fluid and electrolytes

1. Fluid and
Electrolytes
Balance and
Disturbances

2. Fluid and Electrolytes
 60% of body consists of fluid
 Intracellular space [2/3]
 Extracellular space [1/3]
 Electrolytes are active ions:
positively and negatively
charged

5. Mechanisms controlling fluid
and electrolyte movement:
1) Electrolyte moves by - Simple diffusion
- Facilitated diffusion
- Active transport
2) Water moves by - Hydrostatic pressure
- Osmotic pressure

6. DIFFUSION
 Diffusion is the movement of a substance
from area of higher concentration to one of
lower
concentration
 “Downhill
Movement”

7. FACILITATED DIFFUSION
The molecules from an area of high
concentration to one of low
concentration
 It is passive. Requires no energy
other than that of the concentration
gradient
Ex- glucose transport into the cell

8. ACTIVE TRANSPOTATION
 Active transport is a process in
which molecules moves against
the concentration gradient

9. Sodium-Potassium Pump
 Sodium concentration is higher in
ECF than ICF
 Sodium enters cell by diffusion
 Potassium exits cell into ECF

10. OSMOSIS
 Osmosis is the diffusion of water
caused by fluid gradient

11. Fluid and Electrolytes 2

12.  Tonicity is the ability of solutes to
cause osmotic driving forces

13. Osmotic pressure:
Osmotic pressure is the amount of
pressure needed to stop the flow of
water

14. Fluid shifts
 If capillary interstitial pressure altered fluid
abnormally shift from one compartment to
another
Shift of plasma to interstitial –
Accumulation of fluid in the interstitial
occurs if venous hydrostatic pressure raises,
plasma oncotic pressure decreases

15.  Elevation of venous hydrostatic pressure
– causes fluid overload, heart failure, liver
failure, obstruction to venous return to the
heart
 Decrease in plasma oncotic pressure –
results excessive protein loss, deficient
protein synthesis.
 Elevation of interstitial oncotic pressure –
trauma, burn, inflammation

16. Shift of interstitial fluid to
plasma
 Fluid is drawn into the plasma whenever
there is an increase in the oncotic pressure
Ex- administration of colloids, dextral,
Manito, hypertonic solutions
 Increasing the hydrostatic pressure in the
way of causing shift of fluid into the plasma
Ex- wearing stockings

17. Fluid movement between
Extra cellular and intra
cellular:
 1. Increased ICF osmolarity (water
deficit)
 2. Decreased ESF osmolarity (water
excess)

18. Fluid spacing
 The distribution of water:
 first spacing – normal distribution of body
water
 second spacing – abnormal accumulation
of interstitial fluid Ex- edema
 Third spacing – fluid accumulate in a
portion of the body from which it is not
freely. Exchanged with the rest of ECF Ex-
ascites, peritonitis.

19. FLUID
IMBALANCES

20. Fluid Volume Disturbances
2
 Fluid Volume Excess
(Hypervolemia)

21. Nursing Diagnosis and
Goal
 Fluid volume excess r/t CHF, excess sodium
intake, renal failure:
Weight gain of 6 lb. in 24 hours; lungs with
crackles in bases bilaterally; 2+ edema in
ankles bilaterally
Goal: Client will have normal fluid volume within
48 hours :
Decreased weight of 1 lb. per day, lung sounds
clear in all fields, ankles without edema

22. Fluid Volume
Disturbances
 Fluid Volume Deficit
(Hypovolemia)

23. Fluid Volume Deficit
 Mild – 2% of body weight loss
 Moderate – 5% of body weight loss
 Severe – 8% or more of body
weight loss

24. Nursing Diagnosis
 Fluid volume Deficit r/t
Insufficient intake, vomiting, diarrhea,
hemorrhage m/b dry mucous membranes, low
BP, BUN 28, Na 152, urine dark amber; Intake
200mL/Output 450mL over 24 hours
Goal: Client will have adequate fluid volume
within 24 hours :
Moist tongue, mucous membranes, BUN
between 8-20, Na 135-145, Urine clear yellow,
balanced I/O

