Fluids and Electrolytes

FluidsFluids
andand
ElectrolytesElectrolytes
Ma. Tosca Cybil A. Torres, RN

OBJECTIVESOBJECTIVES
After this lecture/discussion, the learner should be able to:After this lecture/discussion, the learner should be able to:
1.1. Describe the mechanisms that maintain fluid, electrolyteDescribe the mechanisms that maintain fluid, electrolyte andand
acid-base balance.acid-base balance.
2.2. Compare the mechanisms and effects of fluid deficit andCompare the mechanisms and effects of fluid deficit and
excess.excess.
3.3. Discuss the mechanisms and effects of deficits and excess.Discuss the mechanisms and effects of deficits and excess.
4.4. Describe the mechanisms that maintain acid-base balance.Describe the mechanisms that maintain acid-base balance.
5.5. Differentiate between metabolic and respiratory acidosis andDifferentiate between metabolic and respiratory acidosis and
alkalosis.alkalosis.
6.6. Apply the pathophysiologic principles of acid-base balance toApply the pathophysiologic principles of acid-base balance to
the interpretation of ABG measurements.the interpretation of ABG measurements.
7.7. Analyze the components of ABGs to identify the type of acid-Analyze the components of ABGs to identify the type of acid-
base balance.base balance.
8.8. Describe the causes and effects of each type of acid-baseDescribe the causes and effects of each type of acid-base
balance.balance.
9.9. Use ABG findings in formulating the care of the patient with anUse ABG findings in formulating the care of the patient with an
acid-base imbalance.acid-base imbalance.
10.10. Describe the management of patients with a fluid, electrolyte, orDescribe the management of patients with a fluid, electrolyte, or
acid-base imbalance.acid-base imbalance.

HOW IMPORTANT IS WATER?HOW IMPORTANT IS WATER?
• Between 50% and 60% of the humanBetween 50% and 60% of the human
body by weight is waterbody by weight is water
• Water provides a medium forWater provides a medium for
transporting nutrients to cells and wastestransporting nutrients to cells and wastes
from cells and for transportingfrom cells and for transporting
substances such as hormones, enzymes,substances such as hormones, enzymes,
blood platelets, and red and white bloodblood platelets, and red and white blood
cellscells
• Water facilitates cellular metabolism andWater facilitates cellular metabolism and
proper cellular chemical functioningproper cellular chemical functioning
• Water acts as a solvent for electrolytesWater acts as a solvent for electrolytes
and nonelectrolytesand nonelectrolytes
• Helps maintain normal body temperatureHelps maintain normal body temperature
• Facilitates digestion and promotesFacilitates digestion and promotes
eliminationelimination
• Acts as a tissue lubricantActs as a tissue lubricant

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

VARIATIONS IN FLUID CONTENTVARIATIONS IN FLUID CONTENT
AGEAGE

AVENUES BY WHICH WATERAVENUES BY WHICH WATER
ENTERS AND LEAVES THE BODYENTERS 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 MECHANISMSANTIDIURETIC 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-Angiotensin-
convertingconverting
enzymeenzyme
ALDOSTERONE
Intestine, sweat
glands, Salivary
glands
Via vasoconstriction of arterial smooth muscle
ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEMALDOSTERONE-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
• Has a higher solute
concentration than
another solution
• Fluid from the second
solution would shift
into the hypertonic
solution until the two
solutions had equal
concentrations
• Ex. D5NSS

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 Movements
• Types of Transport
–A. Active transport
–B. Passive transport
• Diffusion
• Osmosis
• Filtration

Assessment• CLINICAL MEASUREMENT
– Daily weights
• Each kg = 1 L of fluid
• To gain accuracy:
– Balance the scale before each use and weigh the client;
» At same time each day before breakfast after the first void
» Wear the same or similar clothing
» On the same scale
– Vital signs
• Tachycardia – first sign of hypovolemia
– Fluid I & O
• Oral fluids
• Ice chips
• Foods that tend to become fluid at room temperature
• Tube feedings
• Parenteral fluids
• IV meds
• Catheter or tube irrigant
• Urinary output – if with diaper, 1 g = 1 mL
• Vomitus or liquid feces
• Diaphoresis
• Tube drainage
• Wound dressing or wound fistula

LABORATORY TESTS FOR EVALUATING
FLUID STATUS
• Osmolality – measures the solute concentration per
kilogram in blood and urine.
• Osmolarity – concentration of solution per liter.
• BUN – (10-20 mg/dL)made up of urea, an end product of
protein metabolism by the liver.
• Creatinine (0.7 to 1.5 mg/dL)- end product of muscle
metabolism
• Serum electrolytes
• CBC

Diagnosis
• Fluid volume deficit
• High risk for Fluid volume deficit
• Fluid volume excess
• Altered oral mucous membrane

FLUID BALANCEFLUID 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 IMBALANCEFLUID 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/HYPOVOLEMIAFLUID DEFICIT/HYPOVOLEMIA
• May occur as a result of:May occur as a result of:
– Reduced fluid intakeReduced fluid intake
– Loss of body fluidsLoss of body fluids
– Sequestration (compartmentalizing) of body fluidsSequestration (compartmentalizing) of body fluids
Pathophysiology and Clinical ManifestationsPathophysiology and Clinical Manifestations
DECREASED FLUID VOLUMEDECREASED FLUID VOLUME
Stimulation of thirstStimulation of thirst
center in hypothalamuscenter in hypothalamus
Person complains of thirstPerson complains of thirst
↑↑ ADH SecretionADH Secretion
↑↑ Water resorptionWater resorption
↓↓ Urine OutputUrine Output
Renin-Angiotensin-Renin-Angiotensin-
Aldosterone SystemAldosterone System
ActivationActivation
↑↑ Sodium andSodium and
Water ResorptionWater Resorption
↑↑ Urine specific gravityUrine specific gravity

Pathophysiology and Clinical ManifestationsPathophysiology and Clinical Manifestations
UNTREATED FLUID VOLUME DEFICITUNTREATED FLUID VOLUME DEFICIT
Depletion of fluids availableDepletion of fluids available
↑↑ BODY TEMPERATUREBODY TEMPERATURE
Dry mucous membranesDry mucous membranes
Difficulty with speechDifficulty with speech
Cells become unable to continueCells become unable to continue
providing water to replace ECFproviding water to replace ECF
losseslosses
Signs of circulatory collapseSigns of circulatory collapse
↓↓ blood pressureblood pressure
↑↑ heart rateheart rate
↑↑ respiratory raterespiratory rate
Restlessness and ApprehensionRestlessness 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
• Warning Signs
– Cool pale skin over the arms and legs
– Decreased central venous pressure
– Delayed capillary refill
– Deterioration in mental status flat jugular veins
– Orthostatic hypotension
– Tachycardia
– Urine output initially more than 30ml/min, then dropping below
10ml/hour
– Weak or absent peripheral pulses
– Weight loss

