Obstructive Lung Disease Flashcards
Preoperative pulmonary testing is indicated for which of the following patients? A. baseline NaHCO3 35 mEq/L B. planned pneumonectomy C. suspected pulmonary hypertension D. hypoxemia on room air (PaO2 <60 mmHg) E. all of the above
E. all of the above should have preoperative pulmonary testing.
What is obstructive lung disease?
pulmonary conditions characterized by airflow limitation (inside the lumen, bronchial wall, and peri-bronchial region) can be reversible (asthma) or irreversible (COPD)
What is OSA?
Obstructive Sleep Apnea
it is a mechanical obstruction of breathing that occurs during sleep when pharyngeal muscles relax that is more common in males and obese patients being the most precipitating factor
Obstructed airways lead to ___
chronic hypoxemia and hypercarbia
low FRC
Clinical features and hallmark signs of OSA
habitual snoring, fragmented sleep and daytime somnolence
present with comorbidities related to obesity and hypoxemia (systemic and pulmonary HTN, ischemic heart disease, CHF)
How is OSA diagnosed? and significance of AHI value
Polysomnography which records the number of abnormal respiratory events (apnea) per hour
AHI - hypo apnea index
>5 associated with sleep related symptoms
>15 moderate OSA
>30 severe OSA
Berlin or STOP BANG questionnaires
STOP BANG
Snore loudly, daytime Tiredness, Observed stop breathing, high blood Pressure, BMI > 35 kg/m2, Age >50, Neck circumference >40 cm, Gender - male
How would a flow volume loop look for a restrictive airway disease?
smaller volumes, same ratio, looks normal (just smaller)
How would a flow volume loop look for an obstructive airway disease?
“scooping” on exhalation, flow taking longer to get out, normal inspiration
Spirometry testing includes
Forced expiratory volume in 1 second (FEV1), Forced vital capacity (FVC), FEV1 to FVC ratio, FEV25-75%, MVV, DLCO
Normal FEV1 to FVC ratio
75-80%
Forced vital capacity (FVC)
volume of air forcefully exhaled after a deep inhalation
3.7 L in females, 4.8 L in males
Forced expiratory volume in 1 second (FEV1)
volume of air forcefully exhaled in one second (80-120% of predicted value)
obstructive disease usually <50% usually
FEV 25-75%
measurement of air flow at midpoint of a forced exhalation
Maximum voluntary ventilation (MVV)
max amount of air that can be inhaled and exhaled in 1 minute
males: 140-180, females: 80-120 L/min
Diffusing capacity (DLCO)
volume of carbon monoxide transferred across the alveoli into the blood per minute per unit of alveolar partial pressure
single breath of 0.3% CO and 10% helium held for 20 seconds
normal value 17-25 mL/min/mmHg
Acute upper respiratory infection
common cold
diagnosed based on S/S (nonproductive cough, sneezing, rhinorrhea)
bacterial URIs
more serious and include fever, purulent nasal discharge, productive cough, malaise, tachypneic, wheezing
Anesthetic considerations for acute URIs (pediatrics)
pediatric patients higher risk for complications (higher parasympathetic tone and more reactive airways), they are usually actively sick, have reactive airway disease, having their airway manipulated from ETT intubation and airway surgery
If surgery is cancelled when should surgery be rescheduled?
