This document provides an overview of fluid and electrolyte homeostasis and imbalances. It defines key terms like extracellular fluid, intracellular fluid, and body fluid. It describes the functions of body fluid and the mechanisms that regulate fluid intake, distribution, and excretion. It discusses abnormalities that can occur in fluid volume, concentration, and electrolyte composition. Specifically, it examines extracellular fluid volume deficits and excesses, as well as imbalances in body fluid concentration seen in hyponatremia and hypernatremia. Clinical manifestations and etiologies of various fluid and electrolyte disorders are presented.

1. CHAPTER 24
FLUID AND ELECTROLYTE
HOMEOSTASIS
AND IMBALANCES

2. INTRODUCTION
• The fluid of the body flows in arteries, veins,
and lymph vessels
• Body fluids are secreted into specialized
compartments
• Joints
• Cerebral ventricle
• Intestinal lumen

3. FUNCTION OF BODY FLUID
• Surrounds and permeates the cells
• Lubricant and solvent for metabolic chemical
reactions
• Transports oxygen, nutrients, chemical
messengers, and waste products to their
destinations
• Important in regulating body temperature

4. ABNORMALITIES IN BODY FLUID
• Can occur in:
• Volume
• Concentration
• Electrolyte composition of body fluid
• Can cause clinical problems or death
• Occur as a result of many different
pathophysiologic conditions

5. BODY FLUID HOMEOSTASIS
• Important terminology
• Body fluid
• Extracellular fluid
• Intracellular fluid

6. BODY FLUID
• Pertains to water within the body and the
particles dissolved in it

7. EXTRACELLULAR FLUID
• Contained outside the cells
• Interstitial compartment (between cells)
• Relatively rich in sodium, chloride, bicarbonate ions,
and proteins
• Relatively low in potassium, magnesium, and
phosphate ions
• Vascular compartment (in blood vessels)
• Also relatively rich in proteins
• Dense connective tissue and bone
• Other compartments (synovial, cerebrospinal, GI
fluids)

8. INTRACELLULAR FLUID
• Contained inside the cells
• Relatively rich in potassium and magnesium ions,
inorganic and organic phosphates, and
proteins
• Relatively low in sodium and chloride ions

9. TOTAL BODY WATER
• Total of the water in all fluid compartments
• Percentage of body weight that is water
varies
• According to a person’s age
• In proportion to body fat
• See Figure 24-2

10. 0
10
20
30
40
50
60
70
80
90
1st Qtr 2nd Qtr 3rd Qtr 4th Qtr
East
West
North

11. FLUID HOMEOSTASIS
• Dynamic process results from interplay of four
sub-processes
• Fluid intake
• Fluid absorption
• Fluid distribution
• Fluid excretion
• See Figure 24-3

13. FLUID INTAKE
• Fluid intake is entry of fluid into the body by
any route
• Healthy people ingest fluids orally
• Drinking
• Eating (water contained in food)
• Small amount of water synthesized through cellular
metabolism

14. FLUID INTAKE (CONT.)
• Influenced by:
• Habit
• Social factors
• Thirst triggered by:
• Increased concentration of extracellular fluid
• Decreased circulating blood volume
• Dryness of mucous membranes of mouth
• Possibly other visceral signals
• In older adults, thirst diminishes; they may have
insufficient fluid intake

15. OTHER POSSIBLE ROUTES OF
INTAKE
• Controlled by health professionals
• Intravenous intake
• Intake tubes in GI tract and other body cavities
• Subcutaneous tissue or bone marrow infusion
• Rectal intake (tap water enema)
• Accidental
• Lungs (near-drowning)

16. FLUID DISTRIBUTION
• Vascular fluid distribution
• Much fluid within vascular compartment distributes
into other fluid compartments
• Net result of filtration across permeable capillaries
(capillary forces)

17. CAPILLARY FORCES
• Move fluid from capillaries into interstitial
compartment
• Capillary hydrostatic pressure: outward push of
vascular fluid against capillary walls
• Interstitial fluid osmotic pressure: inward-pulling force
of particles in the interstitial fluid
• Move fluid from interstitial compartment into
capillaries
• Capillary osmotic pressure: inward-pulling force of
particles in vascular fluid

18. CAPILLARY FORCES (CONT.)
• Interstitial hydrostatic pressure: outward push of
interstitial fluid against outside of capillary walls
• See Figure 24-1

19. FIGURE 24-1

20. INTERSTITIAL AND
INTRACELLULAR
FLUID DISTRIBUTION
• Fluid distribution between the vascular and
interstitial compartments is net result of
differences in particle concentration
(osmolality)

21. OSMOLALITY AND OSMOSIS
• Cell membranes are permeable to water but
not to electrolytes
• Water crosses the cell membrane rapidly to
equalize particle concentration inside and
outside the cells (osmosis)

22. DIRECTION OF WATER
MOVEMENT
• Determined by the particle concentrations on
the two sides of the semipermeable cell
membrane
• Changes in the osmolality of the interstitial
and intracellular compartments control the
distribution of water between them

