5.1.

FLUIDS AND ELECTROLYTES INTRODUCTION

Learning Objectives
 Describe variables that influence fluid and electrolyte balance
 Identify factors related to fluid/electrolyte balance across the life span
 Assess a patient’s nutritional and fluid/electrolyte status
 Outline specific nursing interventions to promote fluid and electrolyte balance
 Base decisions on the signs and symptoms of fluid volume excess and fluid volume
deficit
 Base decisions on the interpretation of diagnostic tests and lab values indicative of a
disturbance in fluid and electrolyte balance
 Identify evidence-based practices
The human body maintains a delicate balance of fluids and electrolytes to help ensure proper
functioning and homeostasis. When fluids or electrolytes become imbalanced, individuals are at
risk for organ system dysfunction. If an imbalance goes undetected and is left untreated, organ
systems cannot function properly and ultimately death will occur. Nurses must be able to
recognize subtle changes in fluid or electrolyte balances in their patients so they can intervene
promptly. Timely assessment and intervention prevent complications and save lives.
Go to:

15.2. BASIC FLUID AND ELECTROLYTE CONCEPTS

Before learning about how to care for patients with fluid and electrolyte imbalances, it is
important to understand the physiological processes of the body’s regulatory mechanisms. The
body is in a constant state of change as fluids and electrolytes are shifted in and out of cells
within the body in an attempt to maintain a nearly perfect balance. A slight change in either
direction can have significant consequences on various body systems.

Body Fluids
Body fluids consist of water, electrolytes, blood plasma and component cells, proteins, and other
soluble particles called solutes. Body fluids are found in two main areas of the body called
intracellular and extracellular compartments. See Figure 15.1[1] for an illustration of intracellular
and extracellular compartments.
Figure 15.1
Intracellular and Extracellular Compartments
Intracellular fluids (ICF) are found inside cells and are made up of protein, water, electrolytes,
and solutes. The most abundant electrolyte in intracellular fluid is potassium. Intracellular fluids
are crucial to the body’s functioning. In fact, intracellular fluid accounts for 60% of the volume
of body fluids and 40% of a person’s total body weight![2]
Extracellular fluids (ECF) are fluids found outside of cells. The most abundant electrolyte in
extracellular fluid is sodium. The body regulates sodium levels to control the movement of water
into and out of the extracellular space due to osmosis.
Extracellular fluids can be further broken down into various types. The first type is known as
intravascular fluid that is found in the vascular system that consists of arteries, veins, and
capillary networks. Intravascular fluid is whole blood volume and also includes red blood cells,
white blood cells, plasma, and platelets. Intravascular fluid is the most important component of
the body’s overall fluid balance.
Loss of intravascular fluids causes the nursing diagnosis Deficient Fluid Volume, also referred to
as hypovolemia. Intravascular fluid loss can be caused by several factors, such as excessive
diuretic use, severe bleeding, vomiting, diarrhea, and inadequate oral fluid intake. If
intravascular fluid loss is severe, the body cannot maintain adequate blood pressure and
perfusion of vital organs. This can result in hypovolemic shock and cellular death when critical
organs do not receive an oxygen-rich blood supply needed to perform cellular function.
A second type of extracellular fluid is interstitial fluid that refers to fluid outside of blood
vessels and between the cells. For example, if you have ever cared for a patient with heart failure
and noticed increased swelling in the feet and ankles, you have seen an example of excess
interstitial fluid referred to as edema.
The remaining extracellular fluid, also called transcellular fluid, refers to fluid in areas such as
cerebrospinal, synovial, intrapleural, and gastrointestinal system.[3]

Fluid Movement
Fluid movement occurs inside the body due to osmotic pressure, hydrostatic pressure, and
osmosis. Proper fluid movement depends on intact and properly functioning vascular tissue
lining, normal levels of protein content within the blood, and adequate hydrostatic pressures
inside the blood vessels. Intact vascular tissue lining prevents fluid from leaking out of the blood
vessels. Protein content of the blood (in the form of albumin) causes oncotic pressure that holds
water inside the vascular compartment. For example, patients with decreased protein levels (i.e.,
low serum albumin) experience edema due to the leakage of intravascular fluid into interstitial
areas because of decreased oncotic pressure.
Hydrostatic pressure is defined as pressure that a contained fluid exerts on what is confining it.
In the intravascular fluid compartment, hydrostatic pressure is the pressure exerted by blood
against the capillaries. Hydrostatic pressure opposes oncotic pressure at the arterial end of
capillaries, where it pushes fluid and solutes out into the interstitial compartment. On the venous
end of the capillary, hydrostatic pressure is reduced, which allows oncotic pressure to pull fluids
and solutes back into the capillary.[4],[5] See Figure 15.2[6] for an illustration of hydrostatic pressure
and oncotic pressure in a capillary.

Figure 15.2
Hydrostatic Pressure
Filtration occurs when hydrostatic pressure pushes fluids and solutes through a permeable
membrane so they can be excreted. An example of this process is fluid and waste filtration
through the glomerular capillaries in the kidneys. This filtration process within the kidneys
allows excess fluid and waste products to be excreted from the body in the form of urine.
Fluid movement is also controlled through osmosis. Osmosis is water movement through a
semipermeable membrane, from an area of lesser solute concentration to an area of greater solute
concentration, in an attempt to equalize the solute concentrations on either side of the membrane.
Only fluids and some particles dissolved in the fluid are able to pass through a semipermeable
membrane; larger particles are blocked from getting through. Because osmosis causes fluid to
travel due to a concentration gradient and no energy is expended during the process, it is referred
to as passive transport.[7] See Figure 15.3[8] for an illustration of osmosis where water has moved
to the right side of the membrane to equalize the concentration of solutes on that side with the
left side.

Figure 15.3
Osmosis
Osmosis causes fluid movement between the intravascular, interstitial, and intracellular fluid
compartments based on solute concentration. For example, recall a time when you have eaten a
large amount of salty foods. The sodium concentration of the blood becomes elevated. Due to the
elevated solute concentration within the bloodstream, osmosis causes fluid to be pulled into the
intravascular compartment from the interstitial and intracellular compartments to try to equalize
the solute concentration. As fluid leaves the cells, they shrink in size. The shrinkage of cells is
what causes many symptoms of dehydration, such as dry, sticky mucous membranes. Because
the brain cells are especially susceptible to fluid movement due to osmosis, a headache may
occur if adequate fluid intake does not occur.

Solute Movement
Solute movement is controlled by diffusion, active transport, and filtration. Diffusion is the
movement of molecules from an area of higher concentration to an area of lower concentration to
equalize the concentration of solutes throughout an area. (Note that diffusion is different from
osmosis because osmosis is the movement of fluid whereas diffusion is the movement of
solutes.) See Figure 15.4[9] for an image of diffusion. Because diffusion travels down a
concentration gradient, the solutes move freely without energy expenditure. An example of
diffusion is the movement of inhaled oxygen molecules from alveoli to the capillaries in the
lungs so that they can be distributed throughout the body.

Figure 15.4
Diffusion
Active transport, unlike diffusion, involves moving solutes and ions across a cell membrane
from an area of lower concentration to an area of higher concentration. Because active transport
moves solutes against a concentration gradient to prevent an overaccumulation of solutes in an
area, energy is required for this process to take place.[10] An example of active transport is the
sodium-potassium pump, which uses energy to maintain higher levels of sodium in the
extracellular fluid and higher levels of potassium in the intracellular fluid. See Figure 15.5[11] for
an image of diffusion and the sodium-potassium pump regulating sodium and potassium levels in
the extracellular and intracellular compartments. Recall that sodium (Na+) is the primary
electrolyte in the extracellular space and potassium (K+) is the primary electrolyte in the
intracellular space.

Figure 15.5
Sodium-Potassium Pump

Fluid and Electrolyte Regulation

The body must carefully regulate intravascular fluid accumulation and excretion to prevent fluid
volume excesses or deficits and maintain adequate blood pressure. Water balance is regulated by
several mechanisms including ADH, thirst, and the Renin-Angiotensin-Aldosterone System
(RAAS).
Fluid intake is regulated by thirst. As fluid is lost and the sodium level increases in the
intravascular space, serum osmolality increases. Serum osmolality is a measure of the
concentration of dissolved solutes in the blood. Osmoreceptors in the hypothalamus sense
increased serum osmolarity levels and trigger the release of ADH (antidiuretic hormone) in the
kidneys to retain fluid. The osmoreceptors also produce the feeling of thirst to stimulate
increased fluid intake. However, individuals must be able to mentally and physically respond to
thirst signals to increase their oral intake. They must be alert, fluids must be accessible, and the
person must be strong enough to reach for fluids. When a person is unable to respond to thirst
signals, dehydration occurs. Older individuals are at increased risk of dehydration due to age-
related impairment in thirst perception. The average adult intake of fluids is about 2,500 mL per
day from both food and drink. An increased amount of fluids is needed if the patient has other
medical conditions causing excessive fluid loss, such as sweating, fever, vomiting, diarrhea, and
bleeding.
The Renin-Angiotensin-Aldosterone System (RAAS) plays an important role in regulating
fluid output and blood pressure. See Figure 15.6[12] for an illustration of the Renin-Angiotensin-
Aldosterone System (RAAS). When there is decreased blood pressure (which can be caused by
fluid loss), specialized kidney cells make and secrete renin into the bloodstream. Renin acts on
angiotensinogen released by the liver and converts it to angiotensin I, which is then converted to
angiotensin II. Angiotensin II does a few important things. First, angiotensin II causes
vasoconstriction to increase blood flow to vital organs. It also stimulates the adrenal cortex to
release aldosterone. Aldosterone is a steroid hormone that triggers increased sodium reabsorption
by the kidneys and subsequent increased serum osmolality in the bloodstream. As you recall,
increased serum osmolality causes osmosis to move fluid into the intravascular compartment in
an effort to equalize solute particles. The increased fluids in the intravascular compartment
increase circulating blood volume and help raise the person’s blood pressure. An easy way to
remember this physiological process is “aldosterone saves salt” and “water follows salt.” [13]

