Chapter 16

Friday, September 30, 2022 11:00 AM

1. Describe the composition of the major body fluid compartments.

- 2 fluid compartments: Intracellular space and the extracellular space.
- Intracellular space: about two thirds of body water is found within cells. Makes
up 40% of body weight of an adult.
- Extracellular fluid: contains the interstitial fluid (fluid in the spaces between cells)
and the plasma (intravascular fluid, liquid part of blood). Other compartments
include lymph and transcellular fluids. Transcellular fluids include cerebrospinal
fluid; fluid in the gastrointestinal (GI) tract and joint spaces. Makes up about one
third of the body water
2. Define processes involved in regulating the movement of water and electrolytes
between the body fluid compartments.
- Simple Diffusion: Diffusion is the movement of molecules from an area of high
concentration to low concentration. Requires no energy
- Facilitated Diffusion: Facilitated diffusion involves the use of a protein carrier in
the cell membrane. High to low concentration. No energy.
- Active Transport: Molecules move against the concentration gradient. External
energy is needed for this process.
- Osmosis: Osmosis is the movement of water “down” a concentration gradient,
that is, from a region of low solute concentration to one of high solute
concentration, across a semipermeable membrane. Osmosis requires no outside
energy sources.
3. Describe the etiology, laboratory diagnostic findings, clinical manifestations, and
nursing and interprofessional management of the following disorders:
a. Extracellular fluid volume imbalances: fluid volume deficit (hypovolemia) and fluid
volume excess (hypervolemia):
Fluid volume deficit
Etiology:
Diagnostic findings/laboratory findings:
• Fluid imbalance
• Impaired cardiac output
• Acute confusion
• Potential complication: hypovolemic shock
Increased Blood Urea Nitrogen, sodium, and hematocrit levels with increased plasma
and urine osmolality
Reference range
Risk factors:
Nursing Implementations:
• Daily Weights: Obtain the weight under standardized conditions. Weigh
patient at the same time every day, wearing the same clothes and on th
same carefully calibrated scale
• Intake and Output: Intake and output records give valuable information
about fluid and electrolyte problems. Intake should include oral and IV f
tube feedings, and retained irrigation solutions. Output includes urine,
excess perspiration, wound or tube drainage, vomitus, and diarrhea. am
and color of the urine and measure the urine specific gravity.
• Cardiovascular Care: In fluid volume excess, the pulse is full, bounding, a
not easily obliterated. Increased volume causes distended neck veins (ju
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• Acute confusion
• Potential complication: hypovolemic shock
Increased Blood Urea Nitrogen, sodium, and hematocrit levels with increased plasma
and urine osmolality
Reference range
Risk factors:
• ↑ Insensible water loss or perspiration (high fever, heatstroke)
• Diabetes insipidus
• Osmotic diuresis
• Hemorrhage
• GI losses: vomiting, NG suction, diarrhea, fistula drainage
• Overuse of diuretics
• Inadequate fluid intake
• Third-space fluid shifts: burns, pancreatitis
Assessment and clinical manifestations:
• Restlessness, drowsiness, lethargy, confusion
• Thirst, dry mucous membranes
• Cold clammy skin
• Decreased skin turgor, ↓ capillary refill
• Postural hypotension, ↑ pulse, ↓ CVP
• ↓ Urine output, concentrated urine
• ↑ Respiratory rate
• Weakness, dizziness
• Weight loss
• Seizures, coma
Treatment: Replacing both water and any needed electrolytes. Mild losses: oral
rehydration. More severe and rapid volume replacement: replace volume with blood
products or balanced IV solutions such as isotonic sodium chloride (0.9%) or lactated
ringer's solution. Blood is given when volume loss is due to blood loss.
Complications: heart attack, acute renal failure, liver failure, ischemic stroke, shock

Fluid Volume Excess (hypervolemia)