23. WATER MOVEMENT OUT OF
CELLS
• Occurs when particle concentration
(osmolality) of the interstitial fluid becomes
higher than the particle concentration inside
cells
• Water moves from the cells to the interstitial
fluid to equalize the osmolality in the two
compartments

24. WATER MOVEMENT INTO
CELLS
• Occurs when the osmolality of the interstitial
fluid becomes lower than the osmolality of
the intracellular fluid
• Water moves from the interstitial
compartment to the intracellular
compartment to equalize the osmolality

25. FLUID EXCRETION
• Occurs through:
• Urinary tract
• Largest volume excreted
• Bowels
• Normal bowel function
• Increases with diarrhea
• Lungs
• Exhalation
• Skin
• Visible sweat
• Insensible perspiration

26. URINE
• Amount of fluid excreted in the urine is
controlled primarily by hormones
• Antidiuretic hormone (ADH)
• Aldosterone
• Natriuretic peptides (ANP and BNP)
• Other minor hormones

27. SECRETION AND RELEASE OF
ADH
• Synthesized by cells in the supraoptic and
paraventricular nuclei of the hypothalamus
• Release of ADH occurs from the posterior
pituitary gland
• Factors that increase release of ADH into the
blood include increased osmolality
(concentration) of the extracellular
fluid, decreased circulating fluid volume,
pain, nausea, and physiologic and
psychological stressors.

28. FUNCTION OF ADH
• Causes reabsorption of water, which:
• Decreases urine volume
• Makes urine more concentrated
• Decreases fluid excretion
• Concentrates the urine thus decreasing fluid
excretion
• If ADH release is decreased, result is large
dilute urine volume
• Decreased osmolality of extracellular fluid
• Ethanol intake

29. ALDOSTERONE
• Synthesized and secreted by cells in the
adrenal cortex
• Major stimulus for its release
• Angiotensin I
• From the renin-angiotensin system
• Activated by decreased circulating blood volume and
increased concentration of potassium ions in the
plasma

30. FUNCTION OF ALDOSTERONE
• Causes renal tubules to reabsorb sodium and
water (saline)
• Decreases fluid excretion, although by a
different mechanism than ADH
• When more aldosterone is secreted, urine
volume is smaller; decreased secretion of
aldosterone causes a larger urine volume

31. COMPARISON OF ADH AND
ALDOSTERONE
• ADH is the tap water hormone
• Causes the kidneys to reabsorb water
• Renal reabsorption of water due to ADH makes a
smaller volume of more concentrated
urine
• Aldosterone is the saltwater hormone
• Causes the kidneys to reabsorb sodium and water
• Renal reabsorption of sodium and water due to
aldosterone makes a smaller volume of urine

32. ANP
• Normally secreted from cells in the heart
when the atria are stretched

33. BNP
• B-type natriuretic peptide
• Released from ventricular cells when
ventricular diastolic pressure
increases abnormally, as in heart failure

34. FUNCTION OF ANP AND BNP
• Promote fluid excretion in the urine by:
• Causing natriuresis (sodium excretion in the urine)
• Sodium excretion is accompanied by water
excretion

35. REGULATION OF NPS
• When vascular volume increases:
• Heart is stretched
• More NPs released to cause renal excretion of the
excess
• When vascular volume is decreased:
• Heart is less stretched
• Fewer NPs released
• Kidneys excrete less fluid
• NPs oppose the action of aldosterone, but
they are not as strong as aldosterone

36. ADEQUATE URINE VOLUME
• Highly dependent on:
• Adequate blood pressure to perfuse the kidneys
• Glomerular filtration rate (GFR)

37. ABNORMAL FLUID LOSS
• May be a significant factor in disturbing fluid
status
• Types of abnormal fluid loss
• Emesis
• Tubes in the GI tract or other body cavities
• Hemorrhage
• Drainage from fistulas, wounds, or open skin
• Paracentesis

38. CATEGORIES OF FLUID
IMBALANCES
• Extracellular (saline) imbalances
• Imbalances of body fluid (water)
concentration
• Extracellular and body fluid imbalances can
occur simultaneously
• Both volume and serum sodium concentration are
abnormal

39. EXTRACELLULAR FLUID
IMBALANCES
• Too much or too little extracellular fluid
• Involve a change in the amount or volume of
extracellular fluid
• Also termed saline imbalances because they
are disorders of isotonic salt water (in the
same concentration as the normal plasma
concentration)
• May lead to hypovolemic shock, which can
be fatal if not treated effectively (fluid
replacement)

40. VOLUME DEFICIT
• Caused by removal of a sodium-containing
fluid from the body
• Decrease in saline in the same concentration
as normal extracellular fluid
• Condition sometimes termed saline deficit

41. UNCOMPLICATED VOLUME
DEFICIT
• Serum sodium concentration is normal
• Concentration of extracellular fluid is normal
• Amount of extracellular fluid is abnormally
decreased
• See Figure 24-4

