Transcript Oxygenation lecturex

OXYGENATION LECTURE
M. Catherine Hough, Ph.D, RN
University of North Florida
COH - Department of Nursing
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

Alveolar Dead Space



+ ventilation
- perfusion
Intrapulmonary Shunting


- ventilation
+ perfusion
OBSTRUCTIVE SLEEP APNEA
 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
(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


More underdiagnosed in women than men.
Mean duration of s/s before dx in one series of women was
10years
Pathogenesis
There is normally a moderate degree of hypoventilation during
sleep resulting from partial pharyngeal collapse and
resulting increase in upper airway resistance.
1.
2.
3.
This is due to decreased activity of the "upper airway dilator
musculature" during sleep.
Occasional apneic or hypopneic episodes are normal, esp. in elderly.
Prolonged and repetitive apneic/hypopneic episodes are not normal.
Structural factors
In most OSA patients, there are no evident structural abnormalities.
Most experts, however, believe that subtle underlying structural
factors are involved:
a.
b.
Narrower upper airway (OSA patients
have narrower upper airways on average,
but there' much overlap)
More "collapsible" airways (+/- evidence
for this)
Structural factors …
In rare instances, clear structural abnormalities are found
1.
2.
3.
4.
5.
nasal obstructing lesions
Deviated nasal septum
chronic rhinitis
masses of the soft palate
large T & A's
Structural abnormalities may play a larger role in women
1.
2.
3.
48% of women with OSA in one series had abnormalities of the hard
palate
>70% with mild OSA
In one series of women with OSA, most weren't overweight, but BMI
was correlated with severity (freq. of apneic/hypopneic episodes)
Functional factors
1. OSA pts may have altered sleep
2. Influences on palatal muscle control, e.g. the reflexes which
normally keep palate open during inspiration
3. May have impaired ventilatory drive or arousal mechanisms
(Sources: Disease-a-month, 4/94; Lancet 344:653, 1994; 344: 656, 1994;
Ann. Int. Med. 122: 493, 1995)
TREATMENT
1. Surgical - Remove obstruction
2. Mechanical - Nasal CPAP
3. Support Groups
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 consumption and lower
achievement
 Advertising targets fantasies and insecurities of teens
and young adults
Obstructive & Restrictive
Lung Disorders
Obstructive Lung
Disorders
 Asthma
 COPD


head injuries, tumors, OD
Neuromuscular
 GB, ALS, MD, Polio
Chest Wall
 trauma
Pleural Disorders
 pleural effusion, pleurisy
Parenchmal
 atelectasis, pneumonia,
TB, pulmonary fibrosis


Acute Bronchitis
Chronic Bronchitis
Emphysema

Intrapulmonary

Restrictive Lung
Disorders
 General


Characteristics of Lung Disorders
Obstructive
Restrictive
 Decreased resistance
to airflow
 Normal or decreased
Vital Capacity
 Increased Total Lung
Capacity
 Increased Functional
Residual Capacity
 Increased Residual
Volume
 Reduced Vital Capacity
 Reduced Total Lung
Capacity
 Normal or reduced
Functional Residual
Capacity
 Cause difficulty with
inspiration
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
Emphysema …
 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
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
Healthy Lung
Emphysema Lung

The destruction of elastin that occurs in
emphysema is believed to result from an imbalance
between two proteins in the lung:
1.
2.

