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CH 13 Electrolytes

Terms in this set (47)

ELECTROLYTES
Substances whose molecules dissociate into ions
when placed in water
• Cations: positively charged
• Anions: negatively charged
Concentration of electrolytes is often expressed in
milliequivalents (mEq)/L
Electrolyte concentrations differ depending on
fluid compartments
Normal serum ranges can vary depending on
facility*
• Follow facility ranges
ELECTROLYTE IMBALANCES
An abnormality in the concentration of electrolytes in the body
Electrolytes help to regulate
cardiac and neurological function
fluid balance
oxygen delivery
acid-base balance
-most important function
SODIUM (NA)
Plays a major role in
• ECF volume and concentration (osmolality)
• Generation and transmission of nerve impulses
• Muscle contractility
• Acid-base balance
Sodium Facts
-Serum level reflects the ratio of sodium to water
-Major cation of ECF
-Obtained from food/fluids in GI tract
-Excreted through urine, sweat, feces
-Kidneys primary regulator
-Imbalances typically associated with equivalent changes in osmolality
Hypernatremia
>145 mEq/L
• Elevated serum level occurring with water loss or gain of this electrolyte
• Causes hyperosmolality leading to cellular dehydration
• Primary protection is thirst from hypothalamus
Hypernatremia Causes
Excess intake
• Diet high in this electrolyte
• Hypertonic IVF
--contain a higher concentration of solute compared to plasma and interstitial fluid; this creates an osmotic gradient and drives fluid from the interstitial space into the intravascular space.
• Fluid deprivation
• Heat Stroke
• Diabetes Insipidus
Hypernatremia Occurence
• normal fluid volume
• Fluid Volume Deficiency
• Fluid Volume Excess
• Most affected are the very old, very young, and cognitively impaired
Hypernatremia Clinical Manifestations
• Thirst
• Elevated body temperature
• Lethargy
• Agitation
• Seizures
• Coma
Hypernatremia Nursing Implementation
• Treat underlying cause
• Primary water deficit—
• replace fluid orally or IV with isotonic or hypotonic
fluids
• D5W or 0.45 NS
• Excess of this electrolyte—
• dilute with IV fluids that do not contain this electrolyte and promote excretion with diuretics
• Diuretics
• Monitor serum levels carefully
• Monitor for CNS changes
Hypernatremia Treatment Concerns
• The body (in particular the brain) adapts to the
higher concentration of this electrolyte.
• Rapidly lowering concentration of this electrolyte causes water to flow into brain cells (swelling)
• This can lead to cerebral edema, potentially
resulting in seizures, permanent brain damage, or
death.
• This risk is greatest in the patient who has
developed this condition over several days or
longer.
Hyponatremia
<135 mEq/L
• Insufficient amount of this electrolyte in serum
• Loss of more of this electrolyte than water
• Inadequate intake of this electrolyte
• Fasting, starvation, confusion
• Excess water intake
• fluid overload in surgical/sepsis patient
Hyponatremia Causes
• Disease processes/symptoms
• SIADH (Syndrome of inappropriate antidiuretic hormone secretion), N/V/D, adrenal insufficiency
• Acute: Fluid overload in surgical/sepsis patient
• Chronic: outpatient, longer duration
• Exercise associated: extreme temperature,
excess water intake, prolonged exercise
Hyponatremia Clinical Manifestations
• Hypovolemic
• Irritability, personality changes, dry mucous
membranes, postural hypotension, increased HR
• Hypervolemic
• Headache, apathy, N/V/D, abdominal cramps,
weight gain, increased BP
Hyponatremia Nursing Implemenation
Treat Underlying Condition
*Caused by water excess - Fluid restriction is needed
*Severe symptoms (seizures) - IV hypertonic solution with this electrolyte (3% NaCl)
*Abnormal fluid loss - Fluid replacement solution containing this electrolyte
*Drugs that block vasopressin (ADH) - Convaptan (Vaprisol) & Tolvaptan (Samsca)
POTASSIUM
Major ICF cation
• Primary source is food
• Kidneys primary regulator (also GI tract and
sweat)
• Necessary for
• Transmission and conduction of nerve and smooth
