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Ca Mg
Cl
HCO3 -
Measurement of electrolyte
Milli equivalents (meq) per liter)
a measure of chemical activity
equal in msq /L
Approximate Major Electrolyte Content in Body
Fluid
ELECTROLYTES MEQ/L
Extracellular Fluid (Plasma)
Cations
Sodium (NA) 142
Potassium (K) 5
Calcium (CA++) 5
Magnesium (MG++) 2
Total cations 154
Anions
Chloride(CI-) 103
Bicarbonate(HCO 3-) 26
Phospate (HPO4--) 2
Sulfate (SO4--) 1
Organic Acids 5
Proteinate 17
Total anions 154
Intracellular Fluid
Cations
Potassium (K+) 150
Magnesium (MG++) 40
Sodium (Na+) 10
Total cations 200
Interpreting serum electrolyte
test result
Electrolyte Result Implications Common
Causes
Calcium 8.9 to 10.1 Normal
mg/dl
Chloride 96 to Normal
106
mEq/L
Magnesium1.5 to Normal
2.5
mEq/L
Implementation:
a. vital sign assessed every 2 to 4 hours and compared with
baseline vital signs
b. positional blood pressure should be assessed to determine
degree of ostotrasis,
c. Urine output be assesses hourly if success per shift in mild cases
and per day should be compared with intake for the same time
frame absence of urine output in 8 to 12 hours may indicate
renal insufficiency because of decrease renal perfusion.
with fluid volume excess (fluid overload) the fluid pressure is even greater than
usual at arterial end of the capillary. Fluid is pushed into the tissue spaces
with greater force because venous pressure exceeds oncotic pressure.
Peripheral and pulmonary edema may result.
When fluid overload result from renal Disorder there is in sodium and
water retentions fluid volume rises and heart must compensate for
the increasing pressure heart failure can result.
Clients with cerihosis of the liver sodium protein and albumin levels are
decreased the oncotic pressure is decreased in the vascular
fluids
which results in less fluid reabsorption from the tissue spaces peripheral
edema and ascites result
Assessment
Cardiovascular
Bounding, increase pulse rate
Elevated blood pressure
Distended neck and hand veins
Elevated central venous pressure
Respiratory
Increased respiratory rate (shallow respiration)
Dyspnea
Moist crackles on auscultation
Assessment
Neuromuscular
Altered level of consciousness
Headache
Visual disturbance
Skeletal muscle weakness
Paresthesias
Integumentary
Pitting edema in dependent area
Skin pale and cool to touch
Increase motility in the gastrointestinal tract
Assessment
Isotonic overhydration results in liver
enlargement and ascites.
Hypotonic overhydration
Polyuria
Diarrhea
Nonpitting edema
Dysrhythmias
Projectile vomiting
Laboratory Findings
Decreased serum osmolality
Decreased hematocrit
Decreased BUN level
Decreased serum sodium level
Decreased urine specific gravity
Intervention
Monitor
Prevent fluid excess
Administer diuretics, osmotic diuretics
typically are prescribed first to prevent
severe electrolyte imbalance.
Restrict fluids and sodium intake
Monitor I & O, weight
Monitor electrolytes values
Regulating sodium and
Serum sodium level
water Serum Sodium level
(water excess) (water deficit)
Diarrhea
Fistulas
Gastric suctioning
Excessive sweating
Cystic fibrosis
Burns
Wound drainage.
Classification
Renal
Osmotic diuresis
Salt losing nephritis
Adrenal insufficiency
Diuretics
Causes sodium loss and volume depletion from
the blood vessels, causing the patient feel thirsty
and his kidneys to retain water. Drinking large
quantities of water can worsen hyponatremia.
Classification
Hypervolemic hyponatremia
Both water and sodium levels increase
in the extracellular area, but the water
gain is more noticeable and has a
greater impact on the patient.
Serum sodium level are diluted, and
edema occurs causes include heart
failure, live failure, nephrotic syndrome,
excessive administration of hypotonic
I.V fluids and hyperaldosreroism.
