LEARNING OU COMES

Following completion of this chapter, the Ieamer will be able to

1 Apply knowledge of fluid volume deficit when caring for the high-acuity patient.

2 Demonstrate knowledge of fluid volume excess when delivering patient care.

3 Discuss alterations in sodium balance that affect patient care.

4 Apply knowledge of alterations in calcium balance when caring for the high-acuity patient.

.:, Demonstrate understanding of alterations in potassium balance.

6 Use knowledge of alterations in magnesium balance when delivering patient care.

7 Apply knowledge of alterations in phosphorus/phosphate balance.

luid and electrolyte balance are essential to maintaining (ECF) volume deficit is an abnormally low volume of body fluid

F physiologic homeostasis. The body is composed largely of

fluids (about 60% in the adult). Fluids serve critical func­
tions, such as acting as a solvent for metabolic chemical reac­
tions; transporting nutrients, oxygen, and waste products to their
appropriate destinations; moistening and lubricating skin and mu­
cous membranes; and regulating body temperature (Felver, 2010).
Fluids are located in and constantly shift between the extracellular
and intracellular compartments to carry out their functions.
Electrolytes are positively (cation) and negatively (anion)
charged salts that are dissolved in the body's fluids and dispersed
throughout the body in all compartments. Electrolytes play essen­
tial roles in electrical conduction, chemical reactions, production
of energy, and regulation of body fluids. Imbalances in fluid or
electrolytes can have profoundly negative effects on essentially all
body systems. High-acuity patients, by virtue of their disease states,
are at high risk for fluid or electrolyte imbalance, and these imbal­
ances can result in serious or even life-threatening complications.
It is recommended that Chapter 24, Determinants and
Assessment of Fluid and Electrolyte Balance, be reviewed prior to
beginning this chapter to enhance understanding of this material.
SECTION ONE: Fluid Volume Oeficit
There are two major fluid compartments in the body: extracel­
lular (composed of intravascular and interstitial fluids) and
intracellular (composed of fluid within cells). Extracellular fluid
608
in the intravascular and interstitial compartments from loss of
sodium and fluid (Felver, 2010). This produces a state of extra­
cellular dehydration, which can then cause intracellular dehy­
dration as fluid shifts out of the cells to increase intravascular
volume. For the purposes of this chapter, fluid volume deficit
(FVD) refers to hypovolemia, an abnormally low circulating
fluid volume, which is specific to the intravascular compartment.
Etiology
Many clinical problems can cause or contribute to the develop­
ment of FVD, which is a common and potentially serious prob­
lem in the high-acuity patient. These factors are summarized in
Table 25-1.
As discussed in Chapter 24, loss of extracellular fluid volume
can be due to third spacing, a unique fluid-shifting situation
that can lead to significant FVD if the fluids are shifting into a
serous cavity in conditions such as liver failure, pancreatitis, or
peritonitis. The fluid shifts of third spacing result from altered
capillary membrane permeability secondary to tissue injury, isch­
emia, or inflammation; or they can develop because of increased
hydrostatic pressure or decreased oncotic pressure in the intra­
vascular space. The resulting trapped fluid is essentially unavail­
able for functional use within the body and may accumulate
rapidly because of protein-rich contents, which causes increased
tissue colloidal osmotic pressure, attracting more fluids.
 CHAP T E R 25 � Alterations in Fluid and Electrolyte Balance 609

Intravenous Fluid Resuscitation Early and rapid

fluid resuscitation with isotonic solutions is the cornerstone of
management. There is still no clear consensus over the choice
of resuscitation fluid. Colloids have not been shown to improve
Related Factors
survival compared with crystalloids; thus, either may be used
Gastrointestinal Diarrhea, vomiting, nasogastric for volume resuscitation (Perel, Roberts, and Ker, 2013) .
suction, fistulas, bleeding Intravenous fluids are classified according t o their osmolar­
Urinary Drug therapy (e. g., diuretics) . hyper­ ity or tonicity. Osmolarity refers to the number of milliosmoles
glycemia, diabetes insipidus, diuretic (mOsm) per liter of solution. Tonicity refers to the effect the
phase of acute tubular necrosis (ATN) solution has on the extracellular fluid and intracellular fluid com­
Burns, diaphoresis, increased capillary
partments and is sometimes used instead of osmolarity (Metheny,
Integumentary
permeability 2010). Intravenous solutions are classified as isotonic, hypotonic,
or hypertonic. The nurse should be aware of the reason a patient
Insensible Hyperventilation, fever, hypermetab­
is receiving a particular IV fluid and what complications are asso­
olism, tachypnea, mechanical ventilation
ciated with that fluid based on tonicity.
Hemorrhage, wound drainage
Isotonic solutions. The term isotonic means that the osmolar­
ity of the solution on one side of a membrane is the same as the
Clinical Manifestations osmolarity on the other side. Isotonic solutions have the same
osmolarity as body fluids (Metheny, 2010). The osmolarity of iso­
Assessing the high-acuity patient for FVD is an important part
tonic fluid closely approximates normal serum plasma osmolality
of the daily nursing assessment, and patients with existing FVD
(solute concentration of body fluids, expressed in mOsm/liter).
require close monitoring. These patients have higher serum osmo­
For this reason, a steady osmolar state is maintained between
lality (greater than 300 mOsm/kg) due to FVD. The critical (panic)
intracellular fluid (ICF) and extracellular fluid (ECF); therefore,
value for hyperosmolality is 390 mOsm/kg or greater. Table 25-2
fluids do not shift from one compartment to another. Isotonic
lists assessment data associated with fluid volume deficit.
fluids C• Fig. 25-1a) are used when rapid ECF expansion is
needed. The most common reason for administration of iso­
Medical Treatment
tonic solutions is intravascular dehydration (intravascular FVD).
The primary goals of medical treatment are to identify and con­ Normal saline (0.9%) and lactated Ringer's solutions are com­
trol the source of fluid loss and to correct the deficit by replen­ monly used for fluid resuscitation in shock (Phillips et al., 2009).
ishing fluids. Fluids can be replaced by intravenous (IV), oral,
or enteral routes, depending on the severity of the FVD and the Hypotonic Solutions. Hypotonic solutions (e.g., 0.45% NS,
acuity level of the patient. Intravenous fluids are generally pre­ and 0.2% NS, 2.5% dextrose) contain a lower concentration of
ferred for acute situations. particles than exists in the ICF and ECF. The low osmolarity

�TABLE. 2s-2" • • F.luid Volume Deficit

..

Assessment : Parameter � Data

Physical assessment � Neurologic : Altered mental status, anxiety, restlessness, diminished alertness/cognition,
: possible coma
: Mucous membranes : Dry, decreased tongue size with longitudinal furrows
il::_.: Integumentary
����fi�G,;__
: Poor skin turgor, dry skin, pale/cool extremities
: Urinary : Decreased urinary output, oligura (severe FVD)
: Cardiovascular : Flat neck veins, decreased pulse volume and capillary refill, decreased venous filling
: Other : Thirst, weight loss (mild FVD 2-5%, moderate FVD
= = 6-9%, severe
� FVD greater than 10%), fatigue
=

Vital signs and : HR, BP, Temperature : Tachycardia, hypotension, orthostatic hypotension, hypothermia (isotonic FVD)
hemodynamic : or hyperthermia (dehydration)
pressures

: CVP and PA pressures .: Decreased CVP and PA pressures, decreased CO

.
: :

Laboratory data � Hct, urine osmolality, : Increased Hct, high serum osmolality, high urine specific gravity (increased
� specific gravity � concentration) . increased BUN

CVP = central venous pressure; P A = pulmonary artery; C O = cardiac output

610 PART 7 � Fluid and Electrolytes

(a) Isotonic solution (b) Hypotonic solution (c) Hypertonic solution

• FIGURE 25-1 Tonicity. (a) Isotonic solutions (same osmolarity as plasma,
and IV fluids remain in intravascular space). (b) Hypotonic solutions (lower
osmolarity than plasma, and IV fluids shift into the cells) . (c) Hypertonic
solutions (higher osmolarity than plasma, and IV fluids pull fluid from intracel­
lular and extracellular compartments into intravascular compartment) .

