Fluid and Electrolytes

Intracellular Electrolytes vs. Extracellular

o Intracellular K, Mg, Phos
o Extracellular Na, Chl, Bricarb
Serum Values
o Na 135-145
o K 3.5-5.5
o Chl 95-105
o Mg 1.8-3.0
o PO4 2.5-4.5
o Ca 8.5-10.5
Fluid Volume Deficits/Excesses
o Hypertonic characterized by a state of high amounts of electrolytes lost.
Hypertonic dehydration can be caused by conditions that increase fluid
loss such as excessive perspiration, hyperventilation, ketoacidosis,
prolonged fevers, diarrhea, and DI.
Includes:
D51/2NS used for patients with DKA after theyve receives isotonic
fluids
Hypertonic Overhydration can be seen with excessive sodium intake.
Causes include: excessive sodium bicarbonate therapy.
o Isotonic state of equal loss and gain of electrolytes.
Isotonic Dehydration caused by inadequate intake of fluids and solutes,
excessive loss of isotonic body fluids through trauma or what-have-you.
Includes:
Normal Saline 0.9% - used for fluid resuscitation and shock
Lactated Ringers used for acute blood loss.
Isotonic Overhydration known as hypervolemia. Causes of this include
HF, ESRD, liver Disease, and also inadequately controlled IV therapy.
Complications include: crackles in the lungs, increased ICP, and
bradycardia.
o Hypotonic characterized by a state of high amounts of electrolytes gained.
Hypotonic dehydrated is caused by chronic illness, excessive fluid
replacement, renal failure, and chronic malnutrition.
Includes:
D5W becomes hypotonic in the blood stream and this raises total
volume quickly.
0.45%NS given to renal transplant pts, people with DKA also. NOT
commonly given to liver pts.
Hypotonic Overhydration known as water intoxication. Complications are
diluted electrolytes in the blood vessels. Causes include: SIADH, CHF,
early renal failure.
Fluid Volume Deficit Assessments
o First we see tachycardia and lowered BP, Dysrhythmias, and flattened venous
systems.
o RR increased respiratory rate.
o Neuro altered mental status and a decrease in LOC.
 o GU decreased urine output and increased concentration.
o GI decreases motility, constipation, thirst.
o Hct increased, BUN increase, Na increase.
o Notify HCP if fluid resuscitation is implemented and no urine is produced. Can
also check bladder for retention.
o Vasopressor drips may be initiated for patients that may go into shock.
Nursing Implications
o We want to replace fluids lost, we want to treat the shock symptoms, we want
to monitor urine output and blood pressure, take daily weights.
MAP is used to measure the pressure being used to perfuse organs and we
get this through an arterial line which gives us a continuous accurate
reading.
Fluid Volume Excesses Assessments
o Cardiac elevated BP, distended veins
o Neuro altered mental status, headache
o RR increased shallow breathing, dyspnea, crackles.
o GI diarrhea, liver enlargement ascites.
o Skin cold, clammy skin. Ptential pitting edema.
o Renal increased urine output, If working with a damaged kidney, you can
have decreased output because with chronic kidney disease youre not
producing urine anyway
o Labs decreased Hct, BUN depends on underlying kidney status (with no
kidney issues, BUN would be decreased), NA decrease.
Nursing Implications for Excess
o Monitor I/Os, daily weights, change body positions appropriately, and watch
potassium levels.
Electrolyte Imbalances
o Sodium (Na) essential for nerve impulse transmission, muscle contraction
and the movement of glucose, insulin and amino acids.
Hyponatremia Na less than 135.
Assessment findings: altered mental status, personality changes,
increased GI motility, and some respiratory involvement.
Nursing Implications - If the client is taking lithium, monitor lithium
level because hyponatremia can cause diminished lithium excretion,
resulting in toxicity.
Hypernatremia Na over 145. Can be caused by a decrease in secretion
seen in patients with Cushing s syndrome, Renal Failure, and
Hyperaldosteronism.
Assessment findings neuro twitches, increased HR, and pulmonary
edema.
Nursing Implications assess neurological status, if we see neuro
changes, we give 0.45% NS or D5W.
o Potassium (K) Major cation of ICF. Helps maintain acid base balance. Note
that insulin drops potassium and insulin needs glucose and potassium to go
into the cell.
 Hypokalemia K less than 3.5. Causes include: SABAs, LABAs, vomiting,
diarrhea, increased secretion of aldosterone, non-potassium sparing
diuretics.
Assessment Findings Cardiac arrhythmias, peripheral pulses weak,
prominent U waves, breathing is impacted, nausea and vomiting,
abdominal distention.
Nursing Interventions telemetry, administer K supplements
Potassium IV NEVER give K as an IV push. Can only be given slowly
through IV, we want to shake the bag to make sure its all evenly
distributed. Maximum infusion of 20 mEq/hr. monitor for phlebitis, if it
occurs, stop the infusion.
Hyperkalemia K more than 5.5. Causes include overingestion of K
containing foods, ACEs, ARBs, potassium sparing diuretics, acidosis, and
tissue damage.
Assessment Findings Elevated T waves on ECG, paralysis, irregular
heart rhythm, chest pain, n/v.
Nursing Interventions place pt on cardiac monitor, restrict K in diet,
use of kayaxelate (must monitor BMs to be sure its being excreted),
can give Calcium IV and sodium bicarb. Can give Gluvose with regular
insulin to help potassium back into the cell.
o Calcium (Ca) helps with bone and tooth formation, muscle contraction
(including the heart), and transmission of neural impulses.
Hypocalcemia Ca less than 8.5. Causes: hyperproteinemia, acture
pancreatitis, hyperphosphatemia, diarrhea, lactose intolerance,
malabsorption syndrome.
Assessment Findings tetany, muscles twitching, Chvosteks Sign
(twitching of facial muscles), Trousseaus sign (twitching of arm),
arrhythmias with prolonged ST interval and prolonged QT interval.
Nursing Interventions cardiac monitor, administer calcium
supplements, Calcium IV (must be warmed to body temp, given
slowly), place client on seizure precautions (if they have one, ask about
an aura).
Hypercalcemia Ca more than 10.5. Causes: excessive oral intake, renal
failure, excessive oral intake of vitamin D, immobility, and
hyperparathyroidism.
Assessment fndings: kidney function alteration causing excessive thirst
and urination, n/v, constipation, bone density decrease if it was pulled
from there, confusion, fatigue.
Nursing Interventions place client on cardiac monitoring, administer
medications that inhibit calcium resorption (such as phosphorus,
calcitonin, and prostaglandin synthesis inhibitors). Monitor for kidney
stones.
o Magnesium (Mg) bone and tooth constituent, muscle nerve irritability, and
intracellular.
Hypomagnesemia Mg less than 1.5. Causes: diuretics, chronic
alcoholism, sepsis, hyperglycemia, diarrhea, vomiting, Chrons disease,
celiac disease.
 Assessment Findings tall T waves, convulsions, paresthesias, muscle,
positive Trousseaus, Chvosteks sign, and tetany or seizures.
Nursing Interventions increase intake of mg, monitor pt for laryngeal
stridor, initiate seizure precautions.
Hypermagnesemia Mg more than 2.5. Causes excessive IV magnesium
and decreased renal excretion of mg.
Assessment Finding lethargy, nausea and vomiting, muscle
weakness, and decreased deep tendon reflexes.
Nursing Intervention diuretics prescribed to increase renal excretion
of magnesium. Notify MD if patellar reflexes are absent.
o Phosphate has an inverse relationship with calcium
Hypophosphatemia Phos less than 2.7. Causes: hyperparathyroidism,
malignancy, respiratory alkalosis.
Assessment Findings slowed peripheral pulses, irritability, confusion,
immunosuppression, decreased bone density, decrease deep tendon
reflexes.
Nursing Intervention administer IV Phos, move client carefully and
monitor for possible fractures.
Hyperphosphatemia Pos more than 4.5. Causes: tumor lysis syndrome,
increased intake, and hypoparathyroidism.
Nursing Intervention manage hypocalcemia, administer phosphate
binding medication.
