fluid & electrylyte tables
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Table 46-2 Major Electrolytes
Electrolyte Functions Sources and Losses Regulation
Sodium (Na+): chief
electrolyte of ECF that
moves easily betweenintravascular and
interstitial spaces and
moves across cell
membranes by activetransport; influential in
many chemical reactions
in the body, particularly
in nervous tissue cells
and muscle tissue cells
Controls and regulates the
volume of body fluids
Maintains water balancethroughout the body
Is the primary regulator of
ECF volume
Influences ICF volumeParticipates in the
generation and transmission
of nerve impulses
Is an essential electrolyte in
the sodium-potassium pump
The average daily requirements
for sodium not known
Precisely; 2,400 mg (approx. 1tsp) as the Daily Value cited on
the Nutrition Facts label; RDA
for sodium for adults about 500
mg, or 0.5 gSodium found in many foods;
typically present in large
amounts, particularly in bacon,
ham, sausage, catsup, mustard,
relish, processed cheese, canned
vegetables, bread, cereal, and
salted snack foods; also in table
salt (sodium chloride; about46% sodium)
Sodium excesses eliminated
primarily by the kidneys; small
amounts lost in feces and
perspiration
Sodium normally maintained
in the body within a
relatively narrow range;deviations quickly resulting
in a serious health problem
Sodium concentrations
affected by salt, as well aswater, intake
Sodium conserved through
reabsorption in the kidneys, a
process stimulated by
aldosterone
The normal extracellular
concentration of sodium:
135–145 mEq/L (mmol/L).
Potassium (K +): major
cation of ICF working in
reciprocal fashion with
sodium (eg, an excessive
intake of sodium
resulting in an excretion
of potassium, and vice
versa)
Is the chief regulator of
cellular enzyme activity and
cellular water content
Plays a vital role in such
processes as the
transmission of electric
impulses, particularly in
nerve, heart, skeletal,intestinal, and lung tissue;protein and carbohydrate
metabolism; and cellular
building
Assists in regulation of
acid-base balance by
cellular exchange with H+
The average daily requirements
not known precisely; an intake
of 50 to 100 mEq daily enough
to maintain K + balance
Adequate quantities usually in a
wellbalanced diet
Leading food sources: bananas,
peaches, kiwi, figs, dates,apricots, oranges, prunes,melons, raisins, broccoli, and
potatoes. Meat and dairy
products also with adequate
amounts of potassium
Potassium excreted primarily by
the kidneys (no effective
method of conserving
potassium); deficits occur if potassium excretion in excess
without being replaced
simultaneously.
Gastrointestinal (GI) secretionscontain potassium in large
quantities; also some in
perspiration and saliva
Conservation of cellular K +
by the sodium pump
(described later in the
chapter) when Na+ is
excluded; conservation by
kidneys when cellular K +
decreased.
Aldosterone secretiontriggering K + excretion inurine
Normal range for serum
potassium: 3.5 to 5 mEq/L
Calcium (Ca2+): most Is necessary for nerve Average daily requirement Increased secretion of
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abundant electrolyte in
the body, with up to 99%
of the total amount of calcium in the body
found in bones and teethin ionized form; close
link between
concentrations of calcium
and phosphorus
impulse transmission and
blood clotting
Is a catalyst for musclecontraction
Is needed for vitamin B12absorption and for its use
by body cells
Acts as a catalyst for many
cell chemical activities
Is necessary for strong
bones and teethDetermines the thickness
and strength of cellmembranes
about 1 g for adults; higher
amounts according to body
weight required for children andpregnant and lactating women
Consumption of 1,500 mg/dayrecommended for older adults,
particularly postmenopausal
women and men older than 65
years of age
Sources include milk, cheese,
and dried beans; some presentin meats and vegetables
The use of calcium stimulatedby vitamin D; most active form
of vitamin D (calcitriol)
responsible for promoting
calcium absorption and limiting
calcium excretion when levels
are inadequate
Movement out of bones and
teeth to maintain normal bloodcalcium levels, if necessary.
Excretion via urine, feces, bile,
digestive secretions, and
perspiration
parathyroid hormone (PTH),
to increase the release of
calcium from bones into theblood and to increase
reabsorption from kidneysand intestine when ECF
levels are decreased
A high serum phosphate
concentration, resulting in
decreased serum calcium
level; a low serum phosphateconcentration leading to
increased serum calciumCalcitonin, a hormone
secreted by the thyroid gland,
exerting an effect on calcium
opposite that of PTH.
