Pulmonary I Flashcards

1
Q

Pulmonary perfusion

A

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

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2
Q

Ventilation

A

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

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3
Q

Work of breathing

A

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

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4
Q

Alveolar diffusion

A

Exchange of O2 and Co2

Oxygen diffuses down the concentration gradient

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5
Q

Remember oxygen bound to heme is…

A

Useless

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6
Q

Right shift

A
Oxygen is released more easily
decreased pH
Increased temp
sickle cell
pregnancy
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7
Q

Left shift

A
Oxygen is held on more tightly
increased pH
PaCo2 decreases
decreased temperature
hypophosphatemia
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8
Q

Causes of hypoxemia

A
Hypoventilation (obesity, narcotics, weakness)
V/Q mismatch (
R-L shunt
Diffusion limitation
reduced inspired O2 tension
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9
Q

Normal A-a gradient on room air

A

7-14

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10
Q

Causes of hypercapnia

A

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)

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11
Q

Dyspnea

A

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)

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12
Q

Dyspnea and associated disease states

A
asthma
COPD
ILD
Myocardial dysfunction
Obesity
Deconditioning
HF
Pulmonary edema
PE
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13
Q

Respiratory dyspnea

A

Asthma, COPD
Diseases of chest wall
Diseases of lung parenchyma

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14
Q

Cardiac dyspnea

A

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

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15
Q

Other dyspnea

A

anemia
obesity
deconditioning
medically unexplained

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16
Q

Cough

A

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

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17
Q

Acute

A

Less than 3 weeks
infections
aspirations
inhaled chemicals

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18
Q

subacute

A

3-8 weeks

post viral syndrome

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19
Q

chronic cough

A

> 8 weeks
cough variant asthma
medications (ACE)
GERD

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20
Q

Hemoptysis

A

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

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21
Q

Massive hemoptysis

A

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

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22
Q

Oxygen supplementation

A

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

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23
Q

Nasal prongs

A
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
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24
Q

Face mask

A

imprecise
low flow
40-60%

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25
Q

Venturi mask

A

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

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26
Q

Non-rebreather

A

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

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27
Q

Pulmonary function testing

A

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)

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28
Q

Pulmonary function testing

A

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

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29
Q

PFTs and the geriatric patient

A

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

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30
Q

PFTs equation variables to figure out normal lung volumes

A

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

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31
Q

What is abnormal value for FVC

A

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

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32
Q

Two problems with lungs found on PFTs

A

Restriction- problem with volume of lungs

Obstruction- problem with airways

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33
Q

FVC stands for

A

Forced Vital Capacity

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34
Q

How do you perform an FVC

A

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

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35
Q

The initial flow of the FVC comes from

A

The large airways

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36
Q

The latter flow of the FVC comes from the

A

Small airways, alveoli

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37
Q

FVC is

A

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

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38
Q

FVC is decreased with

A

Restriction

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39
Q

Restriction is caused by

A
Fibrosis (intrinsic)
scoliosis (extrinsic)
neuromuscular disease (ex)
obesity (ex)
Pulmonary edema (in)
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40
Q

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

A

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

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41
Q

FEV1 stands for

A

Forced expiratory volume in 1 second

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42
Q

FEV1 is a volume but shows

A

a flow rate

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43
Q

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

A

flow

44
Q

Small airways are…

A

effort independent

you can blow as hard as you want but you can’t effect the flow coming from the small airways

45
Q

FEV1/FVC- normal

A

70%

46
Q

< 70% of FEV1/FVC shows

A

Obstruction

47
Q

On inhalation, intrathoracic airways get…

A

bigger

48
Q

On exhalation, intrathoracic airways get…

A

Smaller

49
Q

On inhalation, extrathoracic airways get…

A

smaller

50
Q

On exhalation, extra thoracic airways get…

A

bigger

51
Q

Obstructions always manifest themselves when the airways are…

A

small

52
Q

therefore obstructions manifest intrathoracic on… and extrathoracic on…

A

exhalation

inhalation

53
Q

What is the DlCO?

A

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

54
Q

High DLCO is

A

normal > 80%

55
Q

Low DLCO is

A

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
Q

How can you tell the cause of the low DLCO?

