Table 46-2 Major Electrolytes

Electrolyte Functions Sources and Losses Regulation

Sodium (Na+): chief Controls and regulates the The average daily requirements Sodium normally maintained
electrolyte of ECF that volume of body fluids for sodium not known in the body within a
moves easily between Maintains water balance Precisely; 2,400 mg (approx. 1 relatively narrow range;
intravascular and throughout the body tsp) as the Daily Value cited on deviations quickly resulting
interstitial spaces and Is the primary regulator of the Nutrition Facts label; RDA in a serious health problem
moves across cell ECF volume for sodium for adults about 500 Sodium concentrations
membranes by active Influences ICF volume mg, or 0.5 g affected by salt, as well as
transport; influential in Participates in the Sodium found in many foods; water, intake
many chemical reactions generation and transmission typically present in large Sodium conserved through
in the body, particularly of nerve impulses amounts, particularly in bacon, reabsorption in the kidneys, a
in nervous tissue cells Is an essential electrolyte in ham, sausage, catsup, mustard, process stimulated by
and muscle tissue cells the sodium-potassium pumprelish, processed cheese, canned aldosterone
vegetables, bread, cereal, and The normal extracellular
salted snack foods; also in table concentration of sodium:
salt (sodium chloride; about 135–145 mEq/L (mmol/L).
46% sodium)
Sodium excesses eliminated
primarily by the kidneys; small
amounts lost in feces and
perspiration

Potassium (K+): major Is the chief regulator of The average daily requirements Conservation of cellular K+
cation of ICF working in cellular enzyme activity and not known precisely; an intake by the sodium pump
reciprocal fashion with cellular water content of 50 to 100 mEq daily enough (described later in the
sodium (eg, an excessive Plays a vital role in such to maintain K+ balance chapter) when Na+ is
intake of sodium processes as the Adequate quantities usually in a excluded; conservation by
resulting in an excretion transmission of electric wellbalanced diet kidneys when cellular K+
of potassium, and vice impulses, particularly in Leading food sources: bananas, decreased.
versa) nerve, heart, skeletal, peaches, kiwi, figs, dates, Aldosterone secretion
intestinal, and lung tissue; apricots, oranges, prunes, triggering K+ excretion in
protein and carbohydrate melons, raisins, broccoli, and urine
metabolism; and cellular potatoes. Meat and dairy Normal range for serum
building products also with adequate potassium: 3.5 to 5 mEq/L
Assists in regulation of amounts of potassium
acid-base balance by Potassium excreted primarily by
cellular exchange with H+ the kidneys (no effective
method of conserving
potassium); deficits occur if
potassium excretion in excess
without being replaced
simultaneously.
Gastrointestinal (GI) secretions
contain potassium in large
quantities; also some in
perspiration and saliva

