Part 2: Electrolytes

Electrolytes
 Charged particles in solution
 Cations (+)
 Anions (-)
 Integral part of metabolic and
cellular processes
Positive or Negative?
 Cations (+)  Anions (-)
 Sodium  Chloride
 Potassium  Bicarbonate
 Calcium  Phosphate
 Magnesium  Sulfate
Major Cations
 EXTRACELLULAR
 SODIUM (Na+)

 INTRACELLULAR
 POTASSIUM (K+)
Electrolyte Imbalances
 Hyponatremia/  Hypocalcemia/
hypernatremia Hypercalcemia
 Hypokalemia/ Hyperkalemia  Hypophosphatemia/
 Hypomagnesemia/ Hyperphosphatemia
Hypermagnesemia  Hypochloremia/
Hyperchloremia
Sodium
 Major extracellular cation

 Attracts fluid and helps preserve fluid volume

 Combines with chloride and bicarbonate to help

regulate acid-base balance
 Normal range of serum sodium 135 - 145 mEq/L
Sodium and Water
 If sodium intake suddenly increases, extracellular
fluid concentration also rises
 Increased serum Na+ increases thirst and the
release of ADH, which triggers kidneys to retain
water
 Aldosterone also has a function in water and
sodium conservation when serum Na+ levels are
low
Sodium-Potassium Pump
 Sodium (abundant  Pump uses ATP,
outside cells) tries to get magnesium and an
into cells enzyme to maintain
sodium-potassium
 Potassium (abundant concentrations
inside cells) tries to get  Pump prevents cell
out of cells swelling and creates
 Sodium-potassium an electrical charge
pump maintains normal allowing
concentrations neuromuscular
impulse transmission
Hyponatremia
 Serum Na+ level < 135 mEq/L
 Deficiency in Na+ related to amount of body fluid
 Several types
 Dilutional
 Depletional
 Hypovolemic
 Hypervolemic
 Isovolumic
Types of Hyponatremia
 Dilutional - results from Na+ loss, water gain
 Depletional - insufficient Na+ intake
 Hypovolemic - Na+ loss is greater than water
loss; can be renal (diuretic use) or non-renal
(vomiting)
 Hypervolemic - water gain is greater than Na+
gain; edema occurs
 Isovolumic - normal Na+ level, too much fluid
Assessment
 Primarily neurologic symptoms
 Headache, N/V, muscle twitching,
altered mental status, stupor, seizures,
coma
 Hypovolemia - poor skin turgor, tachycardia,
decreased BP, orthostatic hypotension
 Hypervolemia - edema, hypertension, weight
gain, bounding tachycardia
Interventions
 MILD CASE  SEVERE CASE
 Restrict fluid intake for  Infuse hypertonic NaCl
hyper/isovolumic solution (3% or 5%
hyponatremia NaCl)
 IV fluids and/or  Furosemide to remove
increased po Na+ excess fluid
intake for hypovolemic  Monitor client in ICU
hyponatremia
Hypernatremia
 Excess Na+ relative to body water
 Occurs less often than hyponatremia
 Thirst is the body’s main defense
 When hypernatremia occurs, fluid shifts outside the
cells
 May be caused by water deficit or over-ingestion of
Na+
 Also may result from diabetes insipidus
Assessment
 Think S-A-L-T
 Skin flushed
 Agitation
 Low grade fever
 Thirst
 Neurological symptoms
 Signs of hypovolemia
Interventions
 Correct underlying  Monitor for s/s of
disorder cerebral edema
 Gradual fluid  Monitor serum Na+
replacement level
 Seizure precautions
Potassium
 Major intracellular cation
 Untreated changes in K+ levels can lead to serious neuromuscular and
cardiac problems
 Normal K+ levels = 3.5 - 5 mEq/L
Balancing Potassium
 Most K+ ingested is excreted by the kidneys
 Three other influential factors in K+ balance :
 Na+/K+ pump
 Renal regulation
 pH level
Sodium/Potassium Pump
 Uses ATP to pump potassium into cells
 Pumps sodium out of cells
 Creates a balance
Renal Regulation
 Increased K+ levels ⇒ increased K+ loss in urine
 Aldosterone secretion causes Na+ reabsorption and
K+ excretion
pH
 Potassium ions and hydrogen ions exchange freely across cell
membranes
 Acidosis ⇒ hyperkalemia (K+ moves out of cells)
 Alkalosis ⇒ hypokalemia (K+ moves into cells)
Hypokalemia
 Serum K+ < 3.5 mEq/L
 Can be caused by GI losses, diarrhea, insufficient intake, non-K+
sparing diuretics (thiazide, furosemide)
Assessment
 Think S-U-C-T-I-O-N
 Skeletal muscle weakness
 U wave (EKG changes)
 Constipation, ileus
 Toxicity of digitalis glycosides
 Irregular, weak pulse
 Orthostatic hypotension
 Numbness (paresthesias)
Interventions
 Increase dietary K+
 Oral KCl supplements
 IV K+ replacement
 Change to K+-sparing diuretic
 Monitor EKG changes
IV K+ Replacement
 Mix well when
adding to an IV
solution bag NEVER GI VE I V
 Concentrations PUSH POTASSI UM
should not exceed
40-60 mEq/L
 Rates usually 10-
20 mEq/hr
Hyperkalemia
 Serum K+ > 5 mEq/L  Caused by altered
 Less common than kidney function,
hypokalemia increased intake (salt
substitutes), blood
transfusions, meds (K+-
sparing diuretics), cell
death (trauma)
Assessment
 Irritability
 Paresthesia
 Muscle weakness (especially legs)
 EKG changes (tented T wave)
 Irregular pulse
 Hypotension
 Nausea, abdominal cramps, diarrhea
Interventions
 Mild  Emergency
 Loop diuretics (Lasix)  10% calcium gluconate
 Dietary restriction for cardiac effects

