Fluid and Electrolytes — Presentation Transcript

 Fluids andElectrolytes
Ma. Tosca Cybil A. Torres, RN, MAN

 OBJECTIVES
After this lecture/discussion, the learner should be able to:
1. Describe the mechanisms that maintain fluid, electrolyte and acid-base balance.
2. Compare the mechanisms and effects of fluid deficit and excess.
3. Discuss the mechanisms and effects of deficits and excess.
4. Describe the mechanisms that maintain acid-base balance.
5. Differentiate between metabolic and respiratory acidosis and alkalosis.
6. Apply the pathophysiologic principles of acid-base balance to the interpretation of ABG
measurements.
7. Analyze the components of ABGs to identify the type of acid-base balance.
8. Describe the causes and effects of each type of acid-base balance.
9. Use ABG findings in formulating the care of the patient with an acid-base imbalance.
10. Describe the management of patients with a fluid, electrolyte, or acid-base imbalance.

 Fluids

 HOW IMPORTANT IS WATER?

o Between 50% and 60% of the human body by weight is water

o Water provides a medium for transporting nutrients to cells and

wastes from cells and for transporting substances such as
hormones, enzymes, blood platelets, and red and white blood
cells

o Water facilitates cellular metabolism and proper cellular chemical

functioning

o Water acts as a solvent for electrolytes and nonelectrolytes

o Helps maintain normal body temperature

o Facilitates digestion and promotes elimination

o Acts as a tissue lubricant

 VARIATIONS IN FLUID CONTENT

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

 VARIATIONS IN FLUID CONTENT

50%
Adult Female
60%
Adult Male
 45%
Elderly
77%
Infants
AGE

 AVENUES BY WHICH WATER ENTERS AND LEAVES THE BODY

 ANTIDIURETIC HORMONE REGULATION MECHANISMS

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

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

 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 BALANCE
The desirable amount of fluid intake and loss in adults ranges from 1500 to 3500 mL each 24
hours. Ave= 2500 mL
Normally INTAKE = OUTPUT
FLUID IMBALANCE

o Changes in ECF volume = alterations in sodium balance

o Change in sodium/water ratio = either hypoosmolarity or

hyperosmolarity

o Fluid excess or deficit = loss of fluid balance

o As with all clinical problems, the same pathophysiologic change is

not of equal significance to all people

o For example, consider two persons who have the same viral
syndrome with associated nausea and vomiting

Man with renal failure

Life threatening E+ disturbances
ECF Volume Depletion
No Significant E+ disturbances
 FLUID DEFICIT/HYPOVOLEMIA
May occur as a result of:
Reduced fluid intake
Loss of body fluids
Sequestration (compartmentalizing) of body fluids
Pathophysiology and Clinical Manifestations
DECREASED FLUID VOLUME
Stimulation of thirst center in hypothalamus
↑ ADH Secretion
Renin-Angiotensin-Aldosterone System Activation
↑ Water resorption
Person complains of thirst
↑ Sodium and Water Resorption
↓ Urine Output
↑ Urine specific gravity

 Pathophysiology and Clinical Manifestations

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

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

 Hypovolemia
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 Management

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

 Collaborative Care Key Points

1 Liter of water = 1 kg of water by weight
Fluid replacement are calculated according to this ratio plus 1.5 L to fulfill the current daily needs
For 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 1 kg=1 L, fluid replacement therapy for him will involve 1 L
of fluids + 1500 L.
Oral fluid resuscitation is preferable but if the patient is unable to tolerate fluids, IV Therapy may be
ordered
Vital signs should be assessed regularly
Postural hypotension is common for postural persons with fluid volume deficit. How do we assess
this?
For 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 lying down. 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, you get 80. This
 is consistent with intravascular volume depletion.
Daily weighing is also useful to monitor fluid and electrolyte balance
Laboratory results should be reviewed for various fluid and electrolyte disturbances so that
appropriate adjustments to therapy can be initiated

