Fluid & Electrolyte Imbalance

ANTIDIURETIC HORMONE REGULATION MECHANISMS

Osmoreceptors in
hypothalamus

Osmolarity

Hypothalamus
Blood
volume
or BP

Volume receptor
Atria and great veins

ADH

Posterior
pituitary gland

Kidney
tubules
H2O
reabsorption

Narcotics, Stress,
Anesthetic agents, Heat,
Nicotine, Antineoplastic
agents, Surgery

vascular
volume and
osmolarity

ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM

Serum Sodium
Blood volume

RENIN

Juxtaglomerular
cells-kidney

Angiotensinogen in
plasma

Angiotensin I
Angiotensinconverting
enzyme

Sodium
resorption
(H2O resorbed
with sodium);
Blood volume

Via vasoconstriction of arterial smooth muscle

Angiotensin II
Kidney tubules

ALDOSTERONE

Adrenal Cortex
Intestine, sweat
glands, Salivary
glands

Fluid Types
Fluids in the body generally arent 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
1

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 bodys
compartments from the cell to the interstitial spaces, to the blood vessels and back again
Types of Transport
A. Active transport
B. Passive transport
Diffusion
Osmosis
Filtration
FLUID BALANCE
The desirable amount of fluid intake and loss in adults ranges from 1500 to 3500 mL each
24 hours. Ave= 2500 mL
Normally INTAKE = OUTPUT
FLUID IMBALANCE
Changes in ECF volume = alterations in sodium balance
Change in sodium/water ratio = either hypoosmolarity or hyperosmolarity
Fluid excess or deficit = loss of fluid balance
As with all clinical problems, the same pathophysiologic change is not of equal
significance to all people
For example, consider two persons who have the same viral syndrome with associated
nausea and vomiting
FLUID DEFICIT/HYPOVOLEMIA
May occur as a result of:
Reduced fluid intake
Loss of body fluids
Sequestration (compartmentalizing) of body fluids

Pathophysiology and Clinical Manifestations

DECREASED FLUID VOLUME

Stimulation of thirst
center in hypothalamus

Renin-AngiotensinAldosterone System
Activation

ADH Secretion

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
Difficulty with speech

blood pressure
heart rate
respiratory rate

Restlessness and Apprehension

Hypovolemia
Fluid Imbalance
Fluid Volume Deficit
(Hypovolemia, Isotonic Dehydration)

Common Causes

Hemorrhage

Vomiting

Diarrhea

Burns

Diuretic therapy

Fever

Impaired thirst
Clinical Manifestations

Signs/Symptoms

Weight loss

Thirst

Orthostatic changes in pulse rate and bp

Weak, rapid pulse

Decreased urine output

Dry mucous membranes

Poor skin turgor

Treatment/Interventions (FVD)

Fluid Management

Diet therapy Mild to moderate dehydration. Correct with oral fluid replacement.

Oral rehydration therapy Solutions containing glucose and electrolytes. E.g., Pedialyte,
Rehydralyte.

IV therapy Type of fluid ordered depends on the type of dehydration and the clients
cardiovascular status.
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
Warning Signs
Cool pale skin over the arms and legs
Decreased central venous pressure
4

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
states
adequate food and fluids

*
* Disease
* Limited access to

Development of a plan of care

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

Collaboration with the nurse,

patient, family members, and
other health care providers for
continued assessment and
treatment of problems

Family members should be

educated about the importance
of fluid and nutrition intake

FLUID EXCESS/HYPERVOLEMIA
Psychiatric Disorders,
SIADH, Certain head injuries

Overhydration

Dietary Sodium Indiscretion

Excessive Sodium Intake

Renal and endocrine disturbances,

malignancies, adenomas

Failure of renal or hormonal

regulatory functions

FLUID VOLUME EXCESS/HYPERVOLEMIA

Since ECF becomes hypoosmolar, fluid moves into the cells to equalize the concentration
on both sides of the cell membrane
Thus there, is an increase in intracellular fluid
The brain cells are particularly sensitive to the increase of intracellular water, the most
common signs of hypoosmolar overhydration are changes in mental status. Confusion,
ataxia, and convulsions may also occur.