Classification
Isovolumic hyponatremia
Sodium levels may appear low because
there’s too much fluids in the body.
However the patient has no physical
signs of fluids volume excess and total
body sodium remain stable.
Causes include glucocorticoid deficiency,
hypothyroidism and renal failure.
Assessment
Cardiovascular
Symptoms vary with changes in vascular
volume
Normavolemic: rapid pulse rate; normal
blood pressure
Hypovolemic: thready, weak rapid pulse
rate; hypotension; flat neck veins, normal or
low central venous pressure
Hypervolemic: rapid, bounding pulse; blood
pressure normal or elevated; normal or
elevated central venous pressure.
Assessment
Respiratory: shallow, ineffective respiratory
movements as a late manifestation related to
skeletal muscle weakness.
Neuromuscular
Generalized skeletal muscle weakness that is worse in
the extremities
Diminished deep tendon reflexes
Cerebral function
Headache
Personality changes
Confusion
Seizures
coma
Assessment
Gastrointestinal
Increased motility and hyperactive
bowel sounds
Nausea
Abdominal cramping and diarrhea
Renal
Decreased urinary specific gravity
Increased urinary output
Intervention
1. Monitor cardiovascular, respiratory, nueromuscular, cerebral,
renal and gastrointestinal status.
2. If hyponatremia is accompanied by a fluid deficit, IV sodium
chloride infusions are administered.
3. If hyponatremia is accomapnied by fluids excess, osmotic
diuretics are administered.
4. If the cause is inappropriate or excessive secretions of
antidiuretic hormone, such as lithium and demeclocycline
(Declomycin), may be administred.
5. Instruct client to increase oral sodium intake and inform the
client about the foods to include in the diet.
6. If the client is taking lithium, monitor the lithium level, because
hyponatremia can cause diminished lithium excretion, resulting
in toxicity.
HYPERNATREMIA
Is a serum sodium level that exceeds
145 mEq/L
Causes
Decrease sodium excretion
Corticosteroids
Cushing’s syndrome
Renal failure
Hyperaldosteroism
Causes
Increased sodium intake: excessive
oral sodium ingestion or excessive
administration of sodium containing IV
fluids.
Decreased water intake: nothing by
mouth
Increased water loss; increased rate of
metabolism, fever, hyperventilation,
infection, excessive diaphoresis,
watery diarrhea, diabetes insipidus.
Assessment
Cardiovascular: heart rate and blood
pressure that respond to vascular
volume status.
Respiratory: Pulmonary edema if
hypervolemia is present.
Neuromuscular
Early: spontaneous muscle twitches;
irregular muscle contraction
Late: skeletal muscle weakness; deep
tendon reflexes diminished or absent.
Assessment
Central nervous system
Altered cerebral functions is the most common
manifestation of hypenatremia.
Normovolemia or hypovolemia: agitation,
confusion, seizures
Hypervolemia: lethargy, stupor, coma
Renal
Increased urinary specific gravity
Decreased urinary output
Integumentary
Dry skin
Presence or absence of edema, depending on fluid
volume changes.
Intervention
Monitor cardiovascular, respiratory,
neuromuscular, cerebral, renal and
integumentary status.
If the cause is fluid loss, prepare to
administered IV infusions.
If the cause is inadequate renal excretion
of sodium, prepare to administer diuretics
that promote sodium loss.
Restrict sodium and fluid intake as
prescribed.
ECG
An electrocardiogram (EKG, ECG) translates the heart's electrical
activity into line tracings on paper. The spikes and dips in the line
tracings are called waves.
The P wave is a record of the electrical activity through the upper
heart chambers (atria).
The QRS complex is a record of the movement of electrical
impulses through the lower heart chambers (ventricles).
The ST segment shows when the ventricle is contracting but no
electricity is flowing through it. The ST segment usually appears as a
straight, level line between the QRS complex and the T wave.
The T wave shows when the lower heart chambers are resetting
electrically and preparing for their next muscle contraction.
HYPOKALEMIA
Serum potassium level lower than
3.5 mEq/L
Deficit is pontentially life threatening
because every body system is
affected.