25. Fluid Volume Deficit 5
 Nursing management
- Restore fluids by oral or IV
- Treat underlying cause
- Monitor I & O at least every 8 hours
- Daily weight
- Vital signs
- Skin turgor
- Urine concentration

26. Good afternoon

27. III. Extra cellular fluid
volume shift
Third space fluid
Definition
“A fluid shift basically a change in
the location of ECF between the
intracellular and interstitial space”

28. Types
 vascular fluid to interstitial space
 interstitial fluid to vascular fluid
space
 (Third space fluid physiologically useless
because it does not circulate nutrients to
cells.)

29. Etiology
 Any pathological process that triggers the
inflammatory or ischemic process can
leads to fluid shifting.
 Crushing injury
 Extensive burns
 Acid base imbalance
 Bowl obstruction: that reduce protein
absorption can reduce sodium levels

30.  Perforated peptic ulcer
 Intestinal obstruction
 Lymphatic obstruction,
 Large venous thrombosis: it impaired fluid
return to the right atrium, thus promoting
third- spacing
 Pleural and pericardial shifts are secondary
to inflammatory responses to infectious, non
infectious, autoimmune disorders

31. Risk factors
 Client at risk of third space fluids
are those who have sustained
major trauma or major surgery

32. Pathophysiology
Tissue injury
↓
Release of histamine and bradikinin
↓
Increases capillary permeability
↓
Shift of fluid, protein and other solutes to interstitial
space
↓ ↓
1st phase 2sd phase
Hypovolemia Hypervolemia

33. Clinical manifestations
 Mostly similar to the manifestations of hypovolemia
because the fluid is not in the vascular system.
 Pale and cold limbs
 Pallor
 Weak and rapid pulse
 Hypotension
 Increased skin turgor
 Decreased level of conscious
 Enlargement of peripheral and jugular veins
 Crackles
 If sever it leads to hypovolemic shock

34. Diagnosis
 History
 Physical examination
 Laboratory tests – if fluid collects and
obstruct any organs, blood, or veins there
is increase hematocrit, sodium, BUN,
urine specific gravity

35. Medical management
 Paracenthesis
# If third space causing bowel obstruction
Paracenthesis is done
 Replace the fluids
# Hypervolemia – a large volume of isotonic IV
fluids administered to replace intravascular
volume. This is to maintain kidney perfusion.
# Albumin may be given to replace protein lost
from trauma and to promote restoration of
capillary oncotic pressure

36.  Stabilize other problems
Diagnosis of sepsis by culture and treatment
is with antibiotics
Vaso active medication to maintain blood
pressure
Repair of bowel obstruction
Treatment of inflammatory bowel disorders –
administer steroids to stabilize the mast cell
membrane

37. Nursing management
 Assess the vital signs every 1-8 hrs , if
shock is present assess vital signs every
hour
 Monitor IV fluid replacement
 Assess for early signs of fluid over load
 Measure abdominal girth every 8 hrs in case
of ascites
 Monitor urine out put every 1 hr and report
an output less than 30ml / hr
 Monitor plasma levels of BUN

38. IV. Intracellular fluid
volume excess
 Water intoxication
The cells are quite resistant to
fluid shifts, certain conditions can
lead to an intracellular fluid volume
excess (ICFVE)

39. Causes
 Administration of excessive amounts of
hypo-osmolar IV fluids such as 0.45 % NS,
5% D water
 Older clients who consume more tap water
without nutrient intake.
 Psychiatric disorders (schizophrenia) –
often have compulsive water consumption
behaviors (80% cases)

