OXYGENATION LECTURE
Respiratory System...
Structure & Function
Lower Respiratory Tract…
 Alveolar ducts
 Alveoli - FUNCTIONAL UNIT OF THE LUNG
– ~300,000,000 ALVEOLI IN THE LUNG
– Total Volume of ~ 2500 ml
– Surface area for gas exchange that is about the size of a tennis court
– SURFACTANT
NURSING DIAGNOSIS (definition and defining characteristics:
 Ineffective
 Gas
airway clearance
Exchange, Impaired
NOCs
Review the following:
 Respiratory
status:
Gas Exchange
Ventilation
 Tissue
Perfusion:
Pulmonary
 Acid-Base
Balance
NICs
 Acid-Base
 Gas
Management
exchange, Impaired
Ventilation and Perfusion
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Alveolar Dead Space
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+ ventilation
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- perfusion
Intrapulmonary Shunting
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- ventilation
+ perfusion
OBSTRUCTIVE SLEEP APNEA
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Periodic apneic or hypopneic episodes during sleep associated with
Upper airway obstruction due to pharyngeal collapse, leading to
Awakening and resulting restoration of airway patency
Sleep recurs almost immediately and the cycle repeats itself, often hundreds of times
each night
Epidemiology
 Prevalence estimated at 4% male; 2% female
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(NEJM 328:1230, 1993)
May be as much as 40-50% of hypertensive Pts
90% of pts with nocturnal angina (Lancet 4/29/95)
 Incidence greatest age 40-60
 Highly underdiagnosed, perhaps due to the gradual onset of s/s
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More underdiagnosed in women than men.
Mean duration of s/s before dx in one series of women was 10years
There is normall a moderate degree of hypoventilation during sleep resulting from partial
phyarngeal collapse and resulting increase in upper airway resistance.
Structural factors: can possibly be a structural abnormality.
There is a larger role of women that have structural abnormalities that cause SA.
Functional factors: 1. Altered sleep
2. influences on palatal muscle control
3. may have impaired ventilator drive or arousal mechanisms
Treatment:
1. Surgical / remove obstruction
2. CPAP
3. Support group
Problems of the LOWER AIRWAY
Statistics:
 Decrease number of deaths R/T acute & chronic respiratory infections due to
antibiotics
 Increase in TB over last ten years, especially the last 5years due to AIDS/HIV
 More people living with COPD (>17 million)
 ^ incidence of lung cancer, especially among women
 ^ number of teenagers starting to smoke
 Pneumonia is the leading cause of death by infectious disease in the U.S.
PREVENTION
 Education/advocacy for smoke-free environment (The use of tobacco is the #1 risk to
developing COPD and lung cancer
 Most people start smoking in high school
 Nicotine addiction results in withdrawal symptoms
 Smoking is tied to ETOH (alcohol) consumption and lower achievement
 Advertising targets fantasies and insecurities of teens and young adults
Obstructive & Restrictive
Lung Disorders
Restrictive Lung Disorders
 General (extrapulmonary)
 head injuries, tumors, OD (overdose)
 Neuromuscular (extrapulmonary)
 GB (guillian barre), ALS, MD, Polio
 Chest Wall (intrapulmonary/extrapulmonary)
 trauma
 Pleural Disorders (intrapulmonary)
 pleural effusion, pleurisy
 Parenchmal (parenchmal)
 atelectasis, pneumonia, TB, pulmonary fibrosis
Obstructive Lung Disorders
 Asthma
 COPD
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Acute Bronchitis
Chronic Bronchitis
Emphysema
Characteristics of Lung Disorders
Restrictive
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Reduced Vital Capacity
Reduced Total Lung Capacity
Normal or reduced Functional Residual Capacity
Cause difficulty with inspiration
Obstructive
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Decreased resistance to airflow
Normal or decreased Vital Capacity
Increased Total Lung Capacity
Increased Functional Residual Capacity
Increased Residual Volume
We will not be tested on normal pulmonary function
(total lung capacity is total amount we can get in. vital capacity is a normal breath)
OBSTRUCTIVE
Characterized by:
INCREASED TO AIR FLOW
RESTRICTIVE
Characterized by:
DECREASED COMPLIENCE OF THE LUNG OR CHEST WALL OR BOTH
OBSTRUCTIVE LUNG DISORDERS
EMPHYSEMA
 Loss of elastic recoil secondary to breakdown of lung tissue and enlargement of alveolar
spaces - leads to retention of CO2
 Emphysema is the most severe form of COPD is characterized by abnormal, permanent
enlargement of the air spaces past the terminal bronchioles, resulting in the destruction of the
alveolar walls
 The affected terminal bronchioles contain mucus plugs and the eventual resulting loss of
elasticity of the lung parenchyma resulting in difficulty in exhaling
Use tripod or pursed lip breathing to get them to increase the breath.
