FLUIDS AND ELECTROLYTES

Fluids
and
Electrolytes
BY: ROMMEL LUIS C. ISRAEL III
1

HOW IMPORTANT IS WATER?
• Between 50% and 60% of the human body by weight is water
• Water provides a medium for transporting nutrients to cells and
wastes from cells and for transporting substances such as
hormones, enzymes, blood platelets, and red and white blood cells
• Water facilitates cellular metabolism and proper cellular chemical
functioning
• Water acts as a solvent for electrolytes and nonelectrolytes
• Helps maintain normal body temperature
• Facilitates digestion and promotes elimination
• Acts as a tissue lubricant

VARIATIONS IN FLUID CONTENT
BODY FAT
Because fat cells contain little water and lean
tissue is rich in water, the more obese the
person, the smaller the percentage of total
body water compared with body weight.
This is also true between sexes because
females tend to have proportionally more
body fat than males.
There is also an increase in fat cells in older
people

VARIATIONS IN FLUID CONTENT
AGE

AVENUES BY
WHICH
WATER
ENTERS AND
LEAVES THE
BODY

↓Blood
volume
or ↓BP
Volume receptor
Atria and great veins
Hypothalamus
↓
Posterior
pituitary gland
Osmoreceptors in
hypothalamus
↑Osmolarity
↑ADH Kidney
tubules
↑H2O
reabsorption
↑vascular
volume and
↓osmolarity
Narcotics, Stress,
Anesthetic agents, Heat,
Nicotine, Antineoplastic
agents, Surgery
ANTIDIURETIC HORMONE REGULATION MECHANISMS

Juxtaglomerular
cells-kidney
↓Serum Sodium
↓Blood volume
Angiotensin I
Kidney tubules
Angiotensin II
Adrenal Cortex
↑Sodium
resorption
(H2O resorbed
with sodium); ↑
Blood volume
Angiotensinogen in
plasma
RENIN
Angiotensin-
converting
enzyme
ALDOSTERONE
Intestine, sweat
glands, Salivary
glands
Via vasoconstriction of arterial smooth muscle
ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM

Fluid Types
• Fluids in the body
generally aren’t
found in pure
forms
• Isotonic,
hypotonic, and
hypertonic types
• Defined in terms
of the amount of
solute or dissolve
substances in the
solution
• Balancing these
fluids involves the
shifting of fluid
not the solute
involved

Isotonic
Solutions
• No net fluid shifts
occur between
isotonic solutions
because the
solution are equally
concentrated
• Ex. NSS or 0.9SS

Hypotonic
Solutions
• Has a lower solute
concentration than
another solution
• Fluid from the
hypotonic solution
would shift into the
second solution until
the two solutions had
equal concentrations
• Ex. Half normal or
0.45%SS

Hypertonic
Solutions
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Fluid
Movements
• Fluids and solutes constantly
move within the body, which
allows the body to maintain
homeostasis
• Fluids along with nutrients and
waste products constantly shift
within the body’s compartments
from the cell to the interstitial
spaces, to the blood vessels
and back again

Fluid
Moveme
nts
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Assessment
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LABORATORY TESTS FOR
EVALUATING FLUID STATUS
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FLUID BALANCE
• The desirable amount of fluid intake and loss in adults ranges from
1500 to 3500 mL each 24 hours. Ave= 2500 mL
• Normally INTAKE = OUTPUT
FLUID IMBALANCE
• Changes in ECF volume = alterations in sodium balance
• Change in sodium/water ratio = either hypoosmolarity or
hyperosmolarity
• Fluid excess or deficit = loss of fluid balance
• As with all clinical problems, the same pathophysiologic change is
not of equal significance to all people
• For example, consider two persons who have the same viral
syndrome with associated nausea and vomiting

FLUID DEFICIT/HYPOVOLEMIA
• May occur as a result of:
– Reduced fluid intake
– Loss of body fluids
– Sequestration (compartmentalizing) of body fluids
Pathophysiology and Clinical Manifestations
DECREASED FLUID VOLUME
Stimulation of thirst
center in hypothalamus
Person complains of thirst
↑ ADH Secretion
↑ Water resorption
↓ Urine Output
Renin-Angiotensin-
Aldosterone System
Activation
↑ Sodium and
Water Resorption
↑ Urine specific gravity

Pathophysiology and Clinical Manifestations
UNTREATED FLUID VOLUME DEFICIT
Depletion of fluids available
↑ BODY TEMPERATURE
Dry mucous membranes
Difficulty with speech
Cells become unable to continue
providing water to replace ECF
losses
Signs of circulatory collapse
↓ blood pressure
↑ heart rate
↑ respiratory rate
Restlessness and Apprehension

Hypovolemia
• Nursing Intervention
• Monitor fluid intake and output
• Checked daily weight (a 1lb(0.45kg) weight loss equals a 500 ml fluid loss)
• Monitor hemodynamic values such as CVP
• Monitor results of laboratory studies
• Assess level of consciousness
• Administer and monitor I.V. fluids
• Apply and adjust oxygen therapy as ordered
• If patient is bleeding, apply direct continuous pressure to the area and elevate it
if possible
• Assess skin turgor
• Assess oral mucous membranes
• Turn the patient at least every 2 hours to prevent skin breakdown
• Encourage oral fluids

Hypovolemia
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Collaborative Care Management
Identification of vulnerable patients and risk factors:
* Compromised mental state
* Physical limitations
* Disease states
* Limited access to adequate food and fluids
Development of a plan of care
Family members should
be educated about the
importance of fluid and
nutrition intake
Collaboration with the
nurse, patient, family
members, and other
health care providers
for continued
assessment and
treatment of problems
Ongoing assessment and
detailed action plan of
fluid and serum
electrolyte balance.
Factors such as
medications (particularly
diuretics),
hyperventilation, fever,
burns, diarrhea, and
diabetes with
appropriate referral

Collaborative
Care Key
Points
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Fluid
Replacement
Therapy
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Fluid Replacement Therapy
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Composition of Different Intravenous Solution
IVF Dextrose
(g/L)
Na
(meq/L)
Cl
(meq/L)
K
(meq/L)
Lactate
(meq/L)
D5 0.9% NaCl 50 154 154
D5 0.15% NaCl 50 25 25
D5 0.3% NaCl 50 51 51
D5 0.45% NaCl 50 77 77
D5 IMB 50 25 22 20 23
LRS 0 130 109 4 28
NSS 0 154 154
D5LRS 50 130 109 4 28
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ISOTONIC SOLUTION
Facts Examples Uses
-same osmolality as plasma (app.
275 to 295 mOsm/kg)
-vascular space osmolality not
altered by infusion
-expand intracellular and
extracellular space equally;
degree of expansion correlates
with amount of fluid infused
-no solution-related shifting
between ICF and ECF spaces
-cells neither shrink nor swell with
fluid movement
Dextrose 5% in water,
Normal Saline Solution,
Lactated Ringers
Solution
-Fluid loss and dehydration
-Hypernatremia
-Blood transfusion, fluid
challenges, resuscitation,
shock, metabolic alkalosis,
hypercalcemia,
hyponatremia
-Acute blood loss, burns,
dehydration, hypovolemia
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HYPOTONIC SOLUTION
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HYPERTONIC SOLUTION
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FLUID EXCESS/HYPERVOLEMIA
Psychiatric
Disorders, SIADH,
Certain head injuries
Dietary Sodium
Indiscretion
Renal and endocrine
disturbances,
malignancies, adenomas
Overhydration
Excessive Sodium
Intake
Failure of renal or
hormonal regulatory
functions
FLUID VOLUME EXCESS/HYPERVOLEMIA