40. Pathophysiology
 Hypo-osmolar fluids in the vessels move by osmosis to
region of higher concentration of sodium in the cells in an
attempt to maintain equilibrium.
 Unfortunately too much fluid accumulates in the cells
causing cellular edema.
 Cerebral cells absorb hypos molar fluid more quickly
that do other cells.
 Thus these cell changes lead to Intracellular fluid
volume excess

41. Clinical manifestations
 Increasing intracranial pressure
 Altered vital signs : when pressure is
at the level of the hypothalamus and
brain stem
 Decreased level of consciousness
 Altered papillary changes

42. Diagnosis
 History
 Physical examination
 Laboratory tests – increased plasma
sodium, decreased hematocrit.
 Computed tomography
 Magnetic resonance imaging

43. Management
Medical management
 To reduce ICP
 Steroids and osmotic diuretics
 Administration of IV fluids containing
Nacl, Administration of saline solutions
ex – 5%D, 0.45% Nacl increases
osmolarity
 Elevate the head end of the bed 30-45
degrees

44. Nursing management
 Perform neurological checks every 1hr
 level of consciousness
 vital signs
 reflexes
 papillary responses
 Monitor intake and out put hourly
 Notify the physician if the client sensorial changes
and if systolic blood pressure less than 100 mmHg
or greater than 150 mmhg
 Monitor weight daily

45.  Administer antiemetic prophylactic ally – to promote
food and fluid ingestion and to decrease the risk of
vomiting, which worsens the increased ICP
 Provide safety measures , if behavioral changes
occur such as confusion or disorientation
 Keep the bed in low position with bed side rails
raised
 Keep the suction equipment at the bed side in
anticipation of seizures
 If the patient has seizures, turn the client to one side
to displace the tongue
 Document all phase’s seizures
 Monitor increased ICP improving

46. Electrolyte
Imbalances

47. Hyponatremia (Sodium)
Normal range – 135 to 145 m E q/L
- Primary regulator of ECF volume (a loss
or gain of sodium is usually accompanied
by a loss or gain of water)
 Sodium level less than 135 m E q/L

48. Critical Thinking Exercise: Nursing
Management of the Client with
Hyponatremia
 Situation: An 87 year old man was
admitted to the acute care facility for
gastroenteritis, 2 day duration. He is
vomiting, has severe, watery diarrhea
and is c/o abd cramping. His serum
electrolytes are consistent with
hyponatremia r/t excessive sodium loss.

49. Critical Thinking Exercise: Nursing
Management of the Client with
Hyponatremia 2
 1. What is the relationship between
vomiting, diarrhea, and hyponatremia?
 2. What s/s should the client be
monitored for that indicate the presence
of sodium deficit?
 3. In addition to examining the client’s
serum electrolyte findings, how will the
nurse know when the client’s sodium
level has returned to normal?

50. Hypernatremia
 Sodium level is greater than 145 mEq/L
 Can be caused by a gain of sodium in
excess of water or by a loss of water in
excess of sodium

52. Critical Thinking Exercise:
Nursing Management of the
Client with Hypernatremia
 Situation: A 47 year old woman was taken to
the ER after she developed a rapid heart rate
and agitation. Physical assessment revealed
dry oral mucous membranes, poor skin turgor,
and fever of 101.3 orally. The client’s daughter
stated her mother had been very hungry
recently and drinking more fluids than usual.
Suspecting DM, the practitioner obtained
serum electrolytes and glucose levels, which
revealed serum sodium of 163 mEq/L and
serum glucose of 360 mg/dL.

53. Critical Thinking Exercise:
Nursing Management of the
Client with Hypernatremia 2
 1. Interpret the client’s lab data.
 2. Why are clients with DM prone to the
development of hypernatremia?
 3. What precautions should the nurse take
when caring for the client with hypernatremia?
 4. List 4 food items this client should avoid and
why.
 5. Identify 3 meds that could have an increased
effect on the client’s sodium level.