Increases in calcitonin
resulting in reduced serum
calcium concentration
primarily by opposingosteoclast bone resorption
Magnesium (Mg2+): most
of cation magnesium
found within body cells
—heart, bone, nerve, and
muscle tissues; secondmost important cation in
the ICF
Is important for the
metabolism of
carbohydrates and proteins
Is important for many vital
reactions involvingenzymes
Is necessary for protein and
DNA synthesis, DNA andRNA transcription, and
translation of RNA
Maintains normal
intracellular levels of
potassium
Helps maintain electrical
activity in nervous tissue
membranes and muscle
membranes
The average daily adult
requirement about 18–30 mEq,
with children requiring larger
amounts
Magnesium found in mostfoods, but especially in
vegetables, nuts, fish, whole
grains, peas, and beans
Intestinal absorption and
excretion by kidneys
Plasma concentrations of
magnesium ranging from
1.3–2.1 mEq/L, with aboutone third of that amount
bound to plasma proteins
Chloride (Cl-): chief
extracellular anion, found
in blood, interstitial fluid,
and lymph and in minute
amounts in ICF
Acts with sodium to
maintain the osmotic
pressure of the blood
Plays a role in the body's
acid-base balanceHas important buffering
The average daily requirements
of chloride unknown
Found in foods high in sodium,
dairy products, and meat
Normally paired with
sodium; exerted and
conserved with sodium by the
kidneys
Chloride deficits lead topotassium deficits, and vice
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action when oxygen and
carbon dioxide exchange in
red blood cellsIs essential for the
production of hydrochloricacid in gastric juices
versa
Normal serum chloride
levels: from 95–105 mEq/L(mmol/L)
Bicarbonate (HCO3-): an
anion that is the major
chemical base buffer
within the body; found in
both ECF and ICF
Is essential for acid-basebalance; bicarbonate and
carbonic acid constitute the
body's primary buffer
system
Losses possible via diarrhea,diuretics, and early renal
insufficiency; excess possible
via overingestion of acid
neutralizers, such as sodium
bicarbonate
Bicarbonate levels regulatedprimarily by the kidneys
Bicarbonate readily available
as a result of carbon dioxide
formation during metabolism
Normal bicarbonate levels
range between 25 and 29
mEq/L (mmol/L)
Phosphate (PO4-): the
major anion in body
cells; a buffer anion in
both ICF and ECF
Helps maintain the body's
acid-base balance
Is involved in important
chemical reactions in the
body; eg, phosphorus is
necessary for many B
vitamins to be effective,helps promote nerve and
muscle action, and plays a
role in carbohydrate
metabolism
Is important for cell
division and for the
transmission of hereditarytraits
Average daily requirements for
phosphorus similar to those for
calcium
Found in most foods but
especially in beef, pork, and
dried peas and beans
Metabolism the same ascalcium
Regulation by PTH and by
activated vitamin D
Calcium and phosphate
inversely proportional; an
increase in one results in a
decrease in the other
Normal range of phosphate:2.5 to 4.5 mEq/L (mmol/L)
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Table 46-3 Homeostatic Mechanisms That Maintain the Composition and Volume of Body Fluid
Within Narrow Limits of Normal
Organs of
Homeostasis Functions
Kidneys • Regulate extracellular fluid (ECF) volume and osmolality by selective retention and
excretion of body fluids
• Regulate electrolyte levels in the ECF by selective retention of needed substances and
excretion of unneeded substances
• Regulate pH of ECF by excretion or retention of hydrogen ions
• Excrete metabolic wastes (primarily acids) and toxic substances
Heart and
blood vessels
• Circulate blood through the kidneys under sufficient pressure for urine to form (pumping
action of the heart)
• React to hypovolemia by stimulating fluid retention (stretch receptors in the atria and
blood vessels)
Lungs • Eliminate about 13,000 mEq of hydrogen ions (H+) daily, as opposed to only 40 to 80
mEq excreted daily by the kidneys
• Act promptly to correct metabolic acid–base disturbances; regulate H+ concentration (pH)
by controlling the level of carbon dioxide (CO2) in the extracellular fluid as follows:
1. Metabolic alkalosis causes compensatory hypoventilation, resulting in CO2
retention (increases acidity of the extracellular fluid).
2. Metabolic acidosis causes compensatory hyperventilation, resulting in CO2
excretion (decreases acidity of the extracellular fluid).
• Remove approximately 300 mL of water daily through exhalation (insensible water loss)
in the normal adult
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Adrenal
glands• Regulate blood volume and sodium and potassium balance by secreting aldosterone, a
mineral corticoid secreted by the adrenal cortex
1. The primary regulator of aldosterone appears to be angiotensin II, which is
produced by the renin–angiotensin system. A decrease in blood volume triggers
this system and increases aldosterone secretion, which causes sodium retention(and thus water retention) and potassium loss.
2. Decreased secretion of aldosterone causes sodium and water loss and potassium
retention.
• Cortisol, another adrenocortical hormone, has only a fraction of the potency of
aldosterone.
• However, secretion of cortisol in large quantities can produce sodium and water retention
and potassium deficit.
Pituitary
gland• Stores and releases the antidiuretic hormone (ADH), which makes the body retain water;
functions of ADH include:
1. Maintains osmotic pressure of the cells by controlling renal water retention or excretion
a. When osmotic pressure of the ECF is greater than that of the cells (as in
hypernatremia—excess sodium—or hyperglycemia), ADH secretion is
increased, causing renal retention of water.
b. When osmotic pressure of the ECF is less than that of the cells (as in
hyponatremia), ADH secretion is decreased, causing renal excretion of
water.
2. Controls blood volume (less influential than aldosterone)a. When blood volume is decreased, an increased secretion of ADH results
in water conservation.
b. When blood volume is increased, a decreased secretion of ADH results
in water loss.
