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.

References

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“Cellular​_Fluid_Content.jpg” by Welcome1To1The1Jungle is licensed under CC BY 3.0 ↵.

2.

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

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4.

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

8.

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

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

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“2626​_Renin_Aldosterone_Angiotensin.jpg” by OpenStax is licensed under CC BY 3.0. Access for free at https://openstax​.org​/books/anatomy-and-physiology​/pages/25-4-microscopic-anatomy-of-the-kidney ↵.

13.

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

15.

Lewis, J. L., III. (June 2020). Volume overload. Merck Manual Professional Version. https://www​.merckmanuals​.com/professional​/endocrine-and-metabolic-disorders​/fluid-metabolism​/volume-overload ↵.

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MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US); Dehydration; [updated 2020, Oct 1; reviewed 2016, Apr 15; cited 2020, Aug 5]. https://medlineplus​.gov/dehydration.html ↵.

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MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US); Dehydration; [updated 2020, Oct 1; reviewed 2016, Apr 15; cited 2020, Aug 5]. https://medlineplus​.gov/dehydration.html ↵.

18.

MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US); Dehydration; [updated 2020, Oct 1; reviewed 2016, Apr 15; cited 2020, Aug 5]. https://medlineplus​.gov/dehydration.html ↵.

19.

Forciea, B. (2017, April 21). Fluids and electrolytes: Water. [Video]. YouTube. All rights reserved. Video used with permission. https://youtu​.be/VMxmDeduKR0 ↵.

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

References

1.

“Blausen​_0685_OsmoticFlow_Isotonic.png” by BruceBlaus.com staff is licensed under CC BY 3.0 ↵.

2.

“Blausen​_0684_OsmoticFlow_Hypotonic.png” by BruceBlaus.com staff is licensed under CC BY 3.0 ↵.

3.

“Blausen​_0683_OsmoticFlow_Hypertonic.png” by BruceBlaus.com staff is licensed under CC BY 3.0 ↵.

4.

Harris, H. (2011). I.V. fluids: What nurses need to know. Nursing2017, 41(5), 30-38. ↵. [PubMed: 21487274]

5.

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

6.

Harris, H. (2011). I.V. fluids: What nurses need to know. Nursing2017, 41(5), 30-38. ↵. [PubMed: 21487274]

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]

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.

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]

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

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

14.

"1814​_The_Parathyroid_Glands.jpg” by OpenStax is licensed under CC BY 3.0. Access for free at https://openstax​.org​/books/anatomy-and-physiology​/pages/17-5-the-parathyroid-glands ↵.

15.

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

16.

Lewis, J. L., III. (April 2020). Hypercalcemia. Merck Manual Professional Version. https://www​.merckmanuals​.com/professional​/endocrine-and-metabolic-disorders​/electrolyte-disorders​/hypercalcemia ↵.

17.

Lewis, J. L., III. (April 2020). Hypocalcemia. Merck Manual Professional Version. https://www​.merckmanuals​.com/professional​/endocrine-and-metabolic-disorders​/electrolyte-disorders​/hypocalcemia ↵.

18.

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

19.

Lewis, J. L., III. (April 2020). Hyperphosphatemia. Merck Manual Professional Version. https://www​.merckmanuals​.com/professional​/endocrine-and-metabolic-disorders​/electrolyte-disorders​/hyperphosphatemia ↵.

20.

Lewis, J. L., III. (April 2020). Hypophosphatemia. Merck Manual Professional Version. https://www​.merckmanuals​.com/professional​/endocrine-and-metabolic-disorders​/electrolyte-disorders​/hypophosphatemia ↵.

21.

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

22.

Lewis, J. L., III. (April 2020). Hypermagnesemia. Merck Manual Professional Version. https://www​.merckmanuals​.com/professional​/endocrine-and-metabolic-disorders​/electrolyte-disorders​/hypermagnesemia ↵.

23.

Lewis, J. L., III. (April 2020). Hypomagnesemia. Merck Manual Professional Version. https://www​.merckmanuals​.com/professional​/endocrine-and-metabolic-disorders​/electrolyte-disorders​/hypomagnesemia 7/7/20 ↵.

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).

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.

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]

References

1.

Mitchel, J. H., Wildenthal, K., & Johnson Jr., R. L. (1972). The effects of acid-base disturbances on cardiovascular and pulmonary function. Kidney International, 1, 375-389. https://www​.kidney-international​.org/article​/S0085-2538(15)31047-4/pdf ↵

2.