Calcium (Ca2+): most Is necessary for nerve Average daily requirement Increased secretion of
abundant electrolyte in
the body, with up to 99%
of the total amount of
calcium in the body
found in bones and teeth
in ionized form; close
link between
concentrations of calcium
and phosphorus
Magnesium (Mg2+): most
of cation magnesium
found within body cells
—heart, bone, nerve, and
muscle tissues; second
most important cation in
the ICF
Chloride (Cl-): chief
extracellular anion, found
in blood, interstitial fluid,
and lymph and in minute
amounts in ICF
impulse transmission and
blood clotting
Is a catalyst for muscle
contraction
Is needed for vitamin B12
absorption and for its use
by body cells
Acts as a catalyst for many
cell chemical activities
Is necessary for strong
bones and teeth
Determines the thickness
and strength of cell
membranes
Is important for the
metabolism of
carbohydrates and proteins
Is important for many vital
reactions involving
enzymes
Is necessary for protein and
DNA synthesis, DNA and
RNA transcription, and
translation of RNA
Maintains normal
intracellular levels of
potassium
Helps maintain electrical
activity in nervous tissue
membranes and muscle
membranes
Acts with sodium to
maintain the osmotic
pressure of the blood
Plays a role in the body's
acid-base balance
Has important buffering
about 1 g for adults; higher parathyroid hormone (PTH),
amounts according to body to increase the release of
weight required for children and calcium from bones into the
pregnant and lactating women blood and to increase
Consumption of 1,500 mg/day reabsorption from kidneys
recommended for older adults, and intestine when ECF
particularly postmenopausal levels are decreased
women and men older than 65 A high serum phosphate
years of age concentration, resulting in
Sources include milk, cheese, decreased serum calcium
and dried beans; some present level; a low serum phosphate
in meats and vegetables concentration leading to
The use of calcium stimulated increased serum calcium
by vitamin D; most active form Calcitonin, a hormone
of vitamin D (calcitriol) secreted by the thyroid gland,
responsible for promoting exerting an effect on calcium
calcium absorption and limiting opposite that of PTH.
calcium excretion when levels Increases in calcitonin
are inadequate resulting in reduced serum
Movement out of bones and calcium concentration
teeth to maintain normal blood primarily by opposing
calcium levels, if necessary. osteoclast bone resorption
Excretion via urine, feces, bile,
digestive secretions, and
perspiration
The average daily adult Intestinal absorption and
requirement about 18–30 mEq, excretion by kidneys
with children requiring larger Plasma concentrations of
amounts magnesium ranging from
Magnesium found in most 1.3–2.1 mEq/L, with about
foods, but especially in one third of that amount
vegetables, nuts, fish, whole bound to plasma proteins
grains, peas, and beans
The average daily requirements Normally paired with
of chloride unknown sodium; exerted and
Found in foods high in sodium, conserved with sodium by the
dairy products, and meat kidneys
Chloride deficits lead to
potassium deficits, and vice
 action when oxygen and versa
carbon dioxide exchange in Normal serum chloride
red blood cells levels: from 95–105 mEq/L
Is essential for the (mmol/L)
production of hydrochloric
acid in gastric juices

Bicarbonate (HCO3-): an Is essential for acid-base Losses possible via diarrhea, Bicarbonate levels regulated
anion that is the major balance; bicarbonate and diuretics, and early renal primarily by the kidneys
chemical base buffer carbonic acid constitute the insufficiency; excess possible Bicarbonate readily available
within the body; found in body's primary buffer via overingestion of acid as a result of carbon dioxide
both ECF and ICF system neutralizers, such as sodium formation during metabolism
bicarbonate Normal bicarbonate levels
range between 25 and 29
mEq/L (mmol/L)

Phosphate (PO4-): the Helps maintain the body's Average daily requirements for Regulation by PTH and by
major anion in body acid-base balance phosphorus similar to those for activated vitamin D
cells; a buffer anion in Is involved in important calcium Calcium and phosphate
both ICF and ECF chemical reactions in the Found in most foods but inversely proportional; an
body; eg, phosphorus is especially in beef, pork, and increase in one results in a
necessary for many B dried peas and beans decrease in the other
vitamins to be effective, Metabolism the same as Normal range of phosphate:
helps promote nerve and calcium 2.5 to 4.5 mEq/L (mmol/L)
muscle action, and plays a
role in carbohydrate
metabolism
Is important for cell
division and for the
transmission of hereditary
traits
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 • Circulate blood through the kidneys under sufficient pressure for urine to form (pumping
blood vessels 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
Adrenal • Regulate blood volume and sodium and potassium balance by secreting aldosterone, a
glands 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 • Stores and releases the antidiuretic hormone (ADH), which makes the body retain water;
gland 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 • Inhibits and stimulates mechanisms influencing fluid balance; acts chiefly to regulate
system sodium and water intake and excretion

• Regulates oral intake by sensing intracellular dehydration, which triggers thirst (thirst
center located in hypothalamus)

Parathyroid • Regulate calcium (Ca2+) and phosphate (HPO42-) balance by means of parathyroid
glands 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

