b. Signs and Symptoms
1. Decreased neuromuscular irritability:
muscle weakness, depressed deep
 23

tendon reflexes (DTR), advances to

confusion, lethargy to coma
2. GI: anorexia, nausea, vomiting,
constipation
3. Cardiac: heart conduction
disturbances: bradycardia, heart
block
4. Polyuria and increased thirst
5. Complications: peptic ulcer disease,
pancreatitis, renal calculi (kidney
stones)
6. Hypercalcemic crisis; acute Ca
excess, can lead to cardiac arrest
7. Diagnostic test findings
a. Serum calcium >10.0 mg/dL
b. Serum Parathyroid level
c. Electrocardiogram: changes
including shortened QT,
bradycardia, heart blocks
c. Collaborative Care
Goal: to promote Ca elimination by
kidneys; to reduce Ca reabsorption from
bone
1. Medications
a. Intravenous fluids: usually
isotonic saline
b. Loop diuretic (e.g. Furosemide
(Lasix) Calcitonin)
c. For hypercalcemic crisis: IV
sodium phosphate or potassium
phosphate
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d. For inhibiting bone

reabsorption: Plicamycin
(Mithracin)
e. Glucocorticoids
2. Dietary Management: Increase
intake of acid ash foods, fiber, fluid
intake
3. Health Promotion
a. Identify persons at risk
b. Encourage weight-bearing
activity
c. Fluids up to 3 -4 quarts, if not
contraindicated
d. Limit calcium foods and
supplements and calcium
containing antacids
4. Assessment
a. Nursing history for precipitating
factors as stimuli
b. Vital signs
c. Neuro assessment
d. Cardiac status, continuous
cardiac monitoring if indicated
e. Reassess lab results (increased
risk for digitalis toxicity)
d. Nursing Diagnoses
1. Risk for Injury
2. Risk for Excess Fluid Volume
D.Magnesium
1. Characteristics
a. Mainly intracellular and in bone
 25

b. Normal serum level 1.6 – 2.6 mg/dL

c. Obtained through diet (green vegetables,
meat, grains, nuts)
d. Excreted by kidneys
e. Vital to cellular processes, enzyme,
protein synthesis
f. Sedative effect on neuromuscular junction
g. Affected by potassium and calcium levels
2. Hypomagnesemia
Magnesium level < 1.6 mg/dL
Common in critically ill patients
a. Common stimuli
1. Usually occurs along with K and Ca
deficiencies
2. Loss of GI fluids as with diarrhea,
ileostomy
3. Impaired nutrition absorption from
gut; starvation, NPO status
4. Chronic alcoholism
5. Medications such as loop or thiazide
diuretics, some antibiotics
b. Signs and Symptoms
1. Increased neuromuscular
excitability: tremors, hyperactive
reflexes, tetany, mood changes
2. Cardiac: dysrhythmias and sudden
death; increased risk of digitalis
toxicity
3. GI: nausea, vomiting, diarrhea,
anorexia, abdominal distention
4. Diagnostic test findings:
 26

a. Electrolyte levels; low

magnesium often with low Ca
and K
b.Electrocardiogram: delayed
conduction with dysrhythmias,
cardiac arrest, sudden death
c. Collaborative Care
1. Medications: if symptomatic, treated
with IV Magnesium Sulfate, and/or
oral supplements
2. Dietary Management: encourage
balanced diet including green
vegetables, meat, grains, nuts,
seafood
3. Health Promotion
a. Identify persons at risk (post-
surgery clients, clients with
malnutrition, alcoholics)
b. Encourage well-balanced
nutrition
4. Assessment
a. Nursing history for precipitating
factors as stimuli
b. Vital signs
c. Neuro status
d. Cardiac status, continuous
cardiac monitoring
e. GI assessment
f. Reassess lab results (increased
risk for digitalis toxicity)
d. Nursing Diagnoses: Risk for Injury
 27