WakeMed Pathology Laboratories. (2016). Critical values. https://www​.wakemed.org​/assets/documents​/pathology/lab-critical-values.pdf ↵

3.

Forciea, B. (2017, May 10). Acid-base balance: Bicarbonate ion buffer. [Video]. YouTube. All rights reserved. Video used with permission. https://youtu​.be/5_S5wZks9v8 ↵

4.

RegisteredNurseRN. (2015, May 6). ABGs made easy for nurses w/ tic tac toe method for arterial blood gas interpretation. [Video]. YouTube. All rights reserved. Video used with permission. https://youtu​.be/URCS4t9aM5o ↵

5.

Feller-Kopman, D. J., & Schwartzstein, R. M. (2020). The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure. UpToDate. https://www​.uptodate​.com/contents/the-evaluation-diagnosis-and-treatment-of-the-adult-patient-with-acute-hypercapnic-respiratory-failure ↵

6.

A.D.A.M. Medical Encyclopedia [Internet]. Atlanta (GA): A.D.A.M., Inc.; c1997-2021. Respiratory acidosis; [updated 2021, February 8]. https://medlineplus​.gov​/ency/article/000092.htm ↵

7.

Feller-Kopman, D. J., & Schwartzstein, R. M. (2020). The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure. UpToDate. https://www​.uptodate​.com/contents/the-evaluation-diagnosis-and-treatment-of-the-adult-patient-with-acute-hypercapnic-respiratory-failure ↵

8.

Schwartzstein, R. M., Richards, J., Edlow, J. A., & Roy-Byrne, P. P. (2020). Hyperventilation syndrome in adults. UpToDate. https://www​.uptodate​.com/contents/hyperventilation-syndrome-in-adults ↵

9.

Schwartzstein, R. M., Richards, J., Edlow, J. A., & Roy-Byrne, P. P. (2020). Hyperventilation syndrome in adults. UpToDate. https://www​.uptodate​.com/contents/hyperventilation-syndrome-in-adults ↵

10.

Emmett, M., & Szerlip, H. (2020). Approach to the adult with metabolic acidosis. UpToDate. https://www​.uptodate​.com/contents/approach-to-the-adult-with-metabolic-acidosis ↵

11.

A.D.A.M. Medical Encyclopedia [Internet]. Atlanta (GA): A.D.A.M., Inc.; c1997-2021. Metabolic acidosis; [updated 2021, February 8]. https://medlineplus​.gov​/ency/article/000335.htm ↵

12.

Emmett, M., & Szerlip, H. (2020). Approach to the adult with metabolic acidosis. UpToDate. https://www​.uptodate​.com/contents/approach-to-the-adult-with-metabolic-acidosis ↵

13.

Emmett, M., & Szerlip, H. (2020). Causes of metabolic alkalosis. UpToDate. https://www​.uptodate​.com/contents/causes-of-metabolic-alkalosis ↵

14.

Emmett, M., & Szerlip, H. (2020). Causes of metabolic alkalosis. UpToDate. https://www​.uptodate​.com/contents/causes-of-metabolic-alkalosis ↵

15.

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

16.

Emmett, M., & Szerlip, H. (2020). Causes of metabolic alkalosis. UpToDate. https://www​.uptodate​.com/contents/causes-of-metabolic-alkalosis ↵

17.

This work is a derivative of StatPearls by Castro and Keenaghan and is licensed under CC BY 4.0 ↵

18.

Woodruff, D. W. (2012). 6 easy steps to ABG analysis. Ed4Nurses, Inc. http://www​.profcaseyscudmorern​.org/uploads​/4/5/0/4/45049193/abgebook.pdf ↵

Assessment

A thorough assessment provides valuable information about a patient’s current fluid, electrolyte, and acid-base balance, as well as risk factors for developing imbalances. Performing a chart review or focused health history is a good place to start collecting data, with any identified gaps or discrepancies verified during the physical assessment. It is also important to consider pertinent life span or cultural considerations that impact a patient’s fluid and electrolyte status.

Objective Assessment

Objective assessment data is information that the nurse directly observes. This data is obtained through a physical examination using inspection, auscultation, and palpation. A complete head-to-toe assessment should be performed to avoid missing clues to the patient’s condition.