Neuro Lectures
Diagnostic Testing
o CT Scan Quickest and more accurate, also cheaper. Provides images of
cross sectional sliced 3D images of the brain. Can use contrast. Helps
diagnose tumors, infarction, hemorrhage, hydrocephalus, and bone
malformations.
o MRI provides images of layering of the brain. Identifies abnormalities of soft
tissue. Anything metal is contraindicated except for titanium. Standard for
spinal cord evaluation.
o Cerebral Agniography (Aterirogram) contrast medium is injected and shows
vascular aneurysms, AVM, occluded and leaking blood vessels. Need to be
NPO 8 hours prior, and neuro checks during and after procedure.
o EEG (Electroencephalogram) records electrical activity in the cerebral
hemispheres. Used for diagnosis of seizure activity, cerebral activity, sleep
disorders, and brain death.
Nursing care
Pre-Procedure withhold CNS depressants 24 hrs prior, hair clean with
no pins or oils, and sedation for pediatric patients.
During Procedure monitor for seizure activity and they must lie still.
o EMG (Electromyography) records electrical activity of the peripheral nerves
motor and sensory.
o Lumbar Puncture insertion of a needle into the subarachnoid space to
obtain a CSF specimen.
Contradiction in patients that have increased ICP that causes herniation.
 Must place a patient flat after a lumbar puncture for 4-8 hours.
Monitor for leakage.
o Intracranial Dynamics cranial vault has three components that maintain the
equilibrium. Brain is 80%, CSF is 8%, and Blood is 12%.
Monroe-Kellie Hypothesis if volume of any one increases the volume of
one or both of the other must decrease to maintain normal pressure within
the cranial vault.
o Intracranial Pressure there is little room for brain and the contents to
expand. CSF may be shunted from cranial compartment to subarachnoid
space.
If increased ICP is left untreated, it may lead to herniation downward to
the brainstem. If there is herniation of the brainstem and there is pressure
on the 3rd cranial nerve we will see pupillary dilation. Along with
deteriorating LOC and possibly death.
Normal ICP is between 5-15.
The difference between MAP and ICP = cerebral perfusion pressure. This
is the pressure needed to perfuse cells in the brain. Normal Cerebral
Perfusion Pressure (CPP) is 80-100.
Causes of Increased ICP defecation, coughing, vomiting, airway
obstruction, suctioning, hypercapnia, stress, pain, seizures, hyperthermia,
and poor neck alignment.
Signs and Symptoms
Early changes in LOC, pupillary change, there may be no change in
vitals, worsening headache, and change in speech.
Late difficult to arouse, posturing, change in respiratory pattern,
abnormal reflexes, cardiac changes, and Cushings Response.
Diagnostic Tests
CT Scan and MRI = identify possible cause and evaluate therapeutic
options.
Serum Osmo used as indicator of hydration status, usually
maintained slightly elevated to draw excess fluid into vascular system
from brain tissue.
ABG monitors pH, CO2, PO2 levels and effect on cerebral circulation.
Hydrogen ions and carbon dioxide are potent vasodilators. Hypoxemia
also causes vasodilation.
Diuretics osmotic diuretics increase osmolality of blood and draw fluid
from edematous brain tissue into vascular bed where it can be eliminated.
Mannitol is commonly used for increased ICP.
Loop diuretics such as furosemide are used, in addition, to further
promote diuresis.
You can get a recess panel from an ABG instead of having to pull extra
labs.
Medications
Antipyretics or hypothermia blanket if acetaminophen is prescribed
but says its for headaches, we dont use it for temp. we can an order
for temp.
 Anticonvulsants will most likely be a standing order.
Histamine H2 Receptor Blockers protonix and pantoprazole.
Vasoactive Medications Levophed or epinephrine.
Surgery May be indicated to treat underlying cause of increased ICP.
ICP Monitoring continuous ICP monitor is used for continual assessment
of ICP and to monitor effects of medical therapy and nursing interventions.
These include the subarachnoid bolt, epidural catheters, or
intraventricular catheter. These can also be used to drain CSF. Biggest risk
is infection.
Craniotomy used to remove accumulated blood or tumor. Possible
complications include increased ICP from edema, hemorrhage, or
obstruction of CSF.
Craniectomy removal of the bone.
Traumatic Brain Injury (TBI)
o Most common to be affected are the frontal and temporal lobes from an
impact that can be direct, indirect, if it rebounds it may rotate the brainstem.
o Open: scalp lacerations, fractures in the skull, and interruptions of the dura
matter.
o Closed: concussions (jarring of the brain within the skull with temporary loss
of consciousness), contusion (bruising type of injury to the brain), and
fractures.
o Edema brain injuries may result in swelling of the brain tissue with or
without associated hemorrhage. Swelling results from humoral and metabolic
responses to injury which lead to a marked increase in ICP. Increased ICP may
lead to decreased cerebral perfusion or herniation.
o Ischemia can result from vascular injuries, vascular spasms, increased ICP,
and focal or more global infarcts can result.
Skull Fractures
o Linear Fracture 80% of skull fractures. Usually an isolated in jury.
o Depressed Skull Fracture usually results from a small object striking the
head at high speeds. Most common are frontal and parietal lobes.
o Open Vault Fracture commonly associated with multitraumas and have a
high mortality rate. These have a high risk of infection because the meninges
are exposed.
o Basilar Skull Fractures Signs of these are the battle sign and the raccoon
eyes. The fracture occurs at the base of the skull. Common diagnosis criteria
is a CT scan. Could also have Anosmia which is that they cant smell. Could
also cause cranial nerve 1 and 2 damage (Olfactory and optic nerves).
A CSF leak can occur. Assess ABCs, neuro changes for changes in LOC,
alterations in taste, smell, and hearing.
We use Halo sign to test for CSF leak. A yellow ring that appears
around the bloody drainage would represent CSF.
Bruising may not develop for a few hours.
Nose and ears can leak CSF. And they are at risk for increased ICP.
Treatment keep HOB elevated, use mustache dressing to absorb
drainage,
 Avoid coughing, sneezing, blowing nose, and we dont want
to put anything through the nose. Such as nasal cannula, NGT, or
suction.
Spinal Cord Injury
o Random Note: the neurological disease that we look at sensory points to
pinpoint outliers is fibromyalgia.
o Tetraplegia paralysis of upper and lower extremities.
o Paraplegia paralysis of the lower extremities only. These pts get a lot of PT
and we promote arm strength.
o Central Cord Syndrome lesions occurring almost exclusively in the
cervical region. Mostly experience upper extremity weakness. Associated with
fractures, dislocations, and compression fractures.
o Brown-Sequard Syndrome lesion that produces ipsilateral proprioceptive
and motor loss and contralateral loss of sensitivity to pain and temp. They
will have petechial hemorrhage. The cause can or can not be trauma. Usually
recover in 1 to 2 months but can be up to two years.
o Anterior Cord Syndrome lesions that produce variable loss of motor
function and loss of sensitivity while preserving proprioception.
o Cauda Equina Syndrome injury to the lumbosacral nerve roots within the
neurocanal resulting in areflexive bladder, bowel and lower limbs. extreme
pressure of the nerves at the end of the spinal cord. Can be acute or gradual.
Acute: can have severr lower back pain, loss of bladder and bowel function
within the first 24 hours. Gradual: can take weeks to months to develop, can
be partial or intermittent loss of bowel and bladder function in addition to
lower back pain, muscle weakness.
o Hyperflexion Injury jerking forward very roughly, usually seen with a head
on collision. And diving accidents.
o Hyperextension Injury seen with whiplash and collisions where you are hit
from behind.
o Emergency Assessment of Sensation
Respiratory status first
C3-c5 innervates phrenic nerve = we need to emergency intubate.
Glascow Coma Scale for LOC eye opening, motor response, verbal
response.
Score 15 is normal.
Score of 3 is a deep coma.
At 5 or less we notify organ harvesters.
o Spinal Shock a sudden depression of reflex activity occurs below the level of
injury. Occurs within the first hour of injury and can last days to months.
Causes hypotension, bradycardia, flaccid paralysis, paralytic ileus, and
urinary retention.
Spinal shock ends when reflexed are regained.
Nursing interventions monitor for signs of spinal shock, monitor for
hypotension and bradycardia, reflex activity, and assess bowel sounds.
o Autonomic Dysreflexia this can occur any time after spinal shock has been
resolved. These individuals present with severe headaches and flushing.
Causes of this can be a full bladder or constipation.
 Treatment catheterize their bladder to empty it, stool evacuation,
elevate HOB to 90 degrees, and monitor BP. Can give Hydralazine or
Apresoline for this.