Figure 15.6
Renin Angiotensin Aldosterone System (RAAS)
Fluid output occurs mostly through the kidneys in the form of urine. Fluid is also lost through the
skin as perspiration, through the gastrointestinal tract in the form of stool, and through the lungs
during respiration. Forty percent of daily fluid output occurs due to these “insensible losses”
through the skin, gastrointestinal tract, and lungs and cannot be measured. The remaining 60% of
daily fluid output is in the form of urine. Normally, the kidneys produce about 1,500 mL of urine
per day when fluid intake is adequate. Decreased urine production is an early sign of dehydration
or kidney dysfunction. It is important for nurses to assess urine output in patients at risk. If a
patient demonstrates less than 30 mL/hour (or 0.5 mL/kg/hour) of urine output over eight hours,
the provider should be notified for prompt intervention. See Figure 15.7[14] for an illustration of
an average adult’s daily water balance of 2,500 mL fluid intake balanced with 2,500 mL fluid
output.

Figure 15.7
Water Balance
Fluid Imbalance
Two types of fluid imbalances are excessive fluid volume (also referred to as hypervolemia) and
deficient fluid volume (also referred to as hypovolemia). These imbalances primarily refer to
imbalances in the extracellular compartment, but can cause fluid movement in the intracellular
compartments based on the sodium level of the blood.

Excessive Fluid Volume

Excessive fluid volume (also referred to as hypervolemia) occurs when there is increased fluid
retained in the intravascular compartment. Patients at risk for developing excessive fluid volume
are those with the following conditions:
 Heart Failure
 Kidney Failure
 Cirrhosis
 Pregnancy[15]
Symptoms of fluid overload include pitting edema, ascites, and dyspnea and crackles from fluid
in the lungs. Edema is swelling in dependent tissues due to fluid accumulation in the interstitial
spaces. Ascites is fluid retained in the abdomen.
Treatment depends on the cause of the fluid retention. Sodium and fluids are typically restricted
and diuretics are often prescribed to eliminate the excess fluid. For more information about the
nursing care of patients with excessive fluid volume, see the “Applying the Nursing Process”
section.

Deficient Fluid Volume

Deficient fluid volume (also referred to as hypovolemia or dehydration) occurs when loss of
fluid is greater than fluid input. Common causes of deficient fluid volume are diarrhea, vomiting,
excessive sweating, fever, and poor oral fluid intake. Individuals who have a higher risk of
dehydration include the following:
 Older adults
 Infants and children
 Patients with chronic diseases such as diabetes mellitus and kidney disease
 Patients taking diuretics and other medications that cause increased urine output
 Individuals who exercise or work outdoors in hot weather[16]
In adults, symptoms of dehydration are as follows:
 Feeling very thirsty
 Dry mouth
  Headache
 Dry skin
 Urinating and sweating less than usual
 Dark, concentrated urine
 Feeling tired
 Changes in mental status
 Dizziness due to decreased blood pressure
 Elevated heart rate[17]
In infants and young children, additional symptoms of dehydration include the following:
 Crying without tears
 No wet diapers for three hours or more
 Being unusually sleepy or drowsy
 Irritability
 Eyes that look sunken
 Sunken fontanel[18]
Dehydration can be mild and treated with increased oral intake such as water or sports drinks.
Severe cases can be life-threatening and require the administration of intravenous fluids.
For more information about water balance and fluid movement, review the following video.

Video Review of Fluid and Electrolytes[19]

References
1.

3.0 ↵.
“Cellular_Fluid_Content.jpg” by Welcome1To1The1Jungle is licensed under CC BY

Fluid. (2012). In Britannica. https://www.britannica.com/science/fluid-biology ↵.

2.

3.

under CC BY 4.0 ↵.
This work is a derivative of StatPearls by Brinkman, Dorius, and Sharma and is licensed

4.

under CC BY 4.0 ↵.
This work is a derivative of StatPearls by Brinkman, Dorius, and Sharma and is licensed

"Hydrostatic Pressure" by Ann Lawrie is licensed under CC BY-NC 2.0 ↵.

5.

6.
 “Capillary_microcirculation.jpg” by Kes47 is in the Public Domain ↵.
7.

.bbc.co.uk/bitesize/guides/zc9tyrd/revision/5 ↵.
BBC. (n.d.) Movement across cell membranes. https://www

8.

at https://openstax.org/books/anatomy-and-physiology/pages/3-1-the-cell-membrane ↵.
“0307_Osmosis.jpg” by OpenStax is licensed under CC BY 4.0. Access for free

“Simple_Diffusion.png” by Elizabeth2424 is licensed under CC BY-SA 3.0 ↵.

9.

10.

.bbc.co.uk/bitesize/guides/zc9tyrd/revision/5 ↵.
BBC. (n.d.) Movement across cell membranes. https://www

11.

under CC BY 3.0 ↵.
“Sodium-potassium_pump_and_diffusion.png” by BruceBlaus.com staff is licensed

12.
“2626_Renin_Aldosterone_Angiotensin.jpg” by OpenStax is licensed under CC BY 3.0.

microscopic-anatomy-of-the-kidney ↵.
Access for free at https://openstax.org/books/anatomy-and-physiology/pages/25-4-

13.

BY 4.0 ↵.
This work is a derivative of StatPearls by Fountain and Lappin and is licensed under CC

"Water_balance.png" by David Walsh and Alan Sved is licensed under CC BY-SA 4.0 ↵.
14.

15.
Lewis, J. L., III. (June 2020). Volume overload. Merck Manual Professional

disorders/fluid-metabolism/volume-overload ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

16.
MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US);

5]. https://medlineplus.gov/dehydration.html ↵.
Dehydration; [updated 2020, Oct 1; reviewed 2016, Apr 15; cited 2020, Aug

17.
MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US);

5]. https://medlineplus.gov/dehydration.html ↵.
Dehydration; [updated 2020, Oct 1; reviewed 2016, Apr 15; cited 2020, Aug

18.
MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US);

5]. https://medlineplus.gov/dehydration.html ↵.
Dehydration; [updated 2020, Oct 1; reviewed 2016, Apr 15; cited 2020, Aug

19.

rights reserved. Video used with permission. https://youtu.be/VMxmDeduKR0 ↵.

Forciea, B. (2017, April 21). Fluids and electrolytes: Water. [Video]. YouTube. All

Go to:

15.3. INTRAVENOUS SOLUTIONS

When patients experience deficient fluid volume, intravenous (IV) fluids are often prescribed. IV
fluid restores fluid to the intravascular compartment, and some IV fluids are also used to
facilitate the movement of fluid between compartments due to osmosis. There are three types of
IV fluids: isotonic, hypotonic, and hypertonic.

Isotonic Solutions
Isotonic solutions are IV fluids that have a similar concentration of dissolved particles as blood.
An example of an isotonic IV solution is 0.9% Normal Saline (0.9% NaCl). Because the
concentration of the IV fluid is similar to the blood, the fluid stays in the intravascular space and
osmosis does not cause fluid movement between compartments. See Figure 15.8[1] for an
illustration of isotonic IV solution administration with no osmotic movement of fluid with cells.
Isotonic solutions are used for patients with fluid volume deficit (also called hypovolemia) to
raise their blood pressure. However, infusion of too much isotonic fluid can cause excessive fluid
volume (also referred to as hypervolemia).

Figure 15.8
Lack of Fluid Movement When Isotonic IV Solution Is Administered

Hypotonic Solutions
Hypotonic solutions have a lower concentration of dissolved solutes than blood. An example of
a hypotonic IV solution is 0.45% Normal Saline (0.45% NaCl). When hypotonic IV solutions are
infused, it results in a decreased concentration of dissolved solutes in the blood as compared to
the intracellular space. This imbalance causes osmotic movement of water from the intravascular
compartment into the intracellular space. For this reason, hypotonic fluids are used to treat
cellular dehydration. See Figure 15.9[2] for an illustration of the osmotic movement of fluid into a
cell when a hypotonic IV solution is administered, causing lower concentration of solutes (pink
molecules) in the bloodstream compared to within the cell.

Figure 15.9
Hypotonic IV Solution Causing Osmotic Movement of Fluid Into Cell
However, if too much fluid moves out of the intravascular compartment into cells, cerebral
edema can occur. It is also possible to cause worsening hypovolemia and hypotension if too
much fluid moves out of the intravascular space and into the cells. Therefore, patient status
should be monitored carefully when hypotonic solutions are infused.

Hypertonic Solutions
Hypertonic solutions have a higher concentration of dissolved particles than blood. An example
of hypertonic IV solution is 3% Normal Saline (3% NaCl). When infused, hypertonic fluids
cause an increased concentration of dissolved solutes in the intravascular space compared to the
cells. This causes the osmotic movement of water out of the cells and into the intravascular space
to dilute the solutes in the blood. See Figure 15.10[3] for an illustration of osmotic movement of
fluid out of a cell when hypertonic IV fluid is administered due to a higher concentration of
solutes (pink molecules) in the bloodstream compared to the cell.

