Obstructive Lung Diseases Flashcards
What is obstructive lung disease?
pulmonary conditions characterized by airflow limitation
- inside lumen
- bronchial wall
- peribronchial region (reversible vs non-reversible)
OSA define
mechanical obstruction of breathing that occurs during sleep when pharyngeal muscles relax
What does OSA lead to?
increased morbidity
chronic hypoxemia & hypercarbia
other pathologies: artherosclerosis, HTN, stroke, insulin resistance, DM
LOW FRC
Cardiac effects of OSA
chronically hypoxic –> changes in vasculature –> RHF
systemic & pulmonary HTN
IHD
CHF
these pt are very unstable
Diagnosis of OSA
polysomnography
> 5 sleep-related symptoms
> 15 dx for moderate OSA
> 30 severe OSA
Obstructive diseases & peak flow rates
Peak flow rates are decreased b/c small airways close on expiration, thus decreasing flow
FEV1
forced expiratory volume in 1 second
normal: 80-120%
COPD: 20%
FVC
forced vital capacity
the volume of air forcefully exhaled after a deep inhalation
normal: 3.7L (Female), 4.8L (male)
FEV1 to FVC ratio
normal: 75 - 80%
FEV25-75
measurement of air flow at midpoint of a forced exhalation
most effort independent and most sensitive indicator of small airway disease
Maximum voluntary ventilation
usually do it for 15m and extrapoalte it
-maximum amount of air that can be inhaled and exhaled in 1 minute
MVV male
140 - 180L
MVV female
80 - 120 L
Diffusing capacity
Volume of carbon monoxide transferred across the alveoli into the blood per minute per unit of alveolar partial pressure
DLCO normal value
17 - 25 mL/m/mmHg
What are some things that could affect DLCO?
Fick’s Law of Diffusion
- emphysema (increased SA)
- fibrosis (increased thickness)
How long do you wait after an acute upper respiratory infection?
6 weeks (only if ACTIVELY febrile)
Acute Upper Respiratory Infection case tips
avoid OPA, run them deep to avoid bronchospasm, extubate deep (turn on side)
- hydrate
- reduce secretions
- limit airway manipulation (best thing you can do)
- LMA
adverse respiratory events
bronchospasm
laryngospasm
airway obstruction
postoperative croup
Asthma (3)
REVERSIBLE airway obstruction characterized by
- bronchial hyperactivity
- bronchoconstriction
- chronic inflammation of lower airways
Pathophys of asthma
activation of the inflammatory pathway leads to infiltration of airway mucosa w/ eosinophils, neutrophils, mast cells, T cells & B cells
inflammatory mediators include: histamine, prostaglandin D, leukotrienes
airway edema results = thickened basement membrane
S/S Asthma (4)
EPISODIC (may lasts minutes to hours but pt completely recovers)
- wheezing
- productive and non-productive cough
- dyspnea & chest discomfort –> air hunger
- eosinophilia (sputum)
Severe bronchospasm VS
RR > 30, HR > 120
Dx asthma
- wheezing, chest tightness, SOB
- airflow obstruction that is partially reversible w/bronchodilators
- PFTS (FEV1 < 35%)
Expiratory limb of loop w/asthma
scoooooping
What happens w/FRC and TLC in asthma?
FRC increases (usually RV) TLC normal
DLCO in asthma?
