AACN Clinical Issues

Volume 15, Number 4, pp. 607-621

© 2004, AACN

Assessment of Fluids and

Electrolytes
Heidi Nebelkopf Elgart, RN, MSN, CRNP

tracellular fluid (ICF) accounts for approxi-

■ Bedside evaluation of a patient’s mately two-thirds of total body water.
Potassium, phosphorus, magnesium, and
intravascular volume status is challenging,
even for the seasoned practitioner. There
protein compose the majority of the ele-
is no single diagnostic test to determine
ments in the intracellular space. The extra-
whether a patient is hypovolemic,
cellular fluid (ECF) is divided into the in-
hypervolemic, or euvolemic. Often,
travascular fluid (plasma) and interstitial
underlying or concomitant disease states,
fluid (lymph fluid, transcellular fluid). Of
medications, and other therapeutics can
the one-third of total body water found in
make available data difficult to interpret.
the extracellular compartment, 25% is lo-
Therefore, a combination of clinical
cated in the intravascular space and 75% is
evaluation, laboratory studies, and other
located in the interstitial space. Sodium and
diagnostics are required to make a clinical
chloride are the primary electrolytes found
judgment regarding volume status.
in the extracellular compartment (Figure 2).
Patients who demonstrate alterations in
their volume status are likely to have

Fluid Movement
electrolyte abnormalities as well, and
assessment of serum electrolyte values
and potential therapeutic interventions is a
Fluid movement between the intracellular
vital piece in caring for critically ill patients.
and extracellular compartments is main-
(KEYWORDS: electrolytes, intravascular
tained by the cell wall, which functions as a
volume, intravenous fluids)
semipermeable membrane. Through active
and passive transport, electrolytes and water
move between the ICF and ECF. The cell
membrane is completely permeable to wa-
ter, thus any condition that alters the osmotic

Normal Distribution of Water pressure in either compartment will cause a
redistribution of water. Electrolytes have an
Total Body Water Composition “osmotic potential,” which refers to the affin-
ity an electrolyte has for water—its ability to
In healthy adults, the total body water is ap-
proximately 60% of body weight (Figure 1). ▪▪▪▪▪▪▪▪▪▪
The proportion tends to be less in women
From St Luke’s Hospital, Department of Trauma,
and the elderly because of decreased mus- Bethlehem, Pa.
cle mass and increased fat stores. Water in Reprint requests to Heidi Nebelkopf Elgart, St Luke’s
the body is distributed between the intra- Hospital, Dept of Trauma, 801 Ostrum St, Bethlehem, PA
cellular and extracellular compartments. In- 18015 (nebelkh@ slhn.org).

607
608  NEBELKOPF ELGART
2.8 L plasma (intravascular)
11.2 L interstitial
28.0 L intracellular
_____
42.0 L total body water
Figure 1. Example fluid distribution of 70 kg adult with
60% water content.
pull water into a compartment. Sodium and
dextrose have high osmotic potentials, and
movement of these solutes can result in ma-
jor fluid shifts between the ICF and ECF.
Within the extracellular compartment, the
electrolyte concentration is fairly similar be-
tween the interstitial fluid and intravascular
fluid. The one main difference is the large
amount of plasma proteins found in the in-
travascular space. Proteins (predominantly
albumin) in the plasma exert an osmotic
pressure that prevents fluid from leaving the
intravascular space and exerts a “pull” from
the interstitial space. This is referred to as
the colloid osmotic pressure. Simultane-
ously, the volume of blood exerts a pressure
within the blood vessel to exceed the pres-
sure in the interstitial space. Hydrostatic
pressure is the “pushing” force that is ex-
erted on the compartment wall which causes
water and electrolytes to move through the
capillary wall into the interstitial space. Col-
loid osmotic pressure and hydrostatic pres-
sure represent the “pull” and “push” re-
quired to maintain homeostasis between the
interstitial and intravascular spaces.
Intracellular
Potassium 150 mEq/L
Magnesium 40 mEq/L
Sodium 10 mEq/L
Phosphate and sulfate 150 mEq/L
Bicarbonate 10 mEq/L
Protein 40 mEq/L
AACN Clinical Issues

Osmolality
Osmolality is the concentration of solute par-
ticles in solution related to the concentration
of water molecules in solution. It is ex-
pressed as osmotic activity per volume of
water. The number of osmotically actively
particles within any given compartment is
between 290 and 310 mOsm/L.

Tonicity
Tonicity refers to the fluid tension within the
ECF or ICF and describes the relationship be-
tween the total solutes and water within these
compartments. Tonicity is determined by fluid
osmolality—the weight of particles in the
compartment or solution that can attract fluid.
When fluid tension of a compartment or solu-
tion is equal, the fluid is considered “iso-
tonic.” When a compartment or solution is
more dilute, it is considered “hypotonic.”
Compartments or solutions that are more con-
centrated are said to be “hypertonic.”