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

Common Causes:

Congestive Heart Failure

Early renal failure

IV therapy

Excessive sodium ingestion

SIADH

Corticosteroid
Clinical Manifestations

Signs/Symptoms

Increased BP

Bounding pulse

Venous distention

Pulmonary edema

Dyspnea

Orthopnea (diff. breathing when supine)

crackles
Treatment/Interventions (FVE)

Drug therapy

Diuretics may be ordered if renal failure is not the cause.

Restriction of sodium and saline intake

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

ElectrolyteImbalance

Anions and Cations

Cations

Anions
Bicarbonate
Chloride
Phosphorous

Calcium
Magnesium
Potassium
Sodium

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 potassiumsparing 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 int Diffusion of water into the interstitial spaces
o the interstitial spaces
Sodium in the interstitial
interstitial Sodium in the interstitial space is diluted
odium in the interstitial space is diluted
Decreased osmolarity of ECF
ial space is diluted

eased osmolarity of ECF

Water moves into the Water moves into the cell as a result of sodium loss
cell as a result of sodium loss
Extracellular compartment is depleted of water
t is depleted of water
CLINICAL SYMPTOMS
LINICAL SYMPTOMS

Hyponatremia (<135mEq/L)
Contributing Factors

Excessive diaphoresis

Wound Drainage

NPO

CHF

Low salt diet

Renal Disease

Diuretics
Hyponatremia (<135mEq/L)

Assessment findings:

Neuro - Generalized skeletal muscle weakness. Headache / personality changes.

Resp.- Shallow respirations

CV - Cardiac changes depend on fluid volume

GI Increased GI motility, Nausea, Diarrhea (explosive)

GU - Increased urine output

Hyponatremia (<135mEq/L)

Interventions/Treatment

Restore Na levels to normal and prevent further decreases in Na.

Drug Therapy

(FVD) - IV therapy to restore both fluid

and Na. If severe may see 2-3% saline.

(FVE) Administer osmotic diuretic (Mannitol) to excrete the water rather than the
sodium.

Increase oral sodium intake and restrict oral fluid intake.

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

Hypernatremia (>145mEq/L)

Contributing Factors

Hyperaldosteronism

Renal failure

Corticosteroids

Increase in oral Na intake

Na containing IV fluids

Decreased urine output with increased urine concentration

Hypernatremia (>145mEq/L)

Contributing factors (contd):

Diarrhea

Dehydration

Fever

Hyperventilation
Hypernatremia (>145mEq/L)

Assessment findings:

Neuro - Spontaneous muscle twitches. Irregular contractions. Skeletal muscle wkness.

Diminished deep tendon reflexes

Resp. Pulmonary edema

CV Diminished CO. HR and BP depend on vascular volume.

Hypernatremia (>145mEq/L)
GU Dec. urine output. Inc. specific gravity
Skin Dry, flaky skin. Edema r/t fluid volume changes.
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Hypernatremia (>145mEq/L)

Interventions/Treatment

Drug therapy

(FVD) .45% NSS. If caused by both Na and fluid loss, will administer NaCL. If
inadequate renal excretion of sodium, will administer diuretics.

Diet therapy

Mild Ensure water intake

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

Known as a low level of serum potassium, less than 3.5 mEq/L

Decreased Intake
Food and Fluids as in
starvation,, Failure to replace
GI losses

Increased Loss
Aldosterone
Gastrointestinal losses
Potassium-losing diuretics
Loss from cells as in trauma,
burns

Shift of Potassium
into Cells
(No change in total
body potassium)

HYPOKALEMIA

GI Tract
Anorexia
N&V
Abdominal
distention

CNS
Lethargy,
Diminished deeptendon reflexes,
Confusion, Mental
depression

Muscles

CV SystemDecrease in standing
BP, Dysrhythmias,
Weakness, Flaccid
ECG changes,
paralysis, Weakness
Myocardial damage,
of respiratory
muscles, Respiratory
Cardiac arrest
arrest

10

Kidneys
Capacity to
concentrate
waste, water
loss, thirst,
kidney damage

PATHOPHYSIOLOGY OF HYPOKALEMIA
= Action Potential

Nerve and Muscle Activity

Low Extracellular K+

Increase in resting
membrane potential

The cell becomes

less excitable

Aldosterone is secreted
Sodium is retained in the body through resorption by the kidney tubules