Collaborative Care ManagementCollaborative Care Management
Identification of vulnerable patients and risk factors:Identification of vulnerable patients and risk factors:
* Compromised mental state* Compromised mental state
* Physical limitations* Physical limitations
* Disease states* Disease states
* Limited access to adequate food and fluids* Limited access to adequate food and fluids
Development of a plan of careDevelopment of a plan of care
Family members shouldFamily members should
be educated about thebe educated about the
importance of fluid andimportance of fluid and
nutrition intakenutrition intake
Collaboration with theCollaboration with the
nurse, patient, familynurse, patient, family
members, and othermembers, and other
health care providershealth care providers
for continuedfor continued
assessment andassessment and
treatment of problemstreatment of problems
Ongoing assessment andOngoing assessment and
detailed action plan ofdetailed action plan of
fluid and serumfluid and serum
electrolyte balance.electrolyte balance.
Factors such asFactors such as
medications (particularlymedications (particularly
diuretics),diuretics),
hyperventilation, fever,hyperventilation, fever,
burns, diarrhea, andburns, diarrhea, and
diabetes withdiabetes with
appropriate referralappropriate referral

Collaborative Care Key PointsCollaborative Care Key Points
• 1 Liter of water = 1 kg of water by weight1 Liter of water = 1 kg of water by weight
• Fluid replacement are calculated according to this ratio plus 1.5 L toFluid replacement are calculated according to this ratio plus 1.5 L to
fulfill the current daily needsfulfill the current daily needs
• For example, JUAN, a one-year-old, lost 1 kg of water from diarrhea asFor example, JUAN, a one-year-old, lost 1 kg of water from diarrhea as
weighed from his diaper over the last 24 hours. Therefore, since 1weighed from his diaper over the last 24 hours. Therefore, since 1
kg=1 L, fluid replacement therapy for him will involve 1 L of fluids +kg=1 L, fluid replacement therapy for him will involve 1 L of fluids +
1500 L.1500 L.
• Oral fluid resuscitation is preferable but if the patient is unable toOral fluid resuscitation is preferable but if the patient is unable to
tolerate fluids, IV Therapy may be orderedtolerate fluids, IV Therapy may be ordered
• Vital signs should be assessed regularlyVital signs should be assessed regularly
• Postural hypotension is common for postural persons with fluidPostural hypotension is common for postural persons with fluid
volume deficit. How do we assess this?volume deficit. How do we assess this?
• For example, in the care of LOIDA, a 31 year old with severe DHN, youFor example, in the care of LOIDA, a 31 year old with severe DHN, you
take her blood pressure (130/80) and pulse (75) while she’s lyingtake her blood pressure (130/80) and pulse (75) while she’s lying
down. Then you ask her to sit at the edge of bed. When you take herdown. Then you ask her to sit at the edge of bed. When you take her
blood pressure again, you get 115/80 and when you take her pulse,blood pressure again, you get 115/80 and when you take her pulse,
you get 80. This is consistent with intravascular volume depletion.you get 80. This is consistent with intravascular volume depletion.
• Daily weighing is also useful to monitor fluid and electrolyte balanceDaily weighing is also useful to monitor fluid and electrolyte balance
• Laboratory results should be reviewed for various fluid and electrolyteLaboratory results should be reviewed for various fluid and electrolyte
disturbances so that appropriate adjustments to therapy can bedisturbances so that appropriate adjustments to therapy can be
initiatedinitiated

Fluid Replacement Therapy
• Aimed at restoring and maintaining homeostasis
• Methods:
– Oral and gastric feeding
– Parenteral therapy
• Choice of therapy affected by several factors
– Type and severity of imbalance
– Patient’s overall health status, age, renal and
cardiovascular status
– Usual maintenance requirements

Advantages
– Provides the patient with life-sustaining
fluids, electrolytes, and drugs
– Immediate and predictable therapeutic
effects
– Preferred for administering fluids,
electrolytes, and drugs in emergency
situations
– Allows fluid intake when a patient has GI
malabsorption
– Permits accurate dosage titration for
analgesics and other drugs

Disadvantages
– Solution incompatibility
– Adverse reactions
– Infection

Administration routes
– Oral route : oral ingestion of fluids and electrolytes as
liquids or solids administered directly into the GI tract
– Nasogastric route: instillation of fluids and electrolytes
through feeding tubes, such as NG, gastrostomy and
jejunostomy tubes
– I.V. route: administration of fluids and electrolytes
directly into the bloodstream using continuous
infusion, bolus, or I.V. push injection through peripheral
or central venous site

Which among the following IV
solutions contains the highest
potassium content?
A. D5 IMB
B. Lactated Ringer's Solution
C. D5 LRS
D. D5 0.3 NaCl

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

ISOTONIC SOLUTION
FactsFacts ExamplesExamples UsesUses
-same osmolality as plasma-same osmolality as plasma
(app. 275 to 295 mOsm/kg)(app. 275 to 295 mOsm/kg)
-vascular space osmolality not-vascular space osmolality not
altered by infusionaltered by infusion
-expand intracellular and-expand intracellular and
extracellular space equally;extracellular space equally;
degree of expansion correlatesdegree of expansion correlates
with amount of fluid infusedwith amount of fluid infused
-no solution-related shifting-no solution-related shifting
between ICF and ECF spacesbetween ICF and ECF spaces
-cells neither shrink nor swell-cells neither shrink nor swell
with fluid movementwith fluid movement
Dextrose 5% inDextrose 5% in
water,water,
Normal SalineNormal Saline
Solution,Solution,
Lactated RingersLactated Ringers
SolutionSolution
-Fluid loss andFluid loss and
dehydrationdehydration
-HypernatremiaHypernatremia
-Blood transfusion,Blood transfusion,
fluid challenges,fluid challenges,
resuscitation, shock,resuscitation, shock,
metabolic alkalosis,metabolic alkalosis,
hypercalcemia,hypercalcemia,
hyponatremiahyponatremia
-Acute blood loss,Acute blood loss,
burns, dehydration,burns, dehydration,
hypovolemiahypovolemia

HYPOTONIC SOLUTION

HYPERTONIC SOLUTION

FLUID EXCESS/HYPERVOLEMIAFLUID EXCESS/HYPERVOLEMIA
PsychiatricPsychiatric
Disorders, SIADH,Disorders, SIADH,
Certain head injuriesCertain head injuries
Dietary SodiumDietary Sodium
IndiscretionIndiscretion
Renal and endocrineRenal and endocrine
disturbances,disturbances,
malignancies, adenomasmalignancies, adenomas
OverhydrationOverhydration
Excessive SodiumExcessive Sodium
IntakeIntake
Failure of renal orFailure of renal or
hormonal regulatoryhormonal regulatory
functionsfunctions
FLUID VOLUME EXCESS/HYPERVOLEMIAFLUID VOLUME EXCESS/HYPERVOLEMIA

• Since ECF becomes hypoosmolar, fluid moves into the cells to equalizeSince ECF becomes hypoosmolar, fluid moves into the cells to equalize
the concentration on both sides of the cell membranethe concentration on both sides of the cell membrane
• Thus there, is an increase in intracellular fluidThus there, is an increase in intracellular fluid
• The brain cells are particularly sensitive to the increase ofThe brain cells are particularly sensitive to the increase of
intracellular water, the most common signs of hypoosmolarintracellular water, the most common signs of hypoosmolar
overhydration are changes in mental status. Confusion, ataxia, andoverhydration are changes in mental status. Confusion, ataxia, and
convulsions may also occur.convulsions may also occur.
• Other clinical manifestations include: hyperventilation, sudden weightOther clinical manifestations include: hyperventilation, sudden weight
gain, warm, moist skin, increased ICP: slow bounding pulse with angain, warm, moist skin, increased ICP: slow bounding pulse with an
increase in systolic and decrease in diastolic pressue and peripheralincrease in systolic and decrease in diastolic pressue and peripheral
edema, usually not markededema, 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-
remobilization
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
a. Partial thickness burns are no greater than 15% of the
TBSA in the adult
b. Full thickness burns are < 2% 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 preexisting medical condition at the
time of the burn injury
g. 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