Traction
o Halo Traction always needs to have the wrench for it on hand. Do not turn
the patient by holding onto the traction bars. Teach patients to wear a shirt
under the vest. We assess skin, we must do sterile procedure when cleaning
the pin sites.
Myasthenia Gravis chronic neuromuscular autoimmune disease involving a
decrease in the number and effectiveness of acetylcholine receptors art the
neuromuscular junction.
o Key abnormal thymus gland, they have issues maintaining acetylcholine
receptors and this is an auto immune disease. Could range from mild ocular
disturbances to rapidly developing weakness and respiratory muscle failure
and death.
o Clinical Presentation Extraoccular muscles changes including ptosis,
diplopia, and incomplete eye closure. Speech becomes weak but do not have
any changes in LOC.
o Diagnostic Evaluation
Tensilon Testing baseline assessment of cranial muscle strength. Give
tensilon IV. A marked improvement in muscle strength that lasts for 5
minutes means its positive. Positive results if given to a client
experiencing a myasthenia crisis.
o Drug Therapy
Cholinesterase inhibitors blocks action of enzyme that breaks down
acetylcholine.
Pyridostigmine (Regonol)
Immunosuppression prednisone is used to induce remission and control
symptoms.
Azanthioprine (Immuran) used for long term management.
o Nursing Care
Occupational and Physical Therapy is used for most neuro pts.
Need small, frequent, and high caloric meals because these individuals
need extra energy.
o Myasthenic Crisis Vs. Cholinergic Crisis
Myasthenic Crisis muscle weakness, respiratory insufficiency with SOB,
extreme difficulty swallowing, and risk for respiratory arrest.
Cholinergic Crisis caused by anticholinesterase drug toxicity. We see
increased intestinal motility therefore diarrhea, cramping. Bradycardia,
increase salivation, and increased sweating.
Multiple Sclerosis no cure, unknown etiology, and is marked sensory and motor
deficits increased with age. Pathophysiology includes a demyelination of the
neurons in the CNS with inflammation and plaques in the white matter.
o Clinical Presentation fatigue, muscle weakness, unsteady gait, dysphagia,
anxiety, muscle spasticity.
o Diagnostic Testing CSF will show high protein and increased WBCs.
MRI showing plaques.
 CT showing increased density in white matter.
o Nursing Care encourage fluid intake to decrease risk of UTI, monitor
cognitive changes, assist with mobility.
Guillan Barre Syndrome acute destruction of myelin sheaths due to
autoimmune disorder that results in varying degreeM of muscle weakness and
paralysis. Death can occur from respiratory arrest.
o Has 3 phases:
Initial onset and progression of symptoms.
Plateau no change in status.
Recovery takes 4-6 months and up to 2 years.
o Risk factors include: acute illnesses, vaccines, surgery, and viruses such as
CMV or EBV.
o Signs and Symptoms ascending bilateral lower extremity weakness.
Acute progressive muscle weakness to muscle flaccidity without muscle
atrophy.
o Diagnostic Procedure
EMG is used, prepare client for discomfort, monitor needle sites for
hematoma.
White cell count shows leukocytosis.
Lumbar puncture shows increase in protein.
o Nursing care monitor pt airway, keep head of bed elevated, monitor ABGs
and provide oxygen as needed.
Amyotophic Lateral Sclerosis (ALS) or Lou Gehrig Disease there is no cure and
these people usually die within 2-5 years of diagnosis. This is a deterioration of
the motor systems characterized by muscle weakness progressing to muscle
atrophy and eventually paralysis and death.
o Diagnostic Tests
Creatine Kinase levels are elevated
EMG showing muscle fasciculation.
o Clinical Manifestations weakness begins in any or all muscles of the body.
Dysphagia, paralysis occurs with progressive muscle atrophy, no associated
mental, sensory, or autonomic systems are present. Normal intellectual
function.
o Nursing Care maintain patent airway. Monitor ABGs, provide support,
keep HOB elevated.
Parkinsons Disease
o Stages:
1 Minimal weakness. Hand and arm trembling and unilateral limb
involvement.
2 Bilateral limb movement, mask like expressions, slow steps.
3. increased gait disturbances.
4. Severe disability. Akinesis and rigidity.
o Presentation tremor, mask like facial expression, pill rolling, slow speech,
drooling, and echolalia.
o Pharmacological Interventions
Anticholinergic used for younger pts with tremors (Carbex, Eldepryl)
 Dopamine Agonists stimulate dopamine receptors: levodopa +
Carbidopa (Sinemet).
Therapy goal is to restore dopamine function, block acetylcholine, and
avoid EPS.
Side Effects of anticholinergic therapy monitor for hypotension, changes
in mental status, dizziness, insomnia, and anorexia. Pts with narrow-
agnle- glaucoma should not take Revastigmine (Exelon).
o Nursing Care provide high calorie, high protein, and high fiber soft diet with
small frequent feedings. Instruct client to rock back and forth to initiate
movement. Avoid foods high in B6.
o Client Teaching for Anticholinergic Drug Therapy take with food or milk to
avoid GI upset, and teach signs of symptoms of overdose: nausea, vomiting,
sweating, salivating, hypotension, bradycardia, convulsions, and increased
muscle weakness.
Meningitis infection of the meninges from bacteria, virsues, fungus, parasites,
or toxins.
o Bacterial common contributing factors are Strep, H. Flu (least common),
meningococcus (most contagious). Portals of entry are CSF, Resp tract, pr
fetal maternal.
Clinical Manifestations Kernig sign (inability to extend leg at hip flexion),
Bruzinski sign (neck comes forward), photophobia, nuchal rigidity,
projectile vomiting.
o Aseptic (Viral) limited only to meninges.
Clinical Manifestations mild symptoms, generalized throbbing headache,
mild photophobia, mild neck pain, stiffness, fever, generalized malaise.
o Fungal chronic, less common, most commonly seen in immunocompromised
patients.
Clinical Manifestations develops slowly and insidiously, dementia, and
afebrile.
o Diagnostic Procedures
Lumbar Puncture make sure the pt lays flat for 4-8 hours after.
With viral meningitis the CSF will be clear. With bacterial CSF will be
cloudy.
Results indicative of meningitis elevated WBC, protein, and CSF
pressure, decreased glucose if its bacterial.
o Nursing Interventions maintain isolation precautions of droplet. Report to
the public department, decrease environmental stimuli, maintain bed rest,
and administer meds.
Cerebrovoscular Disorders account for more than 50% of admitted pts. Two
types: Ischemia with or without infarction or Hemorrhage.
o Ischemic Strokes
Thrombotic Strokes blood flow to the brain is occluded by thrombi that
arise from arterial occlusion. Increased coagulation can lead to thrombus
formation.
Embolic Strokes involves fragments that break from a thrombus formed
outside the brain, in the heart, aorta, or common carotid.
 o Hemorrhagic Stroke most common causes are hypertension and weakening
of the walls of intracerebral vessels. This can be caused be ruptured
aneurysms, vascular malformations, bleeding into a tumor, drug use, and
head trauma.
o Transient Ischemic Attack (TIA) like a small stroke, definitely a warning sign
for a severe one.
Look for FAST Facial drooping, arm weakness, slurred speech, and Time.
We need to act fast to give them TPA.
Signs and Symptoms hemiparesis, headache, LOC decrease, dysarthia
(slurred speech), aphasia, vertigo, and some other shit who cares.
Left Cerebral hemisphere responsible for language, math, and analytic
skills. So we can anticipate to see alexia (difficulty reading), depression,
agraphia, aphasia, and slow behavior if they have a TIA on this side.
Right Cerebral Hemisphere responsible for visual and spatial awareness
and proprioception. A TIA here would show an unawareness of deficits,
disorientation, poor judgment, left hemiplegia, visual changes, or difficulty
with impulse control.
Nursing interventions maintain patent airway, monitor for changes in
LOC, elevate head to reduce ICP, seizure precautions, meds, assist with
safe feedings.
o Pharmacological Therapy
Anticoagulation therapy Heparin, Enoxaporin (Lovenox), Aspirin,
Coumadin.
Antiplatelet Therapy clopidigrol (Plavix), Ticlopidine (Ticlid),
Dipyridamole (Persantine).
Carotid Artery Disease carotid narrowing or occlusion can cause TIAS and
strokes.
o Endarterectomy to remove plaques from the CA. Post procedure we do
antiplatelet therapy.
