NURSING CARE OF THE ADULT PATIENT
EXPERIENCING FLUID AND ELECTROLYTE
DISTURBANCES: SCIENTIFIC PRINCIPLES,
NURSING INTERVENTIONS AND HEALTHCARE
PROMOTION
NSG. 3088
LauriAnne Martin
READING ASSIGNMENT:

Black, J.M. & Hawks, J.H. (2005). MedicalSurgical Nursing: Clinical Management for
Positive Outcomes (7th ed.) St. Louis:
Elsevier Saunders. Unit 3 (p 196); Ch 13-15
(p 205-261)
Lecture Objectives:

1.
Define intracellular fluid (ICF), extracellular fluid
(ECF), intravascular fluid, interstitial fluid,
hypertonic (hyperosmolar), hypotonic
(hyposmolar),
diffusion, osmolality, and
osmolarity.

2.
Describe fluid movement by diffusion and
osmosis.

5.
Differentiate the hypotonic, isotonic and
hypertonic intravenous water and electrolyte
solutions.
Apply the nursing process to extracellular fluid
volume deficit (dehydration) and extracellular fluid
volume excess: assessment, analyze, plan,
implement and evaluate.
Distinguish the etiology, pathophysiology, clinical
manifestation, and medical management of
extracellular fluid volume deficit and excess.
1
Lecture Objectives: (cont.)

6.
Outline situations in which hypotonic, isotonic and
hypertonic intravenous water and electrolyte
solutions are used.

8.
Analyze the modifications of management of fluid
volume excess in elderly clients.

9.
Describe intracellular fluid volume excess (water
intoxication).

10.
Apply the nursing process to extracellular fluid
volume shift (third spacing); assessment,
analyze, plan, implement, and evaluate.
Discuss aspects of care that may be appropriately
delegated to unlicensed assistant personnel and
family members in the management of fluid
volume deficit.
Lecture Objectives: (cont.)

11. Identify the etiology, pathophysiology, clinical
manifestations, and medical management of
extracellular
fluid volume shift.

12. Formulate a nursing care plan for the client with
extracellular fluid volume deficit or excess, intracellular
volume excess, and extracellular fluid volume shift.
fluid

13. Identify normal serum ranges for electrolyte: sodium,
chloride, potassium, calcium, phosphorus, magnesium,
and calcium.

14. Formulate a diet for imbalances of sodium, potassium, and
calcium.
Lecture Objectives: (cont.)

15.
Compare electrolyte imbalances in terms of
etiology, risk factors, clinical manifestations, and
pathophyisology then apply the nursing process to
such imbalances.
A.
B.
C.
D.
E.

Hyponatremia
Hypernatremia
Hypokalemia
Hyperkalemia
Hypocalcemia
F.
G.
H.
I.
J.
Hypercalcemia
Hypophosphatemia
Hyperphosphatemia
Hypomagnesemia
Hypermagnesemia
16.
Discuss concepts of acid-base balance to include
regulation and compensation to correct
imbalances by the respiratory, urinary, and blood buffer
systems.
17.
Describe the etiologic factors and
pathophysiology that underlie respiratory acidosis,
respiratory
alkalosis, metabolic acidosis, and
metabolic alkalosis.
18.
Apply the nursing process to each acid-base
imbalance: assessment, analyze, plan,
implement,
and evaluate.
2
Physiology Review
Normal body fluid function

Intracellular (ICF) : fluid within the cells- 2/3 of total
Extracellular (ECF) : fluid outside the cells- 1/3 total

Interstitial: third spaces around the cells
Intravascular: in the bloodstream
Hydrostatic pressure : pressure within the capillary
Osmotic( oncotic) pressure : pressure resulting
from the presence of plasma proteins (albumin) that
draws fluid to it; pulls fluid back into the vessel
Physiology Review (cont)

Fluid movement

Diffusion- movement of fluids or substances
across a membrane because of differences in
concentration
Osmolality and osmolarity- measured by the
number of dissolved particles per kg. of water

Sodium used to measure osmolality
Normal osmolality is 275- 295 mOsm/kg.
Hyperosmolar (hypertonic) state that is the result of
osmolality > 295
Hyposmolar (hypotonic) state that results when
oxmolality is < 275
Extracellular Fluid Volume Deficit:
Dehydration