Assessment of Burn Injury
Takes several weeks to heal.
Scarring may occur.
Takes several weeks to heal.
Scarring may occur.
Superficial:
Pink or red; blisters form (vesicles);
weeping, edematous, elastic.
Superficial layers of skin are
destroyed; wound moist and painful.
Deep dermal:
Mottled white and red: edematous
reddened areas blanch on pressure.
May be yellowish but soft and elastic
– may or may not be sensitive to
touch; sensitive to cold air.
Hair does not pull out easily
Second
degree
In about 5 days, epidermis peels, heals
spontaneously.
Itching and pink skin persist for about a
week.
No scarring.
Heals spont. If it does not become
infected w/in 10 days - 2 weeks.
Pink to red: slight edema, which
subsides quickly.
Pain may last up to 48 hours.
Relieved by cooling.
Sunburn is a typical example.
First Degree
Reparative ProcessAssessment of ExtentExtent / Degree

Eschar must be removed. Granulation
tissue forms to nearest epithelium from
wound margins or support graft.
For areas larger than 3-5 cm, grafting is
required.
Expect scarring and loss of skin
function.
Area requires debridement, formation
of granulation tissue, and grafting.
Destruction of epithelial cells –
epidermis and dermis destroyed
Reddened areas do not blanch with
pressure.
Not painful; inelastic; coloration
varies from waxy white to brown;
leathery devitalized tissue is called
eschar.
Destruction of epithelium, fat,
muscles, and bone.
Third degree
Reparative ProcessAssessment of ExtentExtent / Degree
Assessment of Burn Injury

59
Burn:Classification
Superficial (1° burns)
• Involve only the epidermal layer of the skin.
• sunburns are commonly first-degree burns.

61
Superficial burn (1° burn)

62
• 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)

64
Partial thickness (2°burn)

65
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.

67
Eschar:composed of
denatured protein

69
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.

70
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.

72
Age in yearsAge in years 00 11 55 1010 1515 AdultAdult
A-head (back orA-head (back or
front)front)
9½9½ 88
½½
6½6½ 5½5½ 4½4½ 3½3½
B-1 thigh (back orB-1 thigh (back or
front)front)
2¾2¾ 33
¼¼
44 4¼4¼ 4½4½ 4¾4¾
C-1 leg (back orC-1 leg (back or
front)front)
2½2½ 22
½½
2¾2¾ 33 3¼3¼ 3½3½
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
• Hyperkalemia / Hypokalemia
• Hypocalcemia
• Hyponatremia / Hypernatremia
• Metabolic acidosis
• Respiratory acidosis

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 icenot 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

WHAT DO ELECTROLYTES DO?WHAT DO ELECTROLYTES DO?

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

HYPONATREMIAHYPONATREMIA
• 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 HYPONATREMIAPATHOPHYSIOLOGY OF HYPONATREMIA
Sodium loss from the intravascular compartmentSodium loss from the intravascular compartment
Diffusion of water into the interstitial spacesDiffusion of water into the interstitial spaces
Sodium in the interstitial space is dilutedSodium in the interstitial space is diluted
Decreased osmolarity of ECFDecreased osmolarity of ECF
Water moves into the cell as a result of sodium lossWater moves into the cell as a result of sodium loss
Extracellular compartment is depleted of waterExtracellular compartment is depleted of water
CLINICAL SYMPTOMSCLINICAL SYMPTOMS

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

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

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

PATHOPHYSIOLOGY OF HYPERNATREMIAPATHOPHYSIOLOGY OF HYPERNATREMIA
Increased Sodium concentration in ECFIncreased Sodium concentration in ECF
Osmolarity risesOsmolarity rises
Water leaves the cell by osmosis and entersWater leaves the cell by osmosis and enters
the the extracellular compartmentsthe the extracellular compartments
Dilution of fluids in ECFDilution of fluids in ECF Cells are water depletedCells are water depleted
Suppression of aldosteroneSuppression of aldosterone
secretionsecretion
Sodium is exreted in theSodium is exreted in the
urineurine
CLINICAL SYMPTOMSCLINICAL SYMPTOMS

CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
Dry, sticky mucousDry, sticky mucous
membranesmembranes
Firm, rubberyFirm, rubbery
tissue turgortissue turgor
Manic excitementManic excitement
TachycardiaTachycardia
DEATHDEATH

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

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

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

PATHOPHYSIOLOGY OF HYPOKALEMIAPATHOPHYSIOLOGY OF HYPOKALEMIA
= Action Potential= Action Potential
Nerve and Muscle ActivityNerve and Muscle Activity
LowLow
ExtracellularExtracellular
K+K+
Increase inIncrease in
restingresting
membranemembrane
potentialpotential
The cellThe cell
becomesbecomes
lessless
excitableexcitable

Sodium is retained in the body through resorption bySodium is retained in the body through resorption by
the kidney tubulesthe kidney tubules
Potassium is excretedPotassium is excreted
Aldosterone is secretedAldosterone is secreted
Use of certain diuretics such as thiazides and furosemide, andUse of certain diuretics such as thiazides and furosemide, and
corticosteroidscorticosteroids
Increased urinary outputIncreased urinary output
Loss of potassium in urineLoss of potassium in urine

• 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 HYPERKALEMIACAUSES AND EFFECTS OF HYPERKALEMIA
• Serum potassium level greater than 5.5 mEq/LSerum potassium level greater than 5.5 mEq/L
Excess IntakeExcess Intake
Dietary intake of excess
of kidney’s ability to
excrete; Excess
parenteral administration
Decreased LossDecreased Loss
Potassium-sparing diuretics;Potassium-sparing diuretics;
Renal failure; AdrenalRenal failure; Adrenal
insufficiencyinsufficiency
Shift of PotassiumShift of Potassium
out of the Cellsout of the Cells
Extensive injuries,Extensive injuries,
crushing injuries,crushing injuries,
metabolic acidosismetabolic acidosis
HYPERKALEMIAHYPERKALEMIA
GI TractGI Tract
N&V
Diarrhea,
Colic
CNSCNS
Numbness,
paresthesias
MusclesMuscles
Early: irritability
Late: weakness
leading to flaccid
paralysis
CV SystemCV System
Conduction
disturbance,
ventricular
fibrillation,
Cardiac Arrest
KidneysKidneys
Oliguria
leading to
anuria

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

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

CAUSES AND EFFECTS OF HYPOCALCEMIACAUSES AND EFFECTS OF HYPOCALCEMIA
DecreasedDecreased
Ionized CaIonized Ca
Large
tranfusion with
citrated blood
Excess LossExcess Loss
Kidney DiseaseKidney Disease
Decrease in GI TractDecrease in GI Tract
and Bone Absorptionand Bone Absorption
↑↑MagnesiumMagnesium
↑↑CalcitoninCalcitonin
↓Vitamin D
↓Parathyroid Hormone
HYPOCALCEMIAHYPOCALCEMIA
BonesBones
Osteoporosis
leading to
Fractures
CNSCNS
Tingling
↓
convulsions
OtherOther
Abnormal
deposits
of calcium
in body
tissues
MusclesMuscles
Muscle spasm
↓
Tetany
CardiovascularCardiovascular
SystemSystem
Dysrhythmias
↓
Cardiac arrest
InadequateInadequate
IntakeIntake
Dietary DeficitDietary Deficit