Causes
Actual total body potassium loss
Excessive use of medication such as diuretics or
corticosteroids
Increased secretion of aldosterone such in
Cushing syndrome
Vomiting, diarrhea
Wound drainage, praticualry gastrointestinal
Prolong nasogastric suction
Excessive diaphoresis
Renal disease impairing reabsorption of
potassium
Causes
Inadequate potassium intake: nothing by
mouth
Movements of potassium from the
extracelluar fluids to the intracellular fluids
Alkalosis
Hyperinsulinism
Dilution of serum potassium
Water intoxication
Intravenous therapy with potassium poor
solutions.
Assessment
Cardiovascular
Thready, weak, irregular pulse
Peripheral pulse weak
Orthostatic hypotension
Electrocardiogram changes: ST depression,
shallow, flat or inverted T wave, and prominent U
wave.
Respiratory
Shallow, ineffective respiration that result from
profound weakness of the skeletal muscles of
respiration.
Diminished breath sounds.
Assessment
Neuromuscular
Anxiety, lethargy, confusion, coma
Skeletal muscle weakness, eventual flaccid paralysis
Loss of tactile discrimination
Deep tendon hyporeflexia
Gastrointestinal
Decreased motility, hypoactive to absent bowel sounds
Nausea, vomiting, constipation, abodminal distention
Paralytic ileus
Renal
Decreased urinary specific gravity
Increased urinary outout
Intervention
Monitor cardiovascular, respiratory,
neuromuscular, gastrointestinal and renal
status and place on a cardiac monitor.
Monitor electrolyte values.
Administer potassium supplements orally
or intravenously as prescribed.
Oral potassium supplements
Institutes safety measure for the clients
experiencing muscle weakness
Intervention
Take the following precaution with
intravenously administered potassium:
Never given by IV push or by the intramuscular
or subcutaneous route.
Dilution of no more than 1mEq/ 10 ml of
solution is recommended.
After adding potassium to an IV solution, rotate
and invert the bag to ensure that the potassium
is distributed evenly throughout the IV solution.
Ensure that the IV bag containing potassium is
properly labeled.
The maximum recommended infusion rate is 5
to 10 mEq/hr, never to exceed 20 mEq/hr under
any circumstances.
Intervention
A client receiving more than 19 mEq/hr should
be placed on a cardiac monitor and monitored
far cardiac changes, and the infusion should be
controlled by an infusion device.
Potassium infusion can cause phlebitis.
The nurse should assess renal function before
administering potassium and monitor intake and
output during administration.
If the client is taking a potassium losing
diuretic, it may be discontinued; a
potassium sparing diuretic may be
prescribed.
Instruct the client about the food that are
high in potassium
HYPERKALEMIA
Is a serum potassium level that
exceeds 5.1 mEq/L
Causes
Excessive potassium intake
Over ingestion of potassium containing foods
or medications such as potassium chloride or
salt substitutes.
Rapid infusion of potassium containing IV
solution
Causes
Decreased potassium excretion
Potassium sparing diuretics
Renal failure
Adrenal insufficiency, such as in addison’s
disease.
Movements of potassium from the
intracellular fluid to the extracelluar fluid
Tissues damage
Acidosis
Hyperuricemia
Hypercatabolism
Assessment
Cardiovascular
Slow, weak, irregular heart rate
Decreased blood pressure
Electrocardiographic changes: tall peaked I waves,
flat P waves, widened QRS complexes, and
prolong PR intervals.
Respiratory: profound weakness of the
skeletal muscles leading to respiratory
failure.
Assessment
Neuromuscular
Early: muscle twitches, cramps,
parasthesias
Late: profound weakness, ascending
flaccid paralysis in the arms and legs
Gastrointestinal
Increased motility, hyperactive bowel
sounds
Diarrhea
Interventions
Monitor cardiovascular, respiratory,
neuromuscular, renal, and gastrointestinal
status; place the client on a cardiac monitor.
Discontinue IV potassium and hold oral
potassium supplements.
Initiate a potassium restricted diet.
