Condition
Hyponatremia (<135mEq/L)
- Fluid shifts from extracellular to
intracellular compartments
- Inability for cells to depolarize and
repolarize
Causes
- Excess retention of water
- Inadequate Na intake
- Loss of Na rich fluids that
are replaced with water
- Vomiting
- Diarrhea
- GI suctioning
- Adrenal insufficiency
- Loss of fluids from wounds
- Excessive use if dextrose 5%
IV fluids (free water being
created when glucose is
metabolized)
- At risk:
- Athletes, heavy labor in
hot temps, elderly in hot
weather, heavy perspiration,
vomiting, diarrhea
- Dillutional hyponatremia d/t
inappropriate IV fluid admin
Hypernatremia (>145mEq/L)
Deficit of water in relation to Na levels
- Cushing’s (aldosterone
excess) causing Na retention
- Diabetes Insipidus (excess
fluid loss)
- Admin of IV fluids too
quickly causes fluids to move
into brain cells too quickly
causing cerebral edema
(cellular dysfunction and
increased intracranial pressure
resulting in seizures and
permanent brain damage)
Signs and Symptoms
- Early:
- Muscle cramps
- Weakness
- Abdominal cramps
- Fatigue
- Anorexia
- N/V
- Diarrhea
- Anorexia
- Neurologic:
- Na drops <120mEq/L
- Late:
- Lethargy, HA, confusion,
depression, dulled sensorium,
personality changes, apprehension,
seizure and coma, hyperreflexia,
muscle twitching, tremors,
hypotension, shock
- Serum <115mEq/L or corrected
too rapidly—CNS demyelination
(flaccid paralysis, dysarthria, and
dysphagia)
Labs/Diagnostics
- Decreased serum osmolality,
hematocrit, BUN
- 24hr urine specimen
(elevates Na excretion)
- Early:
- Thirst, oliguria, weight gain,
increased specific gravity, dry skin
and mucous membranes, decreased
skin turgor, low-grade fever,
furrowed tongue, HA, restlessness
- Late:
- Third spacing (peripheral and
pulmonary edema), tachycardia,
hypotension (and postural),
vascular collapse
- Neurologic:
- Altered mental status,
neuromuscular irritability, coma &
seizures
- Health Hx: duration of
manifestations, precipitation
factors (water deprivation,
perspiration, elevated temp,
rapid breathing, diarrhea,
excessive Na intake, diabetes
Insipidus); current meds,
perception of thirst
- Physical assessment: VS,
mucous membranes, mental
status, LOC
- Increase in serum osmolality
(>295mOsm/kg), hematocrit,
and BUN, elevated serum Na,
possible increase in specific
gravity (d/t water conserving
effects of ADH)
Nursing Considerations
- Health Hx for cause; chronic
diseases (HF, renal failure, liver
cirrhosis, endocrine disorders);
current meds
- Physical assessment: LOC, mental
status, VS, orthostatic BP, peripheral
pulses, presence of edema or weight
gain
- IV fluids only enough to correct
problem, not return serum level to
135mEq/L; give processed foods if
not NPO
- I&O of all fluids (IV fluids and
fluids used to dilute meds, oral)
- Weigh pt daily
- Assess pt muscle strength and tone,
and deep tendon reflexes
- Explain fluid restriction
- Offer ice chips for dry mouth
- Freq. oral care
- Sugarless gum to reduce thirst
sensation
- Education:
- Early s/s and when to report
- Types of fluids and foods to
replace Na orally
- Replace fluids slowly over 48 to
72hrs (oral is preferred route)
- Lower Na at a rate not to exceed
0.5-1mEq/hr
- Assess mental status and changes
- Injury prevention:
- Monitor and maintain fluid
replacement as ordered
- Serum Na and osmolality levels
- Monitor neurological function
- Monitor for cerebral bleeding
(HA, N/V, HTN, bradycardia)
- Keep bed in lowest position
(side rails up)
- Keep an airway at BS
- Decreased mental status: orient
patient regularly (clock, calendar,
familiar objects within view)
- Promote family involvement to
reduce anxiety
- Education:
- Importance of responding to
thirst and consume adequate fluids;
low Na diet
- Early s/s and when to report to
HCP
- Low Na diet as ordered
Treatment
- IV Fluids:
- Isotonic LR or NS when
both Na and water are lost
- 3% or 5% NS used
cautiously in clients with Na
levels <115mEq/L
(overtreatment can lead to
excessive expansion of
intravascular (plasma)
compartment, fluid overload,
and HTN)
- Loop diuretics to promote
isotonic diuresis and fluid
volume loss without
hyponatremia
- Thiazide diuretics are
avoided because they cause a
greater sodium loss in
relation to water loss
- IV fluids:
- 0.45% NS
- D5W
- Diuretics to promote Na
excretion
Hypokalemia (<3.5mEq/L)
- Affects the transmission of nerve
impulses by interfering with the
contraction of smooth, skeletal, and
cardiac muscle.
