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Clinical Nursing Skills

19.1 Fluid and Electrolytes

Clinical Nursing Skills19.1 Fluid and Electrolytes

Learning Objectives

By the end of this section, you will be able to:

  • Identify factors affecting fluid balance
  • Recognize factors affecting electrolyte balances
  • Describe the homeostatic mechanisms of fluid and electrolyte balance

The nurse makes inferences about the amount and location of fluid in the patient’s body by assessment of subjective and objective data, including laboratory test values. 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, or homeostasis, the maintenance of equilibrium of two or more interdependent elements. In this chapter, the interdependent elements are fluids and electrolytes. A slight change in either direction—high or low—can have significant consequences on various body systems. This unit reviews how fluid is regulated in the body and the importance of electrolyte balance.

Fluid Balance

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 (Figure 19.2).

A chart showing the percentages of bodily fluids.
Figure 19.2 Although cerebral spinal fluid is extremely important in protecting the brain and spinal cord, it makes up less than 1 percent of total body fluid. The remaining total body fluid is composed of 7 percent blood plasma, 26 percent interstitial fluids, and 67 percent intracellular fluids. (credit: modification of “Cellular Fluid Content” by “Welcome1To1The1Jungle”/Wikimedia Commons, CC BY 4.0)

The intracellular compartment contains intracellular fluid (ICF) that is made up of protein, water, electrolytes, and solutes. The most abundant electrolyte in ICF is potassium. Intracellular fluids are crucial to the body’s functioning. In fact, ICF accounts for 60 percent of the volume of body fluids and 40 percent of a person’s total body weight (Lorenzo et al., 2019).

Fluid outside of cells is called extracellular fluid (ECF). The most abundant electrolyte in ECF 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 and it is found in the vascular system that consists of arteries, veins, and capillary networks. Intravascular fluid is whole blood volume and 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 functions.

A second type of ECF is interstitial fluid which 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. This is because heart failure is ineffective pumping of blood, which causes the pooling of blood, which increases the pressure on vessels, which “leak” fluid into the interstitial spaces. The remaining ECF, also called transcellular fluid, refers to fluid in areas such as cerebrospinal, synovial, and intrapleural spaces, and the gastrointestinal (GI) system.

Intravascular fluid volume is assessed through perfusion indicators. Perfusion is the delivery of blood and, therefore, essential oxygen and nutrients to organs and tissues. External indicators of intravascular fluid delivery include blood pressure, peripheral pulse characteristics, and end organ function. End organ function assessment includes collecting data to determine if the organ is manifesting adequate blood delivery. Within fluid and electrolyte assessments, end organ assessment often is focused on the kidneys and includes monitoring kidney function measurements such as serum blood urea nitrogen (BUN) and creatinine levels and glomerular filtration rate, monitoring urine output quantity and characteristics, and monitoring urine laboratory data (Table 19.1).

Organ or Body System Objective Assessment Data
Kidney BUN and creatinine levels
Electrolyte levels
Urine output
Urine specific Gravity
Heart Atrial natriuretic peptides
Cardiac biomarkers
Liver Bilirubin levels
Liver enzyme levels
Nervous Level of orientation
Muscle strength
Table 19.1 Examples of End Organ Perfusion Assessment Data

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. Oncotic pressure refers to the condition in which the osmotic force that allows fluid to remain in the vascular space is predominantly proteins. For example, patients with decreased protein levels (such as low serum albumin) experience edema due to the leakage of intravascular fluid into interstitial areas because of decreased oncotic pressure.

The pressure that a contained fluid exerts on what is confining it is called hydrostatic pressure. 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 (Figure 19.3).

Graphic showing capillary microcirculation.
Figure 19.3 Capillary microcirculation involves hydrostatic and osmotic pressures that move molecules across the capillary wall. (credit: “Capillary microcirculation” by “Kes47”/Wikimedia Commons, Public Domain)

The process of 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 can 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.

Osmosis causes fluid movement among the intravascular, interstitial, and ICF compartments on the basis of solute concentration. For example, recall a time when you have eaten a large amount of salty food. 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. 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.) Because diffusion travels down a concentration gradient, the solutes move freely without energy expenditure (Figure 19.4). 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.

Graphic showing diffusion of uncharged substances, like oxygen and carbon dioxide, passing through the cell membrane.
Figure 19.4 The structure of the cell membrane allows diffusion of uncharged substances, like oxygen and carbon dioxide, to pass through the cell membrane down their concentration gradient in a process known as diffusion. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Unlike diffusion, active transport 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. An example of active transport is the sodium-potassium pump, which uses energy to maintain higher levels of sodium in the ECF and higher levels of potassium in the ICF (Figure 19.5). Recall that sodium ion (Na+) is the primary electrolyte in the extracellular space and potassium ion (K+) is the primary electrolyte in the intracellular space.

Graphic showing the cellular diffusion and sodium-potassium pump regulation.
Figure 19.5 Diffusion and the sodium-potassium pump regulate sodium and potassium levels in the extracellular and intracellular compartments. (credit: modification of “Sodium-potassium pump and diffusion” by “BruceBlaus”/Wikimedia Commons, CC BY 3.0)

Fluid and Electrolyte Regulation

The body must carefully regulate intravascular fluid accumulation and excretion to prevent FVEs or deficits and maintain adequate blood pressure. Water balance is regulated by several mechanisms, including antidiuretic hormone (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 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 approximately 2,500 mL/d 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 RAAS plays an important role in regulating fluid output and blood pressure (Figure 19.6). 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.

Graphic showing the Renin-Angiotensin-Aldosterone System (RAAS) and how it regulates fluid and blood pressure.
Figure 19.6 The RAAS is vital in regulating fluid and blood pressure. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

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.”

Fluid output occurs mostly through the kidneys in the form of urine. Fluid is also lost through the skin as perspiration, through the GI 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, GI tract, and lungs and cannot be measured. The remaining 60 percent of daily fluid output is in the form of urine. Normally, the kidneys produce approximately 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 outputs less than 30 mL/h (or 0.5 mL/kg/h) of urine output over 8 hours, the provider should be notified for prompt intervention.

Fluid Imbalance

Two types of fluid imbalances are deficient fluid volume (referred to as hypovolemia) and excessive fluid volume (referred to as hypervolemia). These imbalances primarily refer to imbalances in the extracellular compartment, but they can cause fluid movement in the intracellular compartments, depending on the sodium level of the blood.