Seizures - Abrupt, uncontrolled electrical brain discharges that cause alterations
in level of consciousness and changes in motor and sensory behavior. We ask the
patient if they had an aura, if its happened before, if there were any witnesses
that can account for if they hit their head or how long they seized for.
o Triggers increased physical activity, stress, fatigue, alcohol, Caffeine, Some
chemicals.
o Diagnostic Procedures
EEG no caffeine, wash their hair because they cant have any oils or
sprays, take deep breaths, and possibly withhold sleep prior to test.
o Nursing Interventions maintain patent airway, protect client from injury,
prepare to suction, turn client to the side, loosen clothing, and administer
oxygen.
o Status Epilepticus we use valium and Ativan as standing orders for status
epilepticus. Followed by a continuous infusion of Phenytoin (Dilantin) which
the normal levels are 10-20.
Endocrine
1. Endocrine Glands
 a. Hypothalamus, pituitary gland, parathyroid gland, thyroid gland, thymus, adrenal gland,
pancreas, ovary, and testis
b. Effects of aging:
i. General changes include:
1. Increased connective tissue in glands
2. Decreased blood supply
3. Decreased metabolism resulting in increased half-life of medications
c. Assessments
i. Hormones affect ALL body tissues
ii. Diversity in S/S and are often vague
1. Fatigue, depression, energy level, alertness, sleep patterns, mood, affect, weight, skin, hair,
personal appearance, sexual function
iii. Physical Assessment
1. Inspection: head to toe
2. Palpation: only thyroids and testes
3. Auscultation: cardiac baseline, bruits (turbulent blood flow)
4. Psychosocial: body image depending on the age, support groups, mood changes,
losing hair/thinning of hair
iv. Questions to ask
1. Past history: why is this important? Gives us baseline
2. Family history: genetic disorders
3. General state of health; any noticeable changes:
4. Medications: meds could increase TSH levels, could cause hyperglycemia, calcium levels that
could stimulate parathyroid
5. Changes in: hair, skin, nails, weight, appetite, memory, sleep:
6. Visual changes: diabetes, thyroid
7. Size of extremities: cushing's
8. Trauma (head/neck): SIADH, DI, leads to a bunch of complications
9. Growth and development: dwarf, gianticatism
10. Past surgeries: parathyroidectomy
11. Secondary sex characteristics
12. Menstruation: can have symptoms that have outward appearance, and menopause
13. Stressors and coping patterns: how you eat, your metabolism, college 15
2. Diagnostic Tests
a. Routine x rays
i. Evaluates dysfunction and effect on body tissue
b. CT scans
i. Assesses endocrine gland structure
c. MRI
i. Helps to diagnose thyroid disorders
d. Radioactive iodine (RAI) uptake
i. Radioactivity is measured 2, 6, and 24 hours after ingestion of the capsule
ii. Normal value: 5 to 35% in 24 hours
iii. Increased RAI: hyperthyroidism, thyrotoxicosis, decreased iodine intake, or increased iodine
excretion
iv. Decreased RAI: low T4, the use of antithyroid medications, thyroiditis, myxedema, or
hypothyroidism
e. Stimulation Test #ntk
i. Suspected underactivity of an endocrine gland
ii. Stimulates to evaluate normal function
 iii. Failure to stimulate production hypofunction
f. Suppression Test #ntk
i. Stimulates to evaluate normal function
ii. Failure to suppress hyperfunction
g. T3 and T4 resin uptake test
i. Blood tests for the diagnosis of thyroid disorders
ii. T3 and T4 regular thyroid-stimulating hormone
iii. T3 and T4 is increased in hyperthyroidism and decreased in hypothyroidism.
iv. T3 decreased in aging process
v. Normal values dont need to know levels
1. T3: 80-230
2. T4 (iodized): 5-12
3. Thyroxine (free T4): 0.8-2.4 nanograms/dL
h. Thyroid Stimulating Hormone (TSH)
i. Differentiate the diagnosis of primary hypothyroidism
ii. Normal value: 0.2 to 5.4 microunits/mL
iii. Elevated values indicate primary hypothyroidism
iv. Decreased values indicate primary hyperthyroidism or secondary hypothyroidism
v. TSH levels are monitored, the endocrinologist schedules their meetings in 3,6,9, 12 months
when they are experiencing active thyroid issues.
i. Thyroid scan #ntk
i. Identify nodules or growths in the thyroid gland
ii. A radioisotope of iodine or technetium is administered prior to the scanning of the thyroid gland
iii. Reassure the client that the level of radioactive medication is not dangerous to self or others
iv. Contraindicated with pregnancy: pregnancy tests
v. Pre procedure
1. Determine whether the client has received radiographic contrast agents within the past 3
months not contraindicated but HCP needs to know because it may alter results
2. Discontinue iodine medication for 14 days prior to the test
3. Discontinue thyroid medication 4 to 6 weeks before the test: may alter results
4. NPO status after midnight
5. Iodine is used: fast for an additional 45 minutes after ingestion of the oral isotope and the
scan will be performed in 24 hours
6. Technetium is used: administered IV 30 minutes before the scan
j. Needle aspiration of thyroid
i. Aspiration of thyroid tissue for cytological examination
ii. No client preparation is necessary
iii. Light pressure is applied to the aspiration site after the procedure
k. Glucose tolerance test (GTT)
i. Diagnostic tool for diabetes mellitus
ii. Glucose levels peak after injection or ingestion
iii. HbA1C: used for long term glucose monitoring
iv. Fasting glucose: can use this for anyone, pregnant women because of gestational diabetes
v. Three days prior: eat a high carbohydrate (200 to 300 g) diet
vi. 36 hours: avoid alcohol, coffee, and smoking for 36 hours before testing
vii. 10-12 hours before: fast
viii. 8 hours before and after test: avoid strenuous exercise
ix. Insulin and oral hypoglycemic medication avoid
x. Procedure: minimum of 2 hours (30 minute interval), oral administration of glucose, and labs
l. Glycosylated hemoglobin
 i. Glycosylated hemoglobin is blood glucose bound to hemoglobin
ii. HbA1c is a reflection of how well blood glucose levels have been controlled for up to the prior 3-
4 months
iii. Hyperglycemia in a client with diabetes mellitus is usually a cause of an increase in HbA1c
iv. Patients do not have to fast
v. Values are expressed as a percentage of total hemoglobin
1. Diabetic with good control: 7% or less
2. Non-diabetic: 4-6%
3. Hypopituitarism (Dwarfism-less than four feet ten inches)
a. Low secretion of GH by the anterior pituitary gland, impact on GH, LH, FSH, TSH, ADH, and
ACTH
b. Assessment
i. Growth: weight and height
ii. Aging
iii. Fertility
iv. Cardiac function: low BP and reduced cardiac output
v. Tumors: visual disturbances and headaches
c. Nursing interventions
i. Psychosocial and body image
ii. Education
iii. Medication/hormone replacement
4. Hyperpituitarism (Giantism and acromegaly)
a. High secretion of GH by the anterior pituitary gland
b. Assessment
i. Extremities and jaw: thickening and protrusion of the jaw
ii. Arthritis of joints
iii. Skin: oil, rough
iv. Organomegaly
v. Hypertension
vi. Aspiration precautions: dysphagia
vii. Vocal patterns: deepening of the voice
c. Nursing interventions
i. Skin care
ii. Psychosocial support
iii. Medication/treatment/ hypophysectomy
1. Hypophysectomy: the removal of the pituitary gland via craniotomy or transsphenoidal
(preferred)
2. Complications
a. Increased intracranial pressure
b. Bleeding
c. Meningitis/ infection
d. Hypopituitarism
e. CSF leak check glucose from leakage
3. Post procedure
a. Monitor vital signs, neurological status, and LOC
b. Elevate the head of bed. Do not lay flat!!