42. FIGURE 24-4

43. ETIOLOGY OF VOLUME DEFICIT
• Removal of a sodium-containing fluid from
the extracellular compartment
• Usually fluid is removed from body
• In some instances, fluid is sequestered in a “third
space” in the body, outside the extracellular
compartment
• Example: ascites, fluid in the peritoneal cavity
• If this develops rapidly, may deplete extracellular
volume

44. CLINICAL MANIFESTATIONS
• Sudden weight loss
• Postural blood
pressure decrease
with concurrent
increased heart rate
• Flat neck veins (or
veins collapsing with
inspiration) when a
patient is supine
• Prolonged small vein
filling time
• Prolonged capillary
refill time
• Lightheadedness
• Dizziness
• Syncope
• Oliguria or small
volume of
concentrated urine
(if kidneys are
responding
normally)

45. OTHER CLINICAL
MANIFESTATIONS
• Decreased skin
turgor
• Dryness of oral
mucous membranes
between cheek and
gum
• Hard stools
• Soft sunken eyeballs
• Longitudinal furrows
in the tongue
• Absence of tears
and sweat
• In infants
• Fontanel may be
sunken
• Neck veins are not
reliably assessed in
infants

46. WEIGHT LOSS
• Sudden weight loss is a sensitive measure of
ECV deficit
• One liter of saline weighs 1 kg
• A person who loses 1 kg in 24 hours has excreted 1 L
of fluid or lost it through an abnormal route

47. THIRD SPACE SEQUESTRATION
• ECV deficit may occur without a weight loss if
fluid is sequestered in a third space
somewhere in the body, as with ascites or
intestinal obstruction
• Can be detected with shifts in orthostatic
blood pressure

48. EXTRACELLULAR VOLUME
EXCESS
• Opposite of extracellular volume deficit
• Amount of extracellular fluid is abnormally
increased
• Vascular and interstitial areas have too much
fluid
• See Figure 24-5

50. UNCOMPLICATED ECV EXCESS
• Concentration of extracellular fluid is normal
• Excessive amount of that fluid is present

51. ETIOLOGY
• Caused by addition or retention of isotonic
saline; sometimes termed saline excess
• Hormone aldosterone causes kidneys to
retain saline; therefore, ECV excess may be
caused by conditions that involve excessive
aldosterone secretion
• Compensatory mechanism that can accompany
chronic heart failure

52. CAUSES OF EXTRACELLULAR
FLUID VOLUME EXCESS
• Excessive
intravenous infusion
of sodium-
containing isotonic
solutions
• Normal saline (0.9%
sodium chloride)
• Ringer injection
• Lactated Ringer
injection
• Renal retention of
sodium and water
• Primary
hyperaldosteronism
• Chronic heart failure
• Cirrhosis
• Acute
glomerulonephritis
• Chronic renal failure
• Cushing disease
• Corticosteroid
therapy

53. CLINICAL MANIFESTATIONS
• Sudden weight
gain: a sensitive
measure of
extracellular
volume excess
• Manifestations of
circulatory
overload
• Bounding pulse
• Neck vein distention
in upright position
• Crackles in
dependent portions
of lungs
• Dyspnea
• Edema
• If advanced, frothy
sputum of
pulmonary edema
• In infant
• Bulging fontanel
• Assessment of neck
veins is not effective
in infants

54. BODY FLUID CONCENTRATION
• Imbalances of body fluid concentration are
disorders of concentration and not amount of
extracellular fluid
• Also called water imbalances
• Serum sodium concentration reflects osmolality of
blood
• Recognized by abnormal serum sodium
concentration

55. HYPONATREMIA
• A serum sodium concentration below the
lower limit of normal
• When present the extracellular fluid contains
relatively too much water for the amount of
sodium ions present
• Extracellular fluid is more dilute than normal

56. ETIOLOGY OF HYPONATREMIA
• Factors that produce a relative excess of water
in proportion to salt in the extracellular fluid
• Because serum sodium concentration reflects
the osmolality of the blood, reduced serum
sodium indicates that extracellular fluid has a
reduced osmolality; it is too dilute
• Also called:
• Hypotonic syndrome
• Hypo-osmolality
• Water intoxication

57. ETIOLOGY OF EXCESS WATER
IN EXTRACELLULAR FLUID
• Excessive intravenous infusion of 5% dextrose
in water (D5W)
• Hypotonic irrigating solutions
• Tap water enemas
• Psychogenic polydipsia (compulsive water
drinking)
• Forced excessive water ingestion (child abuse
or club initiation)
• Excessive beer ingestion (beer potomania)

58. ETIOLOGY OF EXCESS WATER
IN EXTRACELLULAR FLUID
(CONT.)
• Near-drowning in fresh water
• Selective serotonin reuptake inhibitors (SSRIs)
• Loss of relatively more salt than water
• Diuretics, especially thiazides
• Salt-wasting renal disease
• Replacement of water but not salt lost
through emesis, diarrhea, gastric suction,
diaphoresis, or burns