Nervous
system• Inhibits and stimulates mechanisms influencing fluid balance; acts chiefly to regulate
sodium and water intake and excretion
• Regulates oral intake by sensing intracellular dehydration, which triggers thirst (thirst
center located in hypothalamus)
Parathyroid
glands• Regulate calcium (Ca2+) and phosphate (HPO4
2-) balance by means of parathyroid
hormone (PTH); PTH influences bone reabsorption, calcium absorption from the
intestines, and calcium reabsorption from the renal tubules.
1. Increased secretion of PTH causes:a. Elevated serum calcium concentration
b. Lowered serum phosphate concentration
2. Conversely, decreased secretion of PTH causes:a. Lowered serum calcium concentration
b. Elevated serum phosphate concentration
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Table 46-4 Acid–Base Parameters for Arterial Blood Gas Studies
Normal Acid Base
pH 7.35–7.45 <7.35 >7.45
PaCO2 35–45 mm Hg >45 mm Hg <35 mm Hg
HCO3- 22–26 mEq/L <22 mEq/L >26 mEq/L
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Focused Assessment Guide 46-1 Fluid, Electrolyte, and Acid–Base Balance
Factors to Assess Questions and Approaches
Usual patterns of fluid intake Describe the amount and types of fluids you usually drink in a 24-hour period. Have there been any recent changes?
Usual pattern of fluid elimination Describe your usual voiding/urination habits.
Any recent changes in frequency or amount?
Is your body losing fluids in any other major way?
• Vomiting
• Diarrhea
• Excessive perspiration
• Fistula
Patient's evaluation of hydration
status
Do you think there is an approximate balance between your fluid
intake and output?
Have you noticed any signs that your body is experiencing too
much or too little hydration (difficulty breathing, edema, dry skin
and mucous membranes, thirst)?
History of disease process Is there any history of disease process or injury that might disrupt
fluid and electrolyte balance (eg, diabetes mellitus, cancer, burns)?
Medication/nutrition history Do you take any medications or treatments that might disrupt fluid
and electrolyte balance (eg, steroids, diuretics, total parenteral
nutrition, dialysis)?
Have you been trying to lose weight by dieting, using diuretics,
laxatives, or diet aids?
Have you been following a high-protein, low-carbohydrate diet?
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Fluid, electrolyte, and acid–base
imbalances and contributing
factors
Are you aware of any other fluid balance problems you may be
experiencing?
• Nature
• Onset of problem and frequency• Causes
• Severity
• Symptoms
• Intervention attempted and results
Table 46-5 Imbalances Resulting From Loss of Specific Body Fluid
Fluid Lost Imbalances Likely to Occur Fluid Lost Imbalances Likely to Occur
Gastric juice Extracellular fluid volume deficit
Metabolic alkalosis
Sodium deficitPotassium deficit
Pancreatic juice Metabolic acidosis
Sodium deficit
Calcium deficitExtracellular fluid volume deficit
Tetany (if metabolic alkalosis is present) Sensible perspiration Extracellular fluid volume deficit
Sodium deficit
Ketosis of starvation
Magnesium deficit
Insensible water loss Water deficit (dehydration)
Sodium excess
Intestinaljuice
Extracellular fluid volume deficit
Metabolic acidosis
Sodium deficit
Potassium deficit
Wound exudate Protein deficit
Sodium deficit
Extracellular fluid volume deficit
Bile Sodium deficit
Metabolic acidosis
Ascites Protein deficit
Sodium deficitPlasma-to-interstitial fluid shift
Extracellular fluid volume deficit
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Table 46-6 Parameters to Be Considered in Clinical Assessment for Fluid, Electrolyte, and Acid–Base Balance
Assessment
Parameters Nursing Considerations Findings in Healthy Adult Significant Findings
Comparison of
total intake and
output of fluids
Records may be initiated by the nurse
for any patient with a real or potential
water or electrolyte problem.
Intake should include all fluids
taken into the body.
Output should include urine,
vomitus, diarrhea, drainage from
fistulas, and drainage from suction
apparatus. Perspiration and drainage
from lesions should be noted andestimated. Prolonged
hyperventilation should also be
noted because it is an important
route of water vapor loss.
Fluid intake about equals fluid
output—when averaged over 2 or 3
days.
Range of 1500–3500 mL fluid
intake and loss; 2000 mL is average
adult intake and loss per day.
Output of urine normally
approximates the ingestion of
liquids; water from food and
oxidation is balanced by the water loss through feces, the skin, and the
respiratory process.
When the total intake is substantiall
less than the total output, the patient
in danger of fluid volume deficit.
When the total intake is substantiall
more than the total output, the patien
in danger of fluid volume excess.
Urine volume and
concentration
All fluid losses are measured
according to routes.
A device calibrated for small
volumes of urine is used when
hourly urine volumes need to be
measured.
Factors that can alter urinary output
must be accounted for:
Amount of fluid intake
Losses from skin, lungs, and GI tract
Amount of waste products for
excretions
Normal urinary output is about 1
mL/kg of body weight per hour (for
the average adult: 1500 mL/24 hr,
which is equivalent to about 40–80
mL/hr).
Stress may diminish the 24-hour urine volume in the adult to 750–
1000 mL (or 30–50 mL/hr) because
of increased aldosterone and ADH
secretion.