54. GOOD MORNING

55. All About Potassium
 Major Intracellular electrolyte
 98% of the body’s potassium is inside the
cells
 Influences both skeletal and cardiac
muscle activity
 Normal serum potassium
concentration –
3.5 to 5.5 mEq/L.

56. Hypokalemia
 Serum Potassium below 3.5 mEq/L

57. Cause
 Actual total body potassium loss
 Excessive use of diuretics and corticosteroids
 Increased secretion of aldosterone Ex Cushing’s
syndrome
 Vomiting, diarrhea, Prolonged NG tube suction
 Excessive diaphoresis
 Renal disease impairing reabsorption of potassium
 Inadequate potassium intake – nothing by mouth
 Movement of potassium from ECF to ICF
 Alkalosis
 Hyperinsulism

58. Clinical manifestations
Cardiovascular
 Thready, weak, irregular pulse
 Peripheral pulse weak
 Orthostatic hypotension
 ECG changes – ST depression, shallow.
Flat or inverted T wave. Prominent U wave

59. Respiratory
 Shallow ineffective respiration that results
in profound weakness of skeletal muscle
of respiration
 Diminished breath sounds
Neuromuscular
 Anxiety, lethargy, confusion, coma
 Skeletal muscle weakness, flaccid
paralysis
 Loss of tactile discrimination

60. Gastrointestinal
 Decreased motility
 Hypoactive to absent bowel sound
 Nausea vomiting, constipation,
abdominal distension
 Paralytic ileus
Renal
 Decreased specific gravity
 Increased urinary output

61. Management
 Monitor cardiovascular, respiratory status
 Place the client on a cardiac monitor
 Monitor electrolyte value
 Administer potassium supplements orally
or IV as prescribed
 Oral potassium supplements – should not
be taken on empty stomach
 Liquid potassium supplements – should
be taken with juice or other liquids

62.  Take the following precautions with IV
administration of potassium
 Potassium never given by IV push, IM, Sc
 The dilution not more than1mEq / 10ml of solution
 After adding potassium to IV solution shake the
bag and invert it to ensure that potassium is
distributed evenly throughout the IV solution
 The maximum recommended infusion rate is 5-10
mEq/hr, never exceed 20 mEq / hr
 A client receiving more than 10 mEq / hr should be
placed on a cardiac monitor and monitor for
cardiac changes

63.  Potassium infusion can cause phlebitis or infiltration. If
it occurs stop the infusion immediately
 The nurse should asses the renal function before
administering potassium and monitor intake and
output during administration
 Institute safety measures for the client experiencing
muscle weakness
 If the client is taking potassium losing diuretic, it may
be discontinued; a potassium sparing diuretic may be
prescribed
 Instruct the client about foods that are high in
potassium content
 Ex – bananas, carrots, oranges, tomatoes, potatoes.

64. Hyperkalemia
 Serum Potassium greater than 5.5 mEq/L
- More dangerous than hypokalemia
because cardiac arrest is frequently
associated with high serum K+ levels

65. Causes
 Excessive potassium
 Over ingestion of potassium containing
potassium
 Medications – Kcl, salt substitutes
 Decrease potassium excretion
 Potassium sparing diuretics
 Renal failure
 Adrenal insufficiency

66.  Movement of fluid from the ICF to ECF
fluid
 Tissue damage
 Acidosis
 Hyperuricemia
 Hyper catabolism

67. Hyperkalemia 3
 Clinical manifestations:
- Skeletal muscle weakness/paralysis
- EKG changes – such as peaked T
waves, widened QRS complexes
- Heart block

68. Clinical manifestation
Cardiovascular
 Slow, weakness, irregular heart rate
 Decreased blood pressure
 ECG changes – tall peaked T wave,
widened QRS complex, prolonged PR
intervals, flat P wave
Respiratory
 Weakness of skeletal muscle causes
respiratory failure