Fluid Volume Deficit

A fluid volume deficit (FVD) can occur from a loss of body fluids or fluid that becomes unavailable in the body for use. The next section discusses the differences between hypovolemia and third spacing. Fluid volume deficit (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.

The nurse must also understand that because fluid can move between compartments, one compartment may be adequate while, at the same time, another compartment is volume deficient or volume excessive. Several terms are used to describe a deficient fluid volume. The term dehydration is used when fluid volume deficiency exists in the interstitial space. When dehydration occurs, the patient may complain of being thirsty, and mucus membranes, especially those in the oral cavity, will look and feel sticky or dry. If dehydration is significant, enophthalmos (or sunken eyes) may be visible, skin turgor may be poor, and skin may look dry.

Dehydration can lead to headaches, and some studies indicate even mild dehydration can decrease cognitive function. As tissue size decreases, pain receptors are stimulated, and patients experience pain. In severe cases, cerebral tissue can shrink, damaging the protective meningeal layers, and cause cerebral bleeding.


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 (Table 19.2):

  • individuals who exercise or work outdoors in hot weather,
  • infants and children,
  • older adults,
  • patients taking diuretics and other medications that cause increased urine output, and
  • patients with chronic diseases such as diabetes mellitus and kidney disease.
Adults Infants and Young Children
Changes in mental status
Dark, concentrated urine
Dizziness due to decreased blood pressure
Dry mouth
Dry skin
Elevated heart rate
Feeling tired
Feeling very thirsty
Urinating and sweating less than usual
Additional symptoms include:
  • being unusually sleepy or drowsy
  • crying without tears
  • eyes that look sunken
  • irritability
  • no wet diapers for three hours or more
  • sunken fontanel
Table 19.2 Signs and Symptoms of Dehydration

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 (IVFs).

Third-Spacing Fluid Shift

The term third spacing refers to a type of hypovolemia in which total body fluid may be adequate or even excessive but fluid has moved out of the intravascular space and into the interstitial space, making it unavailable. Third spacing can be consequence of inflammation or a loss of intravascular oncotic pressure.

Inflammation is an immune system response that results in many of the traditional manifestations we experience when we get sick, such as runny nose, cough, and body aches, among others. Certain kinases and cytokines that are released in the body as part of the inflammatory process cause capillary leaking. Capillary leaking is a normal and useful response for the body to deliver white blood cells, red blood cells, platelets, and other immune mediators to the site of an injury or infection. However, on a larger scale, capillary leaking can potentially cause large amounts of fluid to leak out of the capillary networks and into the tissues. Patients experiencing significant trauma or severe infections and sepsis can become hypovolemic as fluid leaves the intravascular space and stays in the interstitial space.

Intravascular oncotic pressure derives from the number of intravascular solutes compared with the amount of intravascular fluid. The most abundant intracellular solute is sodium, and the largest intravascular solutes are plasma proteins and glucose, in that order. When a disease causes the concentration of intravascular sodium, proteins, or glucose to decrease, there is not adequate oncotic pull to keep fluid in the vascular system, and fluid leaks into the interstitial space. Whether third spacing is a result of inflammation or loss of oncotic pressure, the manifestations are like that of hypovolemia, except with the addition of interstitial space congestion and swelling, which is called edema.

Fluid Volume Excess

Hypervolemia, also referred to as fluid volume excess (FVE), occurs when there is increased fluid retained in the intravascular compartment. Patients at risk for developing FVE are those with the following conditions:

  • cirrhosis
  • heart failure
  • kidney failure
  • pregnancy

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.

Clinical Judgment Measurement Model

Form a Hypothesis: Differentiating FVE and Edema from Third Spacing

A patient presents to the emergency department with complaints of a headache and swollen ankles. Although headache and peripheral edema are both manifestations of FVE, there is not enough information to determine if these manifestations are from FVE due to increased hydrostatic pressure or from third spacing due to a loss of intravascular oncotic pressure. To gather additional pertinent assessment data, the nurse should ask the patient questions and obtain a health history. The patient indicates no history of cardiac or kidney disease and states “I have been very healthy until I was recently diagnosed with meningitis. I have been on antibiotics and was feeling better, but now I have no energy and my feet are swelling.”

The nurse analyzes the patient’s health history information in conjunction with the presenting manifestations and determines it is unlikely the patient’s headache and edema are caused by FVE. The nurse understands that fluid shifting from the intravascular space into the interstitial space can also cause headache and edema.

The nurse performs a physical assessment and determines the patient’s blood pressure is 92/56 mm Hg and apical heart rate is 115 bpm. The nurse analyzes these data and determines the patient is hypovolemic. The nurse reports this information to the provider and then obtains results from a serum electrolyte panel. The patient’s serum sodium level is 130 mEq/L. Subsequently, the patient is diagnosed with meningitis-induced syndrome of inappropriate antidiuretic hormone (SIADH).

Initially, the patient appeared to be experiencing FVE. However, further assessment data did not support FVE.


Hypervolemia is an FVE specific to fluid in the intravascular space. Fluid will remain in the intravascular space if intravascular oncotic pressure is high. If the normal mechanisms that control intravascular solutes are not optimal (in this case mainly sodium and glucose), high levels will pull fluid into the intravascular space.

Hypervolemia manifests with an increase in vascular pressure. Vascular pressure can be assessed through internal or external blood pressure monitoring, by auscultating cardiac heart sounds, assessing arterial pulse characteristics, and assessing for the presence of jugular venous distention. Hypervolemia manifests as high blood pressure (hypertension), the addition of a third heart sound (S3), bounding peripheral pulses, and visible jugular veins when the patient is sitting at a 45° angle or greater (Table 19.3).