Potassium is excreted
Use of certain diuretics such as thiazides and furosemide, and corticosteroids
Increased urinary output
Loss of potassium in urine

Hypokalemia (<3.5mEq/L)

Pathophysiology

Decrease in K+ causes decreased excitability of cells, therefore cells are less responsive
to normal stimuli
Hypokalemia (<3.5mEq/L)

Contributing factors:

Diuretics

Shift into cells

Digitalis

Water intoxication

Corticosteroids

Diarrhea

Vomiting

Interventions

Assess and identify those at risk

Encourage potassium-rich foods

K+ replacement (IV or PO)

Monitor lab values

D/c potassium-wasting diuretics

Treat underlying cause

11

Hyperkalemia (>5.0mEq/L)
CAUSES
EFFECTS
HYPERKALEMIA
Serum potassium
levelAND
greater
thanOF
5.5
mEq/L
Excess Intake
Intake Dietary intake
of excess of kidneys ability to
excrete; Excess parenteral
administration

Decreased Loss
Loss Potassiumsparing diuretics; Renal failure;
Adrenal insufficiency

Shift of Potassium
out of the CellsExtensive injuries,
crushing injuries,
metabolic acidosis

HYPERKALEMIA

GI
Tract
Tract N&V
Diarrhea,
Colic

CNS
CNS Numbness
, paresthesias

Muscles
Muscles Early:
irritability..Late:
weakness leading to
flaccid paralysis

CV
System
System Conductio
n disturbance,
ventricular fibrillation,
Cardiac Arrest

Kidneys
Kidneys Olig
uria leading to
anuria

Pathophysiology An inc. in K+ causes increased excitability of cells.

Hyperkalemia (>5.0mEq/L)

Contributing factors:

Increase in K+ intake

Renal failure

K+ sparing diuretics

Shift of K+ out of the cells

Hyperkalemia (>5.0mEq/L)

Interventions

Need to restore normal K+ balance:

Eliminate K+ administration

Inc. K+ excretion

Lasix

Kayexalate (Polystyrene sulfonate)

Infuse glucose and insulin

Cardiac Monitoring

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

Close link between calcium and phosphorus. High PO4, Low Ca
Necessary for nerve impulse transmission and blood clotting and is also a catalyst for
muscle contraction and other cellular activities
Needed for Vitamin B12 absorption and use
Necessary for strong bones and teeth and thickness and strength of cell membranes
RDA: 1g for adults. Higher for children and pregnant and lactating women according to
body weight, older people, esp. post-menopausal
Found in milk, cheese, and dried beans; some in meat and vegetables
12

Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive secretions, and
perspiration
Normal value 8.5 10.5 mg/dl
PATHOPHYSIOLOGY OF HYPOCALCEMIA
CAUSES AND EFFECTS OF HYPOCALCEMIA

Decreased Ionized
Ca
Ca Large
tranfusion with
citrated blood

Excess Loss

Inadequate Intake

Kidney Disease

Dietary Deficit

Decrease in GI Tract and Bone

Absorption
Magnesium, Calcitonin
Vitamin D,, Parathyroid
Hormone

HYPOCALCEMIA

Bones
Osteoporosis
leading to
Fractures

CNS

Other

Tingling

Abnormal
deposits of
calcium in
body tissues

convulsions

Muscles
Muscle spasm
Tetany

Cardiovascular
System
System Dysrhyt
hmias

Cardiac arrest

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

Contributing factors:

Dec. oral intake

Lactose intolerance

Dec. Vitamin D intake

End stage renal disease

Diarrhea
Contributing factors (contd):
Acute pancreatitis
Hyperphosphatemia
Immobility
13

Removal or destruction of parathyroid gland

Hypocalcemia (<9.0mg/dL)

Assessment findings:
CLINICAL MANIFESTATIONS OF HYPOCALCEMIA
PAINFUL MUSCULAR SPASMS (TETANY) ESPECIALLY OF FEET AND HANDS
(CARPOPEDAL SPASMS), MUSCLE TWITCHING AND CONVULSIONS MAY FOLLOW
Hypocalcemia (<9.0mg/dL)

Neuro Irritable muscle twitches.

