Obstructive Lung Diseases Flashcards
(97 cards)
1
Q
What is obstructive lung disease?
A
pulmonary conditions characterized by airflow limitation
- inside lumen
- bronchial wall
- peribronchial region (reversible vs non-reversible)
2
Q
OSA define
A
mechanical obstruction of breathing that occurs during sleep when pharyngeal muscles relax
3
Q
What does OSA lead to?
A
increased morbidity
chronic hypoxemia & hypercarbia
other pathologies: artherosclerosis, HTN, stroke, insulin resistance, DM
LOW FRC
4
Q
Cardiac effects of OSA
A
chronically hypoxic –> changes in vasculature –> RHF
systemic & pulmonary HTN
IHD
CHF
these pt are very unstable
5
Q
Diagnosis of OSA
A
polysomnography
> 5 sleep-related symptoms
> 15 dx for moderate OSA
> 30 severe OSA
6
Q
Obstructive diseases & peak flow rates
A
Peak flow rates are decreased b/c small airways close on expiration, thus decreasing flow
7
Q
FEV1
A
forced expiratory volume in 1 second
normal: 80-120%
COPD: 20%
8
Q
FVC
A
forced vital capacity
the volume of air forcefully exhaled after a deep inhalation
normal: 3.7L (Female), 4.8L (male)
9
Q
FEV1 to FVC ratio
A
normal: 75 - 80%
10
Q
FEV25-75
A
measurement of air flow at midpoint of a forced exhalation
most effort independent and most sensitive indicator of small airway disease
11
Q
Maximum voluntary ventilation
A
usually do it for 15m and extrapoalte it
-maximum amount of air that can be inhaled and exhaled in 1 minute
12
Q
MVV male
A
140 - 180L
13
Q
MVV female
A
80 - 120 L
14
Q
Diffusing capacity
A
Volume of carbon monoxide transferred across the alveoli into the blood per minute per unit of alveolar partial pressure
15
Q
DLCO normal value
A
17 - 25 mL/m/mmHg
16
Q
What are some things that could affect DLCO?
A
Fick’s Law of Diffusion
- emphysema (increased SA)
- fibrosis (increased thickness)
17
Q
How long do you wait after an acute upper respiratory infection?
A
6 weeks (only if ACTIVELY febrile)
18
Q
Acute Upper Respiratory Infection case tips
A
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
19
Q
adverse respiratory events
A
bronchospasm
laryngospasm
airway obstruction
postoperative croup
20
Q
Asthma (3)
A
REVERSIBLE airway obstruction characterized by
- bronchial hyperactivity
- bronchoconstriction
- chronic inflammation of lower airways
21
Q
Pathophys of asthma
A
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
22
Q
S/S Asthma (4)
A
EPISODIC (may lasts minutes to hours but pt completely recovers)
- wheezing
- productive and non-productive cough
- dyspnea & chest discomfort –> air hunger
- eosinophilia (sputum)
23
Q
Severe bronchospasm VS
A
RR > 30, HR > 120
24
Q
Dx asthma
A
- wheezing, chest tightness, SOB
- airflow obstruction that is partially reversible w/bronchodilators
- PFTS (FEV1 < 35%)
25
Expiratory limb of loop w/asthma
scoooooping
26
What happens w/FRC and TLC in asthma?
```
FRC increases (usually RV)
TLC normal
```
27
DLCO in asthma?