Fluid Volume Alteration Manifestations Laboratory Data
Dehydration Dry, sticky mucus membranes
Dry skin, skin tenting
Serum sodium level normal or high
If intravascular volume is maintained, most serum and urine laboratory measurements will be normal.
Hypovolemia Decreased blood pressure with tachycardia
Concentrated and darkening urine
Increased respiratory rate
Possible decrease in end organ perfusion
Prolonged capillary refill
Weak peripheral pulses, skin may feel cool
Serum values indicate:
  • increased BUN level
  • Increased hematocrit
  • possibly increased creatinine level
Urine values indicate:
  • increased urine osmolality
  • increased urine specific gravity
  • increased urine osmolality
Hypervolemia Increased blood pressure
Jugular vein distension
Strong or bounding peripheral pulses
With increased kidney excretion, urine has lighter color and output is increased.
Serum laboratory values may be low due to dilution.
Urine values indicate:
  • decreased urine osmolality
  • decreased urine specific gravity
Table 19.3 Summary of the Manifestations of Fluid Volume Alterations


Edema is the presence of excess fluid in the interstitial space. As discussed earlier, edema can exist due to third spacing. The nurse must assess multiple indicators to determine if edema is the result of third spacing or FVE. When edema results from FVE, hydrostatic pressure has forced fluid out of the vascular space and into the interstitial space. Hydrostatic pressure is pressure exerted on the sides of capillaries as blood flows through them. If hydrostatic pressure is elevated due to hypervolemia, water will be forced out of the capillaries into the interstitial space to evenly distribute hydrostatic pressure between these two spaces. If hydrostatic pressure is equal, there is no movement of fluid back into the vascular space, and fluid remains stagnant in the interstitial space.

Edema will manifest differently depending on where it is located. In the peripheral tissue, edema presents as visibly swollen tissues (Figure 19.7). Often, edema is first visible in the lower extremities, due to gravity increasing the hydrostatic pressure in the feet, ankles, and lower legs. However, in bed-bound patients, gravitational pull may well be greatest in the buttocks, back, or backs of the legs. When edema is severe and generalized throughout the body, the term anasarca is used.

Image showing edema, which is an excess of fluid buildup in tissues.
Figure 19.7 Edema is an excess of fluid buildup in tissues. When buildup is substantial, an indentation will remain when pressure is applied. This is called pitting edema. (credit: “Oedema, finger marks” by John Campbell/Flickr, Public Domain)

Edema can be present in interstitial spaces that are not visible. When fluid leaks out of the capillaries surrounding the alveoli, fluid can enter the alveoli. This edema is referred to as pulmonary edema and will manifest with coarse crackles heard during auscultation, pink and frothy respiratory secretions, and a decline in the assessment indicators of adequate respiratory gas exchange. (Refer to Chapter 23 Assessment of the Thorax, Lungs, Breast, and Lymphatic System for further information on lung and oxygenation assessment.) When edema is in the interstitial space within brain tissue, the cranium limits brain tissue expansion. That pressure can compress the arteries and nerves inside brain tissue, resulting in decreased blood flow and nerve activity that will manifest as headache, seizure activity, decreased level of consciousness, and other indications of increasing intracranial pressure. This edema is called cerebral edema.

Unfolding Case Study

Unfolding Case Study #3: Part 9

Refer back to Chapter 15 General Survey, Anthropometric Measurement, and Vital Signs, Chapter 17 Nutrition Assessment, and Chapter 18 Oxygenation and Perfusion for Unfolding Case Study Parts 1–8 to review the patient data.

Mrs. Ramirez, a 68-year-old female, is brought to the emergency room by her husband. The patient reports shortness of breath with exertion and feeling “off” for the last 3 days. She has been admitted to the medical-surgical unit for observation.

Past Medical History Patient reports shortness of breath “gets worse with walking and only gets better after sitting down for at least 15 minutes.”
Medical history: Myocardial infarction with stents 10 years ago, heart failure, COPD [chronic obstructive pulmonary disease], GERD (gastroesophageal reflux disease), and hypertension.
Family history: Married for 50 years, three grown children. Mother died because of Alzheimer’s disease. Father alive, with hypertension and prostate cancer, currently undergoing treatment.
Social history: Former 1 pack/day smoker, quit 20 years ago. Social drinker, 1 drink/week.
Allergies: None
Current medications:
  • aspirin (e.g., Bayer) 81 mg PO [orally] daily
  • carvedilol (e.g., Coreg) 6.25 mg PO twice daily
  • furosemide (brand name, Lasix) 40 mg PO daily
  • lisinopril (e.g., Zestril) 10 mg PO daily
Assessment 1900:
Abdominal: Abdomen soft and nontender. Bowel sounds present in all four quadrants. Patient reports last bowel movement was yesterday.
Cardiovascular: Sinus tachycardia on monitor, S1 and S2 present, no murmurs noted. Capillary refill <2 seconds. Peripheral +1 pitting edema noted in bilateral lower extremities.
HEENT [head, eyes, ears, nose, and throat]: Symmetrical, no lesions noted. Jugular venous distension present at rest.
Integumentary: Skin warm and intact. Mild diaphoresis noted.
Musculoskeletal: 4/5 muscle strength in bilateral lower extremities. Limited range of motion in bilateral arms that patient reports is from old shoulder injuries.
Neurological: Alert and oriented ×4, no deficits noted.
Respiratory: Increased respiratory rate with labored breathing observed. Crackles in lung bases bilaterally. Patient reports dyspnea with exertion.
Flow Chart 2000:
Blood pressure: 145/82 mm Hg
Heart rate: 115 bpm
Oxygen saturation: 93 percent on 2 L nasal cannula
Pain: 3/10 with breathing
Respiratory rate: 29 breaths/minute
Temperature: 99.6 °F (37.5°C)
Recognize cues: What findings from the case study indicate the patient may have a fluid imbalance?
Analyze cues: Based on the recognized cues, what kind of fluid imbalance does the patient most likely have?

Electrolyte Balance

Fluid balance and electrolyte balance share many regulatory mechanisms. Through blood sodium concentrations, the hypothalamus detects FVE or FVD and either stimulates or suppresses the patient’s thirst response and the pituitary gland’s secretion of ADH. Other hormones that play a role in managing fluid volume are aldosterone from the adrenal gland and natriuretic peptide hormones released by myoendocrine cells of the atria in the heart.

The kidneys have a major role in managing fluids and electrolytes. Any electrolyte level can be altered in patients with kidney injury or disease. Additionally, calcium also has a hormonal mechanism of regulation through the thyroid hormone calcitonin and parathyroid hormone (PTH).