3. Hypermagnesemia
Magnesium level >2.6 mg/dL
Less common
a. Common Stimuli: renal failure, especially
clients receiving parenteral or oral
supplements
b. Signs and Symptoms
1. Neuromuscular: weakness, lethargy
leading to weak or absent deep
tendon reflexes (DTR), drowsiness
as level rises
2. Cardiovascular: hypotension,
flushing, sweating, brady-
dysrhytmias leading to heart block,
cardiac arrest as level rises;
respiratory depression with high
levels
3. GI: nausea and vomiting
4. Diagnostic test findings
a. Magnesium level elevated
b. Electorcardiogram: changes
with bradycardia, heart block
c. Collaborative Care
1. Medications
a. Withhold medications
containing magnesium
b. Dialysis for clients with renal
failure
c. Calcium Gluconate IV for
reversal or neuro and cardiac
effects
 28

2. Health Promotion
a. Identify clients at risk (those
with renal failure, receiving
magnesium supplements)
b. Teach to avoid laxatives,
antacids, and enemas containing
magnesium
3. Assessment
a. Nursing history for precipitating
factors as stimuli
b. Neuromuscular assessment
c. Cardiac assessment, continuous
cardiac monitoring and airway
support if indicated
d. Reassess lab results
d. Nursing Diagnoses
1. Decreased Cardiac Output
2. Risk for Ineffective Breathing
Pattern
3. Risk for Injury
E. Phosphate
1. Characteristics
a. Mostly in bone; intracellular anion
b. Normal serum level 2.5 – 4.5 mg/dL
c. Essential to intracellular processes,
including muscle contraction and nerve
conduction, metabolism, acid base
balance
d. Source is from diet, excreted by kidneys
e. Inverse relationship with calcium
2. Hypophosphatemia
 29

Serum phosphorus < 2.5 mg/dL

Total body deficit or cellular shift
a. Common Stimuli
1. Usually iatrogenic (related to
treatment)
2. Refeeding syndrome: occurs with
beginning enteral or total parenteral
feedings to malnourished clients
3. Medications: intravenous glucose
solutions, diuretics, aluminum or
magnesium-based antacids
4. Alcoholism
5. Hyperventilation with respiratory
alkalosis
b. Signs and Symptoms
1. Neuromuscular: irritability,
weakness, paresthesias, confusion,
and seizures leading to respiratory
failure
2. Cardiac: dysrhythmias, chest pain
3. GI: anorexia, dysphagia, nausea,
vomiting, decreased GI motility
4. Diagnostic test findings: serum
phosphate is <2.5 mg/dL
c. Collaborative Care
1. Medications
a. Oral phosphate supplements
(Neutra-Phos)
b. Intravenous phosphorus such as
Na Phosphate, K Phosphate
 30

c. Eliminate phosphate depleting

medications, if possible
2. Dietary Management: stress well-
balanced diet
3. Health Promotion
a. Identify clients at risk
b. Teach, including avoidance of
phosphorus-binding antacids
4. Assessment
a. Nursing history for precipitating
factors as stimuli
b. Neuromuscular
c. GI
d. Cardiac with cardiac monitoring
and respiratory support if
indicated
e. Reassess lab results, especially
electrolytes
d. Nursing Diagnoses
1. Impaired Physical Mobility
2. Ineffective Breathing Pattern
3. Decreased Cardiac Output
4. Risk for Injury
3. Hyperphosphatemia
Serum phosphorus > 4.5 mg/dL
Impaired excretion, total body excess or
cellular shift
a. Common Stimuli
1. Acute or chronic renal failure
2. Excess or rapid intake of phosphates
 31

3. Phosphate shifts from chemotherapy,

trauma, heat stroke
4. Accompanies altered calcium
concentrations
b. Signs and Symptoms
1. Neuromuscular: muscle cramps,
paresthesias, muscle spasms, tetany
2. Calcification of soft tissues
3. Diagnostic test findings: serum
phosphate is >4.5 mg/d/L
c. Collaborative Care
1. Treat cause
2. Promote renal excretion by IV saline
or dialysis for client in renal failure
3. Dietary Management: eliminate
phosphate rich foods, such as organ
meats, milk, and milk products
4. Health Promotion
a. Identify clients at risk
b. Teach, including avoidance of
phosphate sources, foods or
medications
5. Assessment
a. Nursing history for precipitating
factors as stimuli
b. Neuromuscular
c. Reassess lab results, especially
electrolytes
d. Nursing Diagnoses: Risk for Injury
 32