We might see: barrel chest, hyperresonance, clubbing.
Spacer on an inhaler helps to prevent person who doesn’t lose any of the medication.
Have patient inhale & hold it in… try to hold it as long as they can. Then they need to rinse their
mouth to prevent thrush.
 1963 - Discovery of deficiency of AAT (Alpha Protease Inhibitor) which is associated with
serous and premature development of emphysema. These enzymes (Pancreatic Elastase,
Trypsin, Chymotrypsin,
Granulocyte Elastase) defend the
lungs against destructive processes
R/T Neutrophil Elastase which
destroys tissue.
 Bullous Emphysema is the result (cavernous)
If a patient has been diagnosed w/ AAT they really need to not smoke, don’t get second hand
smoke…
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AAT (alpha-1-protease inhibitor)
Familial emphysema have a hereditary deficiency of AAT
Number of Americans with this genetic deficiency small (~70,000)
1 in 3,000 newborns have a genetic deficiency of AAT
1 to 3 percent of all cases of emphysema are due to AAT deficiency
 Critical that these people not smoke
 The destruction of elastin that occurs in emphysema is believed to result from an
imbalance between two proteins in the lung:
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An enzyme called elastase which breaks down elastin, and
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AAT which inhibits elastase.
 In normal individuals, there is enough AAT to protect elastin so that abnormal
elastin destruction does not occur
 Permanent destruction of the alveoli
 Due to irreversible destruction of the protein elastin
 Elastin is important for maintaining the strength of the alveolar walls
 The loss of elastin also causes collapse or narrowing of the bronchioles
 End result of above sequence limits airflow out of the lungs. (air is trapped… purse
lipped breathing helps to expire a little more)
ETIOLOGY
 Precise cause is unknown, but thought to involve destruction of the
connective tissue of the lung by protease's that may be facilitated by the
effects of cigarette smoking
EPIDEMIOLOGY
 Symptoms usually occur in the fifth or sixth decade of life
 Typical patient is male over the age of 55 with a history of tobacco
smoking
 Heredity
 Environmental irritants/pollution
PATHOPHYSIOLOGY
Centrilobular Emphysema (CLE)
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Distention and damage of the respiratory bronchioles
Uneven disease distribution throughout the lung
Usually more severe in the upper portions
More common than Panlobular emphysema (PLE)
Panlobular Emphysema (PLE)
 More uniform enlargement and destruction of the alveoli in the pulmonary acinus
 More diffuse and is more severe in the lower lungs
ASSESSMENT
S&S
Subjective
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Hx and onset of symptoms (how old were you when you started to cough?
Smoking Hx (how many years? Pack year history?)
Family Hx
Past or present exposure to environmental irritants (working around coal mines or shipyards)
Activity intolerance, fatigue
Anorexia, weight loss
Symptoms of hypoxemia - restlessness, confusion
 Medications and therapies and their effectiveness
Assessment...