Evaluation of Volume Status
Physical Examination
In a vast majority of patients, careful physical
examination will allow an assessment of
whether a patient’s volume status is normal,
increased, or decreased.
VOLUME OVERLOAD. Weight gain is the most
sensitive and consistent sign of volume ex-
cess.2 Gravity-dependent edema, another
Extracellular (Plasma)
Sodium 142 mEq/L
Potassium 4 mEq/L
Calcium 5 mEq/L
Magnesium 3 mEq/L
Chloride 103 mEq/L
Bicarbonate 27 mEq/L
Phosphate 2 mEq/L
Sulfate 1 mEq/L
Organic acids 5 mEq/L
Protein 6 mEq/L Figure 2. Electrolyte composi-
tion of body compartments.2
Vol. 15, No. 4 Oct.-Dec. 2004
important finding, is not usually apparent
until 2 to 4 kg of fluid have been retained. In
patients who are ambulatory, edema is gen-
erally seen in the lower extremities; in pa-
tients who are bedridden, it is often evident
in the sacrum and buttocks. Patients may ex-
hibit dyspnea and auscultation of the lungs
may reveal crackles or wheezing. Cardiovas-
cular signs of volume expansion include
jugular vein distension, increased pulse pres-
sure, hypertension, and an S3 gallop. The
presence of hepatic congestion—hepato-
jugular reflux—may be evident. Hepatojugu-
lar reflux is an increased jugular venous
pressure induced by manual pressure over
the liver. Patients may also demonstrate
vomiting and diarrhea from bowel and in-
testinal edema (Table 1).
VOLUME DEPLETION. One of the most sensitive
tests to determine volume depletion is the
evaluation of orthostatic hypotension (the
measurement of the arterial blood pressure
and pulse rate of a patient in the supine and
standing positions). A fall in the systolic
blood pressure by
15 mmHg or an in-
crease in the pulse by
15 beats per minute
immediately after the position change is
suggestive of intravascular volume deficit.1 A
repeat reading after 2 to 3 minutes may
identify orthostatic hypotension not seen in
the first reading.2 Orthostatic hypotension
unrelated to vascular volume can also occur
in patients with Parkinson’s disease, dia-
betes mellitus, and other conditions produc-
ing autonomic neuropathy, as well as pa-
tients taking antihypertensive medications.
TABLE 1  Physical Examination Finding of Volume Depletion and Overload
Body System Exam Findings Volume Depletion
Skin Decreased turgor; cool, clammy, pale;
absence axillary sweat; dry mouth and
mucous membranes
Central nervous Weakness, syncope, lethargy, coma,
system decreased deep tendon reflexes
Cardiovascular Orthostatic hypotension; tachycardia;
weak, thready pulse; hypotension;
flat jugular veins
Pulmonary Nonspecific findings
Renal Oliguria or Anuria (prerenal from
hypovolemia)
Gastrointestinal Thirst, anorexia, nausea, vomiting
FLUIDS AND ELECTROLYTES  609
Other cardiovascular findings of volume de-
pletion may include tachycardia; weak,
thready pulse; narrow pulse pressure; hy-
potension; and flat jugular neck veins that
represent decreased venous filling. Early
signs of peripheral vasoconstriction (eg,
cool, clammy, pale skin) may also indicate
fluid depletion.3 Other skin findings include
dry mucous membranes, absence of axillary
sweat, and decreased or delayed capillary
refill. Mottled skin is a late finding of hypov-
olemia. Thirst is another finding in fluid vol-
ume deficit. The thirst center in the hypo-
thalamus is sensitive to changes in
osmolality—an increase in osmolality by
only 1 to 2% is sufficient to stimulate thirst.2
Decreased skin turgor due to loss of skin
elasticity may also be a clinical finding;
however, this is not of diagnostic value in
the elderly or chronically ill. Skin turgor is
also difficult to assess in obese
patients. Neurologic findings related to re-
duced cerebral perfusion may include dizzi-
ness, weakness, syncope, lethargy, de-
creased deep tendon reflexes, or coma.
Patients may exhibit anorexia, nausea, or
vomiting. Urine output may be reduced to
0.5 mg/kg/hr or may be absent4 (Table 1).
Laboratory Data
Laboratory studies may be helpful in con-
firming physical examination findings, espe-
cially when determining volume depletion.
URINE STUDIES. Urine sodium and chloride
excretion often reflect renal perfusion. With
Exam Findings Volume Overload
Dependent pitting edema
Anxiety, agitation
S3 gallop, hypertension, bounding pulse,
jugular vein distention, hepatojugular reflex
Dyspnea, crackles, wheezing
Nonspecific findings
Vomiting, diarrhea
610  NEBELKOPF ELGART
volume depletion, aldosterone is secreted
which causes reabsorption of sodium and
chloride, resulting in decreased urinary
sodium and chloride 20 mEq/L each.3 Ex-
ceptions may occur with patients receiving
diuretic therapy, salt-wasting disease states,
and adrenal insufficiency. In these condi-
tions, lab data may be misleading as the kid-
neys cannot maximally reabsorb sodium and
chloride, despite the presence of hypov-
olemia, resulting in higher levels of urinary
sodium and chloride. Urine chloride is more
reflective of volume status in patients with
sodium losses such as vomiting, certain di-
uretics, or those in ketoacidosis.
The fractional excretion of sodium (FENa)
is another marker for renal perfusion. FENa is
defined as the percentage of filtered sodium
that is excreted in the urine. Under normal
circumstances the FENa is 1%. This indi-
cates that
99% of filtered sodium is reab-
sorbed by the nephrons. In hypovolemic
states, the FENa is usually 1% and can be as
low as 0.5%.5 FENa is most helpful in deter-
mining prerenal hypovolemia (FENa 1%)
from renal causes of acute oliguric renal fail-
ure (FENa
2%).
A microscopic urinalysis may show hya-
line casts and rare granular casts in patients
with hypovolemia due to the relative con-
centration of the urine. Urine-specific gravity
is the relative density of urine to water, a
measurement of
1.020 and a urine osmo-
larity of 500 to 600 mOsm/L reflects volume
depletion. Again, renal failure or diuretic
therapy may impair the renal response to
volume depletion, resulting in altered urine
study results.
SERUM STUDIES. Typically, volume depletion
causes increased urea absorption, causing an
elevated blood urea nitrogen (BUN) level
disproportionate to the serum creatinine.
This results in a BUN-to-creatinine ratio of