shifts fluid from the intravascular compartment into the intra­
cellular compartments. Hypotonic fluids (Fig. 25-1b) are used
primarily in the treatment of cellular dehydration because they
expand the intracellular volume; however, they are also useful
for the prevention of dehydration or for hydration. Hypotonic
solutions must be used with caution, however, because their
overuse causes cells (including blood cells) to expand and
potentially burst, resulting in cellular destruction. Cellular over­
expansion will result in increased intracranial pressure (ICP)
and mental status deterioration; therefore, it is important to
avoid administering hypotonic solutions to patients with neuro­
logical problems associated with increased ICP (Metheny, 2010).
Hypertonic Solutions. Hypertonic solutions (e.g., DlOW, D5
in 0.45 NS, 3% NS) have a high osmolarity because they contain
a higher concentration of particles than exists in the ICF and
ECF. The high osmolarity shifts fluids from the ICF and ECF
into the intravascular compartment, expanding blood volume.
Hypertonic solutions (Fig. 25-1c) are used in the treatment of
water intoxication (intracellular fluid volume excess) (Metheny,
2010). Water intoxication can be caused by administration of
large amounts of electrolyte-free water, overuse of hypotonic
solutions (e.g., 0.45% sodium chloride), elevated ADH secretion,
or renal failure. Hypertonic saline has been shown to be an effec­
tive first-line therapeutic alternative for treatment of intracranial
hypertension and cerebral edema. Beyond its osmotic and hemo­
dynamic properties, compelling laboratory and clinical data indi­
cate that hypertonic saline-dextran exerts immunomodulatory
and anti-inflammatory effects, including blunted cellular activa­
tion and cytokine production (Rhind et al., 2010). Hypertonic
saline not only offers the advantages of more rapid administra­
tion and almost instantaneous hemodynamic stability, it also
downregulates neutrophil activation and organ injury in com­
parison with lactated Ringer's (Costantini et al., 2010).
Nursing Considerations
Nursing diagnoses for patients with FVD may include Deficient
Fluid Volume, Ineffective Tissue Perfusion, Decreased Cardiac
Output, and Diarrhea. Nursing interventions may include mea­
sures to decrease vomiting, diarrhea, or fever; increasing oral
fluid intake or administration of intravenous solutions; and
monitoring of fluid and electrolyte status. Desired patient out­
comes include pulse, blood pressure, central venous pressure
(CVP), and pulmonary artery wedge pressure (PAWP) within
acceptable ranges for the patient; normal serum osmolality;
increased urine output with normal specific gravity; improved
skin turgor; balanced intake and output; stable weight; moist
mucous membranes; hematocrit and blood urea nitrogen
(BUN) within acceptable limits; and absence of other dehydra­
tion manifestations.

Section One Review

1 . Where are third-spaced fluids most commonly 3. Which IV solution is commonly used for patients in a shock
located? state?
A. Joints A. Lactated Ringer's
B. A serous cavity B. 0.45% normal saline
C. The cranial vault C. 2.5% dextrose
D. Interstitial fl uid D. 3% normal saline
2. Which statement is correct regarding 4. Which IV solution can cause cells to expand and burst,
extracellular FVD? resulting in cellular destruction?
A. It can lead to transcellular expansion. A. Isotonic
B. It can lead to intracellular expansion. B. Hypertonic
C. It is associated with low serum osmolality. C. Hypotonic
D. It is associated with high serum osmolality. D. Lactated R inger s
'

Answers: 1. B, 2. D, 3. A, 4. C
 CHA PTER 25 � Alterations in Fluid and Electrolyte Balance 611

SECTION TWO: Fluid Volume

Excess
Fluid volume excess (FVE), also called fluid overload or � Data
hypervolemia, produces a state of overhydration in the intra­
vascular compartment. FVE results when both water and Physical assessment : Mental status changes
sodium are retained. : Weight gain
: Distended neck veins
: Periorbital edema, pitting edema
Etiology
: over bony prominences
Many high-acuity patients are at moderate to high risk for : Adventitious lung sounds, moist
development of FVE. Common causes of FVE include such : crackles
disorders as heart, liver, or kidney failure; and overhydration : Shortness of breath
secondary to excessive or too rapid delivery of IV therapy. : Generalized or dependent
FVE can also occur as a side effect of drugs such as cortico­ : edema
steroids. A growing body of evidence strongly suggests that
fluid overload, especially in critically ill patients, worsens Vital signs : Elevated blood pressure
patient prognosis ( Lee, 2010). It is associated with fewer con­ : Elevated CVP and pulmonary
: artery pressures
tributing factors than in FVD. These factors are summarized
in Table 25-3. : Increased cardiac output
____
_ ._.,.
Laboratory data : Decreased hematocrit
Clinical Manifestations : (dilutional)

Extracellular FVE can be generalized or localized. The : Low serum osmolality

assessment procedures are essentially the same as those used
to assess for FVD. The findings, however, are in almost com­
plete opposition, with the exception of urinary output. A low
urine output can be indicative of either a deficit or an excess.
For example, a low urine output (less than 0.5 mL!kg/hr)
may be indicative of dehydration or kidney injury. Decreased
urinary ·output in the patient with dehydration is a protec­
tive mechanism for the body to preserve volume. Decreased
urinary output in the patient with kidney injury, however,
causes fluid volume excess. Nursing assessment of the patient
for FVE is summarized in Table 25-4. Altered serum labora­
tory values may include decreased hematocrit and hemoglo­
bin as well as a low serum osmolality, resulting from plasma
dilution from excess extracellular fluid. The critical (panic)
value for serum osmolality is 190 mOsm/Kg or less.
: Radiography: pulmonary
: vascular congestion,
: pleural effusion, pericardia!
: effusion, ascites
: Low urine-specific gravity
: (decreased concentration)
Medical Treatment
The treatment for FVE is aimed at correcting the underlying
cause and treating the manifestations. This is accomplished
through restriction of sodium and water intake and admin­
istration of diuretics. Diuretics inhibit sodium and water
reabsorption and increase urine output and are commonly
administered to patients with FVE. Diuretics are summa­
rized in the box Related Pharmacotherapy: Diuretics. Each
diuretic drug group works on a different part of the kidney
tubule.

Nursing Considerations
Related Factors Nursing diagnoses pertinent to patients with fluid overload
may include: Excess Fluid Volume, Risk for Impaired Skin
Cardiovascular Heart failure
Integrity, and Impaired Gas Exchange. Nursing interventions
Urinary may include monitoring adherence to fluid or salt restrictions,
administration of diuretics, or dialysis. Monitoring should
Hepatic Cirrhosis also include daily weight, intake and output, and location and
Liver failure severity of edema, if present; as well as vital signs, chest x-ray,
and possibly central venous pressures or pulmonary artery
Other Cancer
pressures (Lee, 2010). The desired patient outcomes for intra­
Thrombus
vascular fluid excess include pulse, blood pressure, and central
Peripheral vascular disease
venous pressure (CVP) within acceptable ranges for the patient;
Drug therapy (e.g., corticosteroids)
lung sounds clear to auscultation; balanced intake and output;
High sodium intake
weight loss and resolution of edema; and hematocrit and blood
Protein malnutrition
urea nitrogen (BUN) within acceptable limits.
 612 PART 7 � Fluid and Electrolytes

RELATED PHARMACOTHERAPY Diuretics

Loop Diuretics Major Side Effects

Furosemide (Fumide, Furomide, Lasix, Luramide) Hyperglycemia
Hypokalemia
Action and Uses
Inhibits reabsorption of sodium and chloride in the loop of Nursing Implications
Henle; decreases edema and intravascular volume. Monitor vital signs, especially during dosage adjustment.
Monitor for manifestations of hypokalemia.
Dosages (Adult)
Edema: 20-40 mg up to 600 g/day ( IV) (administering in one
Potassium-Sparing Diuretics
or divided doses). May be given undiluted or dilute in D5 W,
Spironolactone (Aldactone, Novo-Spiroton)
NS, or LR. Undiluted-administer at no faster than 20 mg over
1-2 minutes. Action and Uses
Major Side Effects Competes with aldosterone for cellular receptor sites in distal
Circulatory collapse renal tubule. Promotes sodium and chloride excretion without
Hypokalemia loss of potassium. Used for diuresis in cases of refractory
edema due to heart failure or cirrhosis.
Nursing Implications
Monitor vital signs, especially during dosage adjustment. Dosage (Adult)
Monitorfor manifestations of hypokalemia. Edema: 25-200 mg/day (PO) in divided doses
Hypertension: 25-100 mg/day (PO) in one or divided doses,
Thiazide Diuretics dose adjusted as needed
Hydrochlorothiazide (Apo-Hydro, Esidrix, Oretic, HCTZ, Urozide)
Major Side Effects
Action and Uses Hyponatremia
Interferes with absorption of sodium ions across distal renal tubu­ Hyperkalemia
lar segment to enhance excretion of sodium, chloride, potassium,
bicarbonate, and water. Used in adjunct treatment of edema asso­ Nursing Implications
ciated with heart failure, cirrhosis, and renal failure. Monitor serum electrolytes (sodium, potassium) during
therapy.
Dosages (Adult)
Edema: 25-200 mg/day ( PO) in 1 to 3 divided doses Dosages from Wilson, Shannon, & Shields (2011) and Wilson, Shannon, &
Hypertension: 12.5-100 mg/day (PO) in 1 to 2 divided doses Shields (2012).