Etiology: excess intake of fluids, abnormal retention of fluids, or a shift of fluid from
interstitial fluid into plasma fluid.
Diagnostic Findings/Laboratory findings:
• Fluid imbalance
• Impaired gas exchange
• Impaired tissue integrity
• Activity intolerance
• Disturbed body image
• Potential complications: pulmonary edema, ascites
Decreased blood urea nitrogen, sodium, hematocrit, plasma and urine osmolality
Reference Range
 about fluid and electrolyte problems. Intake should include oral and IV f
tube feedings, and retained irrigation solutions. Output includes urine,
excess perspiration, wound or tube drainage, vomitus, and diarrhea. am
and color of the urine and measure the urine specific gravity.
• Cardiovascular Care: In fluid volume excess, the pulse is full, bounding, a
not easily obliterated. Increased volume causes distended neck veins (ju
venous distention), increased central venous pressure, and high BP. In m
to moderate fluid volume deficit, sympathetic nervous system compens
increases the heart rate and results in peripheral vasoconstriction to try
keep BP within normal limits. Pulses may be weak and thready. change i
position from lying to sitting or standing may decrease BP or further incr
the heart rate. Severe deficits, hypotension may be present.
• Respiratory Care: ECF excess can cause pulmonary congestion and
pulmonary edema, patient will have shortness of breath and moist crack
on auscultation. ECF deficit will have an increased respiratory rate becau
decreased tissue perfusion and resultant hypoxia. Give O2 as ordered.
• Patient Safety: fluid volume deficit is at risk for falls because of orthosta
hypotension, muscle weakness, and changes in level of consciousness. T
the patient to change positions slowly when rising from a bed or chair. P
alarm monitors on patients who are confused and try to get out of bed
without help.
• Skin care: ECF volume deficit, there is diminished skin turgor with tentin
a lag in the pinched skinfold’s return to its original state. In mild fluid de
the skin may appear warm, dry, and wrinkled. More severe deficits, the
may be cool and moist if there is vasoconstriction to compensate for the
decreased fluid volume. Oral mucous membranes will be dry, the tongue
may be furrowed, and the person often is thirsty.
• Fluid Therapy: fluid volume deficit, you can use several interventions to
maintain adequate oral intake. Offer fluids every 1 to 2 hours and at sele
times.
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• Impaired tissue integrity
• Activity intolerance
• Disturbed body image
• Potential complications: pulmonary edema, ascites
Decreased blood urea nitrogen, sodium, hematocrit, plasma and urine osmolality
Reference Range
Risk Factors/causes:
• Excess isotonic or hypotonic IV fluids
• Heart failure
• Renal failure
• Primary polydipsia
• SIADH
• Cushing syndrome
• Long-term use of corticosteroids
Clinical Manifestations:
• Headache, confusion, lethargy
• Peripheral edema
• Jugular venous distention
• S3 heart sound
• Bounding pulse, ↑ BP, ↑ CVP
• Polyuria (with normal renal function)
• Dyspnea, crackles, pulmonary edema
• Muscle spasms
• Weight gain
• Seizures, coma
Treatment: Treating the cause and removing fluid without producing abnormal changes
in the electrolyte composition or osmolality of ECF. Primary form of therapy: Diuretics
and fluid restriction. Sodium restrictions. If it leads to ascites or pleural effusion,
abdominal paracentesis or thoracentesis may be needed.