Figure 15.10
Hypertonic IV Solution Causing Osmotic Fluid Movement Out of a Cell
When administering hypertonic fluids, it is essential to monitor for signs of hypervolemia such
as breathing difficulties and elevated blood pressure. Additionally, if hypertonic solutions with
sodium are given, the patient’s serum sodium level should be closely monitored.[4] See Table
15.3 for a comparison of types of IV solutions, their uses, and nursing considerations.

Table 15.3
Comparison of IV Solutions[6]
See Figure 15.11[5] for an illustration comparing how different types of IV solutions affect red
blood cell size.
Figure 15.11
Comparison of Osmotic Effects of Hypertonic, Isotonic, and Hypotonic IV Fluids on Red Blood
Cells

Osmolarity is defined as the proportion of dissolved particles in an amount of

fluid and is generally the term used to describe body fluids. As the dissolved
particles become more concentrated, the osmolarity increases. Osmolality refers
to the proportion of dissolved particles in a specific weight of fluid. The terms
osmolarity and osmolality are often used interchangeably in clinical practice.

References
1.

under CC BY 3.0 ↵.
“Blausen_0685_OsmoticFlow_Isotonic.png” by BruceBlaus.com staff is licensed

2.

under CC BY 3.0 ↵.
“Blausen_0684_OsmoticFlow_Hypotonic.png” by BruceBlaus.com staff is licensed

3.

under CC BY 3.0 ↵.
“Blausen_0683_OsmoticFlow_Hypertonic.png” by BruceBlaus.com staff is licensed

Harris, H. (2011). I.V. fluids: What nurses need to know. Nursing2017, 41(5), 30-38. ↵.
4.

[PubMed]

“Osmotic pressure on blood cells diagram.svg” by LadyofHats is in the Public Domain ↵.

5.

Harris, H. (2011). I.V. fluids: What nurses need to know. Nursing2017, 41(5), 30-38. ↵.
6.

[PubMed]
Go to:
15.4. ELECTROLYTES
Electrolytes play an important role in bodily functions and fluid regulation. There is a very
narrow target range for normal electrolyte values, and slight abnormalities can have devastating
consequences. For this reason, it is crucial to understand normal electrolyte ranges, causes of
electrolyte imbalances, signs and symptoms of imbalances, and appropriate treatments.

Sodium
Sodium levels in the blood typically range from 136-145 mEq/L.[1] Refer to each agency’s
normal reference range on the lab report. Sodium is the most abundant electrolyte in the
extracellular fluid (ECF) and is maintained by the sodium-potassium pump. Sodium plays an
important role in maintaining adequate fluid balance in the intravascular and interstitial spaces.
See the “Fluid and Electrolyte Regulation” section of this chapter for more information about
how the body regulates sodium and water balance.
Hypernatremia refers to an elevated sodium level in the blood. Typically, hypernatremia is
caused by excess water loss due to lack of fluid intake, vomiting, or diarrhea. As you recall,
elevated sodium levels in the blood cause the osmotic movement of water out of the cells to
dilute the blood. This causes the body’s cells to shrink, referred to as cellular dehydration. This
fluid shift can have a significant impact on various organs within the body and is especially
notable in the patient’s neurological function. As fluid shifts out of the brain cells, the nurse may
notice symptoms such as confusion, irritability, lethargy, and even seizures. Other signs and
symptoms of hypernatremia include severe thirst and sticky mucous membranes. See Figure
15.12[2]for an illustration of a patient with severe thirst due to hypernatremia. Treatment for
hypernatremia includes decreasing sodium intake, increasing oral water intake, and rehydrating
with a hypotonic IV solution.[3],[4]

Figure 15.12
Hypernatremia
Hyponatremia refers to a decreased sodium level in the blood. Hyponatremia can be caused by
excess water intake or excessive administration of hypotonic IV solutions. For example, a
marathon runner who only rehydrates with water (without other fluids with solutes like
Gatorade) can develop hyponatremia. As with hypernatremia, altered sodium levels often cause
neurological symptoms due to the movement of water into brain cells, causing them to swell.
Symptoms of hyponatremia are headache, confusion, seizures, and coma. Treatment for
hyponatremia depends on the cause and often consists of limiting water intake or discontinuing
administration of hypotonic IV fluids. If hyponatremia is severe, a hypertonic IV saline solution
may be prescribed to gradually raise the patient’s sodium level.[5]

Video Review of Fluids and Electrolytes: Sodium [6]

Potassium
Potassium levels normally range from 3.5 to 5.1 mEq/L.[7] Refer to each agency’s normal
reference range on the lab report. Potassium is the most abundant electrolyte in intracellular fluid
and is maintained inside the cell by the sodium-potassium pump. Potassium is regulated by
aldosterone in the kidneys and is obtained in the diet through consumption of foods such as
bananas, oranges, and tomatoes. See Figure 15.13[8] for an illustration of potassium regulation by
aldosterone. Recall that aldosterone causes reabsorption of sodium and excretion of potassium in
the distal tubule of the kidneys. In response to potassium levels rising or sodium levels falling in
the bloodstream, the adrenal cortex releases aldosterone and targets the kidneys. In response, the
kidneys excrete potassium and reabsorb sodium. Potassium is also impacted by the hormone
insulin that moves potassium into the cells from the ECF.[9]

Figure 15.13
Potassium Regulation by Aldosterone
Potassium is necessary for normal cardiac function, neural function, and muscle contractility,
including effective contractility of the cardiac muscles. Abnormal potassium levels can cause
significantly abnormal heart rhythms and contractility. Potassium is poorly conserved by the
body and much is lost with urine output. For this reason, it is often necessary to provide
potassium supplements when administering loop and thiazide diuretics because potassium is
excreted from the kidneys along with water.[10] Potassium supplementation can be given orally or
by IV infusion mixed with fluids. Potassium must NEVER be administered IV push because it
can immediately stop the heart.
Hyperkalemia refers to increased potassium levels in the blood. Hyperkalemia can be caused by
kidney failure, metabolic acidosis, and administration of potassium-sparing diuretics or
oral/intravenous potassium supplements. Signs and symptoms of hyperkalemia are generally
cardiac in nature and include irritability, cramping, diarrhea, and electrocardiogram (ECG)
abnormalities. As hyperkalemia worsens, ECG abnormalities may progress to cardiac
dysrhythmias and cardiac arrest.
Treatment for hyperkalemia depends on the severity of the hyperkalemia symptoms. For mild
symptoms, decreased potassium intake in the diet is helpful. Adjustment to medications
contributing to increased levels of potassium may be indicated. For severe symptoms,
administration of sodium polystyrene sulfonate (Kayexalate) orally or rectally helps bind excess
potassium so it is excreted through the GI tract. Insulin may be administered to push potassium
into cells and decrease serum potassium levels. When administering an insulin infusion, it is
important to monitor blood glucose levels closely, often hourly per agency policy. The patient
often requires supplemental IV dextrose to prevent low blood sugar levels when insulin is used
for potassium reduction. IV calcium gluconate may also be given to prevent excess potassium
from affecting cardiac muscle. This is a temporary measure and wears off quickly but allows
time for other treatments to take effect and lower potassium levels before cardiac arrest develops.
For severe symptomatic hyperkalemia, temporary hemodialysis may also be used to quickly
decrease potassium levels.[11]
Hypokalemia refers to decreased potassium level in the blood. Hypokalemia can be caused by
excessive vomiting, diarrhea, potassium-wasting diuretics, and insulin use, as well as lack of
potassium in the diet. Signs and symptoms of hypokalemia include weakness, arrhythmias,
lethargy, and a thready pulse. View helpful mnemonics for hypokalemia using the following
hyperlink. Treatment for hypokalemia includes increasing oral intake of potassium in the diet
and oral or IV potassium in fluids supplementation. It is important to remember that
administering IV potassium too quickly can cause cardiac arrest. In fact, potassium is one of the
ingredients used during lethal injection to stop the heart.

View helpful mnemonics for hypokalemia at Hypokalemia NCLEX Review Notes.

Video Review About Potassium[12]

Calcium
Calcium levels normally range from 8.6-10.2 mg/dL.[13] Refer to each agency’s normal reference
range on the lab report. Calcium circulates in the bloodstream, but the majority is stored in
bones. Calcium is important for bone and teeth structure, nerve transmission, and muscle
contraction. Calcium excretion and reabsorption are regulated by the parathyroid hormone (PTH)
that is secreted from the parathyroid glands near the thyroid. See Figure 15.14[14] for an
illustration of the parathyroid glands. As PTH is secreted in response to low calcium levels in the
blood, calcium is reabsorbed in both the kidneys and the intestine and released from the bones to
increase serum calcium levels. Calcium is also affected by dietary intake and physical activity.
Activity causes calcium to move into bones whereas immobility causes the release of calcium
from bones, which cases them to become weak. Dietary sources of calcium include dairy
products, green leafy vegetables, sardines, and whole grains.[15]