: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •

Section Two Review

1. Which assessments are consistent with fluid volume excess? 3. Which drug works on the distal convoluted tubule?
(Select all that apply.) A. Furosemide
A. Weight loss B. Spironolactone
B. Elevated CVP C. Hydrochlorothiazide
C. Elevated blood pressure D. Loop diuretics
D. S inus bradycardia 4. Which patient outcome would be appropriate for a patient who
E. Decreased hematocrit is experiencing fluid volume excess? (Select all that apply.)
2. Treatment for fluid volume excess may include restricting A. CVP within normal range for patient
which intake? (Select all that apply.) B. Weight gain of2-3%
A. Fluids C. Balanced intake and output
B. Protein D. BUN within acceptable limits
C. Carbohydrates Answers: 1. (B, C, E), 2. (A, D), 3. B, 4. (A, C, D)
D. Sodium

SECTION THREE: Sodium Critical (or panic) values are laboratory measurements that are
potentially life-threatening and require immediate attention.
Imbalances
Sodium is the major extracellular cation whose major function Hyponatremia
is regulation of body water. Therefore, imbalances in sodium Hyponatremia, or abnormally low serum sodium, occurs when the
result in fluid imbalances. Normal ranges and critical values of serum sodium level falls below 135 mmol!L and a critical value of
the electrolytes discussed in this chapter are listed in Table 25-5. 120 mmol!L or less (Kee, 2010; Mayo Medical Laboratories, 2012).
 CHAPTER 25 � Alterations in Fluid and Electrol y te Balance
.TABLE 25-5
Critical (Panic)
Parameter : Normal Range Values
Sodium (mmoi/L} : 135 to 145 s 120 or<:: 160
Calcium (total} (mg/dU : 9 to 11 s 6.5 or<:: 13.0
Potassium (mmoi/L} : 3.5 to 5.3 :;; 2.5 or<:: 6.0
Phosphorus (mg/dU : 2.5 to 4.5 :;; 1.0
Magnesium (mg/dU : 1.8 to 3.0 :;; 1.0 or<:: 9.0
'Normal laboratory ranges and critical values vary between agencies.
Normal ranges from Kee (2010) and critical values from Mayo Medical
Laboratories (2012).
Etiology Hyponatremia is the most common electrolyte
disorder in hospitalized patients (Andreoli & Safirstein, 2010),
with many cases developing postadmission. Hyponatremia can
result from excessive salt loss relative to water loss, excessive
water gain in relation to salt gain, or both (Felver, 2010).
Excessive Salt Loss Relative to Water Loss. A variety
of problems can cause an imbalance in salt and water excre­
tion. Persistent sodium excretion can occur with continuous
release of antidiuretic hormone (ADH) from the pituitary or
ectopic production of ADH. This unregulated production of
ADH is associated with the syndrome of inappropriate release
of antidiuretic hormone (SIADH), which can result from
cerebral trauma, narcotic use, lung cancer, and certain drugs
(Metheny, 2010). Many diuretic agents, particularly thiazides,
block the reabsorption of salt (NaCl) in the distal convoluted
tubules of the kidneys, causing it to be excreted (Felver,
2010). Water and electrolytes are not necessarily excreted in
the same ratio as they exist in the blood, however; relatively
more salt can be excreted than water, resulting in hypona­
tremia (and hypochloremia) (Lehne, 2010). Other possible
causes include replacement of water without replacement of
salt-for example, overuse of dextrose 5% in water ( D5W)
intravenous fluid.
Excessive Water Gain Relative to Salt Gain. Hyponatremia
can result from a net gain of water in the extracellular fluid
compartment without an equivalent increase in sodium, which
causes the plasma to become hypotonic. Normal functioning
kidneys are able to excrete about 16 to 20 liters of free water
every day (Andreoli and Safirstein, 2010). When the rapid
ingestion or administration of large quantities of water exceeds
the ability of the kidneys to excrete it, this form of hyponatre­
mia can develop (M�theny, 2010).
Clinical Manifestations Symptoms develop when
plasma sodium drops to less than 125 mEq/L ( Humphries &
Stone, 2011). The speed of hyponatremia onset influences the
severity of symptoms. Rapid onset is associated with more
severe symptoms because the body has less time to muster
613
� Hypematremia
Cardiovascular : Hypotension : Severe: hypertension,
: tachycardia
Neurologic : Confusion, : Moderate:
: headache, lethargy, : confusion, thirst
: possible coma : Severe:
: restlessness, coma
Gastrointestinal : Anorexia, vomiting, : Nausea and vomiting
: diarrhea, cramps
: Seizures, muscle : Hyperreflexia,
: cramps or spasms : muscle twitching,
:seizures
Fluid balance � Deficit � Excess, edema
Data from Lee (2010).
compensatory mechanisms; a slow onset is associated with
less severe symptoms secondary to compensation. Clinical
manifestations primarily reflect alterations in central nervous
system function. Seizures and coma develop with a rapid
decrease in sodium to less than 110 mEq/L. The most severe
complication of hyponatremia is cerebral edema caused by
intracellular swelling (Lee, 2010). Cerebral edema develops
when the sodium concentrations inside brain cells is greater
than sodium concentration in the extracellular fluid due to
hyponatremia. Osmotic forces pull water from the blood into
the brain cells, resulting in cerebral edema. Hyponatremia
is also associated with early changes in muscle tone because
sodium plays a role in the transmission of neuromuscular
impulses. The clinical manifestations of hyponatremia are
summarized in Table 25-6.
Medical Treatm ent The treatment of hyponatremia de­
pends on the cause; therefore, it is important to determine the
underlying cause and correct it when possible. For example,
if the patient has SIADH, water restriction is implemented.
The aggressiveness with which the sodium imbalance is
corrected depends on the severity of symptoms and duration
of the imbalance (Andreoli & Safirstein, 2010) . Patients with
severe hyponatremia may be given hypertonic fluids, such as
3% or 5% NaCl solution at a rate of 1-2 mL/kg/hr to raise the
serum sodium by 1-2 mEq/hr, but this should be limited to
the initial phase of treatment. The overall correction should
not exceed 8-12 mEq/L in 24 hours; otherwise there is a
risk of demyelination (Lee, 2010). Conivaptan hydrochloride
(Vaprisol) may be ordered. Conivaptan blocks ADH in the
kidneys to cause excretion of water and retention of sodium
(Ghali, Farah, Daifallah, Zabalawi, & Zmily, 2009) . Fluid
restriction and reassessment of patient medications are also
cornerstones of therapy. The box Related Pharmacotherapy:
Sodium provides a summary of intravenous sodium solution
information.
 614 PART 7 � Fluid and Electrolytes

RELATED PHARMACOTHERAPY Sodium

Example Ag ents Major Side Effects

0.9 NaCI, 0.45 NaCl, 0.25 NaCl, and 3% and 5% sodium Cellular edema, confusion, seizures, coma
solution (IV)
Nursing Implications
Action and Uses Monitor serum sodium values. Replace sodium carefully.
Major intracellular cation, used in the sodium-potassium pump Diuresis or sodium replacement performed too quickly can
to maintain cellular homeostasis. Has a significant role in water result in severe neurologic disturbances.
balance and distribution between cells and vascular spaces. Weigh patients daily
Used for sodium and volume replacement therapy. Monitor intake and output

Dosages (Adult)
Hyponatremia: No recommended doses. Treatment of severe
hyponatremia depends on the underlying cause, whether
patient is symptomatic, and severity of symptoms.

· · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · •

Nursing Considerations The major manifestations adrenocorticotropin hormone (ACTH) secretion (e.g., Cushing's
of hyponatremia are related to CNS dysfunction. Therefore, syndrome).
the nurse should focus assessments on CNS functions,
and changes in the patient's mental status should be fol­ Clinical Manifestations As with hyponatremia, the
lowed up immediately. Nursing diagnoses for patients with clinical manifestations of hypernatremia are predominantly
hyponatremia may include Risk for Imbalanced Fluid Volume, neurologic because brain cells are especially sensitive to sodium
Risk for Ineffective Cerebral Tissue Perfusion, and Risk for levels. However, in severe cases, multiple body systems are
Complication of Electrolyte Imbalances. If hypertonic fluids are affected. If hypernatremia develops rapidly, cellular shrinkage
given, the nurse must monitor the patient for pulmonary and also contributes to the neurologic symptoms. In addition, the
cerebral edema related to water retention. The nurse should patient will report extreme thirst if sufficiently awake to com­
also closely monitor the patient's response to therapy, because municate. The clinical manifestations of hypernatremia are
correcting sodium levels too quickly can cause osmotic demy­ summarized Table 25-6.
elination syndrome, a complication that can lead to spastic pa­
resis, dysarthria, dysphagia, occasionally seizures, and possibly Medical Treatment Detection and treatment require
death (Humphries & Stone, 2011). recognition of symptoms, identification of underlying defects
of water metabolism, correction of volume disturbances, and
Hypernatremia correction of serum sodium. The primary medical treat­
Hypernatremia, abnormally elevated serum sodium, is clini­ ment for hypernatremia is water replacement. The FVD may
cally defined as a serum sodium level above 145 mmol!L and be corrected with administration of hypotonic IV fluids.
a critical value of 160 mmol!L or higher (Kee, 2010; Mayo The rate of correction depends on the rate of development
Medical Laboratories, 2012). It develops when the extracel­ and the presence of symptoms. It is recommended that
lular volume of water is low relative to the amount of sodium half the water deficit be corrected in 12-24 hours while the
ions available, causing sodium concentration. Hypernatremia neurologic status is monitored. The maximum hourly rate
results in the shift of water from the intracellular space into the of plasma sodium decrease should not exceed 2 mEq/L!hr
extracellular compartment. The cells shrink and shrivel as fluid (Lee, 2010). Diuretics may also be given to enhance sodium
moves out of them, causing cellular dehydration; and the extra­ excretion.
cellular compartment becomes overloaded with water.
Nursing Considerations The patient should be
Etiology In the high-acuity patient, causes of hypernatremia monitored for neurologic deterioration. This is especially
include administration of sodium bicarbonate solutions to important when administering water replacement, as
correct metabolic acidosis, renal water loss through a defect in changes in serum sodium or osmolality can cause rapid
the renal concentration system, the use of diuretics or diuresis fluid and electrolyte shifts in the brain. The nurse should
from glucose (such as in diabetic ketoacidosis), gastrointestinal also monitor fluid volume replacement in intake and out­
losses through nasogastric suction, water losses from fever, and put as well as the therapeutic and nontherapeutic effects of
drainage from open wounds (Lee, 2010). therapies. Nursing diagnoses appropriate for patients with
Hypernatremia caused by excess water loss can result hypernatremia are Risk for Injury and Risk for Electrolyte
from renal dysfunction, profuse diaphoresis, or increased Imbalances.
 CHA PTER 25 � Alterations in Fluid and Electrolyte Balance 615