Acid-Base Balance
I. Background
A. Facts and Definitions
1. Acid-base homeostasis is necessary to maintain life.
2. Acid base balance must be within a definite range for
cellular function to occur.
3. The acidity of a substance, determined by the
hydrogen ion (H+) concentration; is expressed as pH.
4. Acids
a. Release hydrogen ions into solution
b. Have pH < 7
5. Alkalines (bases)
a. Accept hydrogen ions into solution
b. Have pH > 7
B. Body fluids
1. Normally slightly alkaline
2. Normal range is narrow: 7.35 – 7.45 (pH of 7 is
neutral)
3. Arterial blood pH < 7.35 is considered acid
4. Arterial blood pH > 7.45 is considered alkaline
:
C. Acids and Bases in the body
1. Body functions constantly produce acids
2. Most acids and bases in the body are weak
3. Acids include
a. Carbonic acid, which is eliminated as a gas,
carbon dioxide
b. Lactic, hydrochloric, phosphoric, sulfuric
acids, which are metabolized or excreted as
fluids
4. Bicarbonate is the major base

II. Body regulation of acid-base balance

 33

Constant response to changes in pH to maintain the pH in the

normal range
3 systems in the body, with various response times, to maintain
acid-base balance :

A. Buffer System
1. Responds immediately, but has limited capacity to
maintain
2. Buffers: substances that bind or release hydrogen
ions
a. When body fluid becomes acid, buffers bind
with hydrogen ions to raise pH
b. When body fluid becomes alkaline, buffers
release hydrogen ions to lower pH
3. Buffer systems
a. Bicarbonate-carbonic acid buffer system

CO2 + H20 H2C03  H+ + HC03

weak acid weak base

Process is reversible but the ratio of 20

(bicarbonate) to 1 (hydrogen) must be
maintained
b. Protein buffer system (intracellular and plasma)
c. Phosphates buffer system
B. Respiratory System
1. Responds within minutes
2. Includes respiratory center of brain stem and lungs
3. Occurs automatically, not under voluntary control
4. Adjusts the depth and frequency of respiration
according to the pH of the blood; increases or
decreases the amount of carbon dioxide in the blood;
 34

controls the amount of carbonic acid formed and

adjusts the pH of the blood
a. Hyperventilation: increased depth and
frequency of respiration; blows off more CO2
in response to an acid pH
b. Hypoventilation: decreased depth and
frequency of respiration; retains more CO2 in
response to an alkaline pH
C. Renal (Metabolic) System
1. Responds within hours to days

2. Adjusts the amounts of hydrogen and bicarbonate

ions
a. Kidneys excrete H+ ions, or generate and
reabsorb bicarbonate ions, in response to an
acid pH
b. Kidneys retain H+ ions, or generate and excrete
bicarbonate ions, in response to an alkaline pH

III. Determination of Acid-Base Balance: Analysis of Arterial

Blood Gases
A. pH
1. Normal: 7.35 – 3.45
2. Acidic: <7.35
3. Alkaline: >7.45
B. pCO2
Pressure of carbon dioxide; respiratory component
1. Normal: 35-45 mm Hg
2. Acidic: > 45 mm Hg (carbon dioxide forms carbonic
acid)
Hypercapnia: elevated levels of carbon dioxide in
blood
3. Alkaline: < 35 mm Hg
 35

Hypocapnia: decreased levels of carbon dioxide in

blood
C. HCO3
Bicarbonate; renal or metabolic component
1. Normal: 22 – 26 mEq/L
2. Acidic: < 22 mEq/L
3. Alkaline: > 26 mEq/L
D. Base Excess
1. Calculated value for buffer base capacity: the
amount of acid or base added to blood to obtain a pH
of 7.4
2. Normal: -3 -- +3
E. pO2
Pressure of oxygen in blood
1. Gives data about level of oxygenation; not used to
calculate acid-base status of blood
2. Normal: 80 – 100 mm Hg
3. Hypoxemia: < 80 mm Hg

IV. Acid-Base Imbalance

A. Classifications
1. Acidosis or alkalosis
a. Acidosis: Hydrogen ion concentration in blood
increases above normal and pH is below 7.35
b. Alkalosis: Hydrogen ion concentration in blood
decreases below normal and pH is above 7.45
2. Origin of the problem
a. From the respiratory system
b. From the metabolic system