Average daily fluid intake 1500 to 2000 ml.
Etiology

Lack of fluid intake
Excess fluid loss
Alteration in the fluid balance regulators

Thirst
Hormones
Lymphatic system
Kidneys
3
Degrees of Dehydration

Mild – 1 to 2 L of water loss (2% body wt.)
Moderate- 3 to 5 L water loss (5% body wt)
Severe- 5 to 10 L water loss (8% body wt)
Lack of Fluid Intake

Causes

Cognitive and physical impairments reduce
fluid intake
Impaired thirst mechanisms
Hyperosmolarity conditions
Excess Fluid Losses

Potential causes of excess fluid loss

Unmonitored use of diuretics
Severe vomiting and diarrhea
Fever and diaphoresis
GI suction and fistula drainage
Blood loss and burns
Third spacing of fluids
4
Pathophysiology of a Fluid Deficit

Fluids that are lost from the intravascular
spaces contribute to the following
compensatory mechanism:

Interstitial fluids move to restore volume
Antidiuretic hormone and aldosterone secretion
causes the reabsorption of sodium and water
Baroreceptors are stimulated, leading to
vasoconstriction and an increased HR
Osmoreceptors signal the thirst mechanism
Fluid deficit (dehydration) occurs when
compensation fails to restore blood volume
Types of Extracellular Fluid Volume
Deficit

Hyperosmolar or hypertonic deficit

Iso-osmolar or isotonic deficit

Water loss is greater than electrolyte (sodium)
loss
Water and electrolyte (sodium) losses are
equal
Hypotonic deficit

Electrolyte loss is greater than fluid loss
Clinical Manifestations of a Fluid
Deficit

Loss of body weight

Changes in intake and output

Thirst, decreased uop, concentrated urine
Changes in vital signs

Daily weight most accurate measure of fluid lo
May not occur d/t trapped fluid in third space
Decrease in blood pressure, central venous pressure
(CVP), etc.
Increased heart rate and temperature
Other: dry mucous membranes, decreased skin
turgor– tenting of skin not diagnostic in elderly
5
Diagnostic Findings During a Fluid
Deficit

Indicators of hemoconcentration

Osmolality above 295 mOsm/kg

(Rough estimate- 2 X Na = osmolality)
Plasma sodium > 145mEq/L
BUN > 25 mg/dl
Glucose > 120 mg/dl
Hematocrit > 55%
Urine specific gravity > 1.030
Outcome Management of a Fluid
Deficit

Fluid Restoration

Oral rehydration

IV rehydration

Used if loss is mild and pt. can drink—oral glucose
and electrolyte solutions
Used in severe situations--- volume calculated on wt.
and presence of co-morbidities
Monitor for complications
Correct the underlying problem
Outcome Management of a
Fluid Deficit (cont.)

Nursing Management

Assessments

Vital signs
Peripheral vein filling
Intake, output, and daily weights
Lab values
Oral cavity
Skin turgor
Restore fluids
Control underlying problem
Monitor for complications
6
Diagnosis and Outcomes for Fluid
Deficits

Nursing Diagnosis

Deficient Fluid Volume R/T insufficient fluid intake,
diarrhea, hemorrhage, or third-space fluid loss
Outcomes: return of levels of body fluids

Oral intake 1500-2500 ml/24 hours
Urine output > 0.5 ml/kg/hr
Stable blood pressure and pulse
Increase body weight by 0.5- 1 pound/ day
Absence of crackles
Moist tongue and mucus membranes
Lab values within normal ranges in 48-72 hours
Diagnosis, Outcomes, and
Interventions for Fluid Deficits

Nursing Diagnosis

Impaired Oral Mucous Membranes R/T lack of
oral intake or other causes
Outcomes: mucous membranes are restored

Lips, tongue, and gums are moist
Lips, tongue, and gums are free of dried mucus
Interventions

Assessments
Oral care every 2-4 hours
Diagnosis, Outcomes and
Interventions for Fluid Deficits (cont)

Nursing Diagnosis

Risk for Injury
Outcomes
Client will remain free of injury
Interventions

Provide safety in position changes
Place bed alarms if confused
7
Interventions for Fluid Deficits