Section Three Review

1. Hyponatremia is associated with which symptom? 3. Hypernatremia can be caused by which conditions? (Select all
A. Edema that apply.)
B. Hyperreflexia A. Hyperthyroidism
C. Lethargy B. Profuse diuresis
D. Restlessness C. Cushing's syndrome
2. Patients with hyponatremia may require IV fluids. Which D. Diabetes insipidus
type of IV fluid would the nurse expect to be ordered to treat 4. What is a sign or symptom of hypernatremia?
severe hyponatremia? A. Diarrhea
A. Isotonic B. Muscle twitching
B. Hypotonic C. Stomach cramps
C. Hypertonic D. Decreased muscle tone
D. Lactated Ringer's Answers: l. C, 2. C, 3. (B, C, D), 4. B

SECTION FOUR: Calcium Imbalances
Circulating blood normally contains very little calcium; the
normal value range is 9-11 mg/dL (Kee, 2010). Calcium imbal­
ances can result in complications primarily of the neurologic,
skeletal, hematopoietic, and cardiovascular systems.
Hypocalcemia
Hypocalcemia, or abnormally low serum calcium, is defined as a
total calcium level less than 9 mg/dL, with a critical value of 6.5
mg/dL or greater (Kee, 2010; Mayo Medical Laboratories, 2012).
Hypocalcemia is one of the most frequent electrolyte distur­
bances encountered in the high-acuity patient. Low total serum
calcium has been reported to affect up to 90% of critically ill
patients and is associated with increased mortality (Lee, 2010).
Etiology There are many potential causes of hypocalcemia,
including trauma, acute kidney injury and chronic kidney dis­
ease, sepsis, hypoparathyroidism, hypomagnesemia, vitamin D
deficiency, and the administration of citrate. Hypocalcemia can
be induced by the administration of large amounts of stored
blood because stored blood is preserved with citrate. When
blood is administered, the citrate binds with calcium, which
lowers ionized calcium. Other causes include decreased bone
resorption, drug binding of calcium, decreased secretion of
parathyroid hormone with or without hypomagnesemia, and
decreased urinary calcium excretion (Lee, 2010).
Clinical Manifestations Normally, calcium stabilizes
neuromuscular cell membranes. When calcium is low, neuro­
muscular irritability increases, with multiple related signs and
symptoms. In addition, cardiovascular manifestations include
specific ECG changes (Table 25-7) (Lee, 2010).
Medical Treatment Medical management of hypocalcemia
is aimed at correcting the underlying cause and restoring normal
calcium balance. Intravenous calcium should be administered as
calcium gluconate or calcium chloride; however, calcium gluco­
nate is the preferred drug for calcium replacement. Use of calcium
chloride should be reserved for emergent situations only, as it

Hypocalcemia Hypercalcemia

Cardiovascular Hypotension, decreased myocardial Hypertension, cardiovascular calcification

contractility ECG changes: shortened OTinterval, decreased STsegment,
ECG changes: prolonged QTinterval, long heart block, cardiac dysrhythmias (bradycardia, first- and
STsegment second-degree heart block)

Neurologic Irritability, reduced cognitive ability Lethargy, depression, fatigue, impaired memory, emotional lability
Severe: confusion, stupor, and coma

Neuromuscular Cramps (abdominal and extremities), Muscle weakness

paresthesias
Severe: positive Chvostek's or Trousseau's
sign, tetany, seizures

Gastrointestinal Anorexia, constipation, peptic ulcer disease, abdominal

discomfort

Skeletal Bone fractures possible Pathologic bone fractures, bone thinning (osteopenia,
osteoporosis)

Other Abnormal clotting Kidney stones, polyuria, polydipsia

Data from Lee (2010).

 616 PART 7 � Fluid and Electrolytes

RELATED PHARMACOTHERAPY Calcium

Example Ag ents Major Side Effects

Calcium chloride, calcium gluconate Cardiac arrest, hypotension, bradycardia with rapid
infusion
Action and Uses
Restores serum calcium levels in acute hypocalcemia, improves Nursing Implications
myocardial contractility. Calcium chloride contains more Monitor ECG and BP closely during administration.
calcium than does calcium gluconate. Can be irritating to veins when given in peripheral IV
Dosages (Adult) Can cause necrosis and sloughing of tissue if extravasation
Calcium chloride (IV): Hypocalcemia: 0.5-1 g at 1-3 day intervals occurs.
based on patient data. Hypocalcemic tetany: 4.5-16 mEq/kg Must be administered slowly when given IV (0.5-1 mL/min).
3-4 x/day. CPR: 2-4 mglkg (repeat in 10 min if needed) Calcium chloride is three times more potent than calcium glu­
Calcium gluconate (IV): Hypocalcemia: 2-15 g/day (divided conate; carefully check label.
or continuous dose). Hypocalcemic tetany: 1-3 g as needed;
Dosages from Wilson, Shannon, & Shields (2011).
may repeat every 6 hrs as needed (max. dose: 15 g/day).
CPR: 2.3-3.7 mEq x 1 dose.
: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •

provides significantly more elemental calcium than does calcium complex and varies with the type of tumor, usually breast and lung
gluconate. Severe symptomatic hypocalcemia should be treated cancers and multiple myelomas. Hyperparathyroidism accounts
with 1000 mg of calcium chloride or 3 grams of calcium gluconate for about half of the cases of hypercalcemia, and it results from
over 10 minutes for symptom control. After that, a continuous IV increased release of calcium from bone, augmented intestinal reab­
infusion may be required with close monitoring of serum calcium sorption, and renal reabsorption of calcium.
levels (Lee, 2010). The box Related Pharmacotherapy: Calcium Calcium is absorbed in the intestines only under the
provides a summary of calcium therapy. influence of activated vitamin D (calcitriol); therefore, a high
level of vitamin D in the body can lead to hypercalcemia from
Nursing Considerations Hypocalcemia is commonly increased intestinal absorption. Excessive ingestion of vita­
seen in the presence of other electrolyte disorders. For example, min D is commonly associated with overly aggressive treat­
hypomagnesemia is common, and should be corrected by ment of hyperthyroidism, rickets, or osteomalacia (Metheny,
calcium administration. It is hypothesized that magnesium 2010). Hypercalcemia usually accompanies hypophosphatemia
deficiency may impair the release or activity of parathyroid because calcium and phosphate levels shift in opposite direc­
hormone. If metabolic acidosis is present, hypocalcemia should tions (i.e., they maintain an inverse relationship).
be corrected first because the treatment of acidosis decreases
the concentration of ionized calcium, which can precipitate Clinical Manifestations The signs and symptoms of
problems such as tetany and cardiac arrest. Patients with hypo­ hypercalcemia generally are proportional to the serum calcium
calcemia will have concomitant hyperphosphatemia, as calcium level. Serum calcium levels of 11.5 mg/dL rarely produce symp­
and phosphorus are inversely related (Lee, 2010). Nursing toms, but levels between 11.5 and 13 mg/dL may be associated
diagnoses appropriate for the patient with hypocalcemia are with lethargy, anorexia, and nausea. Higher calcium levels are
Risk for Injury and Risk for Electrolyte Imbalances. The nurse associated with more profound neurologic and neuromuscular
should monitor the patient with hypocalcemia for signs and changes. Hypercalcemia decreases neuromuscular excitability
symptoms of decreased cardiac output, ECG changes, and neu­ because it acts as a sedative at the myoneural junction. Altered
rologic and neuromuscular changes. GI motility associated with hypercalcemia results in delayed
gastric emptying and vomiting; patients are predisposed to
Hypercalcemia duodenal ulcer disease because of increased gastric acid secre­
Hypercalcemia, or abnormally elevated serum calcium, is defined tion. Disturbed renal function from hypercalcemia can cause
as a serum calcium level above 11 mg/dL with a critical level of 13 polyuria and polydipsia, and is considered a form of nephro­
mg/dL or higher (Kee, 2010; Mayo Medical Laboratories, 2012). genic diabetes insipidus that is usually reversible. Calcium exerts
Hypercalcemia occurs when calcium enters the extracellular fluid a positive inotropic effect on the heart and reduces heart rate
more rapidly than it can be excreted by the kidneys. similar to the effect of cardiac glycosides (e.g., digoxin).
The signs and symptoms of hypophosphatemia can accom­
Etiology Primary hyperparathyroidism and malignancy account pany hypercalcemia, as they are inversely related. Alterations in
for more than 90% of the cases of hypercalcemia in ambulatory phosphorus are presented separately in this section.
and non-critically-ill patients. A small percentage of cases develop
from immobilization, vitamin A or D intoxication, and lithium or Medical Treatment Treatment focuses on correcting the
thiazide diuretic use. Malignancy as a cause of hypercalcemia is underlying cause and reducing serum calcium levels. For example,
 CHA PTER 25 � Alterations in Fluid and Electrolyte Balance 617

hyperparathyroidism is managed by parathyroidectomy, and
malignant tumors may be managed through surgical removal,
chemotherapy, and radiation therapy. Strategies to lower serum
calcium levels include the promotion of calcium elimination by
the kidneys and the reduction of calcium reabsorption from the
bone. Large volumes of IV fluids and diuretic therapy may be
given to promote the elimination of calcium. Other drugs used to
reduce calcium include bisphosphonates, calcitonin, and sodium
phosphate or potassium phosphate.
Nursing Considerations Nursing diagnoses appropriate
for the patient with hypercalcemia may include Risk for Injury
as a result of a loss of calcium from bones (falls, pathological
fractures), Impaired Memory, Decreased Cardiac Output, and
Risk for Electrolyte Imbalances. The nurse should be aware of
patients at risk for hypercalcemia, increase patient mobilization
if possible, and encourage the oral intake of fluids if possible
or administer IV fluids as ordered if sufficient oral intake is
not feasible. The nurse should also monitor the patient's diet
to ensure it contains sufficient fiber to prevent constipation.
Furthermore, the increased risk of pathologic fractures war­
rants taking steps to reduce the risk of falls through careful
environmental assessment and patient/family teaching regard­
ing environmental and mobility safety.

