Fluid and Electrolytes: Balance and Disturbance

Chapter 14
Fluid and Electrolytes: Balance

and Disturbance
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
Fluid and Electrolyte Balance

Necessary for life, homeostasis
Nursing role: help prevent, treat fluid, electrolyte
disturbances
Fluid
Approximately 60% of typical adult is fluid
Varies with age, body size, gender
Intracellular fluid
Extracellular fluid
Intravascular
Interstitial
Transcellular
Third spacing: loss of ECF into space that does not
contribute to equilibrium
Electrolytes
Active chemicals that carry positive (cations), negative
(anions) electrical charges
Major cations: sodium, potassium, calcium,
magnesium, hydrogen ions
Major anions: chloride, bicarbonate, phosphate,
sulfate, and proteinate ions
Electrolyte concentrations differ in fluid compartments
Regulation of Fluid
Movement of fluid through capillary walls depends on
Hydrostatic pressure: exerted on walls of blood
vessels
Osmotic pressure: exerted by protein in plasma
Direction of fluid movement depends on differences of
hydrostatic, osmotic pressure
Regulation of Fluid
Osmosis: area of low solute concentration to area of high
solute concentration
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: physiologic pump that moves fluid from
area of lower concentration of one of higher
concentration
Active Transport
Physiologic pump that moves fluid from area of lower
concentration to one of higher concentration
Movement against concentration gradient
Sodium-potassium pump: maintains higher concentration
of extracellular sodium, intracellular potassium
Requires adenosine (ATP) for energy
Question
Tell whether the following statement is true or false:
Osmosis is the movement of a substance from an area of
higher concentration to one of lower concentration.
Answer
False.
Rationale: Diffusion is the movement of a substance from
an area of higher concentration to one of lower
concentration. The concentration of dissolved substances
draws fluid in that direction. Osmosis is the movement of
fluid, through a semipermeable membrane, from an area
of low solute concentration to an area of high solute
concentration until the solutions are of equal
concentration.
Routes of Gains and Losses

Gain
Dietary intake of fluid, food or enteral feeding
Parenteral fluids
Routes of Gains and Losses (contd)

Loss
Kidney: urine output
Skin loss: sensible, insensible losses
Lungs
GI tract
Other
Question
What is the average daily urinary output in an adult?
0.5 L
1.0 L
1.5 L
2.5 L
Answer
C. 1.5 L
Rationale: Vital to the regulation of fluid and electrolyte
balance, the kidneys normal filter 170 L of plasma every
day in the adult, while excreting only 1.5 L of urine.
Gerontologic Considerations
Reduced homeostatic mechanisms: cardiac, renal,
respiratory function
Decreased body fluid percentage
Medication use
Presence of concomitant conditions
Fluid Volume Imbalances

Fluid volume deficit (FVD): hypovolemia
Fluid volume excess (FVE): hypervolemia
Fluid Volume Deficit

Loss of extracellular fluid exceeds intake ratio of water
Electrolytes lost in same proportion as they exist in
normal body fluids
Dehydration: loss of water along with increased serum
sodium level
May occur in combination with other imbalances
Fluid Volume Deficit (contd)

Dehydration
Causes: fluid loss from vomiting, diarrhea, GI
suctioning, sweating, decreased intake, inability to
gain access to fluid
Risk factors: diabetes insipidus, adrenal insufficiency,
osmotic diuresis, hemorrhage, coma, third space
shifts

Manifestations: rapid weight loss, decreased skin turgor,
oliguria, concentrated urine, postural hypotension, rapid
weak pulse, increased temperature, cool clammy skin
due to vasoconstriction, lassitude, thirst, nausea, muscle
weakness, cramps
Laboratory data: elevated BUN in relation to serum
creatinine, increased hematocrit
Serum electrolyte changes may occur

Medical management: provide fluids to meet body needs
Oral fluids
IV solutions
Fluid Volume Deficit - Nursing

Management
I&O, VS
Monitor for symptoms: skin and tongue turgor, mucosa,
UO, mental status
Measures to minimize fluid loss
Oral care
Administration of oral fluids
Administration of parenteral fluids
Question
What is a major indicator of extracellular FVD?
Full and bounding pulse
Drop in postural blood pressure
Elevated temperature
Pitting edema of lower extremities
Answer
B. Drop in postural blood pressure
Rationale: FVD signs and symptoms include acute weight
loss; decreased skin turgor; oliguria; concentrated urine;
orthostatic hypotension due to volume depletion; a weak,
rapid heart rate; flattened neck veins; increased
temperature; thirst; decreased or delayed capillary refill;
decreased central venous pressure; cool, clammy, pale
skin related to peripheral vasoconstriction; anorexia;
nausea; lassitude; muscle weakness; and cramps.
Clinical manifestations of FVE result from expansion of
the ECF and include edema, distended neck veins, and
crackles (abnormal lung sounds).
Fluid Volume Excess