Focused assessments such as trends in weight, 24-hour intake and output, vital signs, pulses, lung sounds, skin, and mental status are used to determine fluid balance, electrolyte, and acid-base status.

• Accurate daily weights can provide important clues to fluid balance. Weights must be taken on the same scale, at the same time of day, with the patient wearing similar clothing in order to be accurate. A one kilogram change in weight in 24 hours is considered significant because this represents a one liter fluid gain or loss and should be reported to the provider.
• Accurate measurement of 24-hour intake and output helps validate weight findings. Averaged urine output of less than 30 mL/hour or 0.5mL/hr/kg of concentrated urine should be reported to the provider.
• Vital signs should be analyzed. An elevated blood pressure and bounding pulses are often seen with fluid volume excess. Decreased blood pressure with an elevated heart rate and a weak or thready pulse are hallmark signs of fluid volume deficit. Systolic blood pressure less than 100 mm Hg in adults, unless other parameters are provided, should be reported to the health care provider.
• Lung crackles can signify fluid volume excess and are often first auscultated in the lower posterior lung fields.
• Tight, edematous, shiny skin indicates fluid volume excess. See Figure 15.15^[1] for an image of edema. Conversely, skin tenting, dry mucous membranes, or dry skin indicate fluid volume deficit.
• New mental status changes such as confusion or decreased level of consciousness can indicate fluid, electrolyte, or acid-base imbalance, especially hypo- or hypernatremia, acid-base imbalances, or fluid volume deficit.
• Cardiac arrhythmias can be seen with acid-base imbalances and electrolyte imbalances, especially with hypo- or hyperkalemia and alkalosis. See Table 15.6a for a comparison of expected and unexpected findings and those that require notification of a health care provider.

Figure 15.15

Edema

Table 15.6a

Expected Findings Versus Unexpected Findings Indicating a Fluid Imbalance^[2]

Review additional details about assessing these body systems in Open RN Nursing Skills.

Diagnostic and Lab Work

Diagnostic tests and lab work provide important information about fluid status, electrolyte, and acid-base balance and should be used in conjunction with a thorough subjective and objective assessment to form a complete picture of the patient’s overall status. It is important to cluster diagnostic and lab assessment data with subjective and objective assessment data to ensure a complete assessment picture. This will help ensure correct information is reported to the provider as necessary.

Lab work provides important clues to overall fluid status. Common lab tests used to evaluate fluid status include serum osmolarity, urine specific gravity, hematocrit, and blood urea nitrogen (BUN).

Serum osmolarity (often interchanged with the term serum osmolality) measures the concentration of particles in the blood with a normal range of 275 to 295 mmol/kg). Normal value ranges may vary slightly among different laboratories. In healthy people, when serum osmolality in the blood becomes high, the body releases antidiuretic hormone (ADH). This hormone causes the kidneys to reabsorb water, resulting in dilution of the blood and the return of serum osmolarity to normal range. An elevated serum osmolarity level means the blood is more concentrated than normal and often indicates deficient fluid volume deficit. A decreased serum osmolarity means the blood is more dilute than normal and may indicate a fluid volume excess.^[3]

Urine osmolarity measures the concentration of particles in the urine. An increased urine osmolarity result means the urine is concentrated and can indicate fluid volume deficit. A decreased urine osmolarity result means the urine is dilute and can indicate excess fluid intake.^[4] Urine specific gravity is a urine test that commonly measures hydration status by measuring the concentration of particles in urine. Normal urine specific gravity levels are between 1.010 and 1.020. A urine specific gravity above 1.020 indicates concentrated urine and can indicate a fluid volume deficit, similarly to an elevated urine osmolarity. A urine specific gravity below 1.010 indicates dilute urine, which can occur with excessive fluid intake.^[5]

When a condition called “Excessive Fluid Volume” occurs, altered physiological mechanisms impact the kidney’s ability to increase urine output to eliminate excessive fluid volume, causing urine output to decrease. As a result, the serum osmolarity decreases as fluid is retained but the urine specific gravity is elevated because urine is concentrated.

Hematocrit (HCT) is a blood test that measures how much of your blood is made up of red blood cells compared to the liquid component of blood called plasma. It is often part of a complete blood count (CBC), a routine test that measures different components of your blood. The normal hematocrit for men is 42 to 52%; for women it is 37 to 47%, but these ranges may vary slightly across labs.