b. Sodium imbalances: hypernatremia and hyponatremia

Hypernatremia
Etiology: inadequate water intake, excess water loss, or rarely sodium gain. Leads to
cellular dehydration.
Diagnostic Findings/Laboratory findings:
• Electrolyte imbalance
• Fluid imbalance
• Risk for injury
• Potential complications: Seizures and coma
Reference range: (Na+ >145 mEq/L [mmol/L])
Risk factors/causes: synthesis or release of ADH from the posterior pituitary gland &
• Electrolyte imbalance
• Fluid imbalance
• Risk for injury
• Potential complications: Seizures and coma
Reference range: (Na+ >145 mEq/L [mmol/L])
Risk factors/causes: synthesis or release of ADH from the posterior pituitary gland &
decrease in kidney responsiveness to ADH. Uncontrolled diabetes or giving
concentrated hyperosmolar tube feedings. Excess sodium intake with inadequate water
intake.
Excess sodium intake:
• IV fluids: hypertonic NaCl, excess isotonic NaCl, IV sodium bicarbonate
• Hypertonic tube feedings without water supplements
• Near-drowning in salt water
Excess water loss due to increased sodium concentrations:
• ↑ Insensible water loss (high fever, heatstroke, prolonged hyperventilation)
• Osmotic diuretic therapy
• Diarrhea
Clinical manifestation:
Decreased ECF volume:
• Restlessness, agitation, lethargy, seizures, coma
• Intense thirst, dry swollen tongue, sticky mucous membranes
• Postural hypotension, ↓ CVP, weight loss, ↑ pulse
• Weakness, muscle cramps, tachycardia, confusion
Normal or increased ECF Volume:
• Restlessness, agitation, twitching, seizures, coma
• Intense thirst, flushed skin
• Weight gain, peripheral and pulmonary edema, ↑ BP, ↑ CVP
Treatment: primary water deficit, fluid replacement is given either orally or IV with
isotonic solutions such as 0.9% sodium chloride. If the problem is sodium excess, expect
diluting the high sodium concentration with sodium-free IV fluids, such as 5% dextrose
in water, and promoting sodium excretion with diuretics. Dietary sodium intake is often
restricted. serum sodium level should not decrease by more than 8 to 15 mEq/L in an 8-
hour period. (Rapid reduction can lead to neurologic complications and cerebral
edema)
Complications: impaired level of consciousness or inability to obtain fluids.
• Diabetes insipidus
• Primary hyperaldosteronism
• Cushing syndrome
• Uncontrolled diabetes

Hyponatremia
Etiology: loss of sodium-containing fluids, water excess in relation to the amount of
sodium or a combination of both.
Diagnostic Findings/Laboratory findings:
Hyponatremia
Etiology: loss of sodium-containing fluids, water excess in relation to the amount of
sodium or a combination of both.
Diagnostic Findings/Laboratory findings:
• Electrolyte imbalance
• Risk for injury
• Acute confusion
• Potential complication: seizures and coma
Reference range: (Na+ <136 mEq/L [mmol/L])
Risk factors/causes: Causes due to loss of sodium-rich body fluids include draining
wounds, diarrhea, vomiting and primary adrenal insufficiency. Inappropriate use of
sodium-free or hypotonic IV fluids causes hyponatremia from water excess. Syndrome
of inappropriate antidiuretic hormone secretion (SIADH) results in dilutional
hyponatremia caused by abnormal retention of water.
Excess sodium loss:
• GI losses: diarrhea, vomiting, fistulas, NG suction
• Renal losses: diuretics, adrenal insufficiency, Na+ wasting renal disease
• Skin losses: burns, wound drainage
Inadequate sodium intake: fasting diets.
Excess water gain: excess hypotonic IV fluids, primary polydipsia
Clinical manifestation: cellular swelling and first appear in the central nervous system
(CNS). Mild hyponatremia: headaches, irritability, difficulty concentrating. Severe
hyponatremia: confusion, vomiting, seizures, coma. Death can occur if hyponatremia
develops rapidly and is severe.
With decreased ECF volume:
• Irritability, apprehension, confusion, dizziness, personality changes, tremors, seizures,
coma
• Dry mucous membranes
• Postural hypotension, ↓ CVP, ↓ jugular venous filling, ↑ pulse, thready pulse
• Cold and clammy skin
With normal or increased ECF volume
• Headache, apathy, confusion, muscle spasms, seizures, coma
• Nausea, vomiting, diarrhea, abdominal cramps
• Weight gain, ↑ BP, ↑ CVP
Treatment: From fluid loss includes replacing fluid using isotonic sodium-containing
solutions, encouraging oral intake, and withholding all diuretics. Mild hyponatremia
caused by water excess, fluid restriction may be the only treatment. Loop diuretics and
demeclocycline may be given. Acute or more serious, small amounts of IV hypertonic
saline solution (3% sodium chloride) can restore the serum sodium level while the body
is returning to a normal water balance. Vasopressor receptor antagonists (drugs that
block the activity of ADH) are used to treat patients who cannot tolerate fluid
restrictions or have more severe symptom. Tolvaptan is given orally to treat
hyponatremia from heart failure or SIADH. level should not increase by more than 6 to
demeclocycline may be given. Acute or more serious, small amounts of IV hypertonic
saline solution (3% sodium chloride) can restore the serum sodium level while the body
is returning to a normal water balance. Vasopressor receptor antagonists (drugs that
block the activity of ADH) are used to treat patients who cannot tolerate fluid
restrictions or have more severe symptom. Tolvaptan is given orally to treat
hyponatremia from heart failure or SIADH. level should not increase by more than 6 to
12 mEq/L per hour in the first 24 hours and 18 mEq/L or less per hour within 48 hours.
Complications:
• SIADH
• Heart failure
• Primary hypoaldosteronism
• Cirrhosis