PATHOPHYSIOLOGY OF HYPOCALCEMIAPATHOPHYSIOLOGY 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 HYPOCALCEMIACLINICAL MANIFESTATIONS OF HYPOCALCEMIA
COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE,COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE,
FINGERTIPS OR TOESFINGERTIPS OR TOES
TREATMENTTREATMENT
PAINFUL MUSCULAR SPASMS (TETANY)PAINFUL MUSCULAR SPASMS (TETANY)
ESPECIALLY OF FEET AND HANDSESPECIALLY OF FEET AND HANDS
(CARPOPEDAL SPASMS), MUSCLE TWITCHING(CARPOPEDAL SPASMS), MUSCLE TWITCHING
AND CONVULSIONS MAY FOLLOWAND CONVULSIONS MAY FOLLOW

TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCYTESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY

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

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

HOW IT HAPPENSHOW IT HAPPENS
HYPERCALCEMIAHYPERCALCEMIA
DEPRESSED NERVEDEPRESSED NERVE
AND MUSCLEAND MUSCLE
ACTIVITYACTIVITY
DEEP TENDONDEEP TENDON
REFLEXES MAY BEREFLEXES MAY BE
DECREASED ORDECREASED OR
ABSENTABSENT
MYOCARDIALMYOCARDIAL
FUNCTION ISFUNCTION IS
ALTEREDALTERED

CLINICAL MANIFESTATIONS OF HYPERCALCEMIACLINICAL MANIFESTATIONS OF HYPERCALCEMIA
Decreased GIDecreased GI
MotilityMotility
Cardiac DysrhythmiasCardiac Dysrhythmias
ConstipationConstipation
NauseaNausea
Mental status changes:Mental status changes:
lethargy, confusion,lethargy, confusion,
memory lossmemory loss

CLINICAL MANIFESTATIONS OF HYPERCALCEMIACLINICAL MANIFESTATIONS OF HYPERCALCEMIA
ImmobilizationImmobilization BoneBone
DemineralizationDemineralization
CalciumCalcium
accumulates inaccumulates in
the ECF andthe ECF and
passes throughpasses through
the kidneysthe kidneys
Ca PrecipitationCa PrecipitationCalcium StonesCalcium Stones

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

HYPOMAGNESEMIA: Serum level < 1.5 mEq/LHYPOMAGNESEMIA: Serum level < 1.5 mEq/L
• Usually coexists with hypokalemia and less often with hypocalcemia
Decreased IntakeDecreased Intake
Prolonged
malnutrition,
Starvation
Impaired absorption from GI TractImpaired absorption from GI Tract
Malabsorption syndrome, Alcohol WithdrawalMalabsorption syndrome, Alcohol Withdrawal
Syndrome, Hypercalcemia, Diarrhea,Syndrome, Hypercalcemia, Diarrhea,
Draining gastrointestinal fistulaDraining gastrointestinal fistula
ExcessiveExcessive
ExcretionExcretion
↑↑Aldosterone,Aldosterone,
ConditionsConditions
causing largecausing large
losses of urinelosses of urine
HYPOMAGNESEMIAHYPOMAGNESEMIA
Mental ChangesMental Changes
Agitation,
Depression,
Confusion
CNSCNS
Convulsions,
Paresthesias,
Tremor, Ataxia
MusclesMuscles
Cramps,
Spasticity, Tetany
CV SystemCV System
Tachycardia,
Hypotension,
Dysrhythmias
HYPOKALEMIAHYPOKALEMIA

PATHOPHYSIOLOGY OF HYPOMAGNESEMIAPATHOPHYSIOLOGY OF HYPOMAGNESEMIA
Low serum magnesium levelLow serum magnesium level
Increased acetylcholine releaseIncreased acetylcholine release
Increased neuromuscular irritabilityIncreased neuromuscular irritability
Increased sensitivity to acetylcholine at the myoneural junctionIncreased sensitivity to acetylcholine at the myoneural junction
Diminished threshold ofDiminished threshold of
excitation for the motorexcitation for the motor
nervenerve
Enhancement of myofibrilEnhancement of myofibril
contractioncontraction

High Serum CalciumHigh Serum Calcium
Increased acetylcholine releaseIncreased acetylcholine release
Increased neuromuscular irritabilityIncreased neuromuscular irritability
Increased sensitivity to acetylcholine at the myoneural junctionIncreased sensitivity to acetylcholine at the myoneural junction
Diminished threshold ofDiminished threshold of
excitation for the motorexcitation for the motor
nervenerve
Enhancement of myofibrilEnhancement of myofibril
contractioncontraction
High Serum CalciumHigh Serum Calcium
Excretion of MagnesiumExcretion of Magnesium
By the GI tractBy the GI tract

MAGNESIUMMAGNESIUM
INHIBITS TRANSPORT OF PTHINHIBITS TRANSPORT OF PTH
DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASEDDECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED
FROM THE BONEFROM THE BONE
POSSIBLE CALCIUM DEFICITPOSSIBLE CALCIUM DEFICIT

CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIACLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA
CONFUSIONCONFUSION
DEPRESSIONDEPRESSION
CRAMPSCRAMPS
TETANYTETANY CONVULSIONSCONVULSIONS

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

HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/LHYPERMAGNESEMIA: Serum Mg level 2.5 mEq/L
• Seldom develops in the presence of normal renal functionSeldom develops in the presence of normal renal function
• May occur as a result of Mg replacementMay occur as a result of Mg replacement
• May occur when MgSO4 is administered to prevent seizuresMay occur when MgSO4 is administered to prevent seizures
resulting from eclampsiaresulting from eclampsia
• Careful monitoring is imperativeCareful monitoring is imperative

PATHOPHYSIOLOGYPATHOPHYSIOLOGY
Renal failure, Excessive IV infusion ofRenal failure, Excessive IV infusion of
magnesium, Decreased GI eliminationmagnesium, Decreased GI elimination
and/or absorption, etc.and/or absorption, etc.
Accummulation of Mg in the bodyAccummulation of Mg in the body
Diminishing of reflexes, drowsiness, lethargyDiminishing of reflexes, drowsiness, lethargy
Mg Level RisesMg Level Rises
Severe Respiratory DepressionSevere Respiratory Depression
RESPIRATORY ARREST may occurRESPIRATORY ARREST may occur
Altered Electrical ConductionAltered Electrical Conduction
Slowed heartSlowed heart
rate and AVrate and AV
BlockBlock
PeripheralPeripheral
vasodilationvasodilation
Hypotension, flushing, andHypotension, flushing, and
increased skin warmthincreased skin warmth

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

NURSING MANAGEMENT OFNURSING MANAGEMENT OF
PATIENT WITH FLUID ANDPATIENT WITH FLUID AND
ELECTROLYTE IMBALANCESELECTROLYTE IMBALANCES

