Transcript Transition Resp ppt

Selected Respiratory Disorders: COPD, Asthma,
Pneumonia, and Pulmonary Tuberculosis
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By the end of this lecture the student should be
able to
Demonstrate knowledge of pathophysiology of
clients experiencing COPD, Asthma, TB, GERD, and
PUD
Nursing interventions, treatment modalities
including pharmacological therapy of clients
experiencing COPD, Asthma, TB, GERD, and PUD
Nutritional needs of clients experiencing COPD,
Asthma, TB, GERD, and PUD
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Upper airway includes nasopharynx,
oraophyarnx, laryngopharynx. The function is
to warm, filter, and humidfy inspired air
Lower airway includes trachea, bronchi,
bronchioles, and alveoli. The function is
prevention of aspiration, location of vocal
cords, passage way for air, gas exchange
Lungs are prefused by bronchial arteries
small amt. of blood to lungs. Pulmonary
arteries bring the entire cardiac output to the
right ventricle to the aveoli for gas exchange
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Ventilation is the process of moving air into
the lungs and distribution of air within the
lungs to gas exchange units
Airway reisitance is determined by the
diameter of the airway.
Lung compliance the lungs expandibility &
ease of lung inflations
The mechanicas of breathing include airway
resistance, lung compliance, opposing lungs
forces(elastic recoil vs chest wall expansion.)
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Chronic Obstructive Pulmonary Disease
A disease state characterized by airflow
limitation that is not full reversible (GOLD).
COPD is the currently is 4th leading cause of
death and the 12th leading cause of disability.
COPD includes diseases that cause airflow
obstruction (emphysema, chronic bronchitis)
or a combination of these disorders.
Asthma is now considered a separate
disorder but can coexist with COPD.
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Chronic Bronchitis > chronic productive
 cough X 3 mo in 2 consecutive yrs
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Emphysema > abnormal enlargement &
destruction of alveoli walls
◦ COPD leads to pulmonary insufficiency, pulmonary
hypertension, and cor pulmonale
◦ In emphysema, the stimulus to breathe is a low PO2
instead of increased PCO2
Stage
Manifestation
Pulmonary Function Test Results
I (Mild)
±Chronic cough,
±Sputum production
FEV1/FVC<70%
FEV1>80% of predicted
II (Mod.)
±Dyspnea, ±Chronic
cough, ±Sputum
production
FEV1/FVC<70%
FEV1<80% But at least 50% of
predicted
III (Severe)
±Dyspnea, ±Chronic
cough, ±Sputum
production
FEV1/FVC<70%
FEV1<50% But at least 30% of
predicted
IV (Very
Severe)
±Dyspnea, ±Chronic
cough, ±Sputum
production
FEV1/FVC<70%
FEV1<30% of predicted OR
FEV1<50% of predicted with
either respiratory or heart failure
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A fifth category--Stage 0: At Risk--that appeared in
the 2001 report is no longer included as a stage of
COPD, as there is incomplete evidence that the
individuals who meet the definition of “At Risk”
(chronic cough and sputum production, normal
spirometry) necessarily progress on to Stage I:
Mild COPD.
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Tobacco smoke causes 80-90% of COPD
cases!
Passive smoking
Occupational exposure
Ambient air pollution
Genetic abnormalities
◦ Alpha1-antitrypsin
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Higher among African-Americans. Blue collar
workers, and less educated people in the US
Highest among Northern Plains American
Indians/Native Americans and Alaskan
Natives
Decrease overall for men and women, but
decrease less for women than men
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The presence of a cough and sputum
production for at least 3 months in each of 2
consecutive years.
Irritation of airways results in inflammation
and hypersecretion of mucous.
Mucous-secreting glands and goblet cells
increase in number.
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Ciliary function is reduced, bronchial walls
thicken, bronchial airways narrow, and
mucous may plug airways.
Alveoli become damaged, fibrosed, and
alveolar macrophage function diminishes.