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

Foc used As sessme nt G ui de 46 -1 Fl uid, Electrolyte, and Acid– Base Balance
Factors to Assess
Usual patterns of fluid intake
Usual pattern of fluid elimination
Patient's evaluation of hydration
status
History of disease process
Medication/nutrition history
Questions and Approaches
Describe the amount and types of fluids you usually drink in a 24-
hour period. Have there been any recent changes?
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
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)?
Is there any history of disease process or injury that might disrupt
fluid and electrolyte balance (eg, diabetes mellitus, cancer, burns)?
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?
 Fluid, electrolyte, and acid–base Are you aware of any other fluid balance problems you may be
imbalances and contributing experiencing?
factors
• 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 Pancreatic juice Metabolic acidosis
Metabolic alkalosis Sodium deficit
Sodium deficit Calcium deficit
Potassium deficit Extracellular fluid volume deficit

Tetany (if metabolic alkalosis is present) Sensible perspiration Extracellular fluid volume deficit
Sodium deficit

Ketosis of starvation Insensible water loss Water deficit (dehydration)

Magnesium deficit Sodium excess

Intestinal Extracellular fluid volume deficit

juice

Metabolic acidosis Wound exudate Protein deficit

Sodium deficit Sodium deficit
Potassium deficit Extracellular fluid volume deficit

Bile Sodium deficit Ascites Protein deficit

Metabolic acidosis Sodium deficit
Plasma-to-interstitial fluid shift
Extracellular fluid volume deficit
 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 Records may be initiated by the nurseFluid intake about equals fluid When the total intake is substantially
total intake and for any patient with a real or potentialoutput—when averaged over 2 or 3 less than the total output, the patient is
output of fluids water or electrolyte problem. days. in danger of fluid volume deficit.

Intake should include all fluids Range of 1500–3500 mL fluid When the total intake is substantially
taken into the body. intake and loss; 2000 mL is average more than the total output, the patient is
adult intake and loss per day. in danger of fluid volume excess.
Output should include urine,
vomitus, diarrhea, drainage from Output of urine normally
fistulas, and drainage from suction approximates the ingestion of
apparatus. Perspiration and drainage liquids; water from food and
from lesions should be noted and oxidation is balanced by the water
estimated. Prolonged loss through feces, the skin, and the
hyperventilation should also be respiratory process.
noted because it is an important
route of water vapor loss.

Urine volume and All fluid losses are measured Normal urinary output is about 1 A low urine volume with a high
concentration according to routes. mL/kg of body weight per hour (for specific gravity indicates fluid volume
the average adult: 1500 mL/24 hr, deficit.
A device calibrated for small which is equivalent to about 40–80
volumes of urine is used when mL/hr). A low urine volume with a low specific
hourly urine volumes need to be gravity indicates renal disease.
measured. Stress may diminish the 24-hour
urine volume in the adult to 750– A high urine volume suggests fluid
Factors that can alter urinary output 1000 mL (or 30–50 mL/hr) because volume excess.
must be accounted for: of increased aldosterone and ADH
secretion. Urine volume is increased in conditions
Amount of fluid intake with high solute loads, such as diabetes
The range of specific gravity is from mellitus.
Losses from skin, lungs, and GI tract1.003 to 1.035. Urine osmolality
ranges between 500 mOsm and 800 Hypovolemia causes decreased renal
mOsm/ kg (mmol/kg). perfusion and thus oliguria;
Amount of waste products for
excretions hypervolemia causes increased urinary
volume if the kidneys are functioning
 Renal concentrating ability
Blood volume
Hormonal influences (primarily
aldosterone and ADH)
Body weight Because of the common
inaccuracies in recording intake and remain relatively stable.
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, portable
scale.
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
normally.
Rapid variations in weight closely
reflect changes in body fluid volume.
A rapid loss of body weight occurs
when the total fluid intake is less than
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 TBW
indicates 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 mild
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) of
body weight is about equal to the gain
or loss of 1 L of fluid.
Skin turgor The patient's skin over the sternum, Pinched skin immediately falls back In a person with a fluid volume deficit,
(elasticity) inner aspect of the thighs, or to its normal position when the skin flattens more slowly after the
forehead is pinched. released. pinch is released; the skin may remain
elevated for many seconds.
Some prefer to test skin turgor in Reduced skin turgor is common in
children over the abdominal area older patients (those more than 55– Severe malnutrition, particularly in
and on the medial aspect of the 60 years of age) because of a infants, can cause depressed skin turgor
thighs. primary decrease in skin elasticity. even in the absence of fluid depletion.