Figure 15.14
Parathyroid Glands
Hypercalcemia refers to an increased calcium level. It can be caused by prolonged
immobilization that allows calcium to leach out of the bones and into the serum. Additionally,
there are many types of cancers that may cause excessive calcium release from bones.
Hypercalcemia can also be caused by hyperparathyroidism and parathyroid tumors, which can
cause too much PTH secretion, causing too much calcium to be reabsorbed in the kidneys and
intestines and released from bone.
Signs and symptoms of hypercalcemia often impact the gastrointestinal and musculoskeletal
systems. These symptoms include nausea, vomiting, constipation, increased thirst and/or
urination, and skeletal muscle weakness. Treatment for hypercalcemia includes decreasing
calcium intake in the diet, phosphate supplementation (which has an inverse relationship to
calcium), hemodialysis, surgical removal of the parathyroid gland (if hyperparathyroidism is
causing the hypercalcemia), and weight-bearing exercises as tolerated.[16]
Hypocalcemia refers to a decreased calcium level in the blood. Hypocalcemia can be caused by
hypoparathyroidism where not enough PTH is excreted, causing a decreased reabsorption of
calcium and decreased release of calcium from the bones. Hypocalcemia is also caused by
vitamin D deficiency and renal disease. Because phosphorus is inversely related to calcium, an
abnormally high phosphorus level as seen with renal failure can also result in hypocalcemia.
Signs and symptoms of hypocalcemia often impact the musculoskeletal and nervous systems.
These include paresthesias (numbness and tingling) of the lips, tongue, hands and feet, muscle
cramps, and tetany. Chvostek’s sign is a classic sign of acute hypocalcemia and is an
involuntary twitching of facial muscles when the facial nerve is tapped. A second classic sign of
acute hypocalcemia is Trousseau’s sign where a hand spasm is caused by inflating a blood
pressure cuff to a level above systolic pressure for 3 minutes. See a video of a patient
experiencing Chvostek’s and Trousseau’s signs in the hyperlink below. Treatment of
hypocalcemia includes increasing oral intake of dietary calcium and vitamin D and oral or IV
calcium supplementation and decreasing the phosphorus level if it is elevated.[17]

View a video of a patient exhibiting Chvostek’s Sign and Trousseau’s Signs of

hypocalcemia.

Phosphorus
Phosphorus levels typically range from 2.5-4.0 mg/dL. Refer to each agency’s normal reference
range on the lab report. Phosphorus is stored in the bones and is predominantly found in the ICF
with small amounts in the ECF. Phosphorus is important in energy metabolism, RNA and DNA
formation, nerve function, muscle contraction, and for bone, teeth, and membrane building and
repair. Phosphorus is excreted by the kidneys and absorbed by the intestines. Dietary phosphorus
sources include dairy products, fruits, vegetables, meat, and cereal.[18]
Hyperphosphatemia refers to an increased phosphorus level in the blood and can be caused by
kidney disease, crush injuries, or overuse of phosphate-containing enemas. Hyperphosphatemia
itself is usually asymptomatic, but signs of associated hypocalcemia may be present due to the
inverse relationship between phosphorus and calcium. Treatment for hyperphosphatemia
includes decreasing intake of phosphorus, administration of phosphate-binder medications to
help with excretion, and hemodialysis.[19]
Hypophosphatemia is a decreased phosphorus level in the blood. Acute hypophosphatemia can
be caused by acute alcohol abuse, burns, diuretic use, respiratory alkalosis, resolving diabetic
ketoacidosis, and starvation. Chronic hypophosphatemia is caused by hyperparathyroidism,
vitamin D deficiency, prolonged use of phosphate binders, and hypomagnesemia or
hypokalemia. Hypophosphatemia is usually asymptomatic, but in severe cases, it can cause
muscle weakness, anorexia, encephalopathy, seizures, and death. Treatment for
hypophosphatemia includes treating what is causing the imbalance, oral or IV phosphorus
replacement, and increased phosphate-containing foods in the diet.[20]

Magnesium
Magnesium levels typically range from 1.5-2.4 mEq/L. Refer to each agency’s reference range
on the lab report. Magnesium is essential for normal cardiac, nerve, muscle, and immune system
functioning. About half of the body’s magnesium is stored in the bones. About 1% is stored in
ECF and the rest is found in ICF.[21] Dietary sources of magnesium include green leafy
vegetables, citrus, peanut butter, almonds, legumes, and chocolate.
Hypermagnesemia refers to an elevated magnesium level in the blood. It is usually the result of
renal failure, excess magnesium replacement, or use of magnesium containing laxatives or
antacids. Signs and symptoms of hypermagnesemia include bradycardia, weak and thready pulse,
lethargy, tremors, hyporeflexia, muscle weakness, and cardiac arrest. Treatment for
hypermagnesemia involves increasing fluid intake, discontinuing magnesium-containing
medications, and in severe cases, hemodialysis or peritoneal dialysis. Additionally,
administration of calcium gluconate can be helpful to reduce the cardiac effects of
hypermagnesemia until the magnesium level can be lowered.[22]
Hypomagnesemia refers to decreased magnesium level in the blood. It typically results from
inadequate magnesium in the diet, or from loop diuretics that excrete magnesium. Patients with
alcohol use disorder often have hypomagnesemia due to concurrent poor diet and impaired
nutrient absorption that occurs with alcohol consumption. Chronic proton pump inhibitor use can
also cause hypomagnesemia due to impaired nutrient absorption.
Signs and symptoms of hypomagnesemia include nausea, vomiting, lethargy, weakness, leg
cramps, tremor, dysrhythmias, and tetany that is associated with concurrent hypocalcemia that
can occur with hypomagnesemia. Treatment for hypomagnesemia consists of increasing dietary
intake of magnesium containing foods and oral or IV magnesium supplementation.[23]
See Table 15.4 for a comparison of causes, symptoms, and treatments of different electrolyte
imbalances. As always, refer to agency lab reference ranges when providing patient care.

Table 15.4
Comparison of Causes, Symptoms, and Treatments of Imbalanced Electrolyte Levels

References

Lab Tests Online. (2019). Sodium. https://labtestsonline.org/tests/sodium ↵.

1.
 “thirsty-4294629_960_720.png” by Conmongt is licensed under CC0 ↵.
2.

3.
Lewis, J. L., III. (April 2020). Hypernatremia. Merck Manual Professional

disorders/electrolyte-disorders/hypernatremia ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

4.

under CC BY 4.0 ↵.
This work is a derivative of StatPearls by Brinkman, Dorius, and Sharma and is licensed

5.
Lewis, J. L., III. (April 2020). Hyponatremia. Merck Manual Professional

disorders/electrolyte-disorders/hyponatremia ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

6.

Rights Reserved. Video used with permission. https://youtu.be/ar-WrfC7SJs ↵.

Forciea, B.(2017, April 24). Fluids and electrolytes sodium. [Video]. YouTube. All

Lab Tests Online. (2019). Potassium. https://labtestsonline.org/tests/potassium ↵.

7.

8.
“2711_Aldosterone_Feedback_Loop-01.jpg” by OpenStax College is licensed under CC

3-electrolyte-balance ↵.
BY 3.0. Access for free at https://openstax.org/books/anatomy-and-physiology/pages/26-

9.
This work is a derivative of Anatomy & Physiology by OpenStax and is licensed

/pages/1-introduction ↵.
under CC BY 4.0. Access for free at https://openstax.org/books/anatomy-and-physiology

10.
Lewis, J. L., III. (April 2020). Overview of disorders of potassium concentration. Merck
Manual Professional Version. https://www.merckmanuals.com/professional/endocrine-

concentration ↵.
and-metabolic-disorders/electrolyte-disorders/overview-of-disorders-of-potassium-

11.
Lewis, J. L., III. (April 2020). Hyperkalemia. Merck Manual Professional

disorders/electrolyte-disorders/hyperkalemia ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

12.

rights reserved. Video used with permission. https://youtu.be/SNAiGaaYkvs ↵.

Forciea, B. (2017, April 26). Fluids and electrolytes potassium. [Video]. YouTube. All

Lab Tests Online. (2017). Calcium. https://labtestsonline.org/tests/calcium ↵.

13.

14.
"1814_The_Parathyroid_Glands.jpg” by OpenStax is licensed under CC BY 3.0. Access

parathyroid-glands ↵.
for free at https://openstax.org/books/anatomy-and-physiology/pages/17-5-the-

15.
 Lewis, J. L., III. (April 2020). Overview of disorders of calcium concentration. Merck
Manual Professional Version. https://www.merckmanuals.com/professional/endocrine-

concentration ↵.
and-metabolic-disorders/electrolyte-disorders/overview-of-disorders-of-calcium-

16.
Lewis, J. L., III. (April 2020). Hypercalcemia. Merck Manual Professional

disorders/electrolyte-disorders/hypercalcemia ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

17.
Lewis, J. L., III. (April 2020). Hypocalcemia. Merck Manual Professional

disorders/electrolyte-disorders/hypocalcemia ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

18.
Lewis, J. L., III. (April 2020). Overview of disorders of phosphate concentration. Merck
Manual Professional Version. https://www.merckmanuals.com/professional/endocrine-

concentration ↵.
and-metabolic-disorders/electrolyte-disorders/overview-of-disorders-of-phosphate-

19.
Lewis, J. L., III. (April 2020). Hyperphosphatemia. Merck Manual Professional

disorders/electrolyte-disorders/hyperphosphatemia ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

20.
Lewis, J. L., III. (April 2020). Hypophosphatemia. Merck Manual Professional

disorders/electrolyte-disorders/hypophosphatemia ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

21.
Lewis, J. L., III. (April 2020). Overview of disorders of magnesium concentration. Merck
Manual Professional Version. https://www.merckmanuals.com/professional/endocrine-

concentration ↵.
and-metabolic-disorders/electrolyte-disorders/overview-of-disorders-of-magnesium-

22.
Lewis, J. L., III. (April 2020). Hypermagnesemia. Merck Manual Professional

disorders/electrolyte-disorders/hypermagnesemia ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

23.
Lewis, J. L., III. (April 2020). Hypomagnesemia. Merck Manual Professional

disorders/electrolyte-disorders/hypomagnesemia 7/7/20 ↵.
Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-

Go to:

15.5. ACID-BASE BALANCE

As with electrolytes, correct balance of acids and bases in the body is essential to proper body
functioning. Even a slight variance outside of normal can be life-threatening, so it is important to
understand normal acid-base values, as well their causes and how to correct them. The kidneys
and lungs work together to correct slight imbalances as they occur. As a result, the kidneys
compensate for shortcomings of the lungs, and the lungs compensate for shortcomings of the
kidneys.