c. Monitor for increased ICP, bleeding, postnasal drip
d. Instruct patient to avoid sneezing, coughing, and blowing the nose
e. Monitor electrolyte values, temporary DI and SIADH, I&O and avoid water intoxication
f. Administer: glucocorticoids, antibiotics, analgesics, antipyretics
 g. Educate medication and oral care (soft bristle brush for the first 2 weeks because risk of
bleeding)
5. Diabetes Insipidus
a. Hyposecretion of ADH, disorder of water metabolism
b. ADH is produced by hypothalamus, stored and released by posterior pituitary. Decreased ADH
leads to distal renal tubules not retaining water
c. Assessments
i. Large volumes of urine excreted (Polyuria)
ii. Massive dehydration, decrease skin turgor, dry mucous membranes
iii. Increased plasma osmolality and urine osmolality decreases
iv. Stimulates thirst response if intact polydipsia
v. Increased serum sodium inability to concentrate urine
vi. Abrupts onset (1-2 days after injury)
vii. Fatigue, muscle pain/weakness, headache, tachycardia, postural hypotension, weight loss,
constipation, anorexia
d. Classifications
i. Nephrogenic
1. No deficiency in hormone, inherited disorder where kidneys do not respond to ADH
ii. Primary (neurogenic)
1. Defect in pituitary or hypothalamus
2. Lack of ADH production or secretion
iii. Drugs
1. Any drug that might interfere with kidneys response to ADH
2. Example: Lithium carbonate
iv. Psychogenic
1. Client ingests large quantities of water, usually 5 liters or more which in turn depresses ADH
production/secretion
e. Diagnostic tests
i. Serum sodium increases
ii. Plasma osmolality increase
iii. Specific gravity of urine decreased. <1.006
iv. Water deprivation test: looking at the inability of the kidneys to concentrate urine despite the
increased plasma
v. Vasopressin test: given SQ which produces urine output
vi. Hypertonic saline test: 3% NS is used and theres a sudden decrease urine output which
means there is a sign of ADH release
f. Interventions
i. Maintain fluid and electrolyte balance, daily weights!!
ii. Identify and correct cause
iii. IV fluids (hypotonic)
iv. Unrestricted access to fluids
v. Administer vasopressin
vi. Severe cases administer desmopressin acetate DDAVP-synthetic form of ADH
6. Syndrome of Inappropriate antidiuretic hormone secretion (SIADH)
a. Hypersecretion of ADH resulting in water intoxication
b. causes: tumors, CNS injury, pituitary surgery, drugs
c. Assessment
i. Serum: decrease Na, dilute osmol = neurological effects, heart failure, cramping, vomiting
ii. Urine: increased Na and concentrated osmol
iii. Fluid overload, change in LOC and mental status
iv. Weight gain, hypertension
v. Positive feedback: elevated ADH release persists even with increased plasma volume and
decreased osmolality
d. Diagnostic Tests
i. Serum sodium-decreased, serum calcium-decreased, BUN/Cr-normal, plasma osmolality-
decreased, urine osmolality-elevated
e. Interventions
i. Monitor I&O, daily weights, F&E balance, restrict fluids to 500-600ml/24hr
ii. Administer hypertonic saline(3%) use with caution (water intoxication) and diuretics
7. Disorders of the Adrenal glands
a. Adrenal cortex
i. Cushings syndrome: hypercortisolism
1. Cortisol excess, affects more women than men
2. Primary: usually a neoplasm
3. Secondary: pituitary or hypothalamus disorder causing increased ACTH; adrenal hyperplasia
4. Assessment
a. Truncal obesity with thin extremities
b. Moonface and buffalo hump
c. Supraclavicular fat pads
d. Generalized muscle wasting and weakness pathological fractures
e. Fragile skin that easily bruises skin assessment
f. Reddish-purple striae on the abdomen and upper thighs
g. Hirsutism(abnormal growth of hair), hypertension
h. Elevated blood glucose, sodium, and WBC
i. Decreased calcium and potassium levels
5. Diagnostic tests
a. Cortisol: high with no circadian variation
b. Urinary levels of steroid metabolites: high
c. RBC and granulocytes: high
d. X rays, MRI, and CAT scans
e. Dexamethasone suppression test: give 1 mg at night, test at 8 am, high level!
6. Interventions
a. Treat underlying cause, stop steroids, taper it down, do not stop abruptly, remove tumors
b. Monitor: vital signs (BP), I&O, daily weights, lab values (Blood glucose, WBC, sodium,
potassium, calcium)
ii. Addisons disease
1. Hyposecretion of adrenal cortex hormones glucocorticoids and mineralocorticoids
2. Impairs stress response by reducing cortisol, aldosterone, and androgens
3. This condition is fatal if left untreated
4. Assessment
a. Lethargy and fatigue
b. Menstrual changes in women and impotence in men
c. Dehydration, weight loss, postural hypotension
d. Hypoglycemia, hyperkalemia
e. Leg and muscle weakness, GI disturbances, emotional disturbances
5. Diagnostics
a. Serum cortisol: low
b. Urinary metabolites: low
c. ACTH stimulation: low cortisol=Addisons, high cortisol= secondary disease
d. Hyperkalemia, hyponatremia, hypochloremia
 e. Fasting hypoglycemia
f. BUN elevated; hematocrit HCT elevated
6. Interventions
a. Pharmacological intervention: lifelong therapy with replacement
i. Cortisone: twice daily BID, increase dose for stressful times
ii. Florinef: aldosterone replacement
iii. Carry emergency kit with 100 mg hydrocortisone for injection
b. Other interventions
i. Salt food liberally and avoid fasting
ii. Eat high carbs, high proteins, normal sodium
iii. Always wear medic alert identification
iv. Observe for Addisonian crisis secondary to stress, infection, trauma, or surgery
c. Addisonian Crisis
i. Precipitated by: stress, infection, trauma, or surgery
ii. Potentially lethal, due to insufficiency; can occur gradually or abruptly (acute adrenal
insufficiency)
iii. Can cause hyponatremia, hyperkalemia, hypoglycemia, and shock
iv. ALWAYS WITHDRAW STEROIDS THERAPY GRADUALLY
v. Assessment: irritability, confusion, severe hypotension, shock, generalized weakness, severe
abdominal, leg, and lower back pain
vi. Treatment: prepare to administer IV glucocorticoids as prescribed; hydrocortisone sodium
succinate (Solu-Cortef) is usually prescribed initially
1. Following resolution of the crisis, administer oral glucocorticoids and mineralocorticoid as
prescribed, monitor vitals (BP), monitor nero status
iii. Conns syndrome (hyperaldosteronism)
1. Primary: called Conns syndrome, usually benign aldosterone producing adenoma
2. Secondary: excess renin-angiotensin stimulation, stimulation occurs with conditions involving
low circulating blood volume: pregnancy, oral contraceptives, hypovolemia, CHF, cirrhosis,
chronic renal failure
3. Diagnostics: decreased potassium, elevated aldosterone, elevated sodium, x rays, cat scan,
MRI
4. Assessment: sodium & water retention, increased fluid volume, hypertension, headache, visual
disturbances (spots), hypokalemia, metabolic alkalosis (finger tingling and paresthesia), and
increased urine output
5. Monitoring: VS, signs for hypokalemia, sodium restriction
6. Treatment: reduce BP, correct hypokalemia, surgical removal of tumor (adrenalectomy),
potassium supplements, administer Spironolactone
b. Adrenal medulla
i. Pheochromocytoma: a catecholamine- producing tumor
1. It causes hypersecretion of the hormones of adrenal medulla and secretions of excessive
amounts of epinephrine and norepinephrine
2. Benign tumor but can be malignant usually in the abdomen, but can be in the
adrenal gland
3. Assessment :
a. Exaggerated flight or fight reaction
b. HALLMARK: high blood pressure 200/150
c. End organ damage, CVA, heart disease, kidney damage
d. Attack occurs with sporadic release of catecholamines
e. Pounding heartbeat, deep breathing, headache
 f. Peripheral vasoconstriction
g. Tremors and anxiety
4. Must rule out all other disorders
5. Do a 24 hour urine collection for catecholamine and their metabolites
6. CAT scan shows tumor
7. Interventions
a. Surgical
i. Surgical removal
ii. Prior to surgery, drugs to reduce the excessive adrenergic action (2 weeks)
iii. Surgery alternative: Demser prevents NE synthesis
b. Nursing
i. Keep phentolamine (Regitine) at the bedside
ii. During attack, maintain bed rest, HOB elevated at 30 degrees
iii. Instruct the client not to smoke, drink caffeine-containing beverages, or change position
suddenly
iv. BP meds, monitor blood glucose and urine for glucose and acetone, promote rest and a non
stressful environment, provide a diet high in calories, vitamins, and minerals, prepare the client
for adrenalectomy
8. Adrenalectomy: surgical removal of an adrenal gland
a. Bilateral med therapy: glucocorticoids for life
b. Unilateral med therapy: temporarily on glucosteroids up to 2 years
c. Catecholamine levels drop as a result of surgery cardiovascular collapse
hypotension and shock close monitoring of the patient hemorrhage can also
occur because of the high vascularity of the adrenal glands
d. Pre op
i. Monitor electrolytes, correct any imbalances
ii. Assess for dysrhythmias, monitor for hyperglycemia
iii. Protect the client from infections
iv. Administer glucocorticoids
e. Post op
i. Vitals, I&O, daily weight, electrolytes
ii. Monitor for signs of shock and hemorrhage, particularly first 24 to 48 hours
iii. Assess dressing for drainage, monitor for paralytic ileus
iv. Administer IV fluids to maintain blood volume
v. Administer glucocorticoids, pain medication
vi. Patient education: glucocorticoid therapy, medic alert bracelet
8. Thyroid
a. Functions:
i. Metabolism: increase rate, accelerate food utilization for energy, excites mental processes
ii. Growth: in children accelerates growth
iii. Carbohydrate: stimulates metabolism, including insulin secretion
iv. Fat: enhances fat metabolism
v. Body weight: production relates inversely to body weight (does not stimulate appetite)
vi. CV: increased cardiac output and heart rate, increased systolic BP by 10-20 mm
vii. Respiration: increases O2 use, rate, and depth
viii. GI: increases appetite, absorption, and motility
ix. CNS: speeds mental processes
x. Thyroid hormones affect nearly all body tissues
xi. Dysfunctions cause profound effects
xii. Three hormones: T3, T4, calcitonin
xiii. Thyroid hormones main component is iodine
xiv. Minimum daily requirement of I=80 mcg; more like 500mcg (contained in bread, water, and
iodized salt)
xv. Diagnostic tests:
1. Thyroid panel: T3, T4, free and bound
2. Radioisotope scan and uptake-- will be less than 10% in a 24 hr period. In secondary
hypothyroidism, intake increased with administration of exogenous TSH.