The patient is more susceptible to respiratory
infections
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Chronic bronchitis causes ↑in the number and
size of mucous glands→ produce large
amount of thick mucus ↑ bronchial wall
thickness (2X the normal thickness)→ impair
airflow
Block small airway and narrows large ones
Small airways are affected before large ones
get involved
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Inflammation of the bronchi and bronchioles
caused by chronic exposure to irritants,
especially tobacco smoke
Irritants trigger inflammation,
vasodilatation→ congestion→ mucosal
edema→ bronchospasm
Bronchitis affects only the airway
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Chronic bronchitis ↓ airflow and gas
exchange because of mucous plugs and
infection narrowing the airways
Result is ↓ PaO2 (hypoxemia) an the arterial
blood carbon dioxide level PaCO2 ↑
(respiratory acidosis)
◦ Exertional dyspnea (late)
◦ Frequent productive cough
◦ Bluish/red color
◦ Hypoxemia
◦ Hypercapnia
◦ Normal wt/heavy
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Abnormal distention of air spaces beyond the
terminal bronchioles with destruction of the
walls of the alveoli.
Decreased alveolar surface area causes an
increase in “dead space” and impaired oxygen
diffusion.
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Reduction of the pulmonary capillary bed
increases pulmonary vascular resistance and
pulmonary artery pressures.
Hypoxemia result of these pathologic
changes.
Increased pulmonary artery pressure may
cause right-sided heart failure (cor
pulmonale).
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Emphysema →hyperinflation , destruction ,
collapse alveoli →Centrilobular/panlobular
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Major two changes are
◦ Loss of elasticity
◦ Hyperinflation of the lungs
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Dyspnea
Exertion/rest
Min. nonproductive
Barrel chest
Hypoxemia
Hypercapina (late)
Underweight (↑ BMR/ ↑ work breathing)
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Client with a late-stage has a low arterial
oxygen (PaO2) level
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Air trapped in lungs
Increase the work of breathing
Use accessory muscles in neck, chest wall and
abdominal
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Gas exchange is affected
Often inhalation starts before exhalation is
completed, resulting in uncoordinated
pattern of breathing
Air hunger
Client ↑ respiration rateCO2 is produced
faster than can be eliminated resulting in →
CO2 retention and chronic respiratory
acidosis
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Panlobular
Centrilobular
Each type can occur along or in combination
in the same lung
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Panlobular emphysema (PLE) has destruction
of the entire alveolus uniformly
Diffuse and more severe in the lower lung
area
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Occur in the bronchioles
Allow spaces to develop as tissue walls
breakdown
Often seen in longstanding cigarette smokers
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Enzyme made by the liver and is normally
present in the lungs
Purpose is to regulate other enzymes
(protease) that are present to break down
inhaled pollutants and microorganisms
AAT prevent the protease from working on
lung structures
AAT is dependent on the inheritance of a pair
of normal gene alleles
About 100,000 American have this deficiency
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COPD affects the delivery of oxygen to all
tissue
Complication of COPD can lead to organ
anoxia and tissue death
Major problems are:
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Hypoxemia and acidosis
Respiratory infections
Cardiac failure
Cardiac dysrhythmias
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↓ gas exchange ↓ oxygenation ↑ carbon
dioxide→ hypoxemia and acidosis
Most tissue have decreased function
Hypoxemia refers to deficient blood oxygen
Hypoxia refers to decrease in tissue
oxygenation
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Infection from ↑ mucous and poor
oxygenation
Acute respiratory infections make COPD
worse by ↑ inflammation and mucus
production and induce more bronchospasm
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Acute exac. of chronic bronchitis due to
impaired mucocillary system
Acute respiratory failure from acute URI &
indiscriminate use of sedatives/narcotics
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Peptic Ulcer/GERD> meds / stress of disease
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Pneumonia
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Cor pulmonale or right-sided hart failure
Key features of Cor Pulmonale