Teach

Appropriate fluid replacement
Exercise with adequate fluid replacement

Cool water before exercise
150-200 ml q 15 min. during exercise
Do not decrease fluid intake for incontinence
Drink fluids even in the absence of thirst
Evaluation: volume deficits usually
resolve in 8-24 hours
Intracellular Fluid Volume Deficit

Caused by severe dehydration
Rare in healthy adults—occurs often in
elderly and in conditions resulting from
acute water loss
Compensatory mechanisms similar to
ECFVD
Manifestations: Fever, CNS changes
Outcome management: Restoration of
fluid volume via IV replacement
Extracellular Fluid Volume Excess:
Fluid Overload

Fluid overload or overhydration
Hypervolemia

Excess fluids in the vascular system
Third-spacing

Excess fluids in the interstitial spaces
8
Extracellular Fluid Volume Excess:
Fluid Overload (cont.)

Etiology

Simple overloading of fluids
Failure to excrete fluids

Renal failure
Edema
Pathophysiology

Hydrostatic pressure increases, pushing
fluids into the interstitial spaces
Peripheral vascular resistance increases
Pulmonary and/or peripheral edema and
heart failure develop
Clinical Manifestations of Fluid
Excess

Respiratory and cardiovascular

Cough, dyspnea, crackles, pallor, etc.
Bounding pulse, elevated B/P, increased CVP
JVD
Other

Peripheral edema
Weight gain
Confusion, seizure, coma
9
Clinical Manifestations of Fluid Excess
(cont.)

Indicators of hemodilution

Osmolality < 275 mOsm/kg
Sodium < 135 mEq/l
Hematocrit , 45%
Urine specific gravity < 1.010
BUN < 8 mg/dl
Outcome Management of Fluid
Excess

Restrict dietary sodium

Restrict fluid
Promote urine output

Mild- 4-5 gm Na
Moderate- 2 gm Na
Severe- 0.5 gm Na
Diuretics- usually combination of potassium sparing
and potassium wasting diuretics
Improve myocardial function

Digitalis
Angiotensin-converting enzyme (ACE) inhibitors and
beta-blockers
Outcome Management for Fluid
Excesses (cont.)

Nursing management

Assessments

Vital signs, lung sounds
Edema
Intake and output
Lab values- plasma osmolality, sodium level,
hematocrit, urine specific gravity
Observe for changes in level of consciousness
10
Diagnosis and Outcomes for Fluid
Volume Excess

Nursing Diagnosis

Excess Fluid Volume R/T specific cause
Outcomes: return of normal levels of body
fluids

Stable blood pressure and pulse
Decrease body weight of .05- 1 lb./ day
Absence of confusion, coughing, crackles,
edema
Lab values, normal levels in 48-72 hours
Interventions for Fluid Volume Excess

Reduce sodium and fluid intake
Mobilize fluids

Turning, positioning
Prevent complications

Elevate head of bed
Monitor lab values
Provide skin care
Interventions for Fluid Volume Excess
(cont.)

Teach

Low-sodium diet
Use of alternative seasonings
Fluid restriction
Daily weights
11
Modifications for Older Patients

Response time to treatment is slower
Increased risk for side effects

Decreased renal and liver function
Drug interactions
Some lab studies not as accurate in this age
group

Creatinine levels more accurate at assessment of
renal function than BUN
Intracellular Fluid Volume Excess:
Water Intoxication

Etiology

Water excess or solute (sodium) deficit

Excessive administration or intake of hypo-osmolar
fluids (especially 5% dextrose or 0.45% saline)
Pathophysiology

Hypo-osmolar fluids in the ECF compartment
move by osmosis to the region of higher
sodium concentration in the cells (ICF
compartment) to equalize concentration of Na
Clinical Manifestations of a Fluid
Volume Excess: Water Intoxication

Neurologic

Increased intracranial pressure
Altered level of consciousness
Pupillary changes
Lab indicators of hemodilution

Plasma sodium less than 125 mEq/L
Decreased hematocrit
12
Outcome Management of Fluid
Volume Excess: Water Intoxication