Objective
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Increased airway resistance
Decreased Expiratory Force
Mild hypoxemia (pick up w/ O2 sat monitor)
Barrel Chest
Increased AP diameter
Increased Accessory Muscles
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ABG’s show compensation (pH is normalizing & CO2 will start to drop)
Increased respiratory rate
Dyspnea
Decreased breath sounds
Late inspiratory crackles
Decreased O2 saturation
LAB FINDINGS
 ABG’s may be normal due to compensation for the destruction by increased resp rate
Even in the presence of hypoxemia overcompensation may result in respiratory
alkalosis
 PO2 normal or slightly low at rest, but drops with activity
 CBC usually normal
DIAGNOSTIC TESTS
 Chest X-Ray -- positive findings indicate increased radiolucency of lungs with
diaphragm in low position
 AAT assay to check for deficiency
 Pulmonary functions tests -
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Increased residual volume, functional residual capacity, total lung capacity
Diffusing capacity is reduced because of tissue destruction
Decreased Forced Expiratory Volume
Vital Capacity may be normal or slightly reduced until late state of disease
INTERVENTIONS
Bronchodilators may provide relief from symptoms but will not cure the disease
Antibiotics if there is an infectious process occurring
Steroids during acute exacerbation's (get them weaned off as soon as possible)
Low flow oxygen (1-2 liters)
Breathing exercises
Respiratory therapy & CPT (chest physiotherapy)
Lung reduction surgery
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Performed only on pts with severe emphysema
Avg. hospital LOS ~ 2 weeks
Require pre and post op extended pulmonary rehab
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Falling out of favor in the prior year
Patients with COPD can help
themselves in many ways
Stop smoking
Avoid work-related exposures to dust & fumes
Avoid air pollution, and curtail physical activity during alerts
Refrain from contact with people that have URI… (upper respiratory infection)
Get pneumonia vaccination and yearly influenza shots
Avoid excessive heat, cold and high altitudes
Drink fluids (to help thin the secretions)
Maintain good nutrition – high protein
Consider allergy shots
Another Nursing Diagnosis
Altered nutrition: less than body requirements related to dyspnea, sputum
production, or fatigue
Interventions:
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Explain importance of consuming adequate amounts of nutrients
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Provide a pleasant, relaxed atmosphere for eating (small meals several times a day, wear oxygen
while eating)
Expected Outcomes:
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Pt will verbalize & understand importance of adequate nutrition
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Pt will use a comfortable environment for meals
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Pt will eat slower and smaller meals
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More NURSING DIAGNOSIS
Ineffective airway clearance
Altered Gas Exchange Breathing pattern, Ineffective
Activity Intolerance
Infection: Actual or Potential
Risk for Nutrition: Less than Body Requirement
Fear
Anxiety
Knowledge Deficit
Nursing Diagnoses
 Ineffective airway clearance r/t bronchospasm, ineffective cough,
excessive mucus production,
 Anxiety r/t difficulty breathing, perceived or actual loss of control, and fear
of suffocation and restlessness
 Ineffective therapeutic regimen management r/t lack of information about
COPD and its treatment
Nursing Diagnoses
 Activity intolerance r/t fatigue, energy shift to meet muscle needs for
breathing to overcome airway obstruction
 Disturbed body image r/t decreased participation in physical activities
 Impaired home maintenance r/t deficient knowledge regarding control of
environmental triggers
 Ineffective coping r/t personal vulnerability to situational crisis
Nursing Interventions
 Airway Management
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Administer humidified air or oxygen immediately
Regulate fluid intake
Monitor respiratory and oxygenation status
Administer drug therapy (bronchodilators, corticosteroids)
Auscultate lung sounds before and after treatments (first time you listen they
sound horrible, have them take deep breaths & then lungs should sound better)
 Cough Enhancement
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Positioning for chest expansion
Deep breathing, hold for 2 seconds, and cough 2-3 times
These interventions will help them to maintain their airway.
Often the secretions are worse in the morning…
Nursing Interventions
 Respiratory Monitoring
 Rate, rhythm, depth, and effort (overall patterns)
 Monitor for increased restlessness, anxiety, and air
 Note changes in SaO2, ABG values
hunger
Nursing Interventions
 Anxiety Reduction
 Calming
& reassuring attitudes (help w/ fear & anxiety of not being
able to breathe).
 Stay with patient
 Encourage slow breathing (pursed lips)
Nursing Interventions
 Teaching: Disease Process & Prescribed Medication
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Identify level of knowledge (make sure patient understands what is going on, why
you are giving the meds, we need to determine their level of understanding)
Instruct on measure to prevent/minimize side effects of treatment (how to properly
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do a nebulizer treatment, etc…)
Evaluate patient’s ability to self-administer medications
Instruct patient on purpose, action, dosage, and duration of each medication
Include family and significant others
Pulmonary Function Tests
Arterial Blood Gases (ABGs)
 Arterial Blood Gases (ABGs)
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Determines how much oxygen is available to perfuse peripheral tissues
Normal values:
 pH: 7.35 - 7.45
 PaCO2: 35 - 45
 PaO2: 80 - 100
 HCO3: 22 - 26
 SaO2: 95 - 100
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Hypoxemia occurs with early respiratory alkalosis, or in severe cases, respiratory
acidosis.