samesies
28
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%
29
CXR in asthma
normal
| severe - hyperinflation, hilar congestion d/t mucus plugging and pulmonary HTN
30
EKG in asthma
only in severe attacks
- RV strain (d/t increased pulmonary pressures)
- T wave inversion (V1-V4, II, III, avF)
31
Treatment of asthma
treat inflammation & bronchospasm
1. corticosteroids
2. long-acting bronchodilators
3. leukotriene modifiers
4. anti-igE monoclonal antibody (omalizumab)
5. methylxanthines (theophylline)
6. mast cell stabilizer (cromolyn)
32
corticosteroid example
beclomethasone
give 1-2h preop (ideally 5 days)
alters gene transcription, inhibits mast cells, apoptosis of inflammatory cells, increase B2 agonist effectiveness
33
long-acting bronchodilator example
salmetrol (50 mcg) DOA 12 - 24 h
combination (symbicort & advair) = LABA + steroid
34
leukotriene modifier
singulair
35
PFT's & ASTHMA
if FEV1 > 50% of normal, symptom free
36
Status asthmaticus
life threatening emergency in which bronchospasm does not respond to treatment
37
Status asthmaticus s/s
```
low oxygen
blunted CO2 waveform
wheezing
mucus hypersecretion
PIPs increased
```
38
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
39
Terbutaline
0.25 mg SQ q15m (beta agonist)
40
Bronchospasm tx
1. deepen (propofol)
2. 100% O2
3. SABA
4. Epi 10 mcg/kg
5. Hydrocort 2-4 mg/kg
6. ipraprotium 0.25 - 5 mg
41
What increases risk for perioperative event for asthma (think PFTS)
FVC < 70%
| FEV1/FVC < 65%
42
When do you stress dose steroids?
only IF systemic therapy in the last six months
43
Anesthesia considerations for asthma
1. deep induction
2. IV or transtracheal lidocaine
3. VA (sevo)
4. avoid histamine releasing drugs (no morphine, no succinylcholine)
5. Adequately hydrated
6. avoid acei?
7. use PEEP
44
COPD define
non-reversible loss of alveolar tissue and progressive airway obstruction
45
COPD RF:
```
cigarette smoking
occupational exposures
pollution
recurrent respiratory infections
low birth weight
a1 antitrypsin deficiency
```
46
type B COPD
bronchitis
| blue bloater
47
type A COPD
emphysema
| pink puffer
48
emphysema pathophys
destruction of parenchyma
loss of SA, elastic recoil & structural support
inability to maintain airway patency
49
bronchitis pathophys
narrowing of small airways by inflammation & mucuous production
50
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
51
what is an acinus
tissue distal to terminal bronchioles
52
centriacinar (centrilobular) emphysema
more common in apex
| *proximal*
53
panacinar (panlobular) emphysema location & cause
more common distally d/t a1 antitrypsin deficiency
54
paraseptal emphysema
regional
55
bullae emphysema
one big sac
56
what does elastase do?
degrades pulmonary connective tissue
| it is released by smoking
57
what does alpha 1 antitriptase do
blocks elastase
58
chronic bronchitis definition
dx characterized by excessive sputum production (expectoration of sputum most days for at least 3 mo for 2 successive years)
59
hallmark findings of chronic bronchitis (5)
1. hypertrophy of mucus glands of large bronchi
2. inflammatory changes in small airways
3. granulation of tissue, smooth muscle increases
4. peribronchial fibrosis
5. chronically hypoxic (paO2 < 60)
60
COPD diagnosis
SPIROMETRY
| severity determined by GOLD
61
FEV1/FVC for COPD
decrease < 70% of predictive
| not reversible w/bronchodilators
62
FEV25-75 for COPD
decreased
63
FRC and TLC for COPD
increased *RV*
64
COPD treatment
smoking cessation
long term O2 admin (2LPM)
hct > 55%, paO2 < 55, usually have corpulmonale
65
Drug treatment of COPD
```
O2
long acting B2agonist
steroids
long acting anticholinergic (ipaprotrium)
vaccines
diuretics
theophylline
```
66
Sx treatment COPD
lung volume reduction surgery for severe COPD cases
-increases pel, decreases hyperinflation, improves diaphragmatic/chest wall movement, decreases V/Q mismatch
67
COPD anesthetic considerations for lung volume reduction
double lumen tube
avoid nitrous
avoid excessive positive pressure (low Vt, high RR)
68
what is most predictive of COPD pulmonary compliactions
clinical symptoms (wheezing, cough)
69
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
```
70
smoking cessation
at least six weeks
| or morning of only
71
COPD malnutrition leads to --->
increases risk of pleural leaks after surgery
72
interscalene block risks
ipsilateral phrenic nerve palsy
73
why do you avoid NO for COPD pt
attenuates HPV, increases V/Q MISMATCH
74
PIP
< 30 CM H2O
75
Why does air trapping occur?
