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Fluids and Electrolyte

S.Y. 2009 – 2010


San Juan de Dios Educational
Foundation Inc.
Third- Spacing
 Is the accumulation and sequestration of trapped
intracellular fluid in an actual or potential body
space as a result of disease or injury.
 Trapped fluids represent a volume loss and is
unavailable for normal physiological process.
 Fluid may be trapped in body space such as the
pericardial, pleural, peritoneal, or joint cavities,
the bowel, or the abdomen, or within soft tissues
after trauma or burns.
 Assessing the intravascular fluid loss caused by
third-spacing is difficult. The loss may not be
reflected in weight changes or intake and output
records and may not become apparent until after
organ malfunction occurs.
Body Fluids Excretion
 Skin
 Water is lost through skin in the amount f
about 400ml/day
 Water lost by perspiration varies
according to the temperature of the
environment and of the body, but the
average amount of loss by perspiration
alone is 100ml/day.
 Water lost through the skin is called
insensible loss
Body Fluids Excretion
 Lungs
 Water is lost from the lungs through expired air
that s saturated with water vapor.
 The amount of water lost from the lungs varies
with the rate and the depth of respiration.
 The average amount of water lost from the lungs
is about 350 ml/day
Body Fluids Excretion
 Gastrointestinal Tract
 Large quantities of water are secreted into the
gastrointestinal tract, but almost all this fluid is
reabsorbed.
 A large volume of electrolyte containing liquids
moves into the gastrointestinal tract and then
returns again into the extracellular fluids.
 150 ml/ day – feces, equal to the amount of
water gained through oxidation of foods.
Body Fluids Excretion
 Kidneys
 Play major role in regulating fluids and
electrolyte balance.
 Normal kidneys can adjust the amount of
water and electrolytes leaving the body.
 The quantity of fluids excreted by the kidneys
is determined by the amount of waste and
solutes excreted.
 Urine output – 1500ml/day
Electrolyte Balance
 Ions – electrically charged particles
Two kinds of Ions
(+) Cation
 Calcium
 Magnesium
 Potassium
 Sodium
(-) Anions
 Bicarbonate
 Chloride
 Phosphorus
 Neural electrical charge called
electroneutrality
Calcium (Ca)
 A major cation
 Found in teeth and bones and unfairly equal
concentrations in intracellular fluid (ICF) and
extra cellular fluids (ECF)
 Also found in cell membranes, where it help cells
adhere to one another and maintain their shapes.
 Acts as an enzyme activator within cells (muscle
must have Ca to contract)
 Aids coagulation
 Affects cell membrane permeability and firing
level
Magnesium (Mg)
 A leading ICF cation
 Contributes to many enzymatic and
metabolic processes, particularly protein
synthesis.
 Modifies nerve impulse transmission and
skeletal muscle response (unbalanced Mg
concentration dramatically affect
neuromuscular process)
Potassium (K)
 Main ICF cation
 Regulates cell excitability
 Permeates cell membranes, thereby
affecting the cell’s electrical status
 Helps to control ICF osmolality and
consequently, ICF osmotic pressure.
Sodium (Na)
 Main ECF cation
 Helps govern normal ECF osmolality
(a shift in Na concentration triggers a
fuild volume change to restore
normal solute and water ration)
 Helps maintain acid-base balance
 Influences water distribution (with
chloride)
Chloride (Cl)
 Main ECF anion
 Helps maintain normal ECF osmolality
 Affects body pH
 Plays a vital role in maintaining acid-
base balance; combines with hydrogen
ions to produce hydrochloric acid.
Bicarbonate (HCO3-)
 Present in ECF
 Regulates acid – base balance
Phosphorus (P)
 Main ICF anion
 Promotes energy storage and
carbohydrate, protein, and fat
metabolism.
 Acts as a hydrogen buffer
Ca
Ca
P K Ca
Na

Ca Mg
Cl
HCO3 -
Measurement of electrolyte
Milli equivalents (meq) per liter)
 a measure of chemical activity

 being equivalent to the


electrochemical activity of 1mg of
hydrogen
 in a solution, cations and anions are

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

< 8.9 mg/dl Hypocalcemia Acute


pancreatiti
>10.1 md/dl
Hypercalcemi s
a Hyperparat
hyroidism
Electrolyt Result Implications Common
e Causes
Calcium, 4.5 to Normal
ionized 5.1
mg/dl
< 4.5 Hypochloremi Prolonged
mg/dl a vomiting
> 5.1 Hyperchloremi Hypernatre
mg/dl a mia
Electrolyte Result Implications Common
Causes

Chloride 96 to Normal
106
mEq/L

< 96 Hypochloremi Prolonged


mEq/L a vomiting
> 106 Hypernatre
mEq/L Hyperchloremi mia
a
Electrolyte Result Implications Common
Causes

Magnesium1.5 to Normal
2.5
mEq/L

< 1.5 Hypomagnese Malnutrition


mEq/L mia
> 2.5 Hypermagnes Renal
mEq/L emia Failure
ElectrolyteResult Implication Common
s Causes
Magnesium2.5 to 4.5 Normal
mg/dl1.8
to 2.6
mEq/L

