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2019 NUR307 TEST 2 - Break down of lecture notes for NUR
307 test 2
Nurs Care Adults (Gwynedd Mercy University)
Studocu is not sponsored or endorsed by any college or university
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2019 NUR307 TEST 2
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COPD
#1 cause of COPD: smoking
o Others contributing factors: air pollution, occupational hazards, h/o lung disease, allergies, recent
pulmonary infections & sometimes viruses can create irreversible damage to the lungs that leads
to COPD
COPD is a problem with expiration, air trapping and increased CO2
#1 cause of a COPD exacerbation is Infection
Airflow limitation not fully reversible
o The airways get obstructed, when they get obstructed there is a hyperobstruction of airflow related
to mucous
o Hypersecretion that is what causes the actual cough-alveolar edema (pt will have a cough and
eventually have bronchospasm)
CO2 retention: hypercapnia (hypercapnic respiratory failure) from increased CO2
Normal CO2: 35-45
Normal oxygen saturation: 95-100%
3 steps in oxygenation: Ventilation, Perfusion & Diffusion
o Ventilation: the movement of air in and out of the body
 We move about 500mL in and out of our lungs
 Dependent on rate and depth
 Acid based balance effects our ventilation
o Perfusion: movement of oxygen to the cells. Want the oxygen saturating the cell
 Need O2, CO2, hemoglobin
 More hemoglobin is made for pts with COPD because they are staved with oxygen
o Diffusion: oxygen that is carried across the capillary membrane
Work of breathing: the effort required to expand and contract the lungs
o Increase work of breathing = increased oxygen demand
o Determined by:
 Compliance: elasticity of the lungs, how expandable the lungs are (think of balloon hard
when you first try to blow it up then easier the second time)
 Airway resistance: any process that changes the bronchial diameter
 Presence of active expiration: blowing off CO2
 Use of accessory muscles: not normal, a sign of struggle, need help and quickly
 Seen in sternocleomastoid, coastal, intercoastal, abdomen (frequently)
Respiratory disease: obstructive or restrictive (ALS, sarcoidosis)
o Obstructive: difficulty exhaling air from lungs
 Asthma
 Chronic Obstructive Pulmonary Disease (COPD): a group of conditions causing the
chronic or recurrent obstruction of airflow. It can result from the combination of
symptoms associated with:
 Emphysema (PINK PUFFER): severe destruction and remodeling of the lungs
o Distention & destruction of gas-exchanging portion of the lung
o Abnormal permanent to the air sacs (alveoli)
o Systemic effects:
 skeletal muscles: loss of muscle mass, osteoporosis
 malnutrition, anemia
 Depression
 Pulmonary hypertension, right sided heart failure
(corpulmonale)
 Typically will die from this
 Chronic Bronchitis (BLUE BLOATER): the presence of a cough for 3 months
for 2 consecutive years, chronic cough/sputum production
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o Seen as chronic inflammatory response due to damage to the lung
 Not everyone that has COPD had emphysema
 Everyone who has COPD has Chronic bronchitis
COPD Nursing Assessment
o Nasal flaring, Cyanosis, Dyspnea, decreased respiratory effort (ineffective breathing pattern),
Decreased LOC (due to not having enough oxygen to the brain) “CO2 Head”, Accessory muscle
use, decreased breath sounds (typically decreased in the bases), decreased oxygen saturation
o Hyperventilation is your blowing off CO2
o If CO2 is rising an increase in breath rate and volume will be the only thing to bring it back down
o Palpation: chest expansion, tracheal position, retractions
o Percussion: hyper-resonance, tactile fremitus
o Auscultation: crackles, gurgles, wheezes
 Wheezing: bronchoconstriction
 Pt needs bronchodilators
 Crackles: typically, some type of fluid
 Rhonchi: inspiratory or expiratory and typically cleared with cough or suction
 Can be cleared with an expectorant
Signs and Symptoms COPD conditions: Chronic bronchitis
o Dyspnea, cyanosis
o Prolonged expiration
 Will be seen when the body is trying to compensate for the high CO2
o Scattered crackles, rhonchi and wheezing
 Crackles indicate fluid
 Rhonchi indicates mucous: will clear with coughing and suctioning
 Wheezing indicates there is bronchoconstriction (narrowing the airways)
o Cardiac dysrhythmias
 From the body being starved from oxygen
o Increased mucous production
 Can help by fluids, chest PT, medication with Mucinex and expectorates (helps to thin the
mucous so that it can be expelled)
o Productive cough
o Increased anterior-posterior diameter
o Peripheral edema
o Normal respiratory rate
Signs and Symptoms COPD conditions: Emphysema
o Dyspnea (all the time)
o Barrel chest
o Use of accessory muscles (typically)
o Increased AP diameter of chest
o Decreased BS with expiratory wheezes
o Patient may look pink and puffy
o Tachypnea
o Leans forward while sitting
Staging of COPD**
o Stage 1: mild- symptoms present, FEV1 greater than 80% predicted
o Stage 2: moderate-worsening airflow limitation, FEV1 less than 80% predicted
o Stage 3: severe- further worsening of airflow limitations, FEV less than 50% predicted
o Stage 4: very severe- severe airflow limitation, FEV1 less than 30% predicted or less than 50 %
with chronic respiratory failure
o FEV1 (Forced expiratory volume): vital capacity of the air
o The lower the FEV1 the worse it is
Diagnostic Procedures
o Chest x-ray: positive findings include hyperinflation of the lung, cardiac enlargement, flattened
diaphragm, congested lung fields
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PEFR (peak expiratory flow rate): will measure the expiratory ability and help assess condition
improvement after treatment
o Pulse Ox
o **ABG (arterial blood gas): decrease pao2, increased pco2
 Decreased oxygen increased CO2
o CBC w/diff: increased WBC indicate infection, eosinophilia indicate asthma
o Sputum cultures: specifically identify infectious agent
 Do as soon as you can before antibiotics is preferred
o Enzymes: may show decreased level of antitrypsin
GOLD guideline recommendations for COPD
o Long-acting bronchodilators: relax airway smooth muscles
 Beta agonist (albuterol, serevent, foradil)
 Anticholinergic (Spiriva)
o Corticosteroids: reduces inflammation in the airways
 It works by decreasing the bodies immune response
 Inhaled (Flovent, Pulmicort, Asmanex)- long term preventative therapy
 Oral for exacerbations
o Combination
 2 bronchodilators with different mechanisms (Combivent, DuoNeb)
 Bronchodilator + corticosteroid (Advair, Symbicort)
o Nebulizers work quicker and more efficiently because it actually gets to the lungs
o Nebulized inhalers and bronchodilators are the most commonly ordered medications
 Need at least 10 liters of oxygen with it on a face mask
o Antibiotics may also be given if an infectious process is suspected
o Do not give a wheezing patient a beta blocker
o Reduce COPD exacerbation by reducing risk of infections
o Vaccines:
 Influenza & pneumonia
o Two ways to get rid of CO2
 Increase respiratory rate
 Increase depth (volume)
o Steroids can: raise your blood sugar
 **Need to be weaned down, cannot stop abruptly
Nursing Interventions
o Allow the patient to be in a position that makes breathing easier
 **#1 priority is sit the head of the bed up, facilitate proper ventilation
o Begin O2 therapy based on pt condition
 High flow oxygen could cause the opposite effect, making the patient lose the drive to
breathe
o **A venturi mask is the MOST precise method of delivering exact amounts of oxygen
 Ventilator
