CHAPTER 10
FLUID AND
ELECTROLYTES
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FLUID AND
ELECTROLYTE
BALANCE
Necessary
for life,
homeostasis
(internal
equilibrium)
Nursing role:
anticipate,
identify, and
respond to
possible
imbalances
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Approximately 60% of typical adult is fluid (water and
electrolytes)
Varies with age, body fat, gender
FLUID
Intracellular fluid (fluid in cells)
2/3 of body fluid, skeletal muscle mass
Extracellular fluid (fluid outside the cells)
Intravascular (fluid within
blood vessels): plasma,
erythrocytes, leukocytes,
thrombocytes
Interstitial (fluid that
surrounds the cell): lymph
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Transcellular: cerebrospinal,
pericardial, synovial
Active chemicals that carry
positive (cations) and negative
(anions) electrical charges
ELECTROLYTES
• Major cations: sodium, potassium,
calcium, magnesium, hydrogen ions
• Major anions: chloride, bicarbonate,
phosphate, sulfate, negatively charged
protein ions
• Expressed in terms of millequivalents
(mEq) per liter
Electrolyte concentrations differ
in ICF and ECF compartments
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Osmosis: area of low solute concentration
to area of high solute concentration
REGULATION
OF FLUID
Diffusion: solutes move from area of
higher concentration to one of lower
concentration
Filtration: movement of water, solutes
occurs from area of high hydrostatic
pressure to area of low hydrostatic
pressure
Active transport:
Sodium–potassium
pump
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Maintains higher
concentration of
extracellular
sodium,
intracellular
potassium
QUESTION
#1
Is the following statement true
or false?
Diffusion is the process by
which solutes move from an
area of higher concentration to
one of lower concentration
and requires energy.
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False
ANSWER TO
QUESTION
#1
Rationale: Although diffusion occurs
when fluid moves from an area of
higher to lower concentration, this
process does not require an
expenditure of energy.
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Gain
GAINS AND
LOSSES OF
FLUID AND
ELECTROLYTES
• Healthy people gain fluids by drinking
and eating
• Daily I&O of water are equal
Loss
• Kidney: urine output of 1mL/kg/hr
• Skin loss: sensible due to sweating
and insensible due to fever, exercise,
and burns
• Lungs: 300 mL everyday, greater with
increased respirations
• GI tract: large losses due to diarrhea
and fistulas
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HOMEOSTATIC MECHANISMS
 MAINTAIN BODY FLUID WITHIN NORMAL LIMITS
• Kidney
• Heart and Blood Vessels
• Renin–Angiotensin–
Aldosterone System
• Lung
• Antidiuretic Hormone
• Pituitary
• Osmoreceptors
• Adrenal
• Natriuretic Peptides
• Parathyroid
• Baroreceptors
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• Clinical manifestations of imbalance
may be subtle
• Fluid deficit may cause delirium
GERONTOLOGIC
CONSIDERATIONS
• Decreased cardiac reserve
• Reduced renal function
• Dehydration is common
• Age-related thinning of the skin and
loss of strength and elasticity
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FLUID VOLUME
DISTURBANCES
FLUID VOLUME
DEFICIT (FVD):
HYPOVOLEMIA
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FLUID VOLUME
EXCESS (FVE):
HYPERVOLEMIA
May occur alone or in
combination with other
imbalances
FLUID VOLUME
DEFICIT
(HYPOVOLEMIA)
Loss of
extracellular fluid
exceeds intake
ratio of water
Electrolyte
s lost in
same
proportion
as they
exist in
normal
body fluids
Dehydration
Not the
same as
FVD
Loss of
water
alone, with
increased
serum
sodium
levels
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Abnormal fluid losses
• Vomiting, diarrhea, sweating, GI
suctioning
CAUSES OF
FVD
Decreased intake
• Nausea, lack of access to fluids
Third-space fluid shifts
• Due to burns, ascites
Additional causes
• Diabetes insipidus, adrenal
insufficiency, hemorrhage
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Can develop rapidly
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS OF
FVD
Severity depends on degree of loss
See Table 10-4 for clinical signs and
symptoms and laboratory findings
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• Assessment
GERONTOLOGIC
CONSIDERATIONS
FOR FVD
• Cognition
• Ambulation
• ADLs
• Gag Reflex
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Oral route is preferred
MEDICAL
MANAGEMENT
OF FVD
IV for acute or severe losses
Types of Solutions
• Isotonic
• Hypotonic
• Hypertonic
• Colloid
• Refer to Table 10-5
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Is the following statement true or
false?