< 2.5 Hypophos Diabetic


mg/dl or phatemia Ketoacidosis
1.8 mEq/L
> 4.5 Hyper Renal
mg/dl 2.6 insufficiency
mEq/L
Maintaining Fluids and
Electrolytes Balance
 Concentration and composition of fluids
must nearly constant.
 Substance deficient either fluids or
electrolytes must be replaced.
 Excess of fluids or electrolytes, therapy
is directed towards assisting the body
to eliminate the excess.
Maintaining Fluids and
Electrolytes Balance
 The kidney plays a major role in controlling all
types of balance in fluids and electrolytes.
 Adrenal gland, through excretion of aldosterone,
also aid in controlling extracellular fluids volume by
regulating the amount of sodium reabsorbed by the
kidneys.
 Antidiuretic hormone from the pituitary gland
regulates the osmotic pressure of extracellular
fluids by regulating the amount of water
reabsorbed by the kidney.
Types of Fluid Volume
Deficit
 Isotonic Dehydration
 Water and dissolved electrolytes are lost
in equal proportions.
 Known as hypovolemia, isotonic
dehydration is the most common type of
dehydration.
 Isotonic dehydration results in decreased
circulating blood volume and inadequate
tissue perfusion
Types of Fluid Volume
Deficit
 Hypertonic dehydration
 Water loss exceeds electrolyte loss.
 Fluids moves from the intracellular
compartment into the plasma and
interstitial fluid spaces, causing cellular
dehydration and shrinkage.
Types of Fluid Volume
Deficit
 Hypotonic Dehydration
 Electrolyte loss exceeds water loss.
 The clinical problems that occurs result from
fluids shifts between compartments, causing a
decrease in plasma volume.
 Fluid moves from the plasma and interstitial
fluids spaces into the cells, causing a plasma
volume deficit and causing the cells to swell.
Causes of Fluids volumes
deficits
 Isotonic Dehydration
 Inadequate intake of fluids and solutes
 Fluids shifts between compartment
 Excessive losses of isotonic body fluids
 Hypertonic Dehydration
 excessive perspiration, hyperventilation,
ketoacidosis, prolonged fevers, diarrhea,
early-stage renal failures, and diabetes
insipidus
Types of Fluid Volume
Deficit
 Hypotonic Dehydration
 Chronic Illness
 Excessive fluid replacement
 Renal Failure
 Chronic Malnutrition
Assessment
 Cardiovascular
 Thready, increased pulse rate
 Decreased blood pressure and
orthostatic hypotension
 Flats neck and hand veins in dependent
positions
 Diminished peripheral pulses.
 Respiratory
 Increased rate and depth of respirations
Assessment
 Neuromuscular
 Decreased CNS activity, from lethargy to coma
 Fever
 Renal
 Decreased urinary output
 Increased urinary specific gravity
 Integumentary
 Dry skin
 Poor turgor
 Dry mouth
Assessment
 Gastrointestinal
 Decreased motility and diminished bowel sounds
 Constipation
 Thirst
 Decreased body weight
 Hypotonic dehydration: skeletal muscle
weakness
 Hypertonic dehydration: Hyperactive deep
tendon reflexes and pitting edema.
Laboratory Findings
 Increased serum osmolality
 Increased hematocrit
 Increased blood urea nitrogen (BUN)
level
 Increased serum sodium level.
Goal
 Restore fluids volume, replace
electrolytes as needed, and eliminate
the cause of the fluids volume deficit.
Intervention
 Monitor
 Prevent further fluids losses and increase
fluids compartment volume to normal
ranges.
 Provide oral rehydration therapy if possible
and IVF if the dehydration severe
 Monitor intake and out put
 Isotonic = isotonic, hypotonic = hyperonic,
hypertonic = hypotoninc
 Administered medication and oxygen as
prescribed.
 Monitor electrolyte values
Nursing diagnosis: fluid volume deficit due to insufficient fluid
intake, vomiting, diarrhea, hemorrhage or third space fluid loss
(ascites, burns)

Planning: client's fluid balance will be restored as evidenced by


vital signs within normal range, return to baseline body weight,
equal intake and output, urine output of greater than 600ml/
day, dim turgos at 2 seconds, or less and moist mucous
membranes

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.

d. Daily weight monitoring, a loss of 1kg is equivalent to 1 liters, a


3.6 kg. weight loss equals approximately 3.L liters which is
indicates of a moderate fluid volume deficit

e. The nurse should apply lotion to the gleim to pressure them


integrity. The client’s position should be changed way 2 hours,
oral care should be given every 2 hours with a nonalcoholic-
based solution. Lips should be moistened frequently.

f. Serum sodium, BUN, glucose and hematocrit levels should be


closely monitored to determine the serum osmolality.