at least 6 weeks
Anesthetic management for acute URIs
hydration, reduce secretions, limit airway maniupulation, decision between LMA vs ETT
adverse respiratory events with acute URIs include
bronchospasm, laryngospasm, airway obstruction, postop croup, desaturation
Asthma
reversible airway obstruction characterized by bronchial hyperreactivity, bronchoconstriction, chronic inflammation of the lower airways
Pathophysiology of asthma
activation of the inflammatory pathway leads to infiltration of airway mucosa with eosinophils, neutrophils, mast cells, T and B cells and inflammatory mediators including histamine, prostaglandin and leukotrienes leading to airway edema and thickening of the basement membrane
Signs and Symptoms of asthma
episodic disease
wheezing, productive and nonproductive cough, dyspnea and chest discomfort, eosinophilia
status asthmaticus = persists despite treatment
Pulmonary function testing in asthma
FEV1 <35% of normal downward scooping of expiratory limb on loop FRC increases TLC remains normal DLCO unchanged (not a diffusion disease)
ABGs in asthma
mild - normal ABG
can see hypocarbia and respiratory alkalosis but once accessory muscle use fatigues = acidosis
severe - PaO2 <60 mmHg, rise in PaCO2 (shunt conditions)
Chest X-Ray and EKG for asthmatics
cxray - may be normal in mild cases but will have hyperinflation and hilar congestion d/t mucus plugging and pulmonary HTN in severe cases
ekg - RV strain d/t increase pulmonary pressures = inferior changes (II, III, aVF) ST depression
Treatment for asthma
treat inflammation and bronchospasm
corticosteroids, long acting bronchodilators, leukotriene modifiers, anti-IgE monoclonal antibody, methylxanthines, mast cell stabilizers
get PFT after treatment to see how responsive they are!
Status Asthmaticus
EMERGENCY
administer B2 agonist, IV corticosteroids, supplemental oxygen, IV Mag, oral leukotriene inhibitor
if resistant to treatment for bronchospasm what are your next thoughts?
airway edema and secretions
Anesthetic considerations for asthma
get thorough history and determine severity of disease
eosinophil counts (indication of inflammation)
PFT results (FVC <70% or FEV1/FVC ratio <65% = increased periop risk!)
use regional whenever possible/safest
use lidocaine!
use Sevoflurane
avoid histamine releasing drugs! (atracurium and succinylcholine)
deep extubation
hydrate
avoid anticholinesterase drugs
What is one ventilator strategy for asthmatics?
increase PEEP and increase expiration (ratio 1:2-3)
COPD
nonreversible loss of alveolar tissue and progressive airway obstruction
risk factors of COPD
cigarette smoking, occupational exposure, pollution, recurrent respiratory infections, low birth weight, a1-antitrypsin deficiency
Emphysema
characterized by enlargement of air spaces distal to the terminal bronchiole with destruction of walls, loss of alveoli and damage to capillaries, small airways are thin, tortuous and atrophied
Centriacinar emphysema
more in apex of lungs
panacinar emphysema
no regional preference, but usually more distally and deals with the a1-antitrypsin deficiency
Chronic bronchitis
disease characterized by excessive sputum production
hallmark findings of chronic bronchitis
hypertrophy of mucus glands of large bronchi, inflammatory changes in small airways, granulation of tissue, smooth muscle increases, peri bronchial fibrosis
COPD PFTs
decrease in FEV1/FVC ratio (<70% and not reversible with bronchodilators)
decrease in FEV25-75%
increase in FRC, RV, and TLC
Severity is determined by GOLD spirometric criteria
COPD treatment goals
relieve symptoms and slow progression
smoking cessation
oxygen administration (2 LPM NC) especially if PaO2 <55, Hct >55%, cor pulmonale
COPD drug treatment
long acting B2 agonists
inhaled corticosteroids
long acting anticholinergic drugs
Severe cases of COPD
may need to have lung volume reduction surgery
increases elastic recoil, decreases amount of hyperinflation, improved diaphragmatic and chest wall movement, decrease in abnormal V/Q
anesthetic considerations for a lung volume reduction surgery
double lumen tube
avoid nitrous oxide
avoid excessive positive pressure ventilation
Examples of who needs PFT
hypoxemia or need for home o2 with no known cause
NaHCO3 > 33 mEq/L
PaCO2 > 50 mmHg
Hx of respiratory failure d/t persistent problem
Severe SOB
Planned pneumonectomy
Difficulty assessing pulmonary status
Differential diagnosis needed
Need to determine response to bronchodilators
If they have pulmonary hypertension
Risk of postoperative complications for COPD
> 60 y/o, ASA III or IV, current smoker, CV involvement (RV function), low albumin <3.5, active S/S (wheezing, low SpO2, edema, crackles)
How long ideally should someone stop smoking before surgery?