An enzyme called elastase which breaks down elastin,
and
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.
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)
 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








Hx and onset of symptoms
Smoking Hx
Family Hx
Past or present exposure to environmental irritants
Activity intolerance, fatigue
Anorexia, weight loss
Symptoms of hypoxemia - restlessness, confusion
Medications and therapies and their effectiveness
Assessment...
Objective
 Increased airway
resistance
 Decreased Expiratory
Force
 Mild hypoxemia
 Barrel Chest
 Increased AP diameter
 Increased Accessory
Muscles
 ABG’s show
compensation
 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 -



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 improve
 Antibiotics if there is an infectious process occurring
 Steroids during acute exacerbation's
 Low flow oxygen (1-2 liters)
 Breathing exercises
 Respiratory therapy & CPT
 Lung reduction surgery

Performed only on pts with severe emphysema
 Avg. hospital LOS ~ 2 weeks
 Require pre and post op extended pulmonary rehab
 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…
 Get pneumonia
vaccination and yearly
influenza shots
 Avoid excessive heat,
cold and high altitudes
 Drink fluids
 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:
1.
Explain importance of consuming adequate amounts of nutrients
2.
Provide a pleasant, relaxed atmosphere for eating
Expected Outcomes:
1.
Pt will verbalize & understand importance of adequate nutrition
2.
Pt will use a comfortable environment for meals
3.
Pat will eat slower and smaller meals
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





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
Cough Enhancement


Positioning for chest expansion
Deep breathing, hold for 2 seconds, and cough 2-3
times
Nursing Interventions
Respiratory Monitoring
 Rate,
rhythm, depth, and effort (overall
patterns)
 Monitor for increased restlessness, anxiety,
and air hunger
 Note changes in SaO2, ABG values
Nursing Interventions
Anxiety Reduction
 Calming
& reassuring attitudes
 Stay with patient
 Encourage slow breathing (pursed lips)
Nursing Interventions
 Teaching: Disease Process & Prescribed
Medication





Identify level of knowledge
Instruct on measure to prevent/minimize side effects
of treatment
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
Asthma
Forced expiratory
volume
Vital capacity
Bronchitis
Emphysema
Expiratory flow
Expiratory flow
rates
rates
Vital capacity
Total lung capacity
Residual volume
Residual volume
Total lung capacity WNL Vital capacity normal or
slightly reduced
Arterial Blood Gases (ABGs)
 Arterial Blood Gases (ABGs)


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

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
 Sympathetic Agents: PO, Inhalation (Albuterol, Terbutaline)

Rescue inhalers – Albuterol…
 Corticosteroids – Solu Medrol – IV or PO to alleviate acute symptoms by
decreasing inflammation
Antibiotics – to manage respiratory tract infections

 Mucolytics and expectorants – to thin and aid in removal of mucus
 Analgesics
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:





>50 years old
Chronic heart or lung
disease
HIV
Anyone living in large
groups
People who may transmit
the flu to high risk groups
 Nurses, doctors, and other
healthcare workers
Flu Shots…
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 a flu shot
PULMONARY EMBOLISM
MEDICAL INTERVENTIONS
 Anticoagulants
 Thrombolytic therapy
SURGICAL INTERVENTIONS
 Embolectomy
NURSING DIAGNOSIS
 Impaired gas exchange
Pulmonary Embolism….
Risk factors for PE











Recent surgery
Recent fx of a lower extremity, especially with immobilization
Immobilization, particularly complete bedrest or LE 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
1.
2.
3.
4.
5.
6.
7.
8.
9.
Prolonged immobility or paralysis
Injury to vascular endothelium
Hypercoagulability
CVP 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
 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



Early ambulation or change position q2h
Compression stockings
Intermittent pneumatic compression stockings
 Pharmacologic agents




Low molecular wt. Heparin
Low dose unit Heparin
Warfarin
Low dose ASA
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)
 MRI
 Pulmonary angiography
 CXR may show evidence of pulmonary infarct
 Lower extremity venous duplex (DVT requires
same tx as PE)
 A negative study does not exclude PE!
Treatment
MEDICAL INTERVENTIONS:
Anticoagulation
 Low molecular wt. Heparin
 Low dose unit Heparin
 Warfarin
SURGICAL INTERVENTIONS
 Embolectomy
 GFF
NURSING DIAGNOSIS
 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)
0 min
0 min
0 min
0 min
60 min
120 min
Rate Change
+4ml/hr (200units/hr)
+2ml/hr (100units/hr)
NO RATE CHANGE
-2ml/hr (100units/hr)
-4ml/hr (200units/hr)
-4mil/hr (200units/hr)
Repeat PTT
6hrs
6hrs
next AM
6hrs
6hrs
6hrs
Greenfield Filter
Venacava
RESTRICTIVE
LUNG DISORDERS
Restrictive Lung Disorders
Restrictive Lung Disorders
Intrapulmnary
 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