 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

 Fluid Replacement Therapy

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

 Fluid Replacement Therapy

Disadvantages
Solution incompatibility
Adverse reactions
Infection

 Fluid Replacement Therapy

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 IMBB.
Lactated Ringer's SolutionC. D5 LRSD. D5 0.3 NaCl

 Composition of Different Intravenous Solution

 Fluid Replacement TherapyISOTONIC SOLUTION

 Fluid Replacement TherapyHYPOTONIC SOLUTION

 Fluid Replacement TherapyHYPERTONIC SOLUTION

 FLUID EXCESS/HYPERVOLEMIA
Renal and endocrine disturbances, malignancies, adenomas
Psychiatric Disorders, SIADH, Certain head injuries
Dietary Sodium Indiscretion
Failure of renal or hormonal regulatory functions
Excessive Sodium Intake
Overhydration
FLUID VOLUME EXCESS/HYPERVOLEMIA
 Sodium
ADH
Extracellular volume expands
Fluid becomes progressively hyponatremic
Normal Extracellular fluid
Normal sodium concentration
Renal Tubules


o Since ECF becomes hypoosmolar, fluid moves into the cells to
equalize the concentration on both sides of the cell membrane

o Thus there, is an increase in intracellular fluid

o The brain cells are particularly sensitive to the increase of

intracellular water, the most common signs of
hypoosmolaroverhydration are changes in mental status.
Confusion, ataxia, and convulsions may also occur.

o Other clinical manifestations include: hyperventilation, sudden

weight gain, warm, moist skin, increased ICP: slow bounding
pulse with an increase in systolic and decrease in diastolic
pressue and peripheral edema, usually not marked

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

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

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

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

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

 BURN

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

 Pathophysiology
Burn phase
Fluid- accumulation phase
Fluid-remobilization phase
Convalescent phase

o Fluid-accumulation phase:

o Last fro 36 to 48 hours after a burn injury

o Fluid shifts from vascular compartment to interstitial space – third-

space shift

o Edema caused by shifted fluid, which typically reaches maximum

within 8 hours after injury
o Circulation possibly compromised and pulses diminished from
severe edema

 Pathophysiology
Burn phase
Fluid- accumulation phase
Fluid-remobilization phase
Convalescent phase
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

 Pathophysiology
Burn phase
Fluid- accumulation phase
Fluid-remobilization phase
Convalescent phase

o Respiratory problems

o Muscle and tissue injuries

o GI problems

o Electrolyte imbalances:

o Common during fluid accumulation phase due to body’s

hypermetabolic needs and priority that fluid replacement takes
over nutritional needs during emergency phase

 Pathophysiology
Burn phase
Fluid- accumulation phase
Fluid-remobilization phase
Convalescent phase

o Fluid- remobilization phase :

o Also known as diuresis stage

o Starts about 48 hours after initial burn

o Fluid shifted back to vascular compartment

o Edema at burn site decreased, blood flow to kidneys increased,

increased urine output

o Fluid and electrolyte imbalances can still occur

 Pathophysiology
Burn phase
Fluid- accumulation phase
Fluid-remobilization phase
Convalescent phase

o Convalescent phase:
o Begins after first two phases has been resolved

o Characterized by healing or reconstruction of burn wound

o Major fluid shifts now resolved but possible further fluid and
electrolyte imbalances exist as a result of inadequate dietary
intake

o Anemia is common – severe burns typically destroy red blood

cells

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

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

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

 Reparative Process
Assessment of Extent
Extent / 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
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
Assessment of Burn Injury

 Reparative Process
Assessment of Extent
Extent / 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
Assessment of Burn Injury

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

 1° burn
2° burn
60

 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)