c. Potassium imbalances: hyperkalemia and hypokalemia

Hyperkalemia
Etiology: may result from impaired renal excretion, a shift of potassium from ICF to
ECF, a massive intake of potassium, or a combination of these factors.
Diagnostic Findings/Laboratory findings:
• Electrolyte imbalance
• Activity intolerance
• Impaired cardiac output
• Potential complication: dysrhythmias
Reference range: (K+ >5.0 mEq/L [mmol/L])
Risk factors/causes: Common cause is renal failure. Adrenal insufficiency with
subsequent aldosterone deficiency leads to potassium retention. Factors that cause
potassium to move from ICF to ECF include acidosis, massive cell destruction (as in burn
or crush injury, tumor lysis, severe infections), and intense exercise. Digoxin-like drugs
and β-adrenergic blockers (e.g., propranolol) can impair entry of potassium into cells,
resulting in higher ECF potassium concentrations. NSAIDS, potassium-sparing diuretics,
angiotensin II receptor blockers and angiotensin-converting enzyme inhibitors reduce
the kidney's ability to excrete potassium.
Excess Potassium Intake
• Excess or rapid parenteral administration
• Potassium-containing drugs (e.g., potassium penicillin)
• Potassium-containing salt substitute
Shift of Potassium Out of Cells
• Acidosis
• Tissue catabolism (e.g., fever, crush injury, sepsis, burns)
• Intense exercise
• Tumor lysis syndrome
Failure to Eliminate Potassium
• Renal disease
• Acidosis
• Tissue catabolism (e.g., fever, crush injury, sepsis, burns)
• Intense exercise
• Tumor lysis syndrome
Failure to Eliminate Potassium
• Renal disease
• Adrenal insufficiency
• Medications: Angiotensin II receptor blockers, ACE inhibitors, heparin, potassium-
sparing diuretics, NSAIDs
Clinical manifestation: most clinically significant problems are the changes in cardiac
conduction. The initial finding is tall, peaked T waves. As potassium increases, cardiac
depolarization decreases. Heart block, ventricular fibrillation, or cardiac standstill may
occur. fatigue, confusion, tetany, muscle cramps, paresthesias, and weakness. As
potassium increases, loss of muscle tone and weakness or paralysis of other skeletal
muscles, including the respiratory muscles, can occur, leading to respiratory arrest.
Abdominal cramping, vomiting, and diarrhea occur from hyperactivity of GI smooth
muscles.
• Fatigue, irritability
• Muscle weakness, cramps
• Loss of muscle tone
• Paresthesias, decreased reflexes
• Abdominal cramping, diarrhea, vomiting
• Confusion
• Irregular pulse
• Tetany
ECG Changes
• Tall, peaked T wave
• Prolonged PR interval
• ST segment depression
• Widening QRS
• Loss of P wave
• Ventricular fibrillation
• Ventricular standstill
Treatment:
When the potassium elevation is mild and the kidneys are functioning, it may be
enough to (1) withhold potassium from the diet and IV sources and (2) increase renal
potassium excretion by giving fluids and loop or thiazide diuretics. Patients with severe
hyperkalemia or symptomatic patients should receive treatment to force potassium
into cells.
Use continuous ECG monitoring for all patients with clinically significant hyperkalemia
to detect dysrhythmias and monitor the effects of therapy. The patient with dangerous
dysrhythmias should receive IV calcium immediately. Monitor BP
Giving insulin monitor hypoglycemia and give glucose as needed.