A common physiological phrase is “where sodium goes, water follows.” Water is attracted to sodium because sodium is the most prevalent ion found in the vascular system, making up about 90 percent of the ECF osmolality (Bernal et al., 2023). Recall that the solute concentration in the intravascular space is what holds water in there. The intravascular, extracellular normal sodium level ranges between 136 and 144 mEq/L (Cleveland Clinic, 2021). As described earlier, sodium levels are influenced by vascular fluid volume and vice versa. Regulated through hypothalamic, pituitary, adrenal, and kidney interactions, sodium balance is necessary to maintain a healthy intravascular fluid volume and to prevent third spacing.

A balanced sodium level is also necessary for nerve and muscle cell conduction and activation through the sodium-potassium pump. These proteins are a part of our cell membranes and allow an uneven exchange of sodium and potassium ions. Three sodium ions leave the cell, and two potassium ions enter the cell. The ion imbalance signals the cell to fire. An excess or deficiency of sodium ions can alter the cell response (Figure 19.8).

Graphic showing sodium, potassium, and phosphate needing to be balanced for the sodium-potassium pump to function.
Figure 19.8 Sodium, potassium, and phosphate balance is necessary for the sodium-potassium pump to function. (credit: modification of Anatomy and Physiology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)


The term hyponatremia refers to an intravascular, extracellular (serum) sodium level of less than 136 mEq/L. Hyponatremia is more commonly related to the loss of serum sodium, which may be due to the use of sodium-wasting diuretics, mainly thiazide diuretics, and is also common in patients experiencing GI loss from significant vomiting or diarrhea. Diuretics and GI loss decrease sodium levels, but also decrease fluid volume. This situation is called “isotonic hyponatremia” and may lead to hypovolemia. In this case, manifestation will look like those of dehydration and hypovolemia, depending on the severity of sodium and fluid loss. Hypovolemic isotonic hyponatremia can also be caused by adrenal insufficiency, in which the adrenal gland does not produce adequate aldosterone. Aldosterone is responsible for sodium retention in the vascular system and for fluid retention the vascular system. For this reason, when aldosterone is deficient, both sodium and water levels are decreased and a hypovolemic isotonic hyponatremia results.

Another type of hyponatremia is hypotonic hyponatremia. In hypotonic hyponatremia, serum sodium levels are decreased due to dilution. The vascular system can become diluted with fluid for several reasons, but a common reason is an abnormal secretion of ADH. The SIADH can be a complication of small cell lung cancer, genetic mutations (nephrogenic SIADH), or brain issues from head injuries or infections. In SIADH, water is retained in the vascular system, diluting sodium levels and causing a decreased intravascular osmotic concentration, in turn resulting in a fluid shift from the vascular space to the interstitial space. Therefore, hypotonic hyponatremia manifests as third spacing.


A serum sodium level greater than 144 mEq/L defines hypernatremia. Hypernatremia is often the result of excess dietary sodium intake. In the United States, most dietary sodium comes from salt (sodium chloride). According to the guideline published by the U.S. Department of Health and Human Services (2021), dietary sodium should not exceed 2,300 mg/d for adults and teenagers aged 14 years or older. However, the average American consumes approximately 3,400 mg of sodium each day (U.S. Food and Drug Administration, 2022).

It is important for nurses to educate the public about the risks of consuming too much sodium. Excess sodium causes the intravascular space to become hyperosmotic and fluid to move from the interstitial space into the intravascular space. As interstitial fluid is replaced, intravascular volume continues to expand, and, thus, hypertension can develop.

Dietary sodium excess is not the only cause of hypernatremia. Water deprivation can occur in people who are unable to respond to thirst or lack access to clean water. One example is a person dependent on enteral feedings for nutrition. If the enteral nutrition preparation is hyperosmolar (or lacking enough water), the vascular space can become hyperosmolar, moving fluid from the interstitial space. Once the interstitial space is depleted, the vascular space can become hypernatremic. Diabetes insipidus is a diminished production of ADH, commonly seen with some types of head injuries, that can cause increased water loss in the urine and a lack of water retention in the body, also resulting in hypernatremia in the vascular space.

Hypernatremia initially will cause fluid to move from the interstitial space into the intravascular space. This causes congestion and an elevated blood pressure in the intravascular space. Over time, hypertension can cause long-term damage to the vasculature, especially that of the kidneys. Meanwhile, the interstitial space is volume depleted. Therefore, hypernatremia will manifest as dehydration and, at least initially, hypertension. As the kidneys filter out excess water from the vascular system, and lost fluid cannot be replaced, hypernatremia can cause hypovolemia.

Clinical Safety and Procedures (QSEN)

QSEN Competency: Safety: Providing Adequate Hydration

Disclaimer: Always follow a provider’s order for administering enteral fluids.

Definition: Reduce the risk of harm to patients through effective, proficient, and competent performance.

Knowledge: Examine human factors that could lead to water being missed, especially during busy shifts. Understand that patients who rely on others for fluid are at high risk for dehydration, hypernatremia, and possibly hypovolemia. Enterally fed patients may be unable to communicate thirst, especially if their need for enteral nutrition is related to a stroke or other conditions that impair swallowing, communicating, and, possibly, cognitive functioning. Enteral nutrition preparations may or may not have water included with the enteral contents. Some tube feedings are premixed with water and others are not. The nurse must be certain to understand if “free water” needs to be included with enteral feedings, and if free water needs to be added, must be careful that no doses are missed (Figure 19.9). It is easy to overlook the importance of water when a patient is receiving nutrition through a gastric or intestinal tube. Water is not considered a medication and is not “scanned” as a medication but must be administered with the same diligence as a medication. When free water doses are missed, the patient may become dehydrated over time. Dehydration, especially in conjunction with decreased independent movement, and urinary and/or fecal incontinence, can dramatically increase the risk for pressure injuries. If dehydration is not corrected, hypovolemia can cause organ damage and death.

Skill: Administer enteral water in the same manner as enteral medications.

  • Review provider’s order for the amount and frequency of free-water administration.
  • Identify patient using two patient identifiers, per institutional medication administration policy.
  • Administer water as ordered by provider.
  • Document water administration per institutional requirements.

Attitude: The nurse will respect the importance of water administration and perform as diligently as if water was a medication.

A nurse administering a feeding tube.
Figure 19.9 Nurses must ensure that in addition to the tube feeding solution, all prescribed free water is administered to patients receiving enteral nutrition. (credit: modification of “At Guantanamo ‘force feeding’ is called ‘enteral feeding’” by Joshua Nistas/Wikimedia Commons, Public Domain)


As mentioned, the sodium-potassium pump is essential for nerve and muscle cell conduction and contraction. Having discussed the role of sodium, the second element in this ion exchange process is potassium. Most potassium in the body is intracellular. For that reason, serum levels of potassium are much lower than serum levels of sodium. The normal range of serum potassium concentration is 3.7 to 5.1 mEq/L (Cleveland Clinic, 2021).