Parameter_____Fluid Excess___Parameter_____Fluid Excess___ Fluid Loss/Electrolyte Imbalance____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 edemaPitting edema
Dependent edemaDependent edema
Refractory EdemaRefractory Edema

LABORATORY VALUESLABORATORY VALUES
FLUID DEFICITFLUID DEFICIT FLUID EXCESSFLUID EXCESS
HemoconcentrationHemoconcentration HemodilutionHemodilution
↑↑ Hct, BUN, E+ levelsHct, BUN, E+ levels ↓↓ Hct, BUN, E+ levelsHct, BUN, E+ levels
↑↑ Urine Specific GravityUrine Specific Gravity ↓ Urine Specific Gravity↓ Urine Specific Gravity

Determined from analysis of patient dataDetermined from analysis of patient data
Diagnostic TitleDiagnostic Title Possible Etiologic FactorsPossible Etiologic Factors
11 Deficient fluid volumeDeficient fluid volume Active fluid volume lossActive fluid volume loss
(hemorrhage, diarrhea, gastric(hemorrhage, diarrhea, gastric
intubation, wounds, diaphoresis),intubation, wounds, diaphoresis),
inadequate fluid intake, failure ofinadequate fluid intake, failure of
regulatory mechanisms,regulatory mechanisms,
sequestration of body fluidssequestration of body fluids
22 Excess Fluid VolumeExcess Fluid Volume Excess fluid intake, excess sodiumExcess fluid intake, excess sodium
intake, compromised regulatoryintake, compromised regulatory
processesprocesses

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

1,21,2Intake and Output MonitoringIntake and Output Monitoring
- Type and amount of fluid the patient has received and the- Type and amount of fluid the patient has received and the
route by which they were administeredroute by which they were administered
-- Record of solid food intake. Gelatin or Popsicles areRecord of solid food intake. Gelatin or Popsicles are
recorded as fluidsrecorded as fluids
-- Ice chips are recorded by dividing the amount of chipsIce chips are recorded by dividing the amount of chips
by ½ (60 mL of chips = 30 mL water)by ½ (60 mL of chips = 30 mL water)
-- Accurate output record and described by color, content,Accurate output record and described by color, content,
and odor (Normally, gastric contents are watery and paleand odor (Normally, gastric contents are watery and pale
yellow-green; they usually have a sour odor)yellow-green; they usually have a sour odor)
-- With acid-base balance upset, gastric secretions mayWith acid-base balance upset, gastric secretions may
have a fruity odor because of ketone bodieshave a fruity odor because of ketone bodies
-- Bile: thicker than gastric juice, dark green to brown,Bile: thicker than gastric juice, dark green to brown,
acrid odor, bitter taste when vomitingacrid odor, bitter taste when vomiting
-- NGT irrigation added to intakeNGT irrigation added to intake
-- Stools: difficult to estimate amount; consistency, color,Stools: difficult to estimate amount; consistency, color,
and number of stools provide a reasonable estimateand number of stools provide a reasonable estimate
-- Peritoneal or pleural fluid drainage is recorded as outputPeritoneal or pleural fluid drainage is recorded as output
as with its amount, color, and clarityas with its amount, color, and clarity
-- Character and volume of urine. Place signs andCharacter and volume of urine. Place signs and
materials somaterials so that an accurate record of UO is maintainedthat an accurate record of UO is maintained

1,21,2 Intake and Output MonitoringIntake and Output Monitoring
- Evaluate and refer urine specific gravity as appropriate- Evaluate and refer urine specific gravity as appropriate
(normal value is 1.003 – 1.030). The implications are:(normal value is 1.003 – 1.030). The implications are:
HighHigh DehydrationDehydration
LowLow SIADH, overhydrationSIADH, overhydration
-- Drainage, fluid aspirated from any body cavity must beDrainage, fluid aspirated from any body cavity must be
measured. With dressings, fluid loss is the differencemeasured. With dressings, fluid loss is the difference
between the wet dressings and the dry weight of thebetween the wet dressings and the dry weight of the
dressingdressing
-- Accurate recording of the temperature to help theAccurate recording of the temperature to help the
physician determine how much fluid should be replacedphysician determine how much fluid should be replaced
1,21,2 Daily WeightDaily Weight
-- Evaluate trends in weight (An increase in 1kg in weightEvaluate trends in weight (An increase in 1kg in weight
is equal to the retention of 1L of fluid in an edematousis equal to the retention of 1L of fluid in an edematous
patient)patient)
Considerations:Considerations:
-- Daily weights early in the morning after voidingDaily weights early in the morning after voiding
but before he or she has eaten or defecatedbut before he or she has eaten or defecated

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

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

** Patients with cardiac and renal impairments arePatients with cardiac and renal impairments are
instructed to avoid foods containing high levelsinstructed to avoid foods containing high levels
of sodium, potassium and bicarbonateof sodium, potassium and bicarbonate
-- Administer replacement solutions through tube feeding as isAdminister replacement solutions through tube feeding as is
** Either water, physiologic solution of NaCl, high proteinEither water, physiologic solution of NaCl, high protein
liquids, or a regular diet can be blended, diluted andliquids, or a regular diet can be blended, diluted and
given by gavagegiven by gavage
** The water content in the tube feeding needs to beThe water content in the tube feeding needs to be
increased if:increased if:
11 the patient complains of thirstthe patient complains of thirst
22 the protein or electrolyte content of the tubethe protein or electrolyte content of the tube
feeding is highfeeding is high
33 the patient has fever or disease causing anthe patient has fever or disease causing an
increased metabolic rateincreased metabolic rate
44 UO is concentratedUO is concentrated
55 signs of water deficit developsigns of water deficit develop
-- Administer parenteral fluids as necessaryAdminister parenteral fluids as necessary

** Types of solutionsTypes of solutions
-- D5W (hypotonic) is given short-term for hyponatremiaD5W (hypotonic) is given short-term for hyponatremia
-- D5NSS may be given depending on the serum levels ofD5NSS may be given depending on the serum levels of
sodium and vascular volume + KCl to meet normalsodium and vascular volume + KCl to meet normal
intake needs and replace losses for hyponatremiaintake needs and replace losses for hyponatremia
-- Dextrose 5% in 0.2% normal saline is generally used asDextrose 5% in 0.2% normal saline is generally used as
a maintenance fluida maintenance fluid
-- Dextrose 5% in ½ normal saline is generally used as aDextrose 5% in ½ normal saline is generally used as a
replacement solution for losses caused byreplacement solution for losses caused by
gastrointestinal drainagegastrointestinal drainage
-- PNSS is given primarily when large amounts of sodiumPNSS is given primarily when large amounts of sodium
have been lost and for patients with hyponatremiahave been lost and for patients with hyponatremia
-- LRS is also isotonic because it remains in theLRS is also isotonic because it remains in the
extracellular spaceextracellular space
-- Fructose or 10-20% glucose in distilled water areFructose or 10-20% glucose in distilled water are
hypertonic solutions and may partially meet bodyhypertonic solutions and may partially meet body
needs for CHOsneeds for CHOs
-- Dextran (commonly-used plasma expander) increasesDextran (commonly-used plasma expander) increases
plasma volume by increasing oncotic pressure. Mayplasma volume by increasing oncotic pressure. May
cause prolonged bleeding time and is CI in patientscause prolonged bleeding time and is CI in patients
with renal failure, bleeding disorders, or severe CHFwith renal failure, bleeding disorders, or severe CHF