Hypokalemia
Use continuous ECG monitoring for all patients with clinically significant hyperkalemia
to detect dysrhythmias and monitor the effects of therapy. The patient with dangerous
dysrhythmias should receive IV calcium immediately. Monitor BP
Giving insulin monitor hypoglycemia and give glucose as needed.

Hypokalemia
Etiology: increased loss of potassium, an increased shift of potassium from ECF to ICF,
or, rarely, from deficient dietary potassium intake.
Diagnostic Findings:
• Electrolyte imbalance
• Activity intolerance
• Impaired cardiac output
• Potential complication: dysrhythmias
Reference range: (K+ <3.5 mEq/L [mmol/L])
Risk factors/causes: Common causes are abnormal losses from either the kidneys or GI
tract. GI tract losses are associated with diarrhea, laxative misuse, vomiting, and
ileostomy drainage. Renal losses occur when a patient is diuresing or has a low
magnesium level. Factors causing potassium to move from ECF to ICF are insulin
therapy. Alkalosis can cause a shift of potassium into cells in exchange for hydrogen,
lowering potassium in ECF.

Clinical manifestation: Changes in cardiac and muscle function.

• Fatigue
• Muscle weakness, leg cramps
• Soft, flabby muscles
Clinical manifestation: Changes in cardiac and muscle function.
• Fatigue
• Muscle weakness, leg cramps
• Soft, flabby muscles
• Paresthesias, decreased reflexes
• Constipation, nausea, paralytic ileus
• Shallow respirations
• Weak, irregular pulse
• Hyperglycemia
ECG Changes
• Flattened T wave
• Presence of U wave
• ST segment depression
• Prolonged QRS
• Peaked P wave
• Ventricular dysrhythmias
• First- and second-degree heart block
Treatment: oral or IV potassium chloride (KCl) supplements and increased dietary
intake of potassium. Consuming potassium-rich foods can usually correct mild
hypokalemia.
Patient teaching:
Preventing hypokalemia:
d. Magnesium imbalances: hypermagnesemia and hypomagnesemia

Hypermagnesemia
Etiology
Reference range: (Mg+ >2.1 mEq/L [1.05 mmol/L])
Risk factors/causes:
• Renal failure
• IV administration of magnesium, especially for treatment of eclampsia
• Tumor lysis syndrome
• Hypothyroidism
• Metastatic bone disease
• Adrenal insufficiency
• Antacids, laxatives
Clinical manifestation:
• Lethargy, drowsiness
• Muscle weakness
• Urinary retention
• Nausea, vomiting
• Diminished deep tendon reflexes
• Flushed, warm skin, especially facial
• ↓ Pulse, ↓ BP
Treatment:
avoiding magnesium-containing drugs and limiting dietary intake of magnesium-
containing foods (e.g., green vegetables, nuts, bananas, oranges, peanut butter,
chocolate). If renal function is adequate, increased fluids and diuretics promote urinary
excretion of magnesium. The patient with impaired renal function may need dialysis

Hypomagnesemia
Etiology: occurs in patients with limited magnesium intake or increased GI or renal
losses.
Reference range: (Mg+ <1.3 mEq/L [0.65 mmol/L])
Risk factors/causes:
• GI tract fluid losses (e.g., diarrhea, NG suction)
• Chronic alcohol use
• Malabsorption syndromes
• Prolonged malnutrition
Reference range: (Mg+ <1.3 mEq/L [0.65 mmol/L])
Risk factors/causes:
• GI tract fluid losses (e.g., diarrhea, NG suction)
• Chronic alcohol use
• Malabsorption syndromes
• Prolonged malnutrition
• Acute pancreatitis
• ↑ Urine output
• Hyperglycemia
• Proton pump inhibitor therapy
Clinical manifestation
Treatment:
Mild magnesium deficiency involves oral supplements and increased dietary intake of
foods high in magnesium. If the deficiency is severe or if hypocalcemia is present, IV
magnesium (e.g., magnesium sulfate) is given.