Potassium is regulated by the kidneys but also moves easily between the intracellular and extracellular spaces. Kidney injury or damage, acid-base imbalances, glucose dysregulation, and some medications can influence serum potassium levels. Because the normal serum level of potassium is low, even slight changes can have a significant impact.


A serum potassium level of less than 3.7 mEq/L defines the condition of hypokalemia. Potassium-wasting diuretics (loop diuretics and thiazide diuretics) are a common cause of hypokalemia. Other medications cause hypokalemia by activating the sodium-potassium pump at a fast rate. Medications that stimulate the sympathetic nervous system (e.g., beta-2 agonists used for bronchodilation and for other reasons) cause rapid smooth-muscle dilation. This rapid dilation requires energy from the sodium-potassium pump but also depletes extracellular potassium as potassium is exchanged for sodium.

Other common causes of hypokalemia include potassium loss from GI sources, including vomiting, gastric suctioning, and diarrhea. Hyperglycemia like that seen with type 2 diabetes mellitus is another cause of hypokalemia. Insulin secretion activates the sodium-potassium pump to change cell membrane structure and allow glucose to enter the cell. This sodium-potassium exchange decreases extracellular potassium levels as both potassium and glucose enter peripheral cells. Diabetic ketoacidosis, in particular, can cause hypokalemia when intracellular potassium is exchanged for extracellular hydrogen and then is eliminated in urine as hyperglycemia creates a hyperosmolar intravascular space and fluid moves from the interstitial space into the intravascular space.

Hypokalemia manifests as fatigue and weakness due to a decrease or slowness in the sodium-potassium pump nerve conduction and muscle contraction. This can include a decrease in GI motility, causing nausea and vomiting, peripheral muscle weakness, and slowed conduction creating muscle cramping, cardiac conduction abnormalities causing dysrhythmias, and impaired nerve conduction resulting paresthesia.


The term hyperkalemia refers to the condition in which serum potassium level is greater than 5.1 mEq/L. There are three main causes of hyperkalemia. First, kidney injury and disease cause an accumulation of intravascular, extracellular potassium. As mentioned, the serum range for potassium is very narrow, so even small accumulations can cause result in hyperkalemia. Second, potassium movement from the intracellular space to the extracellular space occurs during states of acidosis. When extracellular hydrogen ions are excessive secondary to an acidosis in the body, extracellular hydrogen and intracellular potassium will exchange as a way to protect the body from the acidosis, resulting in hyperkalemia. (Diabetic ketoacidosis can be the exception, as discussed in Hypokalemia). Last, aldosterone insufficiency can cause hyperkalemia. When aldosterone promotes sodium’s movement out of the kidney tubules back into the blood, it also causes potassium to move into the kidney tubules for elimination in urine. In the absence of aldosterone, potassium can collect in the serum.

It is estimated that up to 70 percent of clinical decisions are based, at least in part, on laboratory values, and potassium measurement is among the 10 most requested laboratory tests (Khattak et al., 2023). Several factors can contribute to falsely high serum potassium results, termed pseudohyperkalemia. Prolonged tourniquet-application time can damage local tissue cells, and because most potassium is intracellular, cell damage allows intracellular potassium to leak out and become extracellular. Excessive “searching” for a vein can also damage local cells. Using needles that are too small or applying too much negative pressure when drawing blood with a syringe can damage cells. Patients who squeeze their fist too hard can also stimulate potassium release in muscle and that, in turn, can contaminate the blood specimen. For these reasons, it is imperative to correlate laboratory data with clinical assessment findings.

Clinical Judgment Measurement Model

Form a Hypothesis: Correlating Laboratory Data to the Patient’s Clinical Presentation: Pseudohyperkalemia

The nurse reviews morning laboratory data and discovers the patient’s serum potassium level is critically elevated at 7.3 mEq/L. The nurse immediately assesses the patient and determines there are no manifestations of hyperkalemia, the patient is not receiving any medications or IVFs containing potassium, and the patient’s potassium level yesterday was within normal limits. The nurse contacts the provider and obtains a new serum blood sample, recognizing that this laboratory test result is not consistent with the patient’s clinical presentation and that this may be a case of pseudohyperkalemia.

Hyperkalemia manifests as muscle weakness, slowed heart rate, and even paralysis. The manifestations can be similar to those caused by hypokalemia. Both sodium and potassium are essential for the sodium potassium pump to function adequately. Excess potassium makes it harder for nerve and muscle cells to achieve repolarization and the corresponding resting potential, and so causes more frequent firing. This quickly depletes intracellular sodium levels, and the sodium-potassium pump becomes less functional. The most dangerous result of hyperkalemia may be a slowed heart rate with specific T wave, QRS wave, and PR interval changes that can result in ventricular fibrillation and cardiac arrest.


Although people often associate calcium with bone health, calcium also plays a major role in muscle contraction. In all types of muscle, adequate available calcium is necessary to trigger the interaction between actin and myosin. Therefore, calcium regulation is important for cardiac contractility, the dilation and constriction of blood vessels for blood pressure management, respiratory muscle function, GI muscle contraction, and more. Calcium’s role in nerve conduction is multifaceted. It is needed to move electrical signals along axons, and to deposit neurotransmitters into synapsis. Neurologically, calcium is necessary for memory formation (Wood, 2020).

Because calcium is the major component of bone, bone is a source of calcium, if needed. Approximately half of calcium in the serum is in its ionized form, meaning it is a single cation (Ca++) able to bind with calcium cell receptors. However, the other half is not in an ion form but is bound to plasma proteins. Being bound to proteins prohibits this calcium from being able to bind with cell receptors. The normal total serum calcium level in adults is between 8.5 and 10.5 mg/dL (Goyal et al., 2023). Total calcium includes the ionized and bound calcium together. The normal ionized serum calcium range is 4.6 to 5.2 mg/dL, approximately half of the normal total level (Goyal et al., 2023).