3. Scans, ultrasound, biopsy
b. Hypothyroidism
i. Deficiency in thyroid hormone
ii. Leads to low metabolism with buildup of metabolites
iii. Metabolites with water accumulate within cells causes edema called myxedema
iv. A hypothyroid state resulting from hyposecretion of thyroid hormone decreased
rate of body metabolism
v. Assessment
1. Lethargy and fatigue, forgetfulness and loss of memory
2. Weakness, muscle aches, parethesias
3. Intolerance to cold
4. Weight gain
5. Dry skin and hair
6. Loss of body hair
7. Bradycardia, cardiac disorder, menstrual distubances
8. Constipation, generalized puffiness and edema around eyes and face
vi. Diagnostic
1. Decreased T3 and T4, increased TSH, increased TRH
vii. Nursing interventions
1. Monitor vitals, including heart rate and rhythm
2. Administer thyroid replacement; levothyroxine sodium (Synthroid) is most common
3. Instruct patient about thyroid replacement therapy
4. Instruct the client in low-calories, low-cholesterol, low- saturated fat diet
5. Assess the client for constipation Colace
6. Provide a warm environment
7. Avoid sedatives and narcotics
8. Monitor for overdose of thyroid medication characterized by tachycardia, restlessness,
nervousness, and insomnia
9. Instruct to report episodes of chest pain immediately
viii. Myxedema Coma
1. A rare but serious disorder
2. It can be precipitated by:
a. Acute illness
b. Rapid withdrawal of thyroid medication
c. Anesthesia and surgery
d. Hypothermia
e. Sedatives and narcotics
3. Assessment
a. Hypotension, bradycardia, hypothermia, hyponatremia, hypoglycemia, respiratory failure, coma
4. Interventions
a. Airwayyyy, IV fluids or IV glucose as prescribed
b. Give Synthroid IV and corticosteroids as prescribed
c. Assess temperature, keep patient warm
 d. Monitor blood pressure, changes in mental status, monitor electrolytes and glucose level
c. Hyperthyroidism (Graves disease)
i. A hyperthyroid state resulting from a hypersecretion of thyroid hormone
ii. Characterized by an increased rate of body metabolism
iii. Thyrotoxicosis refers to the S/S that appear when body tissues are stimulated by increased
thyroid hormones
iv. Assessment
1. Weight loss, diarrhea, smooth soft skin and hair, nervousness and fine tremors of hands,
personality changes, irritability and agitation, goiter, exophthalmos
2. Elevated T3 and T4, low TSH, no response to TRH(thyrotropin releasing hormone), you would
do a thyroid scan and radioiodine uptake test (RAIU)
v. Nursing interventions:
1. Provide a high calorie diet
2. Avoid the administration of stimulants
3. Treat with drugs to return to near normal thyroid function prior to surgery
a. May receive Inderal to reduce cardiac problems
4. Prepare the client for radioactive iodine therapy as prescribed to destroy thyroid cells
5. Surgical intervention
a. May perform total or subtotal (thyroidectomy) performed when persistent
hyperthyroidism exits
b. Explain about risk for hoarseness and soreness
c. Pre op
i. Obtain vital signs and weight
ii. Assess electrolyte levels and for hyperglycemia and glycosuria
iii. Instruct the client how to perform coughing and deep-breathing exercise and how to support the
neck in the post op period when coughing and moving
iv. Administer antithyroid medications, sodium iodide solution, propranolol (Inderal), and
glucocorticoids as prescribed to prevent the occurrence of thyroid storm
d. Post op
i. Monitor for respiratory distress: oxygen, suction set up, trach at bedside
ii. Emergency equipment at the bedside
iii. Maintain semi-fowlers position
iv. Monitor surgical site: look at the back of neck too
v. Limit client talking and assess level of hoarseness: means they are losing airway
vi. Monitor for:
1. Laryngeal nerve damage: high pitch voice, dysphagia, restlessness, respiratory
obstruction assess for these
2. Hypocalcemia and tetany, which can be due to trauma to the parathyroid glands
vii. Prepare to administer calcium gluconate or calcium chloride as prescribed for tetany
viii. Monitor thyroid storm
e. Thyroid storm
i. Crisis situation -- usually caused by Graves
ii. Life threatening, uncontrolled hyperthyroidism
iii. Develops quickly and triggered by stress; trauma or infection
iv. Fever, hyperthermia, tachycardia, hypertension, abdominal pain, restlessness, confused,
psychotic
v. 25% mortality rate if left untreated
vi. Primary nursing care:
1. Maintain patent airway and adequate ventilation
 2. Administer antithyroid meds, sodium iodide solution, propranolol (Inderal), and glucocorticoids
as prescribed
3. Monitor vitals and cardiac dysrhythmias
4. Administer nonsalicylate/NSAIDS antipyretics Tylenol. NOT ASPIRIN
5. Use a cooling blanket to decrease temperature as prescribed
9. Hypoparathyroidism
a. A condition caused by hyposecretion of the parathyroid hormone by the parathyroid glands
b. Can occur following thyroidectomy from removal of the parathyroid tissue
c. Assessment
i. Hypocalcemia and hyperphosphatemia
ii. Numbness and tingling in the face
iii. Muscle cramps and cramps in the abdomen or in the extremities
iv. Positive Trousseaus sign or Chvosteks
v. Signs of overt tetany such as bronchospasm, laryngospasm, carpopedal spasm, dysphagia,
photophobia, cardiac dysrhythmias, seizures
d. Nursing interventions
i. Monitor vital signs
ii. Monitor for signs of hypocalcemia and tetany
iii. Initiate seizure precautions
iv. Place a tracheotomy set, oxygen, and suctioning at the bedside
v. Prepare to administer IV calcium gluconate or calcium chloride for hypocalcemia
vi. Provide a high-calcium and low-phosphorus diet: give vitamin D supplements, phosphate
binders to decrease the phosphate and help eliminate it
vii. Instruct the client to wear a medic alert bracelet
10. Hyperparathyroidism
a. A condition caused by hypersecretion of parathyroid hormone by the parathyroid gland
b. Assessment
i. Hypercalcemia and hypophosphatemia
ii. Fatigue and muscle weakness
iii. Skeletal pain and tenderness
iv. Bone deformities that result in pathological fractures
v. Anorexia, nausea, vomiting, epigastric pain, constipation
vi. Weight loss
vii. Hypertension, cardiac dysrhythmias
viii. Renal stone: calcium
c. Nursing interventions
i. Monitor
1. Vital signs, particularly the BP
2. Cardiac dysrhythmias
3. I&O and for signs of renal stones
4. Skeletal pain
ii. Encourage fluids
iii. Administer furosemide (Lasix) as prescribed, administer IV normal saline as prescribed
iv. Administer phosphates as prescribed, which interfere with calcium absorption
v. Administer calcitonin (Calcimar) as prescribed to decrease skeletal calcium release and
increase renal clearance of calcium
vi. Administer calcium chelators as prescribed to lower calcium levels
vii. Monitor calcium and phosphorus levels
viii. Prepare patient for parathyroidectomy
1. Preoperative
 a. Monitor electrolytes, calcium, phosphate, and magnesium levels
b. Assure that calcium levels are decreased to near-normal
c. Inform the client that talking may be painful for the first day or two postoperative
2. Postoperative
a. Monitor for respiratory distress
b. Place a tracheotomy set, oxygen, and suctioning at the bedside
c. Monitor vital signs
d. Position the client in semi-Fowlers
e. Assess neck dressing for bleeding; 1 to 5 ml of serosanguineous drainage is expected.