69. Neuromuscular
 Early – muscle switches, cramps,
parasthesia
 Late – profound weakness, ascending
flaccid paralysis in the arms and legs
Gastrointestinal
 Increased motility, hyperactive bowel
sounds
 Diarrhea

70. Management
 Monitor cardiovascular, respiratory,
neuromuscular, renal status
 Place the client on a cardiac monitor
 Discontinue IV potassium
 Hold oral potassium supplements
 Initiate a potassium excreting diuretics if renal
function not impaired
 If renal function not impaired, prepare to
administered Na polystyrene sulfonate, a cation
exchange that promotes gastrointestinal
absorption and potassium excretion

71.  Prepare the client for dialysis if potassium levels
critically high
 Prepare for IV administration of glucose with
regular insulin to move potassium into the cell
 Monitor renal function
 When client requires blood transfusion – should
receive fresh blood because stored blood elevate
the potassium level because breakdown of older
blood cells release potassium
 Teach the client to avoid foods high in potassium
 Instruct the client to avoid use of salt substitutes
or potassium containing substances

72. Calcium
 More than 99% of the body’s calcium is
located in the skeletal system
 Normal serum calcium level is 8.5 to
10mg/dL
 Needed for transmission of
nerve impulses
 Intracellular calcium is needed
for contraction of muscles

73. Calcium 2
 Extracellular needed for blood clotting
 Needed for tooth and bone formation
 Needed for maintaining a normal heart
rhythm

74. Hypocalcemia
 Serum Calcium level less than 8.5 mEq/L

75. Causes
Inhibition of calcium absorption from
gastrointestinal tract
 Inadequate oral intake of calcium
 Lactose intolerance
 Malabsorption syndrome (celiac sprue,
crohn’s disease)
 Inadequate intake of vitamin D
 End stage renal disease

76. Increase calcium excretion
 Renal failure
 Diarrhea
 Steatorrhoea
 Wound drainage

77. Conditions that decrease
the ionized fraction of
calcium
 Hyperprteinemia
 Alkalosis
 Medications – calcium chelators, binders
 Acute pancreatitis
 Immobility
 Removal or destruction of the parathyroid

78. Clinical manifestations
Cardiovascular
 Decreased heart rate
 Hypotention
 Diminished peripheral pulses
 ECG changes – prolonged ST interval,
prolonged QT interval
Respiratory
 Respiratory failure

79. Neuromuscular
 Twitches ,
 cramps ,
 Tatany
 seizures
 Paresthesias
 Spasm in the calf muscles
Gastrointestinal
 Increased motility, hyperactive bowel
sounds
 Abnormal cramping, diarrhea

80. Management
 Monitor cardiovascular, respiratory,
neuromuscular status
 Place the client on cardiac monitor
 Administer calcium supplements orally or IV
 When administering calcium IV – warm the
injection to body temperature
 Administer medication that increase calcium
absorption
 Ex – aluminum hydroxide reduces phosphate
and increase absorption of calcium

81.  Vitamin D aids in the absorption of calcium
from the intestinal tract
 Provide a quite environment to reduce
environmental stimuli
 Initiate seizure precautions
 Move client carefully and monitor for signs of
a fracture
 Keep 10% calcium gluconate available for
treatment of calcium deficit
 Instruct the client to consume foods high in
calcium
 Ex- milk, cheese, spinach, yogurt, sardines

82. Hypercalcemia
 Serum Calcium level greater than 10.5
mEq/L

83. Causes
 Increased calcium absorption
 Excessive oral intake of calcium
 Excessive oral intake of vitamin D

84. Decreased bone reabsorption of
calcium
 Hyperparathyroidism
 Hyperthyroidism
 Malignancy
 Immobility
 Use of glucocorticoids

85. Decreased calcium excretion
 Renal failure
 Use of thiazide diuretics
Hem concentration
 Dehydration
 Use of lithium
 Adrenal insufficiency