• Since ECF becomes
hypoosmolar, fluid moves into
the cells to equalize the
concentration on both sides of
the cell membrane
• Thus there, is an increase in
intracellular fluid
• The brain cells are particularly
sensitive to the increase of
intracellular water, the most
common signs of hypoosmolar
overhydration are changes in
mental status. Confusion, ataxia,
and convulsions may also occur.
• Other clinical manifestations
include: hyperventilation, sudden
weight gain, warm, moist skin,
increased ICP: slow bounding
pulse with an increase in systolic
and decrease in diastolic
pressue and peripheral edema,
usually not marked

Hypervolemia
• Evaluating pitting edema
• Press your fingertip firmly into
the patients skin over a bony
surface for a few seconds. Then
note the depth of the imprint
your finger leaves on the skin
• A slight imprint indicates +1
pitting edema
• A deep imprint, with the skin
slow to return to its original
contour, indicates a +4
pitting edema
• When the skin resists
pressure and appears
distended, the condition is
called brawny edema, which
causes the skin to swell so
much that fluid cant be
displaced

Hypervolemia
• Diagnostic Findings:
• Decreased hematocrit resulting from
hemodilution
• Normal serum Na level
• Low serum K and BUN levels
• either due to hemodilution or higher levels
may indicate renal failure
• Low oxygen level
• Abnormal chest x-ray
• Indicates fluid accumulation
• May reveal pulmonary edema or pleural
effusions

Hypervolemia
• Treatment
• Na and fluid intake restriction
• Diuretics to promote excess fluid excretion
• Morphine and nitroglycerin (Nitro-Dur) for
pulmonary edema
• Dilate blood vessels
• Reduce pulmonary congestion and amount
of blood returning to the heart
• Digoxin for heart failure
• Strengthens cardiac contractions

Hypervolemia
• Treatment
• Supportive measures
• Oxygen administration
• Bed rest
• Hemodialysis or continuous renal
replacement therapy for renal
dysfunction

Hypervolemia
• Nursing Interventions
• Monitor fluid intake and output
• Monitor daily weight
• Monitor cardiopulmonary status
• Auscultate breathe sounds
• Assess for complaints of dyspnea
• Monitor chest x-ray results
• Monitor arterial blood gas values
• Assess for peripheral edema
• Inspect the patient for sacral edema
• Monitor infusion of I.V. solutions
• Monitor the effects of prescribed medications

General Information
• Involve destruction of the
epidermis, dermis, or subcutaneous
layers of the skin
• Can be permanently disfiguring and
incapacitating and possibly life-
threatening

General Information
• Associated imbalances result from
alterations in skin integrity and
internal body membranes, and
from effect of heat on body water
and solute loss that may result
from cellular destruction

General Information
•Type and severity of imbalance
depends on burn type and
depth, percentage body
surface area involved and burn
phase

Pathophysiology
•Burn Phase:
–Refer to stages that
describe physiologic
changes occurring
after a burn
Burn phase
Fluid-
accumulation
phase
Fluid-
remobilization
phase
Convalescent
phase

Pathophysiology
Fluid-accumulation phase:
 Last fro 36 to 48 hours after a burn
injury
 Fluid shifts from vascular
compartment to interstitial space –
third-space shift
 Edema caused by shifted fluid,
which typically reaches maximum
within 8 hours after injury
 Circulation possibly compromised
and pulses diminished from severe
edema
Burn phase
Fluid-
accumulation
phase
Fluid-
remobilization
phase
Convalescent
phase

Pathophysiology
• Several reasons for fluid
imbalances during fluid-
accumulation phase
–Damage to capillaries causing
altered vessel permeability
–Diminished kidney perfusion
–Production and release of stress
hormones such as aldosterone
and ADH
Burn phase
Fluid-
accumulation
phase
Fluid-
remobilization
phase
Convalescent
phase

Pathophysiology
Respiratory problems
Muscle and tissue injuries
GI problems
Electrolyte imbalances:
 Common during fluid accumulation
phase due to body’s hypermetabolic
needs and priority that fluid
replacement takes over nutritional
needs during emergency phase
Burn phase
Fluid-
accumulation
phase
Fluid-
remobilization
phase
Convalescent
phase

Pathophysiology
Fluid- remobilization phase :
 Also known as diuresis stage
 Starts about 48 hours after initial
burn
 Fluid shifted back to vascular
compartment
 Edema at burn site decreased, blood
flow to kidneys increased, increased
urine output
 Fluid and electrolyte imbalances can
still occur
Burn phase
Fluid-
accumulation
phase
Fluid-
remobilizatio
n phase
Convalescent
phase

Pathophysiology
Convalescent phase:
 Begins after first two phases has
been resolved
 Characterized by healing or
reconstruction of burn wound
 Major fluid shifts now resolved but
possible further fluid and electrolyte
imbalances exist as a result of
inadequate dietary intake
 Anemia is common – severe burns
typically destroy red blood cells
Burn phase
Fluid-
accumulation
phase
Fluid-
remobilization
phase
Convalescent
phase

Characteristics
• 1. Minor Burns
• Partial thickness burns are no greater than 15% of the
TBSA in the adult
• Full thickness burns are < 2% of the TBSA in the adult
• Burn areas do not involve the eyes, ears, hands, face,
feet, or perineum
• There are no electrical burns or inhalation injuries
• The client is an adult younger than 60 y.o.
• The client has no preexisting medical condition at the
time of the burn injury
• No other injury occurred with the burn

Characteristics
2. Moderate Burns
a. Partial thickness burns are deep and are 15% to 25% of
the TBSA in the adult
b. Full thickness burns are 2% to 10% of the TBSA in the
adult
c. Burn areas do not involve the eyes, ears, hands, face,
feet, or perineum
d. There are no electrical burns or inhalation injuries
e. The client is an adult younger than 60 y.o.
f. The client has no chronic cardiac, pulmonary, or
endocrine disorder at the time of the burn injury
g. No other complicated injury occurred with the burn

Characteristics
3. Major Burns
a. Partial thickness burns are > 25% of the TBSA in the
adult
b. Full thickness burns are > 10% of the TBSA
c. Burn areas involve the eyes, ears, hands, face, feet,
or perineum
d. The burn injury was an electrical or inhalation injury
e. The client is older than 60 y.o.
f. The client has a chronic cardiac, pulmonary, or
metabolic disorder at the time of the burn injury
g. Burns are accompanied by other injuries

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Burn:Classification
Superficial (1°burns)
• Involve only the epidermal layer
of the skin.
• sunburns are commonly first-
degree burns.

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Superficial burn (1° burn)

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• Present of blisters indicates superficial
partial-thickness injury.
• Blister may ↑size because continuous
exudation and collection of tissue fluid.
• Healing phase of partial thickness, itching
and dryness because ↑vascularization of
sebaceous glands, ↓reduction of secretions
and ↑perspiration.
Partial thickness (2°burn)

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Partial thickness (2°burn)

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Burn:Classification
3.Full thickness (third-degree burn)
• Destruction of the epidermis and the entire
dermis, subcutaneous layer, muscle and
bone.
• Nerve ending are destroyed-painless wound.
• Eschar may be formed due to surface
dehydration.
• Black networks of coagulate capillaries may
be seen.
• Need skin grafting because the destroyed
tissue is unable to epithelialize.
• Deep partial-thickness burn may convert to a
full-thickness burn because of infection,
trauma or ↓blood supply.

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Eschar:composed of
denatured protein

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Extent of surface area burned
Rule of nines-An estimated
of the TBSA involved as a
result of a burn.
The rule of nines measures
the percentage of the body
burned by dividing the body
into multiples of nine.
The initial evaluation is made
upon arrival at the hospital.

