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Presented by : Miss.
Gurleen kaur
1. Hyponatremia is a serum sodium
level lower than 135 mEq/L (135
mmol/L).
2. Sodium imbalances usually are
associated with fluid volume
imbalances
1. Increased sodium excretion
 a. Excessive diaphoresis
 b. Diuretics
 c. Vomiting
 d. Diarrhea
 e. Wound drainage, especially
gastrointestinal
 f. Kidney disease
 g. Decreased secretion of aldosterone
2. Inadequate sodium intake
a.Fasting; nothing by mouth status
b. Low-salt diet
3. Dilution of serum sodium
a.Excessive ingestion of hypotonic fluids or
irrigation with hypotonic fluids
b. Kidney disease
c. Freshwater drowning
d. Syndrome of inappropriate antidiuretic
hormone secretion
e. Hyperglycemia
f. Heart failure
Assessment Findings
 Symptoms vary with changes in vascular
volume
 Normovolemic: Rapid pulse rate, normal
blood pressure
 Hypovolemic: Thready, weak, rapid pulse
rate; hypotension; flat neck veins; normal
or low central venous pressure
 Hypervolemic: Rapid, bounding pulse;
blood pressure normal or elevated;
normal or elevated central venous
pressure
Shallow, ineffective respiratory
movement is a late
manifestation related to skeletal
muscle weakness
Generalized skeletal
muscle weakness that is
worse in the extremities.
Diminished deep tendon
reflexes
Headache
Personality changes
Confusion
Seizures
Coma
Increased motility and
hyperactive bowel sounds.
Nausea
Abdominal cramping and
diarrhea
Increased urinary output
INTEGUMENTARY
Dry mucous membranes
Serum sodium level less
than 135 mEq/L (135
mmol/L)
Decreased urinary specific
gravity
 1. Monitor cardiovascular,
respiratory, neuromuscular,
cerebral, renal, and gastrointestinal
status.
2. If hyponatremia is accompanied
by a fluid volume deficit
(hypovolemia), IV sodium chloride
infusions are administered to restore
sodium content and fluid volume
•3. If hyponatremia is accompanied
by fluid volume excess
(hypervolemia), osmotic diuretics
may be prescribed to promote the
excretion of water rather than
sodium.
•4. If caused by inappropriate or
excessive secretion of antidiuretic
hormone, medications that
antagonize antidiuretic hormone
may be administered
•5. Instruct the client to
increase oral sodium intake as
prescribed and inform the
client about the foods to
include in the diet.
•6. If the client is taking
lithium, monitor the lithium
level, because hyponatremia
can cause diminished lithium
excretion, resulting in toxicity
Hypernatremia is a serum
sodium level that exceeds
145 mEq/L (145 mmol/L)
1. Decreased sodium excretion
 a. Corticosteroids
 b. Cushing’s syndrome
 c. Kidney disease
 d. Hyperaldosteronism
2. Increased sodium intake:
Excessive oral sodium ingestion or
excessive administration of sodium-
containing IV fluids
3. Decreased water intake:
Fasting; nothing by mouth
status
4. Increased water loss:
Increased rate of metabolism,
fever, hyperventilation,
infection, excessive
diaphoresis, watery diarrhea,
diabetes insipidus
Assessment Findings
Heart rate and blood pressure
respond to vascular volume
status
RESPIRATORY
▪ Pulmonary edema if
hypervolemia is present
Early: Spontaneous muscle
twitches; irregular muscle
contractions
Late: Skeletal muscle
weakness; deep tendon
reflexes diminished or absen
Altered cerebral function is the
most common manifestation of
hypernatremia
Normovolemia or hypovolemia:
Agitation, confusion, seizures
Hypervolemia: Lethargy, stupor,
coma
Extreme thirst
Renal
• Decreased urinary output
Dry and flushed skin
Dry and sticky tongue and
mucous membranes
Presence or absence of
edema, depending on fluid
volume changes
▪ Serum sodium level that
exceeds 145 mEq/L(145
mmol/L)
▪ Increased urinary specific
gravity
1. Monitor cardiovascular,
respiratory, neuromuscular,
cerebral, renal, and
integumentary status.
2. If the cause is fluid loss,
prepare to administer IV
infusions
3. If the cause is inadequate
renal excretion of sodium,
prepare to administer
diuretics that promote
sodium loss.
4. Restrict sodium and fluid
intake as prescribed
1. Hypokalemia is a serum
potassium level lower than
3.5 mEq/L (3.5 mmol/L)
2. Potassium deficit is
potentially life-threatening
because every body system is
affected.