muscle impulses
• Cellular growth
• Maintenance of cardiac rhythms
• Acid-base balance
HYPERKALEMIA
>5 mEq/L
• Excessive serum potassium
HYPERKALEMIA CAUSES
• Excess intake
• Salt Substitutes
• Rapid parenteral administration
• Internal shift: K+ shifting out of cells
• Acidosis (DKA*)
• Rhabdomyolysis, severe burns, or crush injuries
• Retention
• Renal Injury or Disease
• ARBs (losartan), ACE inhibitors (Lisinopril), Beta Blocker
(propranolol)
Hyperkalemia clinical manifestations
• Increased cell excitability
• Changes in cardiac conduction (loss of P wave,
prolonged PR interval, widening of QRS)
• Tall, peaked T waves
• Heart block, ventricular fibrillation, cardiac arrest
• Muscle weakness
• Abdominal and/or leg cramps
• Diarrhea
Hyperkalemia Nursing Implementation
• Monitor ECG, apical pulse
• Limit oral and parenteral K+ intake
• Increase elimination of K+
• Potassium wasting diuretics (loop)
• Kayexalate (causes excretion via diarrhea)
• Dialysis (in severe cases)
• Force K+ from ECF to ICF by IV insulin & glucose
(Severe; symptomatic or >6.5)
• Reverse membrane effects of elevated ECF
potassium by administering calcium gluconate IV
Hypokalema
<3.5 mEq/L
• Low serum potassium caused by
• Increased loss of K+ via the kidneys
• Loop or thiazide diuretics
• GI tract losses
• Increased shift of K+ from ECF to ICF
• Magnesium deficiency & Laxative dependency
• Metabolic alkalosis
• Dietary K+ deficiency (anorexia, fasting)
Hypokalemia Clinical Manifestations
• Hyperpolarization of cells impairs muscle
contraction
• Cardiac (ST segment depression, prolonged QRS,
Heart blocks, ventricular dysrhythmias)
• Skeletal muscle weakness (legs), cramps
• Weakness of respiratory muscles
• Decreased GI motility (constipation)
• Impaired regulation of arteriolar blood flow
• Hyperglycemia
Hypokalemia Nursing Implementation
• Monitor:
• ECG for changes
• UOP before administering K+
• KCl supplements orally or IV
• Always dilute IV KCL
• NEVER give KCL via IV push or as a bolus
• Should not exceed 10 mEq/hr
• To prevent hyperkalemia and cardiac arrest
Calcium Functions
Formation of teeth and bone
Blood clotting
Transmission of nerve impulses
Myocardial contractions
Muscle contractions
Calcium
• Obtained from ingested foods
• Vitamin D needed to absorb
• 99% is in bones
• Present in three forms: Ionized calcium is
biologically active
• Changes in pH of the blood
• Serum albumin affects total Ca levels can cause them to be lower
Calcium Balance Control
Parathyroid hormone (PTH)
• production and release stimulated by low
serum calcium levels
• PTH increases bone resorption, increases GI
absorption of calcium, and increases renal
reabsorption of calcium
--movement of calcium out of the bone into the blood
Calcitonin
• produced by the thyroid gland
• stimulated by high serum calcium levels. It
opposes the action of PTH
Hypercalcemia
>10.5 mg/dl
High serum calcium level cause by
Hyperparathyroidism (2/3 of
cases)
Malignancy (1/3 of cases)
Rare causes
-Excessive intake
-Prolonged immobilization (coma, ventilation)
-Excess Vitamin D
Hypercalcemia Clinical Manifestations
• Neuro:
• Fatigue, lethargy, muscle weakness, stupor, coma,
depressed reflexes, decreased memory, confusion,
personality changes, psychosis
• ECG changes
• Anorexia, nausea, vomiting
• Bone pain, fractures
--calcium is leaving the bone & going to bloodstream
• Flank pain from nephrolithiasis (renal calculi)
• Polyuria, dehydration
Hypercalcemia Nursing Implementation
• Increase in fluid intake & increase Ca excretion
with loop diuretics
• Hydration with isotonic saline infusion
--3 to 4 L per day
• Low calcium diet
• Mobilization
• Synthetic calcitonin
• Bisphosphonates (in cases of malignancy)
Hypocalcemia
< 8.5 mg/dL
• Less Ca entering blood:
• Inadequate vitamin D, malnutrition (poor Ca
intake)
• Decreased production of PTH (hypothyroidism,
surgery)
• Chronic Renal Failure
• Excess Excretion
• Renal insufficiency
• Burns, Rhabdo
• Pancreatitis, Cirrhosis
• Diarrhea, laxative abuse
• Multiple blood transfusions
Hypocalcemia Clinical Manifiestations
• Tetany