Skin turgor can vary with age,

nutritional state, and even race and
complexion.

Tongue turgor Unlike skin turgor, tongue turgor is Tongue has one longitudinal furrow.In the person with fluid volume deficit,
not affected appreciably by age and there are additional longitudinal
thus is a useful assessment for all furrows and the tongue is smaller.
age groups. (In an arid climate, this
may not be a reliable parameter.) Sodium excess causes the tongue to
look red and swollen.

Moisture and oral A dry mouth may be the result of Mucous membranes in oral cavity Dryness of the membrane where the
cavity fluid volume deficit or of mouth are moist. cheek and gum meet indicates fluid
breathing. (Exposure to an arid volume deficit.
climate may result in a dry mouth.)
Dry sticky mucous membranes are
noted in sodium excess. (The oral
cavity feels like flypaper.)

Tearing and Tearing and salivation decrease The absence of tearing and salivation in
salivation normally with age. a child is a sign of fluid volume deficit;
it becomes obvious with a fluid loss of
5% of TBW.

Appearance of Metabolic acidosis can cause warm,

skin and skin flushed skin (due to peripheral
temperature vasodilation).

Facial appearance A person with a severe fluid volume

deficit may have a pinched and drawn
facial expression.

Edema (excessive Pitting edema (see Fig. 46-7)
accumulation of
interstitial fluid) 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 the
lower extremities of ambulatory
patients and in the presacral region
of 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.
Body temperature Because fever increases the loss of Baseline temperature: diurnal
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.
Pulse
A fluid volume deficit of 10% of body
weight causes decreased intraocular
pressure, causing the eyes to appear
sunken and to feel soft to the touch.
No edema Clinically edema is not usually
apparent in the adult until the retention
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 localized
(as in thrombophlebitis) or generalized
(as in heart failure, cirrhosis of liver, or
nephrotic syndrome). Edema of
congestive heart failure, liver cirrhosis,
or nephrotic syndrome is the result of
sodium retention.
There is an elevation of body
variations temperature in hypernatremia
(dehydration) probably related to lack
of available fluid for sweating.
There is a decrease in body temperature
in fluid volume deficit, when
uncomplicated by infection.
Fever increases the loss of body fluids.
A temperature elevation between 101°F
(38.3°C) and 103°F (39.4°C) increases
the 24-hour fluid requirement by at
least 500 mL, and a temperature above
103°F increases it by at least 1000 mL.
Baseline pulse rate, rhythm, and Tachycardia is usually the earliest sign
volume of the decreased vascular volume
associated with fluid volume deficit.
Irregular pulse rates also occur with
potassium imbalances and magnesium

Respirations
Blood pressure Whenever a fluid imbalance is
suspected, the patient's blood
pressure is checked while he or she
is lying down, sitting, and standing
(orthostatic).
Neck veins and The jugular veins provide a built-in Normally, when the patient is
central venous manometer for following changes in supine, the external jugular veins fill
pressure (CVP) CVP.
To estimate CVP, the nurse:
Positions the patient in a semi-
Fowler's position (head of bed
elevated to a 30- to 45-degree
angle), keeping the neck straight
Removes any of the patient's
clothing that could constrict the
neck or upper chest
Provides adequate lighting to
visualize effectively the external
jugular veins on each side of the
neck
Baseline respiratory rate, rhythm,
and qualities
Baseline blood pressure
to the anterior border of the
sternocleidomastoid muscle. With
the patient positioned sitting at a 45-
degree angle, the venous distentions
normally should not extend higher
than 2 cm above the sternal angle.
Pressure in the right atrium is
usually 0–4 cm H2O; pressure in the
vena cava is about 4–11 cm H2O.
deficit.
Pulse volume is decreased in fluid
volume deficit and increased in fluid
volume excess.
Deep, rapid respirations may be a
compensatory mechanism for
metabolic acidosis or a primary
disorder causing respiratory alkalosis.
Slow, shallow respirations may be a
compensatory mechanism for
metabolic alkalosis or a primary
disorder causing respiratory acidosis.
Moist crackles, in the absence of
cardiopulmonary disease, indicate fluid
volume excess.
A fall in systolic pressure greater than
15 mm Hg from the lying to the sitting
or standing position (postural
hypotension) usually indicates fluid
volume deficit.
A low CVP may indicate:
Decreased blood volume
Drug-induced
vasodilation (causing
pooling of blood in
peripheral veins)
A high CVP may indicate:
Increased blood volume
Heart failure
Vasoconstriction
 Measures the levels to which the
veins 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 When imbalances in calcium, Negative response