1. Actual total body potassium loss
 a. Excessive use of medications such as
diuretics or corticosteroids
 b. Increased secretion of aldosterone,
such as in Cushing’s syndrome
 c. Vomiting, diarrhea
 d. Wound drainage, particularly
gastrointestinal
 e. Prolonged nasogastric suction
 f. Excessive diaphoresis
 g. Kidney disease impairing reabsorption
of potassium
2. Inadequate potassium
intake:
Fasting; nothing by mouth status
3. Movement of potassium
from the extracellular fluid
to the intracellular fluid
a. Alkalosis
b. Hyperinsulinism
4. Dilution of serum
potassium
a. Water intoxication
b. IV therapy with potassium-
deficient solutions
Assessment Findings
Thready, weak,
irregular pulse
Weak peripheral pulses
Orthostatic hypotension
Shallow, ineffective
respirations that result from
profound weakness of the
skeletal muscles of
respiration
Diminished breath sounds
Anxiety, lethargy, confusion,
coma
Skeletal muscle weakness, leg
cramps
Loss of tactile discrimination
 Paresthesias
 Deep tendon hyporeflexia
Decreased motility,
hypoactive to absent bowel
sounds
 Nausea, vomiting,
constipation, abdominal
distention
Paralytic ileus
Serum potassium level lower
than 3.5 mEq/L (3.5 mmol/
L)
Electrocardiogram changes:
ST depression; shallow, flat,
or inverted T wave; and
prominent U wave
1. Monitor cardiovascular,
respiratory, neuromuscular,
gastrointestinal, and renal
status, and place the client
on a cardiac monitor.
2. Monitor electrolyte
values.
3. Administer potassium supplements orally or
intravenously, as prescribed.
4. Oral potassium supplements
a.Oral potassium supplements may cause
nausea and vomiting and they should not be
taken on an empty stomach; if the client
complains of abdominal pain, distention,
nausea, vomiting, diarrhea, or
gastrointestinal bleeding, the supplement
may need to be discontinued.
b. Liquid potassium chloride has an
unpleasant taste and should be taken with
juice or another liquid.
5. Intravenously administered
potassium
6. Institute safety measures for
the client experiencing muscle
weakness.
7. If the client is taking a
potassium-losing diuretic, it
may be discontinued; a
potassium-retaining diuretic
may be prescribed.
8. Instruct the client about
foods that are high in potassium
content
1. Hyperkalemia is a serum
potassium level that exceeds 5.0
mEq/L (5.0 mmol/L)
2. Pseudohyperkalemia: a condition
that can occur due to methods of
blood specimen collection and cell
lysis; if an increased serum value is
obtained in the absence of clinical
symptoms, the specimen should be
redrawn and evaluate
1. Excessive potassium
intake
a. Over ingestion of potassium-
containing foods or medications,
such as potassium chloride or
salt substitutes
b. Rapid infusion of potassium-
containing IV solutions
2. Decreased potassium
excretion
a.Potassium-retaining diuretics
b. Kidney disease
c. Adrenal insufficiency, such as
in Addison’s disease
3. Movement of potassium
from the intracellular fluid to
the extracellular fluid
a.Tissue damage
b.Acidosis
c.Hyperuricemia
d.Hypercatabolism
Assessment Findings
Slow, weak, irregular
heart
Decreased blood
pressure
Profound weakness of the
skeletal muscles leading to
respiratory failure
Early: Muscle twitches, cramps,
paresthesias (tingling and burning
followed by numbness in the hands
and feet and around the mouth)
Late: Profound weakness,
ascending flaccid paralysis in the
arms and legs (trunk, head, and
respiratory muscles become
affected when the serum potassium
level reaches a lethal level)
Increased motility,
hyperactive bowel sounds
Diarrhea
Serum potassium level that
exceeds 5.0 mEq/L (5.0
mmol/ L
Electrocardiographic
changes: Tall peaked T
waves, flat P waves, widened
QRS complexes, and
prolonged PR intervals
1. Monitor cardiovascular,
respiratory, neuromuscular, renal,
and gastrointestinal status; place
the client on a cardiac monitor.
2. Discontinue IV potassium (keep
the IV catheter patent), and
withhold oral potassium
supplements.
 3. Initiate a potassium-restricted
diet
4. Prepare to administer
potassium-excreting diuretics if
renal function is not impaired.
5. If renal function is impaired,
prepare to administer sodium
polystyrene sulfonate (oral or
rectal route), a cation-exchange
resin that promotes
gastrointestinal sodium absorp
6. Prepare the client for dialysis if
potassium levels are critically high
7. Prepare for the administration
of IV calcium if hyperkalemia is
severe, to avert myocardial
excitability.
8. Prepare for the IV
administration of hypertonic
glucose with regular insulin to
move excess potassium into the
cells.
9. When blood transfusions are
prescribed for a client with a
potassium imbalance, the client should
receive fresh blood, if possible;
transfusions of stored blood may
elevate the potassium level because
the breakdown of older blood cells
releases potassium.