f. Monitor:
i. Hypocalcemic crisis
ii. Assess for positive Trousseaus or Chvosteks signs
iii. Changes in voice pattern and hoarseness
iv. Laryngeal nerve damage
g. Instruct the client in the administration of calcium and vitamin D supplements as prescribed
Cardiac
1. Patho
a. Conduction pathway
i. SA node: main pacemaker, generates 60 to 100 electrical impulses per minute
ii. AV node: will pace the heart in the case where the SA node is inactive. Can only pace at 40-60
bpm.
iii. Bundle of His - conduct electrical activity through the branches. Can be looked at to show left or
right bundle branch blocks.
iv. Purkinje Fibers - can pace at 20-40 bpm.
1. P Wave originates in the SA node.
2. PR interval should be no greater than 0.20. Greater than that can indicate heart block.
3. QRS Complex should be 0.04-0.12. Greater than this shows a widened QRS complex.
b. EKG lead placement.

2.
a. Questions we ask ourselves about a strip:
i. Rate: is it regular or irregular?
ii. What is the Rate? Slow or fast
iii. Is there a P wave for every QRS?
iv. Is there a QRS for every P wave?
v. What is the PR interval length?
vi. Is the R to R interval regular?
vii. What is the QRS duration? Narrow or widened?
b. Look at our patient, what are we assessing for?
i. We look at our patient. Helps us determine if there is something wrong.
ii. Skin warm or dry tells us about circulation.
iii. Short of breath could mean decreased cardiac output.
iv. Lightheadedness could possibly indicate some cardiac involvement.
v. Important questions: have you taken any medication? Have you experienced
this before?
vi. Be sure to obtain vital signs.
3. Cardiac Dysrhythmias
a. Normal Sinus Rhythm
i. Atrial and Ventricular rhythms are regular
ii. Rate: 60 to 100 beats/min
iii. PR interval and QRS width are within standard.
b. Sinus Bradycardia
i. Rate is less than 60bpm.
ii. Regular sinus
iii. Older patients can have pathological bradycardia. Also athletes. We want to determine the
underlying cause. Could be medication.
iv. For severe bradycardia we give atropine.
v. Nursing Interventions - administer O2 as needed, can apply noninvasive transcutaneous pacing
which sets a rate for the patient to ensure they dont go below it. Monitor for hypotension.
c. Sinus Tachycardia
i. Rate is greater than 100 bpm.
ii. Regular sinus.
iii. Causes include: exercise, infection, hypovolemia, hypoxia, MI, and stimulant drugs.
iv. Nursing Intervention - identify the cause of the tachycardia. Treat cause and lower HR.
d. Premature Atrial Complex (PAC)
i. Rate can be slow or fast.
ii. Rhythm is regular except for the PAC. PACs originate in the Atria.
iii. P waves are flattened or lost in T.
iv. QRS may or may not be normal.
v. Pathological PACs - children and teenagers.
vi. These occur before the normal beat is expected. Can be triggered by anxiety, fever, increased
sympathetic input, caffeine, drugs, and heart disease.

vii.
e. Atrial Fibrillation
i. No distinguishable P wave. Rate can be upwards of 350.
ii. This is the most common arrhythmia.
iii. Causes: hypertension, ischemia, mitral valve and pericardial disease, MI, and aging.
iv. The atria quiver which can lead to the formation of thrombi.
 v. We can treat with Heparin and monitor PTT or Warfarin and monitor INR. we must remind the pt
to stop taking these medications before any surgical intervention. We anticipate the HCP order
something to control the rate such as dig or amiodarone.
vi. Nursing Interventions - administer oxygen, anticoagulants, cardiac meds, prepare for
cardioversion.

vii.
f. Atrial Flutter
i. Rate is between 240 and 400.
ii. Regular Rhythm.
iii. No true P wave is shown, there can be 2-4 before the QRS. There is a sawtooth pattern.
iv. PR interval cannot be measured. QRS is normal.
v. Can feel shortness of breath, dizzy, lightheaded, or experience syncope. A person wont be in
this rhythm for long, its a transient rhythm.
vi. Treatment - rate control, cardioversion, or catheter ablation. For ablation they usually go through
the femoral or jugular.

vii.
g. Junctional Rhythm
i. This is an escape rhythm that serves as a protective mechanism when high pacing centers fail.
We wont survive being here for long.
ii. This occurs with with hypoxemia and digitalis toxicity.

iii.
h. Premature Ventricular Contractions
i. Rate is determined by underlying rhythm.
ii. No P waves, QQRS is wide and bizarre.
iii. PVC are early ventricular complexes result from increased irritability of the ventricles. The QRS
complex can be unifocal or multifocal.
iv. Bigeminy - a PVC is seen every other beat.
v. Trigeminy - every third beat is a PVC. 2 regular then PVC.
vi. Quadrigeminy - 3 beats then a PVC.
vii. Multifocal - different shapes and site of origination for the PVCs.
viii.
1. We want to notify the HCP when PVCs are noted, chest pain, PVC increase in frequency, runs
of Vtach, or R on T phenomenon.
2. We want to evaluate electrolytes, particularly potassium because it can cause PVCs when its
off.
3. Nursing Interventions - administer oxygen. Administer amiodarone or lidocaine as prescribed,
correct electrolytes.
ix. If there is a PCV on the T wave, it will initiate Ventricular Tachycardia.

x.
i.
Ventricular Tachycardia
i. Rate typically between 140-250 bpm.
ii. Rhythm is regular. No P waves seen and QRS is wide and bizarre.
iii. These patients need rapid diagnosis and treatment for this because they cannot stay in this for
long, they will go into cardiac arrest.
iv. Caused by: cardiomyopathy, sarcoidosis (inflammatory disease of the skin tissues).
v. Symptoms: dizziness, palpitations, SOb, nausea, changes in LOC, cardiac arrest.
vi. Treatment - defibrillation or ablation.
1. Stable V. Tach - should treat ASAP. they will not tolerate this for long. Give oxygen and
administer antiarrhythmic medications.
 2. Unstable V. Tach - shows hypotensive, SOB, angina, confusion, and can have pulses or be
pulseless. Treatment:
a. Pulse: administer oxygen, give antiarrhythmic meds, and have the patient cough hard.
Coughing hard may help the patient get back into a regular rhythm. This only works for awake
and alert patients.
b. Pulseless: these patients can be defibrillated. Medications that can be given are epinephrine,
amiodarone, or lidocaine.

vii.
j. Torsades de Pointes -- Polymorphic VT
i. Ventricular Rate: > 100 bpm usually >150
ii. P wave: none
iii. QRS: wide bizarre - twisting pattern
iv. Common causes: diarrhea, hypomagnesemia, hypokalemia, malnourished individuals, and
chronic alcoholics

v.
k. Ventricular Fibrillation
i. No recognizable complexes, wavy lines of varying amplitude
ii. Impulses from many irritable foci fire in a totally disorganized manner
iii. Chaotic rapid rhythm in which the ventricles quiver
iv. Rapidly fatal if not successfully terminated with 3 to 5 minutes
v. Causes: heart attack, cardiomyopathy, toxicity, sepsis
vi. Symptoms lack of: pulse, blood pressure, respiratory rate, and heart sounds

vii.