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Lund and Browder
• More precise method of estimating
• Recognizes that the percentage of BSA of
various anatomic parts.
• By dividing the body into very small areas and
providing an estimate of proportion of BSA
accounted for by such body parts
• Includes, a table indicating the adjustment for
different ages
• Head and trunk represent larger proportions of
body surface in children.

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Age in years 0 1 5 10 15 Adult
A-head (back or
front)
9½ 8
½
6½ 5½ 4½ 3½
B-1 thigh (back or
front)
2¾ 3
¼
4 4¼ 4½ 4¾
C-1 leg (back or
front)
2½ 2
½
2¾ 3 3¼ 3½
Lund and Browder chart

TYPES OF BURNS
Thermal Burns:
caused by exposure to
flames, hot liquids, steam
or hot objects
Chemical Burns:
Caused by tissue contact
with strong alkali, or
organic compounds
Systemic toxicity from
cutaneous absorption
can occur
Radiation Burns:
caused by exposure to
UV light, x-rays, or
radioactive source

TYPES OF
BURNS
• Electrical Burns:
• Caused by heat
generated by electrical energy
as it passes through the body
• Results in internal tissue
damage
• Cutaneous burns cause
muscle and soft tissue damage
that may be extensive,
particularly in high voltage
electrical injuries
• Alternating current is
more dangerous than direct
current because it is associated
with CP arrest, ventricular
fibrillation, tetanic muscle
contractions, and long bone or
vertebral fractures

Potential
Imbalance
• Hypovolemia
• Approximately 10% of plasma
volume lost into tissue soon
after a severe burn
• Occurs because of the third
space shift causes multiple
effects:
• With burn’s damage to the
skin surface, decrease in
skins ability to prevent water
loss; patient can lose up to 8L
of fluid per day (400ml/hour)
• Potential for blood loss,
adding to fluid volume losses

Potential
Imbalance
• Hypervolemia
• Usually develops 3 to 5 days
after a major burn injury
• Occurs during the fluid
remobilization phase, as
fluid shifts from the
interstitial space back to the
vascular compartment
• May be exacerbated by
excessive administration of
I.V. fluids

Potential
Imbalance
•
•
•
•
•

Burns
NURSING PRIORITY:
The client with burn injury
is often awake, mentally alert,
and cooperative at first. The
level of consciousness may
change as respiratory status
change or as the fluid shift
occurs, precipitating
hypovolemia. If the client is
unconscious or confused,
assess him or her for the
possibility of a head injury.

Burns
• Assess for
– Patent airway
– Presence of adequate breath
sounds
– Symptoms of hypoxia
– Pulmonary damage
• Burns around the face, neck,
mouth or in the oral mucosal area
– Circulatory status
• Tachycardia and hypotension
occur early
• Elevate UO

Burns
• Assess for
– GI function – check last
time client ate
– Fluid status
• UO (30 ml/hr)
• Hypotension (< 90/60)
• Confusion /
disorientation
– Circulatory status of
the extremities

Burns
Treatment
 Respiratory status takes priority
over the treatment of the burn
injury
 If burn area is small  cold
compress or immerse in cool
water (not ice) to ↓ heat
 May have ointment on the burn
area
 Analgesics IV, IM, SQ. oral forms
may not be absorbed effectively

Burns
• Nursing intervention
– Maintain patent airway; prevent
hypoxia
– Evaluate fluid status; determine
circulatory status
– Prevent of decrease infection
– Maintain nutrition
– Prevent contractures and
scarring
– Promote acceptance and
adaptation to alterations in body
image

Burns
Formula name Electrolyte-
Containing solution
Colloid-Containing
Solution
Dextrose in
Water
Evans NSS 1 ml/kg/%burn NSS 1 ml/kg/%burn 2000 ml
Brooke LR 1.5 ml/kg/%burn 0.5 ml/kg/%burn 2000 ml
Modified Brooke LR 2 ml/kg/%burn None None
Parkland LR 4 ml/kg/%burn None None
Hypertonic
Saline
Fluid containing 250
mEq of Na/L to
maintain hourly urine
output of 70 ml in
adults
None None
First 24 hours

Burns
Formula name Electrolyte-
Containing solution
Colloid-Containing
Solution
Dextrose in
Water
Evans ½ of first 24-hr
requirement
½ of first 24-hr
requirement
2000 ml
Brooke ½ - ¾ of first 24-hr
requirement
½ - ¾ of first 24-hr
requirement
2000 ml
Modified Brooke None 0.3-0.5 ml/kg/%burn Titrate to
maintain
urine output
Parkland None 0.3-0.5 ml/kg/%burn Titrate to
maintain
urine output
Hypertonic
Saline
Same solution to
maintain hourly urine
output of 30 ml in
adults
None None
Second 24 hours

Considerations
AGE AND GENERAL HEALTH
Mortality rates are higher for children < 4 y.o, particularly
those < 1 y.o., and for clients over the age of 60 years.
Debilitating disorders, such as cardiac, respiratory,
endocrine, and renal d/o, negatively influence the client’s
response to injury and treatment.
Mortality rate is higher when the client has a pre-existing
disorder at the time of the burn injury

Which one is not
a cation?
A. Calcium
B. Magnesium
C. Phosphorous
D. Sodium

Anions
and
Cations
• Anions • Cations
Bicarbonate
Chloride
Phosphorous
Calcium
Magnesium
Potassium
Sodium

Controls and regulates volume of body fluids
Its concentration is the major determinant of
ECF volume
Is the chief electrolyte of ECF
Influence ICF Volume
Participates in the generation and transmission
of nerve impulses
Is an essential electrolyte in the sodium-
potassium pump
RDA: not known precisely. 500 mg
Eliminated primarily by the kidneys, smaller in
feces and perspiration
Salt intake affects sodium concentrations
Sodium is conserved through reabsorption in
the kidneys, a process stimulated by aldosterone
Normal value: 135-145 mEq/L
86

HYPONAT
REMIA
Refers to the serum sodium
concentration less than 135 mEq/L
Common with thiazide diuretic use,
but may also be seen with loop and
potassium-sparing diuretics as well
Occurs with marked sodium restriction,
vomiting and diarrhea, SIADH, etc. The
etiology may be mulfactorial
May also occur postop due to temporary alteration in
hypothalamic function, loss of GI fluids by vomiting or
suction, or hydration with nonelectrolyte solutions
Postoperative hyponatremia is a more serious
complication in premenopausal women. The reasons
behind this is unknown
Therefore monitoring serum levels is critical and careful
assessment for symptoms of hyponatremia is important
for all postoperative patients

PATHOPHYSIOLOGY
OF
HYPONATREMIA
Sodium loss from the intravascular compartment
Diffusion of water into the interstitial spaces
Sodium in the interstitial space is diluted
Decreased osmolarity of ECF
Water moves into the cell as a result of sodium loss
Extracellular compartment is depleted of water
CLINICAL SYMPTOMS

CLINICAL MANIFESTATIONS OF HYPONATREMIA
Muscle
Weakness
APATHY
Postural
hypotension
Nausea and
Abdominal
Cramps
Weight Loss
In severe hyponatremia: mental confusion, delirium, shock and coma

COLLABORATIVE CARE
MANAGEMENT
• General goal: correct sodium imbalance and restore normal fluid and
electrolyte homeostasis
• Recognition of people at risk for hyponatremia is essential for its
prevention: athletes, persons working in hot environments
• Salt is always replaced along with water
• Management includes educating vulnerable people to recognize signs
and symptoms of sodium depletion and maintaining sufficient sodium
and water intake to replace skin and insensible fluid loss
• Generally, an increased sodium and water intake provides adequate
treatment
• Education as the importance of sodium and fluid balance and the
rationale for prescription medications to ensure compliance
• Daily weight. MIO
• Monitoring of sodium levels to determine extent of replacement
• Generally, PNSS or PLRS is prescribed
• Too rapid restoration of sodium balance, hypertonic sodium solutions
may provoke brain injury