at least 6 weeks
benefits are seen in as little as 4 hours
Malnutrition increases risk of
pleural leaks after lung surgery
What can be a complication with interscalene blocks in COPD patients?
causes ipsilateral phrenic nerve palsy which can be bad for COPD patients because it can put them into respiratory failure
Why should nitrous oxide be avoided in COPD patients?
it attenuates HPV which will worsen the V/Q mismatch
mechanical ventilation considerations for COPD patients
humidification avoid dynamic hyperinflation Vt 6-8 mL/kg PIP < 30 mmHg FiO2 to maintain Spo2 >90% or their baseline
What can result from positive pressure ventilation without sufficient expiration?
increased intrathoracic pressure (decreases venous return) and increased pulmonary artery pressure = right heart strain!
How does air trapping present?
capnography shows sloped carbon dioxide concentration
expiratory flow does not reach baseline before next breath
Treatment for bronchospasm
deepen anesthetic, deliver short acting bronchodilator, suction, IV steroids, epinephrine
bronchiectasis
irreversible airway dilation and collapse resulting from inflammation d/t chronic infection
can have significant hemoptysis
Distinguishing factors of bronchiectasis
Finger clubbing!, hemoptysis, history of chronic cough w/ purulent sputum, and pleuritic chest pain
General anesthesia with ETT in bronchiectasis considerations
double lumen tube (to prevent cross contamination from one lung to the other)
frequent suctioning
avoid nasally intubating
cystic fibrosis
autosomal recessive disorder from chromosome 7
prevents chloride transport and movement of salt and water in and out of cells = abnormally thick sputum production outside of epithelial cells
primary cause of morbidity and mortality in cystic fibrosis is
chronic pulmonary infection
diagnosis of cystic fibrosis
sweat chloride concentration >70 mEq/L
chronic purulent sputum production
malabsorption with response to pancreatic enzyme therapy, bronchoalveolar lavage high in neutrophils
presence of normal sinuses is strong evidence that
Cystic fibrosis is NOT present
treatment of cystic fibrosis
alleviate symptoms
clearance of secretions, correction of organ dysfunction, nutrition, prevent intestinal obstruction, gene therapy?
anesthetic considerations for cystic fibrosis
delay until optimized (controlling infection and removing secretions) vitamin K GA with volatile agents avoid anticholinergic meds awake extubation! adequate pain control
What may you need to do if you use volatile agents in cystic fibrosis?
SUCTION their airway after turning gas on
primary ciliary dyskinesia
congenital impairment of ciliary activity in respiratory tract epithelial cells and sperm cells
Kartagener’s syndrome triad of
chronic sinusitis
bronchiectasis
situs inversus (organs reversed)
anesthetic considerations for primary ciliary dyskinesia
regional anesthesia preferred
reverse ECG leads if have organ reversal
do a left IJ cannulation for central line insertion
if pregnant place in right uterine displacement
avoid nasal pharyngeal airways (risk of sinusitis)
bronchiolitis obliterans
disease of the small airways and alveoli in children from respiratory syncytial virus (RSV)
adults can develop bronchiolitis obliterans from
viral pneumonia, collagen vascular disease (RA), inhalation of nitrogen dioxide (Silo filler’s disease), graft vs host disease post-transplant
Bronchiolitis obliterans organizing pneumonia (BOOP) shares features of
interstitial lung disease and bronchiolitis obliterans
tracheal stenosis
occurs following prolonged intubation or over inflation of ETT cuff = ischemia of tracheal mucosa = scarring
symptomatic tracheal stenosis in adults
when tracheal diameter < 5 mm (dyspnea at rest, use of accessory muscles in all phases)
what would a flow loop look like for tracheal stenosis?
flattened inspiratory and expiratory curves
“fixed obstruction”
treatment for tracheal stenosis
tracheal dilation (temporary measure) with balloon or stent
laser scarred tissue
tracheal resection with anastomosis (best treatment)
anesthetic considerations with tracheal stenosis
translaryngeal intubation (below stenosis) volatile anesthetics (ensures max inspired oxygen concentration) helium (decreases density of gas mixture and improves flow through narrowing)