86. Clinical manifestations
Cardiovascular
 Increased heart rate
 Bounding , full peripheral pulse
 ECG changes – Shortened ST segment
 Widened T wave

87. Gastrointestinal
 Decreased motility and hypoactive bowel
sounds
 Anoxia, nausea, constipation
Renal
 Increase urinary output
 Renal calculi


88. Management
 Monitor cardiovascular, respiratory,
gastrointestinal status
 Place the client on cardiac monitor
 Discontinue IV infusions of solutions containing
calcium, oral medication containing calcium or
vitamin D
 Discontinue thiazide diuretics and replace with
diuretics that enhance the excretion of calcium
 Administer medications that inhibit calcium
reabsorption for the bone
 Ex – phosphorus, calcitonin, biphosphonates, aspirin

89.  Prepare client with severe Hypercalcemia
for dialysis if medications failed to reduce
 Monitor signs of fracture
 Monitor for flank or abdominal pain
 Strain the urine to check the presence of
urinary stones
 Instruct the client foods high in calcium

90. Magnesium
- Normal serum magnesium level is 1.5 to 2.5
mg/dL
- Helps maintain normal muscle and nerve
activity
- Exerts effects on the cardiovascular system,
acting peripherally to produce vasodilation
- Thought to have a direct effect
on peripheral arteries and
arterioles

91. Hypomagnesemia
 Serum Magnesium level less than 1.5
mEq/L

92. Causes
Insufficient magnesium intake
 Malnutrition and starvation
 Vomiting and diarrhea
 Celiac disease
 Crohn’s disease

93. Increased magnesium secretion
 Chronic alcoholism
 Diuretics
Intracellular movement of magnesium
 Hyperglycemia
 Insulin administration
 Sepsis

94. Clinical manifestation
Cardiovascular
 ECG changes – tall T wave, depressed
ST segments
 Tachycardia
 hypertension
Respiratory
 Shallow respiration
Central nervous system
 Irritability

95. Neuromuscular
 Twitches, Parenthesia
 Tetany
 Seizure
Gastrointestinal
 Decreased motility
 Decreased bowel sounds
 Anorexia
 Nausea
 Distension

96. Hypomagnesemia 7

97. Management
 Monitor cardiovascular, gastrointestinal,
respiratory status
 Place client on a cardiac monitor
 Administer magnesium sulfate IV route in
severe cases
 Monitor serum magnesium levels
 Monitor for deep tendon reflexes
 Instruct the client to increase the intake of
foods that contain magnesium Ex- milk, pork,
potatoes, green leafy vegetables, cauliflower.

98. Hypermagesemia
 Serum Magnesium level greater than 2.5
mEq/L

99. Causes
Increased magnesium intake
 Magnesium containing antacids and
laxatives
 Excessive administration of magnesium
IV
Decreased renal excretion of
magnesium as a result of renal
insufficiency

100. Clinical manifestation
Cardiovascular
 Bradycardia
 Dysarrythmias
 ECG changes – prolonged PR interval,
widened QRS complex
Respiratory
 Respiratory insufficiency

101. Neuromuscular
 Diminished deep tendon reflexes,
 Skeletal muscle weakness
Central nervous system
 Drowsiness
 Lethargy

102. Management
 Monitor cardiovascular, respiratory,
neuromuscular status
 Place client on cardiac monitor
 Diuretics are prescribed to increase excretion of
magnesium
 IV administration of calcium chloride to reverse
the effects of magnesium on cardiac muscle
 Instruct the client to restrict magnesium
containing foods
 Instruct the client to avoid the use of laxatives
and antacid containing magnesium

103. Phosphorus
- Normal serum phosphorus level is 2.5 to
4.5 mg/dL
- Essential to the function of muscle and
red blood cells, maintanence of acid-
base balance, and nervous system
- Phosphate levels vary inversely to
calcium levels
- High Calcium = Low Phosphate