QUESTION #2
An isotonic solution, such as 0.9%
NaCl (Normal Saline), is the only
intravenous solution that may be
administered with blood products.
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True
ANSWER TO
QUESTION #2
Rationale: Tonicity is the tension that
osmotic pressure of a solution with
impermeable solutes exerts on cell
size because of water movement
across the cell membrane. Normal
saline has nearly the same tonicity as
plasma.
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I&O at least every 8 hours, sometimes hourly
Daily weight
NURSING
MANAGEMENT
OF FVD
Vital signs closely monitored
Skin and tongue turgor, mucosa, urine output,
mental status
Measures to minimize fluid loss
Administration of oral fluids
Administration of parenteral fluids
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FLUID VOLUME
EXCESS
(HYPERVOLEMIA)
Expansion of the ECF caused by
the abnormal retention of water
and sodium in approximately the
same proportions in which they
normally exist in the ECF
Secondary to an increase in the
total‐body sodium content
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Due to fluid overload or
diminished homeostatic
mechanisms
CAUSES OF
FVE
Heart failure, kidney injury,
cirrhosis of liver
Contributing factors: Consumption
of excessive amounts of table salt
or other sodium salts
Excessive administration of
sodium-containing fluids
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• Edema
• Distended neck veins
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS OF FVE
• Crackles
• BUN
• HCT
• See Table 10-4 for signs and symptoms
and laboratory findings
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Pharmacologic
MEDICAL
MANAGEMENT
OF FVE
Diuretics
Dialysis
Nutritional
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Dietary
restriction
s of
sodium
NURSING
MANAGEMENT
OF FVE
I&O AND DAILY
WEIGHTS; ASSESS
LUNG SOUNDS,
EDEMA, OTHER
SYMPTOMS
MONITOR
RESPONSES TO
MEDICATIONS—
DIURETICS AND
PARENTERAL FLUIDS
MONITOR, AVOID
SOURCES OF
EXCESSIVE SODIUM,
INCLUDING
MEDICATIONS
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PROMOTE
ADHERENCE TO
FLUID
RESTRICTIONS,
PATIENT TEACHING
RELATED TO
SODIUM AND FLUID
RESTRICTIONS
PROMOTE REST
ELECTROLYTE IMBALANCES
• Sodium: hyponatremia, hypernatremia
• Potassium: hypokalemia, hyperkalemia
• Calcium: hypocalcemia, hypercalcemia
• Magnesium: hypomagnesemia, hypermagnesemia
• Phosphorus: hypophosphatemia, hyperphosphatemia
• Chloride: hypochloremia, hyperchloremia
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• Serum sodium less than 135 mEq/L
• Acute
• Result of fluid overload of a surgical
patient
• Chronic
HYPONATREMIA
• Seen outside of hospital setting, longer
duration, less serious neurologic
sequelae
• Exercise associated
• More common in women of small
stature, extreme temperatures,
excessive fluid intake, prolonged
exercise
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• Hyponatremia
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #1
• Pathophysiology: Imbalance of water,
losses by vomiting, diarrhea, sweating,
diuretics, adrenal insufficiency, certain
medications, SIADH
• Clinical manifestations: poor skin
turgor, dry mucosa, headache,
decreased salivation, decreased blood
pressure, nausea, abdominal cramping,
neurologic changes
• Serum sodium levels
• Refer to Table 10-6
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• Treat underlying condition
• Sodium replacement
• Water restriction
MEDICAL AND
NURSING
MANAGEMENT
OF
HYPONATREMIA
• Medication
• Assessment: I&O, daily weight, lab values,
CNS changes
• Encourage dietary sodium
• Monitor fluid intake
• Effects of medications (diuretics, lithium)
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HYPERNATREMIA
Serum sodium
greater than 145
mEq/L
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Occurs in patients
with normal fluid
volume, FVD, FVE
• Hypernatremia
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS
• Pathophysiology: fluid deprivation,
excess sodium administration, diabetes
insipidus, heat stroke, hypertonic IV
solutions