HYPERNATREMIA
• A serum sodium level above 145 mEq/L is termed hypernatremia
• May occur as a result of fluid deficit or sodium excess
• Frequently occurs with fluid imbalance
• Develops when an excess of sodium occurs without a
proportional increase in body fluid or when water loss occurs
without proportional loss of sodium
• Risk Factors: excess dietary or parenteral sodium intake, watery
diarrhea, diabetes insipidus, damage to thirst center, those with
physical or mental status compromise, and people with
hypothalamic dysfunction

PATHOPHYSIOLOGY OF
HYPERNATREMIA
Increased Sodium concentration in ECF
Osmolarity rises
Water leaves the cell by osmosis and enters
the the extracellular compartments
Dilution of fluids in ECF Cells are water depleted
Suppression of
aldosterone secretion
Sodium is exreted in the
urine
CLINICAL SYMPTOMS

CLINICAL MANIFESTATIONS
Dry, sticky mucous
membranes
Firm, rubbery
tissue turgor
Manic excitement
Tachycardia
DEATH

COLLABORATIVE CARE
MANAGEMENT
Recognition of risk
factors: bedridden and
debilitated patients,
diabetes insipidus, fluid
deprivation, the elderly
and the very young
A careful and accurate
record of MIO permits
quick recognition of
negative fluid balance
People with kidney
failure, CHF, or increased
aldosterone production
may require dietary
sodium intake restriction
Usually, osmolar balance
can be restored with oral
fluids. If not, the
parenteral route may be
necessary
Fluid resuscitation must
be undertaken with
particular caution in
patients with
compromised cardiac or
renal function
The nurse should closely
monitor the patient’s
response to fluids and
be alert to symptoms of
fluid overload

• Major cation of the ICF. Chief regulator of cellular enzyme activity and
cellular water content
• The more K, the less Na. The less K, the more Na
• Plays a vital role in such processes such as transmission of electrical
impulses, particularly in nerve, heart, skeletal, intestinal and lung tissue;
CHON and CHO metabolism; and cellular building; and maintenance of
cellular metabolism and excitation
• Assists in regulation of acid-base balance by cellular exchange with H
• RDA: not known precisely. 50-100 mEq
• Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges,
prunes, melons, raisins, broccoli, and potatoes, meat, dairy products
• Excreted primarily by the kidneys. No effective conserving mechanism
• Conserved by sodium pump and kidneys when levels are low
• Aldosterone triggers K excretion in urine
• Normal value: 3.5 – 5 mEq/L
95

CAUSES AND EFFECTS OF HYPOKALEMIA
• Known as a low level of serum potassium, less than 3.5 mEq/L
Decreased Intake
↓ Food and Fluids as in
starvation
Failure to replace GI
losses
Increased Loss
↑ Aldosterone
Gastrointestinal losses
Potassium-losing diuretics
Loss from cells as in trauma,
burns
Shift of Potassium
into Cells
(No change in total
body potassium)
HYPOKALEMIA
GI Tract
Anorexia
N&V
Abdominal
distention
CNS
Lethargy,
Diminished
deep-tendon
reflexes,
Confusion,
Mental
depression
Muscles
Weakness,
Flaccid paralysis,
Weakness of
respiratory
muscles,
Respiratory arrest
CV System
Decrease in
standing BP,
Dysrhythmias,
ECG changes,
Myocardial
damage, Cardiac
arrest
Kidneys
↓Capacity to
concentrate
waste, water
loss, thirst,
kidney
damage

PATHOPHYSIOLOGY
OF
HYPOKALEMIA
= Action Potential
Nerve and Muscle Activity
Low
Extracellular
K+
Increase in
resting
membrane
potential
The cell
becomes
less
excitable

Aldosterone is secreted
Sodium is retained in the body through resorption by
the kidney tubules
Potassium is excreted
Use of certain diuretics such as thiazides and furosemide, and
corticosteroids
Increased urinary output
Loss of potassium in urine

COLLABORATIVE CARE
MANAGEMENT
• Being alert to the conditions that cause potassium depletion such as vomiting,
diarrhea and diuretics, by monitoring the patient for early warning signs
• No more than 3 enemas without consulting a physician
• Education about the importance of adequate dietary intake of potassium
• In severe hypokalemia, a patient may die unless potassium is administered
promptly
• The safest way to administer K is orally. When K is given IV, the rate of flow
must be monitored closely and should be diluted. Should not exceed 20 mEq/hr
• If PO, taken with at least ½ glass of water
• Cardiac monitoring is useful
• Potassium sparing diuretics such as triamterene, spironolactone, etc
• Symptoms of K depletion: muscle weakness, anorexia, nausea and vomiting =
appropriate referral

CAUSES AND EFFECTS OF HYPERKALEMIA
• Serum potassium level greater than 5.5 mEq/L
Excess Intake
Dietary intake of excess
of kidney’s ability to
excrete; Excess
parenteral administration
Decreased Loss
Potassium-sparing diuretics;
Renal failure; Adrenal
insufficiency
Shift of Potassium
out of the Cells
Extensive injuries,
crushing injuries,
metabolic acidosis
HYPERKALEMIA
GI Tract
N&V
Diarrhea,
Colic
CNS
Numbness,
paresthesias
Muscles
Early: irritability
Late: weakness
leading to flaccid
paralysis
CV System
Conduction
disturbance,
ventricular
fibrillation,
Cardiac Arrest
Kidneys
Oliguria
leading to
anuria

COLLABORATIVE
CARE
MANAGEMENT
• Patients at risk should be identified: impaired renal
function to avoid OTC, esp. NSAIDS which provoke
hyperkalemia; and salt substitutes that are high in
potassium
• Severity guides therapy
– Mild: Withholding provoking agent (i.e., K supp)
– Severe (>6 mEq/L: cation-exchange resin such as
Kayexalate (act by exchanging the cations in the
resin for the potassium in the intestine 
potassium is then excreted in the stool;
Continuous cardiac monitoring
• Bowel function must be maintained if Kayexelate
therapy is to be effective
• Potassium-wasting diuretics may be prescribed to
promote further potassium loss. Dialysis for
patients with renal failure to eliminate excess
potassium
• Intravenous Ca Gluconate may be prescribed to
counteract the cardiac effects of hyperkalemia
• Insulin infusions and IV NaCO3 may be used to
promote intracellular uptake of K

• Most abundant electrolyte in the body. 99% in bones and teeth
• Close link between calcium and phosphorus. High PO4, Low Ca
• Necessary for nerve impulse transmission and blood clotting and is
also a catalyst for muscle contraction and other cellular activities
• Needed for Vitamin B12 absorption and use
• Necessary for strong bones and teeth and thickness and strength of
cell membranes
• RDA: 1g for adults. Higher for children and pregnant and lactating
women according to body weight, older people, esp. post-menopausal
• Found in milk, cheese, and dried beans; some in meat and vegetables
• Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive
secretions, and perspiration
• Normal value 8.5 – 10.5 mg/dl
102