104. Hypophosphatemia
 Serum Phosphorus level less than 2.5 mEq/L

105. Causes
Insufficient phosphorus intake
Increase phosphorus excretion
 Hyperparathyroidism
 Renal failure
 Malignancy
 Use of aluminum hydroxide base
Intracellular shift
 Hyperglycemia
 Respiratory alkalosis

106. Clinical manifestation
Cardiovascular
 Decreased contractility
 Slowed peripheral pulses
Respiratory
 Shallow respiration
Neuromuscular
 Weakness
 Decreased deep tendon reflexes

107. Central nervous system
 Irritability
 Confusion
 Seizures
Hematological
 Decreased platelet aggregation
 Immunosuppression

108. Management
 Monitor cardiovascular, respiratory,
neuromuscular status
 Administer phosphorus IV slowly because of
the risks associated with
hyperphosphatemia
 Monitor for signs of facture
 Instruct the client to increase intake of foods
while decreasing intake of calcium
containing foods
 Ex – fish, nuts, pork, beef, chicken.

109. Hyperphosphatemia
 Serum Phosphorus level greater than 4.5
mEq/L

110. Causes
 Decrease renal excretion resulting from
renal insufficiency
 Tumor lyses syndrome
 Increase intake of phosphorus including
– dietary intake, over use of phosphate
containing laxatives
 Hypoparathyroidism

111. Clinical manifestations
Cardiovascular
 Decrease heart rate
 Hypotension
 ECG changes – prolonged ST interval,
prolonged QT interval


112. Neuromuscular
 Twitches, cramps, tetany, seizures
 Parasthesia, numbness
 Hyperactive deep tendon reflexes
Gastrointestinal tract
 Increased gastric mobility
 Cramping, diarrhea

113. Management
 Administer phosphate binding medication that
increase fecal excretion of phosphorus
 Instruct the client avoid phosphate containing
medications Ex laxatives, enemas
 Instruct the client to decrease intake of
phosphorus
 Instruct the client low intake phosphate binding
medication, emphasizing that should be taken
with meals or immediately after the meals
 Interventions entail the management of
hypocalcaemia

114. DISORDERS OF ACID
BASE BALANCE
 The four general classes of acid based
imbalance are
1. Respiratory acidosis
2. Respiratory alkalosis,
3. Metabolic acidosis, and
4. Metabolic alkalosis.

115. TERMINOLOGY:
 Acidosis: any pathological process that
cause a relative excess of acid in the
body
 Acidemia: excess acid in the blood
 Alkalosis: it indicates a primary condition
resulting in excess base in the body
 Alkalemia: most narrow to elevation of
serum PH

117. Critical Thinking Exercise:
Nursing Management of the
Client with Hypokalemia
 Situation: A 69 year old man has a
history of CHF controlled by Digoxin and
Lasix. Two weeks ago he developed
diarrhea, which has persisted in spite of
his taking OTC antidiarrheal meds. His
partner transported him to the ER when
she found him lethargic and confused.
Initial assessment of the client reveals
heart rate at 86 bpm, respiratory rate 10,
and blood pressure 102/56 mmHg.

118. Critical Thinking Exercise:
Nursing Management of the
Client with Hypokalemia 2
 1. An electrolyte panel shows the client’s
serum potassium is 2.9 mEq/L. Does the nurse
have cause to be concerned about the client’s
serum potassium? Why or why not?
 2. What data supports the presence of
hypokalemia in this client?
 3. What, if anything, should the nurse do?
 4. What foods should the client be advised to
eat that are high in potassium?

119. Calcitonin
 - used to lower serum calcium level
- useful for pts with heart disease or renal
failure
- reduces bone resorption
- increases deposit of calcium and
phosphorus in the bones
- increases urinary excretion of calcium
and phosphorus

120.  Parathyroid pulls, calcitonin keeps
Parathyroid hormone pulls calcium out of
the bone.
Calcitonin keeps it there.