• Clinical manifestations: thirst; elevated
temperature
• Serum osmolality greater than 300
mOsm/kg
• Increased urine specific gravity and
osmolality
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Gradual lowering of serum sodium level via
infusion of hypotonic electrolyte solution
Diuretics
MEDICAL AND
NURSING
MANAGEMENT
OF
HYPERNATREMIA
Assessment for abnormal loss of water and
low water intake
Assess for over-the-counter sources of
sodium
Monitor for CNS changes
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Below-normal serum potassium
HYPOKALEMIA
Less than 3.5 mEq/L
May occur with normal potassium
levels: when alkalosis is present a
temporary shift of serum
potassium into cells occurs
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• Hypokalemia
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS
• Pathophysiology: GI losses,
medications, prolonged intestinal
suctioning, recent ileostomy, tumor of
the intestine, alterations of acid–base
balance, poor dietary intake,
hyperaldosteronism
• Clinical manifestations: ECG changes,
dysrhythmias, dilute urine, excessive
thirst, fatigue, anorexia, muscle
weakness, decreased bowel motility,
paresthesia
• ECG changes
• Refer to Table 10-7
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MEDICAL AND
NURSING
MANAGEMENT
OF
HYPOKALEMIA
• Potassium replacement: Increased dietary
potassium, oral potassium supplements or IV
potassium for severe deficit (unless oliguria
present)
• Monitor ECG for changes
• Monitor ABGs
• Monitor patients receiving digitalis for toxicity
• Monitor for early signs and symptoms
• Administer IV potassium only after adequate
urine output has been established
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HYPERKALEMIA
• Serum potassium greater than 5.0 mEq/L
• Seldom occurs in patients with normal renal function
• Increased risk in older adults
• Cardiac arrest is frequently associated
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• Hyperkalemia
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #3
• Pathophysiology: Impaired renal function,
rapid administration of potassium,
hypoaldosteronism, medications, tissue
trauma, acidosis
• Clinical manifestations: Cardiac changes and
dysrhythmias, muscle weakness, paresthesias,
anxiety, GI manifestations
• ECG changes
• Metabolic or respiratory acidosis
• Refer to Table 10-7
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Monitor ECG, heart rate (apical pulse) and
blood pressure, assess labs, monitor I&O,
obtain apical pulse
MEDICAL AND
NURSING
MANAGEMENT
OF
HYPERKALEMIA
Limitation of dietary potassium and dietary
teaching
Administration of cation exchange resins
(sodium polystyrene sulfonate)
Emergent care: IV calcium gluconate, IV
sodium bicarbonate, IV regular insulin and
hypertonic dextrose IV, beta-2 agonists, dialysis
Administer IV slowly and with an infusion
pump
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HYPOCALCEMIA
• Serum level less than 8.6 mg/dL,
must be considered in conjunction
with serum albumin level
• Serum calcium level controlled by
parathyroid hormone and
calcitonin
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PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #4
• Hypocalcemia
• Pathophysiology: hypoparathyroidism,
malabsorption, osteoporosis,
pancreatitis, alkalosis, transfusion of
citrated blood, kidney injury,
medications
• Clinical manifestations: tetany,
circumoral numbness, paresthesias,
hyperactive DTRs, Trousseau sign,
Chvostek sign, seizures, respiratory
symptoms of dyspnea and
laryngospasm, abnormal clotting,
anxiety
• Ionized calcium levels
• Refer to Table 10-8
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MEDICAL AND
NURSING
MANAGEMENT
OF
HYPOCALCEMIA
• IV of calcium gluconate for emergent
situations (monitor for risk of
extravasation)
• Seizure precautions
• Oral calcium and vitamin D
supplements
• Exercises to decrease bone calcium
loss
• Patient teaching related to diet and
medications
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• Serum level greater than 10.4 mg/dL
HYPERCALCEMIA
• Mild and moderate hypercalcemia
usually asymptomatic.