20:1. In the presence of liver disease or
protein deficiency, BUN may not be ele-
vated. Conversely, patients in a catabolic
state or with gastrointestinal bleeding may
have an elevated BUN as a result of nitrogen
breakdown, which may not imply volume
depletion. Serum studies may reveal a rela-
tive elevation in hematocrit, uric acid, and
serum protein (albumin) due to a depletion
of intravascular volume.
AACN Clinical Issues
The normal range of serum osmolarity is
280 to 295 mosm/kg.5 Plasma osmolarity can
be calculated by accounting for the most
prevalent solutes in the plasma: sodium, glu-
cose, and urea in the equation:
Osmolality (mOsm/kg) = 2 (Na+ [mEq/L]) +
(glucose [mg/dL]  18) + (BUN [mg/dL] + 2.8).6
An osmolar gap is defined by the mea-
sured serum osmolality exceeding the calcu-
lated osmolality by
10 mOsm/kg. An os-
molar gap can occur when significant
quantities of unmeasured solutes are present
in the serum, but not measured or accounted
for in this formula (eg, mannitol, lipids, pro-
teins, alcohols). Sodium is the primary deter-
minant of ECF osmolality, and serum osmo-
lality plays an important role in the
evaluation of hypo- and hypernatremia.
Diagnostic Studies
INVASIVE DIAGNOSTIC STUDIES. It is not uncom-
mon for critically ill patients to have physical
assessment findings and laboratory studies
yield uncertain or contradictory data regard-
ing volume status. This is especially true
when there is evidence of volume overload
in the interstitial or “third spaces” while there
is evidence of intravascular volume deple-
tion. Hemodynamic monitoring may be of
value for these patients, although contro-
versy exists over the validity, accuracy, and
clinical implications of measurements ob-
tained. However, hemodynamic monitoring
may be beneficial to assess response to ther-
apeutic interventions (ie, fluid boluses) and
following trended data. (see Hemodynamic
Assessment by Adams elsewhere in this is-
sue.)
A central venous pressure (CVP) or right
atrial pressure (RAP) is the measurement of
pressure in the right atrium. The average CVP
in a healthy, supine patient is 6 to 8 mmHg,
but up to 10 mmHg may be accepted as nor-
mal in acutely ill patients.7 Controversy exists
over whether the measurement of CVP reli-
ably indicates intravascular volume status. It
is generally accepted that a reduced CVP will
occur during and after acute volume loss.
Therefore, a low CVP may reflect a volume
deficit. However, CVP values depend on ve-
nous wall compliance, which can change
rapidly to accommodate variations in blood
Vol. 15, No. 4 Oct.-Dec. 2004
volume. Therefore, it may be misleading to
assess fluid volume status from a single CVP
reading. CVP can be elevated in a variety of
disease states: right heart failure, infarction,
tricuspid regurgitation, increased intraab-
dominal pressure, pericardial tamponade,
tension pneumothorax, positive pressure
ventilation, or fluid overload. Thus, the find-
ing of a low CVP may support the diagnosis
of hypovolemia, but an elevated CVP does
not necessarily support the diagnosis of vol-
ume overload. It is possible to have a CVP of
20 mmHg caused by any of the above dis-
ease states, and still have an underfilled right
ventricle. CVP values may be most helpful in
patients with single system organ failure (eg,
cardiac) or uncomplicated acute blood loss.
CVP readings may be useful during early re-
suscitation from acute injury with hypoten-
sion by following trends and response to
fluid therapy.7-10
Pulmonary artery occlusion pressure
(PAOP), also referred to as the pulmonary
capillary wedge pressure (PCWP), measured
with a pulmonary artery catheter allows esti-
mation of left atrial pressure, which allows
estimation of the left ventricular end dias-
tolic pressure, an important determinant of
cardiac output and indirect diagnostic tool
to determine intravascular volume. A low
PAOP may indicate hypovolemia, while an
elevated PAOP may indicate impaired car-
diac function. However, PAOP is influenced
by factors such as blood volume, ventricular
function, intrathoracic and intraabdominal
pressures, vasopressors, vasodilators, and
fluid therapy. There are no accepted high
and low PAOP values to definitively diag-
nose hypovolemia versus cardiac dysfunc-
tion. A PAOP 10 mmHg may indicate an
underfilled left ventricle (hypovolemia)
while a PAOP
18 mmHg may suggest a
full, distended, or noncompliant left ventri-
cle. Again, factors such as valvular defects,
ventricular defects, or pulmonary venous re-
sistance (eg, chronic obstructive pulmonary
disease) may elevate the PAOP, even in con-
junction with an underfilled ventricle.7-10
Using the CVP or pulmonary artery
catheter to evaluate a patient’s response to
fluid boluses may be helpful to determine
intravascular volume. This is based upon the
Frank-Starling relationship that describes the
effect of volume loading on cardiac function.
FLUIDS AND ELECTROLYTES  611
Normally, as the ventricular volume is in-
creased by intravenous fluid administration,
the stroke volume will increase until a
plateau is reached. The ventricle will reach
its filling pressure based upon contractility,
compliance, and afterload. Generally, an un-
derfilled ventricle will show a slight increase
in the CVP or PAOP with a constant or slight
increase in the cardiac output/index in re-
sponse to a fluid bolus. Once the ventricle is
filled or at its plateau, small increments of
fluid administration will result in greater in-
creases in the PAOP or CVP and may show a
decrease in the cardiac output. Administer-
ing fluid boluses and observing the cardiac
output (or index), PAOP or CVP can help de-
termine whether the ventricles require addi-
tional intravenous fluids or have reached fill-
ing potential. See Figure 3 for examples of
fluid challenge algorithms.11-14
MINIMALLY INVASIVE DIAGNOSTIC STUDIES. Trans-
thoracic echocardiography (TTE) can be
used in the acute care setting to assess car-
diac output, left ventricular (LV) systolic
function, systolic pulmonary arterial pres-
sure, wall motion, and ejection fraction.15,16
Clinically, the TTE can be used to evaluate
the diastolic function and filling pressures of
the LV, which can be useful in the acute care
setting to determine responsiveness to fluid
administration.17 Limitations of TTE include
operator dependence, a single view in time
rather than continuous trended data, and ex-
pense. TTE images may have poor diagnos-
tic quality in patients who are obese; have
severe chronic obstructive pulmonary dis-
ease; are unable to be properly positioned;
have thoracic incisions, chest tubes, or dress-
ings; or are uncooperative.15,18
Transesophageal doppler uses sonography
within the lumen of the esophagus to deter-
mine pressures within the descending tho-
racic aorta. The device measures the velocity
of blood flow in the aorta and mathematically
translates flow into stroke volume and cardiac
output. Drawbacks to using this technology
in acute care include the bulky size of the
esophageal tube, and time-consuming mea-
surements. Factors such as anemia, tachycar-
dia, or a thick chest wall may interfere with
the data values. Because this is a relatively
new technology, its widespread use is cur-
rently limited.19-22
612  NEBELKOPF ELGART AACN Clinical Issues

With Central Venous Pressure (CVP):

Select bolus: 250 mL-1000 mL
10 minutes
If CVP increases by 2 mmHg Repeat
If CVP increases by 2-5 mmHg Hold until drops within 2 mmHg of baseline
If CVP increases by
5 mmHg Discontinue challenge

With Pulmonary Artery Occlusion Pressure (PAOP):

Initial PAOP Give Bolus (over 10 minutes)
12 mmHg 200 mL
12-16 mmHg 100 mL

16 mmHg 50 mL
PAOP rises 3 mmHg Repeat bolus
PAOP rises
7 mmHg Stop
PAOP rises 3-7 mmHg Observe
After observation remains the same Stop
After observation decreases to within
3 mmHg of baseline Repeat

With PAOP and Cardiac Index (CI):

Boluses as above
PAOP rises 3 mmHg Repeat if CI fails to rise
PAOP rises
7 mmHg Stop if CI adequate, if CI not adequate
consider inotropes
PAOP rises 3-7 mmHg Observe
After observation CI remains the same Repeat measurements in 30 min
After observation CI declines Repeat bolus

Figure 3. Sample fluid challenge algorithms.11-14 RAP, right atrial pressure; PAOP, pulmonary artery occlusive
pressure; CI, cardiac index.