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

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

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

Fluids and Electrolytes
Acid-base
balance

DRAWING ARTERIAL BLOOD GASESDRAWING ARTERIAL BLOOD GASES
ALLEN’S TESTALLEN’S TESTARTERIAL PUNCTUREARTERIAL PUNCTURE

NORMAL ACID-BASE BALANCENORMAL ACID-BASE BALANCE
Estimated HCO3 concentration after fullyEstimated HCO3 concentration after fully
oxygenated arterial blood has beenoxygenated arterial blood has been
equilibrated with CO2 at a PCO2 of 40equilibrated with CO2 at a PCO2 of 40
mmHg at 38C; eliminates the influence ofmmHg at 38C; eliminates the influence of
respiration on the plasma HCO3respiration on the plasma HCO3
concentrationconcentration
22-2622-26 mEq/LmEq/LStandard HCO3Standard HCO3
Partial pressure of CO2 in the arterialPartial pressure of CO2 in the arterial
blood:blood:
PCO2<35 mmHg = respiratory alkalosisPCO2<35 mmHg = respiratory alkalosis
PCO2>45 mmHg = respiratory acidosisPCO2>45 mmHg = respiratory acidosis
35-45 mmHg35-45 mmHgPaCO2PaCO2
Identifies whether there is acidemia orIdentifies whether there is acidemia or
alkalemia:alkalemia:
pH<7.35 = acidosis; pH>7.45 = alkalosispH<7.35 = acidosis; pH>7.45 = alkalosis
7.35-7.457.35-7.45pHpH
Partial pressure of oxygen in arterialPartial pressure of oxygen in arterial
blood (decreases with age)blood (decreases with age)
In adults < 60 years:In adults < 60 years:
60-80 mmHg = mild hypoxemia60-80 mmHg = mild hypoxemia
40-60 mmHg = moderate hypoxemia40-60 mmHg = moderate hypoxemia
< 40 mmHg = severe hypoxemia< 40 mmHg = severe hypoxemia
80-100 Hg80-100 HgPaO2PaO2
Definition and ImplicationsDefinition and ImplicationsNormal ValueNormal ValueParameterParameter

BASIC REGULATION OF ACID-BASE BALANCEBASIC REGULATION OF ACID-BASE BALANCE
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3
The lungs help control acid-base balance by blowing off orThe lungs help control acid-base balance by blowing off or
retaining CO2. The kidneys help regulate acid-base balance byretaining CO2. The kidneys help regulate acid-base balance by
excreting or retaining HCO3excreting or retaining HCO3

TYPES OF ACID-BASE DISTURBANCESTYPES OF ACID-BASE DISTURBANCES
Depression of the centralDepression of the central
nervous system, asnervous system, as
evidenced by disorientationevidenced by disorientation
followed by comafollowed by coma
Overexcitability of theOverexcitability of the
nervous system; musclesnervous system; muscles
may go into a state of tetanymay go into a state of tetany
and convulsioonsand convulsioons

EXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCESEXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCES
↑
↑
↑
↓
↓
↓
Normal
↓
↓
Normal
↑
↑
HCO3HCO3
Normal
↑
↑
↑
↑
Normal
Metabolic Alkalosis
Uncompensated
Partly Compensated
Compensated
Normal
↓
↓
↓
↓
Normal
Metabolic Acidosis
Uncompensated
Partly Compensated
Compensated
↓
↓
↓
↑
↑
Normal
Respiratory Alkalosis
Uncompensated
Partly Compensated
Compensated
↑
↑
↑
↓
↓
Normal
Respiratory Acidosis
Uncompensated
Partly Compensated
Compensated
PCO2PCO2pHpHCONDITIONCONDITION

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

NURSING MANAGEMENT OF RESPIRATORY ACIDOSISNURSING MANAGEMENT OF RESPIRATORY ACIDOSIS
ASSESSMENTASSESSMENT
** Health Hx: complaints of headache, confusion, lethargy,Health Hx: complaints of headache, confusion, lethargy,
nausea, irritability, nausea, irritability, anxiety, dyspnea, andnausea, irritability, nausea, irritability, anxiety, dyspnea, and
blurred vision, preexisting conditionsblurred vision, preexisting conditions
** Physical Examination: lethargy to stupor to coma, tachycardia,Physical Examination: lethargy to stupor to coma, tachycardia,
hypertension, cardiac dysrhythmias, airway patencyhypertension, cardiac dysrhythmias, airway patency
NURSING DIAGNOSES include but are not limited to:NURSING DIAGNOSES include but are not limited to:
11 Impaired gas exchangeImpaired gas exchange HypoventilationHypoventilation
22 Disturbed thought processesDisturbed thought processes Central nervous system depressionCentral nervous system depression
33 AnxietyAnxiety Hypoxia, hospitalizationHypoxia, hospitalization
44 Risk for ineffective familyRisk for ineffective family Illness of a family memberIllness of a family member
copingcoping
55 Ineffective airway clearanceIneffective airway clearance Hypoventilation, secretionsHypoventilation, secretions
66 Ineffective breathing patternIneffective breathing pattern Hypoventilation, dyspneaHypoventilation, dyspnea

NURSING MANAGEMENT OF RESPIRATORY ACIDOSISNURSING MANAGEMENT OF RESPIRATORY ACIDOSIS
EXPECTED PATIENT OUTCOMES include but are not limited to:EXPECTED PATIENT OUTCOMES include but are not limited to:
11 Will maintain airway patency and adequate breathing rate andWill maintain airway patency and adequate breathing rate and
rhythm will return of ABGs to patient’s normal levelrhythm will return of ABGs to patient’s normal level
22 Will be alert and oriented to time, place, and person, or to hisWill be alert and oriented to time, place, and person, or to his
or her normal baseline level of consciousnessor her normal baseline level of consciousness
33 Will cope with anxietyWill cope with anxiety
44 Will exhibit effective coping and awareness of effectiveWill exhibit effective coping and awareness of effective
support systemssupport systems
55 Will have secretions that are normal for self in amount and canWill have secretions that are normal for self in amount and can
be raisedbe raised
66 Will maintain adequate rate and depth of respirations usingWill maintain adequate rate and depth of respirations using
pursed lip and other breathing techniques when necessary (aspursed lip and other breathing techniques when necessary (as inin
the patient with COPD)the patient with COPD)

NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSISNURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
INTERVENTIONSINTERVENTIONS
11 Supporting effective gas exchangeSupporting effective gas exchange
-- Provide a position of comfort to allow ease of respirationProvide a position of comfort to allow ease of respiration
-- Obtain and monitor ABG results and VS. Refer accordinglyObtain and monitor ABG results and VS. Refer accordingly
-- Provide and monitor supplemental oxygen as orderedProvide and monitor supplemental oxygen as ordered
-- Turn the patient q2 and PRNTurn the patient q2 and PRN
-- Provide pulmonary hygiene PRNProvide pulmonary hygiene PRN
-- Maintain adequate hydrationMaintain adequate hydration
-- Provide comfort measures such as mouth careProvide comfort measures such as mouth care
-- Assist with ADLsAssist with ADLs
-- Instruct patient regarding coughing and deep breathing andInstruct patient regarding coughing and deep breathing and
management of disease condition, especially COPDmanagement of disease condition, especially COPD
22 Coping with disturbed thought processesCoping with disturbed thought processes
-- Do frequent neurologic assessmentsDo frequent neurologic assessments
-- Monitor and document person’s baseline LOC frequentlyMonitor and document person’s baseline LOC frequently