 Nasal cannula can go up to 6 Liters (use a mask if cannula is not enough)
 Anything over 2 should be humidified
 Normal FIO2: 21% atmospheric air
 Need a standing order by physician to give oxygen
o Continue to monitor vital signs: 24hr pulse ox, cardiac monitoring
o If they get CO2 head: ventilate them, wipe out Bipap mask
o Bipap: a noninvasive ventilator that delivers both pressure volume oxygen and can deliver a
necessary rate
 Bipap is not appropriate for a patient who is completely confused and unable to protect
their own airway
 If you cant do bipap, the patient can get put on 100% non-rebreather
 ABG tests will need to be done to let us know how to fix the problem
o Call rapid response if the patient is starting to go down hill
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Patient in COPD exacerbation is going to end up in respiratory acidosis
Assess Neuro status: elevated CO2 can cause CO2 head and pt can become very confused
Respiratory failure: low O2, SOB, using accessory method, tachycardic, hyper/hypoventilation
 While waiting for rapid response put them on oxygen, sit the head of the bed up, get ABG
labs* in order to correct it (ph will be low typically around 7.25 when this sick) (CO2 is
high) (PO2 will be low normal range is 80-100)
 How do u fix respiratory acidosis: oxygen with an increased respiratory rate or volume
(achieved by being put on a ventilator) ex. Bipap machine
 Difference between bipap and cpap: bipap is inspiration and expiration
o Obtain IV access
Patient management
o Pursed lip and diaphragmatic breathing
 Pursed lip prolongs expiration to help decrease air trapping and co2 levels
 Diaphragmatic breathing teaches the pt to use their diaphragm
o Change diet habits/exercise
o The need to cough up sputum
 Mucinex is the best one to help thin and liquify secretions so pts can move it up and out
of their lungs
o Staying hydrated
o Avoid triggers
o Medication compliance
COPD exacerbation
o Common causes: infection, air pollution
o Symptoms: increased dyspnea, increased cough, increased sputum
o Fatigue, activity intolerance, disturbed sleep
o Fever is rarely present
o Treatment:
 Mostly managed outpatient
 Indications for hospitalization: pneumonia, sever dyspnea, accessory muscle use,
worsening hypoxemia, change in mental status, peripheral edema
 Medications
 Bronchodilators (short acting beta 2 agonist)
o Consider using a long acting bronchodilator if pt is not using one
 Oral corticosteroids
o Prednisone 30-40mg/d PO for 10-14 days
o Consider using inhaled one
o Rinse mouth after taking to prevent thrush
 Oxygen
 Pt education: smoking cessation, check inhaler technique, consider using a spacer, airway
clearance devices (vibratory peep or flutter valve), pulmonary rehab
o Correct use of metered dose inhaler (MDI)
 Inhaled and oral steroids: reduce inflammation
 Many pts do not benefit from inhaled medications due to incorrect techniques
 Recommended use of spacers
 Common problems with metered dose inhalers:
 Difficulty activating inhaler
 Lack of co-ordination of inspiration with release of medication
 Pts inability to take a slow deep breath
Right lung has 3 lobes and left has 2
Respiratory Acidosis: occurs when the lungs cannot remove all of the carbon dioxide produced by the body
o Symptoms:
 Ph is low, Co2 is high
 Hypoventilation leads to hypoxia
 Rapid, shallow respirations
 Decrease BP with vasodilation
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 Dyspnea
 Headache
 Hyperkalemia
 Dysrhythmias
 Drowsiness, dizziness, disorientation
 Muscle weakness, hyperreflexia
o Causes:
 Decreased respiratory stimuli (anesthesia, drug overdose)
 COPD (major cause)
 Pneumonia
 Atelectasis
o Must be corrected or the pt will die
o May be a sign of respiratory failure with dangerously low blood oxygen levels
Self-management behaviors
o Manage exacerbations
o Smoking cessation
o Proper use of oxygen therapy
o Maintaining functional abilities
Caring for a patient with Asthma
Definition: chronic inflammatory disorder of airways, variable airflow obstruction, leads to
recurrent episodes of wheezing, breathlessness, cough and chest tightness
o #1 priority nursing goal: help them teach them about the disease to prevent
exacerbation
o Women are affected more than men
Pathophysiology: primary response is chronic inflammation from exposure to
allergens/irritants
 Leads to bronchoconstriction, hyperresponsiveness and edema of airways
 Remodeling: occurs in some cases, body adapts to the issue, cells/tissues get
more fibrous, morph into something it wasn’t before
Triggers of Asthma:
 Allergens: seasonal or year-round, furry animals, fungi, molds, cockroaches
 Exercise: exercised induced asthma (EIA), occurs after vigorous exercise, because of
hyperventilation CO2 is released, hypercapnic (CO2 retention) causing, pronounced
with cold/dry air, decrease likelihood of symptoms by breathing through mask/scarf,
premedicate
 Air pollutants: cigarette/wood smoke decreases lung function, vehicle exhaust,
pollution
 Occupational factors: exposure to diverse agents, may take months-years
 Viral respiratory infections: major factor in acute asthma attack, increase
inflammation and hyperresponsiveness of tracheobronchial system, increase airway
narrowing ex. Flu, upper respiratory infection
 Nose/sinus problems: large polyps need to be removed, usually related to
inflammation of mucous membranes which decrease ability to get enough air in and
out
 Drug allergies: aspirin and non-steroidal anti-inflammatory drugs (NSAIDS) block
specific enzymes and increase production of pro-inflammatory, wheezing develops in
2 hours, salicylate sensitivities (found in food, beverages and flavorings), BAdrenergic blockers trigger bronchospasms, ACE inhibitors cause dry non-productive
cough that causes bronchospasms
 Food allergies: may cause asthma symptoms, rare in adults, food challenges to test
what happens when certain food are eaten (controlled environment)
 GERD: reflux can trigger bronchoconstriction or aspiration, asthma meds worsen
GERD because of dilation (foods: spicy, chocolate, alcohol, caffine)
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Emotional stress: attacks can trigger panic and anxiety, pt hyperventilates,
decreasing CO2, airway narrows due to hypocapnia
Acute Asthma Attack: triggers vary, airways narrow
o What to do when it happens:
o Teach them how to use an inhaler
 In acute attack use short acting medication
o Seek help, Administer medications, Take them properly, If it doesn’t work, call
911
o Having an action plan is going to be the most important thing
 Clinical Manifestations:
 recurrent wheezing (hear with expiration), breathlessness, cough and tight
chest, abrupt or gradual, last minutes to hours (miniutes usually means an
acute attack, hours means they are in big trouble and need to get to the ER
asap), ,prolonged expiration (air takes longer to move out), Inspirationexpiration ratio is 1:2 (normal) to 1:3 or 1:4, bronchospasm, edema, mucus in
bronchioles narrow the airway
 Leads to trapped air and difficulty expiring
 *produces wheezing, air trapping and hyperinflation
 Wheezing is unreliable to gauge severity
 Severe attacks may have no audible wheezing because there is no air
moving
 May be described as sounds arising from the nose and upper airways
 silent chest: no wheezing due to no air movement
 Hypoxemia: restlessness, increase anxiety, inappropriate behavior, increased
pulse and BP, O2 sat below 90, hypercapnic (decreased CO2), difficulty
speaking, increases respiratory rate, hyperresonance (percuss lungs, heard bc
air is trapped inside), inspiratory and expiratory wheezing, silent chest