Due to fluid overload or diminished homeostatic
mechanisms
Risk factors: heart failure, renal failure, cirrhosis of liver
Contributing factors: excessive dietary sodium or sodiumcontaining IV solutions
Manifestations: edema, distended neck veins, abnormal
lung sounds (crackles), tachycardia, increased BP, pulse
pressure and CVP, increased weight, increased UO,
shortness of breath and wheezing
Medical management: directed at cause, restriction of
fluids and sodium, administration of diuretics
Fluid Volume Excess - Nursing

Management
I&O and daily weights; assess lung sounds, edema,
other symptoms; monitor responses to medicationsdiuretics
Promote adherence to fluid restrictions, patient teaching
related to sodium and fluid restrictions
Monitor, avoid sources of excessive sodium, including
medications
Promote rest
Semi-Fowlers position for orthopnea
Skin care, positioning/turning
Electrolyte Imbalances
Sodium: hyponatremia, hypernatremia
Potassium: hypokalemia, hyperkalemia
Calcium: hypocalcemia, hypercalcemia
Magnesium: hypomagnesemia, hypermagnesemia
Phosphorus: hypophosphatemia, hyperphosphatemia
Chloride: hypochloremia, hyperchloremia
Hyponatremia
Serum sodium less than 135 mEq/L
Causes: adrenal insufficiency, water intoxication, SIADH
or losses by vomiting, diarrhea, sweating, diuretics
Manifestations: poor skin turgor, dry mucosa, headache,
decreased salivation, decreased BP, nausea, abdominal
cramping, neurologic changes
Medical management: water restriction, sodium
replacement
Nursing management: assessment and prevention,
dietary sodium and fluid intake, identify and monitor atrisk patients, effects of medications (diuretics, lithium)
Hypernatremia
Serum sodium greater than 145mEq/L
Causes: excess water loss, excess sodium administration,
diabetes insipidus, heat stroke, hypertonic IV solutions
Manifestations: thirst; elevated temperature; dry, swollen
tongue; sticky mucosa; neurologic symptoms;
restlessness; weakness
Note: thirst may be impaired in elderly or the ill
Medical management: hypotonic electrolyte solution or
D5W
Nursing management: assessment and prevention,
assess for OTC sources of sodium, offer and encourage
fluids to meet patient needs, provide sufficient water with
tube feedings
Hypokalemia
Below-normal serum potassium (<3.5 mEq/L), may occur
with normal potassium levels with alkalosis due to shift of
serum potassium into cells
Causes: GI losses, medications, alterations of acid-base
balance, hyperaldosterism, poor dietary intake
Manifestations: fatigue, anorexia, nausea, vomiting,
dysrhythmias, muscle weakness and cramps, paresthesias,
glucose intolerance, decreased muscle strength, DTRs
Medical management: increased dietary potassium,
potassium replacement, IV for severe deficit
Nursing management: assessment, severe hypokalemia is
life-threatening, monitor ECG and ABGs, dietary
potassium, nursing care related to IV potassium
administration
Hyperkalemia
Serum potassium greater than 5.0 mEq/L
Causes: usually treatment related, impaired renal
function, hypoaldosteronism, tissue trauma, acidosis
Manifestations: cardiac changes and dysrhythmias,
muscle weakness with potential respiratory impairment,
paresthesias, anxiety, GI manifestations
Medical management: monitor ECG, limitation of dietary
potassium, cation-exchange resin (Kayexalate), IV
sodium bicarbonate , IV calcium gluconate, regular
insulin and hypertonic dextrose IV, -2 agonists, dialysis
Hyperkalemia (contd)
Nursing management: assessment of serum potassium
levels, mix IVs containing K+ well, monitor medication
affects, dietary potassium restriction/dietary teaching for
patients at risk
Hemolysis of blood specimen or drawing of blood above
IV site may result in false laboratory result
Salt substitutes, medications may contain potassium
Potassium-sparing diuretics may cause elevation of
potassium
Should not be used in patients with renal dysfunction
Question
Tell whether the following statement is true or false:
The ECG change that is specific to hyperkalemia is a
peaked T wave.
Answer
True.
Rationale: The ECG changes that are specific to
hyperkalemia are peaked T wave; wide, flat P wave; and
wide QRS complex. The ECG changes that are specific to
hypokalemia are flatted T wave and the appearance of a
U wave.
Hypocalcemia
Serum level less than 8.5 mg/dL, must be considered in
conjunction with serum albumin level
Causes: hypoparathyroidism, malabsorption, pancreatitis,
alkalosis, massive transfusion of citrated blood, renal
failure, medications, other
Manifestations: tetany, circumoral numbness,