10. Teach the client to avoid foods high
in potassium
11. Instruct the client to avoid the use
of salt substitutes or other potassium-
containing substance
Hypocalcemia is a
serum calcium level
lower than 9.0 mg/dL
(2.25 mmol/L)
1. Inhibition of calcium absorption
from the gastrointestinal tract
 a. Inadequate oral intake of calcium
 b. Lactose intolerance
c. Malabsorption syndromes such as
celiac sprue or Crohn’s disease
 d. Inadequate intake of vitamin D
e. End-stage kidney disease
2. Increased calcium excretion
a.Kidney disease, polyuric phase
b.Diarrhea
c. Steatorrhea (the excretion of
abnormal quantities of fat with
the faeces owing to reduced
absorption of fat by the
intestine.)
b.Wound drainage, especially
gastrointestinal
3. Conditions that decrease the
ionized fraction of calcium
a. Hyperproteinemia
b. Alkalosis
c. Medications such as calcium
chelators or binders
d. Acute pancreatitis
e. Hyperphosphatemia
f. Immobility
g. Removal or destruction of the
parathyroid glands
Assessment Findings
Decreased heart rate
Hypotension
Diminished peripheral
pulses
Not directly affected; however,
respiratory failure or arrest can
result from decreased
respiratory movement because
of muscle tetany or seizures
Irritable skeletal muscles:
Twitches, cramps, tetany,
seizures
Painful muscle spasms in the
calf or foot during periods of
inactivity
Paresthesias followed by
numbness that may affect the
lips, nose, and ears in addition
to the limbs
•Positive Trousseau’s and
Chvostek’s signs
• Hyperactive deep tendon
reflexes
•Anxiety, irritability
Increased gastric motility;
hyperactive bowel sounds
Cramping, diarrhea
Urinary output varies
depending on the cause
Serum calcium level less
than 9.0 mg/dL (2.25
mmol/ L)
 Electrocardiographic
changes: Prolonged ST
interval, prolonged QT
interval
1. Monitor cardiovascular,
respiratory, neuromuscular, and
gastrointestinal status; place the
client on a cardiac monitor.
 2. Administer calcium
supplements orally or calcium
intravenously.
3. When administering calcium intravenously,
warm the injection solution to body
temperature before administration and
administer slowly; monitor for
electrocardiographic changes, observe for
infiltration, and monitor for hypocalcaemia.
4. Administer medications that increase
calcium absorption.
a. Aluminum hydroxide reduces phosphorus
levels, causing the counter effect of increasing
calcium levels.
b. Vitamin D aids in the absorption of calcium
from the intestinal tract.
5. Provide a quiet environment to
reduce environmental stimuli.
6. Initiate seizure precautions.
7. Move the client carefully, and
monitor for signs of a pathological
fracture.
8. Keep 10% calcium gluconate
available for treatment of acute
calcium deficit.
9. Instruct the client to consume
foods high in calcium
Hypercalcemia is a serum
calcium level that exceeds
10.5 mg/dL(2.75 mmol/L)
1. Increased calcium absorption
a. Excessive oral intake of
calcium
b. Excessive oral intake of
vitamin D
2. Decreased calcium excretion
a. Kidney disease
b. Use of thiazide diuretics
3. Increased bone resorption
of calcium
a.Hyperparathyroidism
b. Hyperthyroidism
c. Malignancy (bone
destruction from metastatic
tumors)
d. Immobility
e. Use of glucocorticoids
4. Hemoconcentration
a.Dehydration
b. Use of lithium
c. Adrenal insufficiency
Assessment Findings
Increased heart rate in the
early phase; bradycardia
that can lead to cardiac
arrest in late phases
Increased blood pressure
Bounding, full peripheral
pulses
Ineffective
respiratorymovement as a result
of profound skeletal muscle
weakness
Profound muscle weakness
Diminished or absent deep
tendon reflexes
Disorientation, lethargy,
coma
Decreased motility and
hypoactive bowel sounds
Anorexia, nausea, abdominal
distention, constipation
Urinary output varies
depending on the cause
Serum calcium level that
exceeds 10.5 mg/ dL (2.75
mmol/ L)
 Electrocardiographic
changes: Shortened ST
segment, widened T wave
 1. Monitor cardiovascular, respiratory,
neuromuscular, renal, and gastrointestinal
status; place the client on a cardiac
monitor.
 2. Discontinue IV infusions of solutions
containing calcium and oral medications
containing calcium or vitamin D.
 3. Thiazide diuretics may be discontinued
and replaced with diuretics that enhance
the excretion of calcium.
44. Administer medications as
prescribed that inhibit calcium
resorption from the bone, such as
phosphorus, calcitonin,
bisphosphonates, and prostaglandin
synthesis inhibitors (acetylsalicylic
acid, nonsteroidal antiinflammatory
medications).
5. Prepare the client with severe
hypercalcemia for dialysis if
medications fail to reduce the serum
calcium level.
6. Move the client carefully and
monitor for signs of a pathological
fracture.
7. Monitor for flank or abdominal
pain, and strain the urine to check
for the presence of urinary stones.
8. Instruct the client to avoid
foods high in calcium
Hypomagnesemia is a
serum magnesium level
lower than 1.3 mEq/L(0.65
mmol/L)
1. Insufficient magnesium intake
 a. Malnutrition and starvation
 b. Vomiting or diarrhea
 c. Malabsorption syndrome
d. Celiac disease
e. Crohn’s disease
 2. Increased magnesium
excretion
o a.Medications such as diuretics
o b. Chronic alcoholism
 3. Intracellular movement of
magnesium
o a.Hyperglycemia
o b.Insulin administration
o c. Sepsis
Assessment Findings
Tachycardia
Hypertension
RESPIRATORY
Shallow respirations
Twitches, paresthesias
Positive Trousseau’s and
Chvostek’s signs
Hyperreflexia
Tetany, seizures
Irritability
 Confusion
Serum magnesium level
less than 1.3 mEq/ L (0.65
mmol/L)
Electrocardiographic
changes: Tall T waves,
depressed ST segments
 1. Monitor cardiovascular, respiratory,
gastrointestinal, neuromuscular, and
central nervous system status; place the
client on a cardiac monitor.
