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acute bronchitis (infectious)
inflammation of bronchi
most common cause: viral infection
primarily affect bronchi, NOT alveoli
acute bronchitis manifestations
cough
clear sputum - can become purulent
fever
dyspnea
HA & malaise
paroxysmal (sudden violent) coughing
hoarseness, myalgia, chest pain
acute bronchitis diagnosis
H&P
crackles (mucus buildup) and wheezes on exhalation with exertion
chest x-ray
to r/o pneumonia
acute bronchitis treatment goals
symptoms relief
tea, honey, cough drops, menthol
prevent pneumonia
acute bronchitis interventions
droplet precautions
vital signs
TCDB Q2H (turn, cough, deep breathe)
PO fluids (loosen secretions)
prevent spread
wash hands
avoid sharing articles
cover mouth when sneezing or coughing
discard soiled tissues in a plastic bag
if secondary bacterial infection occurs:
persistent cough & thick purulent sputum
obtain a sputum culture followed by antibiotic therapy
see HCP: fever, dyspnea, or duration greater than 4 weeks
antitussives:
dextromethophran (OTC)
benzonatate (Rx)
codeine (Rx)
expectorants:
guaifenesin (OTC)
bronchodilators:
albuterol (Rx)
levalbuterol (Rx)
adrenergic agonists - dilate the bronchioles - cause SE of tachycardia, anxiety, incr HR/RR
pneumonia
infection spread from bronchioles to alveoli → more dangerous
bacterial infection → more serious/painful and needs to treat w antibiotics
organisms reach lung by:
aspiration: impaired swallowing go into the lungs, food/liquid in lungs cause bacterial growth
inhalation
hematogenous spread
community acquired
6th leading cause of death for > 65 yrs old
nosocomial
hospital-associated
ventilator-associated
healthcare-associated
opportunistic and d/t aspiration
pneumonia risk factors
smoking
age (v young and v old)
ETOH
chronic disease
immunosuppression
recent respiratory infection
recent hospitalization
difficulty swallowing
bed rest
prolonged immobility
pneumonia pathophysiology
infection and fluids in lung tissue
infection → inflammatory process (swelling) in alveoli
consolidation of debris, fibrin, fluids in affected area of lung = impaired gas exchange
pneumonia assessment
subjective
fever
chills
cough
productive sputum
chest pain
objective
crackles
rhonchi → very hoarse lung sounds → caused by thick mucus
decreased SaO2
elderly considerations
dehydration
change in LOC
diagnostics
CXR
C&S
CBC
pulse ox
blood cultures if increased fever
pneumonia interventions
pulmonary toilet (TCDB, IS)
O2 to treat hypoxemia
hydration
I&O
administer medications as Rx’d
analgesics for pain
antipyretics for fever
antibiotics for infection
comfort: cough suppressants, mucolytics, bronchodilators, corticosteroids
pertussis (infectious) - AKA whooping cough
highly contagious bacterial disease with uncontrolled, violent cough
gram-negative bacteria attach to cilia, release toxins results in inflammation
inspiratory gasp after cough → “whooping” sound
pertussis symptoms
initial: similar to acute bronchitis
severe coughing, worse at night
vomiting may occur with coughing
runny nose
fever (102 F or lower)
pertussis clinical manifestations
stage 1: 1-2 weeks
low-grade fever, runny nose, watery eyes, general malaise, and mild nonproductive cough
stage 2: 2-10 weeks
paroxysms of cough
stage 3: 2-3 weeks
less severe cough, weak
pertussis diagnosis
initially based on symptoms
sputum culture
CBC
pertussis Rx’s
airborne precautions
antibiotics
macrolides (erythromycin, zithromax)
fluids
expectorants & suppressants are NOT helpful and are not recommended
pertussis prevention
DPT vaccination for children; but all adults > 18 should have TDAP
children under 2 months cannot be vaccinated
tuberculosis
caused by Mycobacterium tuberculosis
lungs are most commonly infected
¼ of world’s population has TB
US prevalence is decreased
TB risk factors
international travel
live in group settings
work in hospitals, jails, shelters, etc
tuberculosis classifications
exposure to TB
inhalation of bacteria
inflammation
usually contained by immune response
active TB
if initial immune response fails, bacteria replicate and disease emerges within 2 years
latent TB infection (LTBI)
positive skin test but asymptomatic and non-transmissible
5-10% risk of developing active TB
tx of LTBI is as critical as managing active TB
tuberculosis manifestations
LTBI
no S/S
does not feel sick
+ skin/blood test
normal CXR
(-) sputum smear
active TB
cough > 3 weeks
chest pain
hemoptysis
weakness/fatigue
weight loss/anorexia
chills
fever
night sweats
feels sick
+ skin/blood test
+ sputum smear
abnormal CXR
tuberculosis diagnostics
H&P examination
tuberculin skin test (TST, aka mantoux test)
quantiFERON-TB gold test
CXR
bacteriologic studies
sputum smear for acid-fast bacilli (AFB)
sputum culture
TB interventions
active TB
most patients treated as outpatients
infectious for first 2 weeks after starting treatment if sputum (+) → airborne precautions
restrict visitors and limit public exposure
hand hygiene and oral hygiene