Planning & Intervention
Medications:
 Bronchodilators – to relax smooth muscles in the airways and reduce congestion
 Xanthine Compounds – Theophylline to reduce mucosal edema and smooth muscle spasms – also strengthens
contractility of the diaphragm (can come in tablet… another form can be given IV)
 Sympathetic Agents: PO, Inhalation (Albuterol, Terbutaline)
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Rescue inhalers – Albuterol… (fast acting broncho dialators… don’t need to be used all the time, pollen)
 Corticosteroids – Solu Medrol – IV or PO to alleviate acute symptoms by decreasing inflammation (hour glass vial, powder
in the top, you take the metal cap off, push on the rubber plunger… pushes the powder through into the fluid in the bottom &
then give a direct IV push. Will start on IV in an acute situation, eventually wean them & get on a PO med)
Antibiotics – to manage respiratory tract infections
Mucolytics and expectorants – to thin and aid in removal of mucus
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 Analgesics (nsaid or Tylenol for aches & pain)
Flu Shots
 Given early October to mid November (however can be given any time during the flu
season
 Given yearly
 Cost for people > 65 is paid by Medicare
 Recommended for:
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>50 years old
Chronic heart or lung disease
HIV (compromised immune system)
Anyone living in large groups
People who may transmit the flu to high risk groups
 Nurses, doctors, and other healthcare workers
You should NOT get the flu shots if
 Allergic to eggs
 Hx of Guillain-Barre Syndrome
 Acute illness or fever
Side effects
 <1 out of 3 develop site soreness
 Rare to have fever, aches
 Recent research shows that flu shots do not increase asthma attacks
NOTE: flu vaccine is made from a virus that is no longer active – NO one can catch the flu from
flu shot.
PULMONARY EMBOLISM
MEDICAL INTERVENTIONS
 Anticoagulants (prevents a clot from forming, coumadin & heparin)
 Thrombolytic therapy (break up a present clot, TPA, streptokinase & eurokinase)
PE usually comes from legs
SURGICAL INTERVENTIONS
 Embolectomy (if it is large enough)
NURSING DIAGNOSIS
 Impaired gas exchange
Pulmonary Embolism….
Risk factors for PE
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Recent surgery
Recent fx of a lower extremity, especially with immobilization
Immobilization, particularly complete bedrest or LE (lower extremity) paralysis
Previous DVT or PE
Family history of DVT or PE
Cancer
Obesity
Cardiovascular disease
Postpartum period
Sub therapeutic heparin dose
Age > 40 years
Pulmonary Embolism….
Predisposing factors & Precipitating Conditions that make some higher risk for
developing DVT/PE
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Prolonged immobility or paralysis
Injury to vascular endothelium
Hypercoagulability
CVP catheter (central venous pressure catheter)
History
CV disease
Cancer
Trauma
Pregnancy & estrogen use
Virchow’s Triad
Three primary factors that predispose to venous thrombosis:
 Venous stasis
 Injury to vascular endothelium
 Hypercoagulability
Typical clinical features
S&S
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Tachypnea
Dyspnea, sudden onset or worsening of chronic dyspnea
Tachycardia
Pleuritic chest pain or chest pain that is nonretrosternal and nonpleuritic
Syncope
Cough
Feeling of impending doom
Hemoptysis
Arterial oxygen saturation < 92% on room air
Low-grade fever (occasionally)
Hemoptysis
Hypoxemia
Pleural friction rub
Clinical evidence of DVT
Sudden hypertension
Prophylaxis for DVT
 Mechanical intervention to decrease venous status
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Early ambulation or change position q2h
Compression stockings (or Ted stockings)
Intermittent pneumatic compression stockings
 Pharmacologic agents
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Low molecular wt. Heparin
Low dose unit Heparin
Warfarin
Low dose ASA (81 mg enteric coated baby aspirin)
Hypoxemia in PE caused by
 V/Q mismatching
 Intrapulmonary shunt
 Dead space ventilation
Clinical features of severe PE:
 Hypotension (from reduced left-heart venous return)
 Right heart failure
Dignostic Evaluation to Confirm PE
 V-Q lung scan (limited specificity) – test will come back saying “limited
specificity”… not really sure if there is a clot.