Arterial Blood Gases

Arterial blood gases (ABG) are measured by collecting blood from an artery, rather than a vein,
and are most commonly collected via the radial artery. ABGs measure the pH level of the blood,
the partial pressure of arterial oxygen (PaO2), the partial pressure of arterial carbon dioxide
(PaCO2), the bicarbonate level (HCO3), and the oxygen saturation level (SaO2).

Prior to collecting blood gases, it is

important to ensure the patient has appropriate arterial blood flow to the hand.
This is done by performing the Allen test. When performing the Allen test,
pressure is held on both the radial and ulnar artery below the wrist. Pressure is
released from the ulnar artery to check if blood flow is adequate. If arterial blood
flow is adequate, warmth and color should return to the hand.

pH
pH is a scale from 0-14 used to determine the acidity or alkalinity of a substance. A neutral pH is
7, which is the same pH as water. Normally, the blood has a pH between 7.35 and 7.45. A blood
pH of less than 7.35 is considered acidic, and a blood pH of more than 7.45 is considered
alkaline.
The pH of blood is a measure of hydrogen ion concentration. A low pH, less than 7.35, occurs in
acidosis when the blood has a high hydrogen ion concentration. A high pH, greater than 7.45,
occurs in alkalosis when the blood has a low hydrogen ion concentration. Hydrogen ions are by-
products of the metabolism of substances such as proteins, fats, and carbohydrates. These by-
products create extra hydrogen ions (H+) in the blood that need to be balanced and kept within
normal range as described earlier.
The body has several mechanisms for maintaining blood pH. The lungs are essential for
maintaining pH and the kidneys also play a role. For example, when the pH is too low (i.e.,
during acidosis), the respiratory rate quickly increases to eliminate acid in the form of carbon
dioxide (CO2). The kidneys excrete additional hydrogen ions (acid) in the urine and retain
bicarbonate (base). Conversely, when the pH is too high (i.e., during alkalosis), the respiratory
rate decreases to retain acid in the form of CO2. The kidneys excrete bicarbonate (base) in the
urine and retain hydrogen ions (acid).

PaCO2
PaCO2 is the partial pressure of arterial carbon dioxide in the blood. The normal PaCO2 level is
35-45 mmHg. CO2 forms an acid in the blood that is regulated by the lungs by changing the rate
or depth of respirations.
As the respiratory rate increases or becomes deeper, additional CO2 is removed causing
decreased acid (H+) levels in the blood and increased pH (so the blood becomes more alkaline).
As the respiratory rate decreases or becomes more shallow, less CO2 is removed causing
increased acid (H+) levels in the blood and decreased pH (so the blood becomes more acidic).
Generally, the lungs work quickly to regulate the PaCO2 levels and cause a quick change in the
pH. Therefore, an acid-base problem caused by hypoventilation can be quickly corrected by
increasing ventilation, and a problem caused by hyperventilation can be quickly corrected by
decreasing ventilation. For example, if an anxious patient is hyperventilating, they may be asked
to breathe into a paper bag to rebreathe some of the CO2 they are blowing off. Conversely, a
postoperative patient who is experiencing hypoventilation due to the sedative effects of receiving
morphine is asked to cough and deep breathe to blow off more CO2.

HCO3
HCO3 is the bicarbonate level of the blood and the normal range is 22-26. HCO3 is a base
managed by the kidneys and helps to make the blood more alkaline. The kidneys take longer
than the lungs to adjust the acidity or alkalinity of the blood, and the response is not visible upon
assessment. As the kidneys sense an alteration in pH, they begin to retain or excrete HCO3,
depending on what is needed. If the pH becomes acidic, the kidneys retain HCO3 to increase the
amount of bases present in the blood to increase the pH. Conversely, if the pH becomes alkalotic,
the kidneys excrete more HCO3, causing the pH to decrease.

PaO2
PaO2 is the partial pressure of arterial oxygen in the blood. It more accurately measures a
patient’s oxygenation status than SaO2 (the measurement of hemoglobin saturation with
oxygen). Therefore, ABG results are also used to manage patients in respiratory distress.

Read more information about interpreting ABG results in the “Oxygen Therapy”
chapter in Open RN Nursing Skills.
See Table 15.5a for a review of ABG components, normal values, and key critical values. A
critical ABG value means there is a greater risk of serious complications and even death if not
corrected rapidly. For example, a pH of 7.10, a shift of only 0.25 below normal, is often fatal
because this level of acidosis can cause cardiac or respiratory arrest or significant hyperkalemia.
[1]
As you can see, failure to recognize ABG abnormalities can have serious consequences for
your patients.

Table 15.5a
ABG Components, Descriptions, Adult Normal Values, and Critical Values[2]

Video Review of Acid-Base Balance[3]

Interpreting Arterial Blood Gases

After the ABG results are received, it is important to understand how to interpret them. A variety
of respiratory, metabolic, electrolyte, or circulatory problems can cause acid-base imbalances.
Correct interpretation also helps the nurse and other health care providers determine the
appropriate treatment and evaluate the effectiveness of interventions.
Arterial blood gasses can be interpreted as one of four conditions: respiratory acidosis,
respiratory alkalosis, metabolic acidosis, or metabolic alkalosis. Once this interpretation is made,
conditions can further be classified as compensated, partially compensated, or uncompensated. A
simple way to remember how to interpret ABGs is by using the ROME method of interpretation,
which stands for Respiratory Opposite, Metabolic Equal. This means that the respiratory
component (PaCO2) moves in the opposite direction of the pH if the respiratory system is
causing the imbalance. If the metabolic system is causing the imbalance, the metabolic
component (HCO3) moves in the same direction as the pH. Some nurses find the Tic-Tac-Toe
method of interpretation helpful. If you would like to learn more about this method, click on the
hyperlink below to view a video.

Review of Tic-Tac-Toe Method of ABG Interpretation [4]

Respiratory Acidosis
Respiratory acidosis develops when carbon dioxide (CO2) builds up in the body (referred to
as hypercapnia), causing the blood to become increasingly acidic. Respiratory acidosis is
identified when reviewing ABGs and the pH level is below 7.35 and the PaCO2 level is above
45, indicating the cause of the acidosis is respiratory. Note that in respiratory acidosis, as the
PaCO2 level increases, the pH level decreases. Respiratory acidosis is typically caused by a
medical condition that decreases the exchange of oxygen and carbon dioxide at the alveolar
level, such as an acute asthma exacerbation, chronic obstructive pulmonary disease (COPD), or
an acute heart failure exacerbation causing pulmonary edema. It can also be caused by decreased
ventilation from anesthesia, alcohol, or administration of medications such as opioids and
sedatives.
Chronic respiratory diseases, such as COPD, often cause chronic respiratory acidosis that is fully
compensated by the kidneys retaining HCO3. Because the carbon dioxide levels build up over
time, the body adapts to elevated PaCO2 levels so they are better tolerated. However, in acute
respiratory acidosis, the body has not had time to adapt to elevated carbon dioxide levels,
causing mental status changes associated with hypercapnia. Acute respiratory acidosis is caused
by acute respiratory conditions, such as an asthma attack or heart failure exacerbation with
pulmonary edema when the lungs suddenly are not able to ventilate adequately. As breathing
slows and respirations become shallow, less CO2 is excreted by the lungs and PaCO2 levels
quickly rise.
Signs of symptoms of hypercapnia vary depending upon the level and rate of CO2 accumulation
in arterial blood:
 Patients with mild to moderate hypercapnia may be anxious and/or complain of mild
dyspnea, daytime sluggishness, headaches, or hypersomnolence.
 Patients with higher levels of CO2 or rapidly developing hypercapnia develop delirium,
paranoia, depression, and confusion that can progress to seizures and coma as levels
continue to rise.
Individuals with normal lung function typically exhibit a depressed level of consciousness when
the PaCO2 is greater than 75 to 80 mmHg, whereas patients with chronic hypercapnia may not
develop symptoms until the PaCO2 rises above 90 to 100 mmHg.[5]
When a patient demonstrates signs of potential hypercapnia, the nurse should assess airway,
breathing, and circulation. Urgent assistance should be sought, especially if the patient is in
respiratory distress. The provider will order an ABG and prescribe treatments based on
assessment findings and potential causes. Treatment for respiratory acidosis typically involves
improving ventilation and respiration by removing airway restrictions, reversing oversedation,
administering nebulizer treatments, or increasing the rate and depth of respiration by using a
BiPAP or CPAP devices. BiPAP and CPAP devices provide noninvasive positive pressure
ventilation to increase the depth of respirations, remove carbon dioxide, and oxygenate the
patient. If these noninvasive interventions are not successful, the patient is intubated and placed
on mechanical ventilation.[6],[7]

Read more details about oxygenation equipment in “Oxygen Therapy” in Open

RN Nursing Skills.

