respiratory Flashcards
obstructive lung dis.
obstruction air flow–>air trapping
airways close premat. at high lung vols–>inc. RV and dec. FVC
v. low FEV1 and low FVC–>dec. FEV1/FVC ratio (
air flow directly prop to…
indirectly prop to…
dir. prop to driving pressure
inv. prop to resistance
obstructive lung disease
airway narrowing w/ inc. airway resistance +/- dec. elastic recoil w/ dec. driving pressure (emphysema)
*pathophys: what defines asthma?
airway inflammation (current med tx) *mucosal edema* inc. mucus production airway narrowing hypersensitivity/hyperreactivity
asthma
hyper reactivity of lungs causes mucosal edema, airway inflammation
why we don’t just give B2s, but steroids–>target inflammation not just dilation
B2 receptors, smooth muscl
adr: dilates
chol: constricts
work of breathing is inc. as air-trapping occurs:
diaphragm flattened
inspiratory musc. fibers shortened, so little opportun. for further contraction
asthma
industrialized country disease (pollution) 3-5% chronic airway inflammation maj. mech hyperreactiv. to triggers sm. musc hypertrophy (extra work) can be fatal
asthma: rev or irrev airway narrowing?
reversible airway narrowing, bronchospasm, bronchoconstr. (type 1 hypersens. rxn of airways)
COPD is not reversible!!
asthma incidence: increasing?
YES: inc. mold, roaches (poop), and pollution
dec. asthma risk with
breastfeeding
Curshcmann’s spirals
spiral shaped mucus plugs in sputum
desquamated/shed epithelium forms whorled MUCUS PLUGS (see pic)
think asthma
Charccot-Leyden crystals
asthma
eosinophilic (allergy related), hexagonal, double pointed needle-like crystals
formed by breakdown of eosinophils in sputum
asthma triggers
infections** (URI, pneumonia)
stress
environ.: insects, pollen, mold, pollution, weather changes, air temp/humid.**
allergens (roach droppings, allergies)
subsets of asthma pts: hypersensitivity to Aspirin, NSAIDS (inc. react. w/ motrin, naprocen, etc.) aspirin as well
symptoms of asthma
persistent wheeze (may be audible (pretty bad) or with auscultation)
need to be able to tell if asthma pt. is sick or not sick!!
chronic episodic dyspnea
cough
CP, tightness, inc. sputum prod, tachypnea, hypoxemia, dec. I/E ratio, pulsus paradoxus, mucus plugging
pulsus paradoxus
systolic will drop during inspiration by =>10mmHg
timeline of wheezing
expiratory wheezes –> add inspiratory when more severe (entire phase is wheezing)
- *end expiratory wheezing** is beginning of asthma
dec. expiratory phase (3-4 sec–>2-3 sec)
asthma: if no wheezing??
usually there is NO air movement
VERY SEVERE
asthma dx
Pulm. Func tests: dec. FEV1 which IMPROVES w. bronchodilator
inc. serum IgE and eosins
allergy testing
asthma: CXR
hyperinflation (hyperexpansion) w/ flat diaphragms
asthma dx studies
measu. of airway reactivity after graded challenge w. inhaled METHACHOLINE or HISTAMINE
bronchoconstriction occurs at LOWER doses in asthma
findings in sev. asthma
-speech difficulty
diaphoresis: implies they are sick!!**
-**fatigue: worrisome when become conversationally dyspnic (“are you feeling ok?”)-check in
-hypoxia: attempt to rip off mask; ominous during breathing tx
orthopnea: can’t lay down, diff. to intubate
agitation, somnolence, confusion
acid/base imbalance with asthma
respiratory acidosis from not blowing off CO2
accessory muscle use in asthma
“belly breathing”, retractions (gut sucks in, ribs stick out)
take shirt off!
tracheal tugging: ant. portion of neck pulls in and out (type of retraction, suprasternal notch)
nasal flaring
questions to ask every pt having an asthma attack
ever been intubated? red flag-high risk how many times?
last ED visit? how often?
last attack?
for you, is this a mild, mod, sev. attack compared to previous? -det. baseline
trigger? document
obstructive lung diseases
asthma bronchiectasis emphysema chronic bronchitis bronchiolitis CF
albuterol inhaler
rescue inhaler! acute tx why use? to quickly bronchodilate, NOT a maintenance program, should not be used every day B2 agonist, relaxes bronch sm. musc SE: tachycardia, tremors inhaler or nebulizing tx
chronic asthma tx
peak flow monitoring: >500 is GOOD (200s is worrisome)
- inhaled corticosteroids: aerobid, azmacort, flovent pulmicort, advair
- B2 agonist-Albuterol
- antichol-Atrovent
- Leukotriene inhib.-singulair
- mast cell stabilizer-cromolyn
salmeterol (serevent), formoterol
B2 agonist
LONG ACTING PPX agent, not for acute
SE: tremor, arrhythmia
inhaled, inc. in deaths in asthmatics???