 Moderate  Sodium bicarbonate for

acidosis
 Kayexalate
Magnesium
 Helps produce ATP
 Role in protein synthesis & carbohydrate
metabolism
 Helps cardiovascular system function
(vasodilation)
 Regulates muscle contractions
Hypomagnesemia
 Serum Mg++ level < 1.5  High risk clients
mEq/L  Chronic alcoholism
 Caused by poor dietary  Malabsorption
intake, poor GI  GI/urinary system
absorption, excessive disorders
GI/urinary losses  Sepsis
 Burns
 Wounds needing
debridement
Assessment
 CNS
 Altered LOC
 Confusion
 Hallucinations
Assessment
 Neuromuscular
 Muscle weakness
 Leg/foot cramps
 Hyper DTRs
 Tetany
 Chvostek’s & Trousseau’s signs
Assessment
 Cardiovascular
 Tachycardia

 Hypertension

 EKG changes
Assessment
 Gastrointestinal
 Dysphagia

 Anorexia

 Nausea/vomiting
Interventions
 Mild
 Dietary replacement
 Severe
 IV or IM magnesium sulfate
 Monitor
 Neuro status
 Cardiac status
 Safety
Mag Sulfate Infusion
 Use infusion pump - no faster than 150 mg/min
 Monitor vital signs for hypotension and respiratory
distress
 Monitor serum Mg++ level q6h
 Cardiac monitoring
 Calcium gluconate as an antidote for treating
Mg++ toxicity
Hypermagnesemia
 Serum Mg++ level > 2.5 mEq/L
 Not common
 Renal dysfunction is most common cause
 Renal failure
 Addison’s disease
 Adrenocortical insufficiency
 Untreated DKA
Assessment
 Decreased neuromuscular activity
 Hypoactive DTRs
 Generalized weakness
 Occasionally nausea/vomiting
Interventions
 Increased fluids if renal function normal
 Loop diuretic if no response to fluids
 Calcium gluconate for toxicity
 Mechanical ventilation for respiratory depression
 Hemodialysis (Mg++ free dialysate)
Calcium
 99% in bones, 1% in serum and soft tissue (measured
by serum Ca++)
 Works with phosphorus to form bones and teeth
 Role in cell membrane permeability
 Affects cardiac muscle contraction
 Participates in blood clotting
Calcium Regulation
 Affected by body stores of Ca++ and by dietary
intake & Vitamin D intake
 Parathyroid hormone draws Ca++ from bones
increasing low serum levels
 With high Ca++ levels, calcitonin is released by the
thyroid to inhibit calcium loss from bone
Hypocalcemia
 Serum calcium < 8.9 mg/dl
 Ionized calcium level < 4.5 mg/Dl
 Caused by inadequate intake, malabsorption,
pancreatitis, thyroid or parathyroid surgery, loop
diuretics, low magnesium levels
Assessment
 Neuromuscular
 Anxiety, confusion, irritability, muscle twitching,
paresthesias (mouth, fingers, toes), tetany
 Fractures
 Diarrhea
 Diminished response to digoxin
 EKG changes
Interventions
 Calcium gluconate for postop thyroid or parathyroid client
 Cardiac monitoring
 Oral or IV calcium replacement
Hypercalcemia
 Serum calcium > 10.1 mg/dl
 Ionized calcium > 5.1 mg/dl
 Two major causes
 Cancer
 Hyperparathyroidism
Assessment
 Fatigue, confusion, lethargy, coma