irritability magnesium, and sodium are
suspected it is important to assess
patients for increased or decreased
neuromuscular irritability.

To test for Chvostek's sign, the Negative response Patients with hypocalcemia or
facial nerve should be hypomagnesemia respond positively
percussed about 2 cm anterior with a unilateral twitching of the facial
to the ear lobe. muscles, including the eyelid and lips.

To test for Trousseau's sign, a The response in the prospective A positive response is the development
blood pressure cuff is placed muscle is a sudden contraction (2+). of carpal spasm.
on the arm and inflated above
systolic pressure for 3 minutes.

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.
The muscle being tested
should be slightly stretched,
and the patient should be
relaxed.
Reflexes usually are graded on a 0 Deep tendon reflexes may be
to 4+ scale. hyperactive in the presence of
0 = no response hypocalcemia, hypomagnesemia,
1+ = somewhat diminished, but hypernatremia, and alkalosis.
present
2+ = normal
3+ = brisker than average and
possibly but not necessarily
indicative Deep tendon reflexes may be
hypoactive in the presence of
of disease hypercalcemia,
4+ = hyperactive hypermagnesemia, hyponatremia,
hypokalemia, and acidosis.

Behavior Because these changes are often

Sensation Fatigue vague, they are best evaluated in
level context with specific imbalances

.
Table 46-7 Acid–Base Disturbances
Risk Factors Assessments Nursing Interventions

Respiratory Acidosis (Carbonic Acid Excess)

Acute respiratory disease: Acute respiratory acidosis Treatment is directed at improving ventilation:
Pulmonary edema Mental cloudiness Pharmacologic measures
Aspiration of a foreign Dizziness Pulmonary hygiene measures
body Muscular twitching Adequate hydration
Atelectasis Unconsciousness Supplemental oxygen
Overdose of sedative or ABGs Mechanical ventilation may be necessary to correct disorder but
anesthetic pH <7.35 must be used cautiously to decrease PaCO2 slowly.
Cardiac arrest PaCO2 >45 mm Hg
Chronic respiratory disease: (primary)
Emphysema HCO3- normal or only
Bronchial asthma slightly elevated
Cystic fibrosis Chronic respiratory acidosis
Inadequate mechanical Weakness
ventilation Dull headache
CNS depression ABGs
Neuromuscular disease pH <7.35 or low N
PaCO2 >45 mm Hg
(primary)
HCO3- >26 mEq/L
(compensatory)

Respiratory Alkalosis (Carbonic Acid Deficit)

Hyperventilation Lightheadedness If anxiety is the cause, the patient should be encouraged to breathe
Extreme anxiety (most Inability to concentrate more slowly (causes accumulation of CO2) or breathe into a closed
common cause) Hyperventilation syndrome system (paper bag). Sedative may also be necessary in extreme
Hypoxemia Tinnitus anxiety.
High fever Palpitations Treatment of other causes is directed at correcting the underlying
Early sepsis Sweating problem.
Excessive ventilation by Dry mouth
mechanical ventilator Tremulousness
CNS lesion involving the Convulsions and loss of
respiratory center consciousness
Thyrotoxicosis ABGs
pH >7.45
PaCO2 <35 mm Hg
(primary)
HCO3- <22 mEq/L
(compensatory)

Metabolic Acidosis (Base Bicarbonate Deficit)

Diarrhea Headache Treatment is directed toward correcting the metabolic deficit. If