- Affects carbohydrate metabolism.
Hypokalemia suppresses insulin
secretion and the synthesis of glycogen
in skeletal muscle and in the liver
- Interferes with cardiac contractility
and transmission of cardiac impulses
which maintain normal cardiac rhythm
(leads to dysrhythmias)—leading to
decreased CO
- Slows peristalsis
- Affects muscles of UE before LE and
trunk
- Kidneys lose ability to concentrate
urine (kidney tubules less responsive to
ADH)
Hyperkalemia (>5.5mEq/L)
- Kidneys:
- Excess K loss d/t Kwasting diuretics,
corticosteroids, amphotericin
B, large doses of antibiotics
-Hyperaldosteronism
- Stress, trauma, metabolic
acidosis, and Mg deficiency
(hypomagnesemia promotes
K excretion from kidneys—
treat first)
- GI:
- Severe vomiting, GI
suctioning, diarrhea, or
ileostomy drainage
- Anorexia nervosa or
alcoholism (vomiting,
diarrhea, or laxative/diuretic
use)
- Transcellular shift:
- beta-2-bronchodilators,
diabetic ketoacidosis (insulin
increases K movement into
cells)
- Cushing’s
- Elevated serum insulin
levels
- Increased serum pH (K-H
exchange)
- ECG:
- Flattened or inverted T waves
- U waves
- Depressed ST segment
- Neuro:
- Confusion, depression,
lethargy
- Respiratory: arrest
- Cardio:
- Decreased CO and
dysrhythmias (vent tachy and
hemodynamic changes
- Irregular pulse
- Postural HTN
- Increased risk of digitalis
toxivity
- Cardiac arrest
GU:
- Polyuria; polydipsia
- Diluted urine
- GI:
- N/V/D
- Anorexia
- Decreased bowel sounds/ileus
Musculoskeletal:
- Muscle weakness and leg
cramps, poor muscle tone,
paresthesia, paralysis
- Serum K in pts at risk for or
Tx for hypoK
- ABGs:
- Determine acid-base status
- Assess for increase in pH
or alkalosis
- Serum creatinine and BUN to
evaluate potential cause of
hypoK
- ECG for effects of cardiac
conduction
- Education:
- Food high in K
- Impact of K-wasting diuretics on
K levels
- Need for regular serum K levels
- Health Hx:
- Current s/s: anorexia, N/V, abd
discomfort, muscle weakness, or
cramping
- Duration of manifestations and
precipitating factors (diuretic use,
prolonged vomiting, or diarrhea)
- Chronic illnesses (DM,
hyperaldosteronism, Cushing’s)
- Current meds
- Physical assessment:
- Mental status
- Activity intolerance: monitor VS
including orthostatic BP; RR, depth,
and effort; HR and rhythm; BP at
rest and w/ activity
- Apical and periph pulse
- Bowel sounds, abd distention
- Muscle strength and tone
- Monitor I&O accurately
- Untreated renal failure
- Adrenal insufficiency
(decreased release of
aldosterone)
- K-sparing diuretics
- Some NSAIDs
- Rapid infusion of K
- Transfusion of older blood
from blood bank
- Metabolic acidosis
- Severe tissue trauma (cells
release K)
- Fever, sepsis, surgery
- Chemo
- Starvation
- Decreased urinary excretion
(chronic renal failure—output
<30mL/hr)
- Inappropriate K supps
- ECG:
- Prolonged depolarization
- Peaked or narrow T waves
- Depressed ST seg
- Prolonged PR interval
- Widening of QRS complex
- Loss of P wave
- Cardio:
- Slowing of HR leading to heart
block
- Development of ventricular
dysrhythmias
- Cardiac arrest
- Neuro:
- HA, restlessness, seizure,
coma
- Early:
- Diarrhea, colic, anxiety,
paresthesias, irritability, muscle
tremors, twitching, cramping, abd
distention
- Late:
- Muscle weakness, flaccid