59. ETIOLOGY OF EXCESS WATER
IN EXTRACELLULAR FLUID
(CONT.)
• Abnormal concentration of extracellular fluid
• Results when normal proportion of salt to
water in extracellular fluid is disrupted
• Gain of relatively more water than salt
• ADH elevation
• Causes kidneys to retain excessive amounts of
water (a gain of water relative to salt)

60. CAUSES OF ADH ELEVATION
• The syndrome of inappropriate secretion of
ADH (SIADH)
• Ectopic synthesis
• For example, small cell (oat cell) carcinoma is a
type of lung tumor that frequently synthesizes and
releases ADH
• Physical or psychological stressors
• Pain, nausea, other symptoms

61. CLINICAL MANIFESTATIONS
• Mild central nervous
system dysfunction
• Malaise
• Anorexia
• Nausea
• Vomiting
• Headache
• Severe central
nervous system
dysfunction
• Confusion
• Lethargy
• Seizures
• Coma
• Fatal cerebral
herniation

62. HYPERNATREMIA
• Serum sodium concentration above upper
limit of normal
• Extracellular fluid contains relatively too little
water for the amount of sodium ions present;
it is too concentrated
• Also called
• Water deficit
• Hypertonic syndrome
• Hyperosmolality

63. ETIOLOGY
• Gain of more salt than
water
• Inadequately diluted
concentrated tube
feedings
• Intravenous infusion of
hypertonic solution
• Near-drowning in
saltwater
• Overuse of salt tablets
• Food intake with
reduced fluid intake
• Difficulty swallowing
fluids
• No access to water
• Inability to respond to
thirst
• Loss of more water
than salt
• Diabetes insipidus
(deficient antidiuretic
hormone)
• Tube feeding (causes
obligate water loss in
urine)
• Osmotic diuresis
• Prolonged emesis,
diarrhea or diaphoresis
without water
replacement

64. CLINICAL MANIFESTATIONS
• Mild
• Thirst
• Oliguria
• Confusion
• Lethargy
• Severe
• Seizures
• Coma
• Death

65. CLINICAL DEHYDRATION
• Combination of two fluid disorders
• Extracellular volume deficit
• Hypernatremia
• Too small a volume of fluid in the extracellular
compartment and too-concentrated body fluids
• See Figure 24-8

66. FIGURE 24-8

67. ETIOLOGY
• Vomiting
• Diarrhea
• Knowledge deficit about salt and fluid
replacement

68. CLINICAL MANIFESTATIONS
• Sudden weight loss
• Postural blood pressure
decrease with
concurrent increased
heart rate
• Lightheadedness,
dizziness, or syncope on
standing
• Flat neck veins when
supine or neck veins
that collapse during
inspiration (older
children and adults)
• Sunken
fontanel
(infants)
• Rapid, thready
pulse
• Prolonged
small-vein filling
time
• Prolonged
capillary refill
time

69. CLINICAL MANIFESTATIONS
(CONT.)
• Decreased skin
turgor
• Dryness of oral
mucous
membranes
• Absence of
sweat and tears
• Hard stools
• Soft, sunken
eyeballs
• Longitudinal furrows in
the tongue
• Thirst
• Increased serum
sodium concentration
• Confusion, lethargy
• Coma
• Hypovolemic shock

70. EDEMA
• Edema: excess fluid in interstitial
compartment
• May be a manifestation of excess extracellular fluid
volume
• May also arise from other mechanisms
• Increased capillary hydrostatic pressure
• Increased interstitial fluid osmotic pressure
• Blockage of lymphatic drainage
• Decreased capillary osmotic pressure
• See Figure 24-9

71. FIGURE 24-9

72. INCREASED CAPILLARY
HYDROSTATIC PRESSURE
• Caused by:
• Increased extracellular fluid volume
• Increased local capillary flow that accompanies
inflammation
• Venous congestion

73. INCREASED INTERSTITIAL
FLUID OSMOTIC PRESSURE
• Occurs when inflammation increases vascular
permeability and proteins leak into interstitial
fluid

74. BLOCKAGE OF LYMPHATIC
DRAINAGE
• Caused by:
• Tumor
• Parasites
• Fibrosis from radiation therapy
• Surgical removal of lymph nodes
• Edema is frequently localized

75. DECREASED CAPILLARY
OSMOTIC PRESSURE
• Occurs when plasma proteins are decreased
• Malnutrition
• Liver disease (decreased protein synthesis)
• Edema may be extensive

76. PRINCIPLES OF ELECTROLYTE
HOMEOSTASIS
• Electrolytes
• Ionized salts dissolved in water
• Most clinically important
• Sodium
• Potassium
• Calcium
• Magnesium
• Chloride
• Bicarbonate
• Phosphate