Medical management

First priority is to reduce intracranial pressure
Nursing management

Frequent vital signs, neuro check
Hourly I&O, daily weights
Prevent increased intracranial pressure
Provide safety
Monitor IV fluids-sodium rich solutions
Extracellular Fluid Volume Shift:
Third-Spacing

A change in the location of ECF between
the intravascular and interstitial spaces
Etiology

Increased capillary permeability
Decreased serum protein levels
Obstructed lymphatic drainage
Pathophysiology

Tissue injury (burns) or protein malnutrition
leading to fluid shift
Clinical Manifestations of Fluid
Volume Shift: Third-Spacing

Cardiovascular

Weak pulse, hypotension, pallor, cool limbs
Other

Oliguria
Decreased level of consciousness
Elevated BUN, hematocrit, and urine specific
gravity
Weight doesn’t change– fluid has only shifted
Fluid may obstruct an organ nerve, or blood
vessel causing additional symptoms
13
Outcome Management for a Fluid
Volume Shift: Third-Spacing

Identify underlying cause
Replace fluids
Stabilize other problems
Nursing management

Assessments
Prevent skin breakdown
Monitor for signs of fluid overload with fluid
replacement
Electrolytes

Chemicals that carry a positive or
negative charge
Impact the electrical impulses in nerves
and muscles
Imbalance is present whenever there is an
excess or deficit in the serum
Plasma Ranges for Electrolytes
Sodium (Na)
135-145 mEq/L
Potassium (K)
3.5-5.0 mEq/L
Chloride (Cl)
98-106 mEq/L
Calcium (Ca)
4.5-5.5 mEq/L
Phosphorus (P)
1.2-3.0 mEq/L
Magnesium (Mg)
1.5-2.5 mEq/L
Ionized calcium (ICa)
1.18-1.30 mEq/L
14
Electrolyte Imbalances

Etiology and risk factors

Decreased intake and availability or increased
loss of an electrolyte
Increased intake and retention or decreased
excretion of an electrolyte
Diagnosis of imbalance

Through plasma levels in lab studies
Through clinical manifestations
Related Nursing Diagnoses

No direct nursing diagnoses for
electrolyte imbalances
Indirect diagnoses

Collaborative problems

Risk for injury
Hyponatremia, hyperkalemia. Etc.
Nursing activities developed for
collaborative problems
Sodium Imbalances: Hyponatremia

Sodium < 135 mEq/L
Etiology and risk factors

Increased loss: diuretics, vomiting, diarrhea,
excessive perspiration, etc.
Inadequate intake
Pathophysiology

Intracellular edema due to fluid shifts
15
Clinical Manifestations:
Hyponatremia

Sodium < 125 mEq/L

Neurologic: headache, confusion
Cardiovascular: decreased BP, tachycardia,
thready pulse
Pulmonary: crackles, dyspnea
Gastrointestinal: nausea, vomiting
Other: dry skin and mucous membranes
Outcome Management: Hyponatremia

Medical and nursing management

Restore sodium levels: replacement
Reduce sodium loss: prevent vomiting and
diarrhea
Restore sodium balance
Outcomes

The nurse will monitor sodium and chloride
levels and for clinical manifestations of
hyponatremia
Sodium Imbalances: Hypernatremia

Sodium > 145 mEq/L
Etiology and risk factors

Excess fluid loss or sodium intake
Inadequate water intake
Pathophysiology

Fluid shift causing cellular dehydration
Increased myocardial depolarization
16
Clinical Manifestations:
Hypernatremia

Early symptoms- Na > 145 mEq/L

Polyuria followed by oliguria, anorexia, N&V,
weakness, restlessness
Late symptoms– Na > 155 mEq/L

Confusion, seizures, coma, tremors, muscle
twitching, rigid paralysis
Outcome Management:
Hypernatremia

Medical/nursing outcome management

Goal is correction of the body water osmolality with
restoration of cell volume, by decreasing the ratio of
sodium to water in the ECF
Replace fluid loss-slow IV administration of
hyposmolar electrolyte solutions (0.2% or 0.45% NaCl
or 5% dextrose in water)
Sodium restriction- know high and low Na foods and
teach accordingly
Outcomes

The nurse will monitor plasma sodium and chloride
levels and for clinical manifestations of hypernatremia
Diagnosis, Outcomes, Interventions