The range of specific gravity is from
1.003 to 1.035. Urine osmolality
ranges between 500 mOsm and 800
mOsm/ kg (mmol/kg).
A low urine volume with a high
specific gravity indicates fluid volum
deficit.
A low urine volume with a low spec
gravity indicates renal disease.
A high urine volume suggests fluidvolume excess.
Urine volume is increased in condit
with high solute loads, such as diabemellitus.
Hypovolemia causes decreased rena
perfusion and thus oliguria;hypervolemia causes increased urina
volume if the kidneys are functionin
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Renal concentrating ability
Blood volume
Hormonal influences (primarily
aldosterone and ADH)
normally.
Body weight Because of the common
inaccuracies in recording intake and
output, body weight is believed to
be a more accurate indicator of fluid
gained and lost.
Guidelines for weighing patients
include:
Using the same scale each time.
Measuring weight at the same time
each day: in the morning before
breakfast and after voiding.
Ensuring the patient is wearing the
same or similar clothing (clothing
should be dry).
Using a bed scale if the patient is
unable to stand on a small, portablescale.
A patient may have a severe fluid
volume deficit even though body
weight is essentially unchanged
when there is a third-space loss of
body fluid.
A patient's dry weight should
remain relatively stable.
Rapid variations in weight closely
reflect changes in body fluid volum
A rapid loss of body weight occurs
when the total fluid intake is less tha
the total fluid output.
Rapid loss of 2% total body weight
(TBW) indicates mild fluid volume
deficit.
Rapid loss of 5% TBW indicates
moderate fluid volume deficit.
Rapid loss of 8% or more of TBWindicates severe fluid volume deficit
A rapid gain of body weight occurs
when the total fluid intake is greater
than the total fluid output.
Rapid gain of 2% TBW indicates m
fluid volume excess.
Rapid gain of 5% TBW indicates
moderate fluid volume excess.
Rapid gain of 8% or more of TBW
indicates severe fluid volume excess
A rapid gain or loss of 1 kg (2.2 lb)
body weight is about equal to the ga
or loss of 1 L of fluid.
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Skin turgor
(elasticity)
The patient's skin over the sternum,
inner aspect of the thighs, or
forehead is pinched.
Some prefer to test skin turgor inchildren over the abdominal area
and on the medial aspect of the
thighs.
Skin turgor can vary with age,
nutritional state, and even race andcomplexion.
Pinched skin immediately falls back
to its normal position when
released.
Reduced skin turgor is common inolder patients (those more than 55–
60 years of age) because of a
primary decrease in skin elasticity.
In a person with a fluid volume defi
the skin flattens more slowly after th
pinch is released; the skin may remaelevated for many seconds.
Severe malnutrition, particularly in
infants, can cause depressed skin tur
even in the absence of fluid depletio
Tongue turgor Unlike skin turgor, tongue turgor is
not affected appreciably by age and
thus is a useful assessment for all
age groups. (In an arid climate, thismay not be a reliable parameter.)
Tongue has one longitudinal furrow.In the person with fluid volume defi
there are additional longitudinal
furrows and the tongue is smaller.
Sodium excess causes the tongue to
look red and swollen.
Moisture and oral
cavity
A dry mouth may be the result of
fluid volume deficit or of mouthbreathing. (Exposure to an arid
climate may result in a dry mouth.)
Mucous membranes in oral cavity
are moist.
Dryness of the membrane where the
cheek and gum meet indicates fluidvolume deficit.
Dry sticky mucous membranes are
noted in sodium excess. (The oral
cavity feels like flypaper.)
Tearing and
salivation
Tearing and salivation decrease
normally with age.
The absence of tearing and salivatio
a child is a sign of fluid volume defi
it becomes obvious with a fluid loss
5% of TBW.
Appearance of
skin and skin
temperature
Metabolic acidosis can cause warm,
flushed skin (due to peripheral
vasodilation).
Facial appearance A person with a severe fluid volume
deficit may have a pinched and drawfacial expression.
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A fluid volume deficit of 10% of boweight causes decreased intraocular
pressure, causing the eyes to appear
sunken and to feel soft to the touch.
Edema (excessive
accumulation of
interstitial fluid)
Pitting edema (see Fig. 46-7)
Measurement of an extremity or
body part with a millimeter tape, in
the same area each day, is a more
exact method of measurement.
An excess of interstitial fluid may
accumulate predominantly in thelower extremities of ambulatory
patients and in the presacral regionof bedridden patients.
The presence of periorbital (around
the eyes) edema or pedal edema
should prompt one to look for
edema in other parts of the body.
No edema Clinically edema is not usually
apparent in the adult until the retent
of 5–10 lb of excess fluid occurs.
Pitting edema is not evident until at
least a 10% increase in weight has
occurred.
Formation of edema may be localize(as in thrombophlebitis) or generaliz
(as in heart failure, cirrhosis of livernephrotic syndrome). Edema of
congestive heart failure, liver cirrho
or nephrotic syndrome is the result o
sodium retention.
Body temperature Because fever increases the loss of
body fluids, it is important that
temperature elevations be detected
early and appropriate interventions
be taken.
Body temperature and other vital
signs should be assessed as ordered
and at the nurse's discretion.