 2. Because hypocalcemia frequently
accompanies hypomagnesemia,
interventions also aim to restore normal
serum calcium levels.
 3. Oral preparations of magnesium may
cause diarrhea and increase magnesium
loss
4. Magnesium sulfate by the IV route
may be prescribed in ill clients when
the magnesium level is low
(intramuscular injections cause pain
and tissue damage); initiate seizure
precautions, monitor serum magnesium
levels frequently, and monitor for
diminished deep tendon reflexes,
suggesting hypermagnesemia, during
the administration of magnesium.
5. Instruct the client to increase the
intake of foods that contain magnesium
Hypermagnesemia is a
serum magnesium level
that exceeds 2.1 mEq/L
1. Increased magnesium intake
a. Magnesium-containing
antacids and laxatives
 b. Excessive administration of
magnesium intravenously
2. Decreased renal excretion of
magnesium as a result of renal
insufficiency
Assessment Findings
Bradycardia, dysrhythmias
Hypotension
RESPIRATORY
Respiratory insufficiency
when the skeletal muscles of
respiration are involved ions
Diminished or absent deep
tendon reflexes
Skeletal muscle weakness
Drowsiness and lethargy
that progresses to coma
Serum magnesium level
that exceeds 2.1 mEq/L
(1.05 mmol/ L)
Electrocardiographic
changes: Prolonged PR
interval, widened QRS
complexes
1. Monitor cardiovascular,
respiratory, neuromuscular,
and central nervous system
status; place the client on a
cardiac monitor.
 2. Diuretics are prescribed
to increase renal excretion of
magnesium.
3. Intravenously administered
calcium chloride or calcium
gluconate may be prescribed to
reverse the effects of magnesium
on cardiac muscle.
4. Instruct the client to restrict
dietary intake of magnesium-
containing foods.
5. Instruct the client to avoid the
use of laxatives and antacids
containing magnesium
1. Hypophosphatemia is a serum
phosphorus (phosphate) level
lower than 3.0 mg/dL (0.97
mmol/L) .
2. A decrease in the serum
phosphorus level is accompanied
by an increase in the serum
calcium level
 1. Insufficient phosphorus intake:
Malnutrition and starvation
 2. Increased phosphorus excretion
 a. Hyperparathyroidism
 b. Malignancy
 c. Use of magnesium-based or aluminum
hydroxide–based antacids
 3. Intracellular shift
 a. Hyperglycemia
 b. Respiratory alkalosis
1. Cardiovascular
 a. Decreased contractility and
cardiac output
 b. Slowed peripheral pulses
2. Respiratory:
Shallow respirations
3. Neuromuscular
a. Weakness
b. Decreased deep tendon reflexes
c. Decreased bone density that can cause
fractures and alterations in bone shape
d. Rhabdomyolysis
4. Central nervous system
a.Irritability
b. Confusion
c. Seizures
5. Hematological
a. Decreased platelet aggregation and
increased bleeding
b. Immunosuppression
1. Monitor cardiovascular,
respiratory, neuromuscular, central
nervous system, and hematological
status.
2. Discontinue medications that
contribute to hypophosphatemia.
3. Administer phosphorus orally
along with a vitamin D supplement.
4. Prepare to administer phosphorus
intravenously when serum phosphorus
levels fall below 1 mg/dL and when
the client experiences critical clinical
manifestations.
5. Administer IV phosphorus slowly
because of the risks associated with
hyperphosphatemia.
6. Assess the renal system before
administering phosphorus.
7. Move the client carefully, and
monitor for signs of a pathological
fracture.
8. Instruct the client to increase the
intake of the phosphorus-containing
foods while decreasing the intake of
any calcium-containing foods
1. Hyperphosphatemia is a serum
phosphorus level that exceeds 4.5
mg/dL (1.45 mmol/L)
2. Most body systems tolerate
elevated serum phosphorus levels
well.
3. An increase in the serum
phosphorus level is accompanied by
a decrease in the serum calcium
level.
4. The problems that occur in
hyperphosphatemia center on the
hypocalcemia that results when
serum phosphorus levels increase.
1. Decreased renal excretion resulting
from renal insufficiency
 2. Tumorlysis syndrome (Tumor lysis
syndrome (TLS) is an oncologic
emergency that is caused by massive
tumor cell lysis with the release of
large amounts of potassium,
phosphate, and nucleic acids into the
systemic circulation)
 3. Increased intake of phosphorus,
including dietary intake or overuse of
phosphate-containing laxatives or
enemas
 4. Hypoparathyroidism
 Refer to assessment of
hypocalcemia
1. Interventions entail the
management of hypocalcemia.