Respiratory Alkalosis
Respiratory alkalosis develops when the body removes too much carbon dioxide through
respiration, resulting in increased pH and an alkalotic state. When reviewing ABGs, respiratory
alkalosis is identified when pH levels are above 7.45 and the PaCO2 level is below 35. With
respiratory alkalosis, notice that as the PaCO2 level decreases, the pH level increases.
Respiratory alkalosis is caused by hyperventilation that can occur due to anxiety, panic attacks,
pain, fear, head injuries, or mechanical ventilation. Overdoses of salicylates and other toxins can
also cause respiratory alkalosis initially and then often progress to metabolic acidosis in later
stages. Acute asthma exacerbations, pulmonary embolisms, or other respiratory disorders can
initially cause respiratory alkalosis as the lungs breath faster in an attempt to increase
oxygenation, which decreases the PaCO2. After a while, however, these hypoxic disorders cause
respiratory acidosis as respiratory muscles tire, breathing slows, and CO2 builds up in the blood.
Patients experiencing respiratory alkalosis often report feelings of shortness of breath, dizziness
or light-headedness, chest pain or tightness, paresthesias, and palpitations as a result of decreased
carbon dioxide levels.[8] Respiratory alkalosis is not fatal, but it is important to recognize that
underlying conditions such as an asthma exacerbation or pulmonary embolism can be life-
threatening, so treatment of these underlying conditions is essential. As the pH level increases,
the kidneys will attempt to compensate for the shortage of H+ ions by reabsorbing HCO3 before
it can be excreted in the urine. This is a slow process, so additional treatment may be necessary.
Treatment of respiratory alkalosis involves treating the underlying cause of the hyperventilation.
Acute management of patients who are hyperventilating should focus on patient reassurance, an
explanation of the symptoms the patient is experiencing, removal of any stressors, and initiation
of breathing retraining. Breathing retraining attempts to focus the patient on abdominal
(diaphragmatic) breathing. Read more about breathing retraining in the following box.

Breathing Retraining
While sitting or lying supine, the patient should place one hand on their abdomen and the other
on the chest, and then be asked to observe which hand moves with greater excursion. In
hyperventilating patients, this will almost always be the hand on the chest. Ask the patient to
adjust their breathing so that the hand on the abdomen moves with greater excursion and the
hand on the chest barely moves at all. Assure the patient that this is hard to learn and will take
some practice to fully master. Ask the patient to breathe in slowly over four seconds, pause for a
few seconds, and then breathe out over a period of eight seconds. After 5 to 10 such breathing
cycles, the patient should begin to feel a sense of calmness with a reduction in anxiety and an
improvement in hyperventilation. Symptoms should ideally resolve with continuation of this
breathing exercise.
If the breathing retraining technique is not successful in resolving a hyperventilation episode and
severe symptoms persist, the patient may be prescribed a small dose of a short-acting
benzodiazepine (e.g., lorazepam 0.5 to 1 mg orally or 0.5 to 1 mg intravenously). Current
research indicates that instructing patients who are hyperventilating to rebreathe carbon dioxide
(CO2) by breathing into a paper bag can cause significant hypoxemia with significant
complications, so this intervention is no longer recommended. If rebreathing is used, oxygen
saturation levels should be continuously monitored.[9]
Metabolic Acidosis
Metabolic acidosis occurs when there is an accumulation of acids (hydrogen ions) and not
enough bases (HCO3) in the body. Under normal conditions, the kidneys work to excrete acids
through urine and neutralize excess acids by increasing bicarbonate (HCO3) reabsorption from
the urine to maintain a normal pH. When the kidneys are not able to perform this buffering
function to the level required to excrete and neutralize the excess acid, metabolic acidosis results.
Metabolic acidosis is characterized by a pH level below 7.35 and an HCO3 level below 22 when
reviewing ABGs. It is important to notice that both the pH and HCO3 decrease with metabolic
acidosis (i.e., the pH and HCO3 move in the same downward direction). A common cause of
metabolic acidosis is diabetic ketoacidosis, where acids called ketones build up in the blood
when blood sugar is extremely elevated. Another common cause of metabolic acidosis in
hospitalized patients is lactic acidosis, which can be caused by impaired tissue oxygenation.
Metabolic acidosis can also be caused by increased loss of bicarbonate due to severe diarrhea or
from renal disease that causes decreased acid elimination. Additionally, toxins such as salicylate
excess can cause metabolic acidosis.[10]
Nurses may first suspect that a patient has metabolic acidosis due to rapid breathing that occurs
as the lungs try to remove excess CO2 in an attempt to resolve the acidosis. Other symptoms of
metabolic acidosis include confusion, decreased level of consciousness, hypotension, and
electrolyte disturbances that can progress to circulatory collapse and death if not treated
promptly. It is important to quickly notify the provider of suspected metabolic acidosis so that an
ABG can be drawn and treatment prescribed (based on the cause of the metabolic acidosis) to
allow acid levels to improve. Treatment includes IV fluids to improve hydration status, glucose
management, and circulatory support. When pH drops below 7.1, IV sodium bicarbonate is often
prescribed to help neutralize the acids in the blood.[11],[12]

Metabolic Alkalosis
Metabolic alkalosis occurs when there is too much bicarbonate (HCO3) in the body or an
excessive loss of acid (H+ ions). Metabolic alkalosis is defined by a pH above 7.45 and an
HCO3 level above 26 on ABG results. Note that both pH and HCO3 are elevated in metabolic
alkalosis.
Metabolic alkalosis can be caused by gastrointestinal loss of hydrogen ions, excessive urine loss,
excessive levels of bicarbonate, or a shift of hydrogen ions from the bloodstream into cells.
Prolonged vomiting or nasogastric suctioning can also cause metabolic alkalosis. Gastric
secretions have high levels of hydrogen ions (H+), so as acid is lost, the pH level of the
bloodstream increases.
Excessive urinary loss (due to diuretics or excessive mineralocorticoids) can cause metabolic
alkalosis due to loss of hydrogen ions in the urine. Intravenous administration of sodium
bicarbonate can also cause metabolic alkalosis due to increased levels of bases introduced into
the body. Although it was once thought that excessive intake of calcium antacids could cause
metabolic alkalosis, it has been found that this only occurs if they are administered concurrently
with Kayexelate.[13]
Hydrogen ions may shift into cells due to hypokalemia, causing metabolic alkalosis. When
hypokalemia occurs (i.e., low levels of potassium in the bloodstream), potassium shifts out of
cells and into the bloodstream in an attempt to maintain a normal level of serum potassium for
optimal cardiac function. However, as the potassium (K+) molecules move out of the cells,
hydrogen (H+) ions then move into the cells from the bloodstream to maintain electrical
neutrality. This transfer of ions causes the pH in the bloodstream to drop, causing metabolic
alkalosis.[14]
A nurse may first suspect that a patient has metabolic alkalosis due to a decreased respiratory
rate (as the lungs try to retain additional CO2 to increase the acidity of the blood and resolve the
alkalosis). The patient may also be confused due to the altered pH level. The nurse should report
signs of suspected metabolic alkalosis because uncorrected metabolic alkalosis can result in
hypotension and cardiac dysfunction.[15]
Treatment is prescribed based on the ABG results and the suspected cause. For example, treat the
cause of the vomiting, stop the gastrointestinal suctioning, or stop the administration of diuretics.
If hypokalemia is present, it should be treated. If bicarbonate is being administered, it should be
stopped. Patients with kidney disease may require dialysis.[16]

Analyzing ABG Results

Now that we’ve discussed the differences between the various acid-base imbalances, let’s review
the steps to systematically interpret ABG results. Table 15.5b outlines the steps of ABG
interpretation.
Table 15.5b
Analyzing ABG Results[17],[18]

Type IV Solution Uses Nursing Considerations

Fluid resuscitation for

hemorrhaging, severe
0.9% Normal vomiting, diarrhea, GI Monitor closely for hypervolemia,
Isotonic Saline (0.9% suctioning losses, wound especially with heart failure or
NaCl) drainage, mild renal failure.
hyponatremia, or blood
transfusions.

Fluid resuscitation, GI Should not be used if serum pH is

tract fluid losses, burns, greater than 7.5 because it will
Lactated Ringer’s
Isotonic traumas, or metabolic worsen alkalosis. May elevate
Solution (LR)
acidosis. Often used potassium levels if used with renal
during surgery. failure.

5% Dextrose in Should not be used for fluid

Water (D5W) Provides free water to resuscitation because after
*starts as isotonic help renal excretion of dextrose is metabolized, it
Isotonic and then changes solutes, hypernatremia, becomes hypotonic and leaves the
to hypotonic when and some dextrose intravascular space, causing brain
dextrose is supplementation. swelling. Used to dilute plasma
metabolized electrolyte concentrations.

Monitor closely for hypovolemia,

hypotension, or confusion due to
Used to treat intracellular fluid shifting into the intracellular
0.45% Sodium dehydration and space, which can be life-
Hypotonic Chloride (0.45% hypernatremia and to threatening. Avoid use in patients
NaCl) provide fluid for renal with liver disease, trauma, and
excretion of solutes. burns to prevent hypovolemia
from worsening. Monitor closely
for cerebral edema.
Type IV Solution Uses Nursing Considerations

Monitor closely for hypovolemia,

hypotension, or confusion due to
Provides free water to
fluid shifting out of the
promote renal excretion
intravascular space, which can be
5% Dextrose in of solutes and treat
Hypotonic life-threatening. Avoid use in
Water (D5W) hypernatremia, as well as
patients with liver disease, trauma,
some dextrose
and burns to prevent hypovolemia
supplementation.
from worsening. Monitor closely
for cerebral edema.