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Hypoxia & hypoxemia
Increasing dyspnea
Enlarged & tender liver
Warm , cyanotic extremities with bounding pulse
Fatigue
Cyanotic lips
Right ventricle enlargement (hypertrophy)
Distended neck veins
weakness
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Key features of Cor Pulmonale
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Lower sternal or epigastric pulsation
GI disturbance such as N/V
Dependent edema
Metabolic and respiratory acidosis
Pulmonary hypertension
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Smoking cessation
Pneumonia/influenza vaccines
Avoidance of environmental irritants/triggers,
extreme in temp, crowds peak URI season &
prompt Tx URI
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History
Physical assessment
Psychological assessment
Laboratory assessment
Radiographic assessment
Other diagnostic assessments
 History
◦ Risk factors
 Consider age
 Gender
 Occupational history
 Ethnic cultural background
 Current problem
 Weight and diet
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General appearance
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Weight in proportion to height
Posture
Mobility
Muscle mass
Overall hygiene
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Respiratory changes
◦ Assess breathing rate and pattern
◦ Assess degree of dyspnea
◦ palpate chest for tenderness and abnormal
retractions
◦ Examine chest for presence of “barrel chest”
◦ Assess for cyanosis, delayed capillary refill and
clubbing of the fingers
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Cardiac changes
◦ Assess heart rate & rhythm
◦ Check for swelling of feet and ankles (dependent
edema)
◦ Examine nail beds and oral mucous membranes
◦ Pallor or frank cyanosis
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Reduced socialization
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Annoying coughs
Excessive sputum
Dyspnea
Exposure to irritants may reduce hobbies
Economic status
Work, family, social and sexual roles affected
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ABGs
Sputum cultures
WBC
HGB & HCT
Serum electrolytes
CXR
PFT
Pulse oximetry
ECG
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Oxygen therapy
Drug therapy
Respiratory therapy
Exercise training
Surgical intervention
Nutrition
Anxiety
Activity intolerance
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Oxygen therapy
◦ Use to treat hypoxemia. COPD pt are CO2 retainers
◦ Their drive to breath is stimulated by hypoxia
◦ Always use humidity & titrate O2 to lowest effective
concentration usually 1 to 2 liters
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Drug Therapy
Bronchodilators- decrease airway resistant &
hyperinflation of lung resulting in decreased
dyspnea & ˄FEV.
Used as maintenance therapy
◦ Inhaled anticholingerics (atrovent most effective
also used in combination B2 agonist (combivent)
◦ B2 agonist (albuterol)
◦ Long acting B2 agonist (theophylline)
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Drug Therapy (cont.)
Corticosteroids used frequent in exac. that
don’t respond to bronchodilators/
bronchospasm/asthma
Mucolytic prescribed for pt with thick
tenacious mucous secretions
◦ Neb with NS or agents such as mucomyst or
mucosil
◦ Guiafenesin is a systemic mucolytic taken orally
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Respiratory Therapy
◦ Breathing retraining
◦ Pursed lip and
diaphragmatic techniques
◦ Coughing technique
◦ Chest physiotherapy
◦ Aerosol/
neubulization/cleaning of
equipment
Pursed lip breathing
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Exercise training
◦ Walk 15-20 min/day. Guideline to avoid over
exerting if SOB return to normal level 5 min after
rest
◦ Use bronchodilator before exercise and 5 min after
stopping activity
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Surgical management
◦ Lung transplantation
◦ Lung reduction
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Preoperative
◦ Selection process requires several criteria
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Post care
◦ Close monitoring for respiratory problems
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Nutrition
◦ Monitor pt weight
◦ Foods easy to chew and non gas forming
◦ High caloric & high protein diet divided in to 5-6
meals /day
◦ Rest and bronchodilators before and after meals
◦ Avoid drinking fluids before and during meals
◦ Avoid milk, chocolate when symptomatic
◦ Fluid intake 3 liters/day between meals
◦ Mouth care before meals
◦ Assist with feeding when tire easy
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Activity intolerance
Encourage pt to pace activities
Provide as much self-care as possible
Instruct not to rush through morning activities
Assess pt response to activities (skin color, vital
signs, etc.)