Positive Trousseaus sign.

Positive Chvosteks sign.

Resp. Resp. failure d/t muscle tetany.

CV Dec. HR., dec. BP, diminished

peripheral pulses

GI Inc. motility. Inc. BS. Diarrhea

Positive Trousseaus Sign
Positive Chvosteks Sign
Hypocalcemia (<9.0mg/dL)

Interventions/Treatment

Drug Therapy

Calcium supplements

Vitamin D

Diet Therapy

High calcium diet

Prevention of Injury

Seizure precautions

Hypercalcemia (>10.5mg/dL)

14

Loss from bones

HYPERCALCEMIA: Serum concentration > 10mg/dL

Causes and Effects

Immobilization, Carcinoma with

bone metastases, Multiple
myeloma

Excess Intake

Increase in factors Causing

Mobilization from bone

Calcium diet (esp. milk)

Antacids containing calcium

PTH, Vitamin D, steroid

therapy

HYPERCALCEMIA

Kidneys

CNS

Bones

Muscles

CV System

Stones

Deep-tendon
reflexes

Bone pain

Muscle fatigue,
hypotonia

Depressed activity

Kidney
Damage

Osteoporosis

Dysrhythmias
GI motility

Lethargy

Fractures

Cardiac Arrest

Coma

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

Contributing factors:
Excessive calcium intake
Excessive vitamin D intake
Renal failure
Hyperparathyroidism
Malignancy
Hyperthyroidism
Assessment findings:
Neuro Disorientation, lethargy, coma, profound muscle weakness
Resp. Ineffective resp. movement
CV - Inc. HR, Inc. BP. , Bounding peripheral pulses, Positive Homans sign.
Late Phase Bradycardia, Cardiac arrest

GI Dec. motility. Dec. BS. Constipation

GU Inc. urine output. Formation of renal calculi

Interventions/Treatment
15

Eliminate calcium administration

Drug Therapy
Isotonic NaCL (Inc. the excretion of Ca)
Diuretics
Calcium reabsorption inhibitors (Phosphorus)
Cardiac Monitoring
Hypophosphatemia (<2.5mg/L)

Contributing Factors:
Malnutrition
Starvation
Hypercalcemia
Renal failure
Uncontrolled DM
Assessment findings: (Chart 13-7)
Neuro Irritability, confusion
CV Dec. contractility
Resp. Shallow respirations
Musculoskeletal - Rhabdomyolysis
Hematologic Inc. bleeding
Dec. platelet aggregation

Interventions

Treat underlying cause

Oral replacement with vit. D

IV phosphorus (Severe)

Diet therapy

Foods high in oral phosphate

Hyperphosphatemia (>4.5mg/L)
Causes few direct problems with body function. Care is directed to hypocalcemia.
Rarely occurs

Mostly found within body cells: heart, bone, nerve, and muscle tissues
Second most important cation in the ICF, 2nd to K+
Functions: Metabolism of CHO and CHON, protein and DNA synthesis, DNA and RNA
transcription, and translation of RNA, maintains normal intracellular levels of potassium,
helps maintain electric activity in nervous tissue membranes and muscle membranes
RDA: about 18-30 mEq; children require larger amounts
Sources: vegetables, nuts, fish, whole grains, peas, and beans
Absorbed in the intestines and excreted by the kidneys
Plasma concentrations of magnesium range from 1.5 2.5 mEq/L, with about one third
of that amount bound to plasma proteins
16

HYPOMAGNESEMIA: Serum level < 1.5 mEq/L

Usually coexists with hypokalemia and less often with hypocalcemia

Decreased Intake

Impaired absorption from GI Tract

Excessive
Excretion

Prolonged malnutrition,
Starvation

Malabsorption syndrome, Alcohol Withdrawal

Syndrome, Hypercalcemia, Diarrhea, Draining
gastrointestinal fistula

Aldosterone,
Conditions causing
large losses of urine

HYPOMAGNESEMIA

Mental Changes
Agitation,
Depression,
Confusion

CNS

Muscles

Convulsions,
Paresthesias,
Tremor, Ataxia

Cramps, Spasticity,
Tetany

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

Enhancement of myofibril
contraction

High Serum Calciu

Excretion of Magnesium
By the GI tract
17

CV System
Tachycardia,
Hypotension,
Dysrhythmias

MAGNESIUM
INHIBITS TRANSPORT OF PTH
DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED FROM THE BONE
POSSIBLE CALCIUM DEFICIT
Hypomagnesemia (<1.4mEq/L)