Intestinal fistulas Confusion the cause of the problem is excessive intake of chloride, treatment
Ureterosigmoidostomy
Hyperalimentation
Excessive intake of acids,
such as salicylates
Diabetic ketoacidosis
Renal failure
Starvational ketoacidosis
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)
Drowsiness obviously focuses on eliminating the source. When necessary,
Increased respiratory rate bicarbonate is administered.
and depth
Nausea and vomiting
Peripheral vasodilation
ABGs
pH <7.35
HCO3- <22 mEq/L
(primary)
PaCO2 <35 mm Hg
Hyperkalemia frequently
present
Dizziness Treatment is aimed at reversal of the underlying disorder.
Tingling of fingers and toes Sufficient chloride must be supplied for the kidney to absorb
Hypertonic muscles sodium with chloride (allowing the excretion of excess
Depressed respirations bicarbonate). Treatment also includes administration of NaCl
(compensatory) fluids to restore normal fluid volume.
ABGs
pH >7.45
HCO3- >26 mEq/L
(primary)
PaCO2 >45 mm Hg
(compensatory)
Hypokalemia may be
present
Table 46-8 Fluid Volume Disturbances
Risk Factors Assessments Nursing Interventions

Fluid Volume Deficit (Hypovolemia)

GI: Vomiting, diarrhea, suction, fistulas Thirst Assess for presence or worsening of FVD.
Hemorrhage Weight loss over short period Administer oral fluids if indicated.
Excessive sweating Weakness, fatigue, anorexia If patient unable to eat and drink, anticipate
Skin trauma, burns, draining wounds Dry mucous membranes TPN or tube feedings to be ordered.
Third-space fluid shifts Poor skin and tongue turgor Monitor patient's response to fluid intake,
Excessive laxative or diuretic use Sunken eyes either oral or parenteral.
Polyuria from renal disease or diuretics Flat neck veins Be alert for signs of fluid overload.
Hyperglycemia Urine output <30 mL/hr Provide appropriate skin care.
Change in mental status (unable to gain access Postural hypotension
to fluids, depression, confusion) Weak, rapid pulse
↑Urine specific gravity
↑Hematocrit
↑BUN
↑Serum sodium
Altered sensorium

Fluid Volume Excess (Hypervolemia)

Compromised regulatory mechanisms: renal Weight gain over short Assess for presence or worsening of FVE.
failure, CHF, cirrhosis of liver, Cushing's period Encourage adherence to sodium-restricted
syndrome Peripheral edema (may be and fluid-restricted diet, if ordered.
GI irrigation with hypotonic fluid pitting) Avoid OTC drugs or check with physician or
Excess IV fluids with sodium Increased BP pharmacist about sodium content.
Corticosteroid therapy Shortness of breath Encourage rest periods.
Excessive ingestion of sodium-containing Crackles and wheezes in Monitor patient's response to diuretics.
substances in diet or sodium-containing lungs Teach self-monitoring of weight and intake
medications Full, bounding pulse and output.
Neck vein distention Attentive skin care.
Polyuria if renal function is Monitor respiratory status.
normal
Ascites, pleural effusion
Pulmonary edema
↓BUN (due to plasma
dilution)
↓Hematocrit
↓Serum sodium
↓Urine specific gravity

Table 46-9 Electrolyte Disturbances

Risk Factors Assessments Nursing Interventions

Hyponatremia

Loss of sodium, as in: Anorexia Monitor fluid losses and gains.

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
Nausea and vomiting Monitor for presence of GI and CNS
Lethargy symptoms.
Confusion Monitor serum Na levels.
Muscle cramps Check urine specific gravity.
Muscular twitching If able to eat, encourage foods and fluids with
Seizures high sodium content.
Coma Be aware of sodium content of common IV
Serum Na below 135 mEq/L fluids.
Urine specific gravity <1.010 Avoid giving large water supplements to
patients receiving isotonic tube feedings.
Take seizure precautions when hyponatremia
is severe.

Hypernatremia

Water deprivation Thirst Monitor fluid losses and gains.