CAUSES AND EFFECTS OF HYPOCALCEMIA
Decreased
Ionized Ca
Large
tranfusion with
citrated blood
Excess Loss
Kidney Disease
Decrease in GI Tract
and Bone Absorption
↑Magnesium
↑Calcitonin
↓Vitamin D
↓Parathyroid Hormone
HYPOCALCEMIA
Bones
Osteoporosis
leading to
Fractures
CNS
Tingling
↓
convulsions
Other
Abnormal
deposits
of calcium
in body
tissues
Muscles
Muscle spasm
↓
Tetany
Cardiovascular
System
Dysrhythmias
↓
Cardiac arrest
Inadequate
Intake
Dietary Deficit

PATHOPHYSIOLOGY OF HYPOCALCEMIA
•Calcium ions are thought to line the
pores of cell membranes, especially
neurons
•Calcium and Sodium repel each other
•When serum calcium levels are low, this
blocking effect is minimized
•When Sodium moves more easily into
the cell, depolarization takes place more
easily
•This results in increased excitability of
the nervous system leading to muscle
spasm, tingling sensations, and if severe,
convulsions and tetany
•Skeletal, smooth, and cardiac muscle
functions are all affected by
overstimulation
Sodium Calcium

CLINICAL MANIFESTATIONS OF HYPOCALCEMIA
COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE,
FINGERTIPS OR TOES
TREATMENT
PAINFUL MUSCULAR SPASMS (TETANY)
ESPECIALLY OF FEET AND HANDS (CARPOPEDAL
SPASMS), MUSCLE TWITCHING AND CONVULSIONS
MAY FOLLOW

TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY

COLLABORATIVE CARE
MANAGEMENT
• Identify risk factors: Inadequate calcium intake, excess calcium loss, Vitamin D deficiency,
patients with poor diets
• Education about the importance of adequate calcium and Vitamin D intake
• Patients undergoing thyroid, parathyroid, and radical neck surgery are particularly
vulnerable to hypocalcemia secondary to parathyroid hormone deficit
• Monitoring of serum calcium levels and correction of deficits
• Citrate is added to store blood to prevent coagulation.
• Citrate + Transfusion = Citrate+Calcium
• Normally, Liver + Citrate = Quick metabolism
• Preexisting calcium deficit/hepatic dysfunction/large amounts of BT very rapidly =
hypocalcemia
• With acute hypocalcemia, Ca Gluconate is used + Continuous cardiac monitoring
• Mild Hypocalcemia: High calcium diet or oral calcium salts
• If PTH or Vit D Deficiency is the cause: aluminum hydroxide gel is used because when serum
phosphate level rises, calcium level falls
• Complication: Bone demineralization
• Therefore, careful ambulation should be encouraged to minimize bone resorption

HYPERCALCEMIA: Serum concentration > 10mg/dL
Causes and Effects
Loss from bones
Immobilization,
Carcinoma with bone
metastases, Multiple
myeloma
Excess Intake
↑ Calcium diet (esp. milk)
Antacids containing calcium
Increase in factors
Causing Mobilization
from bone
↑PTH, ↑ Vitamin D,
steroid therapy
HYPERCALCEMIA
Kidneys
Stones
↓
Kidney
Damage
CNS
↓Deep-tendon
reflexes
↓
Lethargy
↓
Coma
Bones
Bone pain
↓
Osteoporosis
↓
Fractures
Muscles
Muscle fatigue,
hypotonia
↓
↓ GI motility
CV System
Depressed
activity
↓
Dysrhythmias
↓
Cardiac Arrest

HOW IT
HAPPENS
HYPERCALCEMIA
DEPRESSED NERVE
AND MUSCLE ACTIVITY
DEEP TENDON
REFLEXES MAY BE
DECREASED OR
ABSENT
MYOCARDIAL
FUNCTION IS ALTERED

CLINICAL MANIFESTATIONS OF HYPERCALCEMIA
Decreased GI
Motility
Cardiac Dysrhythmias
Constipation
Nausea
Mental status changes:
lethargy, confusion,
memory loss

CLINICAL MANIFESTATIONS OF HYPERCALCEMIA
Immobilization Bone
Demineralization
Calcium
accumulates in
the ECF and
passes through
the kidneys
Ca Precipitation
Calcium Stones

COLLABORATIVE CARE
MANAGEMENT
• Mild hypercalcemia: hydration and education about avoiding foods
high in calcium or medications that promote calcium elevation
• Ambulation as appropriate; weight-bearing exercises as tolerated
• Trapeze, resistance devices
• Marked hypercalcemia: prevention of pathologic fractures,
individualized plan of care
• Prevention of renal calculi: encourage oral fluids to prevent
concentrated urine: 3000 to 4000 mL/day unless contraindicated
• Acid-ash fruit juices: cranberry juice and prune juice
• Severe hypercalcemia: medical emergency: continuous cardiac
monitoring, hydration, IV furosemide, Calcitonin and/or plicamycin
(mithramycin), q2 serum and urinary electrolytes

• Mostly found within body cells: heart, bone, nerve, and muscle tissues
• Second most important cation in the ICF, 2nd to K+
• Functions: Metabolism of CHO and CHON, protein and DNA synthesis,
DNA and RNA transcription, and translation of RNA, maintains normal
intracellular levels of potassium, helps maintain electric activity in nervous
tissue membranes and muscle membranes
• RDA: about 18-30 mEq; children require larger amounts
• Sources: vegetables, nuts, fish, whole grains, peas, and beans
• Absorbed in the intestines and excreted by the kidneys
• Plasma concentrations of magnesium range from 1.5 – 2.5 mEq/L, with
about one third of that amount bound to plasma proteins
113

HYPOMAGNESEMIA: Serum level < 1.5 mEq/L
• Usually coexists with hypokalemia and less often with hypocalcemia
Decreased Intake
Prolonged
malnutrition,
Starvation
Impaired absorption from GI Tract
Malabsorption syndrome, Alcohol Withdrawal
Syndrome, Hypercalcemia, Diarrhea,
Draining gastrointestinal fistula
Excessive
Excretion
↑Aldosterone,
Conditions
causing large
losses of urine
HYPOMAGNESEMIA
Mental Changes
Agitation,
Depression,
Confusion
CNS
Convulsions,
Paresthesias,
Tremor, Ataxia
Muscles
Cramps,
Spasticity, Tetany
CV System
Tachycardia,
Hypotension,
Dysrhythmias
HYPOKALEMIA

PATHOPHYSIOLOGY OF
HYPOMAGNESEMIA
Low serum magnesium
level
Increased acetylcholine release
Increased neuromuscular irritability
Increased sensitivity to acetylcholine at the myoneural
junction
Diminished threshold of
excitation for the motor nerve
Enhancement of myofibril
contraction

PATHOPHYSIOLOGY OF
HYPOMAGNESEMIA
High Serum Calcium
Increased acetylcholine
release
Increased neuromuscular irritability
Increased sensitivity to acetylcholine at the myoneural
junction
Diminished threshold of
excitation for the motor nerve
Enhancement of myofibril
contraction
High Serum Calcium
Excretion of Magnesium
By the GI tract

PATHOPHYSIOLOGY OF HYPOMAGNESEMIA
MAGNESIUM
INHIBITS TRANSPORT OF PTH
DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED
FROM THE BONE
POSSIBLE CALCIUM DEFICIT

CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA
CONFUSION
DEPRESSION
CRAMPS
TETANY CONVULSIONS

COLLABORATIVE CARE
MANAGEMENT
• Recognition of people at risk: people taking loop diuretics and digoxin
should be encouraged to eat foods rich in magnesium, such as fruits,
vegetables, cereals, and milk
• Recognition of signs and symptoms of magnesium deficiency
• Magnesium is essential for potassium resorption, so if hypokalemia
does not respond to potassium replacement, hypomagnesemia should
be suspected
• Treatment of the underlying cause is the first consideration in
hypomagnesemia
• Severe: parenteral magnesium replacement is indicated
• IV therapy: continuous cardiac monitoring
• Safety measures for patients with mental status changes