 2. Administer phosphate-
binding medications that
increase fecal excretion of
phosphorus by binding
phosphorus from food in the
gastrointestinal tract
3. Instruct the client to avoid
phosphate-containingmedications,
including laxatives and enemas.
4. Instruct the client to decrease
the intake of food that is high in
phosphorus
5. Instruct the client in medication
administration: Take phosphate-
binding medications, emphasizing
that they should be taken with
meals or immediately after meals.
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Electrolyte imbalance disorders.pptx

  • 1. Presented by : Miss. Gurleen kaur
  • 2.
  • 3. 1. Hyponatremia is a serum sodium level lower than 135 mEq/L (135 mmol/L). 2. Sodium imbalances usually are associated with fluid volume imbalances
  • 4.
  • 5. 1. Increased sodium excretion  a. Excessive diaphoresis  b. Diuretics  c. Vomiting  d. Diarrhea  e. Wound drainage, especially gastrointestinal  f. Kidney disease  g. Decreased secretion of aldosterone
  • 6. 2. Inadequate sodium intake a.Fasting; nothing by mouth status b. Low-salt diet 3. Dilution of serum sodium a.Excessive ingestion of hypotonic fluids or irrigation with hypotonic fluids b. Kidney disease c. Freshwater drowning d. Syndrome of inappropriate antidiuretic hormone secretion e. Hyperglycemia f. Heart failure
  • 8.  Symptoms vary with changes in vascular volume  Normovolemic: Rapid pulse rate, normal blood pressure  Hypovolemic: Thready, weak, rapid pulse rate; hypotension; flat neck veins; normal or low central venous pressure  Hypervolemic: Rapid, bounding pulse; blood pressure normal or elevated; normal or elevated central venous pressure
  • 9. Shallow, ineffective respiratory movement is a late manifestation related to skeletal muscle weakness
  • 10. Generalized skeletal muscle weakness that is worse in the extremities. Diminished deep tendon reflexes
  • 12. Increased motility and hyperactive bowel sounds. Nausea Abdominal cramping and diarrhea
  • 14. Serum sodium level less than 135 mEq/L (135 mmol/L) Decreased urinary specific gravity
  • 15.  1. Monitor cardiovascular, respiratory, neuromuscular, cerebral, renal, and gastrointestinal status. 2. If hyponatremia is accompanied by a fluid volume deficit (hypovolemia), IV sodium chloride infusions are administered to restore sodium content and fluid volume
  • 16. •3. If hyponatremia is accompanied by fluid volume excess (hypervolemia), osmotic diuretics may be prescribed to promote the excretion of water rather than sodium. •4. If caused by inappropriate or excessive secretion of antidiuretic hormone, medications that antagonize antidiuretic hormone may be administered
  • 17. •5. Instruct the client to increase oral sodium intake as prescribed and inform the client about the foods to include in the diet. •6. If the client is taking lithium, monitor the lithium level, because hyponatremia can cause diminished lithium excretion, resulting in toxicity
  • 18.
  • 19. Hypernatremia is a serum sodium level that exceeds 145 mEq/L (145 mmol/L)
  • 20. 1. Decreased sodium excretion  a. Corticosteroids  b. Cushing’s syndrome  c. Kidney disease  d. Hyperaldosteronism 2. Increased sodium intake: Excessive oral sodium ingestion or excessive administration of sodium- containing IV fluids
  • 21. 3. Decreased water intake: Fasting; nothing by mouth status 4. Increased water loss: Increased rate of metabolism, fever, hyperventilation, infection, excessive diaphoresis, watery diarrhea, diabetes insipidus
  • 23. Heart rate and blood pressure respond to vascular volume status RESPIRATORY ▪ Pulmonary edema if hypervolemia is present
  • 24. Early: Spontaneous muscle twitches; irregular muscle contractions Late: Skeletal muscle weakness; deep tendon reflexes diminished or absen
  • 25. Altered cerebral function is the most common manifestation of hypernatremia Normovolemia or hypovolemia: Agitation, confusion, seizures Hypervolemia: Lethargy, stupor, coma
  • 27. Dry and flushed skin Dry and sticky tongue and mucous membranes Presence or absence of edema, depending on fluid volume changes
  • 28. ▪ Serum sodium level that exceeds 145 mEq/L(145 mmol/L) ▪ Increased urinary specific gravity
  • 29. 1. Monitor cardiovascular, respiratory, neuromuscular, cerebral, renal, and integumentary status. 2. If the cause is fluid loss, prepare to administer IV infusions
  • 30. 3. If the cause is inadequate renal excretion of sodium, prepare to administer diuretics that promote sodium loss. 4. Restrict sodium and fluid intake as prescribed
  • 31.
  • 32. 1. Hypokalemia is a serum potassium level lower than 3.5 mEq/L (3.5 mmol/L) 2. Potassium deficit is potentially life-threatening because every body system is affected.
  • 33.