Increased sensible and insensible
water loss
Ingestion of large amount of salt
Excessive parenteral
administration of sodium-
containing solutions
Profuse sweating
Diabetes insipidus
Elevated body temperature
Tongue dry and swollen, sticky mucous
membranes
Severe hypernatremia
Disorientation
Hallucinations
Lethargy when undisturbed
Irritable and hyperactive
Focal or grand mal seizures
Coma
Serum Na above 145 mEq/L
Urine specific gravity >1.015
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 Fatigue Monitor for occurrence of hypokalemia.

Vomiting or gastric suction
Potassium-wasting diuretics
Steroid administration and
certain antibiotics
Poor intake as in anorexia
nervosa, alcoholism, potassium-
free parenteral fluids
Polyuria
Anorexia, nausea, and vomiting
Muscle weakness
Decreased bowel motility
Cardiac arrhythmias
Increased sensitivity to digitalis
Polyuria, nocturia, dilute urine
Postural hypotension
Serum K below 3.5 mEq/L
ECG changes
Paresthesias or tender muscles
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.
Hyperkalemia
Decreased potassium excretion:
Oliguric renal failure
Potassium-sparing diuretics
Hypoaldosteronism
High potassium intake,
especially in presence of renal
insufficiency
Shift of potassium out of cells
(acidosis, tissue trauma,
malignant cell lysis)
Hypocalcemia
Surgical hypoparathyroidism
Malabsorption
Vitamin D deficiency
Acute pancreatitis
Excessive administration of
citrated blood
Alkalotic states
Hypercalcemia
Hyperparathyroidism
Malignant neoplastic disease
Prolonged immobilization
Large doses of vitamin D
Overuse of calcium supplements
Thiazide diuretics
Hypomagnesemia
Chronic alcoholism
Intestinal malabsorption
Diarrhea
Nasogastric suction
Vague muscle weakness
Cardiac arrhythmias
Paresthesias of face, tongue, feet, and
hands
Flaccid muscle paralysis
GI symptoms such as nausea, intermittent
intestinal colic, or diarrhea may occur
Serum K above 5.0 mEq/L
Trousseau's and Chvostek's signs
Numbness and tingling of fingers and toes
Mental changes
Seizures
Spasm of laryngeal muscles
ECG changes
Cramps in muscles of extremities
Total serum calcium <8.5 mg/dL
Muscular weakness
Tiredness, lethargy
Constipation
Anorexia, nausea, and vomiting
Decreased memory and attention span
Polyuria and polydipsia
Renal stones
Neurotic behavior
Cardiac arrest
Serum calcium >10.5 mg/dL
Neuromuscular irritability
Increased reflexes
Coarse tremors
Seizures
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
Take seizure precautions when hypocalcemia
is 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.
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.
Assess for magnesium deficit because it
predisposes patient to digitalis toxicity.
Take seizure precautions if necessary.
Monitor condition of airway because
Drugs
Thiazide diuretics
Aminoglycoside antibiotics
Excessive doses of vitamin D
Citrate preservative in blood
Hypermagnesemia
Renal failure
Adrenal insufficiency
Excessive magnesium
administration during treatment
of eclampsia
Hemodialysis with hard water or
dialysate high in magnesium
content
Hypophosphatemia
Glucose administration
Refeeding after starvation
Hyperalimentation
Alcohol withdrawal
Diabetic ketoacidosis
Respiratory alkalosis
Hyperphosphatemia
Renal failure
Chemotherapy
Large intake of milk
Excessive intake of phosphate-
containing laxatives (Fleet
phosphosoda)
Large vitamin D intake
Hyperthyroidism
Cardiac manifestations
Tachyarrhythmias
Increased susceptibility to digitalis
toxicity
Mental changes
Disorientation
Mood changes
Serum magnesium <1.3 mEq/L
Early sign is serum magnesium level of 3
to 5 mEq/L
Flushing and sense of skin warmth
Hypotension
Depressed respirations
Drowsiness, hypoactive reflexes, and
muscular weakness
Cardiac abnormalities
Cardiomyopathy
Acute respiratory failure
Seizures
Decreased tissue oxygenation
Joint stiffness
Serum phosphate <2.5 mg/dL
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
laryngeal stridor can occur.
Educate patient if abuse of diuretics or
laxatives is a problem.
Educate about intake of foods rich in
magnesium.
If hypermagnesemia is present, be alert for
low BP and shallow respirations, lethargy,
drowsiness, and coma.
Do not give magnesium-containing
medications to patient with renal failure or
compromised renal function.
Be cautious of OTC drugs.
Check deep tendon reflexes frequently.
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 oral
supplements.
Sudden increase in serum phosphate level can
cause hypocalcemia.
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.
Table 46-10 Selected IV Solutions
 Solution Comments