aggressive antibiotic therapy (4-9 months) → monitor adherence
directly observed therapy preferred, but it is controversial
latent TB
antibiotic therapy (4-9 months)
atelectasis
restrictive
alveolar collapse
caused by shallow breathing, sedation, decreased mobility, post-op
easier to anticipate than to treat
lungs don’t fully expand and secretions occlude alveoli → decreased surfactant and alveolar collapse
atelectasis assessment
physical
RR and rhythm
SOB
dyspnea
cough
breath sounds decreased or absent
diagnostic tests
O2 sat
CXR
ABGs
interventions
re-expand alveoli
cough
suctioning
CPT
monitor for complications
ARDS (acute respiratory distress syndrome)
restrictive
caused by: pneumonia, sepsis, trauma, inhalation injury
risk factors: smoking, alcohol abuse, recent high-risk surgeries
process:
damage to alveoli and pulmonary capillaries
increased permeability of alveolar blood vessels
fluid accumulates in alveolar spaces
alveoli become airless, decreased surfactant, decreased lung compliance, decreased ventilation, hypoxia occurs
respiratory failure
ARDS assessment
early:
may be subtle
increased RR, dyspnea, restlessness, cough
progresses quickly
later:
diaphoresis
increased SOB
cyanosis
ARDS diagnostics
imaging (CXR, CT)
ABGs
SaO2
ARDS interventions
mechanical ventilation (PEEP)
positioning → flip around, mobilize lung fields and move where fluid is settling
pursed lip breathing
strict I&Os
keep patient euvolemic
serial ABG monitoring
pulmonary fibrosis
lung condition characterized by progressive scarring or thickening of the lung tissue surrounding the alveoli
no good expansion of lungs or alveoli
pulmonary fibrosis causes
environmental → long exposure to certain toxins/pollutants
medical treatments → radiation for thoracic CA, some chemo
chronic inflammatory processes → RA or sarcoidosis
genetic factors → familial pulmonary fibrosis
unknown cause: idiopathic pulmonary fibrosis
pulmonary fibrosis assessment
SOB
DOE (dyspnea on exertion)
dry cough that doesn’t go away
fatigue
weakness
chest discomfort
clubbing in fingers/toes
caused by chronic hypoxia to tissues
pulmonary fibrosis diagnostics
imaging
pulmonary function tests (PFTs) → measure lung volume and capacity
biopsy
pulmonary fibrosis interventions
monitoring respiratory status
administering meds
educating abt energy conservation
promote adequate nutrition
assisting with breathing exercises
encouraging smoking cessation
facilitating emotional support
chronic obstructive pulmonary disease
a group of pulmonary disorders with S/S of chronic cough and expectoration, dyspnea, and impaired expiratory airflow
combo of 3 diff diseases: chronic airflow limitation that isn’t fully reversible
emphysema
chronic bronchitis
asthma
COPD defining features
irreversible airflow limitations during forced exhalation due to loss of elastic recoil
airflow obstruction r/t
mucous hypersecretion (bronchitis)
mucosal edema (emphysema)
bronchospasm (asthma)
air goes in easily but remains in the lungs
bronchioles tend to collapse
can cause barrel-chest look
COPD initiation
inhalation of noxious particles
mediators released cause damage to lung tissue
airways inflamed
parenchyma destroyed
COPD risk factors
cigarette smoking
environmental exposures
hx of respiratory infections
hereditary/genetics
age
occupational hazards
socioeconomic status
asthma
COPD complications
oxygenation: hypoxemia, hypoxia, hypercapnia, respiratory acidosis
inflammation of airways → destruction of alveoli → restricted flow of O2 → hypercapnia → respiratory acidosis
hypercapnia looks like lethargy/decreased LOC
use BiPAP → help push air in/out of lungs
respiratory tract infections
more likely to catch colds, pneumonia, or the flu
infection increases the damage to the lung tissue
cardiac dysrhythmias
r/t respiratory and heart failure, HTN, coronary disease
pulmonary hypertension: cor pulmonale, cardiac failure
constriction of pulmonary blood vessels d/t alveolar hypoxia, increased erythropoiesis → polycythemia → increased blood viscosity
air trapping, airway collapse, inelastic alveolar walls
decreased SA for capillaries to exchange gas → increased pressure in pulmonary arteries → RV has to work harder to push blood in to get oxygenated → overtime, RV begins to fail
hypoxia and increased CO2 → pulmonary HTN
cor pulmonale → RV hypertrophy → RV begins to enlarge
R-sided cardiac failure
chest discomfort, dependent edema (feet/ankles), distended neck veins (JVD)
COPD recap
chronic inflammation (chronic bronchitis)
limited exhalation with force (asthma)
air trapping (emphysema)
dyspnea
mucus
fatigue, weight loss, anorexia → body doesn’t have enough O2 to have appetite
pulmonary HTN
right-sided heart failure (cor pulmonale)
respiratory acidosis → resp failure
exacerbations with bacterial infections
emphysema
chronic disease
abnormal distention of the alveoli
alveoli lose elasticity, trapping air that should be expired/exhaled
walls of alveoli break down & form one large sac