 2° burn
63

 64
Partial thickness (2°burn)

 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.
65

 3° burn
66

 Eschar:composed of denatured protein

67

 68
Full thickness (3°burn)

 Extent of surface area burned

Rule ofnines-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.
69

 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.
70

 71

 Lund and Browder chart

72

 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
o Hypovolemia

o Approximately 10% of plasma volume lost into tissue soon after a

severe burn

o Occurs because of the third space shift causes multiple effects:

o 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)

o 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

o Treatment
o Respiratory status takes priority over the treatment of the burn
injury

o cold compress or immerse in cool water (not ice) to ↓ heatIf burn

area is small

o May have ointment on the burn area

o 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
First 24 hours

 Burns
Second 24 hours

 Considerations

o AGE AND GENERAL HEALTH

o Mortality rates are higher for children < 4 y.o, particularly those <
1 y.o., and for clients over the age of 60 years.

o Debilitating disorders, such as cardiac, respiratory, endocrine, and

renal d/o, negatively influence the client’s response to injury and
treatment.

o Mortality rate is higher when the client has a pre-existing disorder

at the time of the burn injury

 Electrolytes

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

 Anions and Cations

Anions
Cations
Calcium
Magnesium
Potassium
Sodium
Bicarbonate
Chloride
Phosphorous

 WHAT DO ELECTROLYTES DO?

Promote neuromuscular irritability
 Maintain body fluid volume and osmolarity
Distribute body water between fluid compartments
Regulate acid-base balance

 Sodium (Na+)

o Controls and regulates volume of body fluids

o Its concentration is the major determinant of ECF volume

o Is the chief electrolyte of ECF

o Influence ICF Volume

o Participates in the generation and transmission of nerve impulses

o Is an essential electrolyte in the sodium-potassium pump

o RDA: not known precisely. 500 mg

o Eliminated primarily by the kidneys, smaller in feces and

perspiration

o Salt intake affects sodium concentrations

o Sodium is conserved through reabsorption in the kidneys, a

process stimulated by aldosterone

o Normal value: 135-145 mEq/L

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

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

 CLINICAL MANIFESTATIONS OF HYPONATREMIA

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

 COLLABORATIVE CARE MANAGEMENT

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

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

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

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

 COLLABORATIVE CARE MANAGEMENT

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

 Potassium (K+)

o Major cation of the ICF. Chief regulator of cellular enzyme activity

and cellular water content

o The more K, the less Na. The less K, the more Na

o Plays a vital role in such processes such as transmission of

electrical impulses, particularly in nerve, heart, skeletal, intestinal
and lung tissue; CHON and CHO metabolism; and cellular
building; and maintenance of cellular metabolism and excitation

o Assists in regulation of acid-base balance by cellular exchange

with H

o RDA: not known precisely. 50-100 mEq

o Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges,

prunes, melons, raisins, broccoli, and potatoes, meat, dairy
products

o Excreted primarily by the kidneys. No effective conserving

mechanism

o Conserved by sodium pump and kidneys when levels are low

o Aldosterone triggers K excretion in urine

o Normal value: 3.5 – 5 mEq/L

 CAUSES AND EFFECTS OF HYPOKALEMIA

Known as a low level of serum potassium, less than 3.5 mEq/L
Decreased Intake
↓ Food and Fluids as in starvation
Failure to replace GI losses
Increased Loss
↑ Aldosterone
Gastrointestinal losses
Potassium-losing diuretics
Loss from cells as in trauma, burns
Shift of Potassium into Cells
(No change in total body potassium)
HYPOKALEMIA
CNS
Lethargy, Diminished deep-tendon reflexes, Confusion, Mental depression
CV System
Decrease in standing BP, Dysrhythmias, ECG changes, Myocardial damage, Cardiac arrest
Muscles
Weakness, Flaccid paralysis, Weakness of respiratory muscles, Respiratory arrest
GI Tract
Anorexia N&V Abdominal distention
Kidneys
↓Capacity to concentrate waste, water loss, thirst, kidney damage
 PATHOPHYSIOLOGY OF HYPOKALEMIA
= Action Potential
Nerve and Muscle Activity
The cell becomes less excitable
Low Extracellular K+
Increase in resting membrane potential