• Hypercalcemia crisis has high mortality
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PATHOPHYSIOLOGY, CLINICAL MANIFESTATIONS,
ASSESSMENT AND DIAGNOSTIC FINDINGS #5
• Hypercalcemia
• Pathophysiology: malignancy and hyperparathyroidism, bone loss related to
immobility, diuretics
• Clinical manifestations: polyuria, thirst, muscle weakness, intractable nausea,
abdominal cramps, severe constipation, diarrhea, peptic ulcer, bone pain,
ECG changes, dysrhythmias
• Refer to Table 10-8
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• Treat underlying cause (Cancer)
MEDICAL AND
NURSING
MANAGEMENT
OF
HYPERCALCEMIA
• Administer IV fluids, furosemide,
phosphates, calcitonin,
bisphosphonates
• Increase mobility
• Encourage fluids
• Dietary teaching, fiber for
constipation
• Ensure safety
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HYPOMAGNESEMIA
• Serum level less than 1.8 mg/dL
• Associated with hypokalemia and hypocalcemia
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• Hypomagnesemia
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #6
• Pathophysiology: alcoholism, GI losses,
enteral or parenteral feeding deficient
in magnesium, medications, rapid
administration of citrated blood
• Clinical manifestations: Chvostek and
Trousseau signs, apathy, depressed
mood, psychosis, neuromuscular
irritability, ataxia, insomnia, confusion,
muscle weakness, tremors, ECG
changes and dysrhythmias
• Ionized serum magnesium level
• Refer to Table 10-9
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• Magnesium sulfate IV is administered with
an infusion pump; monitor vital signs and
urine output
MEDICAL AND
NURSING
MANAGEMENT OF
HYPOMAGNESEMIA
• Calcium gluconate or hypocalcemic
tetany or hypermagnesemia
• Oral magnesium
• Monitor for dysphagia
• Seizure precautions
• Dietary teaching (green, leafy vegetables;
beans, lentils, almonds, peanut butter)
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Serum level greater than
2.6 mg/dL
HYPERMAGNESEMIA
Rare electrolyte
abnormality, because the
kidneys efficiently excrete
magnesium
Falsely elevated levels with
a hemolyzed blood sample
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• Hypermagnesemia
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #7
• Pathophysiology: kidney injury, diabetic
ketoacidosis, excessive administration
of magnesium, extensive soft tissue
injury
• Clinical manifestations: hypoactive
reflexes, drowsiness, muscle weakness,
depressed respirations, ECG changes,
dysrhythmias, and cardiac arrest
• Refer to Table 10-9
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IV calcium gluconate
Ventilatory support for respiratory depression
MEDICAL AND
NURSING
MANAGEMENT OF
HYPERMAGNESEMIA
Hemodialysis
Administration of loop diuretics, sodium chloride,
and LR
Avoid medications containing magnesium
Patient teaching regarding magnesium-containing
over-the-counter medications
Observe for DTRs and changes in LOC
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HYPOPHOSPHATEMIA
Serum level below 2.7
mg/dL
Hypophosphatemia can
occur when total‐body
phosphorus stores area
normal
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Hypophosphatemia
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #8
• Pathophysiology: alcoholism, refeeding of
patients after starvation, pain, heat stroke,
respiratory alkalosis, hyperventilation, diabetic
ketoacidosis, hepatic encephalopathy, major
burns, hyperparathyroidism, low magnesium, low
potassium, diarrhea, vitamin D deficiency, use of
diuretic and antacids
• Clinical manifestations: neurologic symptoms,
confusion, muscle weakness, tissue hypoxia,
muscle and bone pain, increased susceptibility to
infection
• 24-hour urine collection
• Elevated PTH levels
• Refer to Table 10-10
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• Prevention is the goal
MEDICAL AND
NURSING
MANAGEMENT OF
HYPOPHOSPHATEMIA
• Oral or IV phosphorus replacement (only for
patients with serum phosphorus levels less than 1
mg/dL not to exceed 3 mmol/hr), Burosumab,
correct underlying cause
• Monitor IV site for extravasation
• Monitor phosphorus, vitamin D and calcium levels
• Encourage foods high in phosphorus (milk, organ
meats, beans nuts, fish, poultry), gradually
introduce calories for malnourished patients
receiving parenteral nutrition
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HYPERPHOSPHATEMIA
Serum level above 4.5 mg/dL
Can occur with increased