 MRI
 Pulmonary angiography
 CXR may show evidence of pulmonary infarct (also limited specificity)
 Lower extremity venous duplex (DVT requires same tx as PE) –like a
Doppler (study of the leg)
 A negative study does not exclude PE!
MEDICAL INTERVENTIONS:
Anticoagulation
 Low molecular wt. Heparin (lovenox)
 Low dose unit Heparin
 Warfarin
SURGICAL INTERVENTIONS
 Embolectomy
 GFF (green field filter)… looks like an umbrella, goes in the vein to trap the clot)
NURSING DIAGNOSIS
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Impaired gas exchange
…
Heparin Nomogram
Anticoagulation form Venous
Thrombosis/Peripheral Vascular Disease
Adjustment Contingency Table
(25,000 units Heparin/500ml D5W)
PTT
Bolus (units)
Below 41 2000 unit
41-49
1000 units
50-80
0
81-89
0
90-106
0
Above 106
0
Hold (min)
Rate Change
0 min
+4ml/hr (200units/hr)
0 min
+2ml/hr (100units/hr)
0 min NO RATE CHANGE
0 min -2ml/hr (100units/hr)
60 min
-4ml/hr (200units/hr)
120 min
-4mil/hr (200units/hr)
Repeat PTT
6hrs
6hrs
next AM
6hrs
6hrs
6hrs
PTT = partial thrombosin time? Usually check every 6 hours w/ another PTT.
Heparin works very quickly while Coumadin works over a period of days. PTINR is to test
Coumadin. PTINR w/ Coumadin will be 2.5 to 3.5.
Med to reverse heparin… PTT comes back at 118, physician want to take pt to surgery
protamine sulfate is drug given… immed reverses heparin.
Vitamin K will immediately reverse Coumadin. Those patients on Coumadin has to know not to
eat green leafy veggies… too much vitamin K will reverse the effects of Coumadin.
Greenfield Filter
Restrictive Lung Disorders
 General
 head injuries, tumors, OD
 Neuromuscular
 GB, ALS, MD, Polio
 Chest Wall
 Trauma
 Pickwickian syndrome
 Pleural Disorders
 pleural effusion, pleurisy, pneumothorax
 Parenchmal
 atelectasis, pneumonia, TB, pulmonary fibrosis, ARDS
PNEUMONIA
 Acute infection of lung tissue resulting from inhalation or transport via bloodstream of
infectious agents, noxious fumes, or radiation therapy.
 An acute inflammation of the lung parenchyma associated with the production of
exudate
LUNG CANCER
 Primary lung cancer is the leading cause of death in men and women who have
malignant disease in the U.S.
 Mortality rate increasing - in 1994 there were 153,000 deaths from lung cancer
 5-year survival rate is 13%
 Found most frequently in person 40-75 years of age
PATHOPHYSIOLOGY
 > 90% of lung cancer originate from the epithelium of the bronchus (bronchogenic)
 Primary lung cancers are often categorized into histologic types
 Mets occurs primarily by direct extension and via the blood circualtion and the lymph
system
 Common sites for mets are the liver, brain, bones, scalene lymph nodes, and adrenal
glands.