paralysis, bradycardia, irreg. HR
- Serum K to show levels
>5.0mEq/L
- Serum Ca (low in clients
with hyperK)
- Serum Na (low in pts with
hyperK)
- ABGs to determine if
acidosis is present (also
increased RR, BP, and HR)
- ECG to evaluate effects of
hyperK on cardiac conduction
- Monitor for at risk pts:
- K sparing diuretics, supps, salt
substitutes, anabolic steroids
- Education:
- Teach to read food label
- Do not change dose of K supps
unless ordered
- Maintain adequate fluid inake to
maintain renal function and
eliminate K from body
- Health Hx:
- Current s/s: numbness and
tingling, N/V, abd cramping, muscle
weakness, and palpitations
- Duration and precipitating
factors (use of salt subs, K-sparing
diuretics, or reduced urine output
- Chronic illnesses (renal failure
or endocrine disorders)
- Current meds
- Physical assessment:
- Apical and peripheral pulses
- Bowel sounds
- Muscle strength up UE & LE
- ECG pattern (progressive
changes from peaked T wave to loss
of P wave and widening QRS
- IV KCl:
- Dose according to daily
maintainace requirement,
replacement of ongoing
losses, and additional K to
correct deficit
- Do not IV push
- Infuse at a rate not to
exceed 10mEq/hr through
peripheral access; 20mEq/L
may be administered through
central venous access over
1hr; severe admin 40-60mEq
in 1000mL of 0.45%NS at a
rate not to exceed 40mEq/hr.
- Must dilute
- Assess for signs of
infiltration
- Use infusion pump
- Continuous cardiac
monitoring if high doses are
administered
-Oral Supplements:
- Readily absorbed in GI
tract (50-100mEq daily)
- Give KCl and dilute or
dissolve in juice or water
- Diet: bananas, oranges,
avocados, spinach, potatoes,
tomatoes, meat, seafood,
milk, yogurt
- Reduce IV and oral intake
- Diuretics: K-wasting to
enhance renal excretion
(Lasix)
- Insulin, hypertonic
dextrose, NaHCO3
- Emergency Tx for
moderate to severe hyperK
- Insulin promotes K
movement into cell
- Glucose prevents
hypoglycemia while giving
insulin
- NaHCO3 elevates serum
pH—K is moved into cell in
exchange for H ions
- Monitor ECG pattern
closely
- Ca Gluconate/Chloride:
- Temp emergency to
counteract toxic effects of K
on myocardial conduction
and function
- Monitor ECG for
bradycardia
- Monitor for pts on
digitalis—increases
complex indicate increased risk of
dysrhythmias and cardiac arrest
- Monitor skeletal muscle strength
and tone; RR and depth; assess lung
sounds
Hypocalcemia (<8.5mg/dL or ionized
<4.25mg/dL)
Book says <9.0 serum
- Extracellular calcium acts to stabilize
neuromuscular cell membranes. When
there is not enough calcium,
neuromuscular irritability occurs. The
threshold of excitation of sensory nerve
fibers is lowered, leading to
paresthesias. The nervous system
becomes more excitable, and muscle
spasms develop.
- In the heart, the change in the cell
membrane can lead to dysrhythmias
such as ventricular tachycardia (VT)
and cardiac arrest. The contractility of
cardiac muscle fibers decreases,
causing a drop in cardiac output
Hypercalcemia (>10mg/dL or ionized
>5.25mg/dL)
Book says >11 serum
- Hypercalcemia decreases
neuromuscular excitability, leading to
muscle weakness and depressed deep
tendon reflexes. It also causes a
decrease in gastrointestinal motility.
- In the heart, calcium strengthens
contractions and reduces the heart rate.