Methylxanthines
older drug, Marshall dislikes
theophylline: :
bronchodilator,
narrow therapeutic index: SE: cario and neuro tox: arrhythmias, seizures
blocks adenosine*
metab. by P450
inhib. phosphodiesterase–>lowers cAMP hydrolysis–>inc. cAMP
Muscarinic antagonist
atrovent-(ipratropium)
anticholinergic, comp. block competitive block of musc rec, prev. bronchoconstr.
often used simultaneously w. albuterol
DUONEB
Tiotropium
long-acting musc. antagonist
Cromolyn sodium
prev. rel. of mediators from mast cells (mast cell stabilizer, prev. mast cell degranulation)
pox only, QID dosing?? dec. compliance
largely repl. by leukotriene rec. antagonist
corticosteroids
fluticasone, budesonide, prednisone*
(today give out like candy)
can give IV: Solumedrol, about 6 hours to work
corticosteroid action
inhib. syn. of virtually all cytokines
* FIRST LINE THERAPY* for chronic asthma
- txs inflammation, reduces narrowing, most important
- takes about 6 hrs to work
what really helps people
inhaled corticosteroid: prevents asthma attacks
take 1-2x day
antileukotrienes
Zafirlukast, montelukast
-v. expensive, blocks leuk rec, v. good for aspirin-ind. asthma
Zileuton
-v. expensive, liver toxic SE, 5-LOX pathway inhibitor, blocks conversion of arachidonic acid to leukotrienes
prevent attack, do not tx symptoms
cure for asthma?
NO
if using albuterol inhaler few times a week: uncontrolled
Omalizumab
MoAb anti IgE Ab
binds mostly unbound serum IgE
used in allergic asthma resistant to inhaled steroids and long acting B2 agonists
real life management
albuterol +/- atrovent neb: all pts
-if using often, need inh. corticosteroid
asthma pt presents to ER
DUONEB: albuterol + atrovent: all pts
prednisone PO or Solumedrol IV: all pts (95% pts)
Mag 2 gs IV over 20 min (mod–>sev. pts)
-sm. musc relaxer
terbutaline (bronchodil.-B2) SQ, or EPI SQ (v. severe pts) (Marshall dislikes cardiac effects of EPI)
last ditch effort!
O2: all pts
Bipap: sev. and worse pts
Intubation worst cases: difficult, will desat. very fast!
Heliox: combo of helium and oxygen: makes air thinner, into airways w/ less resistance
Bipap
like Cpap: used for sleep apnea control inspiratory and expiratory pressures lets O2 in, sucks CO2 out be careful about barotrauma pts. need to be cooperative!
dx test to consider
consider CXR, ABG (Marshall already knows results)
ensure no pneumonia, no dropped lung, etc
-if following pts, consulting pulmonology
peak flow
how bad is asthma? improving? can take home, know what zone they are in
COPD
emyphsema
chronic bronchitis
will usually co-exist in same pt!** same: PE (lung sounds), etiology, tx, phys. tx and imaging
COPD etiology
SMOKING (if stop: 0% of damage done will be reversed :( )
slowly progressive, pts. blow off bc they get used to sym
-dec. abs response to bronchodilators
-inc. prevalence with age
4th leading cause of death in US!
COPD: rev. or irreversible obstruction?
IRREVERSIBLE obstruction
first sign of COPD
DOE: dyspnea on exertion
COPD is how serious
4th leading COD in US!
COPD signs
pulmonary HTN inc. AP diameter of chest (cough, SOB, wheezing) access. musc use dec. breath sounds prolonged expiratory phase inc. A-P diameter cyanosis (ends up on home O2)
COPD causes
a1-antitrypsin deficiency
smoking accounts for up to 90% (a lot of times called asthma)
air pollution
airway hyperresponsiveness (Dutch hypothesis) : unclear mechanism
COPD lab findings
polycythemia (chr. hypoxemia) (not for asthma)
a1-antitrypsin level (when younger than 40 yo)
sputum: S. pneumo, H. flu most common during exacerbation
ABG shows
hypoxemia, with or without hypercapnia
lung CT shows:
alveolar walls breakdown–>non-func airspace coalesce–>bullae
LONG, DARK AIR COLUMNS : dark: not much long tissue left, air trapping, hyperinflation
flattened diaphragm
narrow hear shadow
COPD PFT’s
essential to dx
FEV1 forced expiratory volume in 1 sec; most common used index of airflow obstruction
TLC, FRC, RV all increased
COPD walking distance
how far can you walk in 6 minutes?