paresthesias, hyperactive DTRs, Trousseaus sign,
Chovstek's sign, seizures, respiratory symptoms of
dyspnea and laryngospasm, abnormal clotting, anxiety
Hypocalcemia (contd)
Medical management: IV of calcium gluconate, calcium
and vitamin D supplements; diet
Nursing management: assessment, severe hypocalcemia
is life-threatening, weight-bearing exercises to decrease
bone calcium loss, patient teaching related to diet and
medications, and nursing care related to IV calcium
administration
Trousseaus Sign
Hypercalcemia
Serum level above 10.5 mg/dL
Causes: malignancy and hyperparathyroidism, bone loss
related to immobility
Manifestations: muscle weakness, incoordination,
anorexia, constipation, nausea and vomiting, abdominal
and bone pain, polyuria, thirst, ECG changes,
dysrhythmias
Medical management: treat underlying cause, fluids,
furosemide, phosphates, calcitonin, biphosphonates
Nursing management: assessment, hypercalcemic crisis
has high mortality, encourage ambulation, fluids of 3 to 4
L/d, provide fluids containing sodium unless
contraindicated, fiber for constipation, ensure safety
Hypomagnesemia
Serum level less than 1.8 mg/dL, evaluate in conjunction
with serum albumin
Causes: alcoholism, GI losses, enteral or parenteral
feeding deficient in magnesium, medications, rapid
administration of citrated blood; contributing causes
include diabetic ketoacidosis, sepsis, burns, hypothermia
Manifestations: neuromuscular irritability, muscle
weakness, tremors, athetoid movements, ECG changes
and dysrhythmias, alterations in mood and level of
consciousness
Medical management: diet, oral magnesium, magnesium
sulfate IV
Hypomagnesemia (contd)
Nursing management: assessment, ensure safety, patient
teaching related to diet, medications, alcohol use, and
nursing care related to IV magnesium sulfate
Hypomagnesemia often accompanied by hypocalcemia
Need to monitor, treat potential hypocalcemia
Dysphasia common in magnesium-depleted patients
Assess ability to swallow with water before
administering food or medications
Hypermagnesemia
Serum level more than 2.7 mg/dL
Causes: renal failure, diabetic ketoacidosis, excessive
administration of magnesium
Manifestations: flushing, lowered BP, nausea, vomiting,
hypoactive reflexes, drowsiness, muscle weakness,
depressed respirations, ECG changes, dysrhythmias
Medical management: IV calcium gluconate, loop
diuretics, IV NS of RL, hemodialysis
Nursing management: assessment, do not administer
medications containing magnesium, patient teaching
regarding magnesium containing OTC medications
Hypophosphatemia
Serum level below 2.5 mg/DL
Causes: 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
Manifestations: neurologic symptoms, confusion, muscle
weakness, tissue hypoxia, muscle and bone pain, increased
susceptibility to infection
Medical management: oral or IV phosphorus replacement
Nursing management: assessment, encourage foods high in
phosphorus, gradually introduce calories for malnourished
patients receiving parenteral nutrition
Hyperphosphatemia
Serum level above 4.5 mg/DL
Causes: renal failure, excess phosphorus, excess vitamin
D, acidosis, hypoparathyroidism, chemotherapy
Manifestations: few symptoms; soft-tissue calcifications,
symptoms occur due to associated hypocalcemia
Medical management: treat underlying disorder, vitaminD preparations, calcium-binding antacids, phosphatebinding gels or antacids, loop diuretics, NS IV, dialysis
Nursing management: assessment, avoid highphosphorus foods; patient teaching related to diet,
phosphate-containing substances, signs of hypocalcemia
Hypochloremia
Serum level less than 96 mEq/L
Causes: Addisons 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
Manifestations: agitation, irritability, weakness,
hyperexcitability of muscles, dysrhythmias, seizures, coma
Medical management: replace chloride-IV NS or 0.45% NS
Nursing management: assessment, avoid free water,
encourage high-chloride foods, patient teaching related to
high-chloride foods
Hyperchloremia
Serum level more than 108 mEq/L
Causes: excess sodium chloride infusions with water loss,
head injury, hypernatremia, dehydration, severe diarrhea,
respiratory alkalosis, metabolic acidosis,
hyperparathyroidism, medications
Manifestations: tachypnea, lethargy, weakness, rapid,
deep respirations, hypertension, cognitive changes
Normal serum anion gap
Medical management: restore electrolyte and fluid
balance, LR, sodium bicarbonate, diuretics
Nursing management: assessment, patient teaching
related to diet and hydration
Maintaining Acid-Base Balance