Section Four Review

1. What are the most common causes of hypocalcemia in 3.Hypercalcemia can be caused by which factors? (Select all
high-acuity patients? (Select all that apply.) that apply.)
A. Administration of large amounts of stored blood A. Bone metastasis
B. Hypoparathyroidism B. Hyperactivity
C. Acute pancreatitis C. Hypothyroidism
D. Malignancy D. T hiazide diuretics
2. Rapid infusion of IV calcium can result in which 4. An appropriate nursing diagnosis for patients with hypercalcemia
manifestations? (Select all that apply.) is Riskfor Injury related to which factor? (Select all that apply.)
A. Tachycardia A. Pathological fractures
B. Hypertension B. Falls
C. Cardiac arrest C. Decreased mental status
D. Hypotension D. Cardiac dysrhythmias
E. Seizures
Answers: 1. (A, B, C), 2. (C, D), 3. (A, D), 4. (A, B, C, D)

SECTION FIVE: Potassium
Imbalances
Potassium is the major intracellular electrolyte, with a normal
serum range of 3.5-5.3 mmol/L. The body does not tolerate
significant alterations in serum potassium, and life-threatening
cardiac complications can arise.
as paralysis and respiratory muscle weakness (Lee, 2010). Because
potassium affects the transmission of nerve impulses, hypokalemia
can result in electrocardiogram (ECG) changes, including flat­
tened or inverted T waves, the development of U waves, and de­
pressed ST segment C• Fig. 25-2b, Hypokalemia). Cardiac distur­
bances can be especially significant in patients with hypertension,

Hypokalemia
Hypokalemia, or abnormally low serum potassium, is clinically
defined as a serum potassium level below 3.5 mmol/L with a
Causes of Hypokalemia Causes of Hyperkalemia
critical value of 2.5 mmol/L or less (Kee, 2010; Mayo Medical
Laboratories, 2012). When hypokalemia occurs, the body does not Loss of gastrointestinal Renal failure
attempt to retain or reabsorb potassium. Because the body does secretions through vomiting, Adrenal insufficiency
not compensate for potassium loss, it is essential that hypokalemia diarrhea, excessive nasogastric
Insulin deficiency and
suction fluid loss, and fistulas
be rapidly detected and corrected through appropriate potassium resistance
Excessive excretion by kidneys
supplementation. The body is intolerant of abnormal serum potas­ Rhabdomyolysis
Movement of potassium into cells
sium levels, and critical derangements (either high or low) can Severe burns
(e.g., diabetic ketoacidosis)
result in cardiac dysrhythmias or cardiac arrest (Kee, 2010). Acidosis
Prolonged fluid administration
Drug-induced (e.g., beta-
without potassium
Etiology High-acuity patients are at significant risk for devel­ supplementation
adrenergic blockers,
opment of hypokalemia for a variety of reasons, particularly re­ ACE inhibitors,
Excessive use of potassium­
cyclosporine, NSAIDs,
lated to compartment shifts, gastrointestinal loss, and therapies. wasting diuretics without
and others)
Table 25-8lists some of the major causes of hypokalemia. adequate potassium
supplementation
Clinical Manifestations Because potassium is important Drug-related loss (e.g.,
in nerve impulse as well as cardiac impulse conduction, muscle amphotericin B, some
penicillins, aminoglycosides)
contraction, and cell membrane function, the signs and symp­
toms of imbalance reflect interference with these activities, such Data from Lee (2010).
618 PART 7 � Fluid and Electrolytes

IR

: Hyperkalemia

Cardiovascular ECG changes: : ECG changes:

flattened or : progression from
inverted Twaves, : tachycardia to
development of : bradycardia to cardiac
U waves, and : arrest is possible;
depressed ST : prolonged PR interval;
segment : flat or absent P wave;
T : sl urring of ORS; tall
p 7
......
.. ..
" : peaked Twave; ST
/ " : segment depression
- r-
--
--
- PR -,
� :nterv:i" 0
ii=:j f
S segment Pulmonary Respiratory
s I 'I I I muscle
(a) Normal ECG weakness

R Musculoskeletal : Muscle weakness or

: cramps

Gastrointestinal : Nausea, vomiting,

: abdominal cramping,
: diarrhea

I'
Acid-base : Metabolic acidosis

Data from Lee (2010).

I
i Flattened T wave
i I LJ
i U wave dysrhythmias or respiratory muscle weakness. Urinary excre­
I •
p ,...--..[ tion of potassium should be measured by obtaining a 24-hour
,' ' i I ..... urine specimen. Hypokalemia is treated with oral or IV ad­
l'oi """ ST segment --
j ministration of potassium. The preferred route of replacement
s depression---
is oral unless the patient is having cardiac disturbances (Lee,
(b) ECG in hypokalemia 2010). The box Related Pharmacotherapy: Potassium provides
a summary of potassium therapy.

JJic�e � Nursing Considerations Nursing diagnoses appropri­

QRS
ate for the patient with hypokalemia include Decreased Cardiac
r-r- Tall tent � Output, Acute Pain, and Risk for Electrolyte Imbalances. The
�
T wave patient with hypokalemia should be monitored closely for
II\ dysrhythmias and the development of characteristic ECG
1/ ' changes. The nurse should be observant of potassium levels
and take action to prevent hypokalemia. The patient receiving
\
/ '\ digitalis should be assessed for symptoms of digitalis toxic­
--- Prolonged I ity (e.g., vision changes, confusion, dizziness, vomiting, and
---
PR I nterval f.-f.- ST segment depression -r- cardiac dysrhythmias). Administration of potassium through
(c) ECG in hyperkalemia a peripheral vein can be painful and cause irritation to the
vein; it is preferable to administer potassium through a central
• FIGURE 25-2 The effects of changes in potassi um levels
on the ECG. (a) normal, (b) hypokalemia, (c) hyperkalemia. venous catheter.

myocardial infarction, ischemia, or heart failure (Lee, 2010). In

patients receiving digoxin therapy, low serum potassium levels
can potentiate the action of digitalis (Metheny, 2010). The clinical
manifestations of hypokalemia are summarized in Table 25-9.
Medical Treatment The major objective of hypokalemia
treatment is to rule out emergencies such as severe cardiac
Hyperkalemia
Hyperkalemia, or abnormally elevated serum potassium, is
clinically defined as a potassium level above 5.3 mmol!L with
a critical value of 6.0 mmol!L or higher (Kee, 2010; Mayo
Medical Laboratories, 2012). Many high-acuity patients are at
risk for development of hyperkalemia related to their disease
process, disease complications, or therapies.
 CHA PT E R 25 � Alterations in Fluid and Electrolyte Balance 619

RELATED PHARMACOTHERAPY Potassium

Example Agents Nursing Implications

Potassium chloride (Slow K, K-Dur, many others) IV potassium chloride is NEVER administered
Potassium gluconate (Kaon, Kaylixir) undiluted.
Always invert IV bag several times when adding KCl
Action and Uses
to thoroughly mix it with IV solution before
Needed for adequate transmission of nerve impulses and
administering.
cardiac contraction, renal function, and intracellular ion
Monitor for dysrhythmias and ECG changes (particularly
maintenance.
at higher doses).
Dosages (Adult) Monitor potassium levels and report abnormalities.
Potassium chloride (IV): Exact dose is based on patient's Monitor intake and output.
potassium level. Generally 3 mEq/kg or less with max dose of Monitor cardiac status and hematologic parameters such
400 mEq/day. Rate of delivery: no higher than 10 mEq/hr typi­ as CVP and pulmonary pressures if monitoring
cally. In emergency, can deliver at higher rate but must closely directly.
watch cardiac rhythm status. IV administration can be painful in peripheral sites.
Major Side Effects Administer 10 mEq/hr. Administer 20 mEq/ hr in central
Cardiac dysrhythmias, cardiac arrest, peaked T waves, lines only.
prolonged P-R intervals, U waves, widened
QRS complex Dosages from Wilson, Shannon, & Shields (2011).

· · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · •

Etiology Severe kidney injury and acidosis are common the underlying cause, such as medications that are known to
risk factors for hyperkalemia in the high-acuity patient. In increase serum potassium (e.g., ACE inhibitors and potassium­
the presence of renal failure, the kidneys cannot excrete sparing diuretics) and substances that contain potassium, such
sufficient amounts of potassium, increasing serum levels. as potassium-containing salt substitutes. Urinary potassium
Acidosis contributes to hyperkalemia because excess hydro­ excretion should be assessed. The treatment of hyperkalemia
gen ions shift into the cells, forcing potassium out into the depends on how high the potassium level is and the presence
serum (Lee, 2010). A variety of medications also can pre­ of any emergent conditions. If ECG changes or dysrhythmias
cipitate hyperkalemia. For example, beta-adrenergic blockers are present, intravenous calcium gluconate should be admin­
such as propranolol interfere with the entry of potassium istered to stabilize the cardiac membrane. The next step is to
into the cells. Captopril (ACE inhibitor) and nonsteroidal drive the potassium back into the cells, usually by administer­
anti-inflammatory drugs (NSAIDS) exert an inhibitory effect ing insulin and 50 grams of glucose. As an alternative therapy,
on aldosterone secretion, which can cause hyperkalemia in intravenous or inhaled albuterol may be used to shift the po­
patients with renal insufficiency. Table 25-8 lists common tassium into the cells.
causes of hyperkalemia. Sodium polystyrene sulfonate (Kayexalate) may be given
to promote bowel excretion of potassium by exchanging
Manifestations Because potassium is important in nerve sodium for potassium in the intestinal tract, but it is slow to
impulse conduction, muscle contraction, and cell membrane exert a potassium-lowering effect and results are somewhat
function, the signs and symptoms of imbalance reflect unpredictable. Kayexalate is usually administered with an
interference with these activities. Manifestations of hyperkale­ osmotic agent such as sorbitol to cause osmotic diarrhea;
mia usually develop when serum potassium levels rise above however, sorbitol has been shown to cause bowel necrosis
6.0 mEq/L. ECG changes associated with hyperkalemia include so it may not be the therapy of choice. The use of sodium
peaked T waves, and in severe hyperkalemia, absent P waves bicarbonate for treatment of hyperkalemia should be avoided
and a widened QRS pattern can occur (Metheny, 2010) (see in patients with fluid overload for treatment of hyperkale­
Fig. 25-2c, Hyperkalemia). The manifestations of hyperkale­ mia and has not been shown to be a predictably effective
mia are summarized in Table 25-9. Care must be taken when a treatment (Lee, 2010). Dialysis is usually reserved for severe
blood sample is taken for evaluating potassium levels, as a false hyperkalemia when other, more conventional treatments have
elevation in serum potassium can occur if the blood sample is not been effective.
hemolyzed and potassium is released or if blood is drawn above
a site where potassium is infusing. Nursing Considerations Nursing diagnoses appropri­
ate for the patient with hyperkalemia may include Decreased
Medical Treatment Medical management of hyperkale­ Cardiac Output, Risk for Imbalanced Fluid Volume, and Risk
mia includes returning the potassium to normal and treating for Electrolyte Imbalances. Severe hyperkalemia can result in
620 PART 7 • Fluid and Electrolytes

ventricular fibrillation and cardiac arrest. The nurse should
notify the healthcare provider of elevated potassium labora­
tory values and ECG changes associated with hyperkalemia.
Measures to prevent hyperkalemia should be taken, such as
identification of at-risk patients, regular evaluation of serum
electrolytes, review of medications for effects on potassium,
and monitoring diet for potassium content. In the presence of
abnormal kidney function, the nurse should monitor blood
urea nitrogen (BUN) and creatinine (Cr) because kidney failure
is a major cause of hyperkalemia. The nurse should also moni­
tor the patient's intake and output and report low urine output
to the healthcare provider.

Section Five Review

1 . For a patient with hypokalemia, the nurse should monitor the 3. Hyperkalemia can be caused by which condition?
ECG for which changes? (Select all that apply.) A. Renal failure
A. Presence of U waves B. Potassium-wasting diuretics
B. Flattened T waves C. Metabolic alkalosis
C. Peaked T waves D. Severe diarrhea
D. Depressed ST segment 4. T he clinical findings of hyperkalemia include which set of
2. What is a common side effect of the administration of signs and/or symptoms?
potassium in a peripheral I V catheter? A. Muscle weakness, T wave inversion on ECG
A. Burning pain B. Muscle twitching, ST segment depression on ECG
B. Dysrhythmia C. Vomiting, peaked T wave on ECG
C. Diarrhea D. Diarrhea, presence of U wave on ECG
D. T issue necrosis Answers: 1. (A, B, D), 2. A, 3. A, 4. C

SECTI O.N SIX: Magnesium should be assessed for renal failure before administering mag­
nesium because the kidneys are primarily responsible for its
Imbalances elimination. Intravenous administration is preferred in patients
Magnesium is an intracellular electrolyte that plays a crucial role with severe hypomagnesemia (less than 1.2 mg/dL) or if neuro­
in ensuring that sodium and potassium are transported across logic changes or cardiac dysrhythmias occur. Infusion time is
cell membranes. It also plays an important role in nerve cell critical because magnesium distributes into tissues slowly and
conduction. The normal range for magnesium is 1.8-3.0 mg/dL. is rapidly excreted by the kidneys, with up to 50% of the infused
magnesium lost in the urine. Severe hypomagnesemia requires
Hypomagnesemia treatment of up to 1.8 mg/kg of magnesium (Lee, 2010). The
Hypomagnesemia, or abnormally low serum magnesium, is box Related Pharmacotherapy: Magnesium provides a sum­
defined as a serum magnesium level of less than 1.8 mg/dL mary of magnesium therapy.
with a critical value of 1.2 mg/dL (Kee, 2010; Mayo Medical
Laboratories, 2012). Nursing Considerations Nursing diagnoses appropri­
ate for the patient with hypomagnesemia may include Risk for
Etiology High-acuity patients are at moderate to high
risk for development of hypomagnesemia. Common causes
of hypomagnesemia include gastrointestinal or renal losses,
surgery, trauma, infections or sepsis, burns, transfusions of blood
preserved with citrate, alcoholism, and malnutrition. In addition, Bod y S ystem Hypomagnesemia Hypennagnesemia
certain medications can cause hypomagnesemia, such as diuret­
Serum Mg level Less than Greater than
ics, aminoglycosides, amphotericin B, digoxin, and cyclosporine
1.8 mg/dl 3.0 mg/dl
(Lee, 2010). Hypoparathyroidism, with resultant hypocalcemia,
can also cause hypomagnesemia because the regulatory mecha­ Cardiovascular ECG changes: Hypotension
nisms of magnesium and calcium are closely related. premature ventricular ECG changes:
contractions, prolonged PR
ventricular intervals, complete
Manifestations The signs and symptoms of magnesium im­ tachycardia and/or heart block, wide
balances are similar to those seen in calcium imbalances, altering fibrillation; Twave ORS complex,
CNS and neuromuscular and cardiac function. Hypomagnesemia flattening, decreased bradycardia, cardiac
is associated with ECG changes and dysrhythmias such as "tor­ STsegment arrest
sades de pointes" and seizures, coma, and death (Lee, 2010).
Respiratory Depression
The clinical manifestations associated with hypomagnesemia are
presented in Table 25-10. Neuromuscular Tremors, tetany, Absent deep
positive Chvostek's tendon reflexes,
Medical Treatment Medical management is directed at and Trousseau's lethargy,
signs drowsiness
raising serum magnesium levels. Goals include preventing fatal
cardiac dysrhythmias and resolving symptoms. The patient Data from Lee (2010}.
 CHA PTER 25 � Alterations in Fluid and Electrolyte Balance 621

RELATED PHARMACOTHERAPY Mag nesium

Example Agents Major Side Effects

Magnesium sulfate, magnesium oxide, magnesium citrate Impaired energy production and utilization of substrates
Dysrhythmias, PR and QT interval prolongation, widened QRS
Action and Uses
complex, ST segment depression.
Significant role in the structure of bones and intracellular fluid
Hypotension if administered too rapidly (IV) .
component. Participates in numerous enzymatic reactions,
many involving adenosine triphosphate (ATP). Important in Nursing Implications
neuronal control, neuromuscular transmission, and cardiovas­ Magnesium level is closely related to levels of calcium,
cular tone. phosphorus, and potassium.
Administer slowly according to directions.
Dosages (Adult)
Monitor blood pressure and EKG for changes.
Magnesium sulfate (IV): seizures- I g (repeat dose if needed).
Severe hypomagnesemia-5 g to run over a 3-hr period. Dosages from Wilson, Shannon, & Shields (2011).

