This document discusses fluid and electrolyte imbalance. It begins by defining electrolytes and homeostasis. It then describes the distribution of body fluids and the mechanisms controlling fluid and electrolyte movement. Key hormones that regulate fluid and electrolyte balance are discussed including aldosterone, antidiuretic hormone, and atrial natriuretic peptide. Abnormalities in fluid volume such as deficits and excesses are explained. Specific electrolyte imbalances like hyponatremia, hypernatremia, and hypokalemia are then defined and their etiologies, pathophysiology, clinical manifestations, and treatment approaches are summarized.

1. Submitted by:
Bharti
M.Sc (N) 1st year
CON,ILBS
1
Fluid and Electrolyte
Imbalance

2. INTRODUCTION
2
Electrolytes are minerals in your body that have an electric
charge. They are in your blood, urine, tissues, and other
body fluids.

3. Homeostasis
3
Homeostasis is the dynamic process in which the body
maintains balance by constantly adjusting to internal and
external stimuli.

4. Water content of the body:
4

5. Body fluids are distributed in two distinct area:
• intracellular fluid (ICF) 40% body weight
• Extracellular fluid (ECF) 20% body weight
• Interstitial fluid 15% body weight
• Plasma -5% body weight
5

6. ELECTROLYTES
6

7. 7

8. Mechanisms controlling fluid &
electrolyte movement
• Diffusion
• Facilitated diffusion
• Active transport
• Osmosis
• Hydrostatic pressure
• Oncotic pressure
8

9. REGULATION OF WATER BALANCE:
9

10. REGULATION OF ELECTROLYTES
AND WATER LOSS:
• Renin angiotensin aldosterone system
• Aldosterone
• Antidiuretic hormone
• Atrial natriuretic peptide
10

11. 11

12. Aldosterone
• Hormone secreted from the zona glomerulosa
cells of adrenal cortex
• Stimulates kidneys
• Retain sodium
• Retain water
• Secrete potassium
12

13. Antidiuretic hormone
• Also called arginine vasopressin (AVP).
• ADH is produced in neuron cell bodies in supra-
optic and para-ventricular nuclei of the
Hypothalamus, and stored in posterior pituitary.
• Promote the re absorption of water in the
collecting duct.
13

14. 14

15. The natriuretic peptide family
Four peptides of this family have been identified,
including:
• Atrial natriuretic peptide (ANP)
• Brain natriuretic peptide (BNP)
• C-type natriuretic peptide (CNP)
• Urodilatin
15

16. Atrial Natriuretic Peptide: Function
16

17. 17

18. FLUID IMBALANCE
18

19. Abnormalities in the Regulation of
Body Fluid:
• Fluid Volume Deficit (ECFVD)-
Dehydration
• Fluid Volume Excess- Over hydration
19

20. Extra Cellular Fluid Volume
Deficit (ECFVD)
• A decrease in intravascular and interstitial
fluids.
• It is a common and serious fluid imbalance that
results in vascular fluid volume loss
(hypovolemia).
20

21. Risk Factors:
• Diarrhea, vomiting
• Fistula drainage
• Diabetic ketoacidosis
• Hemorrhage
• Difficulty to swallowing
• Aged
• Severe mentally ill patient
21

22. PATHOPHYSOLOGY:
22

23. Degrees of dehydration:
• Mild
• Moderate
• Severe
Types of dehydration:
• Hyper-osmolar
• Iso-osmolar
• Hypo-osmolar
23

24. 24

25. 25

26. Laboratory findings:
• Increased Osmolality
• Increased or normal serum sodium level
• BUN (> 25 mg/d1)
• Hyperglycaemia (>120 mg / dl)
• Increased specific gravity of urine
• Elevated hematocrit (>55%)
26

27. Management of Dehydration
• Oral rehydration
• IV fluids
• Correction of the underlying problem
• Dietary management
• Nursing management
27