With hypercalcemia, the conduction
- At risk:
- Removal of parathyroid
gland (thyroidectomy)
- Reduced intake of milk
products
- Lactose intolerance
- Alcoholism
- Decreased sun exp
- Inactivity or immobility
- Postmenopausal
- Hypomagnesemia
- Hyperphosphatemia (P-Ca
exchange in kidneys)
- Hypoalbuminemia
- Alkalosis
- Malabsorption, inadequate
vit D
- Massive transfusions of
citrated blood (citrate
competes with Ca)
- Loop diuretics (Lasix)
- Anticonvulsants (Dilantin)
- Phosphates
- Mg lowering drugs
- Pancreatitis (FFA’s
combine with Ca)
- Airway obstruction
- Respiratory arrest from
laryngospasms
- Vent dysrhythmias
- Prolonged QT interval
- Cardiac arrest
- Dysrhythmias, bradycardia,
hypotension
- HF
- Convulsions
- Numbness and tingling of hands
and fingers
- Hyperactive reflexes around
mouth
- Laryngeal spasms (severe
hypoCa can result in
asphyxiation), bronchospasms
- Confusion, hallucinations
- Mental changes: anxiety,
depression, psychosis
- Pathologic Fx
-
- Serum Ca to determin level
- Serum albumin: albumin
levels can affect serum Ca
(when low serum Ca is low)
- Serum Mg: serum Ca—often
associated with Mg
- Serum phosphate:
hypophosphatemia leads to
hypoCa
- Parathyroid hormone to
identify possible
hyperparathyroidism
- ECG to evaluate effects of
hypoCa on cardiac conduction
- Hyperparathyroidism
- Bone malignancies
- Thaizides: cause renal tubule
dysfunction and prevent Ca
excretion
- Prolonged immobility (bed
rest)—mobilizaton of Ca from
bone
- Lack of weight bearing
- Chronic renal failure
- Adrenal insufficiency
- Hyperthyroidism
- Excessive Vit D & A
- Ca containing antacids
- Excess milk products
- Musculoskeletal:
- Tetany
- Muscle spasms of face and
extremities
- Muscle weakness and fatigue
- Respiratory:
- Bronchial muscle spasms
leading to asthma attacks
- GI:
- Visceral muscle spasms (abd
pain)
- Anorexia
- N/V, constipation
- Cardio:
- Hypotension
- Bradycardia
- Serum Ca to determine level
- Serum parathyroid hormone
level to identify or rule out
hyperparathyroidism
- ECG to determine changes
such as shortened QT interval,
shortened and depressed ST
segment, and widened T wave;
determine bradycardia or heart
block
- Bone density scans to
monitor bone resorption and
effects of Tx on mineralization
of bone
- Education:
- Importance of maintaining
adequate calcium intake through diet
and calcium supplements
- Weight bearing exercise and
bone density relationship
- Health Hx:
- Current manifestations,
including numbness and tingling
around the mouth, hands, and feet;
abdominal pain; and shortness of
breath
- Acute and chronic conditions
such as pancreatitis and liver or
kidney disease
- Current meds
- Physical assessment:
- Muscle spasms
- Deep tendon reflexes
- Chvostek and Trousseau signs
- VS and apical pulse
- Presence of seizures
- Reduce risk for injury d/t muscle
spasms and seizures
- Monitor airway and respiratory
status, HR and rhythm, BP,
peripheral pulses
- Bed in low position, raise side
rails, keep airway at BS
- Monitor Ca levels 1-2days after
thyroid surgery
- Promote mobility and early
ambulation
- Encourage intake of cranberry or
prune juice to inhibit Ca renal stone
formation
- Weight bearing exercises
- Fluid intak of 3-4 quarts/day
- Limit intake of milk
- Limit intake of Ca containing
antacids and sups
- Health Hx:
- Current manifestations,
including weakness, fatigue,
abdominal discomfort, nausea,
vomiting, increased urination, thirst,
and changes in memory or thinking;
cardiotonic effects (toxicity
and dysrhythmias)
- Na Polystyene sulfonate
and sorbitol:
- Moderate to severe
hyperK
- Exchanges Na or Ca for
K in large intestine
- May admin orally, NGT
or retention enema
- Restrict Na intake
- IV:
- CaCl, Ca gluconate (can
cause necrosis and sloughing
off of tissue; rapid admin
can cause bradycardia and
cardiac arrest
- Oral:
- Ca Carbonate
- Ca Gluconae
- Ca Lactate
- Combined with Vit D to
increase GI absorption
- Diet rich in Ca
- IV fluids and furosemide
(Lasix) to promote
elimination of excess Ca
- Cacitonin to rapidly lower
serum Ca
- Biphosphonates to inhibit
bone resorption
- IV Na phosphate or K
phosphate to rapidly remove
excess Ca
- IV plicamycin
(Mithramycin) to inhibit
bone resorption
- Glucocorticoids that
compete with Vit D and
inhibit bone resorption
system of the heart is impacted,
causing bradycardia and heart blocks.