  • 34. 1. Actual total body potassium loss  a. Excessive use of medications such as diuretics or corticosteroids  b. Increased secretion of aldosterone, such as in Cushing’s syndrome  c. Vomiting, diarrhea  d. Wound drainage, particularly gastrointestinal  e. Prolonged nasogastric suction  f. Excessive diaphoresis  g. Kidney disease impairing reabsorption of potassium
  • 35. 2. Inadequate potassium intake: Fasting; nothing by mouth status 3. Movement of potassium from the extracellular fluid to the intracellular fluid a. Alkalosis b. Hyperinsulinism
  • 36. 4. Dilution of serum potassium a. Water intoxication b. IV therapy with potassium- deficient solutions
  • 38. Thready, weak, irregular pulse Weak peripheral pulses Orthostatic hypotension
  • 39. Shallow, ineffective respirations that result from profound weakness of the skeletal muscles of respiration Diminished breath sounds
  • 40. Anxiety, lethargy, confusion, coma Skeletal muscle weakness, leg cramps Loss of tactile discrimination  Paresthesias  Deep tendon hyporeflexia
  • 41. Decreased motility, hypoactive to absent bowel sounds  Nausea, vomiting, constipation, abdominal distention Paralytic ileus
  • 42. Serum potassium level lower than 3.5 mEq/L (3.5 mmol/ L) Electrocardiogram changes: ST depression; shallow, flat, or inverted T wave; and prominent U wave
  • 43. 1. Monitor cardiovascular, respiratory, neuromuscular, gastrointestinal, and renal status, and place the client on a cardiac monitor. 2. Monitor electrolyte values.
  • 44. 3. Administer potassium supplements orally or intravenously, as prescribed. 4. Oral potassium supplements a.Oral potassium supplements may cause nausea and vomiting and they should not be taken on an empty stomach; if the client complains of abdominal pain, distention, nausea, vomiting, diarrhea, or gastrointestinal bleeding, the supplement may need to be discontinued. b. Liquid potassium chloride has an unpleasant taste and should be taken with juice or another liquid.
  • 45. 5. Intravenously administered potassium 6. Institute safety measures for the client experiencing muscle weakness. 7. If the client is taking a potassium-losing diuretic, it may be discontinued; a potassium-retaining diuretic may be prescribed.
  • 46. 8. Instruct the client about foods that are high in potassium content
  • 47.
  • 48.
  • 49. 1. Hyperkalemia is a serum potassium level that exceeds 5.0 mEq/L (5.0 mmol/L) 2. Pseudohyperkalemia: a condition that can occur due to methods of blood specimen collection and cell lysis; if an increased serum value is obtained in the absence of clinical symptoms, the specimen should be redrawn and evaluate
  • 50. 1. Excessive potassium intake a. Over ingestion of potassium- containing foods or medications, such as potassium chloride or salt substitutes b. Rapid infusion of potassium- containing IV solutions
  • 51. 2. Decreased potassium excretion a.Potassium-retaining diuretics b. Kidney disease c. Adrenal insufficiency, such as in Addison’s disease
  • 52. 3. Movement of potassium from the intracellular fluid to the extracellular fluid a.Tissue damage b.Acidosis c.Hyperuricemia d.Hypercatabolism
  • 55. Profound weakness of the skeletal muscles leading to respiratory failure
  • 56. Early: Muscle twitches, cramps, paresthesias (tingling and burning followed by numbness in the hands and feet and around the mouth) Late: Profound weakness, ascending flaccid paralysis in the arms and legs (trunk, head, and respiratory muscles become affected when the serum potassium level reaches a lethal level)
  • 58. Serum potassium level that exceeds 5.0 mEq/L (5.0 mmol/ L Electrocardiographic changes: Tall peaked T waves, flat P waves, widened QRS complexes, and prolonged PR intervals
  • 59. 1. Monitor cardiovascular, respiratory, neuromuscular, renal, and gastrointestinal status; place the client on a cardiac monitor. 2. Discontinue IV potassium (keep the IV catheter patent), and withhold oral potassium supplements.  3. Initiate a potassium-restricted diet
  • 60. 4. Prepare to administer potassium-excreting diuretics if renal function is not impaired. 5. If renal function is impaired, prepare to administer sodium polystyrene sulfonate (oral or rectal route), a cation-exchange resin that promotes gastrointestinal sodium absorp
  • 61. 6. Prepare the client for dialysis if potassium levels are critically high 7. Prepare for the administration of IV calcium if hyperkalemia is severe, to avert myocardial excitability. 8. Prepare for the IV administration of hypertonic glucose with regular insulin to move excess potassium into the cells.
  • 62. 9. When blood transfusions are prescribed for a client with a potassium imbalance, the client should receive fresh blood, if possible; transfusions of stored blood may elevate the potassium level because the breakdown of older blood cells releases potassium. 10. Teach the client to avoid foods high in potassium 11. Instruct the client to avoid the use of salt substitutes or other potassium- containing substance
  • 63.
  • 64. Hypocalcemia is a serum calcium level lower than 9.0 mg/dL (2.25 mmol/L)
  • 65.