77. TABLE 24-1
ElectrolyteElectrolyte Normal Concentration RangeNormal Concentration Range
Calcium (total)Calcium (total) 9-11 mg/dl (4.5 to 5.5 mEq/L)9-11 mg/dl (4.5 to 5.5 mEq/L)
MagnesiumMagnesium 1.5-2.5 mEq/L1.5-2.5 mEq/L
PhosphatePhosphate 2.5-4.5 mg/dl (adults and older2.5-4.5 mg/dl (adults and older
children)children)
4.5-6.5 mg/dl (children)4.5-6.5 mg/dl (children)
4.3-9.3 mg/dl (neonates)4.3-9.3 mg/dl (neonates)
PotassiumPotassium 3.5-5.0 mEq/L3.5-5.0 mEq/L
3.9-5.9 mEq/L (neonates)3.9-5.9 mEq/L (neonates)
SodiumSodium 135-145 mEq/L135-145 mEq/L
135-162 mEq/L (neonates)135-162 mEq/L (neonates)

78. DYNAMIC CONTROL
• Concentration of an electrolyte in plasma is
different from its concentration in the cell
• For body function, electrolyte concentration
must be normal in both the plasma and in the
cells
• Control of electrolyte levels is dynamic
• If intake of specific electrolyte increases, excretion
of that electrolyte may increase to normalize
plasma levels
• Similarly, if electrolyte intake decreases, electrolytes
may be redistributed into the plasma to maintain
normal plasma level

79. MAINTENANCE OF
ELECTROLYTE
CONCENTRATIONS
• Four processes responsible
• Electrolyte intake
• Electrolyte absorption
• Electrolyte distribution
• Electrolyte excretion
• Processes work together to maintain dynamic
control of electrolytes within normal limits

80. FIGURE 24-10

81. ELECTROLYTE INTAKE
• Intake normally occurs
orally, through food
and drink
• Other routes
• Oral medications
(magnesium antacids)
• Intravenous fluids
• Nutritional solutions
• Blood transfusions
• Administration of the
electrolyte
magnesium
• Tubes into body
cavities
• Nasogastric and GI
feeding tube
• Near-drowning in
saltwater

82. ELECTROLYTE ABSORPTION
• Essential if electrolyte is to be useful
metabolically
• Depends on other factors
• Concentration gradients
• Binding proteins (may increase or decrease
absorption)
• pH of intestinal content
• Medications
• Surgical removal of portions of GI tract

83. ELECTROLYTE DISTRIBUTION
• Influenced primarily by hormones
• Epinephrine
• Insulin
• Parathyroid hormone
• Certain medications also influence electrolyte
distribution
• Electrolyte movement may be rapid
• Shift of electrolytes from extracellular fluid into the
electrolyte pools decreases the plasma electrolyte
concentration

84. ELECTROLYTE DISTRIBUTION
(CONT.)
• Shift of electrolyte from an electrolyte pool into the
extracellular fluid increases the plasma electrolyte
concentration

85. ELECTROLYTE EXCRETION
• Occurs through urine, feces, sweat
• Influenced by hormones
• Other factors
• Rate of renal tubular fluid flow
• Medications
• Diarrhea
• Vomiting

86. ELECTROLYTE LOSS THROUGH
ABNORMAL ROUTES
• Exit of electrolytes from the body through
routes other than urine, feces, sweat
• May be controllable or may result from
therapeutic procedures
• Alters electrolyte homeostasis
• Examples
• Vomiting
• Nasogastric suction
• Paracentesis
• Hemodialysis
• Wound drainage
• Fistula drainage

87. ELECTROLYTE IMBALANCES
• Common in many pathophysiologic
conditions
• May be total body imbalance or may be
imbalance in distribution within
compartments
• Excess may be caused by:
• Increased intake
• Increased absorption
• Shift into extracellular fluid

88. ELECTROLYTE IMBALANCES
(CONT.)
• Deficit may be caused by:
• Decreased intake
• Decreased absorption
• Increased excretion
• Loss through abnormal route

89. PLASMA POTASSIUM
• Normal concentration of potassium ions in
serum is 3.5 to 5 mEq/L (may vary slightly with
different laboratories)
• Higher in neonates

90. HYPOKALEMIA
• Decreased potassium ion concentration in
extracellular fluid
• Does not necessarily denote decrease in total
body potassium
• May coexist with:
• Total body potassium deficit
• Total body potassium excess
• Normal total body potassium ion concentration

91. ETIOLOGY
• Decreased intake
• Increased excretion

92. DECREASED POTASSIUM
INTAKE
• Anorexia
• NPO (nothing by mouth) orders and
intravenous solutions without potassium
• Fasting
• Unbalanced diet

93. SHIFT OF POTASSIUM FROM
EXTRACELLULAR FLUID TO
CELLS
• Alkalosis
• Rapid correction of acidosis
• Excess insulin (e.g., during total parenteral
nutrition)
• Excess β-adrenergic stimulation
• Hypokalemic familial periodic paralysis