In addition to measuring red blood cells, hematocrit levels can also be used to evaluate fluid balance. When deficient fluid volume is occurring, the plasma component of the blood also decreases, causing an elevated concentration of red blood cells (and an elevated hematocrit). In this case, drinking more fluid or receiving intravenous fluids will bring the hematocrit level back to normal range. Conversely, if a patient is experiencing “Excessive Fluid Volume,” the plasma component of the blood is increased, causing dilution of the red blood cells and a decreased hematocrit level.^[6],^[7] See Figure 15.16^[8] for an illustration of normal hematocrit, elevated hematocrit, and decreased hematocrit due to fluid imbalance.

Figure 15.16

Effects of Fluid Imbalance on Hematocrit

Blood Urea Nitrogen (BUN) measures the amount of urea nitrogen in your blood. BUN and serum creatinine levels are used to evaluate kidney function, with increased levels indicating worsening kidney function. In general, the normal BUN range is 7 to 20 mg/dL, but normal ranges vary depending on the reference range used by the lab and the patient’s age. Patients with “Deficient Fluid Volume” can also have elevated BUN levels for the same reason that hematocrit is affected; as plasma levels decrease, the blood becomes more concentrated.

In addition to monitoring lab work for results indicating fluid imbalance, electrolytes, specifically sodium, potassium, calcium, phosphorus, and magnesium, should be monitored closely for patients at risk. Refer to Table 15.4 in the “Electrolytes” section for an overview of electrolyte imbalances, common symptoms, and common treatments.

Additional diagnostic tests used to evaluate for signs of fluid and electrolyte imbalances are the chest X-ray and the electrocardiogram. A chest X-ray evaluates for fluid in the lungs, a common complication of excessive fluid volume. An electrocardiogram (ECG) evaluates for cardiac complications resulting from electrolyte imbalances.

Arterial blood gases are used to closely monitor critically ill patients, such as patients in diabetic ketoacidosis or in severe respiratory distress. ABG results provide important clues about respiratory status, oxygenation, and metabolic processes occurring in the body. See Table 15.6b for a summary of laboratory findings associated with fluid, electrolyte, and acid-base imbalances.

Table 15.6b

Lab Values Associated with Fluid and Electrolyte Imbalances

Diagnoses

There are many nursing diagnoses applicable to fluid, electrolyte, and acid-base imbalances. Review a nursing care planning resource for current NANDA-I approved nursing diagnoses, related factors, and defining characteristics. See Table 15.6c for commonly used NANDA-I diagnoses associated with patients with fluid and electrolyte imbalances.^[12]

Table 15.6c

Common NANDA-I Nursing Diagnoses Related to Fluid and Electrolyte Imbalances^[13]

Outcome Identification

Goals for a patient experiencing fluid, electrolyte, or acid-base imbalances depend on the chosen nursing diagnosis and specific patient situation. Typically, goals should relate to resolution of the imbalance. For example, if the nursing diagnosis is Excess Fluid Volume, then an appropriate goal would pertain to resolution of the fluid volume excess. Remember that goals are broad and outcomes should be narrowly focused and written in SMART format (Specific, Measurable, Achievable, Realistic, and Time Oriented).

For the nursing diagnosis of Excess Fluid Volume, an overall goal is, “Patient will achieve fluid balance.” Fluid balance for a patient with Excess Fluid Volume is indicated by body weight returning to baseline with no peripheral edema, neck vein distention, or adventitious breath sounds.^[14] An example of a SMART outcome is, “The patient will maintain clear lung sounds with no evidence of dyspnea over the next 24 hours.”

For patients experiencing Electrolyte Imbalances, an appropriate goal is, “Patient will maintain serum sodium, potassium, calcium, phosphorus, magnesium, and/or pH levels within normal range.” An additional goal is, “The patient will maintain a normal sinus heart rhythm with regular rate,” because many electrolyte imbalances impact the electrical conduction system of the heart and this is a life-threatening complication.

Planning Interventions

Evidence-based interventions should be planned according to the patient’s history and specific fluid, electrolyte, or acid-base imbalance present. Refer to a nursing care planning resource for evidence-based interventions for specific nursing diagnoses. Table 15.6d lists selected interventions for key imbalances.^[15],^[16],^[17],^[18]

Table 15.6d

Interventions for Imbalances

Read more about medications affecting fluid and electrolyte balance, such as diuretics, in the “Cardiovascular and Renal System” chapter in Open RN Nursing Pharmacology.