◦ Provide supplemental oxygen during high energy
activities as necessary
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Anxiety
◦ Develop written plan that states exactly what to do
if symptoms flare
◦ Stress the use of pursed lip and diaphragmatic
breathing technique
◦ Friends, family and support group
◦ Professional counseling id necessary
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Early identifications with spirometry
Individualize the management of stable COPD
Education
Pharmacotherapy
Exercise
exacerbations
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Referral to registered dietitian for COPD pts
Restrict sodium to <2000 mg/day
Consume folate in the form of food and/or a
combination of B6, B12 and supplementation
Drink 48-64 oz of fluid daily
Consume RDA for antioxidants A, C and E,
and adequate intake of omega-3 fatty acids
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Home care management
◦ Oxygen, equipment at home
◦ Financial concerns (disability benefits)
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Health teaching
◦ Knowledgeable of disease process
◦ Drug therapy, manifestation of infection and
avoidance of irritants
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Health care resources
◦ Support group (American Lung Association)
◦ Smoking cessation
◦ Meals on wheels
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Health history
Inspection and examination findings
Review of diagnostic tests
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Impaired gas exchange
Impaired airway clearance
Ineffective breathing pattern
Activity intolerance
Deficient knowledge
Ineffective coping
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Ineffective airway clearance R/T exp airflow
obstruction /ineffective cough
Impaired gas exchange R/T alveolar
hypoventilation
Imbalanced nutrition: less than R/T poor
appetite/fatigue/SOB/sputum production
Disturbed sleep pattern R/T
dyspnea/depression/abnormal ABG
Risk for infection R/T ineffective airway
clearance/lack of knowledge regarding infectious
process
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Smoking cessation
Improved activity tolerance
Maximal self-management
Improved coping ability
Adherence to therapeutic regimen and home
care
Absence of complications
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Respiratory insufficiency or failure
Atelectasis
Pulmonary infection
Pneumonia
Pneumothorax
Pulmonary hypertension
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Proper administration of bronchodilators and
corticosteroids
Reduction of pulmonary irritants
Directed coughing, “huff” coughing
Chest physiotherapy
Breathing exercises to reduce air trapping
◦ diaphragmatic breathing
◦ pursed lip breathing
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Use of supplemental oxygen
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Focus on rehabilitation activities to improve
ADLs and promote independence.
Pacing of activities
Exercise training
Walking aides
Utilization of a collaborative approach
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Set realistic goals
Avoid extreme temperatures
Enhancement of coping strategies
Monitor for and management of potential
complications
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Disease process
Medications
Procedures
When and how to seek help
Prevention of infections
Avoidance of irritants; indoor and outdoor
pollution, and occupational exposure
Lifestyle changes, including cessation of
smoking
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Overall goal for management
Return/maintain baseline resp. function
Ability to perform ADL
Relief of dyspnea
Suffer no or delay complications
Knowledge and ability to implement long-term
treatment plan
◦ Overall improvement in quality of life
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A chronic inflammatory disease of the airways
that causes hyperresponsiveness, mucosal
edema, and mucous production.
Inflammation leads to cough, chest tightness,
wheezing, and dyspnea.
The most common chronic disease of
childhood.
Can occur at any age.
Allergy is the strongest predisposing factor.