End-tidal carbon dioxide (CO2) monitor-
ing (PetCO2) may also give diagnostic clues
regarding volume status. During conditions
of low cardiac output, expired CO2 is re-
duced as a consequence of caused by de-
creased pulmonary perfusion. As circulating
volume is restored, PetCO2 should increase.23
Lastly, an often overlooked and underuti-
lized tool for assessing volume status in
acute care patients is daily patient weight.
Retention of one liter of fluid will result in a
weight gain of approximately 2.2 pounds.24
Obtaining a weight balance will also take
into account insensible losses, such as those
resulting from fever, mechanical ventilation,
and open wounds.

Evaluation of Electrolytes
Serum electrolyte concentrations influence
movement of fluid within and between body
compartments. The major extracellular elec-
trolytes are sodium, calcium, chloride, and
bicarbonate. The most abundant cation is
sodium; chloride is the most abundant an-
Vol. 15, No. 4 Oct.-Dec. 2004
TABLE 2  Composition of Gastrointestinal Secretions
Sodium
Secretion (mEq/L)
Saliva 60
Stomach 30-90
Pancreatic 135-155
Bile 135-155
Jejunal 70-125
Ileostomy 90-140
Diarrhea 25-50
Reprinted with permission from Barke RA. Fluids and electrolytes. In Abrams JH, Cerra FB, eds. Essentials of Surgical Critical
Care (p 481). Copyright by Quality Medical Publishing, Inc.25
ion. Potassium, magnesium, and phosphates
are the major intracellular electrolytes, of
which potassium is the most plentiful cation
and phosphate is the most abundant anion.
Serum electrolyte concentrations affect all
metabolic activity in some way. Abnormal
electrolytes may reflect fluid or acid-base im-
balance, or renal, neuromuscular, endocrine
or skeletal dysfunction. See Table 2 for com-
mon gastrointestinal electrolyte losses.24,25
Sodium
Sodium affects body water distribution, pro-
motes neuromuscular function, maintains
acid-base balance, influences chloride and
potassium levels, and helps the kidneys reg-
ulate water. Serum sodium disorders are al-
ways evaluated in relation to the patient’s
fluid status and may be associated with
hypovolemic, hypervolemic, or isovolemic
states. Normal serum sodium levels are 135
to 145 mEq/L. Maintenance of the plasma
sodium concentration depends on two
mechanisms: the ability of the kidneys to
regulate water and an intact thirst mecha-
nism with access to water. Arginine vaso-
pressin or antidiuretic hormone (ADH) is the
primary hormone that regulates water excre-
tion. ADH is synthesized in the supraoptic
and paraventricular nuclei of the hypothala-
mus. A 1 to 2% reduction in plasma osmolal-
ity inhibits ADH release, while a 1 to 2% in-
crease in plasma osmolality (or a 7-10%
decrease in blood pressure or volume) stim-
ulates ADH release. The presence of ADH
causes the luminal membranes of the corti-
FLUIDS AND ELECTROLYTES  613
Potassium Chloride Bicarbonate
(mEq/L) (mEq/L ) (mEq/L)
20 15 50
4-12 50-150 70-90
4-6 60-100 70-90
4-6 80-100 35-50
3.5-6.5 70-125 10-20
4-10 60-125 15-50
35-60 20-40 35-45
cal and medullary collecting tubules in the
kidney to reabsorb water. Thus, both the hy-
pothalamus and kidneys influence homeo-
static sodium levels.
The most common cause of hypernatremia
is dehydration—a pure water loss or hypo-
tonic fluid loss from the body. Increased wa-
ter loss may be caused by insensible losses
such as sweat, burn injuries, wounds, or pro-
longed hyperventilation. Gastrointestinal
losses include severe vomiting and diarrhea,
and biliary, gastric, or fistula fluid losses. Cen-
tral (neurogenic) and nephrogenic diabetes
insipidus (DI) are both associated with hyper-
natremia from an inadequate replacement of
urinary water losses. Central DI is associated
with a decrease in ADH secretion, which
causes a relatively dilute urine. It may be in-
duced by trauma, pituitary surgery, hypox-
emia, or ischemic encephalopathy. Nephro-
genic DI is classified by normal ADH
secretion in the presence of renal resistance
to ADH’s water-retaining effect. Hyper-
glycemia, osmotic diuretics (ie, mannitol,
glycerol), and urinary concentrating defects
can cause an increase in renal water loss, re-
sulting in serum hypernatremia. Hyperna-
tremia can also result from aldosteronism,
steroid administration, or excessive sodium
intake. Additionally, iatrogenic replacement
of hypotonic losses with isotonic fluids can
result in hypernatremia. Symptoms are most
prominent with a significantly large or rapid
(over hours) increase in the serum sodium
concentration and are generally seen when
the sodium exceeds 160 mEq/L26 (Table 3).
Symptoms are often attributed to either the
614  NEBELKOPF ELGART AACN Clinical Issues

TABLE 3  Hypernatremia Symptoms

Hypovolemic symptoms Thirst, dry mucous membranes, tachycardia, hypotension, cool
extremities
Central nervous system symptoms Muscle weakness, restlessness, lethargy, confusion, delirium,
seizures, hyperreflexia, spasticity

underlying volume depletion or a decrease in 72 hours. It is important to correct the