HYPER
MAGNE
SEMIA:
Serum
Mg
level
2.5
mEq/L
• Seldom develops in the
presence of normal renal
function
• May occur as a result of Mg
replacement
• May occur when MgSO4 is
administered to prevent
seizures resulting from
eclampsia
• Careful monitoring is
imperative

PATHOPHYSIOLOGY
Renal failure, Excessive IV infusion of
magnesium, Decreased GI elimination and/or
absorption, etc.
Accummulation of Mg in the body
Diminishing of reflexes, drowsiness, lethargy
Mg Level Rises
Severe Respiratory Depression
RESPIRATORY ARREST may occur
Altered Electrical Conduction
Slowed heart
rate and AV
Block
Peripheral
vasodilation
Hypotension, flushing, and
increased skin warmth

COLLABORATIVE CARE
MANAGEMENT
• Identification of patients at risk: those with impaired renal
function to avoid OTC that contain magnesium such as Milk of
Magnesia and some Mg-containing antacids
• Any patient receiving parenteral magnesium therapy should be
assessed frequently for signs of hypermagnesemia
• Mild hypermagnesemia: withholding magnesium-containing
medications may suffice
• Renal failure: dialysis
• Severe: may require treatment with calcium gluconate (10-20
mL of 10% Ca Gluconate administered over 10 minutes)
• If cardiorespiratory collapse is imminent, the patient may
require temporary pacemaker and ventilator support

NURSING
MANAGEMENT
OF PATIENT
WITH FLUID
AND
ELECTROLYTE
IMBALANCES

Parameter_____Fluid Excess___ Fluid Loss/Electrolyte Imbalance____
Behavior Tires easily; Change in behavior, confusion, apathy
Head, neck Facial edema, distended neck Headache, thirst, dry mucous
membranes veins
Upper GI Anorexia, nausea, vomiting
Skin Warm, moist, taut, cool feeling Dry, decreased turgor where
edematous
Respiration Dyspnea, orthopnea, productive Changes in rate and depth of respiration
cough, moist breath sounds
Circulation Loss of sensation in edematous Pulse rate changes, dysrhythmia,
postural areas, pallor, bounding pulse,
increased blood pressure hypotension
Abdomen Increased girth, fluid wave Distention, abdominal cramps
Elimination Constipation Diarrhea, constipation
Extremities Dependent edema, “pitting” Muscle weakness, tingling, tetany ,
discomfort from weight of
bedclothes

Pitting edema
Dependent edema
Refractory Edema

LABORATORY VALUES
FLUID DEFICIT FLUID EXCESS
Hemoconcentration Hemodilution
↑ Hct, BUN, E+ levels ↓ Hct, BUN, E+ levels
↑ Urine Specific Gravity ↓ Urine Specific Gravity

Determined from analysis of patient data
Diagnostic Title Possible Etiologic Factors
1 Deficient fluid volume Active fluid volume loss
(hemorrhage, diarrhea, gastric
intubation, wounds, diaphoresis),
inadequate fluid intake, failure of
regulatory mechanisms,
sequestration of body fluids
2 Excess Fluid Volume Excess fluid intake, excess sodium
intake, compromised regulatory
processes

EXPECTED PATIENT OUTCOMES
1. Will maintain functional fluid volume as evidenced by
adequate urinary output, stable weight, normal vital
signs, normal urine specific gravity, moist mucus
membranes, balanced intake and output, elastic skin turgor,
prompt capillary refill, and absence of edema
2. Will verbalize understanding of treatment plan and
causative factors that led to the imbalance

1,2Intake and Output Monitoring
- Type and amount of fluid the patient has received and the
route by which they were administered
- Record of solid food intake. Gelatin or Popsicles are
recorded as fluids
- Ice chips are recorded by dividing the amount of chips
by ½ (60 mL of chips = 30 mL water)
- Accurate output record and described by color, content,
and odor (Normally, gastric contents are watery and pale
yellow-green; they usually have a sour odor)
- With acid-base balance upset, gastric secretions may
have a fruity odor because of ketone bodies
- Bile: thicker than gastric juice, dark green to brown,
acrid odor, bitter taste when vomiting
- NGT irrigation added to intake
- Stools: difficult to estimate amount; consistency, color,
and number of stools provide a reasonable estimate
- Peritoneal or pleural fluid drainage is recorded as output
as with its amount, color, and clarity
- Character and volume of urine. Place signs and
materials so that an accurate record of UO is maintained

1,2 Intake and Output Monitoring
- Evaluate and refer urine specific gravity as appropriate
(normal value is 1.003 – 1.030). The implications are:
High Dehydration
Low SIADH, overhydration
- Drainage, fluid aspirated from any body cavity must be
measured. With dressings, fluid loss is the difference
between the wet dressings and the dry weight of the
dressing
- Accurate recording of the temperature to help the
physician determine how much fluid should be replaced
1,2 Daily Weight
- Evaluate trends in weight (An increase in 1kg in weight
is equal to the retention of 1L of fluid in an edematous
patient)
Considerations:
- Daily weights early in the morning after voiding
but before he or she has eaten or defecated

1 Replacement of Fluid and Electrolytes
General Principles:
- Either by oral intake (healthiest way), tube feeding,
intravenous infusion, and/or total parenteral nutrition
- Normal saline solution and plain water should also be
given by slow drip to replace daily fluid loss
- IV administration per doctor’s orders
- Fluid replacement considerations:
* Most effective when apportioned over 24 hr period
(Better regulation, ↓potential for calculi formation and
subsequent renal damage, ↓potential for circulatory
overload which may cause in fluid and electrolyte
shifts)
* Administer concentrated solutions of Na, Glucose or
protein because they require body fluids for dilution
* Consider the size of the patient (small adult has less
fluid in each compartment, especially in the
intravascular compartment)
- Promote oral intake as appropriate
* Caution with coffee, tea, and some colas

* small amount at frequent intervals is more useful than a
large amount presented less often
* Always give consideration to cultural and aesthetic
aspects of eating
- Give mouth care to a dehydrated patient before and after meals
and before bedtime (Xerostomia may lead to disruption of t
issues in the oral cavity)
- Avoid irritating foods
- Stimulation of saliva may be aided by hard candy or chewing
gum or carboxymethylcellulose (artificial saliva)
- Keep lips moist and well lubricated
- Give salty broth or soda crackers for sodium replacement and
tea or orange juice for potassium replacement as appropriate.
Bananas, citrus fruits and juices, some fresh vegetables,
coffee, and tea are relatively high in potassium and low in
sodium. Milk, meat, eggs, and nuts are high in protein,
sodium and potassium.
- Offer milk for patients with draining fistulas from any portion of the
GI tract. Lactose intolerance is not necessarily a
contraindication (Lactase enzyme preparations are available)
- Increase usual daily requirement of foods when losses must be
restored, as tolerated

* Patients with cardiac and renal impairments are
instructed to avoid foods containing high levels
of sodium, potassium and bicarbonate
- Administer replacement solutions through tube feeding as is
* Either water, physiologic solution of NaCl, high protein
liquids, or a regular diet can be blended, diluted and
given by gavage
* The water content in the tube feeding needs to be
increased if:
1 the patient complains of thirst
2 the protein or electrolyte content of the tube
feeding is high
3 the patient has fever or disease causing an
increased metabolic rate
4 UO is concentrated
5 signs of water deficit develop
- Administer parenteral fluids as necessary