-- Reorient as necessary by providing calendars, clocks, etc.Reorient as necessary by providing calendars, clocks, etc.
33 Relieving anxietyRelieving anxiety
-- Provide a calm, relaxed environmentProvide a calm, relaxed environment
-- Give clear, concise explanations of treatment plansGive clear, concise explanations of treatment plans
-- Encourage expression of feelingsEncourage expression of feelings
-- Provide support and information to patient and familyProvide support and information to patient and family
-- Teach relaxation techniquesTeach relaxation techniques
-- Assist the patient to identify coping mechanisms to deal withAssist the patient to identify coping mechanisms to deal with
anxiety and stressanxiety and stress
44 Enhancing coping mechanismsEnhancing coping mechanisms
-- Provide support and information to family members about theProvide support and information to family members about the
patient’s ongoing conditionpatient’s ongoing condition
-- Reassure them that there is a physiologic cause for theReassure them that there is a physiologic cause for the
patient’s behaviorpatient’s behavior

-- Encourage questions and open communicationEncourage questions and open communication
55 Promote airway clearancePromote airway clearance
-- Implement regular breathing and coughing exercisesImplement regular breathing and coughing exercises
-- Do suctioning as necessaryDo suctioning as necessary
-- Maintain good hydrationMaintain good hydration
-- Do chest physiotherapy as appropriateDo chest physiotherapy as appropriate
66 Promoting an effective breathing patternPromoting an effective breathing pattern
-- Maintain alveolar ventilationMaintain alveolar ventilation
-- Teach the patient proper breathing techniques as well asTeach the patient proper breathing techniques as well as
panicpanic control breathingcontrol breathing

EVALUATION. Achievement of outcomes is successful when the patient:EVALUATION. Achievement of outcomes is successful when the patient:
1a.1a. Demonstrates improved ventilation and oxygenationDemonstrates improved ventilation and oxygenation
1b1b Has vital signs, ABGs, and cardiac rhythm within own normalHas vital signs, ABGs, and cardiac rhythm within own normal
rangerange
22 Returns to baseline LOCReturns to baseline LOC
33 Reports reduced anxietyReports reduced anxiety
44 Family uses adequate coping mechanismsFamily uses adequate coping mechanisms
55 Is able to raise secretions on ownIs able to raise secretions on own
66 Demonstrate effective breathing techniquesDemonstrate effective breathing techniques

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

NURSING MANAGEMENT OF RESPIRATORY ALKALOSISNURSING MANAGEMENT OF RESPIRATORY ALKALOSIS
** Health Hx: anxiety, shortness of breath, muscle cramps orHealth Hx: anxiety, shortness of breath, muscle cramps or
weakness, palpitations, panic, dyspneaweakness, palpitations, panic, dyspnea
** Physical Examination: light-headedness, confusion as a result ofPhysical Examination: light-headedness, confusion as a result of
cerebral hypoxia, hyperventilation, tachycardia or arrhythmia,cerebral hypoxia, hyperventilation, tachycardia or arrhythmia,
muscle weakness, (+) Chvostek’s sign or Trousseau’s signmuscle weakness, (+) Chvostek’s sign or Trousseau’s sign
indicating a low ionized serum calcium level secondary toindicating a low ionized serum calcium level secondary to
hyperventilation and alkalosis, hyperactive deep tendon reflexes,hyperventilation and alkalosis, hyperactive deep tendon reflexes,
unsteady gait, muscle spasms to tetany, agitation, psychosis,unsteady gait, muscle spasms to tetany, agitation, psychosis,
seizures in extreme cases, decreased potassium levelsseizures in extreme cases, decreased potassium levels
11 AnxietyAnxiety Stress, fearStress, fear
22 Ineffective breathing patternIneffective breathing pattern Hyperventilation, anxietyHyperventilation, anxiety
33 Disturbed thought processesDisturbed thought processes CNS excitability; irritabilityCNS excitability; irritability
44 Risk for injuryRisk for injury Change in LOC, and potential forChange in LOC, and potential for
seizuresseizures

NURSING MANAGEMENT OF RESPIRATORY ALKALOSISNURSING MANAGEMENT OF RESPIRATORY ALKALOSIS
11 Will report decreased anxiety; verbalizes methods to copeWill report decreased anxiety; verbalizes methods to cope
withwith anxietyanxiety
22 Will return to normal respiratory rate and rhythm or at leastWill return to normal respiratory rate and rhythm or at least
decreased hyperventilation, with return to baseline ABGsdecreased hyperventilation, with return to baseline ABGs
33 Will exhibit reorientation to person, place, and time as perWill exhibit reorientation to person, place, and time as per
patient’s baselinepatient’s baseline
44 Will be free from injuryWill be free from injury
11 Allay anxietyAllay anxiety
-- Give antianxiety medications as orderedGive antianxiety medications as ordered
-- Have patient breath into a paper bagHave patient breath into a paper bag
-- Teach relaxation techniques when initial anxiety attack isTeach relaxation techniques when initial anxiety attack is
overover

22 Promoting an Effective Breathing PatternPromoting an Effective Breathing Pattern
-- Encourage the patient to slow his or her RREncourage the patient to slow his or her RR
-- Maintain a calm and comforting attitudeMaintain a calm and comforting attitude
-- Position the patient to promote maximal ease of inspirationPosition the patient to promote maximal ease of inspiration
-- Assist the patient with relaxation techniquesAssist the patient with relaxation techniques
33 Coping with Disturbed Thought ProcessesCoping with Disturbed Thought Processes
-- Do frequent reorientationDo frequent reorientation
-- Encourage family to participate in patient’s careEncourage family to participate in patient’s care
-- Use simple, direct statements or directionsUse simple, direct statements or directions
-- Allow the patient adequate time to respondAllow the patient adequate time to respond
44 Preventing injuriesPreventing injuries
-- Perform neurologic assessment frequently and documentPerform neurologic assessment frequently and document
-- Institute safety and seizure precautionsInstitute safety and seizure precautions
-- Assess frequently for muscle strength and coordinationAssess frequently for muscle strength and coordination

11 Reports reduction in anxiety levelsReports reduction in anxiety levels
2a2a Demonstrates effective normal breathing patternsDemonstrates effective normal breathing patterns
2b2b Has ABG results within patient’s normal baselineHas ABG results within patient’s normal baseline
33 Returns to normal baseline LOC and orientation levelReturns to normal baseline LOC and orientation level
44 Remains free from injury; no seizure activityRemains free from injury; no seizure activity