positive pressure ventilation applied w/o sufficient expiration --> increasing intrathoracic pressure --> decreasing VR --> increases PAP
76
Capnography for air trapping
sloped carbon dioxide concentration; expiratory flow does not reach baseline
77
bronchospasm COPD pt
light? deepen anesthetic
| pathologic? bronchodilator, magnesium, epi, IV steroids, suction secretions
78
Name 5 other expiratory outflow obstructions
```
bronchiectasis
cystic fibrosis
primary ciliary dyskinesia
bronchiolitis obliterans
tracheal stenosis
```
79
bronchiectasis
irreversible airway dilation and collapse d/t inflammation d/t chronic infections
80
bronchiectasis s/s
significant hemoptysis (200 mL over a 24 hour period)
dyspnea/wheezing
pleuritic chest pain
FINGER CLUBBING
81
bronchiectasis dx
```
hx chronic cough w/purulent sputum
CT confirms (usually lower lobes)
```
82
anesthetic considerations for bronchiectasis
GETTA w/frequent suctioning
double lumen tube to avoid infecting both sides
avoid nasal intubations
83
cystic fibrosis definition
autosomal recessive d/o affect a single gene on chromosome 7 - this prevents chloride transport and movement of salt and water
84
cystic fibrosis damage
```
lungs (COPD, bronchiestasis)
pancreas (DM)
GI (ileus)
sinusitis
liver (cirrhosis)
reproductive organs
```
85
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
86
CF tx
alleviation of symptoms
1. clear airway secretions
2. correct organ dysfunction
3. nutrition (VIT K)
4. prevent GI obstruction
87
CF anesthesia considerations (6)
1. optimize pt (elective procedures)
2. vit k to help absorb fat soluble vitamins
3. general anesthesia w/VA (increased oxygen concentrations, relax smooth airways)
4. avoid anticholinergic
5. awake extubation
6. pain control
88
primary ciliary dyskinesia
congenital impairment of ciliary activity in respiratory tract epithelial cells and sperm cells
89
what is kartagener's syndrome?
PCD
- chronic sinusitis
- bronchiectasis
- sinus inversus (ORGANS REVERSED)
- decreased fertility
90
primary ciliary dyskinesia anesthesia
```
regional anesthesia
reverse position of EKG leads
left IJ vein cannulation
right uterine displacement
avoid nasal pharyngeal airways
```
91
bronchiolitis obliterans
disease of small airways and alveoli in children from RSV
92
adult bronchiolitis obliterans
d/t viral pneumonia
- collagen vascular dx (RA)
- silo filler's disease (nitrogen dioxide inhalation)
- graft vs host dx
93
Bronchiolitis obliterans organizing pneumonia (BOOP)
shares features of interstitial lung dx and bronchiolitis obliterans
treatment innefective
94
tracheal stenosis
occurs following prolonged intubation or over-inflation of ETT (may not appear for several weeks)
95
when does tracheal stenosis become symptomatic
tracheal diameter decreases < 5 mm
dyspnea prominent at rest
accessory muscles used in all phases of breathing
96
tracheal stenosis tx
1. tracheal dilation (temporary) - balloon or surgical dilators, lasering of scarred tissue
2. Tracheobronchial stent can be short term or long term
3. Tracheal resection w/anastomosis is the best treatment (intubate below resection)
97
tracheal stenosis anesthetic considerations
translaryngeal intubation
VA to ensure maximum inspired oxygen concentration
helium