samesies
ABGs in asthma
- normal in mild dx
- hypocarbia & respiratory alkalosis common (reflecting neural reflex changes in lungs; not hypoxemia)
- severe obstruction associated w/PAO2 < 60
- rises in PaCO2 noted when FEV1 < 25%
CXR in asthma
normal
severe - hyperinflation, hilar congestion d/t mucus plugging and pulmonary HTN
EKG in asthma
only in severe attacks
- RV strain (d/t increased pulmonary pressures)
- T wave inversion (V1-V4, II, III, avF)
Treatment of asthma
treat inflammation & bronchospasm
- corticosteroids
- long-acting bronchodilators
- leukotriene modifiers
- anti-igE monoclonal antibody (omalizumab)
- methylxanthines (theophylline)
- mast cell stabilizer (cromolyn)
corticosteroid example
beclomethasone
give 1-2h preop (ideally 5 days)
alters gene transcription, inhibits mast cells, apoptosis of inflammatory cells, increase B2 agonist effectiveness
long-acting bronchodilator example
salmetrol (50 mcg) DOA 12 - 24 h
combination (symbicort & advair) = LABA + steroid
leukotriene modifier
singulair
PFT’s & ASTHMA
if FEV1 > 50% of normal, symptom free
Status asthmaticus
life threatening emergency in which bronchospasm does not respond to treatment
Status asthmaticus s/s
low oxygen blunted CO2 waveform wheezing mucus hypersecretion PIPs increased
Status asthmaticus tx
B2 agonist (albuterol - 4 puffs (400 mcg total)) IV steroids O2 Mg (1-2 g over 20 m) Oral leukotriene inhibitor
Resistant? think airway edema & secretions
Terbutaline
0.25 mg SQ q15m (beta agonist)
Bronchospasm tx
- deepen (propofol)
- 100% O2
- SABA
- Epi 10 mcg/kg
- Hydrocort 2-4 mg/kg
- ipraprotium 0.25 - 5 mg
What increases risk for perioperative event for asthma (think PFTS)
FVC < 70%
FEV1/FVC < 65%
When do you stress dose steroids?
only IF systemic therapy in the last six months
Anesthesia considerations for asthma
- deep induction
- IV or transtracheal lidocaine
- VA (sevo)
- avoid histamine releasing drugs (no morphine, no succinylcholine)
- Adequately hydrated
- avoid acei?
- use PEEP
COPD define
non-reversible loss of alveolar tissue and progressive airway obstruction
COPD RF:
cigarette smoking occupational exposures pollution recurrent respiratory infections low birth weight a1 antitrypsin deficiency
type B COPD
bronchitis
blue bloater
type A COPD
emphysema
pink puffer
emphysema pathophys
destruction of parenchyma
loss of SA, elastic recoil & structural support
inability to maintain airway patency
bronchitis pathophys
narrowing of small airways by inflammation & mucuous production
emphysema definition
enlargement of air spaces distal to the terminal bronchiole with destruction of walls
- loss of alveoli & damage to capillaries
- small airways are thin, tortuous, atrophied
shunting & deadspace
what is an acinus
tissue distal to terminal bronchioles
centriacinar (centrilobular) emphysema
more common in apex
proximal
panacinar (panlobular) emphysema location & cause
more common distally d/t a1 antitrypsin deficiency
paraseptal emphysema
regional
bullae emphysema
one big sac
what does elastase do?
degrades pulmonary connective tissue
it is released by smoking
what does alpha 1 antitriptase do
blocks elastase
chronic bronchitis definition
dx characterized by excessive sputum production (expectoration of sputum most days for at least 3 mo for 2 successive years)
hallmark findings of chronic bronchitis (5)
- hypertrophy of mucus glands of large bronchi
- inflammatory changes in small airways
- granulation of tissue, smooth muscle increases
- peribronchial fibrosis
- chronically hypoxic (paO2 < 60)
COPD diagnosis
SPIROMETRY
severity determined by GOLD
FEV1/FVC for COPD
decrease < 70% of predictive
not reversible w/bronchodilators
FEV25-75 for COPD
decreased
FRC and TLC for COPD
increased RV
COPD treatment
smoking cessation
long term O2 admin (2LPM)
hct > 55%, paO2 < 55, usually have corpulmonale
Drug treatment of COPD
O2 long acting B2agonist steroids long acting anticholinergic (ipaprotrium) vaccines diuretics theophylline
Sx treatment COPD
lung volume reduction surgery for severe COPD cases
-increases pel, decreases hyperinflation, improves diaphragmatic/chest wall movement, decreases V/Q mismatch
COPD anesthetic considerations for lung volume reduction
double lumen tube
avoid nitrous
avoid excessive positive pressure (low Vt, high RR)
what is most predictive of COPD pulmonary compliactions
clinical symptoms (wheezing, cough)
preop pulmonary functon testing
hypoxemia home O2 NaHCO3 > 33 mEq/L PaCO2 > 50 mm Hg hx resp failure severe SOB planned pneumonectomy difficulty assessing pulmonary status through clinical means differential dx needed determine response to bronchodilators pulmonary htn
smoking cessation
at least six weeks
or morning of only
COPD malnutrition leads to —>
increases risk of pleural leaks after surgery
interscalene block risks
ipsilateral phrenic nerve palsy
why do you avoid NO for COPD pt
attenuates HPV, increases V/Q MISMATCH
PIP
< 30 CM H2O
Why does air trapping occur?