intake, decreased excretion, or
shifting of phosphate from
intracellular to extracellular
spaces
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• Hyperphosphatemia
• Pathophysiology: kidney injury, excess
phosphorus, excess vitamin D, acidosis,
hypoparathyroidism, chemotherapy
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #9
• Clinical manifestations: few symptoms;
soft tissue calcifications, symptoms occur
due to associated hypocalcemia
• X-rays show abnormal bone
development
• Decreased PTH levels
• BUN
• Creatinine
• Refer to Table 10-10
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MEDICAL AND NURSING
MANAGEMENT OF
HYPERPHOSPHATEMIA
TREAT UNDERLYING
DISORDER
VITAMIN D
PREPARATIONS,
CALCIUM-BINDING
ANTACIDS,
PHOSPHATEBINDING GELS OR
ANTACIDS, LOOP
DIURETICS, IV
FLUIDS (NORMAL
SALINE), DIALYSIS
AVOID HIGHPHOSPHORUS
FOODS
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MONITOR
PHOSPHORUS AND
CALCIUM LEVELS
PATIENT TEACHING
RELATED TO DIET,
PHOSPHATECONTAINING
SUBSTANCES, SIGNS
OF HYPOCALCEMIA
Serum level less than 97
mEq/L
HYPOCHLOREMIA
Aldosterone impacts
reabsorption
Bicarbonate has an inverse
relationship with chloride
Chloride mainly obtained
from the diet
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• Hypochloremia
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #10
• Pathophysiology: Addison disease,
reduced chloride intake, GI loss,
diabetic ketoacidosis, excessive
sweating, fever, burns, medications,
metabolic alkalosis
• Loss of chloride occurs with loss of
other electrolytes, potassium, sodium
• Clinical manifestations: agitation,
irritability, weakness, hyperexcitability
of muscles, dysrhythmias, seizures,
coma
• ABG
• Refer to Table 10-11
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• Replace chloride-IV NS or 0.45% NS
• Ammonium chloride
MEDICAL AND
NURSING
MANAGEMENT OF
HYPOCHLOREMIA
• Monitor I&O, ABG values and
electrolyte levels
• Assess for changes in LOC
• Educate about foods high in chloride
(tomato juice, bananas, eggs, cheese,
milk) and avoid drinking free water
(water without electrolytes)
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HYPERCHLOREMIA
Serum level more than
107 mEq/L
Hypernatremia,
bicarbonate loss, and
metabolic acidosis can
occur
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• Hyperchloremia
• Pathophysiology: usually due to
iatrogenically induced hyperchloremic
metabolic acidosis
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS
• Clinical manifestations: tachypnea;
lethargy; weakness; rapid, deep
respirations; hypertension; cognitive
changes
• Normal serum anion gap
• Potassium Levels
• ABGs
• Urine Chloride Level
• Refer to Table 10-11
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• Correct the underlying cause and restore
electrolyte and fluid balance
• Hypertonic IV solutions
MEDICAL AND
NURSING
MANAGEMENT OF
HYPERCHLOREMIA
• Lactated Ringers
• Sodium bicarbonate, diuretics
• Monitor I&O, ABG
• Focused assessments of respiratory,
neurologic, and cardiac systems
• Patient teaching related to diet and
hydration
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MAINTAINING
ACID–BASE
BALANCE
•
Normal plasma pH 7.35 to 7.45: hydrogen ion
concentration
•
Major extracellular fluid buffer system;
bicarbonate–carbonic acid buffer system
•
Kidneys regulate bicarbonate in ECF
•
Lungs, under control of medulla, regulate CO2, and
thus the carbonic acid in ECF
•
Refer to Table 10-12
•
Other buffer systems
•
ECF: inorganic phosphates, plasma proteins
•
ICF: proteins, organic, inorganic phosphates
•
Hemoglobin
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• Low pH <7.35
• Increased hydrogen concentration
ACUTE AND
CHRONIC
METABOLIC
ACIDOSIS
• Low plasma bicarbonate <22 mEq/L
• Normal anion gap is 8 to 12 mEq/L
• With acidosis, hyperkalemia may
occur as potassium shifts out of cell
• Serum calcium levels may be low
with chronic metabolic acidosis
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• Metabolic Acidosis
• Pathophysiology: salicylate poisoning,
renal failure, propylene glycol toxicity,
diabetic ketoacidosis, starvation
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #12
• Clinical manifestations: headache,
confusion, drowsiness, increased
respiratory rate and depth, decreased
blood pressure, decreased cardiac output,
dysrhythmias, shock; if decrease is slow,
patient may be asymptomatic until
bicarbonate is 15 mEq/L or less
• ABG