A total serum calcium level less than 8.5 mg/dL or an ionized calcium level less than 4.6 mg/dL indicates hypocalcemia. During hypocalcemia, the parathyroid gland will release PTH to trigger an increase in GI absorption of dietary calcium in kidney resorption of calcium from the kidney tubules back to the blood. If necessary, it can also stimulate increased osteoclast activity to break apart bone. In healthy people, approximately 98 percent to 99 percent of the calcium filtered through the kidney glomeruli is reabsorbed into the blood (Gallant & Spiegel, 2017). People with chronic kidney disease often have hypocalcemia, but the exact mechanisms that result in this condition are not fully understood. They are suggested to be related to decreased vitamin D absorption in the GI system and decreased calcium reabsorption in the kidney tubules (Gallant & Spiegel, 2017). Other causes of hypocalcemia include:

  • alterations in acid-base balance
  • hypoparathyroidism
  • multiple blood transfusions
  • tissue necrosis from pancreatitis

Hypocalcemia causes decreased muscle contraction that results in hypotension, weakness, and fatigue. However, the deficit in nerve cell attachment by calcium ions increases the sodium channels available, leading to rapid nerve cell depolarization and increased nerve excitability. Signs and symptoms of hypocalcemia include:

  • cognitive decline
  • hyperreflexia
  • muscle cramping
  • muscle tetany
  • numbness and tingling
  • seizures

Two simple, noninvasive assessment techniques check for hyperreflexivity and tetany; positive Trousseau sign and Chvostek sign are indicators of hypocalcemia (Figure 19.10).

Image showing the involuntary wrist flexion after the application of a blood pressure cuff.
Figure 19.10 Involuntary wrist flexion after the application of a blood pressure cuff inflated to greater than systolic blood pressure is called “Trousseau sign” and is an indication of hypocalcemia. (credit: “Troussau’s Sign of Latent Tetany” by “Huckfinne”/Wikipedia, Public Domain)


The term hypercalcemia refers to a serum calcium level greater than 10.5 mg/dL. Approximately two-thirds of people with hypercalcemia also have hyperparathyroidism. The next most common cause of hypercalcemia is malignancies. In some malignancies, excess PTH is secreted (e.g., breast cancer, squamous-cell lung cancer); in other malignancies, the neoplasm physically invades bony structures and damages bone, which results in release of calcium (e.g., breast, prostate, lung cancers); and in yet others, an excess of vitamin D is present (e.g. pancreatic cancer).

Excess calcium decreases nerve stimulation, which can cause a decrease in cognitive responsiveness, and weak, slowed nerve responses. This slowed nervous system response can result in sluggishness that is manifested in the GI system as constipation, nausea, and possibly vomiting; and in the neurological system as lethargy, confusion, and/or coma. However, the increased calcium can bind with smooth-muscle receptors of the vascular system, resulting in hypertension. If the cause of hypercalcemia is related to increased osteoclast activity from excessive PTH, patients may experience significant bone pain as bone is broken down to release calcium.

Life-Stage Context

Osteoporosis in Older Women

Research indicates that bone density can decline as much as 20 percent during and after menopause, and that 10 percent of women in those years will experience a bone fracture (Endocrine Society, 2022). Bone loss in osteoporosis is mainly due to declining estrogen levels. Estrogen is necessary to support osteoblast activity that rebuilds bone following the normal bone turnover cycle. As estrogen levels decrease, osteoclast activity remains constant, but osteoblast activity declines.

Additionally, older women who have completed menopause are more likely to experience hyperparathyroidism (American Association of Family Physicians, 2023). As previously discussed, hyperparathyroidism produces an excess of PTH, which stimulates the body to increase serum calcium levels. Recall that one source of additional calcium is calcium stored in bones.

For these reasons, it is important for the nurse to recognize that serum calcium levels are not a good indicator of bone health, especially for older women. In fact, adequate or high serum calcium levels may mean bone is being broken down and not replaced and may indicate poor bone health. Women 65 years of age or older should be encouraged to have a bone density test to accurately detect bone strength.


Normal serum magnesium levels range between 1.7 and 2.2 mg/dL. This is the narrowest range of all the electrolytes. Approximately half (50 to 60 percent) of the magnesium in the body is stored in bones and muscles and nearly all the rest is inside cells of the muscles and soft tissues; less than 1 percent is in the serum. Magnesium is tightly regulated in the body through kidney tubule filtration and small intestine absorption. Magnesium is involved in more than 300 enzymatic reactions that affect, among other things, muscle and nerve function, blood pressure regulation, and immune response (Ware & Hatanaka, 2023).


Many natural foods are excellent dietary sources of magnesium, but due to the amount of processed food consumed in the United States, many Americans have a dietary deficiency of magnesium. Magnesium deficiency is associated with a host of potential medical conditions, including but not limited to Alzheimer disease, depression, anxiety, headaches, premenstrual syndrome, type 2 diabetes mellitus, osteoporosis, and an array of cardiovascular pathologies (Ware & Hatanaka, 2023). Although hypomagnesemia, defined as a serum magnesium level less than 1.7 mg/dL, often results from poor dietary intake, it can also be due to GI digestive and/or absorptive problems, including pancreatitis, significant diarrhea, excess alcohol use, the use proton pump inhibitors for acid reflux, and some gastric bypass surgeries.

As mentioned, hypomagnesemia contributes to any number of disease processes. However, clinically, the nurse will notice manifestation of hypomagnesemia associated with magnesium’s influence on blood pressure and heart rhythm, due to magnesium’s role in vasodilation and regulation of cardiac rate and rhythm. Hypomagnesemia manifests as hypertension and tachycardia, possibly with serious cardiac dysrhythmias, including torsades de pointes and ventricular fibrillation.

Magnesium is necessary for adenosine triphosphate (ATP) production, which is needed for sodium-potassium pump function. Hypomagnesemia causes the sodium-potassium pump channels to remain open. This prolonged opening can manifest in the nervous system as confusion, hyperreflexia, and positive Chvostek and Trousseau signs, similar to hypocalcemia.


A level of magnesium that is too high, hypermagnesemia, is an uncommon electrolyte imbalance. Magnesium levels significantly greater than 2.2 mg/dL are rare and usually attributed to acute or chronic kidney disease. However, decreased GI motility, as seen in some types of constipation, can cause an increase in magnesium absorption. Coupled with constipation, treatments that contain magnesium such as milk of magnesia or magnesium citrate can cause hypermagnesemia, especially in combination with decreased kidney function.