cellular volume, particularly cerebral cellular
volume. Chronic hypernatremia is much less
likely to cause symptoms due to the brain’s
ability to adapt slowly to volume loss with a
solute gain to restore lost water.26 This re-
sponse normalizes the brain volume and ac-
counts for the milder symptoms of chronic
hypernatremia.
Treatment of hypernatremia starts with
identification of the underlying cause. For pa-
tients with hypovolemic hypernatremia, free
water replacement is required after replace-
ment of the intravascular volume. Fluid ther-
apy with 5% dextrose or hypotonic saline is
guided by the calculation of the amount of
free water deficit. This is calculated by:
Deficit (L) = 0.6  body wt (kg) 
( [Serum Na divided by 140] –1)27
The constant 0.6 represents the normal
body proportion of water in healthy males.
Use 0.5 in young females and elderly males
and 0.4 in elderly females. Markedly obese
patients may require even lower values, with
replacement based on an adjustment body
weight. Overly rapid sodium correction is
potentially dangerous. Rapid reduction of
the plasma sodium concentration may cause
cerebral edema and lead to seizures, perma-
nent neurologic damage, or death. Replace-
ment of half of the free water deficit should
be done in the first 24 hours, with the re-
mainder being replaced over the next 24 to
sodium at a rate no greater than 0.5
mEq/L/hr or 10 to 12 mEq/L/day.26 Therapy
should stop when the serum sodium has
reached 145 mEq/L. To calculate the esti-
mated change in plasma sodium per liter of
infused IV fluid:
 serum Na+/L of IVF =
(Infusate sodium in mEq/L – serum sodium)
divided by ([0.6 x wt (kg)] +1)26,28
The sodium content of normal saline
(0.9%) is 154 mEql/L and Ringer’s lactate is
130 mEq/L. One-half normal saline (0.45%)
has 77 mEq/L, one-quarter normal saline
(0.2%) has 34 mEq/L, and 5% dextrose has
0 mEq/L.26,28 See Figure 4 for patient exam-
ple.
Hyponatremia can be associated with hy-
per, hypo-, and isovolemic states. Hyperv-
olemic hyponatremia is generally seen in
edematous states. Causes include: congestive
heart failure, cirrhosis, nephrotic syndrome,
hypoalbuminemia, and hypothyroidism. Hy-
povolemic hyponatremia can be due to con-
ditions causing volume depletion or losses
where sodium losses are greater than volume
loss. This includes gastrointestinal losses
(vomiting, nasogastric suctioning, diarrhea,
and fistula loss), diuretics, cerebral salt wast-
ing, burn injury, excessive sweating, and
third space fluid losses (eg, peritonitis, pan-
creatitis, bowel obstruction). Renal disease
(eg, nonoliguric renal failure, renal tubular

A. Fluid deficit = (0.6 x 70 kg) x [165/140)-1] = 7.5 L free water deficit

B. Change in serum sodium = Na+ infusate - 165 / [(0.6 x 70 kg) +1)

Using .45 NS = 77-165 divided by 43 = -2 mEq/L reduction in serum sodium per liter of in-
fusate
Using D5W = 0-165 divided by 43 = -3.8 mEq/L reduction in serum sodium per liter of in-
fusate

Figure 4. A 70-kg male with serum sodium level of 165 mEq/L.