 As nurse: try to settle, be calm, give Oxygen, deep breathing
 Diagnostic studies:
 Peak flow: normal ranges are based on height and age, pt needs to know their
normal range, small hand-held device that measures pts fastest flow they can
generate after taking a deep breath in and blowing out as hard and fast as
they can, pt can perform on their own
 Pulmonary function test (PFT): measures lung capacity and ability to move air
in and out of lungs, perform test between asthma attacks, stop taking
bronchodilators 6-12 hours before test, in office
 Chest X-Ray: gives baseline, shows lungs
 Oximetry: gives oxygenation status
 Lung function test: self-administered survey (asthma control test ACT)
 Allergy skin testing, blood levels of eosinophils and IgE
 Sputum culture and sensitivity: perform when pt has increased secretions to
see if bacteria grow
Cough Variant Asthma: associated with GERD pts, bronchospasm is not severe enough to
cause air flow obstruction
 Clinical Manifestations: cough, feeling of suffocation, increased anxiousness, “I can’t
get a deep breath”
 Nurse: make sure pt is sitting up right, tripod position (allows full lung expansion and
exhalation)
Classifications:
 Intermittent: less than or equal to 2 days of exacerbations per week, no limitations
 Mild persistent: greater than 2 days per week of exacerbations, minor limitations
 Moderate persistent: daily exacerbations, some limitation
 Severe persistent: continuous exacerbations from morning to night, extreme
limitations
Complications:
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Respiratory rate >30 per min
Pulse >120 per min
Peak expiratory flow rate (PEFR) is 40% of persons best and less than 150L being
blown out
 ED or hospitalized
 Status asthmaticus: medical emergency, rapid progression, pt has chest tightness,
wheezes, dry cough and SOB
 Life-threatening: too dyspneic to speak, perspiring profusely, drowsy/confused,
requires hospital care (ICU)
Nursing Management/Diagnoses/Problems/Plans:
 Ineffective airway clearance, impaired gas exchange, ineffective breathing pattern,
anxiety, knowledge deficit, risk for aspiration
 Achieve and maintain control of disease, decreased incidence of attacks, reduce
recurrent exacerbations, teach, maintain greater than 80% of personal best PEFR,
minimize symptoms, maintain acceptable activity levels, few or no adverse effects,
attain normal lung function (collaborative)
 Monitor respiratory and cardiovascular systems, assess O2, sit upright, encourage
slow breathing (pursed lip), help decrease panic, administer meds
Medications:
 Delivery systems: inhalers (dry-powder, metered dose), spacer (holding chamber,
easy use), nebulizers (convert liquid med into fine mist), teach pt proper technique,
MUST rinse mouth after corticosteroid inhaler use
 Relievers: relax muscles around airways, dilating, (bronchodilators)
 Preventers: reduce redness and swelling, anti-inflammatories (steroids or
decongestants)
 Symptom Controllers: long active relievers, relax airway, used with corticosteroid
preventives
 Anti-inflammatory drugs: more effective in asthma control than any other long-term
drug
 Corticosteroids: reduce bronchial hyperresponsiveness, block late-phase response,
inhibit migration of inflammatory cells
 Leukotriene Modifiers: block action of leukotrienes
 Leukotrienes: inflammatory mediators, potent bronchoconstrictors, used as
alternative of corticosteroids inhaled, or used in conjunction for severe cases
 Bronchodilators: produce bronchodilation, increase mucociliary clearance
 SABA’s: most effective drug for relieving acute bronchospasms, rescue med,
increase HR and BP
 LABA’s: long-term control of moderate to severe asthma, never use alone, use
with ICS
Severe Exacerbations: most treatment is the same as acute, increase in frequency and dose
of bronchodilators
 IV corticosteroids are administered every 4-6 hours, then give orally, continuous
monitor, IV magnesium sulfate is given as bronchodilator, Heliox (mix of helium and
O)
 Supplemental O2 is given by mask or nasal cannula for 90% sat, arterial catheter
may be used to facilitate frequent ABG monitoring, IV fluids are given
Patients Personal Management:
 Determine triggers, avoid smoking, consider allergen immunotherapy, daily peak flow
monitoring, fluid intake of 2-3L/day, avoid cold air, aspirin, NSAIDS, and nonselective
B-blockers
Action Plans:
 Green zone: breathing is normal, no asthma symptoms, peak flow results are 80100% of personal best, remain on meds
 Yellow zone: some symptoms (SOB, wheezing, coughing, indicates caution,
something is triggering asthma, peak flow rate is 50-80% of personal best
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Red zone: serious problem, symptoms prevent normal activities, action must be
taken with health care provider, peak flow 50% or less than personal best
Caring for a Patient With Pneumonia, page 291-306
What is pneumonia:
● Infection of the lower respiratory tract caused by a variety of microorganisms, including bacteria,
viruses, fungi, protozoa, and parasites.
● It is the most common infectious cause of death.
Three ways organisms reach lungs:
1. Aspiration from nasopharynx or oropharynx,
2. Inhaled of microbes present in the air,
3. Spread from primary infection elsewhere in the body
Community-Acquired Pneumonia (CAP): Occurs either in the community dwelling person, or within the first 48
hours after hospitalization. Most commonly caused by streptococcus pneumonia.
Risk factors:
-Smoking
-Alcohol abuse
-pre-existing hypoxia
-Acidosis
-Toxic inhalations
-Pulmonary edema
-Altered mental status
-Preexisting conditions such as COPD or asthma
-Malnutrition
-Poor dental hygiene
-Older than 65
-IV drug abuse
-10 or more people in one household
-Environmental conditions
-previously having pneumonia
Hospital-Acquired Pneumonia (HAP) (nosocomial): Onset of pneumonia symptoms more than 48 hours after
admission in patients who had no evidence of infection at the time of hospitalization. Most common kind is
Staphylococcus aureus.
● The most common type of hospital acquired pneumonia is VAP, aka ventilator-associated pneumonia. This
involves endotracheal intubation, and mechanical ventilation.
Risk Factors:
-Debilitation (weak to everyday activities)
-Malnutrition
-Altered mental status
-Previous exposure to antibiotics within the last 90 days
-Hospital stay of 5 days or longer
-High rates of antibiotic resistance
-Immunosuppressive therapies or diseases
-Male gender
-Prolonged intubation or a tracheostomy
Health Care-Associated Pneumonia (HCAP): Residents of a nursing home or other type of long term care facility,
acute care hospitalization for 2 or more days within 90 days, IV antibiotic therapy, wound care, or chemotherapy.
Risk Factors:
-Hospitalization for 2 or more days in the last 3 months
-Chronic dialysis
-Home wound care
-Home IV therapy of antibiotics or chemo
-Family member with drug-resistant microorganism
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Clinical Manifestations: Fever, cough, dyspnea, leukocytosis (elevated WBCs), rigors (shaking/chills), pleuritic
chest pain, use of accessory muscles, tachycardia, fatigue and anorexia. Patients might initially have an upper
respiratory tract infection such as nasal congestion and sore throat.
Physical assessment: bronchial breath sounds over consolidation lung areas, crackles, increased tactile fremitus,
percussion dullness, egophony. Purulent sputum (Purulent sputum contains pus, composed of white blood cells,
cellular debris, dead tissue, serous fluid, and viscous liquid (mucus). Purulent sputum is typically yellow or green)
may be the only sign of pneumonia in patients with COPD.