4. Management of Dysrhythmias
 a. Cardioversion
i. Synchronized countershock to convert an undesirable rhythm to a stable rhythm
ii. Performed by physician
iii. A lower amount of energy is used than with defibrillation
iv. Defibrillator is synchronized to the clients R wave
v. If the defibrillator were not synchronized, it would discharge on the T wave and cause VF.
vi. Pre-procedure:
1. Obtain consent
2. Administer sedation as prescribed
3. Hold digoxin (Lanoxin) 48 hours pre-procedures as prescribed to prevent post-cardioversion
ventricular irritability
vii. During the procedure:
1. Ensure that the skin is clean and dry
2. Joules:
a. 50-100 J for narrow or wide regular
b. 120-200 for narrow irregular, wife irregular 200 J
3. Stop the oxygen before because its a fire hazard
4. Prevent healthcare provider injury
viii. Post procedure
1. Maintain airway patency
2. Administer oxygen as prescribed
3. Assess VS, assess LOC
4. Monitor cardiac rhythm
5. Monitor indications for successful response:
a. Conversion to sinus rhythm
b. Strong peripheral pulses
c. Adequate BP
b. Defibrillation
i. It is done as soon as defibrillator is available in a witnessed arrest or after 2 minutes (or 5 cycles
of CPR) in an unwitnessed arrest
ii. Biphasic: 120- 200 J; Monophasic: 360 joules
iii. Resume CPR after defibrillation (no pulse or rhythm check past shock)
iv. Clear completely before delivery of electricity
v. Remove oxygen supply from area to avoid fire
vi. No need to synchronize this electric delivery: no synchronizing to R wave
vii. Use of paddle electrodes
1. Apply conductive pads
2. Paddle locations:
a. Third intercostal space to the right of the sternum
b. Fifth intercostal space on the left midaxillary line
3. Apply firm pressure with the paddles
a. Avoid breast tissue
4. Healthcare provider safety
c. Clinical Dead
i. The client is unresponsive, have a lack of respiration and no palpable pulse or sign of circulation
ii. Call code blue and start CPR immediately!!
iii. Crash cart evaluate clients rhythm
iv. Key to survival quality CPR
d. Automatic External Defibrillator (AED)
i. Prehospital cardiac arrest and lay persons
ii. Questions :
1. What type of surface should the patient be placed?
2. Do continue CPR with AED mode?
3. How do you prevent healthcare provider injury?
4. Place the electrode paddles in the correct position on the clients chest
5. Can you place a pediatric pad on an adult patient? Its uneffective
6. Can you place an adult pad on a pediatric patient? Yes if thats all we have, but they cannot
touch
7. What is the function of the analyze button?
iii. Shocks are recommended for pulseless VF/VT only
iv. If shock is recommended, the shock is initially delivered at an energy of 200 joules (Biphasic)
v. CPR is continued for 2 minute, and then a pulse check and rhythm check can be performed.
e. Implantable Cardioverter Defibrillator (ICD)
i. Monitors cardiac rhythm and detects and terminates episodes of VT and VF
ii. It senses VT or VF and delivers 25 to 30 joules up to four times if necessary
iii. Treatment:
1. Spontaneous sustained VT or VF unrelated to a myocardial infarction
2. Unsuccessful medication therapy for controlling life-threatening dysrhythmias
iv. Electrodes are placed in the right atrium and ventricle and apical pericardium; the generator is
implanted in the abdomen
v. Client education:
1. Basic functioning of the ICD
2. How to take the pulse; the pulse is taken daily and a diary of pulse rates is maintained
3. Wear loose-fitting clothing
4. Avoid contact sports and strenuous activities
5. During shock discharge, the client may feel faint or SOB
6. To sit or lie down if they feel a shock and to notify the physician
7. How to access emergency medical system
8. Encourage the family to learn CPR
9. Maintain a diary of any shocks that are delivered including:
a. Date
b. Preceding activity
c. Number of shocks
d. If the shocks were successful
10. Avoid electromagnetic fields directly over the ICD
11. Move away from the magnetic field immediately if beeping tones are heard, and notify the
physician
12. Keep a pacemaker ID in the wallet and obtain and wear a medic alert bracelet
13. Inform all health care providers that an ICD is inserted
14. Notify the healthcare provider if these symptoms occur:
a. Fever
b. Redness
c. Swelling
d. Drainage from the insertion site
e. Fainting
f. Nausea
g. Weakness
h. Blackouts
i. Rapid pulse
 6. AV Blocks
a. First degree AV Block: pr interval is longer than .20, QRS is usually narrow, p wave present with
every QRS; husband comes home late every night
b. Second degree AV Block
i. Type I Mobitz Wenckebach: progressive lengthening of interval then one p wave is not followed
by a QRS; husband comes home later and later until he doesnt come home one night
ii. Type II Mobitz II: PR wave is constant with no progressive lengthening, p wave not always
followed by QRS, if the QRS is narrow then it is a high block if it is wide then it is a low
block;sometimes husband comes home, sometimes he doesnt. This is more serious than type
1 second degree
c. Third Degree AV Block: no relationship between p and r wave and QRS can be wide or narrow;
husband no longer at home and no longer in a relationship with the wife
d. Treatment: pacemaker
7. Pacemakers
a. Synchronous or demand pacemaker
i. Stimulates depolarization
b. Asynchronous or fixed rate
i. Treats profound bradycardia
c. Overdrive pacing
 i. To suppress the underlying rhythm in tachydysrhythmias
d. Spikes: pacing stimulus that is delivered to the heart
i. What you should expect: p wave indicates atrial depolarization, QRS complex indicates
ventricular depolarization; this pattern is referred to as capture; both locations indicate atrium
and ventricle
e. Types
i. temporary : external transcutaneous or internal transvenous
1. Noninvasive temporary pacing (NTP)
a. Wash the skin with soap and water prior to applying electrodes
b. Do not shave the hair or apply alcohol or tinctures to the skin
c. Place the posterior electrode between the spine and left scapula behind the heart, avoiding
placement over bone
d. Place the anterior electrode between v2 and v5 position over the heart
e. Do not place the anterior electrode over female breast tissue but rather displace breast tissue
and place under the breast
f. Do not take the pulse of bp on the left side
g. Assure that electrodes are in good contact with the skin
h. If loss of capture occurs, assess the skin contact of the electrodes and increase the current
until capture is regained
2. Transvenous invasive temporary pacing
a. Pacing lead wire is placed through antecubital, femoral, jugular, or subclavian vein into the right
atrium for atrial pacing, or through the right ventricle, and positioned in contact with the
endocardium
b. Monitor cardiac rhythm-continuously
c. Monitor vital signs
d. Monitor pacemaker insertion site
e. Restrict client movement to prevent lead wire displacement
3. Reduce the risk of microshock
a. Use only inspected and approved equipment
b. Insulate the exposed portion of wires with plastic or rubber material (fingers of rubber gloves)
when wires are not attached to the pulse generator, and cover the nonconductive tape
c. Ground all electrical equipment using a three pronged plug
d. Wear gloves when handling exposed wires
e. Keep dressings dry
ii. Permanent: internal pulse generator
1. Pulse generator: SubQ pocket under the clavicle or abdominal wall
2. Lead placement: transvenously via the cephalic vein to the endocardium on the right side of the
heart
3. Single chambered: placed in the chamber to be paced
4. Dual chambered: placed in the atrium and right ventricle
5. Can use electrical appliances except when directly over the pacemaker site
6. If any unusual feelings occur when near any electrical devices, move 5 to 10 feet away and to
check the pulse
7. Avoid transmitter towers and anti theft devices in stores
f. Client Education
i. Educate about the pacemaker and programmed rate
1. Reprogrammed if necessary by noninvasive transmission
ii. Pacemakers are powered by either a lithium: 10 year lifespan
iii. The importance of follow up with the physician
iv. Report:
1. The signs of battery failure
2. Fever, redness, swelling, drainage from the insertion site
3. Dizziness, weakness or fatigue, swelling of the ankles or legs, chest pain, or shortness of breath
g. Troubleshooting
i. Failure to pace: pause without spikes
ii. Loss of capture: spike present but no QRS