Vol. 15, No. 4 Oct.-Dec. 2004
acidosis, and other salt-wasting neph-
ropathies) is another cause of hypovolemic
hyponatremia. Symdrome of inappropriate
ADH secretion (SIADH), another cause of hy-
ponatremia, may be caused by increased
ADH secretion, potentiation of the ADH ef-
fect, or a resetting of the hypothalamic osmo-
stat. Other causes of isovolemic hypona-
tremia include water intoxication, thiazide
diuretics, renal failure, and iatrogenic causes
(eg, excessive hypotonic fluid administration,
excess hypotonic irrigation of tube or body
cavities). Hyponatremia is often seen in pa-
tients following transurethral prostatectomy,
lithothripsy, or with uterine irrigation after
endometrial ablation. The hyponatremia is
usually due to large amounts of irrigation
solutions containing glycine, sorbitol, or
mannitol. Absorption of the solutions results
in a dilutional reduction in plasma sodium
concentration.29 Hyperosmolar hyponatremia
may also be seen in patients with plasma hy-
perosmolality. This is most commonly seen
with hyperglycemia, where the osmotic gra-
dient across the cells facilitates water move-
ment out of cells and into the plasma, with
the resulting dilutional hyponatremia. The
following formula can be used to determine
an estimate appropriate sodium level in the
presence of hyperglycemia:
(serum glucose mg/dL – 100)  0.016 =
expected change in serum sodium27
This estimate varies with body size, falling
more in smaller patients.
Pseudohyponatremia is caused by an in-
crease in the plasma concentration of pro-
teins (eg, immunoglobins in multiple
myeloma) or lipids (eg triglycerides) which
can transiently displace water in a given
volume of plasma, but do not effect the
sodium concentration. The result is an arti-
ficially low plasma sodium in relation to the
percentage of plasma water.
Patients who develop severe hypona-
tremia (serum sodium below 120 mEq/L) or
who develop hyponatremia over 24 hours
are most likely to demonstrate signs and
symptoms.29 Signs of hyponatremia are listed
in Table 4. Treatment is directed toward first
determining volume status. The amount of
total body water excess can be calculated:
Water excess = (0.6 x wt [kg]) 
(1-[Serum Na divided by 140])27
FLUIDS AND ELECTROLYTES  615
TABLE 4  Signs and Symptoms
of Hyponatremia
Lethargy Personality changes
Fatigue Confusion
Malaise Seizures
Headaches Ataxia
Muscle cramps Incontinence
Anorexia Depressed reflexes
Nausea Respiratory depression
Vomiting Coma
Treatment for hypovolemic hyponatremia
includes administration of isotonic fluids.
Symptomatic patients may require hypertonic
saline combined with furosemide to decrease
rapid expansion of the ECF volume. Patients
with asymptomatic hypervolemic hypona-
tremia require water restriction (800
mL/day) and close observation. Patients with
severe symptoms may require isotonic or hy-
pertonic saline. Patients with cardiac disease
may benefit from optimization of hemody-
namics including the use of angiotensin-
converting-enzyme (ACE) inhibitors which
increase the excretion of water and improve
hyponatremia. Loop diuretics also promote
free water excretion. For nonhypotonic hy-
ponatremia, treatment is directed at the un-
derlying disorder and includes insulin for di-
abetics, and correction of water, potassium,
and sodium deficits. Hemodialysis may be re-
quired for patients with impaired renal func-
tion. Sodium should not increase by more
than 0.5 to 1 mEq/L/hr (or 8-10 mEq/day)
and should stop when the serum sodium
reaches 125 to 130 mEq/L. For patients with
severe symptoms, initial correction may be 1
to 2 MEq/L for several hours. This rapid cor-
rection should be halted when the life-threat-
ening symptoms have ceased, or the serum
sodium reaches 125 mEq/L.30 The calculation
to determine the change in serum sodium
per liter of intravenous fluid administered is
the same as in hypernatremia (see Figure 4).
Hypertonic (5%) saline contains 855mEq/L
and 3% hypertonic saline contains 513
mEq/L. Hypovolemic patients should be
monitored closely. As the ECF volume is re-
stored, the stimulus to release ADH will
cease. This can cause a rapid diuresis and in-
616  NEBELKOPF ELGART
crease the correction of hyponatremia.
Overly-rapid correction can lead to Osmotic
Demyelination Syndrome, also known as
Central Pontine Myelinolysis, which can re-
sult in severe neurologic sequelae (eg, quad-
riplegia, oculomotor abnormalities, ataxia,
dysarthria, dystonia, coma, or death).31
Potassium
Potassium is the major intracellular cation. It
maintains cellular osmolarity equilibrium,
muscle activity, enzyme activation and plays
a role in acid-base balance. Normal serum
potassium is 3.3 to 5.0 mEq/L while intracel-
lular levels are generally 125 to 140 mEq/L.29
Acute changes in plasma concentration can
have dramatic effects on muscle contractility
and nerve conduction.
Hyperkalemia is often caused by either in-
creased potassium release from cells or de-
creased urinary potassium excretion. Burns,
crush injuries, tumor lysis, and massive he-
molysis can cause transcellular redistribution
of potassium out of the cell and into the vas-
cular space. Beta-adrenergic blockade inter-
feres with the potassium uptake by cells, al-
though this usually results in minor elevations
of serum potassium (0.5 mEq/L) 29 in
healthy patients. Potassium shifts from the
cells into the ECF in the presence of acidosis.
Serum potassium concentration rises approxi-
mately 0.7 mEq/L (range = 0.2-1.7) for every
0.1 pH unit decrease during acidosis.29 The
movement of potassium out of the cells dur-
ing acidosis is primarily governed by chlo-
ride. The inability of chloride to permeate the
cell membrane causes the transcellular ex-
change of hydrogen for potassium. Insulin
deficiency often combined with hyper-
glycemia hyperosmolality frequently leads to
hyperkalemia.
Impaired urinary potassium excretion can
by caused by renal failure, hypoaldostero-
nism, adrenal insufficiency, potassium-spar-
ing diuretics, and type-1 renal tubular acido-
sis. Excessive intake from supplements or
blood transfusions may also cause hyper-
kalemia. Medications can cause hyper-
kalemia through potassium retention (eg,
potassium-sparing diuretics, ACE inhibitors)
or potassium redistribution (eg, succinyl-
choline). Digitalis toxicity can interfere with
the Na+-K+-ATPase pump, resulting in potas-
AACN Clinical Issues
sium release from cells. Pseudohyper-
kalemia, an elevation of measured serum
potassium, is due to potassium movement
out of cells during or after the blood is
drawn. Mechanical or technical causes of
pseudohyperkalemia include hemolyzed
blood sample, drawing blood above a site
where potassium is infusing, and repeated
clenching and unclenching of a fist during
phlebotomy.2 Additionally, potassium moves
out of white blood cells and platelets after
clotting has occurred. Patients with marked
leukocytosis (
100,000 mm3) or thombocy-
tosis (
1,000,000 mm3) may have an ele-
vated measured serum potassium.29
Symptoms of hyperkalemia include weak-
ness, parasthesias, areflexia, ascending paral-
ysis, nausea, and diarrhea. Patients may ex-
hibit bradycardia, prolongation of the AV
conduction leading to complete heart block,
ventricular fibrillation, and asytole (see Table
5).30
Treatment of hyperkalemia includes cor-
recting factors that cause potassium to shift
from the cells into the vascular space (eg,
acidosis, insulin deficiency, hyperosmolal-
ity). Treatment of severe hyperkalemia in-
cludes intravenous calcium to stabilize the
heart by reinstating the delta change re-
quired to move between resting and thres-
hold membrane potential. Other therapies
include intravenous insulin with glucose, al-
buterol, and sodium bicarbonate to drive
potassium back into the cells, and Kayex-
alate, loop diuretics, and dialysis to remove
potassium from the body.
TABLE 5  Electrocardiogram
Findings With
Hyperkalemia
Potassium
Level ECG Findings
5.5-6.0 mEq/L Peaked T waves, shortened QT
interval
6.0-7.0 mEq/L Lengthening of PR interval,
QRS widening
7.0-7.5 mEq/L Flattened P waves, further
widening QRS
> 8.0 mEq/L Fusion of QRS and T wave,
imminent ventricular standstill
ECG, electrocardiogram.
Vol. 15, No. 4 Oct.-Dec. 2004
Hypokalemia is one of the most prevalent
electrolyte abnormalities found in acute care.
There are multiple causes of hypokalemia in-
cluding renal losses from diabetes, acute
tubular necrosis, diuresis, hypercalcemia,
hypochloremia, and multifactorial polyuria.
Other causes include aldosteronism, Cush-
ing’s syndrome, thiazide and loop diuretic
use, postresuscitation, postmyocardial infarc-
tion, and hematologic malignancies. Gastric
losses from vomiting, nasogastric suctioning,
biliary drainage, diarrhea, fistulas, and postin-
testinal bypass surgery can lead to hy-
pokalemia. Transcellular shifts of potassium
can also occur, moving potassium from the
plasma into the cells. Beta-adrenergic ago-
nists (eg, albuterol, terbutaline, dopamine)
can stimulate muscle cell membranes to move
potassium into the cells. This effect changes
the serum potassium by 0.5 to 1.0 mEq/L.
Respiratory or metabolic alkalosis also pro-
motes the transcellular shift of potassium and
can have a variable and unpredictable effect
on serum potassium.29
Clinical signs and symptoms may be unre-
liable for assessment of hypokalemia and are
generally not present until potassium levels
fall below 3.0 mEq/L.2 Patients receiving digi-
talis and patients with hepatic failure may ex-
hibit symptoms with even mild hypokalemia.
Symptoms are often related to skeletal,
smooth, and cardiac muscle weakness (see
Table 6).
Treatment depends on the severity of the
potassium deficit, which must be estimated,
because there is no correlation equation to
determine plasma potassium concentration in
relation to total body potassium stores. The
loss of approximately 200 to 400 mEq/L body
potassium will lower the serum potassium
from 4 to 3 mEq/L, an additional 200 to 400
mEq/L loss will reduce the serum potassium
to approximately 2 mEq/L.29 Approximately
40 to 60 mEq/L of potassium administration
(oral or intravenous) will increase the plasma
concentration by 1 to 1.5 mEq. The serum
potassium will increase by 2.5 to 3.5 mEq/L
after administration of approximately 135 to
160 mEq/L potassium. Intravenous potassium
is irritating to peripheral veins, therefore it
should be administered in a concentration 20
to 40 mEq/L and can be given centrally in
concentrations of 140 to 200 mEq/L (14-20
mEq/mL).2
FLUIDS AND ELECTROLYTES  617
TABLE 6  Symptoms of
Hypokalemia
Cardiovascular Tachydysrthymias, flattened
T waves, prominent U waves,
ST segment depression,
conduction abnormalities
Central nervous Malaise, fatigue, weakness,
system/neuro- hyporeflexia, parasthesias,
musculoskeletal cramps
Gastrointestinal Constipation, paralytic ileus,
vomiting, anorexia, nausea,
prolonged gastric emptying
Pulmonary Respiratory failure
Magnesium
Magnesium helps regulate intracellular me-
tabolism, activates enzymes, affects metabo-
lism of nucleic acids and proteins, helps
transport sodium and potassium across the
cell membrane, and influences intracellular
calcium by its effect on the secretion of the
parathyroid. Normal serum magnesium is 1.3
to 2.2 mEq/L.
Hypermagnesemia can be caused by re-
nal failure, overuse of magnesium-contain-
ing antacids or laxatives, adrenal insuffi-
ciency, or lithium toxicity. Signs and
symptoms generally correspond with serum
levels (see Table 7) and may include hypore-
flexia, lethargy, flushing, EKG changes, res-
piratory depression, and hypotension. Treat-
ment includes administration of calcium
gluconate, hydration to enhance excretion,
intravenous glucose and insulin, and he-
modialysis for severe hypermagnesemia.
Hypomagnesemia can be caused by de-
creased intake, decreased intestinal absorp-
tion, diuretic therapy, chronic alcoholism,
renal or metabolic disorders, gastric losses
(nasogastric suctioning, severe diarrhea, in-
testinal fluids), other electrolyte abnormali-
ties, and severe burns are just a partial list of
the etiologies of magnesium loss. Symptoms
include vertigo, ataxia, nystagmus, altered
mentation, parasthesias, seizures, tetany,
muscle spasms or tremors, weakness, hyper-
reflexia, hypertension, cardiac dysrthymias,
nausea, constipation or ileus, and abdominal
cramps. Treatment includes administering
oral or intravenous magnesium, and correct-
ing other electrolyte deficiencies.
618  NEBELKOPF ELGART
TABLE 7  Effects of
Hypermagnesemia
Magnesium
Level Clinical Findings