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

 COLLABORATIVE CARE MANAGEMENT

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

 CAUSES AND EFFECTS OF HYPERKALEMIA

o Serum potassium level greater than 5.5 mEq/L

Excess Intake
Dietary intake of excess of kidney’s ability to excrete; Excess parenteral administration
Decreased Loss
Potassium-sparing diuretics; Renal failure; Adrenal insufficiency
Shift of Potassium out of the Cells
Extensive injuries, crushing injuries, metabolic acidosis
HYPERKALEMIA
CNS
Numbness, paresthesias
CV System
Conduction disturbance, ventricular fibrillation, Cardiac Arrest
GI Tract
N&V Diarrhea, Colic
Muscles
Early: irritability
Late: weakness leading to flaccid paralysis
Kidneys
Oliguria leading to anuria
 COLLABORATIVE CARE MANAGEMENT
Patients at risk should be identified: impaired renal function to avoid OTC, esp. NSAIDS which
provoke hyperkalemia; and salt substitutes that are high in potassium
Severity guides therapy
Mild: Withholding provoking agent (i.e., K supp)
Severe (> potassium is then excreted in the stool; Continuous cardiac monitoring6 mEq/L: cation-
 exchange resin such as Kayexalate (act by exchanging the cations in the resin for the potassium in
the intestine

o Bowel function must be maintained if Kayexelate therapy is to be

effective

o Potassium-wasting diuretics may be prescribed to promote further

potassium loss. Dialysis for patients with renal failure to eliminate
excess potassium

o Intravenous Ca Gluconate may be prescribed to counteract the

cardiac effects of hyperkalemia

o Insulin infusions and IV NaCO3 may be used to promote

intracellular uptake of K

 Calcium (Ca2+)

o Most abundant electrolyte in the body. 99% in bones and teeth

o Close link between calcium and phosphorus. High PO4, Low Ca

o Necessary for nerve impulse transmission and blood clotting and

is also a catalyst for muscle contraction and other cellular
activities

o Needed for Vitamin B12 absorption and use

o Necessary for strong bones and teeth and thickness and strength
of cell membranes

o RDA: 1g for adults. Higher for children and pregnant and lactating
women according to body weight, older people, esp. post-
menopausal

o Found in milk, cheese, and dried beans; some in meat and

vegetables

o Use is stimulated by Vitamin D. Excreted in urine, feces, bile,

digestive secretions, and perspiration

o Normal value 8.5 – 10.5 mg/dl

 CAUSES AND EFFECTS OF HYPOCALCEMIA

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

 PATHOPHYSIOLOGY OF HYPOCALCEMIA

o Calcium ions are thought to line the pores of cell membranes,

especially neurons

o Calcium and Sodium repel each other

o When serum calcium levels are low, this blocking effect is

minimized

o When Sodium moves more easily into the cell, depolarization

takes place more easily

o This results in increased excitability of the nervous system leading

to muscle spasm, tingling sensations, and if severe, convulsions
and tetany

o Skeletal, smooth, and cardiac muscle functions are all affected by

overstimulation

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

 TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY

TROUSSEAU'S SIGN
CHVOSTEK'S SIGN

 COLLABORATIVE CARE MANAGEMENT

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

 HYPERCALCEMIA: Serum concentration > 10mg/dLCauses and Effects

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

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

 CLINICAL MANIFESTATIONS OF HYPERCALCEMIA

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

 CLINICAL MANIFESTATIONS OF HYPERCALCEMIA

Calcium accumulates in the ECF and passes through the kidneys
Immobilization
Bone Demineralization
Calcium Stones
Ca Precipitation

 COLLABORATIVE CARE MANAGEMENT

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

 Magnesium (Mg2+)

o Mostly found within body cells: heart, bone, nerve, and muscle
tissues

o Second most important cation in the ICF, 2nd to K+

o Functions: Metabolism of CHO and CHON, protein and DNA

synthesis, DNA and RNA transcription, and translation of RNA,
maintains normal intracellular levels of potassium, helps maintain
electric activity in nervous tissue membranes and muscle
membranes