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

NURSING MANAGEMENT OF METABOLIC ACIDOSISNURSING MANAGEMENT OF METABOLIC ACIDOSIS
** Health Hx: anorexia, nausea, vomiting, abdominal pain,Health Hx: anorexia, nausea, vomiting, abdominal pain,
headache, thirst if the patient is dehydratedheadache, thirst if the patient is dehydrated
** Physical Examination: confusion, hyperventilation, warm,Physical Examination: confusion, hyperventilation, warm,
flushed skin, bradycardia and other dysrhythmias, decreasingflushed skin, bradycardia and other dysrhythmias, decreasing
LOC, nausea, vomiting, diarrhea, Kussmaul respirations, andLOC, nausea, vomiting, diarrhea, Kussmaul respirations, and
acetone breath, especially if acidosis is due to ketoacidosis.acetone breath, especially if acidosis is due to ketoacidosis.
Symptoms may progress to coma if untreatedSymptoms may progress to coma if untreated
11 Disturbed thought processesDisturbed thought processes Secondary to CNS depressionSecondary to CNS depression
22 Decreased cardiac outputDecreased cardiac output DysrhythmiasDysrhythmias
33 Risk for injuryRisk for injury Secondary to altered mental stateSecondary to altered mental state
44 Risk for imbalanced fluidRisk for imbalanced fluid Diarrhea, renal failureDiarrhea, renal failure
volumevolume

NURSING MANAGEMENT OF METABOLIC ACIDOSISNURSING MANAGEMENT OF METABOLIC ACIDOSIS
11 Will return to usual baseline LOCWill return to usual baseline LOC
22 Will return to normal baseline parameters for vital signs withWill return to normal baseline parameters for vital signs with
improved CO and decreased or resolved dysrhythmiasimproved CO and decreased or resolved dysrhythmias
33 Will remain in a safe, secure environment without injuryWill remain in a safe, secure environment without injury
44 Will maintain fluid and electrolyte balance and stable renalWill maintain fluid and electrolyte balance and stable renal
statusstatus
-- Monitor LOC and reorient as necessaryMonitor LOC and reorient as necessary
-- Monitor VS, esp. RRR, BP, and TMonitor VS, esp. RRR, BP, and T
-- Monitor ABGs to assess the effects of treatmentMonitor ABGs to assess the effects of treatment
-- Institute cardiac monitoring as orderedInstitute cardiac monitoring as ordered

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSISNURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS
22 Supporting cardiac outputSupporting cardiac output
-- Monitor VS, MIO, and fluid and electrolyte balanceMonitor VS, MIO, and fluid and electrolyte balance
-- Institute cardiac monitoring to evaluate cardiac statusInstitute cardiac monitoring to evaluate cardiac status
33 Promoting safetyPromoting safety
-- Provide a safe, secure and monitored environmentProvide a safe, secure and monitored environment
-- Institute safety precautionsInstitute safety precautions
44 Promoting return of fluid and electrolyte balancePromoting return of fluid and electrolyte balance
-- Monitor MIOMonitor MIO
-- Administer medications per medical orderAdminister medications per medical order

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSISNURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS
11 Exhibits baseline-level consciousness and orientationExhibits baseline-level consciousness and orientation
22 Returns to normal baseline parameters for vital signs andReturns to normal baseline parameters for vital signs and
Cardiac Output with cardiac dysrhythmias resolvedCardiac Output with cardiac dysrhythmias resolved
33 Remains free from injuryRemains free from injury
44 Maintains fluid and electrolyte balance and stable renal functionMaintains fluid and electrolyte balance and stable renal function

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

NURSING MANAGEMENT OF METABOLIC ALKALOSISNURSING MANAGEMENT OF METABOLIC ALKALOSIS
** Health HxHealth Hx: Prolonged vomiting or nasogastric suctioning,: Prolonged vomiting or nasogastric suctioning,
frequent self-induced vomiting, muscle weakness, light-frequent self-induced vomiting, muscle weakness, light-
headedness, ingestion of large amounts of licorice orheadedness, ingestion of large amounts of licorice or
antacids, use of diuretics, muscle cramping, twitching, orantacids, use of diuretics, muscle cramping, twitching, or
tinglingtingling
** Physical ExaminationPhysical Examination: mental confusion, dizziness, changes in: mental confusion, dizziness, changes in
LOC, hyperreflexia, tetany, dysrhthmias, seizurees, respiratoryLOC, hyperreflexia, tetany, dysrhthmias, seizurees, respiratory
failure, positive Chvostek’s or Trosseau’s sign if the patient hasfailure, positive Chvostek’s or Trosseau’s sign if the patient has
a low ionized serum calcium level, decreased hand grasps,a low ionized serum calcium level, decreased hand grasps,
generalized muscle weakness, decreased serum calcium orgeneralized muscle weakness, decreased serum calcium or
potassium level, impaired concentration, seizures, ECG changespotassium level, impaired concentration, seizures, ECG changes
consistent with hypokalemiaconsistent with hypokalemia
11 Disturbed thought processesDisturbed thought processes CNS excitationCNS excitation
22 Decreased cardiac output Dysrhythmias and electrolyteDecreased cardiac output Dysrhythmias and electrolyte
imbalancesimbalances
33 Risk for injuryRisk for injury Muscle weakness, tetany, confusion and possibleMuscle weakness, tetany, confusion and possible
seizuresseizures
44 Risk for imbalanced fluid Nasogastric drainage, diuretic therapyRisk for imbalanced fluid Nasogastric drainage, diuretic therapy
volumevolume fistulafistula

NURSING MANAGEMENT OF METABOLIC ALKALOSISNURSING MANAGEMENT OF METABOLIC ALKALOSIS
11 Will return to usual baseline LOC and orientationWill return to usual baseline LOC and orientation
22 Will return to normal baseline parameters for vital signs withWill return to normal baseline parameters for vital signs with
improved CO with resolution of electrolyte imbalances andimproved CO with resolution of electrolyte imbalances and
decreased or resolved cardiac dysrhythmiasdecreased or resolved cardiac dysrhythmias
33 Will remain in a safe, secure environment without injuryWill remain in a safe, secure environment without injury
44 Will maintain fluid and electrolyte balanceWill maintain fluid and electrolyte balance
-- Monitor LOC and reorient as necessaryMonitor LOC and reorient as necessary
-- Monitor VS, esp. RRR, BP, and TMonitor VS, esp. RRR, BP, and T
-- Monitor ABGs to assess the effects of treatmentMonitor ABGs to assess the effects of treatment
-- Institute cardiac monitoring as orderedInstitute cardiac monitoring as ordered

NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSISNURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS
22 Supporting cardiac outputSupporting cardiac output
-- Monitor VS, MIO, and fluid and electrolyte balanceMonitor VS, MIO, and fluid and electrolyte balance
-- Institute cardiac monitoring to evaluate cardiac statusInstitute cardiac monitoring to evaluate cardiac status
33 Promoting safetyPromoting safety
-- Provide a safe, secure and monitored environmentProvide a safe, secure and monitored environment
-- Institute safety precautionsInstitute safety precautions
44 Promoting return of fluid and electrolyte balancePromoting return of fluid and electrolyte balance
-- Monitor MIOMonitor MIO
-- Administer medications per medical orderAdminister medications per medical order

NURSING MANAGEMENT OF PATIENT WITH METABOLICNURSING MANAGEMENT OF PATIENT WITH METABOLIC
ALKALOSISALKALOSIS
EVALUATION. Achievement of outcomes is successful whenEVALUATION. Achievement of outcomes is successful when
the patient:the patient:
11 Manifests mental status has returned to baselineManifests mental status has returned to baseline
22 Is free from cardiac dysrhythmiasIs free from cardiac dysrhythmias
33 Remains free from injuryRemains free from injury
44 Maintains fluid balance at baseline levelMaintains 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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