Diagnosis:
-Chest X-ray
-Sputum C & S (Have pts do this in the morning)
-Elevate WBC
-Alterations in ABGs
-Thoracentesis
-Bronchoscopy
Nursing Management Problems:
-Ineffective airway clearance
-Impaired gas exchange
-Ineffective breathing pattern
-Acute pain
-Activity Intolerance
-Knowledge deficit
Nursing Management:
Promote rest and conserve energy
Promote fluid intake
Maintain nutrition
Promote pts knowledge
Monitor and manage complications
Pharmacologic Therapy:
-The choice of antibiotics is determined by the classification of pneumonia, results of gram stain, culture
sensitivities, antigen testing, and patients comorbid conditions.
- Prompt admin. Of antibiotics in patients is a key treatment measure.
-The recommended duration of treatment for CAP is a minimum of 5 days. Patients should be afebrile for at least 2
days before antibiotics are discontinued.
Patients with nosocomial pneumonias are treated for 7-10 days, as long as the pt is showing improvement.
Oxygen Inhalation Therapy:
-The goal of using oxygen therapy is to prevent or correct tissue hypoxia, which is decreased oxygen supply to the
tissues.
-When administering oxygen to a pt a nurse must keep in mind that oxygen transport to the tissues is dependant not
only on the arterial oxygen content but also on the cardiac output hemoglobin concentrations, and metabolic
requirements.
-The use of oxygen to treat patients is based on dyspnea, chest pain, ABG analysis, POX, a physical examination,
change is resp rate, change in mental status, change in BP, development of arrhythmias, cyanosis, diaphoresis, and
cool extremities.
Coronary Artery Disease
CAD (coronary artery Disease)
o Chronic stable angina
Atherosclerosis: Hardening of the arteries
o Begins as soft deposits of fat that harden with age
o Characterized by lipid deposits within intimas of the artery
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o Endothelial injury and inflammation play a major role in development
o People with high cholesterol are more at risk to develop this
o Major cause of CAD
CAD etiology and pathophysiology
 C-reactive protein (CRP)
o Nonspecific marker of inflammation
o Increased in many patient with CAD
o Chronic exposure to CRP associated with unstable plaques and oxidation of LDL cholesterol
o Diagnostics we could use with CRP is cholesterol (HDL good, LDL bad)
Collateral Circulation
● Arterial anastomoses (or connections) within the coronary circulation
● Increased with chronic ischemia
● Inadequate with rapid onset CAD
Risk Factors for CAD
● Nonmodifiable risk factors (things your stuck with):
○ Age- men over 45, women over 55 bc of the amount of estrogen (protective effect on all
blood vessels after menopause)
○ Gender: more prevalent in men
○ Ethnicity: african americans at highest risk, Mexican americans are second, caucasions
have the lowest risk
○ Family history: a first degree relative (sister, brother, mother) with CAD you are at higher
risk
○ Genetic predisposition
● Modifiable risk factors
○ Elevated serum lipids (don’t need to know numbers)
■ Cholesterol >200 mg/dL (5.2 mmol/L)
■ Triglycerides >150 mg/dL (3.7 mmol/L)
■ High-density lipoproteins (HDL): want them to be high, over 40-59 mg/dl, less
than 40 you have an increased risk for CAD.
● Carry lipids away from the heart to the liver
■ Low-density lipoproteins (LDL) : want them to be low, 100-129 mg/dl,
considered normal. Over 160 is considered high and at risk for CAD.
● Contain more cholesterol and are attracted to the coronary artery walls
○ Hypertension
■ >140/90 mmhg or >130/80 mmhg if diabetes or CKD
■ Begin lifestyle changes for prehypertension
■ Treat stage 1 or 2 hypertension with drugs
■ Hypertension increases the workload of the heart
○ Tobacco use
■ Increased catecholamine release (make the heart work harder), general term for
the stress hormones (epinephrine and norepnephrine)
■ ↑ LDL, ↓ HDL, ↑oxygen radicals
■ ↑ Carbon monoxide
■ Second-hand smoke
○ Unhealthy diet: WEIGHT
○ Stress
○ Sleep apnea
○ Chronic kidney disease
○ Chronic infections
○ Physical inactivity
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Obesity:as obesity increases so does insulin resistance
Diabetes: risk increased for people who have diabetes even if sugar is under control,
preferably have your hemoglobin A1C under control
Metabolic syndrome: insulin resistance, abdominal obesity, abnormal serum lipids, pro
inflammatory state, and pro thrombotic state
Collaborative and Nursing Management
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Prevention and early treatment
Identification of people at high risk
○ Healthy history, including family history
○ Presence of cardiovascular symptoms
○ Environmental patterns: diet, activity
○ Psychosocial history
○ Values and beliefs about health and illness
Manage high risk persons by controlling modifiable risk factors
Encourage lifestyle changes
○ Education clarify personal values
○ Set realistic goals
■ Decrease amount of smoking
■ Refer to a nutritionist
Physical fitness
○ FITT (frequency, intensity, type & type) formula: 30 minutes most days plus weight
training 2 days a week
Regular physical activity contributes to
○ Weight reduction
○ Reduction of >10% in systolic BP
○ In some men more than women, increase in HDL cholesterol
Nutritional therapy
○ Decrease saturated fats and cholesterol
○ Increase complex carbohydrates and fiber
■ Whole grains, fruit, veggies
○ Decrease red meat, egg yolks, whole milk
○ Increase omega-3 fatty acids
■ Eat at least 2 times per week
■ Salmon, tuna, tofu, soy beans
○ Eliminate alcohol and simple sugars
Lipid-lowering drug therapy
○ If diet and exercise ineffective
○ Statins (means to stop something)
■ Inhibit cholesterol synthesis, decrease LDL, increase HDL
■ Monitor for liver damage and myopathy
● AST & ALT
■ Ex. atorvastatin
○ Niacin (B vitamin)
■ Lowers LDL and triglyceride by inhibiting synthesis
■ Increase HDL
■ Flushing, pruritus, GI side effects, orthostatic hypotension
○ Antiplatelet therapy: clot does not form
■ ASA 81mg reduces the stickiness of the platelets
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Clopidogrel (plavix) can be used in conjunction with ASA
Gerontologic Considerations
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Increased incidence and mortality associated with CAD in older adults
Strategies to reduce risk and treat CAD are effective
Treat hypertension, increase lipids
Smoking cessation
Necessary to modify guidelines for physical activity
○ Longer warm up
○ Longer periods of low level activity
○ Longer rest periods
○ Avoid extremes of temperature
○ 30 minutes most days minimum
Most likely to change when hospitalized or symptomatic
Clinical manifestations of CAD- Angina
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O2 demand> O2 supple -> myocardial ischemia
Angina= reversible ischemia
○ Occurs when arteries are blocked 70% or more
○ Hypoxic within 10 seconds of occlusion
○ Viable for 20 minutes
Lack of oxygen and glucose leads to anaerobic metabolism
Lactic acid irritates nerve fibers -> pain in cardiac nerves
Referred pain from transmission to the upper thoracic posterior nerve roots
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pressure/ache
Squeezing, heavy, choking, or suffocating sensation
Rarely sharp or stabbing
Indigestion or burning
Various locations- shoulder, arms chest, jaw
Angina pain
Chronic stable angina
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Intermittent chest pain that occurs over a long period with the same pattern of onset, duration and
intensity of symptoms.