4 mg/dL Hyporeflexia, anticonvulsant
effects

5 mg/dL Loss of deep tendon reflexes,
flushing, lethargy

6 mg/dL Flushing, diaphoresis,
drowsiness

7 mg/dL Nausea, emesis, weakness,
somnolence

9 mg/dL Diplopia, prolonged PR interval

10 mg/dL Respiratory depression,
hypotension

13 mg/dL Complete heart block,
paralysis, respiratory arrest,
cardiac arrest
Calcium
Calcium helps regulate neuromuscular and
enzyme activity, skeletal development, and
blood coagulation. Calcium is measured as
two forms, either bound to protein or as a
positively charged ion (“ionized calcium”).
Normal serum calcium is 8.9 to 10.1 mg/dL,
assuming normal albumin levels. A decrease
in albumin decreases the amount of total
measured calcium in the plasma, but may
not change the amount of active calcium,
measured by the ionized calcium. The fol-
lowing formula is used to correct calcium in
the presence of abnormal albumin:
Corrected total Ca = measured total Ca + 0.8
 (4.0 – albumin)33
Normal ionized calcium is 1.1 to 1.3
mmol/L. The ionized calcium accounts for ap-
proximately half of the total serum calcium
concentration and is physiologically more rel-
evant than the total calcium level. Ionized cal-
cium represents the physiologically active
portion of calcium in the body; therefore, cal-
cium imbalances should be assessed and
treated by the measured ionized calcium.23
Hypercalcemia can be caused by parathy-
roid disorders, hyperthyroidism, pheochro-
mocytoma, malignancy, renal failure, med-
ications (calcium-containing agents, lithium,
thiazide diuretics, and estrogens), prolonged
immobilization, osteoporosis, and Paget’s
disease.
AACN Clinical Issues
Clinical evaluation of the patient may re-
veal lethargy, stupor, coma, decreased mus-
cle tone and strength, pathological fracture,
anorexia, nausea or vomiting, constipation or
ileus, abdominal pain, hypertension or hypo-
volemia, polyuria, renal insufficiency, inter-
stitial nephritis, electrocardiogram (ECG)
changes including a shortened Q-T interval,
widened T-wave or dysrhythmias, or hyper-
chloremic acidosis. Treatment includes hy-
dration, loop diuretics, and calcitonin.
Hypocalcemia can be related to hypopara-
thyroidism, vitamin D deficiency, chronic al-
coholism, renal disease, sepsis, or hypothy-
roidism. Some medications can cause
hypocalcemia including: bisphosphonates,
calcitonin, furosemide, phenytoin, phenobar-
bitol, estrogens, cimetidine, radiocontrast
agents, heparin, theophylline, and propylth-
ioruacil. Ionized hypocalcemia is a common
finding in ICU patients. Causes include: alka-
losis, pancreatitis, sepsis, renal failure, and
magnesium depletion. Calcium can also bind
to the citrate preservative found in banked
blood. This causes a transient hypocalcemia,
which resolves when the citrate is metabo-
lized by the liver and kidneys. Patients with
renal or hepatic insufficiency will have a pro-
longed hypocalcemia.
Signs and symptoms of hypocalcemia may
include peripheral numbness and tingling,
muscle twitching, tetany, Chvostek’s sign (fa-
cial muscle spasm) or Trousseau’s sign (car-
popedal spasm), seizures, confusion, hy-
potension, ECG changes (Q-T interval
prolongation, ST segment changes, T wave
changes), laryngospasm, bronchospasm, and
papilledema. Treatment includes oral or in-
travenous calcium administration, magne-
sium administration, and oral phosphate
binding agents for renal failure patients.
Phosphorus
Normal phosphorus levels range from 2.5 to
4.5 mg/dL. Phosphorus helps regulate cal-
cium levels, and has a role in carbohydrate
and lipid metabolism and acid-base balance.
Hyperphosphatemia is most often caused
by renal failure. Other causes include: hypo-
volemia, lactic acidosis, severe hypothermia,
tumor lysis syndrome, skeletal disease, in-
testinal obstruction, hypoparathyroidism, or
acromegly. Patients are often asymptomatic.
Vol. 15, No. 4 Oct.-Dec. 2004
Systemic findings may include: muscle
tetany from hypocalcemia, soft tissue calcifi-
cation, corneal clouding, dysrhythmias or
heart failure, nausea, vomiting, or ileus.
Treatment includes oral phosphate binders,
calcium and vitamin D supplements, glucose
and insulin, or hemodialysis.
Hypophosphatemia is often multifactor-
ial. Some identified causes are: chronic al-
coholism, acid-base disturbances, alu-
minum or calcium-containing antacids,
diuretic therapy, gastrointestinal losses, dia-
betes, burn injury, hypothermia, and renal
losses. Clinical manifestations include mus-
cle weakness, myalgias, fractures, respira-
tory muscle weakness, mechanical ventila-
tor dependence, decreased myocardial
contractility, hemolytic anemia, platelet
dysfunction, parasthesias, ataxia, tremors,
and seizures. Treatment is oral or intra-
venous phosphate administration.