positive pressure ventilation applied w/o sufficient expiration –> increasing intrathoracic pressure –> decreasing VR –> increases PAP
Capnography for air trapping
sloped carbon dioxide concentration; expiratory flow does not reach baseline
bronchospasm COPD pt
light? deepen anesthetic
pathologic? bronchodilator, magnesium, epi, IV steroids, suction secretions
Name 5 other expiratory outflow obstructions
bronchiectasis cystic fibrosis primary ciliary dyskinesia bronchiolitis obliterans tracheal stenosis
bronchiectasis
irreversible airway dilation and collapse d/t inflammation d/t chronic infections
bronchiectasis s/s
significant hemoptysis (200 mL over a 24 hour period)
dyspnea/wheezing
pleuritic chest pain
FINGER CLUBBING
bronchiectasis dx
hx chronic cough w/purulent sputum CT confirms (usually lower lobes)
anesthetic considerations for bronchiectasis
GETTA w/frequent suctioning
double lumen tube to avoid infecting both sides
avoid nasal intubations
cystic fibrosis definition
autosomal recessive d/o affect a single gene on chromosome 7 - this prevents chloride transport and movement of salt and water
cystic fibrosis damage
lungs (COPD, bronchiestasis) pancreas (DM) GI (ileus) sinusitis liver (cirrhosis) reproductive organs
cf dx
sweat chloride > 70 mEq/L
chronic purulent sputum, malabsorption
bronchoalveolar lavage high in neutrophils
older adults –> COPD
normal sinuses is strong evidence CF is NOT present
CF tx
alleviation of symptoms
- clear airway secretions
- correct organ dysfunction
- nutrition (VIT K)
- prevent GI obstruction
CF anesthesia considerations (6)
- optimize pt (elective procedures)
- vit k to help absorb fat soluble vitamins
- general anesthesia w/VA (increased oxygen concentrations, relax smooth airways)
- avoid anticholinergic
- awake extubation
- pain control
primary ciliary dyskinesia
congenital impairment of ciliary activity in respiratory tract epithelial cells and sperm cells
what is kartagener’s syndrome?
PCD
- chronic sinusitis
- bronchiectasis
- sinus inversus (ORGANS REVERSED)
- decreased fertility
primary ciliary dyskinesia anesthesia
regional anesthesia reverse position of EKG leads left IJ vein cannulation right uterine displacement avoid nasal pharyngeal airways
bronchiolitis obliterans
disease of small airways and alveoli in children from RSV
adult bronchiolitis obliterans
d/t viral pneumonia
- collagen vascular dx (RA)
- silo filler’s disease (nitrogen dioxide inhalation)
- graft vs host dx
Bronchiolitis obliterans organizing pneumonia (BOOP)
shares features of interstitial lung dx and bronchiolitis obliterans
treatment innefective
tracheal stenosis
occurs following prolonged intubation or over-inflation of ETT (may not appear for several weeks)
when does tracheal stenosis become symptomatic
tracheal diameter decreases < 5 mm
dyspnea prominent at rest
accessory muscles used in all phases of breathing
tracheal stenosis tx
- tracheal dilation (temporary) - balloon or surgical dilators, lasering of scarred tissue
- Tracheobronchial stent can be short term or long term
- Tracheal resection w/anastomosis is the best treatment (intubate below resection)
tracheal stenosis anesthetic considerations
translaryngeal intubation
VA to ensure maximum inspired oxygen concentration
helium