Pain usually lasts for 5 to 15 minute duration and commonly subsides when the precipitating
factor is resolved
ST segment depression and/or T-wave inversion (don’t need to know)
Control with drugs
○ Nitroglycerin is given
Collaborative care for chronic stable angina
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Goal: decrease O2 demand and/or increase O2 supply
Short acting nitrates
○ Dilates peripheral and coronary blood vessels
○ Give sublingual (tablet) or by spray
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If no relief in 5 minutes, call EMS; if some relief, repeat every 5 minutes for maximum 3
doses
○ Patient teaching
○ Can use prophylactically
Long-acting nitrates
○ To reduce angina incidence
○ Main side effects: headache, orthostatic hypotension
○ Methods of administration
■ Oral
■ Nitroglycerin (NTG) ointment
■ Transdermal controlled-release NTG
Angiotensin-converting enzyme inhibitors: causes vasodilation, reduces blood volume and helps
with the oxygenation that the heart needs
○ lisinopril
Beta-adrenergic blockers: decreases the workload of the heart, decreased HR and BP
○ Metoprolol, Lopressor
Calcium channel blockers: decrease myocardial oxygen demand, causes vasodilation, decrease
systemic vascular resistance
○ Cardizem
Sodium current inhibitor: used as a last resort, used when there is no response from any of the
prior drugs listed
○ Ranolazine (ranexa)
Diagnostic studies
○ Chest xray
○ Laboratory studies
○ 12 lead ECG
○ Calcium score screening heart scan
○ Echocardiogram
○ Exercise stress test
○ Pharmacologic nuclear imaging
Nursing/collaborative management
●
Cardiac catheterization/coronary angiography
○ Visualize blockages (diagnostic)
○ Open blockages (interventional)
■ Percutaneous coronary intervention (PCI)
■ Balloon angioplasty
■ Stent: holds it in place
Nursing care post Cardiac Cath/PCI
● Monitor VS and cardiac rhythm
● Monitor insertion site (radial or femoral artery) for signs of bleeding
● Maintain bedrest for prescribed amount of time (pt may also have to lay flat for 1-2 hours)
● Neurovascular checks of extremity distal to insertion site
ACS (acute coronary syndrome)
○ UA (unstable angina)
○ MI (myocardial Infarction)
Etiology and pathophysiology
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Deterioration of once stable plague ruptures turning into platelet aggregation which creates a
thrombus
 Result from this is:
 partial occlusion of coronary artery: UA or NSTEMI
 total occlusion of coronary artery: STEMI (most serious of the two)
Clinical manifestations of ACS unstable angina
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New in onset
Occurs at rest
Worsening pattern
Increase in frequency
Unpredictable
Medical emergency
Symptoms in women may be more vague
Clinical manifestations of ACS Myocardial infarction (MI)
 Result of sustained ischemia
o >20 minutes, causing irreversible myocardial cell death (necrosis)
o 80-90% secondary to thrombus
o Ischemia starts in subendocardium
o Necrosis of entire thickness of myocardium takes 4 to 6 hours
o Loss of contractile function
 Pain
o Severe, immobilizing chest pain not relieved by rest, position change, or nitrate
administration
o Heaviness, pressure, tightness, burning, constriction, crushing
o Substernal, retrosternal, epigastric
o More common in AM
o Atypical in women, elderly
o No pain if cardiac neuropathy (diabetes)
o Common locations: substernal, retrosternal, or epigastric areas; pain may radiate to neck,
jaw, arms
 Catecholamine release: stimulation of SNS
o Release of glycogen
o Diaphoresis
o Vasoconstriction of peripheral blood vessels
o Skin: ashen, clammy, and/or cool to touch
 Cardiovascular
o Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO)
o Crackles
o Jugular venous distention
o Abnormal heart sounds
 S3 or S4
o New murmur
 Swishing sound or echo sound
 Nausea and vomiting
o Vomiting center by severe pain
o Vasovagal reflex
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 Heart rate will decrease severly
Fever
o Up to 100.4° F (38° C) in first 24 hours
o Systemic inflammation - myocardial cell death
Myocardial Infarction Healing Process
 Within 24 hours, leukocytes infiltrate the area of cell death
 Proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by fourth day →
thin wall
 Necrotic zone identifiable by ECG changes and nuclear scanning
 Collagen matrix laid down
 10 to 14 days after MI, scar tissue is still weak
 Myocardium vulnerable to stress
 Monitor patient carefully as activity level increases
 By 6 weeks after MI, scar tissue has replaced necrotic tissue
o Area is said to be healed, but less compliant
 Ventricular remodeling
o Normal myocardium will hypertrophy and dilate in an attempt to compensate for the infarcted
muscle
 Immediate treatment of an MI is MONA
o Morphine: for pain, causes vasodilation to get oxygen to areas that it is needed
o Oxygen: given with chest pain to keep as much oxygen ready available to get it to the heart
o Nitroglycerine: vasodilates, helps get more blood flow to the area that it is needed
o ASA or plavix: antiplatelet, prevents them from sticking together
o In addition to MONA: assess pt, Use ABCs, sit pt upright to breath appropriately, vitals, 12
lead EKG, anticipate IV (minimum a 22 but ideally a 20 and 18), continuous heart monitor,
anticipate blood work
Complications of Myocardial infarction
 Dysrhythmias: most common complication
o Present in 80% of MI patients
o Most common cause of death in the prehospital period
 Heart failure
o Complication that occurs when the pumping power of the heart has diminished
o s/s: mild dyspnea, restlessness, agitation, crackles, extra heart sounds, etc.
 Lethal rhythms: ventricular fibrillation, ventricular tachycardia, & Asystole
Unstable Angina and MI (acute coronary syndrome) Diagnostic studies
 Detailed health history and physical
 12-lead ECG changes
 Serum cardiac markers
 Coronary angiography
 Others: exercise stress testing, echocardiogram
Care for Acute Coronary Syndrome
 Emergency management (preserve cardiac muscle)
o Initial interventions Ongoing monitoring
 Emergent PCI-percutaneous coronary intervention
o Treatment of choice for confirmed MI (open affected artery within 90 minutes or less of arrival to
facility)
o Balloon angioplasty + Drug-eluting stent(s)
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Caring for a Patient With Hypertension, Chap 13
Hypertension Definition: persistent BP elevation of a systolic greater than 140 & diastolic greater than 90, or current
use of antihypertensive meds
 Normal 120/80mmhg or less
 Prehypertension 120-139/80-89mmhg
 Hypertension 140/90mmhg or higher
·
Stage 1: 140-159/90-99, not as severe
·
Stage 2: >180/>120 or greater, severe
Factors Influencing BP:
 Two consecutive high readings with healthcare professional in two different days
 BP = cardiac output multiplied by systemic vascular resistance (SVR)
 Cardiac output: the amount of blood that is pumped out with each heart beat (contraction)
 SVR: pressure the heart has to push the blood out against, the higher the SVR, the harder the heart has to
work to push out blood
Primary (essential or idiopathic) Hypertension: elevated BP w/o identified cause, 90-95% of all cases
-Risk Factors:
● Age (>50 years old)
● Alcohol intake
● Cigarette smoking (added with hypertension = increase CAD risk)
● Diabetes mellitus
● Elevated serum lipids: at risk for CAD
● Excess dietary Sodium (canned/frozen/lunch meat): increases cardiac output
● Gender (men < 64 yrs are at higher risk between both genders, when women hit 65, they are at a higher
risk)
● Triad: diabetes, hypertension & kidney disease
● Family history, obesity, sedentary lifestyle, stress, socioeconomic status
● Ethnicity (African Americans are at a 2x higher risk)
● Oral contraceptive use: 3x more likely to have HTN
Secondary: elevated BP with a specific cause, 5-10% of adult cases
-Contributing Factors:
● Coarctation of aorta (congenital narrowing of aorta)
● Renal disease: not getting waste out, causing back flow, hypervolemic causing HTN
● Endocrine & neurological disorders
● Cirrhosis= chronic liver damage
● Sleep apnea
● Pregnancy induced hypertension (extra fluid is retained)
Gerontological Considerations
 Prevalence increases with age
 More likely to suffer from hypertension complications
 More likely to have uncontrolled disease
 Risk polypharmacy
o Typically in elderly, Average of 6 medications taken
 Orthostatic decline in b/p as we age may increase with some antihypertensive meds
 Na restriction (better effects than in younger adults)
Clinical Manifestations & assessment
● “silent killer” bc pt can have hypertension for years w/o symptoms because symptoms do not arrive until
organ damage which is then irreversible
● Accurate BP measurement is essential (especially to avoid auscultatory gap)
● Typically no symptoms of hypertension but signs of target organ damage may exist over time:
○ Coronary artery disease
○ Left ventricular hypertrophy
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○ Pathologic changes in the kidneys
○ Cerebrovascular involvement
○ Retinal changes
Assessment of Hypertension
 Laboratory tests: urinarlysis Evaluation for microalbuminuria or proteinuria, Blood chemistry (analysis of
sodium, potassium, BUN and creatinine, fasting glucose, and total and high-density lipoprotein [HDL]
cholesterol levels), 12-lead ECG
Blood pressure
 Bilateral BP measurement
o Use arm with higher reading for subsequent measurements.