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Hyperresponsiveness to a trigger which cause
muscosal edema in the bronchi and mucus
production the stagnated muscus in the
bronchi cause inflammation causing
bronchoconstriction Chronic asthma
Acute asthma is caused by triggers that
stimulate beta-adrenergic receptors in the
bronchi which cause bronchoconstriction
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Cough
Dyspnea
Wheezing
Chest tightness
Exacerbation progression
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Diaphoresis
Tachycardia
Wide pulse pressure
Hypoxemia (late sign of poor oxygenation)
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Family and environmental history
Cormobidity conditions (GERD)
Other possible allergic reactions
Sputum
Blood tests (WBC, IeG, ABGs)
Pulmonary function test
◦ Spirometer(preferred test)
◦ Peak flow(not reliable for kids <5yrs old)
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Nursing alert: Normal PaCO2 during an
asthma attack may be a signal of impending
respiratory failure
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Peak flow meter is small hand held device
used to measure amount of air flow out of the
lung
Meter records flow as a number also known
as Peak Expiratory Flow (PEF)
Use of a peak flow meter helps to determine
how well controlled a person’s asthma is and
can help indicate when an attack may happen
Symptoms may be mild to life threatening
 Step 1.-Mild Intermittent-occurs<2
times weekly
 Step 2.-Mild persistent- occurs>2 times
but<1 times day
 Step 3.-Moderate persistent-occurs
daily/use of medicine daily
 Step 4.Severe persistent –Continual
symptoms/limited physical activity
/frequent exacerbations
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Preventions
Complications
Medical Management
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Pharmacologic Therapy
Quick relief medications
Long acting controlling medications
Peak flow monitoring
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Quick-relief medications
◦ Beta2-adrenergic agonists
◦ Anticholinergics
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Long-acting medications
◦ Corticosteroids
◦ Long acting beta2-adrenergic agonists
◦ Leukotriene modifiers
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Assessment
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Assess respiratory status
History
Identify medication
Administrating prescribed medications
Administrating fluids
Promoting home and community-based care
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The nature of asthma as a chronic inflammatory
disease
Definition of inflammation and bronchoconstriction
Purpose and action for each medication
Identification of triggers and how to avoid them
Proper inhalation techniques
How to perform peak flow monitoring
How to implement an action plan
When and how to seek assistance
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The Asthma Action
Plan is a written plan
for the patient
developed with the
HCP to help control
Asthma
It includes:
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Daily treatment regimen
Asthma triggers
Early signs of attack
Peak flow readings
How to prevent an attack
Emergency treatment for
attack
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Pathophysiology
Clinical Manifestation
Assessment and Diagnostic findings
Preventions
Complications
Medical Management
Nursing Management
Client Teaching
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Infectious disease affecting the lung
parenchyma
Other parts of the body: meninges, kidneys,
bones, and lymph nodes
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Infected with mycobacteria organism via airborne
through airway to the alveoli. Immune system
activate which engulfs the organism and cause the
accumulation of exduate in the alveoli within 2 to
10 weeks after exposure. This tissue of live and
dead bacilli forms a protective wall and become
necrotic and later become calcified and form a
collagenous scar. Common site is the apical or
posterior segment of the upper lobe or the
superior segment of the lower lobe of the lung
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Low grade fever
Cough night sweats
Hemoptysis
Anorexia
Weight loss
Present for weeks or months
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History
Physical exam
Tuberculin skin test
Chest Xray
Sputum culture
QuantiFERON-TB Gold Test
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Page 569
Class o- no exposure; no infection
Class 1- exposure no infection
Class 2- latent infection; no disease (positive
PPD, no clinical evidence of active RB
Class 3- disease; clinically active
Class 4- disease; not clinically active
Class 5- suspect disease; diagnosis pending
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Gerontology Consideration
Medical Management
◦ Pharmacologic therapy
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Nursing Management
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Promoting airway clearance
Advocating adherence to treatment regimen
Promoting activity and adequate nutrition
Preventing spread of TB infection
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R RIFAMPIN
I ISONIAZID
S STREPTOMYCIN
E ETHAMBUTOL
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Tx: Multi-drug therapy = to prevent
development of resistance (RIPES)
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Rifampicin – inhibits RNA synthesis of the
bacilli
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Isoniazid – remarkably potent to the bacilli;
prophylaxis; given with Vit. B6
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Pyrazinamide (PZA) – inhibits cell growth
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Ethambutol – inhibits cell growth
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Nursing Management:
1.