Read about intravenous fluids used to treat Fluid Volume Deficit in the “IV Therapy Management” chapter in Open RN Nursing Skills.

Implement Interventions Safely

Patients with fluid and electrolyte imbalances can quickly move from one imbalance to another based on treatments received. It is vital to reassess a patient before implementing interventions to ensure current status warrants the prescribed intervention. For example, a patient admitted with Fluid Volume Deficit received intravenous fluids (IV) over the past 24 hours. When the nurse prepares to administer the next bag of IV fluids, she notices the patient has developed pitting edema in his lower extremities. She listens to his lungs and discovers crackles. The nurse notifies the prescribing provider, and the order for intravenous fluids is discontinued and a new order for diuretic medication is received.

Therefore, assessments for new or worsening imbalances should be performed prior to implementing interventions:^[20]

• Monitor daily weights for sudden changes. A weight change of greater than 1 kg in 24 hours (using the same scale and type of clothing) should be reported to the provider.
• Monitor location and extent of edema using the 1+ to 4+ scale to quantify edema.
• Monitor intake and output over a 24-hour period; note trends of decreasing urine output in relation to fluid intake indicating potential development of Fluid Volume Excess.
• Monitor lab work such as serum osmolarity, serum sodium, BUN, and hematocrit for abnormalities. (For example, a patient receiving IV fluids may develop Fluid Volume Excess, resulting in decreased levels of serum osmolarity, serum sodium, BUN, and hematocrit. Conversely, a patient receiving IV diuretics can quickly become dehydrated, resulting in elevated levels of serum osmolarity, serum sodium, BUN, and hematocrit.)
• For patients receiving intravenous fluids, monitor for the development of excessive fluid volume. Monitor lung sounds for crackles and ask about the presence of dyspnea. Report new abnormal findings to the provider.
• For patients receiving diuretic therapy, monitor for fluid volume deficit and electrolyte imbalances such as hypokalemia and hyponatremia.

Implement fall precautions for patients with orthostatic hypotension, restlessness, anxiety, or confusion related to fluid imbalances.

Evaluation

The effectiveness of interventions implemented to maintain fluid balance must be continuously evaluated. Evaluation helps the nurse determine whether goals and outcomes are met and if interventions are still appropriate for the patient. If outcomes and goals are met, the plan of care can likely be discontinued. If outcomes and goals are not met, they may need to be revised. It is also possible that interventions may need to be added or revised to help the patient meet their goals and outcomes. Table 15.6e provides a list of assessment findings indicating imbalances are improved.

Table 15.6e

Evaluating for Improvement of Imbalances

References

1.

“Combinpedal​.jpg” by James Heilman, MD is licensed under CC BY-SA 3.0 ↵.

2.

El-Sharkawy A. M., Sahota O., Maughan R. J., Lobo D. N. The pathophysiology of fluid and electrolyte balance in the older adult surgical patient. Clinical Nutrition. 2014;33(1):6–13. ↵ [PubMed: 24308897] [CrossRef]

3.

A.D.A.M. Medical Encyclopedia [Internet]. Atlanta (GA): A.D.A.M., Inc.; c1997-2021. Osmolality blood test; [updated 2021, February 8]. https:​//medlineplus​.gov/ency/article/003463.htm ↵.

4.

RnCeus.com. (n.d.). Serum and urine osmolality. https://www​.rnceus.com/renal/renalosmo​.html ↵.

5.

Flasar C. What is urine specific gravity? Nursing. 2008;2008;38(7):14. ↵ [PubMed: 18580635] [CrossRef]

6.

MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US); Hematocrit test; [updated 2020, Jul 31; reviewed 2020, Jul 31; cited 2021, Feb 11]. https://medlineplus​.gov​/lab-tests/hematocrit-test/ ↵.

7.

Billett, H. H. (1990). Hemoglobin and hematocrit. In Walker H. K., Hall W. D., Hurst J. W. (Eds.), Clinical methods: The history, physical, and laboratory examinations (3rd ed.). Butterworths. https://www​.ncbi.nlm​.nih.gov/books/NBK259/ ↵. [PubMed: 21250045]

8.

“1901​_Composition_of_Blood.jpg” by Arabic is licensed under CC BY 3.0 ↵.

9.

Ringer, S. (2020). Fluid and electrolyte therapy in newborns. UpToDate. https://www​.uptodate​.com/contents/fluid-and-electrolyte-therapy-in-newborns ↵.

10.