94. INCREASED POTASSIUM
EXCRETION THROUGH
NORMAL ROUTES
Renal Route
• Potassium-wasting diuretics
• Corticosteroid therapy
• Cushing disease
• Hyperaldosteronism
• Excessive ingestion of black licorice
(glycyrrhizin)
• Hypomagnesemia
• Parenteral carbenicillin or similar agents
• Amphotericin B, cisplatin, and many other
drugs

95. INCREASED POTASSIUM
EXCRETION THROUGH
NORMAL ROUTES (CONT.)
• Fecal route
• Diarrhea (includes laxative abuse)
• Skin route
• Excessive diaphoresis

96. LOSS OF POTASSIUM
THROUGH ABNORMAL
ROUTES
• Emesis
• Gastric suction
• Fistula drainage

97. CLINICAL MANIFESTATIONS
• Altered smooth, skeletal, cardiac muscle
function
• Abdominal symptoms
• Distention
• Diminished bowel sounds
• Paralytic ileus
• Skeletal muscle symptoms
• Bilateral muscle weakness; usually begins in legs
• Respiratory paralysis

98. CLINICAL MANIFESTATIONS
(CONT.)
• Cardiac muscle cell hyporepolarization
• Ectopic beats
• Alterations in conduction
• Dysrhythmias may be severe enough to cause
sudden cardiac death
• Polyuria

99. HYPERKALEMIA
• Rise of serum potassium ion concentration in
the extracellular fluid
• Level above 5 mEq/L (depending on lab)
• Because most potassium ions are inside cells,
total body potassium may be increased or
decreased depending on cause

100. ETIOLOGY
• Increased potassium intake
• Shift of potassium from cells to extracellular
fluid
• Decreased potassium excretion

101. INCREASED POTASSIUM
INTAKE
• Excessive or too-rapid intravenous potassium
infusion
• Insufficiently mixed intravenous potassium
• Large transfusion of stored blood
• Massive doses of potassium penicillin G

102. SHIFT OF POTASSIUM FROM
CELLS TO EXTRACELLULAR
FLUID
• Acidosis caused by nonorganic acids
• Insufficient insulin
• Crushing injury
• Cytotoxic drugs (tumor lysis syndrome)
• Hyperkalemic periodic paralysis
• β-Adrenergic blockade and prolonged
strenuous exercise

103. DECREASED POTASSIUM
EXCRETION
• Oliguria (such as in hypovolemia or renal
failure)
• Potassium-sparing diuretics
• Adrenal insufficiency
• Renin-deficient states
• Drugs that reduce aldosterone effects
• Angiotensin-converting enzyme (ACE) inhibitors
• Angiotensin II receptor antagonists
• Selective aldosterone blockers
• Nephrotoxic drugs

104. CLINICAL MANIFESTATIONS
• Muscle dysfunction
• Early, mild
• Intestinal cramping, diarrhea
• Late, more severe
• Muscle weakness: ascending, beginning in lower
extremities
• Cardiac dysrhythmias and even cardiac
arrest

105. POTASSIUM ADAPTATION
• Patients who have chronic renal failure often
undergo potassium adaptation
• Therefore, relatively mild symptoms at high plasma
potassium concentrations
• Mechanism
• Increased aldosterone levels
• Shift of potassium excretion by colon
• Shift in potassium ions from extracellular fluid into
cells

106. PLASMA CALCIUM
• Present in three forms
• Calcium ions bound to plasma proteins (such as
albumin)
• Bound to small organic ions (such as citrate)
• Unbound
• Only free ionized calcium is physiologically
active

107. PLASMA CALCIUM (CONT.)
Total Serum Calcium
• Measures all of the calcium (bound plus
unbound)
• Normal range of total serum calcium in adults
= 9 to 11 mg/dl or 4.5 to 5.5 mEq/L (may vary
slightly with different laboratories)
• Unless a calcium value specifies ionized
calcium, it is total calcium

108. PLASMA CALCIUM (CONT.)
Ionized Calcium
• Measures only the unbound ionized form
• The normal range of ionized calcium in adults
= 4 to 5 mg/dl, about half of the total calcium
(varies with different laboratories)
• Clinically significant calcium imbalances are
caused by alterations in the plasma
concentration of unbound ionized calcium

109. HYPOCALCEMIA
• Serum calcium concentration drops below
the lower limit of normal
• Fraction of unbound ionized calcium in the
blood ↓ by more calcium binding to plasma
proteins or other organic ions
• The total serum calcium may be normal
• Ionized hypocalcemia is present and may cause
signs and symptoms

110. ETIOLOGY
• Decreased calcium intake or absorption
• Decreased physiologic availability of calcium
• Increased calcium excretion through normal
routes

111. DECREASED CALCIUM INTAKE
OR ABSORPTION
• Diet with insufficient calcium and vitamin D
• Chronic kidney disease (deficient activated
vitamin D)
• Excessive dietary phytates or oxalates
• Steatorrhea
• Pancreatitis
• Chronic diarrhea (includes laxative abuse)
• Malabsorption syndromes