good predictor of mortality
-desat/hypoxic, higher risk
emphysema
distinction does not matter as much clinically
“Pink puffer”
air spaces enlarge as alveolar walls are destroyed
air pockets (non-functioning)
loss of elastic recoil-can’t exhale
inc. air trapping
inc. compliance due to loss of elastic fibers
-lose natural recoil that helps you exhale
bullae in emphysema
alveoli can coalesce to form bullae that compress normal lung, can compress on normal, functioning lungs
emphysema: less alveoli cause
dec. diffusion capacity
inc. elastase activity–>loss of elastic fiber
increased compliance
centriacinar emphysema
smoking
panacinar emphysema
think a1-antitrypsin def.
more diffuse, involving entire acinus
chest shape in emphysema??
barrel shape
emphysema pts breath how
pursed lips : self-taught or learned
increases airway pressure and prevents airway collapse during respirations
why are emphysema pts slender?
takes more work to breathe,
also sit forward
a1-antitrypsin deficiency
principal endogenous antiprotease: protects from elastase: uncont. elastase–>lose elasticity of lungs
-genetic, premature
emphysema CXR
- hyperinflated lung (may see bottom of heart)-low flattened diaphragm
- “arterial deficiency”: don’t see many arteries
- hyperinflation
- bullous disease
- may be mistaken for pneumothorax!*
- ->if not sure, get a CT scan
emphysema lung
pockets of non-func space
-cigarrette tar: carbon deposits
Bullae
pocket of non-func. tissue
may need to be surg. removed
Chronic Bronchitis
“blue bloater”
airway walls become deformed (not “eaten away* like emphysema) and structurally altered due to atrophy, inflammation, smooth muscle hypertrophy, mucus hypersecretion in airway lumen
Productive cough for MORE THAN 3 MONTHS per year, for at least 2 YEARS—does not have to be consecutive
-Small airway disease
-Mucus gland enlargement, (hypertrophy of mucus gland) is histologic hallmark
-Hyperplasia of mucus secreting glands in bronchi
Reid index
gland layer depth/total bronchial wall thickness:
>50% ind. COPD (need to be dead!!)
symptoms of bronchitis
Wheezing Crackles Cyanosis Early onset hypoxemia due to shunting Late onset dyspnea (not as quick as emphysema pts) CO2 retention polychythemia
COPD tx
education oral and inhaled meds (same as asthma..) stop smoking pulm. rehab BiPaP surg (vol. reduction, bullectomy, lung txp) O2
COPD tx: bronchodilators
Beta 2 agonist (albuterol inhaler)
Anticholinergics (atrovent/ipratropium inhaler)
Long acting
COPD tx: anti-inflammation
Steroids (solumedrol, prednisone)
Inhaled corticosteroids
COPD tx: abx?
MAYBE; pot. to be inf-related
COPD O2 therapy
-for supplementation in acute disease, home O2 for chronic lung disease
COPD:chronic hypoxic pt: CAUTION**
**O2 can worsen hypercapnia
**dec. hypoxia resp. drive (“CO2 retainers”)-chronically elevated, small subset of COPD pop
CO2: 50-60! (should be 30-40)
lost ability to breathe due to high CO2 levels (no longer acts as trigger, chron. elevated)–>if goes higher, CO2 narcosis
-need for O2 only stimulation to breathe
never withhold O2 for hypoxic pt
-if give O2: fall asleep slowly, hypoventilate–>resp. arrest
how can you tell if pt. is retaining CO2??
ABG:
- non-CO2 retainer: if elevated CO2, IF ACUTE: low pH, bicarb will be normal (kidneys cannot respond/adapt that quickly! takes days)
- if CO2 retainer: elevated CO2, NORMAL (typ.) pH, bicarb will be HIGH (chronically elevated to comp. for CO2) -corrected resp. acidosis
how to give O2 if CO2 retainer
titrated O2, can’t handle too much, will hypoventilate
BiPaP is awesome for this takes CO2 out
other things about asthma
B blockers can worsen (also COPD)
consider GERD if adult onset asthma
restrictive lung disease
dec. TLC