28. 28

29. Falls Precautions:
• Assess for orthostatic hypotension
• Assess muscle strength in legs
• Orient the client to the environment
• Remind the client to call for help before getting
out of bed or a chair
• Help the client get out of bed or a chair
• Provide, or remind the client to use, a walker or
cane for ambulating
29

30. • Provide adequate lighting at all times, especially
at night
• Keep the call light within reach, and ensure that
the client can use it
• Place the bed in the lowest position with the
brakes locked
• Place objects that the client needs within reach
• Ensure that adequate handrails are present in
the client's room, bathroom, and hall
• Encourage family members or significant other
to stay with the client
30

31. Extra Cellular Fluid Volume Excess/
Over-hydration
• ECFVE is increased fluid retention in the
intravascular & interstitial spaces (third spacing)
31

32. Etiology:
• Administering fluids rapidly or in a large
amount
• Failure to excrete fluids:
o Heart failure
o Renal disorders Decreased excretion
o Venous obstructions
o Decreased plasma proteins
o Excessive fluid ingestion
o Increased ADH & Aldosterone Increased absorption
32

33. PATHOPHYSIOLOGY:
33

34. 34

35. 35

36. Laboratory findings:
• Decreased Osmolality
• Decreased or normal serum sodium level
• BUN (<8 mg/dl)
• Decreased specific gravity of urine
• Decreased hematocrit (<45%)
36

37. Management of over hydration
• ICFVE is treated by the addition of solutes to IV
fluids.
• Use of D5%, 0.45% Nacl will help to correct
ICFVE
• when the cause is water excess.
• Oral fluids such as water and soft drinks should
be given in addition to water and ice chips.
• IV therapy should be monitored every hour.
37

38. • Monitor vital signs and intake- output
• Weight should be checked daily to measure fluid
gain or loss.
• Administer prescribed antiemetic as needed to
allow food and fluids to be ingested.
• Safety measures are necessary when the client
displays behavioral changes.
38

39. NURSING INTERVENTIONS
• Monitor cardiovascular, respiratory, neuromuscular,
renal, integumentary, and gastrointestinal status.
• Prevent further fluid overload and restore normal
fluid balance.
• Administer diuretics; osmotic diuretics typically are
prescribed first to prevent severe electrolyte
imbalances.
39

40. • Restrict fluid and sodium intake as prescribed.
• Monitor intake and output; monitor weight.
• Monitor electrolyte values, and prepare to
administer medication to treat an imbalance if
present.
40

41. ELECTROLYTE
IMBALANCE:
41

42. Electrolyte Balance and Imbalance
• Sodium:
Hyponatremia
Hypernatremia
42

43. Hyponatremia
Definition:
• Commonly defined as a serum sodium
concentration <135 mEq/L
• Hyponatremia represents a relative excess of
water in relation to sodium.
43

44. • Hyponatremia is the most common electrolyte
disorder
• Acute hyponatremia (developing over 48hr or
less) are subject to more severe degrees of
cerebral edema
• sodium level is less than 105 mEq/L, the
mortality is over 50%
• Chronic hyponatremia (developing over more
than 48hr) experience milder degrees of
cerebral edema
44

45. Types of hyponatremia
• Hypovolemic hyponatremia
• Euvolemic hyponatremia
• Hypervolemic hyponatremia
• Redistributive hyponatremia
45

46. Hypovolemic hyponatremia
• Develops as sodium and free water are lost
and/or replaced by inappropriately hypotonic
fluids.
• Sodium can be lost through renal or non-renal
routes.
46

47. Nonrenal loss:
• GI losses
• Vomiting, Diarrhea, fistulas, pancreatitis
• Excessive sweating
• Third spacing of fluids
->ascites, peritonitis, pancreatitis, and burns
• Cerebral salt-wasting syndrome
-> traumatic brain injury, aneurysmal subarachnoid
hemorrhage, and intracranial surgery
->Must distinguish from SIADH
47