Diagnosis

Outcomes

Impaired oral mucous membranes R/T lack of
body water
Maintain moist oral mucous membranes
Interventions

Oral care
Offer low-acid juices
17
Potassium Imbalances: Hypokalemia

Potassium < 3.5 mEq/L
Etiology and risk factors

Inadequate intake of potassium
Excess output of potassium
Medications linked to potassium loss
(especially diuretics)
Pathophysiology

Increased excitability of nerves and muscles
Clinical Manifestations: Hypokalemia

Cardiovascular

Gastrointestinal

Anorexia, abdominal distention
Musculoskeletal

Electrocardiogram (EKG) changes,
dysrhythmias, arrest, decreased myocardial
contraction
Muscle weakness, leg cramps, paralysis
Neurological

Fatigue, hyporeflexia, confusion, convulsions,
coma
Outcome Management: Hypokalemia

Medical/nursng management

Restore potassium levels

Mild or moderate hypokalemia- Administer foods
high in potassium or oral potassium supplements
(give with juice or food to decrease irritation to
gastric mucosa)
Severe hypokalemia- IV replacement- NEVER GIVE
POTASSIUM IV PUSH ( must dilute and give slowly)
Ongoing assessments
18
Diagnosis, Outcomes, Interventions

Diagnosis

Outcome

Risk for injury R/T muscle weakness,
hypotension, seizures
Client will not sustain injury
Interventions

Implement safety precautions
Diagnosis, Outcomes, Interventions
(cont.)

Diagnosis

Outcomes

Imbalanced Nutrition: Less than Body
Requirements R/T insufficient intake of
potassium-rich foods
Adequate intake of potassium-rich foods
Interventions

Educate patient regarding potassium-rich
foods and supplements
Potassium Imbalances: Hyperkalemia

Potassium > 5.0 mEq/L
Etiology and risk factors

Retention of potassium
Excess intake of potassium
Release from cells following trauma
Pathophysiology

Altered excitability of nerves and muscles
19
Clinical Manifestations: Hyperkalemia

Cardiopulmonary

Gastrointestinal

Hypotension, cardiac and respiratory arrest
due to muscle paralysis
Intestinal colic, diarrhea
Musculoskeletal

Paresthesias, muscle irritability
Outcome Management: Hyperkalemia

Medical/nursing management

Restore potassium balance

Dietary restrictions
Administer fluids and encourage diuresis
Utilize cation exchange resin- Kayexalate
Outcomes

The nurse will monitor potassium levels and
report abnormal findings and symptoms or
hyperkalemia
Calcium Imbalances: Hypocalcemia

Calcium < 4.5 mEq/L or 9 mg/dl
Etiology

Inadequate intake of calcium or vitamin D
Parathyroid disease or removal
Pathophysiology

Increased neuromuscular excitability
20
Clinical Manifestations:
Hypocalcemia

Neuromuscular

Cardiovascular

Numbness and tingling of hands, toes, and
lips; facial twitching, seizures; tetany- NEEDS
IMMEDIATE ATTENTION
Hypotension, dysrhythmias, weak pulse
Skeletal

Spontaneous fractures
Outcome Management:
Hypocalcemia

Medical/nursing management

Restore calcium balance

Replacement
Educate regarding calcium-rich foods
Move patient with caution
Careful assessments
Calcium Imbalances:
Hypercalcemia

Calcium > 5.5 mEq/L or 11 mg/dl
Etiology and risk factors

Metastatic malignancy, thiazide diuretic
therapy, hyperparthyroidism
Pathophysiology

Decreased neuromuscular excitability
21
Clinical Manifestations:
Hypercalcemia

Urinary

Polyuria related to an osmotic diuresis
Gastrointestinal
Anorexia, constipation, nausea, abdominal
distention
Neuromuscular

Fatigue, depression, muscle weakness
Outcome Management:
Hypercalcemia

Medical/nursing management

Restore calcium balance

IV hydration and diuretics
Avoid calcium-containing products and foods high
in calcium
Safety precautions
Educate to avoid calcium intake
Phosphate Imbalances:
Hypophosphatemia

Level < 1.2 mEq/L
Etiology and risk factors

Clinical manifestations

Excess loss or lack of intake
Long-term use of antacids
Decreased cardiac and respiratory function,
weakness, confusion, etc.
Outcome management