B. Disorders: Simple or Combined

1. Primary disorders
a. Simple
b. One cause, either respiratory or metabolic
 36

2. Combined disorders
a. More severe
b. Both the respiratory and metabolic systems are
the cause of the same imbalance
C. Compensation
1. Only occurs with primary disorders
2. Response by the system not causing the imbalance to
correct the pH
Example: with respiratory acidosis, the kidneys
would eliminate hydrogen ions in urine to offset the
acidosis caused by hypoventilation of lungs.
3. Complete Compensation occurs if the pH is
corrected to the normal range (7.35 – 7.45)
4. Partial Compensation occurs if there is improvement
in the pH but not to the normal range.
5. Compensation can be determined by analysis of the
arterial blood gas results.
D. Treatment
1. Urgency
a. Mental ability and level of consciousness is
often affected
b. Brain function usually affected; brain cells
need proper conditions to perform cellular
functions
c. Cells cannot function properly if significant
acidosis or alkalosis occurs
2. Indirect treatment
a. Treating and correcting the precipitating
condition often corrects the acid-base
imbalance
b. Directly treating the acid-base imbalance, by
adding or removing hydrogen or bicarbonate
ions, may lead to further imbalances
c. Not usually first line of treatment
 37

V. Types of Acid-Base Imbalances

A. Respiratory Acidosis
pH < 7.35
pCO2 > 45 mm Hg (excess carbon dioxide in the blood)
Respiratory system impaired and retaining CO2; causing
acidosis
1. Common Stimuli
a. Acute respiratory failure from airway
obstruction
b. Over-sedation from anesthesia or narcotics
c. Some neuromuscular diseases that affect ability
to use chest muscles
d. Chronic respiratory problems, such as Chronic
Obstructive Lung Disease
2. Signs and Symptoms
a. Compensation: kidneys respond by generating
and reabsorbing bicarbonate ions, so HCO3 >26
mm Hg
b. Respiratory: hypoventilation, slow or shallow
respirations
c. Neuro: headache, blurred vision, irritability,
confusion
d. Respiratory collapse leads to unconsciousness
and cardiovascular collapse
3. Collaborative Care
a. Early recognition of respiratory status and treat
cause
b. Restore ventilation and gas exchange; CPR for
respiratory failure with oxygen
supplementation; intubation and ventilator
support if indicated
c. Treatment of respiratory infections with
bronchodilators, antibiotic therapy
d. Reverse excess anesthetics and narcotics with
medications such as naloxone (Narcan)
 38

e. Chronic respiratory conditions

a. Breathe in response to low oxygen levels
b. Adjusted to high carbon dioxide level
through metabolic compensation
(therefore, high CO2 not a breathing
trigger)
c. Cannot receive high levels of oxygen, or
will have no trigger to breathe; will
develop carbon dioxide narcosis
d. Treat with no higher than 2 liters O2 per
cannula
f. Continue respiratory assessments, monitor
further arterial blood gas results

4. Nursing Diagnoses
a. Impaired Gas Exchange
b. Ineffective Airway Clearance

B. Respiratory Alkalosis
pH < 7.35
pCO2 < 35 mm Hg.
Carbon dioxide deficit, secondary to hyperventilation
1. Common Stimuli
a. Hyperventilation with anxiety from
uncontrolled fear, pain, stress (e.g. women in
labor, trauma victims)
b. High fever
c. Mechanical ventilation, during anesthesia
2. Signs and Symptoms
a. Compensation: kidneys compensate by
eliminating bicarbonate ions; decrease in
bicarbonate HCO3 < 22 mm Hg.
b. Respiratory: hyperventilating: shallow, rapid
breathing
 39

c. Neuro: panicked, light-headed, tremors, may

develop tetany, numb hands and feet (related to
symptoms of hypocalcemia; with elevated pH
more Ca ions are bound to serum albumin and
less ionized “active” calcium available for
nerve and muscle conduction)
d. May progress to seizures, loss of consciousness
(when normal breathing pattern returns)
e. Cardiac: palpitations, sensation of chest
tightness
3. Collaborative Care
a. Treatment: encourage client to breathe slowly
in a paper bag to rebreathe CO2
b. Breathe with the patient; provide emotional
support and reassurance, anti-anxiety agents,
sedation
c. On ventilator, adjustment of ventilation settings
(decrease rate and tidal volume)
d. Prevention: pre-procedure teaching,
preventative emotional support, monitor blood
gases as indicated
C. Metabolic Acidosis
pH <7.35
Deficit of bicarbonate in the blood NaHCO3 <22 mEq/L
Caused by an excess of acid, or loss of bicarbonate from
the body
1. Common Stimuli
a. Acute lactic acidosis from tissue hypoxia
(lactic acid produced from anaerobic
metabolism with shock, cardiac arrest)
b. Ketoacidosis (fatty acids are released and
converted to ketones when fat is used to supply
glucose needs as in uncontrolled Type 1
diabetes or starvation)
 40