48. Renal Loss:
• Acute or chronic renal insufficiency
• Diuretics
48

49. Euvolemic hyponatremia
Sodium deficit is more and the volume remains
same.
Etiology:
• Psychogenic polydipsia, often in psychiatric
patients
• Administration of hypotonic intravenous (5%
DW) or irrigation fluids ( sorbitol, glycerin) in the
immediate postoperative period
49

50. • Administration of hypotonic maintenance
intravenous fluids
• Infants who may have been given inappropriate
amounts of free water
• Bowel preparation before colonoscopy or
colorectal surgery
50

51. Hypervolemic hyponatremia
• Total body sodium increases, and TBW increases
to a greater extent.
• Can be renal or non-renal
• Acute or chronic renal failure
• Dysfunctional kidneys are unable to excrete the
ingested sodium load
• Cirrhosis, congestive heart failure, or nephrotic
syndrome
51

52. Redistributive hyponatremia
• Water shifts from the intracellular to the
extracellular compartment, with a resultant
dilution of sodium. The TBW and total body
sodium are unchanged.
This condition occurs with hyperglycemia
Administration of mannitol
52

53. PATHOPHYSIOLOGY:
53

54. MEDICAL MANAGEMENT
• Determine cause of hyponatremia and to correct
it.
• If client has hyponatremia due to fluid volume
excess, intake of fluids will be restricted to allow
the sodium to regain balance.
• If the serum sodium level falls below 125
mEq/L, sodium replacement is needed.
54

55. PHARMACOLOGIC MANAGEMENT
• For client with moderate hyponatremia 125 meq/
L I/V saline solution (0.9% Nacl) or lactated
Ringer solution may be ordered.
• When the serum sodium level is 115 meq / L or
less, a concentrated saline solution such as 3 %
Nacl is indicated.
55

56. NURSING INTERVENTIONS
• Monitor cardiovascular, respiratory,
neuromuscular, cerebral, renal, and
gastrointestinal status of the client.
• If hyponatremia is accompanied by a fluid
volume deficit (hypovolemia), IV sodium chloride
infusions are administered to restore sodium
content and fluid volume.
56

57. • If hyponatremia is accompanied by fluid volume
excess (hypervolemia), osmotic diuretics are
administered to promote the excretion of water
rather than sodium.
• Instruct the client to increase oral sodium intake
and inform the client about the foods to include
in the diet.
• If the client is taking lithium (Lithobid), monitor
the lithium level, because hyponatremia can
cause diminished lithium excretion, resulting in
toxicity.
57

58. Hypernatremia
Hypernatremia is usually due to water deficit
Etiology:
Excess water loss : eg- heat exposure
diabetes insipidus
Impaired thirst: eg - primary hypodypsia,
comatose
Excessive Na+ retention
58

59. 59

60. Clinical features of hypernatremia
• Excessive thirst, polyuria, nausea
• Muscular weakness, neuromuscular irritability
• Altered mental status, focal neurological deficit
occasionally coma or seizures
60

61. 61

62. Treatment
• correct water deficit
• Rate of correction :
-Acute hypernatremia- 1mEq/L/hr
-Chronic hypernatremia-1mEq/L/hr or
10mEq/L over 24hr
-rapid correction may lead to cerebral edema
62

63. Dietary management
63

64. POTASSIUM
64

65. HYPOKALEMIA
• Hypokalemia is a serum potassium level of less
than 3.5 mEq /L
65

66. Etiological factors of hypokalemia
66

67. PATHOPHYSIOLOGY
67

68. CLINICAL MANIFESTATION:
68

69. 69

70. Medical management
• Determining & correcting the cause of the imbalance.
• Extreme hypokalemia requires cardiac monitoring.
Pharmacological Management
• Oral potassium replacement therapy is usually
prescribed for mild hypokalemia.
• Potassium is extremely irritating to gastric mucosa;
therefore the drug must be taken with Glass of water or
juice or during meals.
70