: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •

Injury, and Risk for Electrolyte Imbalances. The nurse should neuromuscular and cardiac toxicity of hypermagnesemia can
monitor patients with hypomagnesemia for the development of be antagonized by the administration of 10-20 mL of calcium
ventricular dysrhythmias, seizures, and neurologic deteriora­ gluconate over 10 minutes (Metheny, 2010).
tion. Hypokalemia is relatively common in hypomagnesemic
patients because the kidneys are not able to conserve potassium Nursing Considerations Nursing diagnoses appropri­
when a magnesium deficiency exists. Hypocalcemia and hypo­ ate for patients with hypermagnesemia may include Decreased
phosphatemia can occur in conjunction with hypomagnesemia Cardiac Output as a result of hypotension, bradycardia, and
because severe magnesium depletion interferes with parathy­ ECG changes, and Risk for Electrolyte Imbalances. Nurses
roid hormone, which is needed to return calcium and phospho­ should be aware of patients at high risk for hypermagnesemia,
rus levels to their normal ranges (Metheny, 2010). such as those in renal failure. These patients should also be
assessed for fluid volume excess and respiratory distress. Level
Hypermagnesemia of consciousness should be assessed as well as low blood pres­
Hypermagnesemia, or abnormally elevated serum magne­ sure and apnea. Magnesium-containing solutions should be
sium, results when magnesium levels rise above 3.0 mg/dL avoided.
with a critical value of 9.0 mg/dL (Kee, 2010; Mayo Medical
Laboratories, 2012). This abnormality is not common but can
occur with diminished renal excretion or excessive magnesium Emerging Evidence
intake. Magnesium is primarily excreted by the kidneys, so
patients with renal failure are at risk for hypermagnesemia.
Consumption of large quantities of magnesium-containing • Patients entering the emergency department with
antacids or laxatives can be a source of excessive intake diabetic ketoacidosis should have a serum potassium
level drawn and read prior to initiation of insulin
(Metheny, 2010).
therapy and fluid resuscitation (Arora, Cheng, Wyler,
Manifestations Hypermagnesemia diminishes neuro­ & Menchine, 2012).

muscular transmission and can depress skeletal muscle func­ • In cardiovascular patients experiencing hypomagne­
tion and cause neuromuscular blockade. Cardiovascular effects semia, IV magnesium replacement therapy resulted
are due to the "calcium channel blocker effect" on cardiac in a higher serum magnesium concentration (SMC)
conduction and the smooth muscle of blood vessels. Cardiac at 24 hours of therapy compared to oral replacement
dysrhythmias that can develop include bradycardia, atrioven­ therapy; however, both IV and oral routes improved
tricular block, and asystole. Hypotension can develop due to SMC adequately. Investigators concluded that
the vasodilator effects of magnesium (Metheny, 2010). The the primary advantage of the IV route is a more
clinical manifestations associated with hypermagnesemia are rapid increase in SCM (Reed, Zhang, Marron, &
presented in Table 25-10. Montague, 2012).

Medical Treatment The cause of hypermagnesemia • Hyponatremia in heart failure patients with left
should be identified and treated. Medications containing mag­ ventricular dysfunction is an independent predictor
nesium should be held; if the patient is in renal failure, the of increased rehospitalization and increased mortality
administration of magnesium should be avoided. In severe (all causes) (Bettari et al., 2012).
cases, dialysis may be required to remove magnesium. The
622 PART 7 � Fluid and Electrolytes

Section Six Review

1. Magnesium balance is closely related to which other two 3. Hypermagnesemia is associated with which symptom?
electrolytes? A. Tetany
A. Potassium and phosphorus B. Lethargy
B. Calcium and sodium C. Tremors
C. Sodium and phosphorus D. Positive Chvostek's sign
D. Calcium and p otassium 4. Magnesium plays an active part in which physiologic
2. The symptoms of hypomagnesemia reflect which functions? (Select all that apply.)
alteration? A. Sodium and p otassium t ransport
A. CNS hypoactivity B. Nerve cell conduction
B. Fluid compartment shifts C. Fluid regulation
C. Cardiac depressant effects D. Transference of energy
D. Neuromuscular and CNS hyperactivity Answers: 1 . D, 2. D, 3. B, 4. (A, B)

Other conditions that can cause hypophosphatemia include

SECTION SEVEN: P hosphorus/
P hosphate Imbalance
Phosphorus is an intracellular electrolyte that exists in the body
primarily as phosphate, in combination with calcium as cal­
cium phosphate. In addition to its importance to healthy bones
and teeth, it is also vital to normal neuromuscular function and
the production of adenosine triphosphate (ATP). The normal
range for phosphorus is 2.5-4.5 mg/dL.
Hypophosphatemia
Hypophosphatemia is defined as a serum phosphorus level
below 2.5 mg/dL with a critical value of 1 mg/dL or lower (Kee,
2010; Mayo Medical Laboratories, 2012).
Etiology In the high-acuity patient, hypophosphatemia is
associated with such disorders as gram-negative sepsis, cardiac
surgery, malnutrition, acute respiratory alkalosis, diabetic keto­
acidosis, and alcoholism. Acute respiratory alkalosis can reduce
plasma phosphate concentration as phosphate enters muscle.
The infusion of glucose and the effects of hormones such as
insulin, glucagon, and cortisol can decrease plasma phosphate
concentrations by redistribution to the intracellular space.
hyperparathyroidism, certain renal tubular defects, metabolic aci­
dosis (including diabetic ketoacidosis), and disorders that cause
hypercalcemia (Lee, 2010). Several important factors following
elective cardiac surgery may be associated with hypophosphate­
mia, including an increased requirement for mechanical ventila­
tion, increased use of cardioactive drugs, and longer hospital stay,
which correlates with decreased energy stores (Lee, 2010).
Manifestations Numerous cellular mechanisms require
phosphate. Hypophosphatemia depresses cellular function,
particularly of the hematologic and cardiovascular systems.
This results in symptoms of impaired heart function and poor
tissue oxygenation. Because phosphorus is essential to form
part of ATP, it serves as a reservoir of energy in cells to fuel mus­
cle contractility, neuronal transmission, electrolyte transport
and conversion of dietary nutrients into energy. Phosphorus
also forms part of the 2,3 DPG enzyme in red blood cells that
facilitates the release of oxygen from hemoglobin to the tissues
(Metheny, 2010). Hypophosphatemia is associated with blood
cell dysfunctions as well as neurologic, neuromuscular, and car­
diopulmonary problems. The clinical manifestations associated
with hypophosphatemia are presented in Table 25-11.

Hypophosphatemia Hyperphosphatemia

Cardiovascular Diminished myocardial function Hypotension, tachycardia

Severe: heart failure ECG changes: prolonged OTinterval and ventricular
dysrhythmias

Gastrointestina I N ausea and vomiting, anorexia Diarrhea, nausea, abdominal cramping

Neurologic Disorientation, irritability, coma Altered mental state, delirium, coma

Severe: Severe neurologic dysfunction Positive Chvostek's and Trousseau's signs, paresthesias

N euromuscular Weakness, numbness, and tingling Muscle cramping, tetany, seizures

Severe: seizures

Musculoskeletal Pathologic fractures

Other (severe) Respiratory failure or arrest, hemolysis, blood cell

dysfunction

Data from Lee (20 10).

 CHA PTER 25 � Alterations in Fluid and Electrolyte Balance 623

Medical Treatment Medical management is directed hyperthyroidism, hypoparathyroidism, or severe catabolic states
at treating the underlying cause of the disorder and replac­ can precipitate hypocalcemia, leading to hyperphosphatemia
ing serum levels. Plasma phosphate concentrations should (Metheny, 2010).
be maintained within the normal range. Treatment of hypo­
phosphatemia depends on the magnitude of the deficit and Clinical Manifestations The clinical manifestations
the presence and severity of symptoms. Asymptomatic mild associated with hyperphosphatemia are similar to those of
hypophosphatemia can be treated with oral supplementation if hypocalcemia because they are inversely related. These include
the gastrointestinal tract is functional. Symptomatic or severe signs of increased neuromuscular irritability and ECG changes.
hypophosphatemia (less than 1.0 mg/dL) should be treated High levels of serum inorganic phosphate promote precipita­
with intravenous phosphate (Lee, 2010). IV preparations in­ tion of calcium phosphate in non-osseous sites. For example,
clude sodium phosphate and potassium phosphate. The box one such site is the kidney, where precipitation of calcium
Related Pharmacotherapy: Phosphate provides a summary of phosphate can result in progressive renal failure. Other sites
phosphate therapy. vulnerable to this problem include the heart, lungs, skin, and
cornea (Metheny, 2010). Common clinical manifestations of
Nursing Considerations Patients with hypophospha­ hyperphosphatemia are presented in Table 25-11.
temia should be monitored for Risk for Injury; Impaired Gas
Exchange; Decreased Cardiac Output related to muscle weak­ Medical Treatment Treatment of hyperphosphatemia is di­
ness, inadequate ventilation, and decreased energy stores; and rected at lowering serum levels. Agents that bind phosphate in the
Risk for Electrolyte Imbalances. Weakness of the respiratory GI tract may be administered. Aluminum-containing agents were
muscles can result in ineffective breathing patterns and may used in the past but are now avoided due to their proven toxicity.
cause respiratory failure requiring mechanical ventilation. The Currently, calcium-based salts are commonly used. An IV solution
choice of phosphate treatment depends on factors such as the with saline can also be administered to promote renal excretion of
patient's renal status. If the patient has renal failure, sodium phosphate if the patient has functional kidneys (Metheny, 2010).
phosphate may be the best choice for replacement. Phosphorus
replacements should be infused slowly, usually over 4-6 hours. Nursing Considerations Nursing diagnoses that apply
The nurse should be alert for symptoms of hypercalcemia, as to hyperphosphatemia include Risk for Injury, Decreased
phosphate and calcium are inversely related (Metheny, 2010). Cardiac Output, and Risk for Electrolyte Imbalances. Nursing
care is directed at monitoring serum lab values and ECG
Hyperphosphatemia rhythm status, as well as monitoring for improvements in
Hyperphosphatemia is defined as a serum phosphorus level neuromuscular status. Phosphate supplements, especially IV
above 4.5 mg/dL (Kee, 2010; Mayo Medical Laboratories, 2012) preparations, should be administered cautiously over several
with a critical value of greater than 5.0 mg/dL. It is less com­ hours and the patient monitored for therapeutic and nonthera­
mon than hypophosphatemia in the high-acuity patient. peutic effects. Patients should be instructed that phosphate­
containing laxatives can cause phosphate poisoning and should
Etiology Hyperphosphatemia is predominantly associated be avoided.
with chronic kidney failure. Other causes include shifting of The box Nursing Care: The Patient with Fluid and Electrolyte
phosphorus from the intracellular space into the extracellular Disturbances provides a summary of nursing considerations
space and increased phosphorus uptake. Conditions causing related to the topics covered in this chapter.