c. Acute or chronic renal failure (kidneys unable

to regulate electrolytes)
d. Excessive bicarbonate loss (severe diarrhea,
intestinal suction, bowel fistulas)
e. Usually results from some other disease and is
often accompanied by electrolyte and fluid
imbalances
f. Hyperkalemia often occurs as the hydrogen
ions enter cells to lower the pH displacing the
intracellular potassium; hypercalcemia and
hypomagnesemia may occur
2. Signs and Symptoms
a. Compensation: respiratory system begins to
compensate by increasing the depth and rate of
respiration in an effort to lower the CO2 in the
blood; this causes a decreased level of carbon
dioxide: pCO2 <35 mm HG.
b. Neuro changes: headache, weakness, fatigue
progressing to confusion, stupor, and coma
c. Cardiac: dysrhythmias and possibly cardiac
arrest from hyperkalemia
d. GI: anorexia, nausea, vomiting
e. Skin: warm and flushed
f. Respiratory: tries to compensate by
hyperventilation: deep and rapid respirations
known as Kussmaul’s respirations
g. Diagnostic test findings:
1. ABG: pH < 7.35, HCO3 < 22
2. Electrolytes: Serum K+ >5.0 mEq/L
3. Serum Ca+2 > 10.0 mg/dL
4. Serum Mg+2 < 1.6 mg/dL
3. Collaborative Care
a. Medications: Correcting underlying cause will
often improve acidosis
 41

b. Restore fluid balance, prevent dehydration with

IV fluids
c. Correct electrolyte imbalances
d. Administer Sodium Bicarbonate IV, if acidosis
is severe and does not respond rapidly enough
to treatment of primary cause. (Oral
bicarbonate is sometimes given to clients with
chronic metabolic acidosis) Be careful not to
overtreat and put client into alkalosis
e. As acidosis improves, hydrogen ions shift out
of cells and potassium moves intracellularly.
Hyperkalemia may become hypokalemia and
potassium replacement will be needed.
f. Assessment
1. Vital signs
2. Intake and output
3. Neuro, GI, and respiratory status;
4. Cardiac monitoring
5. Reassess repeated arterial blood gases
and electrolytes
4. Nursing Diagnoses
a. Decreased Cardiac Output
b. Risk for Excess Fluid Volume
c. Risk for Injury
D. Metabolic Alkalosis
pH >7.45
HCO3 > 26 mEq/L
Caused by a bicarbonate excess, due to loss of acid, or a
bicarbonate excess in the body
1. Common Stimuli
a. Loss of hydrogen and chloride ions through
excessive vomiting, gastric suctioning, or
excessive diuretic therapy
b. Response to hypokalemia
 42

c. Excess ingestion of bicarbonate rich antacids or

excessive treatment of acidosis with Sodium
Bicarbonate
2. Signs and Symptoms
a. Compensation: Lungs respond by decreasing
the depth and rate of respiration in effort to
retain carbon dioxide and lower pH
b. Neuro: altered mental status, numbness and
tingling around mouth, fingers, toes, dizziness,
muscle spasms (similar to hypocalcemia due to
less ionized calcium levels)
c. Respiratory: shallow, slow breathing
d. Diagnostic test findings
1. ABG’s: pH> 7.45, HCO3 >26
2. Electrolytes: Serum K+ < 3.5 mEq/L
3. Electrocardiogram: as with hypokalemia
3. Collaborative Care
a. Correcting underlying cause will often improve
alkalosis
b. Restore fluid volume and correct electrolyte
imbalances (usually IV NaCl with KCL).
c. With severe cases, acidifying solution may be
administered.
d. Assessment
1. Vital signs
2. Neuro, cardiac, respiratory assessment
3. Repeat arterial blood gases and
electrolytes
4. Nursing Diagnoses
a. Impaired Gas Exchange
b. Ineffective Airway Clearance
c. Risk for Injury
43