Baseline temperature: diurnal
variations
There is an elevation of body
temperature in hypernatremia
(dehydration) probably related to la
of available fluid for sweating.
There is a decrease in body temperain fluid volume deficit, when
uncomplicated by infection.
Fever increases the loss of body flui
A temperature elevation between 10(38.3°C) and 103°F (39.4°C) increa
the 24-hour fluid requirement by at
least 500 mL, and a temperature abo
103°F increases it by at least 1000 m
Pulse Baseline pulse rate, rhythm, and
volume
Tachycardia is usually the earliest si
of the decreased vascular volumeassociated with fluid volume deficit
Irregular pulse rates also occur with
potassium imbalances and magnesiu
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Measures the levels to which theveins are distended on the neck or
above the level of the manubrium
More accurate assessments of blood
volume are obtained by measuring
CVP by hemodynamic monitoring.
Neuromuscular
irritability
When imbalances in calcium,
magnesium, and sodium are
suspected it is important to assess
patients for increased or decreased
neuromuscular irritability.
Negative response
To test for Chvostek's sign, thefacial nerve should be
percussed about 2 cm anterior
to the ear lobe.
Negative response Patients with hypocalcemia or hypomagnesemia respond positively
with a unilateral twitching of the fac
muscles, including the eyelid and lip
To test for Trousseau's sign, a
blood pressure cuff is placed
on the arm and inflated above
systolic pressure for 3 minutes.
The response in the prospective
muscle is a sudden contraction (2+).
A positive response is the developm
of carpal spasm.
A deep tendon reflex is elicited
by briskly tapping a partially
stretched tendon with a rubber
percussion hammer, preferably
over the tendon insertion of the
muscle.
Reflexes usually are graded on a 0
to 4+ scale.
0 = no response
1+ = somewhat diminished, but
present
2+ = normal
3+ = brisker than average and
possibly but not necessarilyindicative
of disease
4+ = hyperactive
Deep tendon reflexes may be
hyperactive in the presence of
hypocalcemia, hypomagnesemia,
hypernatremia, and alkalosis.
The muscle being tested
should be slightly stretched,
and the patient should be
relaxed.
Deep tendon reflexes may be
hypoactive in the presence of
hypercalcemia,
hypermagnesemia, hyponatremia
hypokalemia, and acidosis.
Behavior
Sensation Fatiguelevel
Because these changes are often
vague, they are best evaluated incontext with specific imbalances
.
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Table 46-7 Acid–Base Disturbances
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Risk Factors Assessments Nursing Interventions
Respiratory Acidosis (Carbonic Acid Excess)
Acute respiratory disease:Pulmonary edema
Aspiration of a foreign
body
AtelectasisOverdose of sedative or
anesthetic
Cardiac arrest
Chronic respiratory disease:
Emphysema
Bronchial asthma
Cystic fibrosis
Inadequate mechanical
ventilation
CNS depressionNeuromuscular disease
Acute respiratory acidosisMental cloudiness
Dizziness
Muscular twitching
UnconsciousnessABGs
pH <7.35
PaCO2 >45 mm Hg
(primary)
HCO3- normal or only
slightly elevated
Chronic respiratory acidosis
Weakness
Dull headache
ABGspH <7.35 or low N
PaCO2 >45 mm Hg
(primary)
HCO3- >26 mEq/L
(compensatory)
Treatment is directed at improving ventilation:Pharmacologic measures
Pulmonary hygiene measures
Adequate hydration
Supplemental oxygenMechanical ventilation may be necessary to correct disorder but
must be used cautiously to decrease PaCO2 slowly.
Respiratory Alkalosis (Carbonic Acid Deficit)
Hyperventilation
Extreme anxiety (most
common cause)Hypoxemia
High fever
Early sepsis
Excessive ventilation by
mechanical ventilator
CNS lesion involving the
respiratory center Thyrotoxicosis
Lightheadedness
Inability to concentrate
Hyperventilation syndromeTinnitus
Palpitations
Sweating
Dry mouth
Tremulousness
Convulsions and loss of
consciousnessABGs
pH >7.45
PaCO2 <35 mm Hg
(primary)
HCO3- <22 mEq/L
(compensatory)
If anxiety is the cause, the patient should be encouraged to breathe
more slowly (causes accumulation of CO2) or breathe into a closed
system (paper bag). Sedative may also be necessary in extremeanxiety.
Treatment of other causes is directed at correcting the underlying
problem.
Metabolic Acidosis (Base Bicarbonate Deficit)
Diarrhea
Intestinal fistulas
Headache
Confusion
Treatment is directed toward correcting the metabolic deficit. If
the cause of the problem is excessive intake of chloride, treatment
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Ureterosigmoidostomy
Hyperalimentation
Excessive intake of acids,such as salicylates
Diabetic ketoacidosisRenal failure
Starvational ketoacidosis
Drowsiness
Increased respiratory rate
and depthNausea and vomiting
Peripheral vasodilationABGs
pH <7.35
HCO3- <22 mEq/L
(primary)
PaCO2 <35 mm Hg
Hyperkalemia frequentlypresent
obviously focuses on eliminating the source. When necessary,
bicarbonate is administered.