Contributing factors:

Malnutrition

Starvation

Diuretics

Aminoglcoside antibiotics

Hyperglycemia

Insulin administration
Assessment findings:
*Neuro - Positive Trousseaus sign. Positive Chvosteks sign. Hyperreflexia. Seizures
*CV ECG changes. Dysrhythmias. HTN
*Resp. Shallow resp.
*GI Dec. motility. Anorexia. Nausea
Hypomagnesemia (<1.4mEq/L)

Interventions:

Eliminate contributing drugs

IV MgSO4

Assess DTRs hourly with MgSO4

Diet Therapy
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
Diminishing of reflexes, drowsiness, lethargy

18

Slowed heart rate

and AV Block

Severe Respiratory Depression

Peripheral vasodilation

RESPIRATORY ARREST may occur

Hypotension, flushing,
and increased skin warmth

Contributing factors:
Increased Mag intake
Decreased renal excretion
Hypermagnesemia (>2.0mEq/L)

Assessment findings:
Neuro Reduced or weak DTRs. Weak voluntary muscle contractions. Drowsy to the
point of lethargy
CV Bradycardia, peripheral vasodilatation, hypotension. ECG changes.

Hypermagnesemia (>2.0mg/dL)

Interventions

Eliminate contributing drugs

Administer diuretic

Calcium gluconate reverses cardiac effects

Diet restrictions
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 membrane
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
Circulation

cough, moist breath sounds

Loss of sensation in edematous
increased blood pressure

Pulse rate changes, dysrhythmia,

postural areas, pallor,

bounding
Abdomen
Elimination
Extremities
,

pulse,
hypotension
Distention, abdominal cramps
Diarrhea, constipation
Muscle weakness, tingling, tetany

Increased girth, fluid wave

Constipation
Dependent edema, pitting
discomfort from weight of
bedclothes

LABORATORY VALUES
FLUID DEFICIT
Hemoconcentration

FLUID EXCESS
Hemodilution
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 Hct, BUN, E+ levels

Urine Specific Gravity

Hct, BUN, E+ levels

Urine Specific Gravity

Determined from analysis of patient data

Diagnostic Title
1
Deficient fluid volume
diaphoresis),
intake, failure of
mechanisms,
fluids
2
Excess Fluid Volume

Possible Etiologic Factors

Active fluid volume loss
(hemorrhage, diarrhea, gastric
intubation, wounds,
inadequate fluid
regulatory
sequestration of body
Excess fluid intake, excess sodium
intake, compromised regulatory
processes

Intake and Output Monitoring

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

20

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
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 doctors 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
o small amount at frequent intervals is more useful than a large amount presented
less often
o 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)
o Avoid irritating foods
Stimulation of saliva may be aided by hard candy or chewing gum or
carboxymethylcellulose (artificial saliva)
o 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.
o 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)
o Increase usual daily requirement of foods when losses must be restored, as
tolerated
o Patients with cardiac and renal impairments are
instructed to avoid foods
containing high levels of sodium, potassium and bicarbonate
o 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:
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1 the patient complains of thirst