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:

Shows increased bronchovascular markings
 Pulmonary functioning tests:

Decreased forced expriatory volume and vital capacity, and increased
residual volume
 Arterial Blood Gas (ABG) studies

respiratory acidosis, hypercapnia, Hypoxia
 Complete Blood Count

Elevated Hbg and Hct (polycythemia)
 Elevated WBC
 Pulse Oximetry

Pt. usually hypoxic
 Sputum C&S:

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
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

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
system.
T=
N=
M=
TNM staging
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

Lobectomy
 pneumonectomy
 Radiation therapy

Curative approach with resectable tumor but poor surgical risk
 Adjuvant with other approaches
 Palliative to reduce symptoms
 Chemotherapy

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:
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.
 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





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
http://www.shirinwadia.com/asthma1.htm
http://www.asthma.ca/adults/about/whatIsAsthma.php
http://www.asthma.ca/adults/about/whatIsAsthma.php
Hyperventilation
 Airway walls are thickened with inflammatory
exudates which enhances bronchospasms
and reduces expiratory flow.


Results in increased work of breathing and hyperinflation
away from the obstruction.
Air trapping inside the lungs causes the individual to
hyperventilate.
http://www.kodomo.co.jp/asthma/ex/x-ray/
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
PHASES…
Late Phase (5-6 hours to 2 days)
 Infiltration (esoinophils and neutrophils)
 Bronchial hyperreactivity
 Imflammation
 Infiltration with monocytes and lymphocytes
ASTHMA TRIGGERS
G
A
S
P
gerd
allergens
smoking, strong odors
pets & pests
B
R
E
A
T
H
beer, wine & deli
resp. infections
emotional/stress
activities
timing
humidity, cold
air or sudden
temp change
Clinical Presentation
 Abrupt or gradual onset
 Wheezing – inspiratory
&/or expiratory
 Nasal flaring
 Dyspnea/SOB
 Anxiety
 Tachypnea
 Tachycardia
 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)

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:

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
 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:

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.

prednisone, prednisolone, methylprednisolone,
and hydrocortisone.
Long acting beta2-agonist and
corticosteriod combination
 Long-acting beta2-agonists, including salmeterol
(Serevent) and formoterol (Foradil)


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
Nursing Dx
Risk for altered respiratory function related to
excessive or thick secretions secondary to asthma
Interventions:
1.
Regulate fluid intake to thin secretions
2.
Administer bronchodilators as appropriate
3.
Encourage slow, deep breathing; turning and coughing
Expected Outcomes:
1.
Pt will consume 2-3 L of fluid per day
2.
Pt will use brondhodilators when short of breath
3.
Pt will practice breathing exercises
Medically Diagnosing Asthma
 Health history & physical exam
 Pulmonary Function Tests (PFTs)

Spirometry
 Peak expiratory flow rates (PEFR)
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Sputum or blood culture for eosinophils
Arterial blood gases (ABGs) & oximetry
Serum IgE levels: elevated
Chest x-ray: hyperinflation during attack
Allergy skin testing
Medically Diagnosing Asthma

Pulmonary Function Tests (PFTs)
1.
2.
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

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

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

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
Plan and Interventions
 See NIC
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Airway Management
Respiratory Monitoring
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:
1.
Encourage verbalization of feelings, perceptions, and fears
2.
Provide objects that symbolize safeness
3.
Identify when level of anxiety changes
Expected Outcomes:
1.
Pt will verbalize feelings
2.
Pt will surround him/herself with a safe environment
3.
Pt will identify the beginning signs of anxiety