Prepare to administered potassium excreting
diuretics if renal function is not impaired.
Prepare the client for dialysis if potassium level
are critically high.
Prepare for the IV administration of hypertonic
glucose with regular insulin to move excess
potassium into the cells.
Intervention
Monitor renal function
When blood transfusions are prescribed for the
client with potassium imbalance, the client should
received fresh blood, if possible transfusions of
stored blood may elevate the potassium level
because the breakdown of older blood cells
releases potassium.
Teach the client to avoid food high in potassium
Instruct the client to avoid the use of salt
substitutes or other potassium containing
substances.
HYPOCALCEMIA
Serum calcium level lower than 8.6
mg/dL
Causes
Inhibition of calcium absorption from the
gastrointestinal tract
Increased calcium excretion
Conditions that decrease the ionized fraction
of calcium
Immobilty
Removal or destruction of the parathyroid glands
Acute pancreatitis
Assessment
Cardiovascular
Decreased heart rate
Hypotension
Diminished peripheral pulses
Electrocardiographic changes: prolonged ST
interval, prolong QT interval
Respiratory: not directly affected; however
respiratory failure or arrest can result from
decreased respiratory movement because
of muscle tetany or seizures.
Assessment
Neuromuscular
Irritable skeletal muscles; twitches, cramps,
tetany, seizures.
Painful muscle spasms in the calf or foot during
periods of inactivity.
Paresthesias followed by numbness that may
affect the lips, nose, and ears in addition to the
limbs.
Positive Trousseau’s and Chvostek’s signs
Hyperactive deep tendon reflexes
Anxiety, irritability
Assessment
Gastrointestinal
Incrased gastrc motility; hypeactive
bowel sounds
Abdominal cramping, diarrhea
Intervention
Monitor cardiovascular, respiratory, neuromuscular, renal,
and gastrointestinal status; place the client on a cardiac
monitor.
Administer calcium supplements orally or calcium
intravenously.
Administered medication that increase calcium absorption.
Provide quite environment to reduce environmental stimuli.
Initiate seizure precautions.
Move the carefully, and monitor for signs of a fracture.
Keep 10% calcium gluconate available for treatment of
acute calcium deficit.
Instruct the client to consume foods high in calcium.
HYPERCALCEMIA
Serum calcium level that exceeds 10.0 md/dL
Causes
Increased calcium absorption
Excssive oral intake of calcium
Excessive oral intake of vitamin D
Neuromuscular
Twiches, paresthesias
Positive trousseu’s and Chvostek’s signs
Hyperreflexia
Tetany, seizures
Central nervous system
Irritability
Confusion
Intervention
Administer magnesium sulfate by the IV
route in severe cases; monitor serum
magnesium levels frequently.
Initiate seizure precaution
Monitor for reduce deep tendon reflexes,
suggesting hypermagnesemia, during the
administration of magnesium.
Oral preparations of magnesium may cause
diarrhea and increase magnesium loss
Instruct the client to increase the intake of
foods that contain magnesium.
HYPERMAGNESEMIA
Serum magnesium level that exceeds 2.6
mg/dL
Causes
Increased magnesium intake
Magnesium containing antacids and laxatives
Excessive administration of magnesium
intravenously
Decreased renal excretion of magnesium as a
result of renal insufficiency
Assessment
Cardiovascular
Bradycardia, dysrhythmias
Hypotension
Electrocardiographic changes: Prolong PR interval,
widened QRS complexes
Respiratory: respiratory insufficiency when
the skeletal muscles of respiration are
involved
Neuromuscular
Diminished or absent deep tendon reflexes
Skeletal muscle weakness
Central nervous system: drowsiness and
lethargy that progresses to coma.
Intervention
Acid – Base Balance
blood test that is performed using blood
from an artery. It involves puncturing an
artery with a thin needle and syringe and
drawing a small volume of blood. The
most common puncture site is the
radial artery at the wrist, but sometimes
the femoral artery in the groin or other
sites are used
PH
pH usually stays slightly alkaline
between 7.35 to 7.45
pH below 7.35 is abnormally acidic