o RDA: about 18-30 mEq; children require larger amounts

o Sources: vegetables, nuts, fish, whole grains, peas, and beans

o Absorbed in the intestines and excreted by the kidneys

o Plasma concentrations of magnesium range from 1.5 – 2.5

mEq/L, with about one third of that amount bound to plasma
proteins

 HYPOMAGNESEMIA: Serum level < 1.5 mEq/L

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

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

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

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

 CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA

DEPRESSION
CONFUSION
CRAMPS
TETANY
CONVULSIONS

 COLLABORATIVE CARE MANAGEMENT

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

 HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/L

Seldom develops in the presence of normal renal function
May occur as a result of Mg replacement
May occur when MgSO4 is administered to prevent seizures resulting from eclampsia
Careful monitoring is imperative
 PATHOPHYSIOLOGY
Renal failure, Excessive IV infusion of magnesium, Decreased GI elimination and/or absorption,
etc.
Accummulation of Mg in the body
Mg Level Rises
Altered Electrical Conduction
Slowed heart rate and AV Block
Diminishing of reflexes, drowsiness, lethargy
Severe Respiratory Depression
Peripheral vasodilation
RESPIRATORY ARREST may occur
Hypotension, flushing, and increased skin warmth

 COLLABORATIVE CARE MANAGEMENT

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

 NURSING MANAGEMENT OF PATIENT WITH FLUID AND ELECTROLYTE IMBALANCES

 Parameter_____Fluid Excess___ Fluid Loss/Electrolyte Imbalance____

Behavior Tires easily; Change in behavior, confusion, apathy
Head, neck Facial edema, distended neck Headache, thirst, dry mucous membranes veins
Upper GI Anorexia, nausea, vomiting
Skin Warm, moist, taut, cool feeling Dry, decreased turgor where edematous
Respiration Dyspnea, orthopnea, productive Changes in rate and depth of respiration cough, moist
breath sounds
Circulation Loss of sensation in edematous Pulse rate changes, dysrhythmia, posturalareas, 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
A

 Refractory Edema
Pitting edema
Dependent edema

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

 Determined from analysis of patient data

Diagnostic TitlePossible Etiologic Factors
1 Deficient fluid volume Active fluid volume loss (hemorrhage, diarrhea, gastric intubation, wounds,
 diaphoresis), inadequate fluid intake, failure of regulatory mechanisms, sequestration of body fluids
2 Excess Fluid Volume Excess fluid intake, excess sodium intake, compromised regulatory
processes
D

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

 1,2 Intake and Output Monitoring

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

 1,2 Intake and Output Monitoring

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

 1 Replacement of Fluid and Electrolytes

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

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

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

 * Types of solutions
- D5W (hypotonic) is given short-term for hyponatremia
- D5NSS may be given depending on the serum levels of sodium and vascular volume + KCl to
meet normal intake needs and replace losses for hyponatremia
- Dextrose 5% in 0.2% normal saline is generally used as a maintenance fluid
- Dextrose 5% in ½ normal saline is generally used as a replacement solution for losses caused by
gastrointestinal drainage
- PNSS is given primarily when large amounts of sodium have been lost and for patients with
hyponatremia
- LRS is also isotonic because it remains in the extracellular space
- Fructose or 10-20% glucose in distilled water are hypertonic solutions and may partially meet
body needs for CHOs
- Dextran (commonly-used plasma expander) increases plasma volume by increasing oncotic
pressure. May cause prolonged bleeding time and is CI in patients with renal failure, bleeding
disorders, or severe CHF
I
 * Administration
- The rate should be regulated according to the patient’s needs and condition per doctor’s orders
- Monitor UO carefully. Refer marked decreases!
- Verify orders for potassium administration in patients with renal failure and untreated adrenal
insufficiency
- Usual rate for fluid loss replacement: 3ml/min
- Recognize signs of pulmonary edema (bounding pulse, engorged peripheral veins, hoarseness,
dyspnea, cough, and rales) that can result from ↑IV rate
- If infiltration occurs, the infusion should be stopped immediately and relocated. Peripheral IV sites
are generally rotated every 72 hours
- For dextran and other plasma expanders, observe for anaphylactic reaction (apprehension,
dyspnea, wheezing, tightness of chest, angioedema, itching, hives and hypotension). If this
happens, switch infusion to nonprotein solution and run at KVO rate, notify physician and monitor
VS
- Pronounced and continued thirst despite administration of fluids is not normal and should be
reported (may indicate DM or hypercalcemia)
I