o BP is highest in early morning, lowest at night.
o The number should be about 5 mmhg difference between both arms
 Office BP measurement
o Use auscultatory method
o Patient should be seated quietly for 5 minutes in a chair, with feet on the floor and arms supported
at heart level.
o Use appropriately sized cuff to ensure accurate readings.
o Obtain at least two measurements.
Medical and nursing management
 Lifestyle Modifications
o Smoking cessation, weight loss, reduce alcohol intake, sodium intake and regular physical activity
o Weight reduction: loss of 10 kg (22lbs), may decrease systolic BP by approximately 5-10 mmHg
 Pharmacologic therapy
o Diuretics, calcium channel blockers, beta blockers, ACE inhibitors
 Encourage self-management
o Written action plan, self monitoring and regular review
DASH Diet: Dietary approaches to stop hypertension
 Limit or avoid Fats & sweets
 4-5 servings/week of legumes & nuts
 2-3 servings/day of Low Fat dairy
 <6 Servings/day of lean protein
 4-5 servings/day of Vegetables
 6-8 servings/ day of whole grains
Complications of Hypertension
 Blood vessel damage (heart, kidneys, brain, and eyes)
 Myocardial infarction
 Heart failure
 Left ventricular hypertrophy
 Renal failure
 Stroke
 Impaired vision
Hypertensive Crisis
 Systolic blood pressure of greater than 180 mmhg or a diastolic blood pressure of greater than 120 mmhg
 Hypertensive emergency: a situation which BP is higher than 180/120mmhg and must be lowered quickly
to halt or prevent damage to the target organs
o Pts have headache, confusion, blurred vision, vomiting and decreased urine output
 Hypertensive urgency: a situation in which BP is severely elevated but there is no evidence of impending or
progressive target organ damage
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Want to decrease our blood pressure by 10 percent in the first hour and in the next 3-12hr want to
decrease it by 15%
Both are managed with continuous intravenous infusion of a short-acting titratable antihypertensive agent
Goal of a MAP (mean arterial pressure): at or above 60
o Meaning you have good perfusion to the organs
#1 reason why people go into this hypertensive crisis is non-compliance or medication adherence
o
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Fractures, chap 41, 42
Definition: a disruption or break in the continuity of the structure of the bone.
Causes: Trauma (MVA, falls, blunt injuries, penetrating injuries), or Disease Pathology (Osteoporosis, Bone cancer).
Description/classification/extent of fractures: Simple or Compound, complete or incomplete.
-Simple- closed fracture, no break in the skin.
-Compound/open- bone comes out of the skin and communicates with the environment, worried about
infection. (pierces through the skin)
-Complete- broken across the width of the bone. Dividing the bone into two distinct pieces
-Incomplete- does not break into two pieces, only through part of the bone (ex. green stick fracture)
Clinical Manifestations:
-Pain/tenderness- localized and immediate
-Muscle Spasm- protective response to injury, muscle reaction. When the bone is fractured and moved
away from where it is supposed to be the bone is pulling muscle with it
-Loss of function- Disruption of bone preventing functional use
-Deformity- Abnormal position of the bones as a result of original forces of injury and action of muscles
pulling bone fragments into abnormal position.
-Edema/swelling- Fluid and blood infiltrate all around the area.
-Ecchymosis- Discoloration of skin as a result of extra-invasion of blood in the subQ tissue.
-Crepitation- Grating or crunching together of bony fragments, producing palpable or audible crunching
sensations.
Diagnosis of a fracture: Clinical manifestations, history and physical, x-ray of extremity or area, CT scan, MRI,
bone scan, Blood tests. Blood tests will show decreased Hct, and Hgb, and an increase in erythrocyte sedimentation
rate due to inflammatory response.
Treatment for Fractures: all healing requires realignment of bone
-Non surgical management: stabilization with splinting, traction or casting, or closed reduction with or without
anesthesia.
-Surgical Management: Open reduction with or without internal fixation (ORIF), external fixation.
-Healing in the healthy adult takes about 6 weeks, elderly do not heal as fast, someone who has impaired circulatory
or nutrition will have an affected healing time.
Goals of treatment of fractures:
-Anatomical alignment of bone segments (reduction of fracture also means realignment)
-Immunization to maintain alignment
-Restoration of normal to near normal function of injured sire
Traction: applies a pulling force on the fractured extremity to attain realignment while counter-traction pulls it in the
opposite direction. Two types of traction are skin traction and skeletal traction. Make sure the weights are freely
suspended and not on floor or chair. Traction and weights are ordered by the physician.
Skin Traction (external, not invasive)- For short term treatment, 48 to 72 hours until patient placed in skeletal
traction or has surgery.
-Equipment used for alignment- tape, boots, splints, ace wrap, weighs, rope, pulleys
-Purpose- Maintaining alignment, assisting in reduction of fracture, diminish muscle spasms.
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-Traction weight- 5-10 lbs, LESS THAN SKELETAL TRACTION
-When patient is on skin traction must be concerned with skin integrity. We as nurses are responsible to
make sure there is good blood flow and the skin is in good condition***
Skeletal Traction (invasive)- Treatment for longer periods than skin traction.
-Fracture can be reduced manually, the physician will pull on the patients foot to help move the bones back
in place. Then look under x-ray to see if they are in place, and then pins will be inserted to keep them there.
-Purpose- align injured bones and joints (reduction)
-Pin is inserted into the bone (partially or completely) to align and immobilize the injured body part.
-Traction weight- 4-45 lbs
-A type of skeletal traction would be a balanced suspension traction and if your pt had this you would make
the bed top to bottom.
Types of casts: Synthetic material, and plaster.
-Because casts are applied wet, these considerations must be taken while it is drying.
-Increased warmth when cast is drying die to cast material
-Keep blankets directly off cast
-Maintain air flow around the cast
-Assess for skin burns on the edges
-No stress on cast while drying, no fingertips, move pt with palms
-No weight bearing on cast until it is dried, so crutches, or wheelchair is needed
-Purpose of cast is to immobilize the bone that has been realigned
Signs and symptoms to educate your pt to look for:
-Increased pain
-swelling
-discoloration of toes and fingers
-burning of tingling under the cast
-sores
-drainage on cast or from cast- draw circle and time around the drainage and keep an eye on it to see if
drainage increases
-foul odor from cast
Types of surgical Interventions: Closed reduction, open reduction internal fixation (ORIF), external fixation
-Closed reduction- under anesthesia with hardwear insertion, manual traction and then hard wear is
inserted.