STATS, CAUSES & RISK FACTORS
 Smoking is responsible for ~ 80-90% of all lung cancers
 ~ 1 out of every 10 heavy smokers develop lung cancer
 The risk of cancer gradually decreases when smoking ceases and continues to decline estimates are that it
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takes ~ 15 years for the risk of lung cancer of former smokers to equal that
of a nonsmoker
 Inhaled carcinogens - such as asbestos, nickel, iron, air pollutants, etc. increase the risk of
lung cancer
DIAGNOSTIC TESTS
 Chest X-Ray:
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Shows increased bronchovascular markings
 Pulmonary functioning tests:
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Decreased forced expriatory volume and vital capacity, and increased residual volume
 Arterial Blood Gas (ABG) studies
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respiratory acidosis, hypercapnia, Hypoxia
 Complete Blood Count
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Elevated Hbg and Hct (polycythemia)
Elevated WBC
 Pulse Oximetry
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Pt. usually hypoxic
 Sputum C&S:
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neutrophils and bronchial epithelial cells present
STATS, CAUSES & RISK FACTORS
 Heredity
 Preexisting pulmonary diseases
 Incidence of lung cancer correlates with the degree of urbanization and population
density
 Second hand smoke exposure
 Risk of developing lung cancer is directly related to total exposure to cigarette smoke
- Pack Year History
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CLINICAL MANIFESTATIONS
General nonspecific & appear late in the disease process
Dependent on the type of lung cancer
Often there is extensive mets before symptoms become apparent
Persistent cough (may or may not be productive)
Chest Pain
Dyspnea
CLINICAL MANIFESTATIONS
Later manifestations:
 anorexia
 fatigue
 weight loss
 hoarseness
 if mediastinal involvement may have
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pericardial effusion
cardiac tamponade
dysrhythmias
DIAGNOSTIC STUDIES
Chest X-ray
CT scans
MRI
PET - (position-emission tomography) - measurement of differential metabolic activity in normal and
diseased tissue
Definitive diagnosis of lung cancer is made by: Identification of
malignant cells
 Radionuclide scans (liver, bone, brain …)
 Pulmonary angiography and lung scans
 Mediastinoscopy
Staging of Tumors
 Staging of nonsmall cell lung cancer (NSCLC) is performed according to the American Joint
Committee’s
T=
N=
M=
TNM staging system.
denotes tumor size. Location, and degree of involvement
indicates regional lymph node involvement
represents the presence or absence of distant metastases
 Staging of small cell lung cancer (SCLC) not useful because the cancer has usually metastasized by
the time the Dx has been made.
THERAPEUTIC MANAGEMENT
 Surgical resection - decision is dependent on type and location of tumor
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Lobectomy
pneumonectomy
 Radiation therapy
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Curative approach with resectable tumor but poor surgical risk
Adjuvant with other approaches
Palliative to reduce symptoms
 Chemotherapy
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Used as adjuvant
 Laser surgery
NURSING MANAGEMENT
Nursing Diagnosis
 Ineffective airway clearance R/T increased tracheobronchial secretions
 Anxiety R/T lack of knowledge of diagnosis or unknown prognosis and Rx
 Ineffective breathing pattern R/T decreased lung capacity
Planning - Overall goals are that the pt with lung cancer will have:
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effective breathing patterns
adequate airway clearance
adequate oxygenation of tissues
minimal to no pain
realistic attitude toward Rx and prognosis
ASTHMA
Impact of Asthma in the U.S.
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Affects 17,000,000 individuals in U.S.
> 20 million outpatient visits/year
> 1.6 million ED visits/year
> 500,000 hospitalizations/year
> 20 million lost work days/year
> 10 million lost school days/year
– NCHS 1998 CDC asthma surveillance
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Affects 24,700,000 individual in U.S
Increased 60% over the prior 10 years
~ 2 million ED visits/year
Mortality has doubled since 1978
African-Americans: death rate is 2 to 5 times that of Caucasian death rate
Account for ~ 20 million lost work days/year
Annual health care costs ~ 12.7 billion $
 American Lung Association Fact Sheet 2002
Hyperventilation
 Airway walls are thickened with inflammatory exudates which enhances
bronchospasms and reduces expiratory flow.
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Results in increased work of breathing and hyperinflation away from the obstruction.
Air trapping inside the lungs causes the individual to hyperventilate.