g. g) Clinical manifestation of fluid overload include dyspnea,


crackles and jugular vein engorgement.
Types
 Isotonic overhydration
 Know as hypervolemia: excessive fluids
in the extracellular fluid compartments.
 ECF is expanded, and fluids doesn’t shift
between the extracellular and
intracellular compartment.
 Cause circulatory overload and
interstitial edema. Severe: congestive
heart failure and pulmonary edema.
Types
 Hypertonic overhydration
 Occurrence is rare: caused by excessive
sodium intake.
 Fluids is drawn from the intracellular
fluid compartment; the extracellular
fluids volume expands, and the
intracellular fluids volume contract.
Types
 Hypotonic overhydration
 Know as water intoxication
 Excessive fluids moves into the
intracellular space, and all body fluids
compartments expands.
 Electrolyte imbalance occur as a result
of dilution
Causes
 Isotonic overhydration
 Inadequately controlled IV therapy
 Renal failure
 Long-term corticosteroid therapy
 Hypertonic overhydration
 Excessive ingestion of sodium
 Rapid infusion of hypertonic saline
 Excessive sodium bicarbonate therapy.
Causes
 Hypotonic overhydration
 Early renal failure
 Congestive heart failure
 Syndrome of inappropriate antidiuretic
hormone secretion
 Inadequately control of IV
 Replacement of isotonic fluid loss with
hypotonic fluids
 Irrigation of wounds and body cavities
with hypotonic fluids.
Pathophysiology

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)

Serum osmolality falls less Serum osmolality falls more


Than 280 mOsm/Kg Than 300 mOsm/Kg

Thirst diminishes, leading to Thirst increase, leading to


Water intake Water intake

Antidiuretic hormone (ADH)


ADH release increase
Release is suppressed

Renal water excretion Renal water excretion


increases diminishes

Serum osmolality normalizes


Hyponatremia
 Serum sodium level lower than 135
mEq/L
 Sodium imbalances usually are
associated with fluid volume
imbalances.
Causes
 Increase sodium excretion
 Excessive diaphoresis
 Diuretics
 Vomiting
 Diarrhea
 Wound drainage, especially gastrointestinal
 Renal disease
 Decreased secretion of aldosterone
 Inadequate sodium intake
 Nothing by mouth
 Low salt diet
Causes
 Dilution of serum sodium
 Excessive ingestion of hypotonic fluids
or irrigation with hypotonic fluids
 Renal failure
 Freshwater drowning
 Syndrome of inappropriate antidiuretic
hormone secretion
 Hyperglycemia
 Congestive heart failure
Classification
 Hypovolemic hyponatremia
 Both sodium and water levels decreased in the
extracelluar area but sodium loss is greater
than water loss.
 Causes may be nonrenal or renal.
 Nonrenal
 Vomiting

 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

 Decreased calcium excretion


 Renal failure
 Use of thiazide diuretics
Causes
 Increased bone resorption of calcium
 Hyperparathyrodism
 Hyperthyroidism
 Maligancy
 Immobility
 Use of glucocorticoids
 Hemoconcentration
 Dehydration
 Use of lithium
 Adrenal insufficiency
Assessment
 Cardiovascular
 Increased heart rate in the early phase,
bradycardia that can lead to cardiac arrest
in late phase.
 Increased blood pressure
 Bounding, full peripheral pulses
 Electrocardiographic changes: shortened ST
segments, widened T wave
 Respiratory
 Ineffective respiratory movements as a
result of profound skeletal muscle
weakness.
Assessment
 Neuromuscular
 Profound muscle weakness
 Diminished or absent deep tendon reflexes
 Disorientation, lethargy, coma
 Renal
 Increased urinary output leading to dehydration
 Formation of renal calculi
 Gastrointestinal
 Decreased motility and hypoactive bowel sounds
 Anorexia, nausea, abdominal distention, constipation.
Intervention
 Discontinue IV infusion of solution containing calcium and
oral medication containing calcium or vitamin D
 Administered medications as prescribed that inhibit calcium
resorption from the bone, such as phosphorus, calcitonin,
bisphosphonates, and prostaglandin synthesis inhibitors
 Prepare the client with sever hypercalcemia for dialysis if
medications fail to reduce the serum calcium level.
 Move the client carefully and monitor for signs of a fracture.
 Monitor for flank or abdominal pain, and strain the urine to
check for the presence of urinary stones.
 Instruct the client to avoid foods high in calcium.
HYPOMAGNESEMIA
 Serum magnesium level lower than 1.6 mg/dL
 Causes
 Insufficient magnesium intake
 Malnutrition and starvation
 Vomiting and diarrhea
 Malabsorption syndrome
 Celiac disease
 Crohn’s disease
 Increase magnesium secretion
 Medication such as diuretics
 Chronic alcoholism
 Intracellular movement of magnesium
 Hyperglycemia
 Insulin administration
 sepsis
Assessment
 Cardiovascular
 Electrocardiographic changes: Tall T waves,
depressed ST segments
 Tachycardia
 Hypertension
 Gastrointestinal
 Decreased motility, decreased bowel sound
 Anorexia, nausea, abdominal distention
 Respiratory: Shallow respiration
Assessment

 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

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