-Open reduction- reduce fracture and immobilize fracture
-Surgical incision with internal fixation devices to realign fracture and contain boney fragments
-Pis, screws, rods, plates to align and immobilize
-External Fixation- Still classified as surgical intervention, anesthesia will be administered. Manual
reduction will take place, and then they visualize under x-ray to make sure bones are aligned, then an external
fixation is put in. Can stay in for weeks. Worried about it getting caught on something and OBVIOUSLY infection.
Bleeding is a concern when it is first put in.
Fracture of the hip- Mostly due to osteoporosis= brittle, lost of calcium, become porous.
Clinical Manifestations of a fractured hip-External rotation= extremity is pointed out
-Muscle spasms= pt will be complaining of this often
-Shortening of affected extremity
-PAIN
ORIF for hip fracture: (open reduction internal fixation)
-ORIF of proximal femur, or hip. Same thing.
-Pt will go to operating room, surgeon will make an incision in hip and goes in with instruments and pulls
the edges together to line them up and then these internal fixation devices are inserted. They stay in.
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-After surgery, make sure you are not rotating that hip, get the pt up and moving.
Healing Mechanism of a Fracture:
-Fracture Hematoma- •Bleeding and edema create a hematoma that surrounds the ends of the fragments,
The hematoma is extravasated blood that changes from liquid to a semi solid clot, Occurs in the first 72 hours of
injury (fracture)
-Granulation Tissue- •Active phagocytosis absorbs the products of local necrosis. The hematoma converts
into granulation tissue, Granulation tissue (consisting of new blood vessels, fibroblasts and osteoblasts) produce the
basis for new bone substance called osteoid, Occurs during the first 3 to 14 days of s/p fracture
-Callus Formation- •As mineral (Ca, Phosphorus, Magnesium and new bone matrix) are deposited in the
osteoid, an unorganized network of bone is formed that is woven about the fracture parts, Callus is primarily
composed of cartilage, osteoblasts, calcium and phosphorous, This usually begins to appear by the end of the 2 nd
week of injury, Evidence of callus formation can be verified by x-ray
-Ossification- •Ossification of the callus occurs from 3 weeks to 6 months of the fracture and continues till
the fracture is healed, Callus ossification is sufficient to prevent movement at the fracture site when the bones are
gently stressed, The fracture will still be seen on X-ray, During this stage the patient may be changed from traction
to casting or cast can be removed, Average time for cast is 6 to 8 weeks dependent on severity of fracture
-Bone remodeling- •Excess bone is reabsorbed in this final stage of bone healing and union is completed,
Preinjury structural strength and shape returns, Weight bearing is gradual introduced, PT and exercise to strength
area and decrease stress, X-ray is complete bone union, Usually up to one year s/p injury
Major Complications of Fractures:
-Acute compartment syndrome- could result in amputation or loss of use of limb
-Osteomyelitis- infection of the bone, tough to treat and cure
-Fat embolism syndrome (FES)-presence of fat globules distributed into tissues and organs. Hen bone
breaks, and fat goes into the body and travels and lodges into lungs, occurs after traumatic skeletal injury.
-Venous thrombosis leading to pulmonary embolism (PE)
-Malunion or non union leading to deformity- heels but not in the way we wanted it too. Pt might have to
be taken back to the OR and re fracture the bone if malunion occurs. Non-unions means the bone is never going to
heal right.
-May see redness, heat, order, drainage, fever, increased heart rate. May have to get a culture of the
drainage, and CBC.
-Elevated pressure within a myofascial compartment- pressure within the area surrounding the bone
-Reduced capillary perfusion-blood is not getting to the fractured area
-Ischemia- occurs from lack of oxygen and blood feeding the area, tissue death.
-6 P’s- Pallor really pale almost grey, pain usually pain is distal to the fracture, pressure, paresthesia pins
and needles, pulselessness, paralysis worse than paresthesia.
Fat Embolism Syndrome: Presence of fat globules distributed into tissues and organs. When bone breaks, and fat
goes into the body and travels and lodges into the lungs. PREVENTION IS KEY.
S&S:
-Feeling of doom-> extreme apprehension
-dyspnea
-SOB
-Chest pain
-Tachycardia
-Confusion/disorientation-> results in hypoxia
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-Petechiae- little red dots, measles like rash in the buckle membrane, across the chest and conjunctiva of the eye.
Nowhere near the fracture
-once pt has a fatty embolism the nurse can only support them, and admin. Oxygen and fluids.
Venous Thromboembolism: Orthopedic patients highly susceptible, at risk for venoustasis which leads to blood
clots.
How to treat this: Compression stockings, ROM, prophylactic anticoagulants such as ASA=aspirin,
heparin/lovenox/arixtra, warfarin=coumadin.
General post op-care for patients with fractures:
-get up and go as quickly as possible. If on traction they can not, so ROM working with therapy. -turning and
positioning. Incentive spirometer for lungs.
-assess extremity, dressing, cast, traction, external fixation devices
-NV assessments ongoing with everytime vital signs are being taken, longest you can go without NV assessment is
4 hours
-Assessment of postoperative complications
Nutritional Therapy:
-Good nutrition essential for repair of injured bones and tissues
-Protein= 1gram/kg
-Calcium sources and supplements
-Fluid intake 2000-3000 ml per day
-High fiber diet with fruits and veggies to prevent constipation
-Eat well balanced meals and prevent overeating to reduce weight gain
Osteoporosis
○ “Silent disease”
○ Porous bone (holes)
○ Characterized by low bone mass
○ Leads to increased bone fragility
○ Can lead to fragile bone leading to fractures
○ Pt can fracture with stepping
○ More common in women bc of menopause bc loss of estrogen
○ 60-80 of people with this is because of genetics: it is hereditary
● Nursing management
○ Education
○ Proper nutrition supports bone health
■ Ice cream, yogurt, sardines and spinach
○ Calcium supplements
■ 1,000 to 1,500mg/day in adolescents
■ Vitamin D 800 to 1000mg/day
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○
○
○
Exercise prevents progression of osteoporosis
■ Moderate exercise is important to build and maintain bone mass (ex.walking)
Medication regime
■ They could take meds that help to build up the bone or prevents the bone from breaking
down
Prevention of fractures
Risk factors
■ Smoker
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■ Utilities alcohol
■ Female
■ >65
○ Once diagnosed educate them that they are prone to fracture and provide them with any assistive
devices. Make them very aware of sudden impacts/movements
Osteoarthritis (OA)
○ Used to be call DJD (degenerative joint disease)
○ Most common form of joint disease in North America
○ Slowly progressive noninflammatory disorder of the synovial joints
○ 20 million americans affected
■ Expected to greatly increase as population ages
○ Progressive destructions of cartilage
○ Systemic manifestation are NOT present in OA
● Etiology and pathophysiology
○ No longer considered a normal part of aging process
○ Growing older is a risk factor
○ Cartilage destruction can begin between ages 20 and 30
○ Majority of adults affected by age 40
○ Single cause of OA has not been identified
○ Factors that are linked to OA
■ Estrogen reduction
■ Genetic factors
■ Obesity
○ Regular moderate exercise decreases risk
● Clinical manifestations
○ Morning stiffness
○ Pain with overuse of joint
○ Knees, hips, cervical/lumbar vertebrae, joints of hands/feet (weight bearing joints)
○ Pain worsens as barometric pressure drops
● Clinical manifestations: Deformity
○ Knee OA can lead to joint malalignment
○ Hip OA can cause one leg to be shorter
○ Heberden’s and bouchard's nodes form on the fingers
○ Can be bowed legged and nodules on their fingers
○ Can affect patient self esteem and put them at a fall risk
● Clinical manifestations: Joints
○ Increased pain can contribute significantly to disability and loss of function
○ Pain may be referred to groin, buttock, or medial side of thigh or knee
○ Sitting down becomes difficult
○ Getting up from a chair when hips are lower than knees is harder
○ Referred pain
■ Pain located somewhere else in other areas
● Pain later in disease results from contract between exposed bony joint surfaces after articular cartilage has
completely deteriorated
● As OA progresses, cartilage disappears and becomes bone on bone, hearing crepitus
● When bone on bone the best treatment is surgical intervention
● Diagnostic studies
○ In early OA tests
■ Detect joint changes
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■ Bone scan, computed tomography (CT scan)
■ Magnetic resonance imaging (MRI)
○ In progressed OA
■ Detect joint space narrowing, bony sclerosis
■ Osteophyte formation
● X rays
Nursing management
○ Highest priority is pain relief
○ Heat and cold applications must be ordered
○ complementary/alternative therapies
■ Herbal and nutrition products
■ Yoga
■ Tai chi
■ Acupuncture
○ Exercise, firm mattress, splints
○ Fall protocol in hospital and at home
Collaborative Care: Nutritional therapy and exercise
○ Weight reduction program is critical for overweight patient
○ Exercise is a fundamental part of OA management
■ Load on joints and degree of joint mobilization are essential to preservation of articular
cartilage integrity
Surgical Intervention
○ Arthroscopy: looking into a joint
○ Arthrodesis: fusion of a joint
○ Arthroplasty: total joint replacement
■ Hip (THA): total hip arthroplasty
■ Knee (TKA): total knee arthroplasty
Priority nursing care
○ ***Preoperative teaching***
○ At great risk for post op complications
■ Infection: due to foreign bodies inside, aseptic technique is extremely important,
infection within the joint itself is very difficult to fight off.