Restore phosphate balance
22
Phosphate Imbalances:
Hyperphosphatemia

Level > 3 mEq/L
Etiology and risk factors

Excessive intake
Clinical manifestations
Early: tachycardia, palpitations
Late: tetany, hyperreflexia
Outcome management

Eliminate excess phosphate
Magnesium Imbalances:
Hypomagnesemia

Level < 1.5 mEq/L or 1.8 mg/dl

Alcoholism, malabsorption syndromes,
medications, history of cocaine abuse
Clinical manifestations

Related to less intake and absorption
Risk factors
Myocardial irritability, convulsions, etc.
Outcome management

Replacement
Magnesium Imbalances:
Hypermagnesemia

Levels > 2.5 mEq/L or 3 mg/dl
Clinical manifestations

Muscle weakness, sedation, areflexia ( loss of
deep tendon reflexes), respiratory paralysis
Outcome management

IV hydration and diuretics
23
Regulation of Acid-Base Balance

Modulation of serum pH blood buffer
systems
Regulation of volatile acid by lungs
Regulation of fixed acids and
bicarbonate by the kidneys
Acid-Base Regulatory Systems

Acid-base compensation

Acid-base correction

Analysis of arterial blood gases

pH normalized by kidneys or lungs
Occurs when problem is resolved
Determines type of imbalance
Evaluates degree of compensation
Respiratory Alkalosis

Etiology

Pathophysiology
Clinical manifestations

Hyperventilatory states
Hyperventilation
Paresthesias, lightheadedness, confusion
High pH and low PaCo2
24
Respiratory Alkalosis

Outcome management

Treatment of underlying disorder
Respiratory support

O2 therapy
Rebreathing
Respiratory Acidosis

Etiology: hypoventilatory status
Pathophysiology
Clinical manifestations

Hypoventilation, hypoxemia
Low pH and high PaCo2
Respiratory Acidosis (cont.)

Outcome management

Treat underlying cause
Respiratory support

Administer exogenous alkali

Mechanical ventilation
Sodium bicarbonate
25
Metabolic Alkalosis

Etiology

Loss of acid or gain of base
Pathophysiology
Clinical manifestations

Adaptive hypoventilation
Lethargy, confusion, seizures
High pH and high HCO3
Metabolic Alkalosis (cont.)

Outcome management

Treat the underlying disorder
Promote loss of bicarbonate

Administer exogenous acid

Acetazolamide sodium (Diamox)
Metabolic Acidosis

Etiology

Pathophysiology
Clinical manifestation

Accumulation of acid or loss of base
Compensatory hyperventilation
Low pH and low HCO3
26
Metabolic Acidosis (cont.)

Outcome management

Treatment of underlying disorder
Respiratory support

Administration of exogenous alkali

Mechanical ventilation
Sodium bicarbonate
Complex Acid-Base Disorder

Nursing management

Assessment of patients at risk

Diabetes, renal disease, the older adult
Vomiting, diarrhea, enteric drainage
Burns, fever, sepsis
Total parenteral nutrition (TPN) or enteral feedings
Mechanical ventilation
Complex Acid-Base Disorders (cont.)

Obtain arterial blood gases

Perform Allen’s test prior to obtaining
Minimize sampling errors
Interpret arterial blood gas values
27
Diagnosis, Outcomes, Interventions

Nursing Diagnoses

Ineffective Breathing Pattern
Ineffective Tissue Perfusion
Risk for Injury

Outcomes

Interventions

Collaborative
Correct the cause
Provide respiratory support
Administer exogenous acid or alkali
Analysis of Arterial Blood Gases

Classify the pH: norm: 7.35 to 7.45

Acidemia: < 7.35
Alkalosis: >7.45
Assess PaCo2: norm: 35 to 45 mm Hg

Respiratory acidosis: > 45 mm Hg
Respiratory alkalosis:< 35 mm Hg
Analysis of Arterial Blood Gases (cont.)

Assess HCO3: norm: 22 to 26 mEq/L

Metabolic acidosis: < 22 mEq/L
Metabolic alkalosis: > 26 mEq/L
Determine if compensated