Acute manifestations of hypermagnesemia typically are not observed until magnesium levels in serum approach greater than 7.0 mg/dL. Hypotension and slowed heart rate with atrioventricular blocks are among the most common and life-threatening manifestations.


Every cell in the body requires phosphorous to function. Phosphorous, along with calcium, is essential for bone strength. Hydroxyapatite is the mineralized form of calcium phosphate that is present in bone. Phospholipids are major structural components of cell membranes. The process of phosphorylation, whereby phosphate groups are added or removed from proteins, enzymes, and hormones, support cellular functions and supply energy, like ATP. Phosphorous acts as an acid-base buffer through the balance of hydrogen phosphate and dihydrogen phosphate. Diphosphoglycerate, another compound made of phosphorous, directly influences the oxyhemoglobin curve and, thereby, oxygen delivery to tissues.

Phosphorous exists in the body as phosphate; therefore, phosphorous and phosphate are often used interchangeably. Laboratory tests measure phosphate levels; the normal serum phosphate level is between 2.5 and 4.8 mg/dL (Cleveland Clinic, 2021). Like calcium, phosphorus is regulated by PTH and through the kidneys. However, phosphate regulation is the opposite of calcium regulation. When PTH is released, phosphorus levels are decreased through an increase in kidney filtration and excretion. For that reason, alterations in phosphorous levels manifest as the opposite of alterations in calcium levels.


Hypophosphatemia is usually caused by extreme states of malnutrition from starvation or significant GI malabsorption of nutrients. A serum phosphate level less than 2.5 mg/dL defines hypophosphatemia. Because of the phosphorus-calcium inverse relationship, hypophosphatemia manifestations resemble those of hypercalcemia. In severe hypophosphatemia, bone pain can be difficult to manage as osteoclast activity increases to elevate serum calcium levels. The subsequent decrease in nerve function can result in numbness and tingling in the extremities, neuropathies, and possibly coma. Muscle weakness can be life threatening when cardiac and respiratory muscles are affected.


Because phosphorus is regulated, in part, by kidney filtration and excretion, most cases of hyperphosphatemia (phosphate level >4.8 mg/dL) are related to decreased kidney function. Concurrently, hyperphosphatemia is associated with worsening kidney function due to the formation of calcium phosphate salt calcifications in the vasculature of the kidneys. In a similar manner, cardiovascular disease risk is increased in the patient with hyperphosphatemia (Zhou et al., 2021).


Chloride is the most abundant anion in the body. Normal serum chloride levels are 97 to 105 mEq/L (Cleveland Clinic, 2021). Chloride is regulated by the kidneys through filtration, excretion, and resorption in the tubule system. Like sodium, there is much more extracellular chloride than other electrolytes, and like sodium, chloride plays an essential role in fluid balance. As a positively charged ion, sodium (Na+) moves into and out of the fluid spaces and changes the overall electric charge in the spaces. Chloride moves along with sodium, and because it is a negatively charged anion (Cl) it maintains charge neutrality. Additionally, chloride is necessary for acid-base balance because it can move more easily in and out of cells than can bicarbonate ions. Negatively charged chloride can accept a positively charged hydrogen and move intracellularly, thus decreasing blood pH, and vice versa. Last, chloride is a component of a main digestive acid, hydrochloric acid. Hydrochloric acid’s acidity helps protect against foodborne illnesses, facilitates nutritional absorption, and stimulates secretion of digestive enzymes and bile from the pancreas and liver.


The term hypochloremia refers to the condition in which the serum chloride level less than 97 mEq/L. Dilutional causes of hypochloremia include FVE from SIADH or heart failure. Other reasons for hypochloremia are increased kidney losses due to loop and thiazide diuretic therapy; states of acidosis in which, to correct the acidosis, kidney bicarbonate is preserved in exchange for chloride; and lastly, hydrochloric acid loss due to vomiting or nasogastric suctioning. Manifestations of hypochloremia are like those of hyponatremia and can include fluid shifting and weakness.

Life-Stage Context

Cystic Fibrosis Is No Longer Just a Childhood Disease

Cystic fibrosis (CF) was named in 1955 and is a serious inherited disease in which chloride transport across epithelial cell membranes of the respiratory tract and GI organs is disrupted and so normal fluid transport is interrupted. This results in respiratory mucus that is thick and difficult to clear, and significant malnutrition. Cystic fibrosis used to be a pediatric disease; children diagnosed with CF rarely lived through elementary school age. However, due to treatment advances, approximately 60 percent of patients with CF in the United States today are adults (Cystic Fibrosis Foundation, n.d.).


A serum chloride level higher than 105 mEq/L defines hyperchloremia. The most common cause is a loss of bicarbonate, most frequently seen in extreme or prolonged diarrhea, or from medications that decrease serum bicarbonate levels, such as acetazolamide (Diamox). Manifestations of hyperchloremia are like those of hypernatremia and include hypertension and tissue dehydration.

Homeostatic Mechanisms of Fluid and Electrolyte Balance

As described throughout this chapter, there are many mechanisms that work together to maintain fluid and electrolyte balances in the body. Osmotic regulation relies on osmoreceptors in the hypothalamus and stimulates water movement in response to changes in sodium levels. Antidiuretic hormone is secreted by the pituitary gland when osmoreceptors recognize high sodium levels in the blood. Antidiuretic hormone directs the kidneys to conserve water and thereby lower serum sodium concentrations.

The hormone aldosterone also acts to increase fluid volume, but aldosterone is released on the basis of pressure inside the glomeruli as the last part of the RAAS. Aldosterone acts to increase the amount of sodium returned to the blood. Where sodium goes, water follows; through this mechanism, fluid volume is increased.

Peptides (e.g., atrial natriuretic peptide [ANP]) also assist in fluid volume regulation. ANP is found in the cells of the atrial endocardium. As fluid volume increases, these cells are stretched and release ANP. ANP works by interrupting the RAAS and decreasing fluid volume. Numerous hormones, peptides, and proteins work to maintain electrolyte balances. Through stimulating the digestive system to absorb more or fewer electrolytes, or through altering cell membrane structure to move more or fewer electrolytes inside or outside of cells, the interchange between these mechanisms maintains a balance of fluids and electrolytes.