Iglesia I., Guelinckx I., De Miguel-Etayo P. M., González-Gil E. M., Salas-Salvadó J., Kavouras S. A., Gandy J., Martínez H., Bardosono S., Abdollahi M., Nasseri E., Jarosz A., Ma G., Carmuega E., Thiébaut I., Moreno L. A. Total fluid intake of children and adolescents: cross-sectional surveys in 13 countries worldwide. European Journal of Nutrition. 2015;54:57–67. ↵ [PMC free article: PMC4473088] [PubMed: 26081646] [CrossRef]

11.

El-Sharkawy A. M., Sahota O., Maughan R. J., Lobo D. N. The pathophysiology of fluid and electrolyte balance in the older adult surgical patient. Clinical Nutrition. 2014;33(1):6–13. ↵ [PubMed: 24308897] [CrossRef]

12.

Herdman, T., & Kamitsuru, S. (2017). NANDA international nursing diagnoses: Definitions & classification 2018-2020 (11th ed.). Thieme Publishers. pp. 182-186. ↵.

13.

Herdman, T., & Kamitsuru, S. (2017). NANDA international nursing diagnoses: Definitions & classification 2018-2020 (11th ed.). Thieme Publishers. pp. 182-186. ↵.

14.

Ackley, B., Ladwig, G., Makic, M. B., Martinez-Kratz, M., & Zanotti, M. (2020). Nursing diagnosis handbook: An evidence-based guide to planning care (12th ed.). Elsevier. pp. 360-363, 406-416. ↵.

15.

Ackley, B., Ladwig, G., Makic, M. B., Martinez-Kratz, M., & Zanotti, M. (2020). Nursing diagnosis handbook: An evidence-based guide to planning care (12th ed.). Elsevier. pp. 360-363, 406-416. ↵.

16.

Fluid overload. (2021). Lippincott advisor. http://advisor​.lww.com ↵.

17.

Dehydration. (2021). Lippincott advisor. http://advisor​.lww.com ↵.

18.

Electrolyte imbalance. (2021). Lippincott advisor. http://advisor​.lww.com ↵.

19.

Centers for Disease Control and Prevention. (2017). Assessment - measuring orthostatic blood pressure. cdc​.gov/steadi/pdf/Measuring​_Orthostatic​_Blood_Pressure-print.pdf ↵.

20.

Ackley, B., Ladwig, G., Makic, M. B., Martinez-Kratz, M., & Zanotti, M. (2020). Nursing diagnosis handbook: An evidence-based guide to planning care (12th ed.). Elsevier. pp. 360-363, 406-416. ↵.

Patient Scenario

Mr. Hernandez is a 54-year-old patient admitted to the medical telemetry floor with a diagnosis of heart failure exacerbation. He tells the nurse, “My breathing has gotten worse the past last three days and I have a lot of swelling in my feet.”

Applying the Nursing Process

Assessment: Vital signs at the start of shift were blood pressure 154/94, heart rate 88, respiratory rate 24, and oxygen saturation 88%. On assessment, the nurse finds fine crackles in bilateral posterior lower lung bases, an S3 heart sound, and 2+ pitting edema in bilateral lower extremities midway to the knee. The nurse reviews the patient’s chart and discovers Mr. Hernandez has gained 10 pounds since his previous office visit last week.

Based on the assessment information that has been gathered, the nurse creates the following nursing care plan for Mr. Hernandez:

Nursing Diagnosis: Excess Fluid Volume related to compromised regulatory mechanism as evidenced by fine crackles in bilateral posterior lung bases, S3 heart sound, weight gain of 10 pounds in the past week, and the patient states, “My breathing has gotten worse the past last three days and I have a lot of swelling in my feet.”

Overall Goal: The patient will demonstrate stabilization in fluid volume.

SMART Expected Outcomes:

• Mr. Hernandez’s vital signs and weight will return to his baseline in the next 48 hours.
• Mr. Hernandez will verbalize three rules of dietary and fluid restriction to follow at home following his educational session.

Planning and Implementing Nursing Interventions:

The nurse will weigh the patient daily and analyze weight trends and 24-hour intake and output. The nurse will closely monitor lung sounds, respiratory rate, and oxygenation status. The nurse will establish a 24-hour schedule for fluid intake and educate the patient regarding fluid restriction. The nurse will closely monitor lab results, especially sodium and potassium, and monitor for symptoms of fluid shifts. The nurse will provide patient education regarding fluid and sodium restrictions.