Metabolic Alkalosis (Base Bicarbonate Excess)
Vomiting or gastric suction
Hypokalemia
Potassium-wasting diuretics
Alkali ingestion
(bicarbonate-containing
antacids)
Renal loss of H+ (eg, from
steroid or diuretic use)
Dizziness
Tingling of fingers and toes
Hypertonic muscles
Depressed respirations
(compensatory)
ABGs
pH >7.45
HCO3- >26 mEq/L
(primary)
PaCO2 >45 mm Hg
(compensatory)
Hypokalemia may be
present
Treatment is aimed at reversal of the underlying disorder.
Sufficient chloride must be supplied for the kidney to absorb
sodium with chloride (allowing the excretion of excess
bicarbonate). Treatment also includes administration of NaCl
fluids to restore normal fluid volume.
Table 46-8 Fluid Volume Disturbances
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Risk Factors Assessments Nursing Interventions
Fluid Volume Deficit (Hypovolemia)
GI: Vomiting, diarrhea, suction, fistulasHemorrhage
Excessive sweating
Skin trauma, burns, draining wounds
Third-space fluid shiftsExcessive laxative or diuretic use
Polyuria from renal disease or diuretics
Hyperglycemia
Change in mental status (unable to gain access
to fluids, depression, confusion)
ThirstWeight loss over short period
Weakness, fatigue, anorexia
Dry mucous membranes
Poor skin and tongue turgor Sunken eyes
Flat neck veins
Urine output <30 mL/hr
Postural hypotension
Weak, rapid pulse
↑Urine specific gravity
↑Hematocrit
↑BUN
↑Serum sodium
Altered sensorium
Assess for presence or worsening of FVD.Administer oral fluids if indicated.
If patient unable to eat and drink, anticipate
TPN or tube feedings to be ordered.
Monitor patient's response to fluid intake,either oral or parenteral.
Be alert for signs of fluid overload.
Provide appropriate skin care.
Fluid Volume Excess (Hypervolemia)
Compromised regulatory mechanisms: renal
failure, CHF, cirrhosis of liver, Cushing's
syndrome
GI irrigation with hypotonic fluid
Excess IV fluids with sodium
Corticosteroid therapy
Excessive ingestion of sodium-containing
substances in diet or sodium-containingmedications
Weight gain over short
period
Peripheral edema (may be
pitting)
Increased BP
Shortness of breath
Crackles and wheezes in
lungsFull, bounding pulse
Neck vein distention
Polyuria if renal function is
normal
Ascites, pleural effusion
Pulmonary edema
↓BUN (due to plasmadilution)
↓Hematocrit
↓Serum sodium
↓Urine specific gravity
Assess for presence or worsening of FVE.
Encourage adherence to sodium-restricted
and fluid-restricted diet, if ordered.
Avoid OTC drugs or check with physician or
pharmacist about sodium content.
Encourage rest periods.
Monitor patient's response to diuretics.
Teach self-monitoring of weight and intakeand output.
Attentive skin care.
Monitor respiratory status.
Table 46-9 Electrolyte Disturbances
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Risk Factors Assessments Nursing Interventions
Hyponatremia
Loss of sodium, as in:Loss of GI fluids
Use of diuretics
Adrenal insufficiency
Gains of water, as in:Excessive administration of
D5W
Water intoxication
Disease states associated with
SIADH (a form of
hyponatremia)
Pharmacologic agents that may
impair water excretion
AnorexiaNausea and vomiting
Lethargy
Confusion
Muscle crampsMuscular twitching
Seizures
Coma
Serum Na below 135 mEq/L
Urine specific gravity <1.010
Monitor fluid losses and gains.Monitor for presence of GI and CNS
symptoms.
Monitor serum Na levels.
Check urine specific gravity.If able to eat, encourage foods and fluids with
high sodium content.
Be aware of sodium content of common IV
fluids.
Avoid giving large water supplements to
patients receiving isotonic tube feedings.
Take seizure precautions when hyponatremia
is severe.
Hypernatremia
Water deprivationIncreased sensible and insensible
water loss
Ingestion of large amount of salt
Excessive parenteral
administration of sodium-
containing solutions
Profuse sweating
Diabetes insipidus
ThirstElevated body temperature
Tongue dry and swollen, sticky mucous
membranes
Severe hypernatremia
Disorientation
Hallucinations
Lethargy when undisturbed
Irritable and hyperactive
Focal or grand mal seizuresComa
Serum Na above 145 mEq/L
Urine specific gravity >1.015
Monitor fluid losses and gains.Observe for excessive intake of high sodium
foods.
Monitor sodium content of prescriptions and
OTC drugs.
Monitor for changes in behavior such as
restlessness, lethargy, and disorientation.
Look for excessive thirst and elevated body
temperature.
Monitor serum Na levels.Check urine specific gravity.
Give sufficient water with tube feedings to
keep serum Na and BUN at normal limits.
Hypokalemia
Diarrhea
Vomiting or gastric suction
Potassium-wasting diureticsSteroid administration and
certain antibioticsPoor intake as in anorexia
nervosa, alcoholism, potassium-
free parenteral fluids
Polyuria
Fatigue
Anorexia, nausea, and vomiting
Muscle weaknessDecreased bowel motility
Cardiac arrhythmiasIncreased sensitivity to digitalis
Polyuria, nocturia, dilute urine
Postural hypotension
Serum K below 3.5 mEq/L
ECG changes
Paresthesias or tender muscles
Monitor for occurrence of hypokalemia.