Signs and Symptoms of Asthma
Abrupt or gradual onset
Inspiratory and/or expiratory wheezing
Shortness of breath
Non-productive cough leading to thick, stringy mucus during attack
Position: High Fowlers, tripod
Percussion: Hyperresonance
Prolonged expiration
Tachycardia
Tachypnea
Use of accessory muscles
Dyspnea
Chest tightness
 Hypoxemia
 Nasal flaring
Asthma …
The high morbidity/mortality rate is due to:
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inaccurate assessment of disease
increased allergens/irritants in the environment
delay in seeking medical help
inadequate medical Rx
limited access to health care
non adherence with prescribed therapy
PATHOPHYSIOLOGY
 Hyperirritability or hyperresponsiveness tracheobronchial tree
 Bronchoconstriction in response to physical, chemical and pharmacolgic
agents
PHASES OF ASTHMA
Early Phase (30-60 minutes)
 Triggered by allergen or irritant
 MAST cell degranulation -- Immune Mediator Release
 Bronchial smooth muscle constriction
 Mucous Secretion
 Vascular Leakage
Late Phase (5-6 hours to 2 days)
 Infiltration (esoinophils and neutrophils)
 Bronchial hyperreactivity
 Imflammation
 Infiltration with monocytes and lymphocytes
ASTHMA TRIGGERS
 G gerd
 A allergens
 S smoking, strong odors
P
B
R
E
A
T
H
pets & pests
beer, wine & deli
resp. infections
emotional/stress
activities
timing
humidity, cold
air or sudden
temp change
Clinical Presentation
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Abrupt or gradual onset
Wheezing – inspiratory &/or expiratory
Nasal flaring
Dyspnea/SOB
Anxiety
Tachypnea
Tachycardia
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Percussion: Hyperresonance
Use of accessory muscles
Sitting upright or forward (tripod)
Hypoxemia
Prolonged expiration
Cough – nonproductive leading to thick, stringy mucus during attack
MANAGEMENT OF ASTHMA
Preventive
 MAST Cell stabilizer
 Long acting beta 2 agonists (serevent)
 Inhaled corticosteroids
 Epinephrine
 Theophylline
Pharmacological Treatment
 Short acting beta2-agonists (Bronchodilators)
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End in –ol
 Theophylline
 Anticholinergic Agents - Atrovent
 Corticosteroids
 Long acting beta2-agonist and corticosteriod combination
 Cromolyn
 Leukotriene-antagonists
Short acting beta2-agonists
 Albuterol, Levalbuterol (Xoponex)
 Side effects:
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Anxiety.
Tremor.
Restlessness.
Headache.
Patients may experience fast and irregular heartbeats.
 Interaction with beta blockers
Theophylline
 Theo-Dur, Theolair, Slo-Phyllin, Slo-bid, Constant-T, Respbid
 Theophylline level
 Toxicity causes the following symptoms: nausea, vomiting,
headache, insomnia, and, in rare cases, disturbances in heart
rhythm and convulsions.
Anticholinergic Agents - Atrovent
 Acts as a bronchodilator over time
 Not for acute attacks
 It may be useful for certain older asthma patients who also have
emphysema or chronic bronchitis.
 A combination with a beta2-agonist might be helpful for patients who do
not initially respond to treatment with a beta2-agonist alone.
Corticosteriods
 Chronic management
 Inhaled:
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The most recent generation of inhaled steroids include:
fluticasone (Flovent), budesonide (Pulmicort), triamcinolone (Azmacort and
others), and flunisolide (AeroBid)
 Oral – last to be used & first to be removed. Used as maintenance in
severe cases.
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prednisone, prednisolone, methylprednisolone, and hydrocortisone.
Long acting beta2-agonist and corticosteriod
combination
 Long-acting beta2-agonists, including salmeterol (Serevent) and formoterol (Foradil)
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Used for prevention of asthma attack
Formoterol has a much faster action than salmeterol and may achieve better control of nighttime asthma.
 Advair is a single device that contains a combination of both drugs.
Cromolyn
 Cromolyn sodium (Intal) serves as both an anti-inflammatory drug and has
antihistamine properties that block asthma triggers such as allergens, cold, or
exercise.
 Side effects:
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nasal congestion
coughing
sneezing
wheezing
nausea
nosebleeds
dry throat.
Leukotriene-antagonists
 zafirlukast (Accolate), montelukast (Singulair), zileuton (Ziflo), and pranlukast
(Ultair, Onon)
 Oral medications that block leukotrienes, powerful immune system factors that, in
excess, produce a battery of damaging chemicals that can cause inflammation and
spasms in the airways of people with asthma.
 Used to prevent asthma attacks.