The ability of the kidneys to
concentrate urine is impacted by
elevated calcium levels, causing excess
sodium and water loss, as well as
increased thirst
Hypomagnesemia (>2.6mg/dL)
Book says >3.0
- Magnesium exerts a sedative effect
on the neuromuscular junction,
decreasing acetylcholine release. This
electrolyte is an essential ion for
neuromuscular transmission and
cardiovascular function. The effects of
magnesium are affected by potassium
and calcium
- Patho includes effects of hypoK and
hypoCa
- Increased neuromuscular excitability
- Increased risk for cardiac
dysrhythmias
- Dysrhythmias
- ECG changes
- HTN
- Cardiac arrest (hyperCa crisis
or acute increase in serum Ca)
- Neuro:
- Seizure and coma
- Numbness and tingling around
mouth, hands, and feet
- Hyperactive deep tendon
reflexes
- Postive Chvostek and
Trousseau sign
- Confusion, lethargy,
behavior/personality changes
- GU: polyuria and increased
thirst; kidney stones
- Deficient Mg intake
- Excessive excretion by
kidneys (loop of Henley)
- Intra and extracellular shifts
- Risks:
- Loss of GI fluids
(diarrhea, ileostomy, intestinal
fistula, malabsorption in small
intestine)
- Alcoholism (deficient
nutrient intake, increased GI
losses, impaired absorption,
increased renal excretion)
- Protein-calorie
malnutrition or starvation,
diabetic ketoacidosis, kidney
disease, diuretics (loops and
thiazides), aminoglycosides,
amphotericin B, cyclosporine,
rapid admin of citrated blood
- Osmotic diuresis
- Loop diuretics
- Neuromuscular:
- Tremors
- Hyperreactve reflexes
- + Chvostek & Trousseau sign
- Tetany
- Paresthesias
- Nystagmus
- Seizures
- CNS:
- Confusion
- Apathy
- Depression
- Agitation
- Hallucinations
- Psychoses
- Cardio:
- Tachycardia (SVT)
- Ventricular dysrhythmias
- HTN
- Sudden death
- Coronary artery spasms
- Paresthesia
- Severe deficiency: confusion,
lethargy, seizures, hyperreflexia of
deep tendon reflexes, tetany,
hallucinations, N/V, hypertension,
cardiac dysrhythmias, and death
- Serum Mg levels
- ECG:
- Prolonged PR intervals
- Widened QRS complex
- Depressed ST segment
- T wave inversion
and duration
- Risk factors such as excessive
intake of milk or calcium products,
prolonged immobility, malignancy,
renal failure, or endocrine disorders
- Current meds
- Physical assessment:
- Mental status and LOC
- VS and apical pulse
- Bowel sounds
- Muscle strength of UE & LE
- Deep tendon reflexes
- Reduce risk for injury:
- At risk d/t mental status changes,
reduced muscle strength, and Ca loss
from bone
- Use caution when turning,
repositioning, and ambulating
(pathologic fractures)
- Fluid volume overload (ensure
adequate kidney fx):
- I&O; assess VS, RR, and heart
sounds; pt in Fowler or semi-Fowler
position
- Auscultate breath sounds for
crackles and rhonchi, and heart
sounds for development of an S3
heart sound with vital signs to detect
fluid overload at earliest onset
- IV NS admin to pts with
severe hyperCa to restore
vascular volue and promote
renal excretion of Ca—
monitor for signs of fluid
overload
- IV or IM admin
- Before admin, assess serum Mg
levels and renal function
- Monitor neurologic status and
deep tendon reflexes during therapy
- Monitor I&O
- Admin IM doses deep into
ventral or dorsal gluteal sites
- Provide IV medication via IVPB
or by continuous infusion
- Education:
- Promote adequate Mg intake
through diet
- Monitor serum Mg levels
- Reduce risk for injury:
- Monitor serum electrolytes,
including Mg, K, and Ca
- Monitoring GI function,
including BS and abd distention
- Initiate cardiac monitoring
- Reporting and treating ECG
changes and dysrhythmias
- Monitor for digitalis toxicity
- Assessing deep tendon reflexes
during Mg infusions and before each
IM dose
- Initiate seizure precautions
- IV or IM Mg sulfate