emphysema causes
smoking/2nd hand smoke
pollution
chronic infection
allergens
emphysema assessment
dyspnea with activity
breathlessness at rest
barrel chest → lungs don’t fully deflate → chronic change
chronic productive cough
inspiration is difficult d/t barrel chest
use accessory muscles to breathe
difficult prolonged expiration (I:E > 1:3)
wheezing
rhonchi → thick mucus in bronchioles → coarse sounding
vs crackles in thin fluid in alveoli
“pink puffers”
advanced emphysema
appears drawn, anxious, pale
speaks in short jerky sentences
leans forward and dyspneic
neck veins distend during inspiration
pursed lip breathing
improves O2 flow by slowing rate of exhalation
emphysema interventions
if CO2 is chronically high → resp center insensitive to CO2
O2 needs to be kept slightly lower than “normal” to maintain drive to breathe → or else body thinks don’t need O2 and don’t need to breathe
KEEP SAO2 BETWEEN 88-92%
if color improves but LOC decreases, stop O2
teach diaphragmatic/abdominal and pursed-lip breathing
bronchodilators to open airways (SABA), corticosteroids to reduce inflammation (budesonide)
pulmonary rehab to improve activity tolerance
meet nutritional needs
monitor & manage exacerbations and complications
barrel chest and tripod position → ribs flare and inhalation/exhalation is difficult
chronic bronchitis
chronic cough
increased mucus for over 3 months/year for 2+ years
bronchial glands hyper-secrete mucus → plugs form in small bronchi → necrosis and fibrosis → trapped air
chronic bronchitis early symptoms
productive cough of thick white mucus esp in morning and evening
bronchospasms during severe coughing
chronic bronchitis late symptoms
as condition worsens, sputum → yellow, purulent, copious and after coughing, blood streaked
chronic bronchitis assessment
cyanosis
dyspnea upon exertion - dyspnea at rest
“blue bloater”
dusky and cyanotic d/t
hypoxemia → cyanosis
hypercapnia → too much CO2
respiratory acidosis
chronic bronchitis interventions
monitor respiratory status
manage risks for infection → flu, pneumonia, RSV, immunizations
O2 therapy (keep O2 above 90%)
bronchodilators to open airways
steroids to reduce inflammation
antibiotics if infection present
balanced diet/increased fluid intake
postural drainage
patient education → avoid environmental irritants, stop smoking, avoid wind/cold, avoi others with resp. infections, breathing exercises (pursed-lip, diaphragmatic)
asthma
exposure to allergens or irritants → inflammation
mast cells release inflammatory mediators (leukotrienes, histamine, cytokines, prostaglandins, nitric oxide)
eosinophils, neutrophils, lymphocytes
result: persistent airway inflammation
limited airflow → bronchoconstriction, hyper-reactive airway, airway edema
asthma triggers
allergens → IgE response
irritants
respiratory infections
exercise-induced asthma
environmental temp (too cold/warm)
drugs and food additives
ASA, NSAIDs, salicylates, beta blockers
emotional stress can worsen symptoms
asthma classifications
mild intermittent
1-2 mild/week, no limitation of activity
mild persistent
2 times/week, activity is affected during episodes
moderate persistent
some sx on most days, mild to moderate reduction in physical activity
severe persistent
can cause rib fractures, pneumothorax, atelectasis, and pneumonia
asthma assessment
RESPIRATORY DISTRESS
anxiety, increased pulse and RR, diaphoresis
hypoxemia
WHEEZING/cough/dyspnea
chest tightness esp night/early AM
every breath is effort
thick, tenacious sputum
exhalation may be prolonged
classic position: body leans forward, arms to at shoulder height
decreased breath sounds with increased RR is ominous findings
may lead to status asthmaticus
status asthmaticus
severe, life-threatening complication of asthma
causes:
abrupt discontinuation of meds
abuse of aerosol meds
hx of poorly controlled asthma over days/weeks
S&S:
more severe and prolonged asthma symptoms
airway obstruction intensifies
hypotention, bradycardia, resp/cardiac arrest
does not respond to common therapy
can cause cor pulmonale, pneumothorax, death
Rx:
IV fluids, bronchodilators, steroids, IV, O2, intubation w/mechanical ventilation
asthma diagnostics
pulmonary function tests
measure lung volumes/airflow
uses spirometer, computer, peak flow meter
interventions:
do not eat a heavy meal prior to the test
no smoking 4-6 hours prior
hold bronchodilators 4-6 hours prior
remind patients these are low-risk, non-invasive, painless tests
asthma medication
goal: treatment of acute exacerbations and control chronic symptoms
control agents:
inhaled corticosteroids → BLACK BOX WARNING → shouldn’t be used as a relief bed.. SABAs first
long-acting bronchodilators (beta-agonists and anticholinergics)
leukotriene modifiers
monoclonal antibiotics for eosinophilic asthma (benralizumab)
anti-IgE therapy (omalizumab)
relief agents:
short-acting bronchodilators (albuterol)
systemic corticosteroids (prednisone)
ipratropium (anticholinergic, reduced mucus production)