Sample Documentation:

The patient was admitted with acute heart failure exacerbation and stated, “My breathing has gotten worse the past last three days and I have a lot of swelling in my feet.” On admission to the unit at 0900, vital signs were blood pressure 154/94, heart rate 88, respiratory rate 24, and oxygen saturation 88%. Fine crackles were present in bilateral posterior lower lung bases, an S3 heart sound was present, and there was 2+ pitting edema in bilateral lower extremities midway to the knee. The chart indicates he has gained 10 pounds since his previous office visit last week. Provider orders and fluid restrictions were implemented. Lab results are within normal ranges. Patient education regarding fluid and sodium restrictions and a handout were provided. At the end of the session, Mr. Hernandez was able to report back three rules of dietary and fluid restrictions to follow at home when discharged.

Evaluation:

By the end of the shift, the second SMART outcome was “met” when Mr. Hernandez was able to report back three rules of dietary and fluid restrictions after the patient education session. The first SMART outcome was not yet met but will be reevaluated every shift for the next 24 hours.

Patient Scenario

Mr. Hernandez is a 54-year-old patient admitted to the medical telemetry floor with a diagnosis of heart failure exacerbation. He tells the nurse, “My breathing has gotten worse the past last three days and I have a lot of swelling in my feet.”

Applying the Nursing Process

Assessment: Vital signs at the start of shift were blood pressure 154/94, heart rate 88, respiratory rate 24, and oxygen saturation 88%. On assessment, the nurse finds fine crackles in bilateral posterior lower lung bases, an S3 heart sound, and 2+ pitting edema in bilateral lower extremities midway to the knee. The nurse reviews the patient’s chart and discovers Mr. Hernandez has gained 10 pounds since his previous office visit last week.

Based on the assessment information that has been gathered, the nurse creates the following nursing care plan for Mr. Hernandez:

Nursing Diagnosis: Excess Fluid Volume related to compromised regulatory mechanism as evidenced by fine crackles in bilateral posterior lung bases, S3 heart sound, weight gain of 10 pounds in the past week, and the patient states, “My breathing has gotten worse the past last three days and I have a lot of swelling in my feet.”

Overall Goal: The patient will demonstrate stabilization in fluid volume.

SMART Expected Outcomes:

• Mr. Hernandez’s vital signs and weight will return to his baseline in the next 48 hours.
• Mr. Hernandez will verbalize three rules of dietary and fluid restriction to follow at home following his educational session.

Planning and Implementing Nursing Interventions:

The nurse will weigh the patient daily and analyze weight trends and 24-hour intake and output. The nurse will closely monitor lung sounds, respiratory rate, and oxygenation status. The nurse will establish a 24-hour schedule for fluid intake and educate the patient regarding fluid restriction. The nurse will closely monitor lab results, especially sodium and potassium, and monitor for symptoms of fluid shifts. The nurse will provide patient education regarding fluid and sodium restrictions.

Sample Documentation:

The patient was admitted with acute heart failure exacerbation and stated, “My breathing has gotten worse the past last three days and I have a lot of swelling in my feet.” On admission to the unit at 0900, vital signs were blood pressure 154/94, heart rate 88, respiratory rate 24, and oxygen saturation 88%. Fine crackles were present in bilateral posterior lower lung bases, an S3 heart sound was present, and there was 2+ pitting edema in bilateral lower extremities midway to the knee. The chart indicates he has gained 10 pounds since his previous office visit last week. Provider orders and fluid restrictions were implemented. Lab results are within normal ranges. Patient education regarding fluid and sodium restrictions and a handout were provided. At the end of the session, Mr. Hernandez was able to report back three rules of dietary and fluid restrictions to follow at home when discharged.

Evaluation:

By the end of the shift, the second SMART outcome was “met” when Mr. Hernandez was able to report back three rules of dietary and fluid restrictions after the patient education session. The first SMART outcome was not yet met but will be reevaluated every shift for the next 24 hours.

References

1.

"HF-RTD.JPG“ by ARISE project is licensed under CC BY 4.0 ↵.

2.

"HF-RTD.JPG“ by ARISE project is licensed under CC BY 4.0 ↵.

3.

"Hospitalized Male“ by ARISE project is licensed under CC BY 4.0 ↵.

4.

"Hospitalized Male“ by ARISE project is licensed under CC BY 4.0 ↵.