  • 66. 1. Inhibition of calcium absorption from the gastrointestinal tract  a. Inadequate oral intake of calcium  b. Lactose intolerance c. Malabsorption syndromes such as celiac sprue or Crohn’s disease  d. Inadequate intake of vitamin D e. End-stage kidney disease
  • 67. 2. Increased calcium excretion a.Kidney disease, polyuric phase b.Diarrhea c. Steatorrhea (the excretion of abnormal quantities of fat with the faeces owing to reduced absorption of fat by the intestine.) b.Wound drainage, especially gastrointestinal
  • 68. 3. Conditions that decrease the ionized fraction of calcium a. Hyperproteinemia b. Alkalosis c. Medications such as calcium chelators or binders d. Acute pancreatitis e. Hyperphosphatemia f. Immobility g. Removal or destruction of the parathyroid glands
  • 71. Not directly affected; however, respiratory failure or arrest can result from decreased respiratory movement because of muscle tetany or seizures
  • 72. Irritable skeletal muscles: Twitches, cramps, tetany, seizures Painful muscle spasms in the calf or foot during periods of inactivity Paresthesias followed by numbness that may affect the lips, nose, and ears in addition to the limbs
  • 73. •Positive Trousseau’s and Chvostek’s signs • Hyperactive deep tendon reflexes •Anxiety, irritability
  • 74. Increased gastric motility; hyperactive bowel sounds Cramping, diarrhea
  • 76. Serum calcium level less than 9.0 mg/dL (2.25 mmol/ L)  Electrocardiographic changes: Prolonged ST interval, prolonged QT interval
  • 77. 1. Monitor cardiovascular, respiratory, neuromuscular, and gastrointestinal status; place the client on a cardiac monitor.  2. Administer calcium supplements orally or calcium intravenously.
  • 78. 3. When administering calcium intravenously, warm the injection solution to body temperature before administration and administer slowly; monitor for electrocardiographic changes, observe for infiltration, and monitor for hypocalcaemia. 4. Administer medications that increase calcium absorption. a. Aluminum hydroxide reduces phosphorus levels, causing the counter effect of increasing calcium levels. b. Vitamin D aids in the absorption of calcium from the intestinal tract.
  • 79. 5. Provide a quiet environment to reduce environmental stimuli. 6. Initiate seizure precautions. 7. Move the client carefully, and monitor for signs of a pathological fracture. 8. Keep 10% calcium gluconate available for treatment of acute calcium deficit. 9. Instruct the client to consume foods high in calcium
  • 80.
  • 81. Hypercalcemia is a serum calcium level that exceeds 10.5 mg/dL(2.75 mmol/L)
  • 82. 1. Increased calcium absorption a. Excessive oral intake of calcium b. Excessive oral intake of vitamin D 2. Decreased calcium excretion a. Kidney disease b. Use of thiazide diuretics
  • 83. 3. Increased bone resorption of calcium a.Hyperparathyroidism b. Hyperthyroidism c. Malignancy (bone destruction from metastatic tumors) d. Immobility e. Use of glucocorticoids
  • 84. 4. Hemoconcentration a.Dehydration b. Use of lithium c. Adrenal insufficiency
  • 86. Increased heart rate in the early phase; bradycardia that can lead to cardiac arrest in late phases Increased blood pressure Bounding, full peripheral pulses
  • 87. Ineffective respiratorymovement as a result of profound skeletal muscle weakness
  • 88. Profound muscle weakness Diminished or absent deep tendon reflexes Disorientation, lethargy, coma
  • 89. Decreased motility and hypoactive bowel sounds Anorexia, nausea, abdominal distention, constipation
  • 91. Serum calcium level that exceeds 10.5 mg/ dL (2.75 mmol/ L)  Electrocardiographic changes: Shortened ST segment, widened T wave
  • 92.  1. Monitor cardiovascular, respiratory, neuromuscular, renal, and gastrointestinal status; place the client on a cardiac monitor.  2. Discontinue IV infusions of solutions containing calcium and oral medications containing calcium or vitamin D.  3. Thiazide diuretics may be discontinued and replaced with diuretics that enhance the excretion of calcium.
  • 93. 44. Administer medications as prescribed that inhibit calcium resorption from the bone, such as phosphorus, calcitonin, bisphosphonates, and prostaglandin synthesis inhibitors (acetylsalicylic acid, nonsteroidal antiinflammatory medications). 5. Prepare the client with severe hypercalcemia for dialysis if medications fail to reduce the serum calcium level.
  • 94. 6. Move the client carefully and monitor for signs of a pathological fracture. 7. Monitor for flank or abdominal pain, and strain the urine to check for the presence of urinary stones. 8. Instruct the client to avoid foods high in calcium
  • 95.