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

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

 Fluids and Electrolytes

Acid-base balance

 DRAWING ARTERIAL BLOOD GASES

ALLEN’S TEST
ARTERIAL PUNCTURE

 NORMAL ACID-BASE BALANCE

Definition and Implications
Normal Value
Parameter
Partial pressure of oxygen in arterial blood (decreases with age)
In adults < 60 years:
60-80 mmHg = mild hypoxemia
40-60 mmHg = moderate hypoxemia
< 40 mmHg = severe hypoxemia
80-100 Hg
PaO2
Identifies whether there is acidemia or alkalemia:
pH<7.35 = acidosis; pH>7.45 = alkalosis
7.35-7.45
 pH
Partial pressure of CO2 in the arterial blood:
PCO2<35 mmHg = respiratory alkalosis
PCO2>45 mmHg = respiratory acidosis
35-45 mmHg
PaCO2
Estimated HCO3 concentration after fully oxygenated arterial blood has been equilibrated with CO2
at a PCO2 of 40 mmHg at 38C; eliminates the influence of respiration on the plasma HCO3
concentration
22-26 mEq/L
Standard HCO3

 BASIC REGULATION OF ACID-BASE BALANCE

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3
Kidney
Lungs
The lungs help control acid-base balance by blowing off or retaining CO2. The kidneys help
regulate acid-base balance by excreting or retaining HCO3

 TYPES OF ACID-BASE DISTURBANCES

Depression of the central nervous system, as evidenced by disorientation followed by coma
ACIDOSIS
Overexcitability of the nervous system; muscles may go into a state of tetany and convulsioons
ALKALOSIS

 EXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCES

HCO3
PCO2
pH
CONDITION
Normal
↑
↑
↑
↑
↑
↓
↓
Normal
Respiratory Acidosis
Uncompensated
Partly Compensated
Compensated
Normal
↓
↓
↓
↓
↓
↑
↑
Normal
 Respiratory Alkalosis
Uncompensated
Partly Compensated
Compensated
↓
↓
↓
Normal
↓
↓
↓
↓
Normal
Metabolic Acidosis
Uncompensated
Partly Compensated
Compensated
↑
↑
↑
Normal
↑
↑
↑
↑
Normal
Metabolic Alkalosis
Uncompensated
Partly Compensated
Compensated

 Compensation

 RESPIRATORY ACIDOSIS: CARBONIC ACID EXCESS

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

 NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS

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

 NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS

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

 NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

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

 NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

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

 NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

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

 NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

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

 RESPIRATORY ALKALOSIS: CARBONIC ACID DEFICIT

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

 NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS

ASSESSMENT
* Health Hx: anxiety, shortness of breath, muscle cramps or weakness, palpitations, panic,
dyspnea
* Physical Examination: light-headedness, confusion as a result of cerebral hypoxia,
hyperventilation, tachycardia or arrhythmia, muscle weakness, (+) Chvostek’s sign or Trousseau’s
sign indicating a low ionized serum calcium level secondary to hyperventilation and alkalosis,
hyperactive deep tendon reflexes, unsteady gait, muscle spasms to tetany, agitation, psychosis,
seizures in extreme cases, decreased potassium levels
NURSING DIAGNOSES include but are not limited to:
Diagnostic TitlePossible Etiologic Factors
1 Anxiety Stress, fear
2 Ineffective breathing pattern Hyperventilation, anxiety
3 Disturbed thought processes CNS excitability; irritability
4 Risk for injury Change in LOC, and potential for seizures

 NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS

EXPECTED PATIENT OUTCOMES include but are not limited to:
1 Will report decreased anxiety; verbalizes methods to cope with anxiety
2 Will return to normal respiratory rate and rhythm or at least decreased hyperventilation, with
return to baseline ABGs
3 Will exhibit reorientation to person, place, and time as per patient’s baseline
4 Will be free from injury
INTERVENTIONS
1 Allay anxiety
- Give antianxiety medications as ordered
- Have patient breath into a paper bag
- Teach relaxation techniques when initial anxiety attack is over

 NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

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

 NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS

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

 METABOLIC ACIDOSIS: BICARBONATE DEFICIT

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

 NURSING MANAGEMENT OF METABOLIC ACIDOSIS

ASSESSMENT
* Health Hx: anorexia, nausea, vomiting, abdominal pain, headache, thirst if the patient is
dehydrated
* Physical Examination: confusion, hyperventilation, warm, flushed skin, bradycardia and other
dysrhythmias, decreasing LOC, nausea, vomiting, diarrhea, Kussmaul respirations, and acetone
breath, especially if acidosis is due to ketoacidosis. Symptoms may progress to coma if untreated
NURSING DIAGNOSES include but are not limited to:
Diagnostic TitlePossible Etiologic Factors
1 Disturbed thought processes Secondary to CNS depression
2 Decreased cardiac output Dysrhythmias
3 Risk for injury Secondary to altered mental state
4 Risk for imbalanced fluid Diarrhea, renal failure
volume

 NURSING MANAGEMENT OF METABOLIC ACIDOSIS

EXPECTED PATIENT OUTCOMES include but are not limited to:
1 Will return to usual baseline LOC
2 Will return to normal baseline parameters for vital signs with improved CO and decreased or
resolved dysrhythmias
3 Will remain in a safe, secure environment without injury
4 Will maintain fluid and electrolyte balance and stable renal status
INTERVENTIONS
1 Coping with disturbed thought processes
- Monitor LOC and reorient as necessary
- Monitor VS, esp. RRR, BP, and T
 - Monitor ABGs to assess the effects of treatment
- Institute cardiac monitoring as ordered

 NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS

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

 NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS

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

 METABOLIC ALKALOSIS: BICARBONATE EXCESS

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

 NURSING MANAGEMENT OF METABOLIC ALKALOSIS

ASSESSMENT
* Health Hx: Prolonged vomiting or nasogastric suctioning, frequent self-induced vomiting, muscle
weakness, light- headedness, ingestion of large amounts of licorice or antacids, use of diuretics,
muscle cramping, twitching, or tingling
* Physical Examination: mental confusion, dizziness, changes in LOC, hyperreflexia, tetany,
dysrhthmias, seizurees, respiratory failure, positive Chvostek’s or Trosseau’s sign if the patient has
a low ionized serum calcium level, decreased hand grasps, generalized muscle weakness,
decreased serum calcium or potassium level, impaired concentration, seizures, ECG changes
consistent with hypokalemia
NURSING DIAGNOSES include but are not limited to:
Diagnostic TitlePossible Etiologic Factors
1 Disturbed thought processes CNS excitation
2 Decreased cardiac output Dysrhythmias and electrolyte imbalances
3 Risk for injury Muscle weakness, tetany, confusion and possible seizures
4 Risk for imbalanced fluid Nasogastric drainage, diuretic therapy
volume fistula

 NURSING MANAGEMENT OF METABOLIC ALKALOSIS

EXPECTED PATIENT OUTCOMES include but are not limited to:
1 Will return to usual baseline LOC and orientation
2 Will return to normal baseline parameters for vital signs with improved CO with resolution of
electrolyte imbalances and decreased or resolved cardiac dysrhythmias
3 Will remain in a safe, secure environment without injury
 4 Will maintain fluid and electrolyte balance
INTERVENTIONS
1 Coping with disturbed thought processes
- Monitor LOC and reorient as necessary
- Monitor VS, esp. RRR, BP, and T
- Monitor ABGs to assess the effects of treatment
- Institute cardiac monitoring as ordered

 NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS

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

 NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS

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

 CRITICAL THINKING EXERCISES

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