Pathophys, Test Iii - 2Nd Part Respiratory Pathophysiology

Front 1

causes of wheezing other than bronchospasm

Back 1

ETT obstruction, inadequate anesthetic depth, endobronchial intubation, pulmonary aspiration, pulmonary edema, pulmonary emboli, pneumothorax

Front 2

what is the most common pulmonary disorder encountered in anesthesia

Back 2

COPD

Front 3

two classifications for COPD are

Back 3

chronic bronchitis or emphysemic

Front 4

PFT values for a COPD will be

Back 4

decreased FEV1,
decreased FEV1/FVC,
decreased MMEF 25-75%

Front 5

COPD prevalence increases

Back 5

with age - normal aging mimics COPD to an extent

Front 6

early changes respond to

Back 6

bronchodilator therapy

Front 7

changes in xray seen in a COPD patient

Back 7

increased TLC, and continued increase in capacity and flattened diaphragm even with exhalation
a normal lung shows some atelectasis with expiration

Front 8

three methods of airflow obstruction in COPD patients

Back 8

secretions in airway lumen
thickening of airway walls in response to damage
loss of tethering parenchyma to the neighbioring cells

Front 9

chronic bronchitis is defined as

Back 9

a productive cough on most days for more than 3 consecutive months for at least 2 consecutive years

Front 10

causes of chronic bronchitis are

Back 10

cigarette smoking, pollutants, pulmonary infection, familial factors

Front 11

describe the pathophysiology of chronic bronchitis (Part I)

Back 11

inspired irritants lead to inflammation of airways causing infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall
bronchial edema, increased size of mucus glands and goblet cells
thick and tenacious mucus can not be cleared because of impaired ciliary function
increased susceptibility to infection and injury

Front 12

describe the pathophysiology of chronic bronchitis (Part II)

Back 12

initially affects large bronchi but eventually affects them all
airways collapse in early expiration, are blocked by mucus, and air is trapped
big V:Q mismatching and hypoxemia
air trapping leads to hypoventilation and hypercarbia and barrel chested ineffective respiratory muscles

Front 13

what does the hypoxemia resulting from chronic bronchitis cause

Back 13

hypoxic pulmonary vasoconstriction (intrapulmonary shunting)
cor pulmonale
lost of central chemoreceptor function
RBC production

Front 14

what is hypoxic pulmonary vasoconstriction

Back 14

vasoconstriction of the pulmonary vasculature due to increased CO2 tension, can cause increased pulmonary tension leading to Cor Pulmonale (right Ventricle failure)
also seen when drop a lung - allow blood to be shunted to a better ventilated area

Front 15

describe the appearance of someone with chronic bronchitis

Back 15

Blue Bloater
ashen colored skin
kleenex everywhere
bit overweight
can't clear secretions
sit in a chair

Front 16

treatment for chronic bronchitis

Back 16

PREVENT because not reversible
smoking cessation halts progression of the disease
bronchodilators, CPT, expectorants
antibiotics, steroids, ventilators if necessary
chronic oral steroids are last resort
home O2

Front 17

emphysema is characterized as

Back 17

an irreversible enlargement of the airways distal to terminal bronchioles and destruction of alveolar septa

Front 18

diagnosis of emphysema is made by

Back 18

CT

Front 19

mild emphysemic changes are associated with

Back 19

aging

Front 20

emphysema is almost always associated with

Back 20

cigarette smoking

Front 21

less common cause of emphysema

Back 21

homozygous deficiency of alpha-1 antitrypsin which prevents excessive activity of elastase - causing a loss of elastic recoil

Front 22

elastase is produced by

Back 22

macrophages in response to infection or pollutants

Front 23

additional effect of smoking

Back 23

reduce protease inhibitors causing a lack of elastic recoil

Front 24

loss of elastic recoil in the lungs causes

Back 24

collapse of the small airways during exhalation because of decreased support and tugging between adjacent structures