 Muscle weakness, hyporeflexia
 Bradycardia ⇒ cardiac arrest
 Anorexia, nausea/vomiting, decreased bowel sounds, constipation
 Polyuria, renal calculi, renal failure
Interventions
 If asymptomatic, treat underlying cause
 Hydrate the patient to encourage diuresis
 Loop diuretics
 Corticosteroids
Phosphorus
 The primary anion in the intracellular fluid
 Crucial to cell membrane integrity, muscle function, neurologic function
and metabolism of carbs, fats and protein
 Functions in ATP formation, phagocytosis, platelet function and
formation of bones and teeth
Hypophosphatemia
 Serum phosphorus < 2.5 mg/dl
 Can lead to organ system failure
 Caused by respiratory alkalosis (hyperventilation), insulin release,
malabsorption, diuretics, DKA, elevated parathyroid hormone levels,
extensive burns
Assessment
 Musculoskeletal  Cardiac
 muscle weakness  hypotension
 respiratory muscle  decreased cardiac
failure output
 osteomalacia  Hematologic
 pathological fractures  hemolytic anemia
 CNS  easy bruising
 confusion, anxiety,  infection risk
seizures, coma
Interventions
 MILD/MODERATE  SEVERE
 Dietary interventions  IV replacement using

 Oral supplements potassium phosphate

or sodium phosphate
Hyperphosphatemia
 Serum phosphorus > 4.5 mg/dl
 Caused by impaired kidney function, cell damage,
hypoparathyroidism, respiratory acidosis, DKA,
increased dietary intake
Assessment
 Think C-H-E-M-O
 Cardiac irregularities
 Hyperreflexia
 Eating poorly
 Muscle weakness
 Oliguria
Interventions
 Low-phosphorus diet
 Decrease absorption with antacids that bind
phosphorus
 Treat underlying cause of respiratory acidosis or
DKA
 IV saline for severe hyperphosphatemia in
patients with good kidney function
Chloride
 Major extracellular anion
 Sodium and chloride maintain water balance
 Secreted in the stomach as hydrochloric acid
 Aids carbon dioxide transport in blood
Hypochloremia
 Serum chloride < 96 mEq/L
 Caused by decreased intake or decreased absorption, metabolic
alkalosis, and loop, osmotic or thiazide diuretics
Assessment
 Agitation, irritability
 Hyperactive DTRs, tetany
 Muscle cramps, hypertonicity
 Shallow, slow respirations
 Seizures, coma
 Arrhythmias
Interventions
 Treat underlying cause
 Oral or IV replacement in a sodium chloride or potassium chloride
solution
Hyperchloremia
 Serum chloride > 106 mEq/L
 Rarely occurs alone
 Caused by dehydration, renal failure, respiratory alkalosis, salicylate
toxicity, hyperparathyroidism, hyperaldosteronism, hypernatremia
Assessment
 Metabolic Acidosis  Hypernatremia
 Decreased LOC  Agitation

 Kussmaul’s respirations  Tachycardia, dyspnea,

 Weakness tachypnea, HTN

 Edema
Interventions
 Correct underlying cause
 Restore fluid, electrolyte and acid-base balance
 IV Lactated Ringer’s solution to correct acidosis