 Gastrointestinal distress is the most common side effect
Risk for altered respiratory function related to excessive or thick secretions
secondary to asthma
Interventions:
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Regulate fluid intake to thin secretions
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Administer bronchodilators as appropriate
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Encourage slow, deep breathing; turning and coughing
Expected Outcomes:
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Pt will consume 2-3 L of fluid per day
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Pt will use brondhodilators when short of breath
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Pt will practice breathing exercises
Medically Diagnosing Asthma
 Health history & physical exam
 Pulmonary Function Tests (PFTs)
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Spirometry
Peak expiratory flow rates (PEFR)
 Sputum or blood culture for eosinophils
 Arterial blood gases (ABGs) & oximetry
 Serum IgE levels: elevated
 Chest x-ray: hyperinflation during attack
 Allergy skin testing
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Medically Diagnosing Asthma
Pulmonary Function Tests (PFTs)
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Reveals a low expiratory flow rate, forced expiratory volume, and forced vital
capacity with functional residual capacity and total lung capacity
Aid in determining degree of obstruction
Medically Diagnosing Asthma
 Arterial Blood Gases (ABGs)
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Determines how much oxygen is available to perfuse peripheral tissues
Normal values:
 pH: 7.35 - 7.45
 PaCO2: 35 - 45
 PaO2: 80 - 100
 HCO3: 22 - 26
 SaO2: 95 - 100
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Hypoxemia occurs with early respiratory alkalosis, or in severe cases, respiratory
acidosis.
Asthma Severity Classification
 Step 1: Mild Intermittent
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S/S < 2x week
Nocturnal s/s < 2x month
PEFR < 20% variability
Exacerbations brief with variable intensity
No daily medication needed
Asthma Severity Classification
 Step 2: Mild Persistent
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S/S > 2x week, but < 1x daily
Nocturnal s/s > 2x month
PEFR 20% - 30% variability
Exacerbations may or may not affect ADLs
One medication daily (low-dose corticosteroid or slow release theophylline)
Asthma Severity Classification
 Step 3: Moderate Persistent
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S/S daily
Nocturnal s/s > 1x week
PEFR > 30% variability
Exacerbations 2x daily
Exacerbations affect ADLs
One or two daily medications (med-dose corticosteroid &/or inhaled
bronchodilator)
Asthma Severity Classification
 Step 4: Severe Persistent
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S/S continuous
Nocturnal s/s frequent
PEFR > 30% variability
Exacerbations frequent
Exacerbations affect and limit ADLs
Two daily medications (high-dose corticosteroid & inhaled bronchodilator)
Status Asthmaticus
Is the most severe form of asthma
A severe life-threatening complication of an asthma attack
Persistent status of acute asthma exacerbation that does not respond to usual treatments
Hypoxemia worsens
Expiratory rate and volume further decrease
May lead to respiratory failure
Repeated attacks may cause irreversible emphysema
Buildup of CO2
acidosis
BP
Airways narrow further making it very difficult to move air in and out of the lungs
Requires intubation and ventilator support
Nursing Diagnoses
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Anxiety r/t inability to breath effectively, fear of suffocation
Ineffective breathing pattern r/t airway obstruction/resistance
Inadequate tissue perfusion r/t impaired gas exchange
Activity intolerance r/t fatigue, tightness of chest, shortness of breath
Risk for infection r/t ineffective airway clearance and decreased pulmonary
function
 See NIC
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Airway Management
Respiratory Monitoring
Plan and Interventions
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Allergy Management
Anxiety Reduction
Positioning
Vital Sign Monitoring
 Per physician order:
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Albuterol via nebulizer
Oxygen therapy
Order ABG’s
Nursing Diagnoses
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Anxiety r/t inability to breath effectively, fear of suffocation
Ineffective breathing pattern r/t anxiety
Anxiety r/t medication side effect
Impaired gas exchange r/t inflammation of airways, ventilation-perfusion imbalance
Ineffective airway clearance r/t excessive mucus production
Inadequate tissue perfusion r/t impaired gas exchange
Impaired spontaneous ventilation r/t asthma
Risk for decreased cardiac output r/t dysrhythmias associated with respiratory acidosis
Risk for infection r/t potential corticosteroid use
Plan and Interventions
 See NIC:
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Airway Management
Respiratory Monitoring
Anxiety Reduction
Positioning
Vital Sign Monitoring
Airway Clearance
 Per physician order:
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40% oxygenation via Venturi Mask
IV
Methylprednisolone
Start transfer to ICU
Nursing Dx
Anxiety related to threat of unknown death secondary to severe asthma attack
Interventions:
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Encourage verbalization of feelings, perceptions, and fears
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Provide objects that symbolize safeness
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Identify when level of anxiety changes
Expected Outcomes:
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Pt will verbalize feelings
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Pt will surround him/herself with a safe environment
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Pt will identify the beginning signs of anxiety