RELATED PHARMACOTHERAPY Phosphate

Example Ag ents Major Side Effects

Sodium phosphate, potassium phosphate (IV) Muscle weakness, impaired cellular energy resources, impaired
oxygen delivery to the tissues, respiratory failure, anemia, car­
Action and Uses
diomyopathy, and dysrhythmias
Important in cellular metabolism. Forms part of compounds
that perform metabolic processes, such as adenosine Nursing Implications
triphosphate and 2,3 diphosphoglycerate (2,3 DPG) . Fuels Replace phosphorus slowly (IV).
muscle contractility, neuronal transmission, electrolyte Monitor patients for respiratory distress.
transport, and conversion of dietary nutrients into energy, Monitor the EKG for changes and dysrhythmias.
and facilitates release of oxygen to the tissues. Watch for signs of calcium disturbances, as phosphorus
Dosages (Adult) and calcium are inversely related.
Potassium phosphate (IV): 0.08-0.16 mmol!kg (dilute in
500 mL of 0.45 NS) to run over 6 hrs. Dosages from Foster, Mistry, Peddi, & Sharma (2010).

· · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · •
 624 PART 7 � Fluid and Electrolytes

'. �"'�· "'. � -.. ' ..� '.

Th e Pat i e nt with F l u i d a n d E l ectro lyte
·,.N URS I N G' CARE
'
s� D i stu rba n ces

Expected Patient Outcomes and Related Weigh daily and monitor intake and output.
· I nterventions Note the color and character of urine, emesis, large
nasogastric output or wound drainage.
Outcome: No complications offluid or electrolyte Measure central venous pressure or pulmonary artery
imbalances pressures if indicated.
Assess and compare to established norms, patient Interventions to prevent complications of fluid and
baseline, and trends. electrolyte imbalances
Obtain thorough patient history: Monitor all of the above on an ongoing basis and note
Note any causes of potential fluid and electrolyte trends.
imbalances; any reports of thirst? Administer related fluid and drug therapy and monitor
Review medications: Are there any that could for therapeutic and nontherapeutic effects.
contribute to fluid or electrolyte imbalance? PO or IV fluids
Review diet: Is the patient receiving adequate nutri­ Diuretic agents
tion and fluids for maintenance of homeostasis? Electrolyte supplements
Monitor laboratory results and compare to baseline labs. Agents that decrease serum electrolyte levels
Assess physical status: (e.g., Kayexalate)
Skin condition, wound healing, and moistness of Related nursing diagnoses
mucous membranes Acute Confusion
Assess lung sounds and heart sounds. Acute Pain
Note dysrhythmias or ECG changes from baseline. Decreased Cardiac Output
Check capillary refill to assess volume status. Note Deficient Fluid Volume
the presence of edema or swelling, especially in Excess Fluid Volume
extremities. Impaired Memory
Note any signs of neuromuscular disturbances such as Impaired Gas Exchange
twitching, tetany. Ineffective Breathing Pattern
Check vital signs. Note deviations from baseline in Risk for Imbalanced Fluid Volume
blood pressure, heart rate and rhythm, respiratory rate, Risk for Injury
rhythm, depth, and effort.

: . . . .. .. . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . _. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •

Section Seven Review

1. Hypophosphatemia is associated with which condition? 3. The clinical picture of hyperphosphatemia frequently reflects
A. Malnourished state which other electrolyte abnormality?
B. Metabolic alkalosis A. Hypermagnesemia
C. Hypocalcemia B. Hypochloremia
D. Hyperthyroidism C. Hypernatremia
2. Severe hypophosphatemia is associated with which D. Hypocalcemia
symptom? 4. Severe hyperphosphatemia is associated with which ECG
A. Joint pain change?
B. Muscle c ramping A. Tachycardia
C. Respiratory arrest B. Bradycardia
D. Peptic ulcer disease C. Flattened T waves
D. Widened QRS complexes
Answers: 1. A, 2. C, 3. D, 4. A

Clinical Reasoning Checkpoint days of nausea and vomiting and has not been eating or drink­
ing much since she got sick. She informs you that she has a
Mrs. T. has just been admitted to your telemetry unit. She is long history of "heart problems" and is taking a heart pill and
82 years old and reports that she has been homebound for a water pill daily but has not been able to take either because
about a week with "the flu:' She also reports that she had several of her nausea. Mrs. T. had a complete lab panel drawn on
 CHA PTER 25 � Alterations in Fluid and Electrolyte Balance 625

admission and you have just been informed that her serum po­ 5. What nursing diagnoses would be most applicable to
tassium level is 2.8 mEq/L. You go to her room to reassess her. Mrs. T.'s hypokalemia?
1. List at least two clinical findings consistent with hypokale­ 6. If Mrs. T. is experiencing FVD from her vomiting, what
mia for each of the assessments below: would you anticipate her serum sodium level would be?
A. Neurologic: 7. It is determined that Mrs. T. is experiencing FVD. The pro­
B. Cardiovascular: vider orders a moderate fluid challenge. What type of IV fluid
C. ECG changes: would the provider likely order?

D. Gastrointestinal: A . D 5W

E. Musculoskeletal: B. 0.9 normal saline

2. Is Mrs. T. is at risk for cardiac emergency? Why or why not? C. Hypertonic saline

3. Should you be concerned about her potassium level because D. 0.225 saline
she has a history of coronary artery disease and is taking a
Answers to the Clinical Reasoning Checkpoint questions can befound
heart pill? Why or why not?
in the Wagner Student Resources at nursing.pearsonhighered.com.
4. From her recent history, what are the most likely causes of
her hypokalemia?

Pearson N u rsing And additional review materials at: nurslng.pearsonhlghered.com

--------�

6) Which patient would the nurse most closely monitor for the
Posttest development of hypermagnesemia?
1 } A patient is admitted with intravascular fluid deficit secondary 1. Patient in renal failure
to third spacing. The nurse would anticipate providing which 2. Patient with burns over 40% of the body
type of IV fluid as the probable best choice for this patient? 3. Patient taking digoxin
1 . A hypertonic solution 4. Patient with histor y of alcoholism
2. An isotonic solution 7} A patient has a phosphate of 1.5 mg/dL. The nurse would
3. A hypotonic solution monitor this patient for which musculoskeletal changes?
4. A colloid solution 1. Muscle spasm
2} A patient is admitted with fluid volume excess (FVE). Which 2. Joint pain
assessment findings would the nurse attribute to this prob­ 3. Muscle weakness
lem? (Select all that apply.) 4. Muscle cramping
1. Shortness of breath 8) A patient who requires IV potassium replacement therapy
2. Orthopnea has a peripheral IV line. The nurse would be confident to
3. 3+ pitting edema administer which order without further collaboration with
4. Hypotension the prescriber?
5. Tachycardia 1 . 10 mEq potassium IV push STAT
3) A patient has a serum sodium of 128 mEq/L. The nurse 2. 20 mEq potassium per hour by continuous IV
should monitor this patient for which problem? 3. 10 mEq potassium per hour by continuous IV
1. Hypertension 4. 80 mEq potassium IVPB ever y 6 hours
2. Tachycardia 9) Which assessment finding would the nurse evaluate as
3. Prolonged QT interval on ECG indicating successful treatment of the patient with fluid
4. Changes in muscle tone volume excess (FVE)?
4) A patient has a total calcium of 8 mg/dL. The nurse should 1 . Lungs are clear to auscultation
monitor this patient for which problems? (Select all that apply.) 2. Input exceeds output
1 . Decreased cardiac output 3. Edema remains at +2
2. Abnormal clotting 4. Weight gain of l kg in24 hours
3. Constipation 10) A patient has hyperphosphatemia. The nurse looks for
4. Pathological fractures manifestations of which other electrolyte imbalance in this
5. Reduced mental abilities
patient?
5) A patient's potassium is 3.3 mEq/L. The nurse should alert 1. Hypokalemia
the technician monitoring the patient's ECG to be watchful 2. Hypocalcemia
for which changes? (Select all that apply.) 3. Hypernatremia
1 . Inversion of the T wave 4. Hypermagnesemia
2. Development of a U wave
3. Depression of the ST segment Answers to Posttest questions can be found in the Wagner Student
4. Prolongation of the PR interval Resources at nursing.pearsonhighered.com.
5. Absence of the P wave
626 PART 7 � Fluid and Electrolytes
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