112. DECREASED PHYSIOLOGIC
AVAILABILITY OF CALCIUM
• Hypoparathyroidism
• Excessive phosphate intake
• Tumor lysis syndrome (high phosphate)
• Hypomagnesemia
• Alkalosis
• Large transfusion of citrated blood
• Rapid infusion of plasma expanders that bind
calcium
• Elevated plasma free fatty acids
• Chronic kidney disease

113. INCREASED CALCIUM
EXCRETION THROUGH
NORMAL ROUTES
• Steatorrhea
• Pancreatitis

114. CLINICAL MANIFESTATIONS
• Alteration in normal neuromuscular
excitability resulting in:
• Positive Trousseau sign
• Positive Chvostek sign
• Paresthesias
• Muscle twitching and cramping
• Hyperactive reflexes

115. CLINICAL MANIFESTATIONS
(CONT.)
• Carpal spasm
• Pedal spasm
• Tetany
• Laryngospasm
• Seizures
• Cardiac dysrhythmias

116. HYPERCALCEMIA
• Increased calcium intake or absorption
• Milk-alkali syndrome
• Vitamin D overdose (includes shark cartilage
supplements)

117. HYPERCALCEMIA (CONT.)
• Shift of calcium from bone to extracellular
fluid
• Hyperparathyroidism
• Immobilization
• Paget disease
• Bone tumors
• Multiple myeloma
• Leukemia
• Nonosseous malignancies that produce bone-
resorbing factors

118. HYPERCALCEMIA (CONT.)
• Decreased calcium excretion
• Thiazide diuretics
• Familial hypocalciuric hypercalcemia

119. PLASMA MAGNESIUM
• Normal serum magnesium concentration =
1.5 to 2.5 mEqL (depending on lab)
• Magnesium ions present in blood and bound
and unbound ionized forms
• Plasma magnesium imbalances may occur
• At same time as total body magnesium imbalances
• In the absence of total body magnesium
imbalances

120. HYPOMAGNESEMIA
• Serum magnesium concentration ↓ below the
lower limit of normal (1.5 mEq/L)
• Indicates a decreased magnesium
concentration of the extracellular fluid
• Does not necessarily indicate a total body
magnesium deficit (although the two may
occur concurrently)

121. DECREASED MAGNESIUM
INTAKE OR ABSORPTION
• Chronic alcoholism
• Malnutrition
• Prolonged intravenous therapy without
magnesium
• Ileal resection
• Chronic diarrhea (includes laxative abuse)
• Malabsorption syndromes
• Steatorrhea
• Pancreatitis

122. DECREASED PHYSIOLOGIC
AVAILABILITY OF MAGNESIUM
• Elevated plasma free fatty acids

123. INCREASED MAGNESIUM
EXCRETION THROUGH
NORMAL ROUTES
• Renal route
• Diabetic ketoacidosis
• Chronic alcoholism
• Hyperaldosteronism
• Diuretic therapy
• Aminoglycoside (e.g., gentamicin) toxicity
• Amphotericin B, cisplatin, and many other drugs
• Fecal route
• Steatorrhea
• Pancreatitis

124. MAGNESIUM LOSS THROUGH
ABNORMAL ROUTES
• Emesis
• Gastric suction
• Fistula drainage

125. CLINICAL MANIFESTATIONS
• Increased neuromuscular excitability
• Insomnia
• Hyperactive reflexes
• Muscle cramps
• Muscle twitching, grimacing
• Positive Chvostek sign
• Positive Trousseau sign
• Nystagmus
• Dysphagia
• Ataxia
• Tetany
• Seizures

126. CLINICAL MANIFESTATIONS
(CONT.)
• Cardiac dysrhythmias

127. FIGURE 24-11

128. HYPERMAGNESEMIA
• Serum magnesium concentration above
upper limit of normal (2.5 mEq/L, depending
on lab)
• Indicates an excess of magnesium in
extracellular fluid

129. ETIOLOGY
• Increased magnesium intake or absorption
• Ingestion or aspiration of seawater
• Excessive ingestion of magnesium-containing
medications (e.g., laxatives, antacids)
• Excessive intravenous infusion of magnesium
• Decreased magnesium excretion
• Oliguric renal failure
• Adrenal insufficiency

130. CLINICAL MANIFESTATIONS
• Depression of neuromuscular function related
to decreased release of acetylcholine at
neuromuscular junctions
• Decreased deep tendon reflexes
• Lethargy
• Hypotension
• Flushing
• Diaphoresis

131. CLINICAL MANIFESTATIONS
(CONT.)
• Drowsiness
• Flaccid paralysis
• Respiratory depression
• Bradycardia
• Cardiac dysrhythmias
• Cardiac arrest

132. FIGURE 24-11

133. HYPOPHOSPHATEMIA
• Present when concentration of phosphate in
plasma decreases below 2.5 mg/dl
• Clinical manifestations often not observed
until severe, until concentration of phosphate
less than 1 mg/dl