71. • Potassium chloride can be administered intravenously for
moderate or severe hypokalemia & must be diluted in IV
fluids.
• Administration of potassium by IV push may result in cardiac
arrests. Potassium can be given in doses of 10 to 20 mEq/
hour diluted in IV fluid if the client is on heart monitor.
• High concentration of potassium is irritating to heart muscle.
Thus correcting a potassium deficit may take several days.
71

72. Dietary management
• The administration of
foods that are high in
potassium help to correct
the problem as well as
prevent further
potassium losses.
72

73. HYPERKALEMIA
• Hyperkalemia is an Elevated potassium level over 5.0 mEq/L.
ETIOLOGY
Retention of Potassium- Renal insufficiency, renal
failure, decreased urine output, potassium sparing
diuretics.
Excessive release of Cellular Potassium - severe
traumatic injuries. Severe burns, severe infection,
metabolic acidosis.
Excessive IV infusions or Oral administration of
potassium.
73

74. PATHOPHYSIOLOGY
74

75. 75

76. 76

77. LABORATORY FINDINGS:
• Serum potassium >5.0 meq/L
• Serum creatinine >1.5mg/L
• BUN >25mg/dl
77

78. MEDICAL MANAGEMENT
• When serum potassium level is 5.0 to 5.5 mEq/L
restrict potassium intake.
• If potassium Excess is due to metabolic
acidosis, correcting the acidosis with sodium
bicarbonate promotes potassium uptake into the
cells.
• Improving urine output decreases elevated
serum potassium level.
78

79. 79

80. 80

81. DIETARY MANAGEMENT
• When hyperkalemia is severe, immediate
actions are needed to be taken to avoid severe
Cardiac disturbances.
• The administration of foods that are low in
potassium help to correct the problem as well as
prevent further potassium excess.
81

82. 82

83. NURSING INTERVENTIONS
• Monitor cardiovascular, respiratory, neuromuscular, renal, and
gastrointestinal status; place the client on a cardiac monitor.
• Discontinue IV potassium and hold oral potassium
supplements.
• Prepare to administer potassium-excreting diuretics if renal
function is not impaired.
• Initiate a potassium-restricted diet.
• If renal function is impaired, prepare to administer sodium
polystyrene sulfonate (Kayexalate).
83

84. • Prepare the client for dialysis if potassium levels are
critically high.
• Prepare for the IV administration of hypertonic glucose
with regular insulin to move excess potassium into the
cells.
• Monitor renal function.
• Teach the client to avoid foods high in potassium.
• Instruct the client to avoid the use of salt substitutes or
other potassium-containing substances.
84

85. Calcium
• Calcium is involved in bone formation/reabsorption
neural transmission/muscle contraction, regulation
of enzyme systems, and is acoenzyme in blood
coagulation.
• Normal serum level are 4.3-5.3meq/L, 8.5-10.5mg/dl (total)
or 2.1-2.6 mEg/L (ionized).
85

86. CALCIUM IMBALANCES:
• Hypocalcemia
• hypercalcemia
86

87. HYPOCALCEMIA
• Hypocalcemia is serum calcium below 4.5 meq/L or 8.5
mg/dl.
Etiology
Malabsorption of fat in intestine.
Metabolic alkalosis
Renal failure with hyperphsophatemia, acute
pancreatitis, Burns, Cushing’s disease,
hypoparathyrodism.
Medications – Magnesium sulfate.
87

88. PATHOPHYSIOLOGY:
88

89. CLINICAL MANIFESTATIONS
• Neuromuscular: Tetany symptoms: Twitching
around mouth, tingling and numbness of fingers,
facial spasm, convulsions.
• Respiratory: Dyspnea, laryngeal spasm.
• Gastrointestinal: increased peristalsis,
diarrhea.
• Cardiovascular: Dysrhythmias, palpitations
89