A

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

57
Q

How to differentiate asthma from COPD

A

both will have low FEV1/FVC

but for COPD the DLCO will be low while it will be normal or high in asthma

58
Q

Interpreting PFTs

A
  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
Q

Gold stages look at…

A

FEV1 only

60
Q

Gold stage I

A

80-100

61
Q

Gold stage 2

A

50-80

62
Q

Gold stage 3

A

30-50

63
Q

Gold stage 4

A

0-30

respiratory failure with an elevated PCO2 level

64
Q

Also need to classify with Obstruction

A

Reactivity or not

65
Q

How to determine reactivity

A

Bronchodilator testing

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

66
Q

DLCO > 80% of predicted?

A

Yes- normal membrane surface area

No- abnormal membrane surface area

67
Q

DLCO/Va > 80% of predicted?

A

Yes- Extrinsic lung disease

No- Intrinsic lung disease

68
Q

Asthma is a

A

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

69
Q

Atopy is..

A

allergies and are a major risk factor for asthma

70
Q

Asthma is diagnosed…

A

with symptoms and objective measurement of lung function

71
Q

Spirometry on asthma shows…

A

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

72
Q

Asthma s/sx

A
episodic wheezing
chest tightness
cough
increased sputum production
nocturnal worsening
73
Q

ABG finding that could show impending respiratory failure

A

PCO2 rising or normalizing

74
Q

Asthma PFTs…

A

decrease of more than 20% of normal is asthma exacerbation.

PEF thats greater than 50% of baseline is considered a severe attack

75
Q

Asthma CXR…

A

CXR will be normal, diaphragmatic flattening shows chronic condition

76
Q

Asthma exacerbation classifications

A

mild, moderate, severe, respiratory arrest

77
Q

Medications for long term asthma control…

A
inhaled corticosteroids
systemic corticosteroids
long acting/short acting beta-2-agonists
Cromolyn and Nedocromil
Inhaled long acting anticholinergic
phosphodiesterase inhibitors
leukotrine modifiers
immunomodulators
78
Q

Asthma medications for quick relief

A

Beta-adrenergic agonists
Anticholinergic agents
corticosteroids

79
Q

All asthma patients should be immunized with

A

pneumococcal vaccination, annual influenza vaccine recommended

80
Q

Mild asthma exacerbation

A

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
Q

Moderate asthma exacerbations

A

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
Q

Severe asthma exacerbations

A

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
Q

Asthma when to refer

A

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
Q

COPD is

A

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
Q

COPD s/sx

A

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

86
Q

Type A COPD

A
"Pink puffers"
c/o dyspnea
less coughing
thin, weight loss
accessory muscle use
chest quiet
oxygenate fine
CXR-hyperinflation, flattened diaphragm
TLC-increased
87
Q

Type B COPD

A
"Blue Bloaters"
loud chronic cough
sputum
chest infections
Mild dyspnea
overweight
cyanotic
peripheral edema
noisy chest
reduced PaO2
CXR- interstitial markings
TLC- normal
88
Q

Spirometry is required to make the diagnosis of…

A

COPD

89
Q

COPD symptoms

A
progressive dyspnea
cough
sputum production
wheezing chest tightness
ankle swelling
syncope
90
Q

COPD spirometry

A

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
Q

Classification of severity of airflow limitation in COPD

A

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

92
Q

Alpha-1 antitrypsin deficiency screening

A

All patients with COPD diagnosis

typically < 45 years with pan lobular basal emphysema

93
Q

Prevention and maintenance therapy for COPD

A

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
Q

Pharmacologic treatments of Alpha-1 antitrypsin disease

A

IV augmentation therapy may slow down the progression of emphysema

95
Q

Pulmonary rehabilitation in COPD patients..

A

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

96
Q

Goals for treatment of stable COPD

A

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

97
Q

Preferred treatment for patients with stable COPD

A

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
Q

Group A patients pharmacologic treatment

A

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
Q

Group B patients pharmacologic treatment

A

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

100
Q

Group C patients pharmacologic treatment

A

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

101
Q

Group D patients Pharmacologic

A

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
Q

Nonpharmcologic treatment in COPD

A
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
Q

Oxygen therapy for COPD

A

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

104
Q

Monitoring and follow up for patients for COPD

A

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
Q

Management of COPD exacerbations

A

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
Q

COPD classification and treatment

A

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