Assessment of Intravenous Fluids
Intravenous Fluid Administration
Intravenous (IV) fluid administration has
several purposes: to replenish fluid com-
partments, replace renal and insensible
losses, correct electrolytes, provide glucose
calories, and correct/maintain acid-base bal-
ance.23,34 The composition of commonly
used crystalloid intravenous fluids can be
found in Table 8.
Fluids are described in terms of their tonic-
ity to plasma. Fluids with lower osmolality
than plasma are considered hypotonic (ie, 5%
dextrose in water). The body distribution of
TABLE 8  Composition of Commonly Used IV Fluids10
Dextrose Na+
Fluid (mg/mL) (mEq/L)
Lactated ringers 0 130
0.9% saline 0 154
5% dextrose 50 0 0
5% dextrose &
.45% saline 50 77
Plasmalyte 0 140
Normosol-R 0 140
Na, sodium; K, potassium; Ca, calcium; Mg, magnesium; Cl, chloride.
FLUIDS AND ELECTROLYTES  619
hypotonic solutions is similar to the distribu-
tion of water in the body. Thus, two-thirds of
fluid given will disperse to the ICF, while one-
third will disperse into the ECF. Figure 5 illus-
trates the example of D5W administration.
Hypotonic fluids will not replace the vascular
space and cannot be used for volume resusci-
tation. Because of the significant accumula-
tion within the cellular space, dextrose is
rarely used as an intravenous fluid indepen-
dently, but can be combined with isotonic
fluids to provide minimal glucose calories.
D5W may also be used to treat hypernatremia
or increased serum osmolality.35
Isotonic fluids such as 0.9 normal saline
(NS) and lactated ringers (LR) have a tonicity
similar to plasma. When administered, these
fluids will distribute into the extracellular
space. The interstitial space is three times
greater than the intravascular space, and fluid
will be dispersed in this ratio (see Figure 5).37
There is a small fluid shift that occurs from
the intracellular space to the extracellular
space because NS is actually slightly more hy-
pertonic than the ECF. Evidence suggests that
after 1 hour of NS administration, approxi-
mately one-quarter of the isotonic fluid re-
mains in the intravascular space.36 Thus, iso-
tonic solutions are the crystalloid of choice
for fluid resuscitation or to replace intravascu-
lar losses. Combination crystalloids such as
5% dextrose with 0.9% normal saline will be
dispersed as an isotonic fluid once the cells
have utilized the glucose in the dextrose con-
tent. Similarly, although 5% dextrose with
0.45% normal saline is slightly hypertonic in
solution, it becomes hypotonic as an infusion
after the glucose is metabolized and will be
K+ Ca+ Mg+ Cl-
(mEq/L) (mEq/L) (mEq/L) (mEq/L) Other
4 3 0 109 28 lactate
0 0 0 154
0 0 0
0 0 0 77
5 0 3 98 27 acetate
5 0 3 90 50 acetate
620  NEBELKOPF ELGART
distributed into the compartments as 50% free
water and 50% isotonic saline.24
For patients requiring fluid volume replace-
ment, the choice of which isotonic fluid to
use, NS or LR, is generally a matter of clinician
preference. The sodium content in NS is
higher than LR, thus NS may be a better op-
tion for hyponatremic patients. The sodium
concentration of NS is 154 mEq/L while LR
contains 140 mEq/L. It is thought that LR has
an advantage over NS in acidotic patients for
several reasons. First, the pH of LR is 6.5 while
the pH of NS is 5.5. Additionally, the added
lactate in LR is converted to bicarbonate in pa-
tients with normal liver function, further rais-
ing the serum pH.36 Lastly, administration of
large amounts of NS can result in a hyper-
chloremic-induced metabolic acidosis, while
large amounts of LR may result in a metabolic
alkalosis.37
Hypertonic solutions (eg, 3% saline, 5%
saline, 7.5% saline) are used occasionally for
osmotic therapy or intravascular volume ex-
pansion. Administration of hypertonic solu-
tions causes significant shifts from the intracel-
lular space to the intravascular space;
however, cellular dehydration is often the re-
sult of such fluid shifts. Hypertonic solutions
should only be used with intensive hemody-
namic and electrolyte monitoring and further
research is needed to determine benefits and
efficacy for the routine use of hypertonic solu-
tions.38.39

Summary
Although hemodynamic monitoring and
laboratory studies offer some assistance in
determining intravascular volume, clinical
examination remains a key component in
the evaluation of fluid status. Controversy
exists over the accuracy and validity of RAP
AACN Clinical Issues
Figure 5. Distribution of D5W and
0.9NS in body.
and PAOP measurements; however, these
parameters are often used as guides to de-
termine the effect of fluid administration.
Sodium is often a key component in deter-
mining fluid distribution within the body.
Electrolyte abnormalities are a common
finding in critically ill patients and need to
be continuously evaluated. Isotonic intra-
venous fluids are the fluid of choice to re-
place intravascular volume losses. Although
hypertonic solutions are effective for vol-
ume replacement, further research is re-
quired to determine benefits and safety of
using these solutions routinely.
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