90. 90

91. 91

92. MEDICAL MANAGEMENT
• Determining & correcting the cause of hypocalcemia.
• Asymptomatic hypocalcemia is usually corrected with
oral calcium gluconate, calcium lactate or calcium
chloride.
• Administer calcium supplements 30 minutes before
meals for better absorption and with glass of milk
because vitamin D is necessary for absorption of
calcium from the intestine.
92

93. • Intravenous calcium chloride or calcium
gluconate (10%) is given slowly to avoid
hypertension, bradycardia & other arrhythmias.
• Chronic or mild hypocalcemia can be treated in
part by having the client consume a diet high in
calcium.
93

94. 94

95. NURSING INTERVENTIONS
• Monitor cardiovascular, respiratory, neuromuscular, and
gastrointestinal status; place the client on a cardiac monitor.
• Administer calcium supplements orally or calcium
intravenously.
• When administering calcium intravenously, warm the injection
solution to body temperature before administration and
administer slowly, monitor for electrocardiographic changes,
and monitor for hypercalcemia.
95

96. • Administer medications that increase calcium
absorption. i.e. Vitamin D aids in the absorption of
calcium from the intestinal tract.
• Initiate seizure precautions.
• Keep 10% calcium gluconate available for treatment of
acute calcium deficit.
• Instruct the client to consume foods high in calcium.
96

97. HYPERCALCEMIA
• Hypercalcemia is a serum level over 5.5 meq/L or 11
mg/L.
97

98. ETIOLOGY
• Metastatic malignancy-lung, breast, Ovarian, Prostatic,
bladder, leukemia, Kidney.
• Hyperparathyroidism.
• Thiazide diuretic therapy.
• Prolong immobilization.
• Excessive intake of calcium supplements and vitamin D.
98

99. CLINICAL MANIFESTATIONS
• Gastrointestinal: Anorexia, Vomiting, Constipation
• Neuromuscular: Mild to moderate hypercalcemia state
–weakness, Severe hypercalcemic state-Extreme
lethargy
• Cardiovascular: Dysrhythmias
• Electro-cardiographic Changes: Shortened ST
Segment and lengthened QT interval.
• Musculoskeletal: Bone pain, fracture.
99

100. LABORATORY FINDINGS:
• Arteial blood gasses- PH<7.45
• Serum calcium >5.5meq/L (11.5mg/dl)
• HCO3>26meq/L
100

101. MEDICAL MANAGEMENT
• Treatment consists of correcting the underlying cause.
• Intravenous normal saline (0.9% Nacl) given rapidly with
furosemide to prevent fluid overload, Promote urinary
calcium excretion.
• Corticosteroid drugs decrease calcium levels by
competing with vitamin D thus resulting in decreased
intestinal absorption of calcium.
101

102. • If the cause is excessive use of calcium or vitamin D
supplements or calcium containing antacids these
agents should be either avoided or used in reduced
dosage.
• A newer form of drug therapy is etidronate di-sodium.
This drug reduces serum calcium by reducing normal
and abnormal bone reabsorption of calcium and
secondarily by reducing bone formation.
102

103. NURSING INTERVENTIONS
• Monitor cardiovascular, respiratory, neuromuscular,
renal, and gastrointestinal status; place the client on
a cardiac monitor.
• Discontinue IV infusions of solutions containing
calcium and oral medications containing calcium or
vitamin D.
• Discontinue thiazide diuretics and replace with
diuretics that enhance the excretion of calcium.
103

104. • Administer medications as prescribed that inhibit calcium
resorption from the bone, such as phosphorus,
calcitonin, bisphosphonates, and prostaglandin
synthesis inhibitors (aspirin, nonsteroidal anti-
inflammatory drugs).
• Prepare the client with severe hypercalcemia for dialysis
if medications fail to reduce the serum calcium level.
• Instruct the client to avoid foods high in calcium.
104