Give meds before meals
2.
Maintenance therapy = after 6months
3.
Client not communicable after 2wks
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Rifampicin’s SE: reddish/orange body secretions
(urine)
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PZA prone to hyperuricemia so ↑oral fluids
6.
Ethambutol - A/E: optic neuritis so √
Streptomycin – 1st drug found to be
vision/visual changes
effective against PTB; given by injection
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C/I: pedia – cannot report any visual
disturbances
7.
Streptomycin – A/E: ototoxic (√ tinnitus)
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nephrotoxic = √ oliguria
neurotoxic = seizure precautions
Nursinglectures.blogspot.com
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Airbone isolation
Negative Pressure Room
N95 masks
Keep door closed at all times
Transport patient with masks
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3 consecutive negative sputum smears
Their symptoms have improved, and
They are adhering to an adequate treatment
regimen for at least two weeks.
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Pathophysiology
Clinical Manifestation
Assessment and diagnostic findings
Classifications
Gerontology consideration
Medical management
Nursing management
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Acute tracheobronchitis
Pneumonia
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Community-acquired pneumonia
Hospital-acquired pneumonia
Pneumonia in immunocompromised host
Aspiration pneumonia
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Chest x-ray
Sputum examination
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Supportive treatment includes fluids, oxygen
for hypoxia, antipyretics, antitussives,
decongestants, antihistamines
Administration of antibiotic therapy
determined by gram-stain results
If etiologic agent is not identified, utilize
empiric antibiotic therapy
Antibiotics not indicated for viral infections
but are used for secondary bacterial infection
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Ineffective airway clearance
Activity intolerance
Risk for fluid volume deficient
Imbalanced nutrition
Deficient knowledge
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Continuing symptoms after initiation of
therapy
Shock
Respiratory failure
Atelectasis
Pleural effusion
Confusion
Superinfection
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Improved airway clearance
Maintenance of proper fluid volume
Maintenance of adequate nutrition
Patient understanding of treatment,
prevention
Absence of complications
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Encourage hydration; 2 to 3 L a day, unless
contraindicated
Humidification may be used to loosen
secretions
◦ By face mask or with oxygen
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Coughing techniques
Chest physiotherapy
Position changes
Oxygen therapy administered to meet patient
needs
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Promoting rest
◦ Encourage rest, avoidance of overexertion
◦ Positioning to promote rest, breathing (Semi-Fowler’s)
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Promoting fluid intake
◦ Encourage fluid intake to at least 2 L a day
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Maintaining nutrition
◦ Provide nutritionally enriched foods, fluids
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Patient teaching
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Oxygenation assessment with ABG or pulse
oximetry within 24 hour prior to or after hospital
arrival
Pneumococcal vaccine
Blood cultures within 24 hours prior to or 24 hours
after hospital arrival
Adult smoking cessation
advice/counseling(including prescriptions for
patches/gum/meds/handouts/video
Initial Antibiotic with 4-6hr of hospital arrival
Influenza vaccination discharged during October
and March
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Risk factors
Pathophysiology
Prevention:
◦ Elevate HOB
◦ Turn patient to side when vomiting
◦ Prevention of stimulation of gag reflex with suctioning
or other procedures
◦ Assessment, proper administration of tube feeding
◦ Rehabilitation therapy for swallowing
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Pleurisy: inflammation of both layers of
pleurae
◦ Inflamed surfaces rub together with respirations,
cause sharp pain intensified with inspiration
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Pleural effusion: collection fluid in pleural
space usually secondary to another disease
process
◦ Large effusions impair lung expansion, cause
dyspnea
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Empyema: accumulation of thick, purulent
fluid in pleural space.
◦ Patient usually acutely ill; fluid, fibrin development,
loculation impair lung expansion
◦ Resolution is a prolonged process
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Cigarette smoking
Air pollution