Monitor closely for hypervolemia,

hypernatremia, and associated
respiratory distress. Do not use it
3% Sodium Used to treat severe
Hypertoni with patients experiencing heart
Chloride (3% hyponatremia and
c failure, renal failure, or conditions
NaCl) cerebral edema.
caused by cellular dehydration
because it will worsen these
conditions.

Monitor closely for hypervolemia,

hypernatremia, and associated
5% Dextrose and respiratory distress. Do not use it
Used to treat severe
Hypertoni 0.45% Sodium with patients experiencing heart
hyponatremia and
c Chloride failure, renal failure, or conditions
cerebral edema.
(D50.45% NaCl) caused by cellular dehydration
because it will worsen these
conditions.
Type IV Solution Uses Nursing Considerations

Monitor closely for hypervolemia,

hypernatremia, and associated
5% Dextrose and respiratory distress. Do not use it
Used to treat severe
Hypertoni Lactated Ringer’s with patients experiencing heart
hyponatremia and
c (D5LR) failure, renal failure, or conditions
cerebral edema.
D10 caused by cellular dehydration
because it will worsen these
conditions.

able 15.4
Comparison of Causes, Symptoms, and Treatments of Imbalanced Electrolyte
Levels

Elevated Level Decreased Level

Hypernatremia Hyponatremia
Sodium
Causes: Excessive salt intake Causes: Excessive water intake and
(Na+)
Symptoms: Lethargy, irritability, diuretics
Normal range
seizures, and weakness Symptoms: Headache, confusion, coma
136-145
Treatments: Rehydrate w/ D5W and Treatments: 3% NS and fluid
mEq/L
increase water intake restriction

Hyperkalemia
Causes: Kidney dysfunction, Hypokalemia
Potassium excessive potassium intake, and ACE Causes: Loop and thiazide diuretics and
(K+) inhibitors IV administration of insulin
Normal range Symptoms: Cardiac arrhythmias, Symptoms: Weakness, arrhythmias,
3.5-5.1 cramping, diarrhea, and irritability lethargy, and thready pulse (WALT)
mmol/L Treatments: Limit potassium in diet, Treatments: PO/IV potassium and
loop diuretic, insulin, dialysis, and increase K+ in diet
kayexalate

Calcium Hypercalcemia Hypocalcemia

 Elevated Level Decreased Level

Causes: Overactive parathyroid

Causes: Diuretic use and removal of
glands and cancer
(Ca++) parathyroid glands
Symptoms: Nausea, vomiting,
Normal range Symptoms: Numbness, tingling,
constipation, and thirst
8.6 -10.2 Chvotek’s sign, and tetany
Treatments: Decrease calcium in diet,
mg/dL Treatments: Increase Ca++ in diet and
increase mobility, and administer
IV/PO calcium
phosphorous

Hypermagnesemia
Causes: Kidney disease and excessive Hypomagnesemia
magnesium intake (i.e., laxatives and Causes: Diuretics, undernutrition, and
Magnesium
antacids) long-term alcohol use disorder
(Mg+)
Symptoms: Muscle weakness, Symptoms: Nausea, vomiting, lethargy,
Normal range
bradycardia, asystole, tremors, and weakness, tetany, leg cramps, tremors,
1.5-2.4
slow reflexes and arrhythmias
mg/dL
Treatments: Dialysis, increased fluid Treatments: Increase Mg+ in diet and
intake, and stopping medications PO/IV magnesium
containing Mg+

From: Chapter 15 Fluids and Electrolytes

Nursing Fundamentals [Internet].

Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors.
Eau Claire (WI): Chippewa Valley Te
Table 15.5a
ABG Components, Descriptions, Adult Normal Values, and Critical Values[2]
 Adult
ABG Critical
Description Normal
Component Value
Value

 Acidity (<7.35) or alkalinity (>7.45) of blood.

 Measure of H+ ions (acids).
<7.25
pH 7.35-7.45
 Affected by the lungs via hypo- or >7.60
hyperventilation or the kidneys through
bicarbonate retention.

80-100 <60
PaO2  Pressure of oxygen in the blood.
mmHg mmHg

 Pressure of carbon dioxide in the blood.

 CO2 is an acid managed by the lungs. <25
PaCO2  As PaCO2 increases, the blood becomes more 35-45 mmHg
acidic and the pH decreases. mmHg >60
mmHg
 As PaCO2 decreases, the blood becomes less
acidic and the pH increases.

 Bicarbonate level in the blood.

 HCO3 is a base managed by the kidneys. <10
HCO3  As HCO3 increases, the blood becomes more 22-26 mEq/L
alkaline and the pH increases. mEq/L >40
mEq/L
 As HCO3 decreases, the blood becomes more
acidic and the pH decreases.

SaO2  Oxygen saturation in the blood. 95-100% <88%

From: Chapter 15 Fluids and Electrolytes

Nursing Fundamentals [Internet].
Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors.
Eau Claire (WI): Chippewa Valley Technical College; 2021.
Copyright Notice

Licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license,

visit https://creativecommons.org/licenses/by/4.0/.

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

able 15.5b
Analyzing ABG Results[17],[18]

Step Action

If pH is out of range, determine if it is acidosis or alkalosis:

Step 1: pH (normal
pH <7.35 is acidosis.
7.35-7.45)
pH >7.45 is alkalosis.

Step 2: PaCO2 Is the PaCO2 normal?

(normal 35-45 PaCO2 <35 is considered alkalotic.
mmHg) PaCO2 >45 is considered acidotic.
If the PaCO2 is abnormal, determine if this is caused by a
respiratory problem. Recall that if the imbalance is caused by a
respiratory problem, the PaCO2 moves in the opposite direction of
the pH:
If the pH is <7.35 (acidosis) and the PaCO2 is >45 (acidotic), this is
respiratory acidosis.
If the pH is >7.45 (alkalosis) and the PaCO2 is <35 (alkalotic), this is
respiratory alkalosis.
**If the imbalance does not appear to be caused by a respiratory
Step Action

problem, move on to evaluate the HCO3.

Is the HCO3 normal?

HCO3 <22 is considered acidotic.
HCO3 >26 is considered alkalotic.
If the HCO3 is abnormal, determine if this caused by a metabolic
Step 3: HCO3 problem. Recall that the HCO3 moves in the same direction as the
(normal 22-26) pH if the imbalance is caused by a metabolic problem:
If pH is <7.35 (acidosis) and the HCO3 is <22 (acidotic), this is
metabolic acidosis.
If the pH is >7.45 (alkalosis) and the HCO3 is >26 (alkalotic), this is
metabolic alkalosis.

After determining the cause of the pH imbalance, determine if

compensation is occurring.
Fully compensated = the body has fixed the imbalance by bringing
the pH back to normal:
pH is normal (7.35-7.45).
PaCO2 and HCO3 are both out of range.
The cause of the disorder is out of range, and the other value is
significantly out of range indicating compensation is occurring.
Recall the respiratory rate quickly compensates for metabolic
disorders, and the kidneys take longer to compensate for
Step 4: Determine respiratory disorders.
level of Partially compensated = the body is working to fix the imbalance
compensation but hasn’t yet brought the pH back to normal:
pH is abnormal (<7.35 or >7.45).
PaCO2 and HCO3 are abnormal.
The CAUSE of the disorder is out of range and the other value is
moving out of range, indicating compensation is occurring.
Uncompensated = the body is not yet working to bring the pH back
to normal:
pH is abnormal (<7.35 or >7.45)
PaCO2 or HCO3 is abnormal, but not both.
The CAUSE of the disorder is out of range but the other value is not
yet out of range, indicating compensation is not yet occurring.
From: Chapter 15 Fluids and Electrolytes

Nursing Fundamentals [Internet].

Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors.
Eau Claire (WI): Chippewa Valley Technical College; 2021.
Copyright Notice

Licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license,

visit https://creativecommons.org/licenses/by/4.0/.

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Hea

able 15.6a
Expected Findings Versus Unexpected Findings Indicating a Fluid
Imbalance[2]

Unexpected Findings
Indicating Excessive Fluid
Volume Unexpected Findings
Expected
Assessment *Bolded items are critical Indicating Deficient Fluid
Findings
conditions that require Volume
immediate health care
provider notification.

Blood pressure,
Elevated blood pressure,
heart rate, and Decreased blood
increased respiratory
Vital signs oxygen saturation pressure or elevated heart
rate, or decreased oxygen
levels within rate
saturation
normal limits

Neurological Alert and Headache Headache, confusion,

 Unexpected Findings
Indicating Excessive Fluid
Volume Unexpected Findings
Expected
Assessment *Bolded items are critical Indicating Deficient Fluid
Findings
conditions that require Volume
immediate health care
provider notification.

decreased level of
oriented consciousness, dizziness, or
weakness

Normal heart rate

and rhythm, Bounding pulses, S3 heart Weak, thready pulses;
Cardiac capillary refill <3 sound, or jugular venous sluggish capillary refill; or
seconds, and distention chest pain
normal pulses

Clear lung
sounds Crackles in lung fields,
throughout, pink frothy sputum,
Respiratory normal shortness of Shortness of breath possible
respiratory rate, breath, or respiratory
and no shortness distress
of breath

Bowel sounds
present x4
quadrants and
Constipation with dry, hard
Gastrointestinal normal stool
stools
consistency and
frequency for
patient

Urinary Clear urine, Decreased urine output Decreased urine output

normal urine <30 mL/hr or < 0.5 <30 mL/hr or <0.5
 Unexpected Findings
Indicating Excessive Fluid
Volume Unexpected Findings
Expected
Assessment *Bolded items are critical Indicating Deficient Fluid
Findings
conditions that require Volume
immediate health care
provider notification.

specific gravity,
mL/kg/hr concentrated
and urine output mL/kg/hr concentrated
urine, or elevated urine
greater than 30 urine
specific gravity
ml/hr

Normal skin
Tenting (poor skin turgor);
turgor and moist Tight, edematous, or shiny
Integumentary dry, sticky mucous
mucous skin
membranes; or dry skin
membranes

<1kg change in
Weight weight over 24 >1kg increase over 24 hours >1kg decrease over 24 hours
hours

From: Chapter 15 Fluids and Electrolytes

Nursing Fundamentals [Internet].

Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors.
Eau Claire (WI): Chippewa Valley Technical College; 2021.
Copyright Notice
Licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license,

visit https://creativecommons.org/licenses/by/4.0/.

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

able 15.6b
Lab Values Associated with Fluid and Electrolyte Imbalances

Lab Value Normal Ranges

Serum osmolarity 275 to 295 mmol/kg

Urine Specific Gravity 1.010 and 1.020

Men: 42 to 52%
Hematocrit
Women: 37 to 47%

BUN 7 to 20 mg/dL

Serum sodium 135-145 mEq/L

Serum potassium 3.5-5 mEq/L

Serum magnesium 1.5-2.4 mEq/L

Serum calcium 8.5-10.3 mg/dL

Serum phosphorus 2.5-4 mg/dL

Lab Value Normal Ranges

pH: 7.35 and 7.45

PaO2: 80-100 mm Hg
ABG
HCO3: 22-26 mEq/L
PaO2: 35-45 mm Hg

From: Chapter 15 Fluids and Electrolytes

Nursing Fundamentals [Internet].

Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors.
Eau Claire (WI): Chippewa Valley Technical College; 2021.
Copyright Notice

Licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license,

visit https://creativecommons.org/licenses/by/4.0/.

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

able 15.6c
Common NANDA-I Nursing Diagnoses Related to Fluid and Electrolyte
Imbalances[13]
NANDA-I Defining
Definition
Diagnosis Characteristics

Excess Fluid Surplus intake and/or retention of fluid. Adventitious breath

Volume sounds
Elevated blood
pressure
Altered mental status
Anxiety
Decreased hematocrit,
serum osmolarity, and
BUN
Dyspnea
Edema
Fluid intake exceeds
output
Jugular vein distension
Restlessness
Weight gain >1 kg/24
hours

Deficient Fluid Decreased intravascular, interstitial, and/or Altered mental status

Volume intracellular fluid. This refers to dehydration, water Decreased skin turgor
loss alone without change in sodium. Decreased blood
pressure
Decreased urine output
Dry skin and mucous
membranes
Increased heart rate
Increased serum
osmolarity, hematocrit,
and BUN
Increased urine
concentration
Sudden weight loss
Thirst
Weakness

Risk for Susceptible to a decrease, increase, or rapid shift Diarrhea

NANDA-I Defining
Definition
Diagnosis Characteristics

Imbalanced from one to the other of intravascular, interstitial, Vomiting

Fluid Volume and/or intracellular fluid, which may compromise Excessive fluid volume
health. This refers to body fluid loss, gain, or both. Insufficient fluid
volume

Risk for Susceptible to changes in serum electrolyte levels, Diarrhea

Electrolyte which may compromise health. Vomiting
Imbalance Excessive fluid volume
Insufficient fluid
volume

From: Chapter 15 Fluids and Electrolytes

Nursing Fundamentals [Internet].

Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors.
Eau Claire (WI): Chippewa Valley Technical College; 2021.
Copyright Notice

Licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license,

visit https://creativecommons.org/licenses/by/4.0/.

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Table 15.6d
Interventions for Imbalances
Nursing
Interventions
Diagnosis

 Administer prescribed diuretics to eliminate excess fluid as appropriate

and monitor for effect. Monitor for side effects of diuretics such as
orthostatic hypotension and electrolyte imbalances.
 Position the patient with the head of the bed elevated to facilitate
respiratory function as needed.
 Implement fluid restrictions if ordered. For comfort, provide ice chips as
appropriate.
 Assist in diet choices to reduce sodium intake.
 Monitor weight and notify the provider for weight gain > 1 kg in 24
hours.
 Accurately measure and monitor fluid intake and output, as ordered.
Notify provider for urine output less than 30 mL/hour or 0.5mL/kg/hour
or as ordered.
 Monitor blood pressure, heart rate, respiratory rate, and pulse oximeter.
Excessive
Monitor lungs sounds for new or worsening crackles. Notify the
Fluid Volume
provider of new abnormal findings.
 Monitor for worsening edema and notify the provider as indicated.
 Monitor for jugular vein distension with the head of bed elevated 30 to
45 degrees.
 Monitor the patient for restlessness, anxiety, or confusion. Implement
safety precautions if present. Notify the provider of new or worsening
findings.
 If edema is present in the extremities, provide care such as elevation and
compression, and reposition to prevent skin breakdown.
 Monitor lab results relevant to fluid status such as serum osmolarity,
urine specific gravity, hematocrit, and BUN.
 Educate the patient and family members about medications, fluid
restrictions, sodium restrictions, and monitoring at home for sudden
weight changes, worsening edema, or worsening dyspnea.

Deficient
Fluid Volume  Encourage oral fluid intake, as tolerated. Provide fluids the patient
prefers within easy reach.
Nursing
Interventions
Diagnosis

 Minimize intake drinks with diuretic or laxative effects (e.g., coffee, tea,
alcohol, prune juice).
 Administer IV fluids as ordered and monitor the patient’s response.
Generally, isotonic fluids are ordered for hydration. Monitor for the
potential development of excessive fluid volume.
 Monitor weight and watch for sudden decreases, especially in the
presence of decreased urine output.
 Monitor total fluid intake and output every four hours. Report urine
output equal or less than 30 mL/hour or 0.5 mL/kg/hour to the provider
because this may indicate kidney injury in addition to deficient fluid
volume.
 Monitor pulse, respirations, and blood pressure every 15 minutes to one
hour for unstable patients and every 4 hours for stable patients.
 Recognize and report signs of impending hypovolemic shock, including
elevated pulse and respirations; decreased blood pressure below
baseline; cold, clammy skin; weak, thready pulse; and confusion.
Patients progressing towards hypovolemic shock require emergent care.
 Check orthostatic blood pressures with the patient lying and standing.
To perform this procedure, have the patient lie down for 5 minutes.
Measure blood pressure (BP) and pulse rate. Have the patient stand.
Repeat the BP and pulse rate measurements after standing 1 and 3
minutes. A decrease in systolic blood pressure > 20 mm Hg or a
decrease in diastolic blood pressure > 10 mm Hg, or if the patient
reports feeling light-headed or dizzy, is considered abnormal.
[19]
Orthostatic hypotension should be reported to the provider and safety
measures implemented to prevent falls.
 Recognize and address factors contributing to deficient fluid volume,
such as diarrhea, vomiting, fever, diuretic therapy, or uncontrolled
diabetes mellitus. Administer medications such as antidiarrheals and
antiemetics as appropriate.
 Monitor lab results relevant to fluid status such as serum osmolarity,
urine specific gravity, hematocrit, and BUN.
 Educate the patient and family members about signs of dehydration to
watch for at home. Remind older adults that thirst sensation often
decreases with age.
Nursing
Interventions
Diagnosis

 Monitor mental status, vital signs, and heart rhythm at least every 8
hours or more frequently as needed. Electrolyte imbalances can cause
confusion, cardiac dysrhythmias, muscle weakness, edema, and
respiratory failure.
 Review associated laboratory results and report abnormal findings to the
provider.
 Review the patient’s medical record for possible causes of altered
electrolyte levels, such as diuretics, kidney disease, gastrointestinal fluid
loss, drainage from wounds or burns, and excessive perspiration.
Address potential causes with the provider.
Risk for
Electrolyte  Administer PO and IV electrolyte supplements as ordered for
Imbalance deficiencies.
 Limit dietary intake of specific electrolyte excesses.
 Administer electrolyte-binding medications, such as Kayexalate for
hyperkalemia, as prescribed.
 Administer IV fluids to promote renal excretion of excess electrolyte
levels, as prescribed.
 Educate the patient and family members about dietary choices
corresponding to the specific electrolyte imbalance. Provide information
about monitoring for potential electrolyte imbalances at home resulting
from their medications.

From: Chapter 15 Fluids and Electrolytes

Nursing Fundamentals [Internet].

Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors.
Eau Claire (WI): Chippewa Valley Technical College; 2021.
Copyright Notice

Licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license,

visit https://creativecommons.org/licenses/by/4.0/.

NCBI Bookshelf. A service of the National Library of Medicine,

Table 15.6e
Evaluating for Improvement of Imbalances

Imbalance Signs and Symptoms of Improvement

Fluid Volume Decreased crackles, decreased edema, decreased shortness of breath,

Excess and/or improved jugular venous distention

Fluid Volume Increased blood pressure, decreased heart rate, normal skin turgor, and/or
Deficit moist mucous membranes

Electrolyte Electrolyte levels return to normal and/or absence of signs or symptoms of

Imbalances deficit or excess

Acid-Base ABGs return to normal or baseline, resolution of vomiting or diarrhea,

Imbalance and/or no respiratory distress

From: Chapter 15 Fluids and Electrolytes

Nursing Fundamentals [Internet].
Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors.
Eau Claire (WI): Chippewa Valley Technical College; 2021.
Copyright Notice

Licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license,

visit https://creativecommons.org/licenses/by/4.0/.