105. Phosphorus
• Hypophosphatemia
• Hyperphosphatemia
105

106. Hypophosphatemia
• Hypophosphatemia is defined as plasma
phosphorus <1.2mEq/L.
106

107. Causes of hypophosphatemia
• Malabsorption syndrome
• TPN
• Alcohol withdrawal
• Phosphate binding anta-acids
• Respiratory alkalosis
• Recovery from DKA
107

108. Clinical manifestations
• Muscle weakness
• Osteomalacia
• Rhabdomyolysis
• Cadiac problems- Dysrhythmias, decreased
stroke volume
• CNS dysfunction
108

109. 109

110. Management:
• Mild cases- treated with dietary restrictions
• Teach client about balanced diet
• Severe cases: phosphate supplementation
110

111. 111

112. Hyperphosphatemia
• Hyperphosphatemia is defined as plasma phosphorus
>3mEq/L.
Causes of hyperphosphatemia
Excess intake of high phosphate foods
Excess vitamine D supplementation especially in renal
insufficiency
Impaired colonic motility
Hypoparathyroidism
Addison’s disease
112

113. Clinical manifestations
• Tachycardia, palpitations
• Restlessness
• Anorexia, nausea, vomiting
• Hyper-reflexia, tetany
• Dysrhythmias
113

114. PATHOPHYSIOLOGY:
114

115. Management:
• Mild cases- limit phosphate rich foods ( milk, ice-cream,
cheese, meat, fish)
• Giving calcium, aluminium products that promotes
binding & excretion of phosphate.
• Dialysis is the TOC in case of hyperphosphatemia with
renal failure.
115

116. Magnesium
• Hypomagnesemia
• Hypermagnesemia
116

117. Hypomagnesemia
Hypomagnesemia is defined as plasma magnesium
<1.8mg/dl
Causes of hypomagnesemia:
• Diarrhea, vomiting
• Chronic alcoholism
• Prolonged malnutrition
• Hyperaldosteronism
• Impaired GI absorption
• NG suction
• Poorly controlled DM
117

118. 118

119. Clinical manifestations
• Myocardial irritability
• Anorexia, nausea
• Abdominal distention
• Severe cases: Chvostek’s & Trousseau’s sign,
tetany, convulsions, stroke
119

120. 120

121. Management:
• Oral magnesium replacement (anta-acids)
• Parenteral magnesium sulphate
• Increase dietary intake of magnesium (chili, tofu, wheat
gram)
• Initiate safety & seizure precautions in severe cases and
monitor all electrolytes.
• Keep watch on rising magnesium levels.
121

122. Hypermagnesemia
Hypermagnesemia is defined as plasma magnesium
>3mg/dl
Causes of hypermagnesemia
• Renal insufficiency
• Excessive anta-acid use
• Adrenal insufficiency
• Ketoacidosis
122

123. 123

124. Clinical manifestations
Clinical manifestations are related to blocked release of
Acetylcholine from myoneronal junction which affects muscle
cell activity.
• Hypotension
• Muscle weakness
• Loss of DTR
• Prolonged QT, PR interval
• Lethargy, drowiness
• Respiratory paralysis, loss of consiosness
124

125. Management:
• Low magnesium diet (eat chicken, eggs, green peas, white
bread, hamburger)
• Decrease magnesium sulphate use
• In severe cases saline infusion with diuretics is give to
promote magnesium excretion
• IV calcium (antagonistic action)
• Drugs: Albuterol
• If renal failure is also present than hemodialysis is done in
severe cases
125

126. Nursing Management
• Nurses may use effective teaching and communication skills
to help prevent and treat various fluid and electrolyte
disturbances.
Nursing Assessment
Close monitoring should be done for patients with fluid and
electrolyte imbalances.
• I&O. the nurse should monitor for fluid I&O at least every 8
hours, or even hourly.
• Daily weight. Assess the patient’s weight daily to measure
any gains or losses.
• Vital signs. Vital signs should be closely monitored.
• Physical exam. Physical exam is needed to reinforce other
data about a fluid or electrolyte imbalance.
126