  • 96. Hypomagnesemia is a serum magnesium level lower than 1.3 mEq/L(0.65 mmol/L)
  • 97. 1. Insufficient magnesium intake  a. Malnutrition and starvation  b. Vomiting or diarrhea  c. Malabsorption syndrome d. Celiac disease e. Crohn’s disease
  • 98.  2. Increased magnesium excretion o a.Medications such as diuretics o b. Chronic alcoholism  3. Intracellular movement of magnesium o a.Hyperglycemia o b.Insulin administration o c. Sepsis
  • 101. Twitches, paresthesias Positive Trousseau’s and Chvostek’s signs Hyperreflexia Tetany, seizures
  • 103. Serum magnesium level less than 1.3 mEq/ L (0.65 mmol/L) Electrocardiographic changes: Tall T waves, depressed ST segments
  • 104.  1. Monitor cardiovascular, respiratory, gastrointestinal, neuromuscular, and central nervous system status; place the client on a cardiac monitor.  2. Because hypocalcemia frequently accompanies hypomagnesemia, interventions also aim to restore normal serum calcium levels.  3. Oral preparations of magnesium may cause diarrhea and increase magnesium loss
  • 105. 4. Magnesium sulfate by the IV route may be prescribed in ill clients when the magnesium level is low (intramuscular injections cause pain and tissue damage); initiate seizure precautions, monitor serum magnesium levels frequently, and monitor for diminished deep tendon reflexes, suggesting hypermagnesemia, during the administration of magnesium. 5. Instruct the client to increase the intake of foods that contain magnesium
  • 106.
  • 107. Hypermagnesemia is a serum magnesium level that exceeds 2.1 mEq/L
  • 108. 1. Increased magnesium intake a. Magnesium-containing antacids and laxatives  b. Excessive administration of magnesium intravenously 2. Decreased renal excretion of magnesium as a result of renal insufficiency
  • 111. Diminished or absent deep tendon reflexes Skeletal muscle weakness
  • 112. Drowsiness and lethargy that progresses to coma
  • 113. Serum magnesium level that exceeds 2.1 mEq/L (1.05 mmol/ L) Electrocardiographic changes: Prolonged PR interval, widened QRS complexes
  • 114. 1. Monitor cardiovascular, respiratory, neuromuscular, and central nervous system status; place the client on a cardiac monitor.  2. Diuretics are prescribed to increase renal excretion of magnesium.
  • 115. 3. Intravenously administered calcium chloride or calcium gluconate may be prescribed to reverse the effects of magnesium on cardiac muscle. 4. Instruct the client to restrict dietary intake of magnesium- containing foods. 5. Instruct the client to avoid the use of laxatives and antacids containing magnesium
  • 116.
  • 117. 1. Hypophosphatemia is a serum phosphorus (phosphate) level lower than 3.0 mg/dL (0.97 mmol/L) . 2. A decrease in the serum phosphorus level is accompanied by an increase in the serum calcium level
  • 118.  1. Insufficient phosphorus intake: Malnutrition and starvation  2. Increased phosphorus excretion  a. Hyperparathyroidism  b. Malignancy  c. Use of magnesium-based or aluminum hydroxide–based antacids  3. Intracellular shift  a. Hyperglycemia  b. Respiratory alkalosis
  • 119. 1. Cardiovascular  a. Decreased contractility and cardiac output  b. Slowed peripheral pulses 2. Respiratory: Shallow respirations
  • 120. 3. Neuromuscular a. Weakness b. Decreased deep tendon reflexes c. Decreased bone density that can cause fractures and alterations in bone shape d. Rhabdomyolysis 4. Central nervous system a.Irritability b. Confusion c. Seizures 5. Hematological a. Decreased platelet aggregation and increased bleeding b. Immunosuppression
  • 121. 1. Monitor cardiovascular, respiratory, neuromuscular, central nervous system, and hematological status. 2. Discontinue medications that contribute to hypophosphatemia. 3. Administer phosphorus orally along with a vitamin D supplement.
  • 122. 4. Prepare to administer phosphorus intravenously when serum phosphorus levels fall below 1 mg/dL and when the client experiences critical clinical manifestations. 5. Administer IV phosphorus slowly because of the risks associated with hyperphosphatemia. 6. Assess the renal system before administering phosphorus.
  • 123. 7. Move the client carefully, and monitor for signs of a pathological fracture. 8. Instruct the client to increase the intake of the phosphorus-containing foods while decreasing the intake of any calcium-containing foods
  • 124.
  • 125. 1. Hyperphosphatemia is a serum phosphorus level that exceeds 4.5 mg/dL (1.45 mmol/L) 2. Most body systems tolerate elevated serum phosphorus levels well. 3. An increase in the serum phosphorus level is accompanied by a decrease in the serum calcium level.
  • 126. 4. The problems that occur in hyperphosphatemia center on the hypocalcemia that results when serum phosphorus levels increase.
  • 127. 1. Decreased renal excretion resulting from renal insufficiency  2. Tumorlysis syndrome (Tumor lysis syndrome (TLS) is an oncologic emergency that is caused by massive tumor cell lysis with the release of large amounts of potassium, phosphate, and nucleic acids into the systemic circulation)  3. Increased intake of phosphorus, including dietary intake or overuse of phosphate-containing laxatives or enemas  4. Hypoparathyroidism
  • 128.  Refer to assessment of hypocalcemia
  • 129. 1. Interventions entail the management of hypocalcemia.  2. Administer phosphate- binding medications that increase fecal excretion of phosphorus by binding phosphorus from food in the gastrointestinal tract
  • 130. 3. Instruct the client to avoid phosphate-containingmedications, including laxatives and enemas. 4. Instruct the client to decrease the intake of food that is high in phosphorus 5. Instruct the client in medication administration: Take phosphate- binding medications, emphasizing that they should be taken with meals or immediately after meals.