Isotonic Solutions

5% dextrose in water Supplies about 170 cal/L and contains 50 g of glucose

(D5W) 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 is
promptly recognized and treated.

0.9% NaCl (normal Not desirable as routine maintenance solution because it provides only Na+ and Cl-, which are provided in excessive
saline) amounts.
May be used to expand temporarily the extracellular compartment if circulatory insufficiency is a problem; also used to
treat diabetic ketoacidosis.

Lactated Ringer's A roughly isotonic solution that contains multiple electrolytes in about the same concentrations as found in plasma (note
solution 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- A hypotonic solution that provides Na+, Cl-, and free water Na+ and Cl- allows kidneys to select and retain needed
strength saline) amounts
Free water desirable as aid to kidneys in elimination of solutes

0.45% NaCl ½-strength A hypotonic solution that provides Na+, Cl- and free water
saline) Often used to treat hypernatremia (because this solution contains a small amount of Na+, it dilutes the plasma sodium
while not allowing it to drop too rapidly)

Hypertonic Solutions

5% dextrose in 0.45% A common hypertonic solution used to treat hypovolemia; used to maintain fluid intake
NaCl

10% dextrose in water Supplies 340 cal/L

(D10W) Used for peripheral parenteral nutrition (PPN)

5% dextrose in 0.9% Replaces nutrients and electrolytes

NaCl (normal saline) Can temporarily be used to treat hypovolemia if plasma expander is not available

Table 46-11 Complications Associated With Intravenous Infusions

Complication/Cause
Infiltration: the escape of fluid into the
subcutaneous tissue Dislodged needle
Penetrated vessel wall
Sepsis: microorganisms invade the
bloodstream through the catheter insertion
site
Poor insertion technique Multilumen
catheters
Long-term catheter insertion
Frequent dressing changes
Phlebitis: an inflammation of a vein
Mechanical trauma from needle or catheter
Chemical trauma from solution
Septic (due to contamination)
Thrombus: a blood clot Tissue trauma from
needle or catheter
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 into
circulation
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
Signs and Symptoms
Swelling, pallor, coldness, or pain around the Check the infusion site several times
infusion site; significant decrease in the flow per shift for symptoms.
rate
Red and tender insertion site Fever, malaise, Assess catheter site daily.
other vital sign changes
Local, acute tenderness; redness, warmth,
and slight edema of the vein above the
insertion site
Symptoms similar to phlebitis IV fluid flow Stop the infusion immediately.
may cease if clot obstructs needle
Pounding headache, fainting, rapid pulse
rate, apprehension, chills, back pains, and
dyspnea
Engorged neck veins, increased blood
pressure, and difficulty in breathing
(dyspnea)
Nursing Considerations
Discontinue the infusion if symptoms
occur.
Restart the infusion at a different site.
Limit the movement of the extremity
with the IV.
Notify physician immediately if any
signs of infection.
Follow agency protocol for culture of
drainage.
Use scrupulous aseptic technique when
starting an infusion.
Discontinue the infusion immediately.
Apply warm, moist compresses to the
affected site.
Avoid further use of the vein.
Restart the infusion in another vein.
Apply warm compresses as ordered by
the physician.
Restart the IV at another site.
Do not rub or massage the affected area.
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.
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.
Air embolus: air in the circulatory system
Break in the IV system above the heart
level allowing air in the circulatory system
as a bolus
Respiratory distress
Increased heart rate
Cyanosis
Decreased blood pressure
Change in level of consciousness
Pinch off catheter or secure system to
prevent entry of air.
Place patient on left side in
Trendelenburg position.
Call for immediate assistance.
Monitor vital signs and pulse oximetry.