e. Calcium imbalances: hypercalcemia and hypocalcemia

Hypercalcemia
Etiology:
Diagnostic Findings:
• Electrolyte imbalance
• Acute confusion
• Impaired physical mobility
• Potential complication: dysrhythmias
Reference range: (Ca2+ >10.5 mg/dL [2.62 mmol/L])
Risk factors/causes:
Increased Total Calcium
• Hyperparathyroidism
• Hematologic cancer
• Cancers with bone metastasis
• Prolonged immobilization
• Vitamin A or D overdose
• Paget’s disease
• Adrenal insufficiency
• Thyrotoxicosis
• Thiazide diuretics
• Excess dairy intake
• Calcium-containing antacids
• Mycobacterium infection
Increased Ionized Calcium
• Acidosis
Clinical manifestation:
• Lethargy, weakness, fatigue
• Decreased memory
• Mycobacterium infection
Increased Ionized Calcium
• Acidosis
Clinical manifestation:
• Lethargy, weakness, fatigue
• Decreased memory
• Depressed reflexes
• ↑ BP
• Confusion, psychosis
• Anorexia, nausea, vomiting
• Bone pain, fractures
• Polyuria, dehydration
• Nephrolithiasis
• Seizures, coma
ECG Changes
• Shortened ST segment
• Shortened QT interval
• Ventricular dysrhythmias
• Increased digitalis effect
Treatment:
mild hypercalcemia should stop any medications related to hypercalcemia, start a diet
low in calcium, increase weight-bearing activity, and maintain adequate hydration. The
patient must drink 3000 to 4000 mL of fluid daily to promote the renal excretion of
calcium and decrease the chance of kidney stone formation.
severe hypercalcemia includes giving IV isotonic saline, a bisphosphonate, and
calcitonin. IV saline therapy requires careful monitoring
Bisphosphonates (e.g., pamidronate, zoledronic acid) are the gold standard in treating
hypercalcemia, particularly when caused by cancer. They interfere with the activity of
osteoclasts, cells that break down bone. patients receive calcitonin injections for an
immediate effect.
denosumab (Prolia) may be used as an alternative treatment.
Dialysis is an option in life-threatening situations.

Hypocalcemia
Etiology
Diagnostic Findings:
• Electrolyte imbalance
• Impaired breathing
• Activity intolerance
• Potential complications: fracture, respiratory arrest
Reference range
Risk factors/causes:
Decreased total calcium
• Primary hypoparathyroidism
• Activity intolerance
• Potential complications: fracture, respiratory arrest
Reference range
Risk factors/causes:
Decreased total calcium
• Primary hypoparathyroidism
• Renal insufficiency
• Acute pancreatitis
• High phosphate level
• Vitamin D deficiency, malnutrition
• Low magnesium level
• Bisphosphonates
• Tumor lysis syndrome
• Loop diuretics
• Chronic alcohol use
• Diarrhea
• ↓ Serum albumin
Decreased Ionized Calcium
• Alkalosis
• Receiving excess citrated blood
Clinical manifestation:
• Weakness, fatigue
• Depression, irritability, confusion
• Hyperreflexia, muscle cramps
• ↓ BP
• Numbness and tingling in extremities and region around mouth
• Chvostek’s sign
• Trousseau’s sign
• Laryngeal and bronchial spasms
• Tetany, seizures
ECG Changes
• Elongation of ST segment
• Prolonged QT interval
• Ventricular tachycardia
Treatment: Treating mild or asymptomatic hypocalcemia involves a diet high in
calcium-rich foods and calcium and vitamin D supplementation. Symptomatic
hypocalcemia is treated with IV calcium gluconate.10 Measures to promote CO2
retention, such as breathing into a paper bag or sedating the patient, can control
muscle spasm and other symptoms of tetany until the calcium level is corrected.