* Types of solutions
- D5W (hypotonic) is given short-term for hyponatremia
- D5NSS may be given depending on the serum levels of
sodium and vascular volume + KCl to meet normal
intake needs and replace losses for hyponatremia
- Dextrose 5% in 0.2% normal saline is generally used as
a maintenance fluid
- Dextrose 5% in ½ normal saline is generally used as a
replacement solution for losses caused by
gastrointestinal drainage
- PNSS is given primarily when large amounts of sodium
have been lost and for patients with hyponatremia
- LRS is also isotonic because it remains in the
extracellular space
- Fructose or 10-20% glucose in distilled water are
hypertonic solutions and may partially meet body
needs for CHOs
- Dextran (commonly-used plasma expander) increases
plasma volume by increasing oncotic pressure. May
cause prolonged bleeding time and is CI in patients
with renal failure, bleeding disorders, or severe CHF

* Administration
- The rate should be regulated according to the patient’s
needs and condition per doctor’s orders
- Monitor UO carefully. Refer marked decreases!
- Verify orders for potassium administration in patients
with renal failure and untreated adrenal insufficiency
- Usual rate for fluid loss replacement: 3ml/min
- Recognize signs of pulmonary edema (bounding pulse,
engorged peripheral veins, hoarseness, dyspnea,
cough, and rales) that can result from ↑IV rate
- If infiltration occurs, the infusion should be stopped
immediately and relocated. Peripheral IV sites are
generally rotated every 72 hours
- For dextran and other plasma expanders, observe for
anaphylactic reaction (apprehension, dyspnea,
wheezing, tightness of chest, angioedema,
itching, hives and hypotension). If this happens,
switch infusion to nonprotein solution and run at KVO
rate, notify physician and monitor VS
- Pronounced and continued thirst despite administration
of fluids is not normal and should be reported (may
indicate DM or hypercalcemia)

* Patient/Family Education
- Include the signs and symptoms of water excess in
discharge instructions
- With drug therapy, instruct patient and family regarding
correct method of administration, correct dose, and
therapeutic and adverse effects
- Instruct to read labels for nutritional content
* For K restriction: avoid organ meats, fresh and dried
fruits, and salt substitutes
- Skin assessment and care, positioning techniques for
patients with mobility restrictions

* Achievement of outcomes is successful in disturbances in fluid
and electrolyte balance:
1 Maintains functional fluid volume level with adequate UO,
VS within the patient’s normal limits, sp gr of urine
within 1.003-1.035, moist mucous membranes, stable
weight, Intake=output, elastic skin turgor, and no edema
2 States possible causes of imbalance and plan to prevent
recurrence of imbalances
3 Reports a decrease or absence of symptoms causing
discomfort

Fluids and Electrolytes
Acid-base
balance

DRAWING ARTERIAL BLOOD GASES
ALLEN’S TEST
ARTERIAL PUNCTURE

BASIC REGULATION OF ACID-BASE BALANCE
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3
The lungs help control acid-base balance by blowing off or
retaining CO2. The kidneys help regulate acid-base balance by
excreting or retaining HCO3

TYPES OF ACID-BASE DISTURBANCES
Depression of the central
nervous system, as
evidenced by disorientation
followed by coma
Overexcitability of the
nervous system; muscles
may go into a state of tetany
and convulsioons

RESPIRATORY ACIDOSIS: CARBONIC ACID EXCESS
Damage to the respiratory center in the medulla, drug or narcotic use, obstruction
of respiratory passages, respiratory and respiratory muscle disorders
Decrease in the rate of pulmonary ventilation
Increase in the concentration of CO2, carbonic acid,
and hydrogen ions
RESPIRATORY ACIDOSIS
Potassium moves out of the cells
HYPERKALEMIA
VENTRICULAR FIBRILLATION

NURSING MANAGEMENT OF
ASSESSMENT
* Health Hx: complaints of headache, confusion, lethargy,
nausea, irritability, nausea, irritability, anxiety, dyspnea, and
blurred vision, preexisting conditions
* Physical Examination: lethargy to stupor to coma, tachycardia,
hypertension, cardiac dysrhythmias, airway patency
NURSING DIAGNOSES include but are not limited to:
• Diagnostic Title Possible Etiologic Factors
1 Impaired gas exchange Hypoventilation
2 Disturbed thought processes Central nervous system depression
3 Anxiety Hypoxia, hospitalization
4 Risk for ineffective family Illness of a family member
coping
5 Ineffective airway clearance Hypoventilation, secretions
6 Ineffective breathing pattern Hypoventilation, dyspnea

NURSING MANAGEMENT OF
EXPECTED PATIENT OUTCOMES include but are not limited to:
1 Will maintain airway patency and adequate breathing
rate and rhythm will return of ABGs to patient’s
normal level
2 Will be alert and oriented to time, place, and person,
or to his or her normal baseline level of
consciousness
3 Will cope with anxiety
4 Will exhibit effective coping and awareness of
effective support systems
5 Will have secretions that are normal for self in amount
and can be raised
6 Will maintain adequate rate and depth of respirations
using pursed lip and other breathing
techniques when necessary (as in the patient
with COPD)

NURSING MANAGEMENT OF PATIENT
WITH RESPIRATORY ACIDOSIS
INTERVENTIONS
1 Supporting effective gas exchange
- Provide a position of comfort to allow ease of
respiration
- Obtain and monitor ABG results and VS. Refer
accordingly
- Provide and monitor supplemental oxygen as
ordered
- Turn the patient q2 and PRN
- Provide pulmonary hygiene PRN
- Maintain adequate hydration
- Provide comfort measures such as mouth care
- Assist with ADLs
- Instruct patient regarding coughing and deep
breathing and management of disease condition,
especially COPD
2 Coping with disturbed thought processes
- Do frequent neurologic assessments
- Monitor and document person’s baseline LOC
frequently

NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
- Reorient as necessary by providing calendars, clocks, etc.
3 Relieving anxiety
- Provide a calm, relaxed environment
- Give clear, concise explanations of treatment plans
- Encourage expression of feelings
- Provide support and information to patient and family
- Teach relaxation techniques
- Assist the patient to identify coping mechanisms to deal with
anxiety and stress
4 Enhancing coping mechanisms
- Provide support and information to family members about the
patient’s ongoing condition
- Reassure them that there is a physiologic cause for the
patient’s behavior

- Encourage questions and open communication
5 Promote airway clearance
- Implement regular breathing and coughing exercises
- Do suctioning as necessary
- Maintain good hydration
- Do chest physiotherapy as appropriate
6 Promoting an effective breathing pattern
- Maintain alveolar ventilation
- Teach the patient proper breathing techniques as well as panic
control breathing

EVALUATION. Achievement of outcomes is successful when the patient:
1a. Demonstrates improved ventilation and oxygenation
1b Has vital signs, ABGs, and cardiac rhythm within own normal
range
2 Returns to baseline LOC
3 Reports reduced anxiety
4 Family uses adequate coping mechanisms
5 Is able to raise secretions on own
6 Demonstrate effective breathing techniques

RESPIRATORY ALKALOSIS: CARBONIC ACID DEFICIT
Anxiety, hysteria, fever, hypoxia, pain, pulmonary disorders, lesions
affecting the respiratory center in the medulla, brain tumor,
encephalitis, meningitis, hyperthyroidism, gram-negative sepsis
Hyperventilation: Excessive pulmonary ventilation
Decrease in hydrogen ion concentration
RESPIRATORY ALKALOSIS

NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS
ASSESSMENT
* Health Hx: anxiety, shortness of breath, muscle cramps or
weakness, palpitations, panic, dyspnea
* Physical Examination: light-headedness, confusion as a
result of cerebral hypoxia, hyperventilation, tachycardia
or arrhythmia, muscle weakness, (+) Chvostek’s sign or
Trousseau’s sign indicating a low ionized serum calcium
level secondary to hyperventilation and alkalosis,
hyperactive deep tendon reflexes, unsteady gait, muscle
spasms to tetany, agitation, psychosis, seizures in
extreme cases, decreased potassium levels
1 Anxiety Stress, fear
2 Ineffective breathing pattern Hyperventilation, anxiety
3 Disturbed thought processes CNS excitability; irritability
4 Risk for injury Change in LOC, and potential for
seizures

NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS
1 Will report decreased anxiety; verbalizes methods to
cope with anxiety
2 Will return to normal respiratory rate and rhythm or at
least decreased hyperventilation, with return to
baseline ABGs
3 Will exhibit reorientation to person, place, and time as
per patient’s baseline
4 Will be free from injury
INTERVENTIONS
1 Allay anxiety
- Give antianxiety medications as
ordered
- Have patient breath into a paper bag
- Teach relaxation techniques when initial
anxiety attack is over

INTERVENTIONS
2 Promoting an Effective Breathing Pattern
- Encourage the patient to slow his or her RR
- Maintain a calm and comforting attitude
- Position the patient to promote maximal ease of
inspiration
- Assist the patient with relaxation techniques
3 Coping with Disturbed Thought Processes
- Do frequent reorientation
- Encourage family to participate in patient’s care
- Use simple, direct statements or directions
- Allow the patient adequate time to respond
4 Preventing injuries
- Perform neurologic assessment frequently and
document
- Institute safety and seizure precautions
- Assess frequently for muscle strength and
coordination

EVALUATION. Achievement of outcomes is successful when the patient:
1 Reports reduction in anxiety levels
2a Demonstrates effective normal breathing patterns
2b Has ABG results within patient’s normal baseline
3 Returns to normal baseline LOC and orientation level
4 Remains free from injury; no seizure activity

METABOLIC ACIDOSIS: BICARBONATE DEFICIT
Increased acid production, uncontrolled diabetes mellitus,
alcoholism, starvation, renal acidosis, lactic acidosis, increased acid
ingestion, ethanol, salicylates, loss of bicarbonate, severe diarrhea,
intestinal fistulas, adrenal insufficiency, hypoparathyroidism
Excess organic acids are added to body fluids or
bicarbonate is lost
Decrease in bicarbonate concentration
METABOLIC ACIDOSIS

NURSING MANAGEMENT OF METABOLIC ACIDOSIS
ASSESSMENT
* Health Hx: anorexia, nausea, vomiting, abdominal pain,
headache, thirst if the patient is dehydrated
* Physical Examination: confusion, hyperventilation, warm,
flushed skin, bradycardia and other dysrhythmias,
decreasing LOC, nausea, vomiting, diarrhea, Kussmaul
respirations, and acetone breath, especially if acidosis is
due to ketoacidosis. Symptoms may progress to coma if
untreated
1 Disturbed thought processes Secondary to CNS depression
2 Decreased cardiac output Dysrhythmias
3 Risk for injury Secondary to altered mental state
4 Risk for imbalanced fluid Diarrhea, renal failure
volume

NURSING MANAGEMENT OF METABOLIC ACIDOSIS
1 Will return to usual baseline LOC
2 Will return to normal baseline parameters for vital
signs with improved CO and decreased or resolved
dysrhythmias
3 Will remain in a safe, secure environment without
injury
4 Will maintain fluid and electrolyte balance and stable
renal status
INTERVENTIONS
- Monitor LOC and reorient as necessary
- Monitor VS, esp. RRR, BP, and T
- Monitor ABGs to assess the effects of
treatment

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS
2 Supporting cardiac output
- Monitor VS, MIO, and fluid and electrolyte
balance
- Institute cardiac monitoring to evaluate
cardiac status
3 Promoting safety
- Provide a safe, secure and monitored
environment
- Institute safety precautions
4 Promoting return of fluid and electrolyte balance
- Monitor MIO
- Administer medications per medical order

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS
EVALUATION. Achievement of outcomes is successful when the
patient:
1 Exhibits baseline-level consciousness and orientation
2 Returns to normal baseline parameters for vital signs and
Cardiac Output with cardiac dysrhythmias resolved
3 Remains free from injury
4 Maintains fluid and electrolyte balance and stable renal function

METABOLIC ALKALOSIS: BICARBONATE EXCESS
Loss of stomach acid, gastric suctioning, persistent vomiting, excess
alkali intake, intestinal fistulas, hypokalemia, Cushing’s syndrome or
aldosteronism, potassium-diuretic therapy
Excessive amounts of acid substance and
hydrogen ions are lost from the body or large
amounts of bicarbonate or lactate are added orally
or IV
Excess of base elements
METABOLIC ALKALOSIS

NURSING MANAGEMENT OF METABOLIC ALKALOSIS
ASSESSMENT
* Health Hx: Prolonged vomiting or nasogastric suctioning,
frequent self-induced vomiting, muscle weakness, light-
headedness, ingestion of large amounts of licorice or
antacids, use of diuretics, muscle cramping, twitching, or
tingling
* Physical Examination: mental confusion, dizziness, changes in
LOC, hyperreflexia, tetany, dysrhthmias, seizurees, respiratory
failure, positive Chvostek’s or Trosseau’s sign if the patient has
a low ionized serum calcium level, decreased hand grasps,
generalized muscle weakness, decreased serum calcium or
potassium level, impaired concentration, seizures, ECG changes
consistent with hypokalemia
1 Disturbed thought processes CNS excitation
2 Decreased cardiac output Dysrhythmias and electrolyte
imbalances
3 Risk for injury Muscle weakness, tetany,
confusion and possible seizures
4 Risk for imbalanced fluid volume Nasogastric drainage, diuretic
therapy volume

NURSING MANAGEMENT OF METABOLIC ALKALOSIS
1 Will return to usual baseline LOC and orientation
2 Will return to normal baseline parameters for vital
signs with improved CO with resolution of electrolyte
imbalances and decreased or resolved cardiac
dysrhythmias
3 Will remain in a safe, secure environment without
injury
4 Will maintain fluid and electrolyte balance
INTERVENTIONS
- Monitor LOC and reorient as necessary
- Monitor VS, esp. RRR, BP, and T
- Monitor ABGs to assess the effects of
treatment
- Institute cardiac monitoring as ordered

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS
2 Supporting cardiac output
- Monitor VS, MIO, and fluid and electrolyte
balance
- Institute cardiac monitoring to evaluate
cardiac status
3 Promoting safety
- Provide a safe, secure and monitored
environment
- Institute safety precautions
4 Promoting return of fluid and electrolyte balance
- Monitor MIO
- Administer medications per medical order

NURSING MANAGEMENT OF PATIENT WITH METABOLIC
ALKALOSIS
EVALUATION. Achievement of outcomes is successful when the
patient:
1 Manifests mental status has returned to baseline
2 Is free from cardiac dysrhythmias
3 Remains free from injury
4 Maintains fluid balance at baseline level

CRITICAL THINKING EXERCISES
A 32-year-old administrative assistant comes to the urgent care
center with a 72-hour history of vomiting secondary to influenza.
She is lethargic and states, “My muscles are twitching.” Her RR is
18/min and HR is 110 bpm, T=100.4F. Her blood pressure is 110/68
which she states “is about normal for me.” Her ABG values are as
follows:
pH: 7.57
PaO2: 92
PaCO2: 41
HCO3: 36
Describe her acid-base status, probable cause for the imbalance
and treatment

FLUIDS AND ELECTROLYTES

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