134. ETIOLOGY OF
HYPOPHOSPHATEMIA
• Decreased phosphate intake or absorption
• Chronic alcoholism
• Chronic diarrhea
• Malabsorption syndromes
• Excessive or long-term use of antacids that bind
phosphate

135. ETIOLOGY OF
HYPOPHOSPHATEMIA (CONT.)
• Shift of phosphate from extracellular fluid to
cells
• Refeeding after starvation (includes anorexia
nervosa)
• Total parenteral nutrition
• Hyperventilation (respiratory alkalosis)
• Insulin
• Epinephrine
• Intravenous glucose, fructose, bicarbonate, or
lactate

136. ETIOLOGY OF
HYPOPHOSPHATEMIA (CONT.)
• Increased phosphate excretion through the
normal renal route
• Alcohol withdrawal
• Diuretic phase after extensive burns
• Diabetic ketoacidosis
• Diuretic therapy

137. ETIOLOGY OF
HYPOPHOSPHATEMIA (CONT.)
• Phosphate loss through abnormal routes
• Emesis
• Hemodialysis

138. CLINICAL MANIFESTATIONS
• Anorexia
• Malaise
• Paresthesias
• Hemolysis
• Diminished reflexes
• Muscle aches, weakness
• Respiratory failure
• Confusion, stupor
• Seizures
• Coma
• Impaired cardiac function

139. HYPERPHOSPHATEMIA
• Increase in serum phosphate concentration
above the upper limit of normal, 4.5 mg/dl

140. ETIOLOGY OF
HYPERPHOSPHATEMIA
• Increased phosphate intake or absorption
• Overzealous phosphate therapy
• Excessive use of phosphate-containing enemas or
laxatives
• Shift of phosphate from cells to extracellular
fluid
• Tumor lysis syndrome
• Crushing injury
• Rhabdomyolysis

141. ETIOLOGY OF
HYPERPHOSPHATEMIA
(CONT.)
• Decreased phosphate excretion
• Chronic kidney disease
• Oliguric renal failure
• Adrenal insufficiency

142. CLINICAL MANIFESTATIONS
• Increased neuromuscular excitability
• If excess phosphate salts deposit in soft tissues
of areas of body where deposits are present
• May cause aching and stiffness of joints
• Itching
• Conjunctivitis

143. VARIATIONS IN INFANTS
• More extracellular fluid than intracellular fluid;
this proportion reverses by a few months of
age
• Body weight is approximately 75% water
• Percentage higher in preterm infants
• Percentage of body weight that is water decreases
as the child grows older

144. INFANT VARIATIONS
• Loss of fluid equivalent to 5%-10% of body
weight within first few days after birth is part of
normal adjustment to extrauterine life
• Neonates have high metabolic rate, thus high
turnover rate of water
• Increased insensible water excretion due to:
• Proportionately large body surface area
• Proportionately large respiratory mucosa surface
area

145. INFANT VARIATIONS (CONT.)
• Vasomotor immaturity
• Increased skin permeability

146. INFANT VARIATIONS (CONT.)
• Glomerular filtration rate (GFR) is lower than in
adults
• Kidneys have limited ability to concentrate
urine; therefore unable to:
• Excrete large load of water effectively
• Conserve fluid when needed
• Communication of thirst by crying may not be
understood by caregivers, resulting in
dehydration

147. INFANT VARIATIONS (CONT.)
• Assessment of extracellular volume
imbalances should focus on tension of
fontanel, not on degree of filling of neck
veins
• If powdered formula not properly diluted, can
result in hypernatremia
• Laboratory normal ranges of electrolytes
generally wider for infants than for older
children or adults

148. ELECTROLYTE IMBALANCES IN
INFANTS
• Hypocalcemia more likely if:
• Resuscitation required at birth
• Infant is premature
• Most reliable physical signs
• Jitteriness
• Hyperactive reflexes
• High-pitched cry
• Hypermagnesemia more likely if mother given
magnesium sulfate before birth

149. GERIATRIC VARIATIONS
• Age-related changes result in:
• Decreased muscle mass
• Increased fat in internal organs
• Less body water
• About 50% of lean older man’s body weight is water
• About 45% of lean older woman’s body weight is water
• Glomerular filtration rate (GFR) is lower in
older adults than in middle-aged adults

150. GERIATRIC VARIATIONS
(CONT.)
• Kidneys less able to concentrate urine, thus
less able to conserve fluid when needed
• Contributes to nocturia  larger volume of urine
produced at night than in younger adults
• Reduced thirst response may lead to
decreased awareness of dehydration
• Age-related changes mean that older adults
may have decreased skin turgor even when
appropriately hydrated

151. GERIATRIC VARIATIONS
(CONT.)
• Older adults who receive tube feedings at
higher risk for hypernatremia than middle-
aged adults
• Older adults absorb more magnesium from
antacids and cathartics than do middle-
aged adults
• With age-related changes in renal excretion, older
adults who use oral magnesium laxatives or
antacids regularly are at high risk for
hypermagnesemia