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Flashcards in Pulmonary I Deck (106):
1

Pulmonary perfusion

movement of mixed venous blood through pulmonary capillary with purpose of exchange between blood and alveolar air
Blood- High volume, low pressure- mean pressure 18
At any time 1/3 of pulmonary vasculature is filled with blood-lung bases, more blood
Mean alveolar pressure
decreased PaO2- shunting blood to areas with increased PaO2

2

Ventilation

Mechanical movement of air into and out of alveoli
Regulation- CNS, Chemical
Hypercapnic ventilatory drive

3

Work of breathing

Amount of effort required to overcome the elastic and resistive properties of the lungs and chest wall
Influenced by elasticity (return to normal shape)
Compliance (ability to expand)
High-COPD
Low-PNA, ARDS

4

Alveolar diffusion

Exchange of O2 and Co2
Oxygen diffuses down the concentration gradient

5

Remember oxygen bound to heme is...

Useless

6

Right shift

Oxygen is released more easily
decreased pH
Increased temp
sickle cell
pregnancy

7

Left shift

Oxygen is held on more tightly
increased pH
PaCo2 decreases
decreased temperature
hypophosphatemia

8

Causes of hypoxemia

Hypoventilation (obesity, narcotics, weakness)
V/Q mismatch (
R-L shunt
Diffusion limitation
reduced inspired O2 tension

9

Normal A-a gradient on room air

7-14

10

Causes of hypercapnia

Drugs
Diseases of medulla
abnormalities in the spine conducting pathways
Diseases of the neuromuscular junction or respiratory muscles
thoracic cage abnormalities
Large airway obstruction (OSA)
Increased web or physiologic dead space (emphysema)

11

Dyspnea

Subjective symptom that only patient can perceive
Mechanisms:
Motor
Sensory afferents (chemoreceptors in carotid bodies, mechanoreceptors in the lungs)
integration: efferent-Reafferent mismatch (COPD and asthma patients)
Contribution of emotional or affective factors to dyspnea (anxiety)

12

Dyspnea and associated disease states

asthma
COPD
ILD
Myocardial dysfunction
Obesity
Deconditioning
HF
Pulmonary edema
PE

13

Respiratory dyspnea

Asthma, COPD
Diseases of chest wall
Diseases of lung parenchyma

14

Cardiac dyspnea

Diseases of the left heart
Ischemic heart disease
Diastolic dysfunction
Diseases of the pulmonary vasculature (PE, PHTN)
Diseases of the pericardium (constructive pericarditis, tamponade)

15

Other dyspnea

anemia
obesity
deconditioning
medically unexplained

16

Cough

complex and triggered by sensory nerve endings that can detect both chemical and mechanical exposure

17

Acute

Less than 3 weeks
infections
aspirations
inhaled chemicals

18

subacute

3-8 weeks
post viral syndrome

19

chronic cough

> 8 weeks
cough variant asthma
medications (ACE)
GERD

20

Hemoptysis

Expectoration of blood from the respiratory tract- must distinguish source (airway, mouth, sinuses, GI)
Causes:
Worldwide- TB
US- Viral/Bacterial PNA

21

Massive hemoptysis

any amount of bleeding that can compromise airway or hemodynamic stability
Will need ETT for airway protection

22

Oxygen supplementation

Diffusion gradient- increases it with supplementation (easier diffusion, lowest amount possible for the shortest amount of time)
Goals of treatment SaO2 > 90

23

Nasal prongs

Assume mouth breathing
Oxygen is stored in nasal cavity and drawn down into lungs (Bernouli's principle)
Sinuses act as a reservoir
1-6 L
Each liter adds 4% O2

24

Face mask

imprecise
low flow
40-60%

25

Venturi mask

More precise
uses velocity to create pressure gradient
40-60%
More expensive

26

Non-rebreather

High flow 11-15 L
Near 100% O2
High flow creates pressure which keeps air from entering from other parts of the mask
Exhaled air into mask move through one way valve preventing rebreathing

27

Pulmonary function testing

Spirometry
FVC- total exhaled volume after a maximal inspiration and expiration
FEV1- The first exhaled second of FVC
FEV1/FVC
Post bronchodilator testing
after 4 puffs of albuterol and waiting 15 minutes (increase of more than 12% in FEV1 is significant)

28

Pulmonary function testing

Exhaled NO
Diffusing capacity of carbon monoxide- is used to assess Pulmonary vascular disease
Maximal inspiratory pressures
Bronchial provocation testing- suspect asthma, but no improvement in bronchodilator testing

29

PFTs and the geriatric patient

TLC usually constant but VC decreases because RV increases
TV may be decreased
Alveoli collapse more easily
Cilia decrease
Decrease in cough and gag reflex
May need more time when performing PFTs with the elderly

30

PFTs equation variables to figure out normal lung volumes

height
Age (declines with age)
Gender
Race (black man has shorter torso so shorter lungs than white man)

31

What is abnormal value for FVC

less than 80% of the predicted normal value given the 4 variables

32

Two problems with lungs found on PFTs

Restriction- problem with volume of lungs
Obstruction- problem with airways

33

FVC stands for

Forced Vital Capacity

34

How do you perform an FVC

take a deep breath in and blow it out as fast and as completely as possible

35

The initial flow of the FVC comes from

The large airways

36

The latter flow of the FVC comes from the

Small airways, alveoli

37

FVC is

The volume of air that you can move in a forced manner

38

FVC is decreased with

Restriction

39

Restriction is caused by

Fibrosis (intrinsic)
scoliosis (extrinsic)
neuromuscular disease (ex)
obesity (ex)
Pulmonary edema (in)

40

How do we know if the number is normal or low?