Assess digitalized patients at risk for
hypokalemia, which potentiates the action of digitalis
Prevent hypokalemia by:Encouraging extra K intake if possible
Educating about abuse of laxatives and
diuretics
Administer oral K supplements if ordered.
Be knowledgeable about danger of IV
potassium administration.
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Hyperkalemia
Decreased potassium excretion:
Oliguric renal failurePotassium-sparing diuretics
Hypoaldosteronism
High potassium intake,
especially in presence of renalinsufficiency
Shift of potassium out of cells
(acidosis, tissue trauma,
malignant cell lysis)
Vague muscle weakness
Cardiac arrhythmiasParesthesias of face, tongue, feet, and
hands
Flaccid muscle paralysis
GI symptoms such as nausea, intermittentintestinal colic, or diarrhea may occur
Serum K above 5.0 mEq/L
Monitor for hyperkalemia, which is life-
threatening.Prevent hyperkalemia by:
Following rules for safe administration of K
Avoiding giving patients with renal
insufficiency K-saving diuretics, K supplements, or salt substitutes
Cautioning about foods high in potassium
content
Hypocalcemia
Surgical hypoparathyroidismMalabsorption
Vitamin D deficiency
Acute pancreatitis
Excessive administration of citrated blood
Alkalotic states
Trousseau's and Chvostek's signsNumbness and tingling of fingers and toes
Mental changes
Seizures
Spasm of laryngeal musclesECG changes
Cramps in muscles of extremities
Total serum calcium <8.5 mg/dL
Take seizure precautions when hypocalcemiais severe.
Monitor condition of airway.
Take safety precautions if confusion is
present.Educate people at risk for osteoporosis about
need for dietary calcium intake.
Discuss calcium-losing aspects of nicotine
and alcohol use.
Hypercalcemia
Hyperparathyroidism
Malignant neoplastic disease
Prolonged immobilizationLarge doses of vitamin D
Overuse of calcium supplements
Thiazide diuretics
Muscular weakness
Tiredness, lethargy
ConstipationAnorexia, nausea, and vomiting
Decreased memory and attention span
Polyuria and polydipsia
Renal stones
Neurotic behavior
Cardiac arrest
Serum calcium >10.5 mg/dL
Increase mobilization when feasible.
Encourage sufficient oral intake.
Discourage excessive consumption of milk products.
Encourage bulk in the diet.
Take safety precautions if confusion is
present.
Be alert for signs of digitalis toxicity in
hypercalcemic patients.
Force fluids to prevent formation of renal
stones.
Hypomagnesemia
Chronic alcoholismIntestinal malabsorption
Diarrhea
Nasogastric suction
Neuromuscular irritabilityIncreased reflexes
Coarse tremors
Seizures
Assess for magnesium deficit because itpredisposes patient to digitalis toxicity.
Take seizure precautions if necessary.
Monitor condition of airway because
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Drugs
Thiazide diuretics
Aminoglycoside antibioticsExcessive doses of vitamin D
Citrate preservative in blood
Cardiac manifestations
Tachyarrhythmias
Increased susceptibility to digitalistoxicity
Mental changesDisorientation
Mood changes
Serum magnesium <1.3 mEq/L
laryngeal stridor can occur.
Educate patient if abuse of diuretics or
laxatives is a problem.Educate about intake of foods rich in
magnesium.
Hypermagnesemia
Renal failure
Adrenal insufficiencyExcessive magnesium
administration during treatmentof eclampsia
Hemodialysis with hard water or
dialysate high in magnesium
content
Early sign is serum magnesium level of 3
to 5 mEq/LFlushing and sense of skin warmth
HypotensionDepressed respirations
Drowsiness, hypoactive reflexes, and
muscular weakness
Cardiac abnormalities
If hypermagnesemia is present, be alert for
low BP and shallow respirations, lethargy,drowsiness, and coma.
Do not give magnesium-containingmedications to patient with renal failure or
compromised renal function.
Be cautious of OTC drugs.
Check deep tendon reflexes frequently.
Hypophosphatemia
Glucose administration
Refeeding after starvation
HyperalimentationAlcohol withdrawal
Diabetic ketoacidosis
Respiratory alkalosis
Cardiomyopathy
Acute respiratory failure
SeizuresDecreased tissue oxygenation
Joint stiffness
Serum phosphate <2.5 mg/dL
Be aware that severely hypophosphatemic
patients are at greater risk for infection.
Administer IV phosphate products cautiously.Introduce hyperalimentation cautiously in
patients who are malnourished.
Monitor for diarrhea when taking oralsupplements.
Sudden increase in serum phosphate level can
cause hypocalcemia.
Hyperphosphatemia
Renal failureChemotherapy
Large intake of milk
Excessive intake of phosphate-
containing laxatives (Fleetphosphosoda)
Large vitamin D intake
Hyperthyroidism
Short-term consequences:Symptoms of tetany, such as tingling of
the fingertips and around the mouth,
numbness, and muscle spasms
Long-term consequences:Precipitation of calcium phosphate in
nonosseous sites, such as the kidneys,
joints, arteries, skin, or cornea.