Front 25

patients with emphysema have lung changes that show

Back 25

increased RV
increased FRC
increased TLC

Front 26

emphysema leads to pulmonary hypertension by

Back 26

destroying the capillaries

Front 27

prominent feature of emphysema

Back 27

increased deadspace (CO2 and O2 levels are normal early on, but progress to hypoxemia dn CO2 retention)

Front 28

blebs look like

Back 28

blisters on the lung surface

Front 29

bulla are found

Back 29

within the parietal pleura

Front 30

danger of blebs and bullas

Back 30

can burst leading to a pneumothorax

Front 31

symptomatic blebs and bullas are fixed by

Back 31

excision from the lung

Front 32

clinical manifestations of emphysema

Back 32

dyspnea, barrel chest, minimal wheezing (wheezing is more bronchitis), prolonged expiration, hypoventilation, polycythemia (late)

Front 33

a person with emphysema looks like

Back 33

a pink puffer
skinny, cachexic, all energy used to breathe, pursed lip breathing

Front 34

patients purse lip breathe to

Back 34

delay closure of small airways

Front 35

in emphysemic patients keeping airways open longer allows for

Back 35

more time for trapped air to get out
prolonged exhalation
more fresh gas can come in
reduction in compensatory respiratory rate
decreased work of breathing

Front 36

treatment for emphysema

Back 36

stop smoking
bronchodilators
low flow O2
diuretics if cor pulmonale

Front 37

range for O2 therapy for emphysemic patients

Back 37

PaO2 >60 torr

Front 38

what should you watch for with O2 therapy in emphysema

Back 38

O2 therapy can dangerously elevate CO2 because they operate on a hypoxic drive, so high O2 reduces respiratory drive

Front 39

if patients with COPD are on inhaled corticosteroids

Back 39

they may not be able to be extubated after surgery

Front 40

recommended management for stage I (mild COPD - FEV1 > 80%

Back 40

smoking cessation
flu vaccine
short acting bronchodilators as needed

Front 41

recommended management for stage II (moderate FEV1 50 - 80%) COPD

Back 41

mild treatments plus
long acting bronchodilators
pulmonary rehabilitation

Front 42

recommended management for stage III (severe FEV1 30 - 50%) COPD

Back 42

inhaled corticosteroids
plus stages I and II treatments

Front 43

recommended management for stage IV (severe FEV1 < 30%) COPD

Back 43

all earlier stage treatments plus
LTOT (Oxygen therapy?)
surgical intervention if split lung function tests are favorable

Front 44

preop evaluation of COPD patient should include

Back 44

any recent changes in dyspnea, sputum, wheezing
how long does it take to recover after exertion
bronchodilators (only work on reversible component of disease)

Front 45

intraop anesthetic considerations

Back 45

no Nitrous
large tidal volumes, slow rates
increased expiratory time (I:E)
do not normalize PaCO2
set parameters by the pH
CVP will only show RV pressures due to cor pulmonale
LMA may be a good thing
deep extubation may prevent bronchospasm but make sure patients have adequate PFTs
may require post op ventilation is FEV1 < 50%

Front 46

adjust ventilation parameters in a patient with COPD to

Back 46

pH

Front 47

the PaCO2 and ETCO2 gradient in COPD patients is

Back 47

wider with an increase in deadspace

Front 48

why is a CVP line in a patient with COPD not so useful

Back 48

patients usually have pulmonary hypertension or cor pulmonale, so CVP will only show RV pressure, not an assessment of LV or fluid status

Front 49

what about airway choice for COPD

Back 49

LMA is thought to decrease incidence of bronchospasm in patients with reactive airways
or deep extubate ETT if patient has adequate pulmonary function to help prevent bronchospasm

Front 50

patients with FEV1 values below what will likely need a period of post op ventilation

Back 50

50% - especially after upper abdominal or thoracic procedures

Front 51

clubbing of fingers is a sign of

Back 51

chronic hypoxemia

Front 52

early, middle, and severe stages of clubbing

Back 52

see page 42 of notes