• Serum electrolytes
• Refer to Table 10-13
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• Correct underlying problem, correct
metabolic imbalance
MEDICAL AND
NURSING
MANAGEMENT
OF METABOLIC
ACIDOSIS
• Bicarbonate may be administered
• Monitor serum electrolytes
• Monitor potassium levels
• Hemodialysis
• Peritoneal dialysis
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ACUTE AND
CHRONIC
METABOLIC
ALKALOSIS
• High pH >7.45
• High bicarbonate >26 mEq/L
• Hypokalemia will produce alkalosis
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• Metabolic Alkalosis
PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS #13
• Pathophysiology: Most commonly due to
vomiting or gastric suction, may also be
due to medications, especially long-term
diuretic use, hyperaldosteronism, Cushing’s
syndrome, and hypokalemia will produce
alkalosis
• Clinical manifestations: symptoms related to
decreased calcium, respiratory depression,
tachycardia, symptoms of hypokalemia
including tingling of toes, fingers, dizziness
and tetany, ECG changes, decreased GI
motility
• Urine chloride levels
• Refer to Table 10-13
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Correct Correct the underlying acid–base disorder
MEDICAL AND
NURSING
MANAGEMENT
OF METABOLIC
ALKALOSIS
fluid volume with sodium chloride
Restore Restore
solutions
Monitor Monitor I&O
Monitor Monitor for ECG and neurologic changes
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ACUTE AND
CHRONIC
RESPIRATORY
ACIDOSIS
• Low pH <7.35
• PaCO2 >42 mm Hg
• Always due to respiratory
problem with inadequate
ventilation, resulting in elevated
plasma levels of CO2
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PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS
• Respiratory Acidosis
• Pathophysiology: Pulmonary edema,
overdose, atelectasis, pneumothorax, severe
obesity, pneumonia, COPD, muscular
dystrophy, multiple sclerosis, myasthenia
gravis
• Clinical Manifestations: With chronic
respiratory acidosis, body may compensate,
may be asymptomatic. With acute
respiratory acidosis may see sudden
increased pulse, respiratory rate, and BP;
mental changes; feeling of fullness in head
(intracranial pressure) and increased
conjunctival vessels.
• Refer to Table 10-13
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MEDICAL AND
NURSING
MANAGEMENT
OF
RESPIRATORY
ACIDOSIS
• Improve ventilation
• Bronchodilators, antibiotics,
anticoagulants
• Pulmonary physiotherapy
• Adequate hydration
• Mechanical ventilation if necessary
• Monitor respiratory status, I&O
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ACUTE AND
CHRONIC
RESPIRATORY
ALKALOSIS
• High pH >7.45
• PaCO2 <35 mm Hg
• Always due to hyperventilation
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PATHOPHYSIOLOGY,
CLINICAL
MANIFESTATIONS,
ASSESSMENT AND
DIAGNOSTIC
FINDINGS
• Respiratory Alkalosis
• Pathophysiology: extreme anxiety, panic
disorder, hypoxemia, salicylate intoxication,
gram-negative sepsis, inappropriate
ventilator settings
• Clinical manifestations: lightheadedness,
inability to concentrate, numbness and
tingling in extremities, tachycardia, and
ventricular and atrial arrhythmias
• ABGs
• ECGs
• Serum electrolyte levels
• Refer to Table 10-13
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MEDICAL AND
NURSING
MANAGEMENT
OF
RESPIRATORY
ALKALOSIS
• Treat the underlying cause
• Antianxiety agent
• Have patient breathe into a bag
• Monitor anxiety and respiratory status
• Educate patient on techniques to
decrease anxiety
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pH 7.35–(7.4)–7.45
PaCO2 35–(40)–45 mm Hg
ASSESSING
ARTERIAL
BLOOD
GASES
HCO3- 22–(24)–26 mEq/L
PaO2 80–100 mm Hg
Oxygen saturation >94%
Base excess/deficit ±2 mEq/L
Refer to Chart 10-3
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Which is the correct interpretation of this
arterial blood gas (ABG)?
pH = 7.5
PaCO2 = 37
QUESTION #3
HCO3 = 30
A.
Respiratory Acidosis
B.
Respiratory Alkalosis
C.
Metabolic Acidosis
D.
Metabolic Alkalosis
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D. Metabolic Alkalosis
ANSWER TO
QUESTION #3
Rationale: The pH is above the
normal range indicating alkalosis. The
CO2 is within normal range
indicating no respiratory involvement.
The HCO3 is above normal range
indicating alkalosis. When the body
absorbs too much bicarbonate, this
creates a metabolic imbalance.
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