Take the four variables and get a number, take the FVC and divide by the "normal" for the 4 variable, If 80% of predictive or better than you are normal. < 80% of predictive then you have a restrictive lung disease

41

FEV1 stands for

Forced expiratory volume in 1 second

42

FEV1 is a volume but shows

a flow rate

43

FEV1- the more volume you can get out in 1 second the better the...

flow

44

Small airways are...

effort independent
you can blow as hard as you want but you can't effect the flow coming from the small airways

45

FEV1/FVC- normal

70%

46

< 70% of FEV1/FVC shows

Obstruction

47

On inhalation, intrathoracic airways get...

bigger

48

On exhalation, intrathoracic airways get...

Smaller

49

On inhalation, extrathoracic airways get...

smaller

50

On exhalation, extra thoracic airways get...

bigger

51

Obstructions always manifest themselves when the airways are...

small

52

therefore obstructions manifest intrathoracic on... and extrathoracic on...

exhalation
inhalation

53

What is the DlCO?

A way of measuring the cross sectional surface area of the lungs and capillaries

54

High DLCO is

normal > 80%

55

Low DLCO is

marker of low pulmonary surface (architectural destruction) area such as
COPD, Emphysema, Pulmonary HTN, Fibrosis

or marker of extrinsic problem such as scoliosis, obesity, chest wall abnormality

56

How can you tell the cause of the low DLCO?

By looking at Va (alveolar ventilation) if the alveolar ventilation is normal than it is caused by architectural destruction and ventilation problem

57

How to differentiate asthma from COPD

both will have low FEV1/FVC
but for COPD the DLCO will be low while it will be normal or high in asthma

58

Interpreting PFTs

1. FVC is it > 80% of predicted (yes, no restriction), (no, then you have restriction or obstruction with air trapping.)
2. Is FEV1/FVC > 0.7? (yes, no obstruction), (no, obstruction)
3. Is TLC > 80% of predicted? (Yes, obstruction) (no, restriction)

59

Gold stages look at...

FEV1 only

60

Gold stage I

80-100

61

Gold stage 2

50-80

62

Gold stage 3

30-50

63

Gold stage 4

0-30
respiratory failure with an elevated PCO2 level

64

Also need to classify with Obstruction

Reactivity or not

65

How to determine reactivity

Bronchodilator testing
If FEV1 or FVC >12% improved and 200 ml than there is reactivity

66

DLCO > 80% of predicted?

Yes- normal membrane surface area
No- abnormal membrane surface area

67

DLCO/Va > 80% of predicted?

Yes- Extrinsic lung disease
No- Intrinsic lung disease

68

Asthma is a

chronic inflammatory condition of the airways, common in young males, adult females

69

Atopy is..

allergies and are a major risk factor for asthma

70

Asthma is diagnosed...

with symptoms and objective measurement of lung function

71

Spirometry on asthma shows...

airflow limitations with reduction in FEV1, FEV1/FVC ration and peak expiratory flow

72

Asthma s/sx

episodic wheezing
chest tightness
cough
increased sputum production
nocturnal worsening

73

ABG finding that could show impending respiratory failure

PCO2 rising or normalizing

74

Asthma PFTs...

decrease of more than 20% of normal is asthma exacerbation.
PEF thats greater than 50% of baseline is considered a severe attack

75

Asthma CXR...

CXR will be normal, diaphragmatic flattening shows chronic condition

76

Asthma exacerbation classifications

mild, moderate, severe, respiratory arrest

77

Medications for long term asthma control...

inhaled corticosteroids
systemic corticosteroids
long acting/short acting beta-2-agonists
Cromolyn and Nedocromil
Inhaled long acting anticholinergic
phosphodiesterase inhibitors
leukotrine modifiers
immunomodulators

78

Asthma medications for quick relief

Beta-adrenergic agonists
Anticholinergic agents
corticosteroids

79

All asthma patients should be immunized with

pneumococcal vaccination, annual influenza vaccine recommended

80

Mild asthma exacerbation

minor changes in PEF (usually more than 80%)
SABA a mainstay of therapy at increased doses
Consider PO steroid in patients on inhaled steroid (7 day coarse)

81

Moderate asthma exacerbations

correct hypoxemia, reverse obstruction and reduce likelihood of recurrence
SABA+systemic corticosteroids
think peak flow less than 70=steroids
how much FEV1 improves after 30 minutes correlates with severity of exacerbation