127. Diagnosis
• The following diagnoses are found in patients with fluid
and electrolyte imbalances.
• Excess fluid volume related to excess fluid intake and
sodium intake.
• Deficient fluid volume related to active fluid loss or
failure of regulatory mechanisms.
• Imbalanced nutrition: less than body
requirements related to inability to ingest food or absorb
nutrients.
• Imbalanced nutrition: more than body
requirements related to excessive intake.
• Diarrhea related to adverse effects of medications or
malabsorption.
127

128. Discharge and Home Care
Guidelines
• After hospitalization, treatment and maintenance of the condition must
continue at home.
• Diet. A diet rich in all the nutrients and electrolytes that a person needs
should be enforced.
• Fluid intake. Fluid intake must take shape according to the
recommendations of the physician.
• Follow-up. A week after discharge, the patient must return for a follow-up
checkup for evaluation of electrolyte and fluid status.
• Medications. Compliance to prescribed medications should be strict to
avoid recurrence of the condition.
128

129. Documentation Guidelines
• Data should be documented for future medical and legal references. The
nurse must document:
• Individual findings, including factors affecting ability to manage body fluids
and degree of deficit.
• I&O, fluid balance, changes in weight, urine specific gravity, and vital signs.
• Results of diagnostic testing and laboratory studies.
• Plan of care.
• Client’s responses to treatment, teaching, and actions performed.
• Attainment or progress toward desired outcome.
• Modifications to plan of care.
129

130. RESEARCH ARTICLE:-
General characteristics of patients with electrolyte imbalance
admitted to emergency department
• Arif Kadri Balcı, Ozlem Koksal, Ataman Kose, Erol
Armagan, Fatma Ozdemir, Taylan Inal, and Nuran Oner
• RESULTS:
• The mean age of the patients was 59.28±16.79, and
55% of the patients were male. The common
symptoms of the patients were dyspnea (14.7%),
fever (13.7%), and systemic deterioration (11.9%);
but the most and least frequent electrolyte
imbalances were hyponatremia and
hypermagnesemia, respectively. Most frequent
130

131. findings in physical examination were confusion (14%), edema
(10%) and rales (9%); and most frequent pathological findings
in ECG were tachycardia in 24%, and atrial fibrillation in 7% of
the patients. Most frequent comorbidity was malignancy
(39%). Most frequent diagnoses in the patients were sepsis
(11%), pneumonia (9%), and acute renal failure (7%).
CONCLUSIONS:
• Electrolyte imbalances are of particular importance in the
treatment of ED patients. Therefore, ED physicians must be
acknowledged of their fluid-electrolyte balance dynamics and
general characteristics.
131

132. SUMMARY
• Electrolytes are minerals in your body that have an electric
charge. They are in your blood, urine, tissues, and other body
fluids. Electrolytes are important because they help
• Balance the amount of water in your body
• Balance your body's acid/base (pH) level
• Move nutrients into your cells
• Move wastes out of your cells
• Make sure that your nerves, muscles, the heart, and the brain
work the way they should
• Sodium, calcium, potassium, chloride, phosphate, and
magnesium are all electrolytes. You get them from the foods
you eat and the fluids you drink.
132

133. • The levels of electrolytes in your body can become too
low or too high. This can happen when the amount of
water in your body changes. The amount of water that
you take in should equal the amount you lose. If
something upsets this balance, you may have too little
water (dehydration) or too much water (over hydration).
Some medicines, vomiting, diarrhea, sweating, and liver
or kidney problems can all upset your water balance.
• Treatment helps you to manage the imbalance. It also
involves identifying and treating what caused the
imbalance.
133

134. CONCLUSION
134

135. 135