2 the protein or electrolyte content of the tube feeding is high
3 the patient has fever or disease causing an increased metabolic rate
4 UO is concentrated
5 signs of water deficit develop
Administer parenteral fluids as necessary
*
Types of solutions
D5W (hypotonic) is given short-term for hyponatremia
D5NSS may be given depending on the serum levels of sodium and vascular volume +
KCl to meet normal intake needs and replace losses for hyponatremia
Dextrose 5% in 0.2% normal saline is generally used as
a maintenance fluid
Dextrose 5% in normal saline is generally used as a replacement solution for losses
caused by gastrointestinal drainage
PNSS is given primarily when large amounts of sodium
have been lost and for
patients with hyponatremia
LRS is also isotonic because it remains in the extracellular space
Fructose or 10-20% glucose in distilled water are hypertonic solutions and may partially
meet body needs for CHOs
Dextran (commonly-used plasma expander) increases plasma volume by increasing
oncotic pressure. May cause prolonged bleeding time and is CI in patients with renal failure,
bleeding disorders, or severe CHF
*Administration
-The rate should be regulated according to the patients
needs and condition per doctors
orders
-Monitor UO carefully. Refer marked decreases!
-Verify orders for potassium administration in patients with renal failure and untreated adrenal
insufficiency
-Usual rate for fluid loss replacement: 3ml/min
-Recognize signs of pulmonary edema (bounding pulse, engorged peripheral veins, hoarseness,
dyspnea, cough, and rales) that can result from IV rate
-If infiltration occurs, the infusion should be stopped immediately and relocated. Peripheral IV
sites are generally rotated every 72 hours
-For dextran and other plasma expanders, observe for anaphylactic reaction (apprehension,
dyspnea, wheezing, tightness of chest, angioedema, itching, hives and hypotension). If this
happens, switch infusion to nonprotein solution and run at KVO rate, notify physician and
monitor VS
-Pronounced and continued thirst despite administration of fluids is not normal and should be
reported (may indicate DM or hypercalcemia)
*Patient/Family Education
-Include the signs and symptoms of water excess in discharge instructions
-With drug therapy, instruct patient and family regarding correct method of administration,
correct dose, and therapeutic and adverse effects
-Instruct to read labels for nutritional content
* For K restriction: avoid organ meats, fresh and dried
fruits, and salt substitutes
-Skin assessment and care, positioning techniques for patients with mobility restrictions
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Acid-base balance
NORMAL ACID-BASE BALANCE
Parameter

Normal Value

PaO2

80-100 Hg

Definition and Implications

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

pH

7.35-7.45

PaCO2

35-45 mmHg

Identifies whether there is acidemia or alkalemia:

pH<7.35 = acidosis; pH>7.45 = alkalosis

Partial pressure of CO2 in the arterial blood:

PCO2<35 mmHg = respiratory alkalosis
PCO2>45 mmHg = respiratory acidosis

Standard HCO3

22-26 mEq/L

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

TYPES OF ACID-BASE DISTURBANCES

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

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CONDITION

pH

HCO3

PCO2

Respiratory Acidosis

Normal

Uncompensated

Normal

Respiratory Alkalosis

Normal

Uncompensated

Normal

Metabolic Acidosis

Normal

Uncompensated

Normal

Metabolic Alkalosis

Normal

Uncompensated

Normal

Partly Compensated
Compensated

Partly Compensated
Compensated

Partly Compensated
Compensated

Partly Compensated
Compensated

RESPIRATORY ACIDOSIS: CARBONIC ACID EXCES

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

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Health Hx: complaints of headache, confusion, lethargy, nausea, irritability, nausea, irritability,
anxiety, dyspnea, and blurred vision, preexisting conditions
*Physical Examination: lethargy to stupor to coma, tachycardia, hypertension, cardiac
dysrhythmias, airway patency
NURSING DIAGNOSES include but are not limited to:
Diagnostic Title
Possible Etiologic Factors
1 Impaired gas exchange
Hypoventilation
2 Disturbed thought processes
Central nervous system depression
3 Anxiety
Hypoxia, hospitalization
4 Risk for ineffective family Illness of a family member
coping
5 Ineffective airway clearance
Hypoventilation, secretions
6 Ineffective breathing pattern
Hypoventilation, dyspnea
NURSING MANAGEMENT OF 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 persons baseline LOC frequently
- 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 patients ongoing condition
- Reassure them that there is a physiologic cause for the
patients behavior
- Encourage questions and open communication
5 Promote airway clearance
- Implement regular breathing and coughing exercises
- Do suctioning as necessary
- Maintain good hydration
- Do chest physiotherapy as appropriate
6 Promoting an effective breathing pattern
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- Maintain alveolar ventilation

- Teach the patient proper breathing techniques as well as panic control breathing
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, (+) Chvosteks sign or
Trousseaus 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
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
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 patients 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

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