f. Phosphate imbalances: hyperphosphatemia and hypophosphatemia

Hyperphosphatemia
Etiology: common in patients with acute kidney injury or chronic kidney disease, which
f. Phosphate imbalances: hyperphosphatemia and hypophosphatemia

Hyperphosphatemia
Etiology: common in patients with acute kidney injury or chronic kidney disease, which
alter the kidney’s ability to excrete phosphate.
Reference range: (PO43− >4.5 mg/dL [1.45 mmol/L])
Risk factors/causes: Long-term, increased phosphate levels result in the development
of calcified deposits outside of the bones.
• Renal failure
• Phosphate enemas (e.g., Fleet Enema)
• Excess ingestion (e.g., phosphate-containing laxatives)
• Rhabdomyolysis
• Tumor lysis syndrome
• Thyrotoxicosis
• Hypoparathyroidism
• Sickle cell anemia, hemolytic anemia
• Hyperthermia
Clinical manifestation:
• Hypocalcemia
• Numbness and tingling in extremities and region around mouth
• Hyperreflexia, muscle cramps
• Tetany, seizures
• Calcium-phosphate precipitates in skin, soft tissue, cornea, viscera, blood vessels
Treatment: Managing hyperphosphatemia involves identifying and treating the
underlying cause. Restrict the intake of foods and fluids high in phosphorus (e.g., dairy
products). Oral phosphate-binding agents (e.g., calcium carbonate) limit intestinal
phosphate absorption and increase phosphate secretion in the intestine. With severe
hyperphosphatemia, hemodialysis may be used to rapidly decrease levels. Volume
expansion and forced diuresis with a loop diuretic may increase phosphate excretion

Hypophosphatemia
Etiology: can result from decreased intestinal absorption, increased urinary excretion,
or ECF to ICF shifts.
Reference range: (PO43− <3.0 mg/dL [0.97 mmol/L])
Risk factors/causes:
• Malabsorption syndromes
• Chronic diarrhea
• Malnutrition, vitamin D deficiency
• Parenteral nutrition
• Chronic alcohol use
• Phosphate-binding antacids
• Diabetic ketoacidosis
• Hyperparathyroidism
• Malnutrition, vitamin D deficiency
• Parenteral nutrition
• Chronic alcohol use
• Phosphate-binding antacids
• Diabetic ketoacidosis
• Hyperparathyroidism
• Refeeding syndrome
• Respiratory alkalosis
Clinical manifestation: Most of the manifestations of hypophosphatemia result from
impaired cellular energy and O2 delivery due to low levels of cellular ATP and 2,3-
diphosphoglycerate.
• CNS depression (confusion, coma)
• Muscle weakness, including respiratory muscle weakness
• Polyneuropathy, seizures
• Heart problems (dysrhythmias, heart failure)
• Osteomalacia, rickets
• Rhabdomyolysis
Treatment: mild phosphate deficiency involves increasing oral intake with dairy
products or phosphate supplements. Symptomatic hypophosphatemia can be fatal and
usually requires IV administration of sodium phosphate or potassium phosphate.
monitor serum calcium and phosphate levels every 6 to 12 hours.