Normal plasma pH 7-35-7.45: 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, carbonic
acid in ECF
Maintaining Acid-Base Balance (contd)

Other buffer systems
ECF: inorganic phosphates, plasma proteins
ICF: proteins, organic, inorganic phosphates
Hemoglobin
Question
What is the most common buffer system in the body?
Plasma protein
Hemoglobin
Phosphate
Bicarbonate-carbonic acid
Answer
D. Bicarbonate-carbonic acid
Rationale: The bodys major extracellular buffer system is
the bicarbonatecarbonic acid buffer system, which is
assessed when arterial blood gases are measured.
Metabolic Acidosis
Low pH <7.35
Low bicarbonate <22 mEq/L
Most commonly due to renal failure
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
Correct underlying problem, correct imbalance
Bicarbonate may be administered
Metabolic Acidosis (contd)

With acidosis, hyperkalemia may occur as potassium
shifts out of cell
As acidosis is corrected, potassium shifts back into cell,
potassium levels decrease
Monitor potassium levels
Serum calcium levels may be low with chronic metabolic
acidosis
Must be corrected before treating acidosis
Metabolic Alkalosis
High pH >7.45
High bicarbonate >26 mEq/L
Most commonly due to vomiting or gastric suction
May also be due to medications, especially long-term
diuretic use
Hypokalemia will produce alkalosis
Manifestations: symptoms related to decreased calcium,
respiratory depression, tachycardia, symptoms of
hypokalemia
Metabolic Alkalosis (contd)

Correct underlying disorder, supply chloride to allow
excretion of excess bicarbonate, restore fluid volume with
sodium chloride solutions
Respiratory Acidosis
Low pH <7.35
PaCO2 >42 mm Hg
Always due to respiratory problem with inadequate
excretion of CO2
With chronic respiratory acidosis, body may compensate,
may be asymptomatic
Symptoms may be suddenly increased pulse,
respiratory rate and BP, mental changes, feeling of
fullness in head
Respiratory Acidosis (contd)

Potential increased intracranial pressure
Treatment aimed at improving ventilation
Respiratory Alkalosis
High pH >7.45
PaCO2 <35 mm Hg
Always due to hyperventilation
Manifestations: lightheadedness, inability to concentrate,
numbness and tingling, sometimes loss of consciousness
Correct cause of hyperventilation
Arterial Blood Gases

pH 7.35 - (7.4) - 7.45
PaCO2 35 - (40) - 45 mm Hg
HCO3 22 - (24) - 26 mEq/L
Assumed average values for ABG interpretation
PaO2 80 to 100 mm Hg
Oxygen saturation >94%
Base excess/deficit 2 mEq/L
IV Site Selection
Complications of IV Therapy
Fluid overload
Air embolism
Septicemia, other infections
Infiltration, extravasation
Phlebitis
Thrombophlebitis
Hematoma
Clotting, obstruction

Fluid and Electrolytes: Balance and Disturbance

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Chapter 14

Fluid and Electrolytes: Balance

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Fluid and Electrolyte Balance

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Routes of Gains and Losses

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Routes of Gains and Losses (contd)

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Fluid Volume Imbalances

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Fluid Volume Deficit

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Fluid Volume Deficit (contd)

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Fluid Volume Deficit (contd)

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Fluid Volume Deficit (contd)

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Fluid Volume Deficit - Nursing

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Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Fluid Volume Excess

Fluid Volume Excess - Nursing

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Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

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Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Maintaining Acid-Base Balance

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Maintaining Acid-Base Balance (contd)

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Metabolic Acidosis (contd)

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Metabolic Alkalosis (contd)

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Respiratory Acidosis (contd)

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Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Arterial Blood Gases

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Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

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