82

Severe asthma exacerbations

Life threatening
Oxygen, SABA, Steroids
+ Ipratropium
IV magnesium-2 g over 20 minutes, smooth muscle relaxation
NO mucolytics (can worsen cough and obstruction)
Avoid anxiolytics
Abx when indicated, not given empirically

83

Asthma when to refer

Atypical presentation
complicated comorbid problems
poor response to therapy
On high dose steroids
Not meeting goals after 3-6 months of treatment
More than 2 course of oral steroids in 2 months
Life threatening asthma exacerbation or hospitalization in last 12 months

84

COPD is

a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema
It is progressive, most patients have features of both
Risk factors- cigarette smoking, environmental exposures, hereditary factors

85

COPD s/sx

4th-5th decade of life
excessive cough, sputum, SOB
Late stages- pneumonia, pulmonary htn, cor pulmonale, chronic respiratory failure

86

Type A COPD

"Pink puffers"
c/o dyspnea
less coughing
thin, weight loss
accessory muscle use
chest quiet
oxygenate fine
CXR-hyperinflation, flattened diaphragm
TLC-increased

87

Type B COPD

"Blue Bloaters"
loud chronic cough
sputum
chest infections
Mild dyspnea
overweight
cyanotic
peripheral edema
noisy chest
reduced PaO2
CXR- interstitial markings
TLC- normal

88

Spirometry is required to make the diagnosis of...

COPD

89

COPD symptoms

progressive dyspnea
cough
sputum production
wheezing chest tightness
ankle swelling
syncope

90

COPD spirometry

early-abnormal closing volume and reduced mid expiratory flow rate
FVC-reduced
RV-increased
FEV1 and FEV1/FVC- decreased later in disease less than 0.7 for diagnosis

91

Classification of severity of airflow limitation in COPD

GOLD 1: mild FEV1 > 80
GOLD 2: moderate 50-80
GOLD 3: Severe30-50
GOLD 4: Very severe < 30

92

Alpha-1 antitrypsin deficiency screening

All patients with COPD diagnosis
typically < 45 years with pan lobular basal emphysema

93

Prevention and maintenance therapy for COPD

Smoking cessation is key
safety of e-cigarettes as a smoking cessation aid is uncertain at this point
Pharmacologic therapy to reduce COPD symptoms, frequency and severity of exacerbations
All therapy should be individualized
Inhaler teaching
Flu and PNA vaccine
Pulmonary rehabilitation
Long-term O2 therapy
Offer palliative approaches in advanced COPD

94

Pharmacologic treatments of Alpha-1 antitrypsin disease

IV augmentation therapy may slow down the progression of emphysema

95

Pulmonary rehabilitation in COPD patients..

improves dyspnea, health status and exercise tolerance in stable patients
reduces hospitalizations among patients who have had a recent exacerbation

96

Goals for treatment of stable COPD

Relieve symptoms, Improve exercise intolerance, improve health status, reduce risk of disease progression, prevent exacerbations, reduce mortality

97

Preferred treatment for patients with stable COPD

Long-acting beta agonists
Long-acting muscurinic agonist are preferred over short acting agents except for in patients with only occasional dyspnea
inhaled corticosteroids are only recommended in association with a LABA for patients with a history of exacerbations

98

Group A patients pharmacologic treatment

A bronchodilator- All group A patients should be offered bronchodilator treatment based on its effect on breathlessness. This can either be short or long acting

99

Group B patients pharmacologic treatment

Initial therapy should consist of a long acting bronchodilator.
LAMA or LAMA/LABA if having severe breathlessness

100

Group C patients pharmacologic treatment

LAMA started first, then step up to LAMA/LABA or LAMA/ICS (alternative)

101

Group D patients Pharmacologic

LAMA/LABA to start- if continuing to have problems, LAMA/LABA/ICS, then you can do additional therapies from there
Consider macrolide in former smokers

102

Nonpharmcologic treatment in COPD

Education and self management
Physical activity
Pulmonary rehabilitation
Exercise training
Self management education
End of life and palliative care
nutritional support
Vaccination
Oxygen therapy

103

Oxygen therapy for COPD

Long term oxygen is indicated for stable patients PaO2 less than 55, < 88%. Prescribe O2 to keep Sat > 90%.

104

Monitoring and follow up for patients for COPD

Spirometry should be preformed once a year
Information on symptoms should be collected at each visit (cough, sputum, breathlessness, fatigue, activity limitation and sleep disturbances)
Exacerbations (frequency, severity, type)
Smoking status

105

Management of COPD exacerbations

can be precipitated by several factors ( most common are respiratory tract infections, viruses)
SABD are recommended as the initial bronchodilators to treat an acute exacerbation
Start maintenance therapy as soon as possible before discharge
systemic corticosteroids can improve lung function, duration of therapy 5-7 days
Antibiotics when indicated

106

COPD classification and treatment

Mild- SABD
moderate- SABD plus antibiotic and/or oral corticosteroids
Severe- patient requires hospitalization