• Positive Trousseau's or Chvostek's sign
• Laryngeal stridor
• Dysphagia
• Perioral Tingling
• Cardiac dysrhythmias
Hypocalcemia Nursing Implementations
• Treat underlying cause
• Oral calcium and vitamin D supplements
• IV calcium gluconate
• Seizure precautions
• Exercise to decrease bone calcium loss
• Treat pain and anxiety to prevent hyperventilationinduced respiratory alkalosis
Phosphate (PO43)
• Normal 2.5 - 4.5 mg/dL
• Primary anion in ICF
• Most phosphorus located in bones & teeth
• Essential to function of muscle, red blood cells,
and nervous system
• Involved in
• acid-base buffering system
• ATP production
• cellular uptake of glucose
• metabolism of carbohydrates, proteins, and fats
Phosphate balance/controls
• Serum levels controlled by parathyroid hormone
• Maintenance requires adequate renal
functioning
• Reciprocal relationship with calcium
• high phosphate level tends to cause a low
calcium concentration in the serum
Hyperphosphatemia causes
Acute Kidney Injury or Chronic Kidney Disease
Chemotherapy
Hypoparathyroidism
-Increase phosphate reabsorption
Tumor lysis, rhabdo
Excessive intake of phosphate or vitamin D
-Laxatives
Hyperphosphatemia Clinical Manifestations
Often asymptomatic unless Ca binds to PO43- (hypocalcemia)
Neuromuscular irritability and tetany (hypocalcemia)
Long term increase results in calcified deposits in soft tissue such as:
Joints
Arteries
Skin
Kidneys
Corneas
Hyperphosphatemia management
• Identify and treat underlying cause
• Restrict foods and fluids containing
phosphorus (dairy products)
• Calcium-binding agents (Calcium carbonate)
• Adequate hydration and correction of
hypocalcemic conditions
• NS IV w loop diuretics
• Hemodialysis (if severe)
Hypophosphatemia
<2.5 mg/dL
Caused by
• Malnourishment/malabsorption
• Diarrhea
• ETOH abuse
• Use of phosphate-binding antacids
• Tums
• During parenteral nutrition with inadequate
replacement
Hypophosphatemia clinical manifestations
• Mild to moderate, often asymptomatic.
• CNS depression, confusion
• Muscle weakness and pain
• Cardiomyopathy
• Respiratory failure
Hypophosphatemia Management
Oral supplementation
-Dairy products or phosphate supplements
Ingestion of foods high in phosphorus
IV administration of sodium or potassium phosphate if severe
Magnesium
1.3 - 2.3 mg/dL
• Required for DNA & protein synthesis
• Necessary for sodium-potassium pump
• Important for normal cardiac function
• 50% to 60% contained in bone
• Absorbed in GI tract
• Excreted by kidneys & stool
Hypermagnesemia Causes
>3 mg/dL
• High serum content caused by
• Increased intake or ingestion of products
containing magnesium when renal insufficiency or
failure is present
• Maalox, MOM
• Treatment of migraines or menstrual cramps
• Excess intravenous magnesium administration
• Tx of eclampsia
• Decreased output
• End Stage Renal Disease (ESRD), AKI, adrenal insufficiency
Hypermagnesemia Clinical Manifestations
• ECG changes
• Hypotension
• Lethargy / Somnolence
• N/V
• Impaired reflexes
--depresses muscle function & deep tendon reflexes
• Respiratory and cardiac arrest
Hypermagnesemia Management
• Prevention first—restrict magnesium intake in highrisk patients
• Emergency treatment (symptomatic)
• IV Calcium gluconate
• Fluids and IV furosemide to promote urinary
excretion
• Dialysis if impaired renal function
Hypomagnesemia Causes
<1.3 mg/dL
Low serum Mg caused by
• Prolonged fasting or starvation
• Chronic alcoholism
• Fluid loss from gastrointestinal tract
• Prolonged parenteral nutrition without
supplementation
• Diuretics
• Large blood transfusion
Hypomagnesemia Clinical Manifestatins
• Hyperactive deep tendon reflexes
• Muscle cramps
--overactive muscles
• Tremors
• Seizures
• Cardiac dysrhythmias
• Torsade de pointes, Vfib
• Corresponding hypocalcemia and hypokalemia
Hypomagnesemia Management
• Treat underlying cause
• Monitor ECG
• Seizure precautions
• Oral supplements
• Increase dietary intake
• green vegetables, nuts, bananas, oranges,
peanut butter, and chocolate
• IV magnesium when severe
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