■ VTE: venous thromboembolism: extremely high in joint replacement patients, leading to
a pulmonary embolism, has a high mortality, prevent it from happening by prophylactic
anticoagulants, range of motion, VT leading to PE
○ Physical therapy and rehab are key for success
○ Patient will be in the hospital for 2 to 3 nights total for both hip and knee replacement
○ Patients will get out of bed the day of surgery
○ Patient may be discharged to home or to a rehabilitation facility or transferred to the rehab until in
the hospital
○ If patient goes home, everyday a physical therapist will come or they will go to a facility
○ Need all special equipment that they need if at home
○ Patient with any joint replacement will be on an antibiotic
Abductor pillow
○ Used when they want the ball to stay in the socket
○ Any equipment that we use post op is very specific to what procedure that they had done
○ Check orders specifically how to move them and how to use equipment
○ Read orders and know equipment
CPM: Continuous Passive motion machine
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○ For total knee replacements, come into the PACU sometimes with this machine
○ It just moves the patient joint up and down so that it doesn’t get stiff
○ Continuous passive motion
● Frozen joint
If the patient doesn't do the motions they are ordered for, the joint could freeze and not work at all
Amputations
Definition:
-Removal of a part of the body resulting in physical impairment
-Associated with a total or partial loss of an extremity
Risk factors
-Ischemia= number one cause. Can occur from arteriosclerosis, PVD, diabetes
-Burn or frostbite
-Cancer/ tumors
-Infections
-Metabolic disorders
-Congenital anomalies
-Trauma
Typical client:
-Elderly
-Diabetic
-Male
-History of smoking
-African American
-History of self care deficit
-history of peripheral vascular disease (PVD)
Types of Amputations: surgeons try to go as distal as possible, in order to remove as little as possible. This is too
preserve as much of the extremity as possible to maintain post operative mobility
1.Surgical Amputations
–Performed in a surgical environment by a surgeon
Elective surgery- impaired circulation of digit or extremity and meds are not working but still in pain, and
elect to have amputation.
Emergency surgery- sudden cut off of circulation to an area.
2.Traumatic Amputations
–An unexpected “severing” of a body part “limb”
–Associated with an accident
–Increased incidence with young men in industrial and motor vehicle accidents
Types of surgical Amputations:
1.
2.
Open or Guillotine: Used for pts who are at risk for infection, or who have a big non-healing infection.
Wound remains open for all the drainage of exudate. Will not be closed. Change dressing constantly.
Closed or Flap method: Wound is closed by a skin flap over the bone with sutures or staples applied to
maintain closure, One or more drains are typically inserted.
Diagnostic Assessment:
•Invasive
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Anterior gram, Angiography- dye is injected into vascular system and then on xray they visualize how the
dye travels through the vascular system, and were it stops. That is how they see where the circulation is imparted.
Most invasive. •Noninvasive- measures the pressure of the extremity to see if the area is perfusing.
Doppler ultrasonography
Segmental arterial pressures
Ankle-Brachial Index (ABI)
Levels of amputations:
-Lower level amputations- more frequent
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AKA=above the knee
BKA=below the knee
Transmetatarsal
Symes
-Upper level amputations●
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AEA=above the elbow
BEA=below the elbow
Hand and distal digits
-Hip disarticulation/ hemipelvectomy= amputations of half the body
Reasons prosthesis fitting may not be indicated or prolonged:
-Contra-indications: chronic or progressive mental deterioration, advancing neuro problems, COPD, cardiac disease
-Prolonged: type of amputation, infection, elderly.
Postoperative Assessment: PROMOTE MOBILITY
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Monitor for signs for circulation to the area and assess for increase bleeding
Neuro assessment: temp, color, sensation/pain, cap refill, proximal pulses, edema
Assessment of tissue perfusion is priority
Dressings: Purpose is to provide compression, decrease bleeding, decrease edema, and mold stump for prosthesis
fitting.
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Dressings and Ace wraps provide compression
Cast
Air Splint
Rigid dressing
Wrapping stump with ace wrap:
Purpose- reduce edema, reduce shrinking of limb, holding the wound dressing in place
-Use correct procedure and method
-Re-apply every 4-6 hours or PRN
-Figure 8 wrapping prevents restriction of blood flow
Promote Mobility:
-ROM
-Prevention of flexion to avoid contraction of joint above amputation
-Proper use of wheelchair, walker, crutches
-Prosthesis fitting, can be done immediately or up to 3 months after
Complications from Amputations:
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-Hemorrhage- occurs by surgical intervention or trauma when major blood vessels are severed. Uncontrolled
hemorrhage will place the client at risk for hypovolemic shock and death
-Infection- assess wound for S&S of inflammation including redness, swelling, warmth. Assess drainage &
document characteristics including color, amount & odor. Change dressing daily until sutures are removed.
Infections of the tissues, wound site, or bone puts the patient at risk for Osteomyelitis. Treatment- prophylactic and
antibiotic therapy. Maintain aseptic wound care.
-Phantom limb pain- Extremity pain below the stump site, where the limb is no longer. Described as burning or
crushing. Opioids show minimal effectiveness for management of phantom limb pain.
-Flexion contractures- freezing of the joint. occurs with decrease movement. Most common are flexion contractures
of the hip, and knee with LE amputations. Can occur in elbow UE amputations. Turning and positioning all 4 ways
helps prevent this.
Problems associated with immobility- promotion of body image and self esteem.
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