4. Identify the processes involved in maintaining acid-base balance.

Buffer System: primary regulator. Buffers act chemically to change strong acids into
weaker ones or bind acids to neutralize them. This minimizes the effect of acids on
blood pH until they can be excreted from the body. Buffers can maintain pH only if the
respiratory and renal systems function adequately.
Respiratory System: lungs help maintain a normal pH by excreting CO2 and water,
which are by-products of cellular metabolism. When released into the circulation, CO2
enters RBCs and combines with H2O to form H2CO3.
Renal System: Under normal conditions, the body depends on the kidneys to reabsorb
and conserve all the HCO3− they filter and excrete some of the acid produced by
cellular metabolism. The 3 mechanisms of acid excretion include (1) secreting small
amounts of free hydrogen into the renal tubule, (2) combining H+ with ammonia (NH3)
to form ammonium (NH4+), and (3) excreting weak acids.
5. Discuss the etiology, diagnostic findings, clinical manifestations, and nursing and
interprofessional management of the following acid-base imbalances: metabolic
acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis.
Metabolic Acidosis:
Etiology: occurs when an acid other than carbonic acid accumulates in the body or
when bicarbonate is lost in body fluids
Diagnostic/causes:
• Diabetic ketoacidosis
• Lactic acidosis
Metabolic Acidosis:
Etiology: occurs when an acid other than carbonic acid accumulates in the body or
when bicarbonate is lost in body fluids
Diagnostic/causes:
• Diabetic ketoacidosis
• Lactic acidosis
• Starvation
• Diarrhea
• Renal tubular acidosis
• Renal failure
• GI fistulas
• Shock
Clinical Manifestation: respiratory and metabolic acidosis, the CNS is depressed.
Headache, lethargy, weakness, and confusion develop, leading eventually to coma and
death.
Interprofessional Management
Metabolic Alkalosis:
Etiology: occurs when a loss of acid (e.g., from prolonged vomiting or gastric suction) or
a gain in HCO3− (e.g., from ingestion of baking soda) occurs
Diagnostic/causes:
• Vomiting
• NG suctioning
• Diuretic therapy
• Hypokalemia
• Excess NaHCO3 intake
• Mineralocorticoid use
Clinical manifestation
Interprofessional management
Respiratory Acidosis
Etiology: when a person has hypoventilation. If CO2 is not eliminated from the bloo
Diagnostic/causes:
• Chronic respiratory disease (e.g., COPD)
• Barbiturate or sedative overdose
• Chest wall abnormality
• Severe pneumonia
• Atelectasis
• Respiratory muscle weakness
• Mechanical hypoventilation
• Pulmonary edema
Clinical Manifestation: respiratory and metabolic acidosis, the CNS is depressed.
Headache, lethargy, weakness, and confusion develop, leading eventually to coma and
death.
Interprofessional Management
Respiratory Alkalosis
Etiology: occurs with hyperventilation, or an increase in respiratory rate or volume.
Clinical Manifestation: respiratory and metabolic acidosis, the CNS is depressed.
Headache, lethargy, weakness, and confusion develop, leading eventually to coma and
death.
Interprofessional Management
Respiratory Alkalosis
Etiology: occurs with hyperventilation, or an increase in respiratory rate or volume.
Diagnostic/ causes: primary cause of respiratory alkalosis is hypoxemia from acute
pulmonary disorders (e.g., pneumonia, pulmonary embolus).
• Hyperventilation (e.g., hypoxia, anxiety, fear, pain, exercise, fever)
• Stimulated respiratory center (e.g., septicemia, stroke, meningitis, encephalitis, brain
injury, salicylate poisoning)
• Liver failure
• Mechanical hyperventilation
Clinical Manifestation
Interprofessional Management

6. Describe the composition of and indications for common IV fluid solutions.

Hypotonic: Infusing a hypotonic solution dilutes ECF, lowering serum osmolality.
Hypotonic solutions (e.g., 0.45% NaCl) are useful in treating patients with
hypernatremia.
Isotonic: This makes isotonic solutions the ideal fluid replacement for patients with ECF
volume deficits. Therefore giving too much isotonic saline has the potential to increase
sodium and chloride levels. Patients with liver dysfunction, hyperkalemia, and severe
hypovolemia should not receive lactated Ringer’s
Hypertonic: It is useful in the treatment of hyponatremia and trauma patients with
head injury.
7. Discuss the types and nursing management of commonly used central venous access
devices.

Centrally Inserted Catheters: Nontunneled catheters: short-term needs in an acute

care setting. Surgically placed tunneled catheters: long term needs.
Peripherally inserted central catheters: inserted into a vein in the arm.
Implanted Infusion Ports: The catheter tip lies in the desired vein. The port lies in a
surgically created subcutaneous pocket on the upper chest or arm.
Midline Catheters: The tip rests right below the axilla, staying below the shoulder joint
to reduce the risk for vein irritation from moving the shoulder. These lines can stay in
place for up to 4 weeks.