Serum phosphate above 4.5 mg/dL
Monitor for signs of tetany.Be aware that soft tissue calcification can be a
long-term complication of chronically
elevated serum phosphate levels.
Instruct patients that use of phosphate-containing laxatives can result in
hyperphosphatemia.
Avoid foods high in phosphorus content.
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Table 46-10 Selected IV Solutions
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Solution Comments
Isotonic Solutions
5% dextrose in water
(D5W)
Supplies about 170 cal/L and contains 50 g of glucose
Should not be used in excessive volumes because it does not contain any sodium; thus the fluid dilutes the amount of sodium in the serum. Brain swelling, or hyponatremic encephalopathy, can develop rapidly and cause death unless it ispromptly recognized and treated.
0.9% NaCl (normalsaline)
Not desirable as routine maintenance solution because it provides only Na+ and Cl-, which are provided in excessiveamounts.May be used to expand temporarily the extracellular compartment if circulatory insufficiency is a problem; also used to
treat diabetic ketoacidosis.
Lactated Ringer's
solution
A roughly isotonic solution that contains multiple electrolytes in about the same concentrations as found in plasma (no
that this solution is lacking in Mg2+ and PO43-)
Used in the treatment of hypovolemia, burns, and fluid lost as bile or diarrhea
Useful in treating mild metabolic acidosis
Hypotonic Solutions
0.33% NaCl 1/3-strength saline)
A hypotonic solution that provides Na+, Cl-, and free water Na+ and Cl- allows kidneys to select and retain neededamounts
Free water desirable as aid to kidneys in elimination of solutes
0.45% NaCl ½-strength
saline)
A hypotonic solution that provides Na+, Cl- and free water
Often used to treat hypernatremia (because this solution contains a small amount of Na+, it dilutes the plasma sodiumwhile not allowing it to drop too rapidly)
Hypertonic Solutions
5% dextrose in 0.45%
NaCl
A common hypertonic solution used to treat hypovolemia; used to maintain fluid intake
10% dextrose in water
(D10W)
Supplies 340 cal/L
Used for peripheral parenteral nutrition (PPN)
5% dextrose in 0.9%
NaCl (normal saline)
Replaces nutrients and electrolytes
Can temporarily be used to treat hypovolemia if plasma expander is not available
Table 46-11 Complications Associated With Intravenous Infusions
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Complication/Cause Signs and Symptoms Nursing Considerations
Infiltration: the escape of fluid into the
subcutaneous tissue Dislodged needlePenetrated vessel wall
Swelling, pallor, coldness, or pain around the
infusion site; significant decrease in the flowrate
Check the infusion site several times
per shift for symptoms.Discontinue the infusion if symptoms
occur.Restart the infusion at a different site.
Limit the movement of the extremity
with the IV.
Sepsis: microorganisms invade the
bloodstream through the catheter insertion
site
Poor insertion technique Multilumen
catheters
Long-term catheter insertion
Frequent dressing changes
Red and tender insertion site Fever, malaise,
other vital sign changes
Assess catheter site daily.
Notify physician immediately if any
signs of infection.
Follow agency protocol for culture of
drainage.
Use scrupulous aseptic technique when
starting an infusion.
Phlebitis: an inflammation of a vein
Mechanical trauma from needle or catheter
Chemical trauma from solution
Septic (due to contamination)
Local, acute tenderness; redness, warmth,
and slight edema of the vein above the
insertion site
Discontinue the infusion immediately.
Apply warm, moist compresses to the
affected site.
Avoid further use of the vein.
Restart the infusion in another vein.
Thrombus: a blood clot Tissue trauma from
needle or catheter
Symptoms similar to phlebitis IV fluid flow
may cease if clot obstructs needle
Stop the infusion immediately.
Apply warm compresses as ordered by
the physician.
Restart the IV at another site.
Do not rub or massage the affected are
Speed shock: the body's reaction to a
substance that is injected into the
circulatory system too rapidly
Too rapid a rate of fluid infusion intocirculation
Pounding headache, fainting, rapid pulse
rate, apprehension, chills, back pains, and
dyspnea
If symptoms develop, discontinue the
infusion immediately.
Report symptoms of speed shock to the
physician immediately.Monitor vital signs if symptoms
develop.
Use the proper IV tubing.
Carefully monitor the rate of fluid flow
Check the rate frequently for accuracy
A time tape is useful for this purpose.
Fluid overload: the condition caused when
too large a volume of fluid infuses into the
circulatory system
Too large a volume of fluid infused into
circulation
Engorged neck veins, increased blood
pressure, and difficulty in breathing
(dyspnea)
If symptoms develop, slow the rate of
infusion.
Notify the physician immediately.
Monitor vital signs.
Carefully monitor the rate of fluid flow
Check the rate frequently for accuracy
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Air embolus: air in the circulatory system
Break in the IV system above the heart
level allowing air in the circulatory systemas a bolus
Respiratory distress
Increased heart rate
CyanosisDecreased blood pressure
Change in level of consciousness
Pinch off catheter or secure system to
prevent entry of air.
Place patient on left side inTrendelenburg position.
Call for immediate assistance.Monitor vital signs and pulse oximetry