Real RN Stories

A Patient Experienced a Motor Vehicle Accident and Diabetes Insipidus

Nurse: Angel, BSN
Clinical setting: Trauma I hospital surgical intensive care unit
Years in practice: 4
Facility location: A medium-sized city in southern Mississippi

My hospital is the only trauma center within about 150 miles, so we admit a lot of trauma patients from around the area. During a significant rainstorm, I received a patient from the emergency department who required life flight to our hospital following a motorcycle versus automobile accident. The patient was a 25-year-old male named Bruce. When Bruce first got to the surgical intensive care unit, he was experiencing a lot of pain from multiple broken ribs, a large pneumothorax, and an open fracture of his humerus. He was alert and oriented and talking to me about how much he wished he hadn’t tried to ride his motorcycle in the rain. He was NPO (not allowed anything by mouth) waiting for surgery to repair his humerus, and we were monitoring him closely for respiratory complications. He had an 18-gauge intravascular access with fluids running at 75 mL/h), an indwelling urinary catheter (IUC), and 2 L of oxygen via a nasal cannula. Compared with other trauma patients, he was easy.

About 4 hours later, I noticed his catheter bag was full of clear, light-yellow urine. I assumed he had received a large amount of IV fluid during life flight and in the emergency room. However, within an hour of emptying his catheter bag, he had another 800 mL, this time of very light-colored urine output. I checked his blood pressure and noted it dropped about 20 mm Hg from his baseline and was now 100/68 mm Hg, with a heart rate of 104 bpm. I was concerned and contacted the admitting physician, who requested a STAT (immediate) urine osmolality measurement and a liter IV bolus of fluid. The urine osmolality returned at 105 mOsm/L, which is very low. By the time I was able to finish the fluid bolus, Bruce had already had a urine output of another 1,200 mL. His neurological assessment had not deteriorated, but the physician ordered a STAT head CT (computed tomography) scan that showed a small subarachnoid bleed. Bruce was immediately sent to the operating room, where a neurosurgeon clipped the bleeding vein. As it turned out, the bleeding was causing inflammation of Bruce’s brain that was preventing his pituitary gland from secreting enough ADH and, therefore, his system was making too much urine. Usually, when a patient has a head injury like Bruce did, you observe a change in his level of consciousness, but in this case all I observed was an increase in urine output.

Organs and Body Systems

Of all the body systems, arguably the kidney system has the most important role in fluid volume regulation and electrolyte, as well as acid-base, balance. Injuries and damage to the kidneys can result in a loss of water and electrolyte filtration and elimination. Chronic kidney disease affects more than 37 million people in the United States (National Institutes of Health, 2023). More than 800,000 people in the United States are living with end-stage kidney disease, with 69 percent of people requiring dialysis and 31 percent receiving a kidney transplant (National Institutes of Health, 2023).

Cardiac control of fluid volume is related to ANP, as described earlier; however, the ability of the heart to generate an adequate cardiac output, coupled with the health of the blood vessels throughout the body, is a main consideration in the kidney’s stimulation of the RAAS. Fluid volume alterations can affect electrolyte levels through simple dilution or concentration.

The GI system, through absorption, affects both fluid and electrolyte balances. Vomiting and nasogastric suctioning can cause sodium and potassium deficits, and diarrhea can lead to chloride deficits. Some weight loss surgeries can decrease both fluid and electrolyte absorption, as can excessive alcohol use. Excessive or deficient electrolyte intake, through mental health issues like anorexia nervosa or bulimia, lack of adequate food sources due to poverty, or lack of access or even knowledge deficits related to dietary sources of essential nutrients can lead to electrolyte imbalances.

Clinical Safety and Procedures (QSEN)

QSEN Competency: Inserting and Removing a Nasogastric Tube and Irrigating a Nasogastric Tube Connected to Suction

See the competency checklists for Inserting and Removing a Nasogastric Tube & Irrigating a Nasogastric Tube Connected to Suction. You can find the checklists on the Student resources tab of your book page on


Osmosis is the movement of water based on a gradient of solutes to water. Water will move to a fluid space that has the highest solute concentration. This is why normalized levels of the most prevalent solutes—sodium, glucose, and protein—are needed to stabilize fluid movement. Elevated serum glucose or sodium levels will cause a shift of fluid into the vascular system, whereas low serum sodium or protein levels will cause fluid to shift out of the vascular system.


Diffusion is the movement of solutes from an area of high solute concentration to an area of low solute concentration to reach an equilibrium. Diffusion is a passive process, which means it does not require energy. This is crucial to remember when considering compensation of other areas. For example, when potassium is exchanged for hydrogen during an acidosis, each electrolyte diffuses across the cell membrane to balance positive ions. Similarly, when electrolytes are absorbed into the blood from the GI tract, the amount of the electrolyte already present will determine, to some degree, how much new electrolyte can diffuse into the blood.

Active Transport

Most diffusion occurs passively. It is a matter of creating an equilibrium on both sides of a permeable membrane. However, it some cases, diffusion requires energy because the movement goes against an existing gradient. This type of diffusion is called active diffusion or active transport. The sodium-potassium pump is an example of active transport. Most sodium is extracellular, and most potassium is intracellular. The sodium-potassium pump moves sodium out of the cell and potassium into the cell, both against the gradient. This alters the cell’s charge and potentiates cell firing, but it requires energy in the form of ATP.


Filtration moves both fluids and solutes, either alone or together. Filtration is caused by variations in hydrostatic pressure. The gradient that drives fluid and/or solute movement in filtration is a pressure gradient that exists between two spaces. When hydrostatic pressure is high, fluid and solutes will be forced into a different space. When that occurs, the pressure is changed, and fluids and solutes can move back (Figure 19.11). This is, in part, how fluid, nutrients, and gasses are exchanged between the blood, via capillaries, and the interstitial and intracellular spaces. During cardiac systole, capillary pressure is high, and fluid, nutrients, and gasses are forced out. During diastole, capillary pressure is low, and fluid, wastes, and gasses are forced out of cells and tissues back into the capillaries. Variances in oncotic pressure as fluid, solutes, and gasses move also contribute to filtration.

Exchange of gasses via capillaries.
Figure 19.11 High arterial hydrostatic pressure forces fluid out of capillaries, whereas lower venous hydrostatic pressure allows fluid to enter capillaries. (credit: modification of work from Anatomy and Physiology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

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