(assess for overcorrection)
- Increased food intake
(green leafy veggies,
seafood, milk, bananas,
citrus fruits, chocolate)
- Oral Mg supps (can cause
diarrhea)
- For seizures: 1-2g IV over
2-4min
Hypermagnesemia (<1.6mg/dL)
Book says <1.8
- HyperMg interferes with
neuromuscular transmission and
depresses CNS
- Affects CV system causing
hypotension and bradydysrhythias
Hypophosphatemia (<2.5mg/dL)
- Decline in renal function or
renal failure
- Adrenal insufficiency
- OTC Mg laxatives or other
containing products
- Slight elevation:
- N/V
- Hypotension
- Facial flushing
- Sweating
- Feeling of warmth
- Moderate elevation:
- Weakness
- Mental health changes:
lethargy, drowsiness
- Weak or absent deep tendon
reflexes (usually lost at 8mg/dL)
- Marked elevation
- Resp. depression (failure at
>10mg/dL)
- Coma
- Bradycardia
- Heart block
- Cardiac arrest (>15mg/dL)
- Serum Mg levels
- ECG to evaluate
bradydysrhythmias, heart
block, and cardiac arrest
- Refeeding syndrome
- Occurs when
malnourished pts revieve
enteral or PTN
- Glucose stimulates insulin
release—promotes transport
of glucose and phosphate into
cells, reducing extracellular
phosphate levels
- Meds: IV glucose, antacids,
anabolic steroids, diuretics
- Alcoholism: affects intake
and absorption of phosphorus
(P)
- Hyperventilation and
respiratory alkalosis:
phosphate shifts out of the
ECF into ICF
- Diabetic ketoacidosis with
excessive phosphate lost in
the urine (P also acts as acid
buffer)
- Stress response
- Excessive burns
- Alcoholism
- Vit D deficiency (promotes
phosphate absorption in GI
tract)
- Bowel disorders leading to
malabsorption
- Excessive use of P-binding
antacids (Aluminum
hydroxide or Mg hydroxide)
- Elevated PTH—kidneys fail
to resorb P
Pathophysiological complications:
- CNS: reduced O2 and ATP
synthesis in the brain
- Intention tremor
- Paresthesia
- Confusion
- Irritability, apprehension
- Weakness, lack of
coordination
- Seizures & coma
- Peripheral neuropathy and
ascending motor paralysis (similar
to Guillain-Barre syndrome)
- Extrapontine myelinolysis
(manifests as movement disorders
similar to Parkinson’s)
- Hematologic: reduced O2
delivery to cells
- Platelet dysfunction
- Impaired WBC function
- Hemolytic anemia (cell
membrane dysfunction-RBC
destruction in spleen)
- Musculoskeletal: decreased ATP
causes release of creatinine
phosphokinase (CPK)
- Acute rhabdomyolysis
- Bone pain
- Joint stiffness
- Resp. Failure d/t muscle
weakness and diaphragmatic
contractile dysfunction
- Skeletal:
- Pathologic fractures d/t P
reabsorption
- Serum phosphate level
- CBC to evaluate RBC and
WBC counts
- ECG to determine presence
of cardiac dysrhythmias
- Creatinine and BUN levels to
determine renal function
- Avoid Mg containing laxatives for
constipation
- Withhold all antacids, IV solutions,
and enemas containing MG
- Prepare pt for hemodialysis or
peritoneal dialysis to remove excess
MG
- During IV admin of Ca Gluconate,
may need to support pts respiratory
function and assist w/ pacemaker
insertion to maintain an adequate
CO
- CO:
- Monitor ECG, BP
- Admin Ca gluconate as ordered
- Assess respiratory function:
- RR and breath sounds
- Reduce risk for injury:
- Assist with ADLs
- Assist with mobility if
experiencing weakness, lethargy, or
drowsiness
- Assess deep tendon reflexes
- Monitor serum P levels in pts with:
- Malnutrition
- IV glucose infusions
- PTN infusions
- Health problems being treated
with diuretics or antacids that bind
with phosphate
- Impaired mobility:
- Assess for muscle weakness,
intention tremors, paresthesias,
- Assist with ambulation
- Provide devices to assist with
ambulation
- Monitor for bone pain or joint
pain
- CO:
- Assess HR and BP
- Assess orthostatic BP changes
- Assess CRT
- Assess for respiratory weakness
- Prevent risk for injury:
- Implement safety precautions
- Monitor serum P levels
- Implement seizure precautions
as indicated
- Instruct to avoid P-binding antacids
- Immediate cessation of Mg
containing products
- Admin 10mL of 10% Ca
Gluconate to reverse
cardiovascular and
neuromuscular effects of
hyperMg IVP
- Dialysis
- With intact kidneys, admin
of 0.45%NS IV with
diuretics to promote renal
excretion of Mg
- Tx of underlying condition
- Diet:
- Encourage milk intake
- Foods high in P: dried
beans, peas, eggs, fish, organ
meat, Brazil nuts, peanuts,
poultry, seeds, and whole
grains
- Oral sups (Neutra-Phos
liquid or Phospho-Soda)
- IV meds (NaPO4 or
KPO4) administered when
serum phosphate levels are
<1mg/dL
- CV: decreased myocardial
contractility and decreased
oxygenation of the heart
- CP
- Dysrhythmias
- GI: decreased O2 to the stomach,
bowel, and accessory digestive
organs
- Anorexia
- Dysphagia
- N/V
- Decreased BS
- Ileus
Hyperphosphatemia (>4.5mg/dL)
- Organ failure: acute or
chronic renal failure decreases
phosphate excretion
- Meds:
- Rapid admin of
phosphate-containing
solutions (ex. enemas)
- Excess intake of Vit D
(promotes absorption of Ca
and P in GI tract)
- Ca imbalance
- Acidosis (extracellular shift
of P in exchange for H ions to
buffer acidosis)
- Cellular destruction (cell
membrane and ICF contains
P)
Hyperchloremia (>105mEq/L)
- Metabolic acidosis
- Hyperparathyroidism
- Dehydration
- Respiratory alkalosis
Hypochloremia (<95mEq/L)
- Loss of gastric fluid (severe
vomiting, suctioning,
duodenal ulcer)
- Serum Cl reduced and
HCO3 elevated (30-40mEq/L)
- Diabetic ketoacidosis
- Cl loss d/t osmotic
diuresis and elevated HCO3
- Bartter’s syndrome
- Prevents renal Cl
reabsorption
- Coronary artery calcification (for
each 1mg/dL increase in serum
phosphate level, the risk of
coronary artery calcification
increases by 21%)
- N/V
- Dysphagia
- Decreased BP
- Cardiac dysrhythmias
- Manifestions are more a resulf of
hypoCa (secondary to elevated
serum phosphate):
- Tetany, muscle spasms of face
and extremities
- Bronchial muscle spasms
causing asthma attack
-Visceral muscle spasm
producing acute abdominal pain
- Hypotension, bradycardia
- Seizures, numbness and
tingling around mouth, face,
hands, and feet; hyperactive deep
tendon reflexes, positive chvostek
and trousseau signs
- Increased RR and depth
- Lethargy
- Stupor
- Disorientation
- Coma (if acidosis is not treated)
- Hypochloremic alkalosis:
- HCO3 retained to maintain
electrical neutrality and buffer
acid-base imbalances
- Paresthesia of face and
extremities, muscle spasms and
tetany, slow and shallow
breathing, dehydratino
- Muscle spasms and tetany
- Slow shallow respirations
- Dehydration
- Serum phosphate levels
- Serum Ca levels to detect a
decreased level (exchange of P
and Ca in kidneys)
- ECG to determine presence
of dysrhythmias
- Decreased cardiac perfusion:
- Assess HR, BP, and CRT
- Assess LOC
- Assess RR and breath sounds
- Monitor ECG rhythm and report
dysrhythmias
- Monitor I&O
- Monitor daily weight
- Prevent risk for injury:
- Implement safety precautions
- Monitor serum P levels
- Monitor serum Ca levels
- Assess for Chvostek and
Troussea signs
- Implement seizure precautions
as indicated
- Impaired health maintainance:
- Instruct to reduce intake of high
P foods
- Discuss importance of adhering
to prescribed dialysis sessions if
indicated
- Tx of underlying condition
- Eliminate all phosphatecontaining drugs
- Restrict intake of
phosphate rich foods
- Provide Ca-containing
antacids that bind
phosphorus in GI tract
- Provide IV infusion of NS
to promote renal excretion
- Dialysis to pts with renal
failure
- Serum Cl level
- Tx of underlying condition
- Admin of saline to repair
volume losses and admin of
K
- Serum Cl levels
- Admin of NS