case 5: COPD Flashcards
1
Q
Lab Test Results
A
- Pulmonary function tests – spirometry
– Diffusing (diffusion) capacity (DL) = 16.0 (ml/min/mmHg) (67%
of predicted)
– FEV1 = 45% of normal, No change in FEV1 with bronchodilator
– decrease FVC, (FEV1/FVC) < 0.7 - decrease Vmax
- A sputum sample showed many neutrophils together with
cellular debris
– Culture of sputum showed positive Streptococcus species - Echocardiogram – enlarged right ventricle
2
Q
CXR Results
A
Chest radiographs – hyperinflated lungs; flattened diaphragms
3
Q
Diagnosis
A
- Chronic obstructive pulmonary diseases (COPD) associated
with emphysema, bronchitis, asthma - COPD, also known as chronic obstructive lung disease
(COLD), chronic obstructive airway disease (COAD)
4
Q
COPD – Introduction
A
- Symptoms – any patient who has dyspnea (shortness of
breath, progressive, persistent and characteristically worse
with exercise), chronic cough or sputum production, plus: - A history of exposure to risk factors for COPD:
– Tobacco (cigarette smoking)
– Occupational dusts (organic & inorganic)
– Indoor air pollution from heating & cooking
– Outdoor air pollution - Usually present in fifth decade of life, with dyspnea (initially
only with exertion) or acute chest illness - Spirometry is required to make the diagnosis
5
Q
Structure of Respiratory System
A
- Airway passages
– Conducting zone and respiratory zone - Conducting zone
– Outside the lungs – nasal passage ->
pharynx -> epiglottis -> larynx (glottis)
– Inside the lungs – trachea (1) ->
bronchus (2 branches) -> bronchiole ->
… -> terminal bronchiole
– Functions of conducting zone –
passage of air, warming, humidification,
and filtration - Respiratory zone
– Respiratory bronchiole -> … -> alveoli
– Functions of respiratory zone –
passage of air, gas exchange
6
Q
The Alveoli
A
- Alveoli
– Total # – ~300 x 106
– .25 - .5 mm in diameter
– Total area – 60 - 80 m2 - Alveolar wall
– Type I alveolar cells – the
major lining cells, accounts
for 95-97% of total surface
area
– Type II alveolar cells –
production of surfactants
– Air-blood barrier – ~0.3 micro m
7
Q
Nature Properties of Lungs & Chest Wall
A
- The lung can be viewed as a passive (no contracting or relaxing), elastic container (can recoil inward)
- The pleural space (air sealed) contains only a film of fluid, so lungs normally remain in contact with the chest walls
- The lung tends to recoil inward and the
chest wall outward - These recoil forces in opposite directions
create a negative (sub-atmospheric)
pleural pressure (always negative) - Lungs expand and contract along with the
thoracic cavity
rib cage can recoil inward
mediasternum is a protection mechanism where if there is a fracture it can protect one lobe and not the other
8
Q
Thoracic Cavity
A
- Diaphragm – separates
thoracic & abdominal cavities - Pleural (intra-pleural) space (air sealed)
– Thin fluid layer between
visceral pleura covering
lungs (visceral) and parietal
pleura lining thoracic cavity
walls
– Air-sealed space - Thoracic cavity surrounded by
rib cage (chest wall) and the
respiratory muscles
9
Q
Respiratory Muscles & Ventilation
A
- Respiratory muscles
– Inspiratory muscles – diaphragm, external
intercostals, scaleneus, sternomastoids and
others
– Expiratory muscles – internal intercostals,
abdominal muscles (oblique, rectus &
transverses), and diaphragm - During inspiration
– Contraction of inspiratory muscles -> increase vertical & horizontal distances of thoracic cavity -> increase volume of thoracic cavity - During quiet expiration
– Relaxation of inspiratory muscles -> decrease vertical & horizontal distances of thoracic cavity -> decrease volume of thoracic cavity - During active (forced) expiration, contracts
expiratory muscles -> accelerate exhalation
10
Q
Sequential Events during Inspiration
A
- Inspiration is an active process (active contraction)
- Mechanics of breathing – interplays of (1)
chest (thoracic cavity, rib cage), (2) pleural
space and (3) alveolar space (lung volume)
– At the end of quiet expiration (FRC, Patm =
Palv) – neural input -> contraction of
inspiratory m. -> increase vertical & horizontal
distance of chest -> increase chest vol
– -> chest “pulls” on pleura -> increase pleural vol -> decrease intra-pleural P (Ppl, more negative) -> pulls lungs to expand more
– -> increase lung vol -> decrease Palv (intra-pulmonary P) -> Palv < Patm -> generates P gradient between atmospheric (originally at 0) (Patm > Palv) -> air flows into lungs -> Palv increase -> until Palv = Patm -> airflow ceases (the end of inspiration) - volume and pressure inversely related
- if pleural pressure is 0 then collapse
- pleural pressure more negative it opens alveolar wall
- increase alveolar space then alveolar pressure decrease/become negative relative to atmosphere
when chest wall expands, pleural space air sealed, there’s an increase in pleural space and there decrease pressure
11
Q
Sequential Events during Expiration
A
- Quiet expiration is a passive process (relax expiratory muscles) (with copd you have to contract expiratory muscle to get air out)
– Can you deduce the pressure and vol changes in the chest, pleural space and alveolar space? - During active (forced) expiration,
expiratory muscles contract -> accelerate exhalation - Intra-pleural P = -4 to -5 mmHg at
the end of quiet expiration (beginning of next inspiration) (FRC)
12
Q
Lung Volumes and Capacities
A
- 4 primary lung volumes – tidal volume (TV), inspiratory reserve volume (IRV), expiratory reserve volume (ERV) and residual volume (RV)
- 4 lung capacities – inspiratory capacity (IC), functional residual capacity (FRC) (ERV + RV), vital capacity (VC) (IRV + TV + ERV) and total lung capacity (TLC) (all 4 vol together)
13
Q
Measurement of Lung Volumes
A
- Lung volumes, capacities & air flow rates
indicate clinical pulmonary functions - Measurement of lung vol – spirometry
– Patient inhales -> air into lungs from spirometer, pen deflects upward
– Patient exhales -> pen deflects downwards
– Limitations of spirometry – cannot measure RV & FRC (RV+ERV) - Dilution method – measure RV & FRC
– Use of radioactive helium (inert gas)
– Takes some breaths to reach equilibrium
– C1 x V1 = C2 x (V1 + V2)
14
Q
Measurement of FVC & FEV1
A
- EFV1 – forced expiratory volume in 1 second
– Is the volume of air that can forcibly be blown out in one second, after full inspiration - FVC (forced vital capacity)
– The patient is asked to take the deepest breath they can
– -> then exhale into the sensor as hard as possible (6-10”)
– The max volume patient expires is FVC
15
Q
Respiration and Pressure Gradient capillaries
A
- How do we get O2 into the body
and CO2 out of the body?
(Ventilation)
– Ventilation results from pressure
differences (gradient) induced by
changes in lung volumes
– Pressure (P) gradient – results in
net gas flow & diffusion from high
P to low P
– For PO2 – alveolar space > blood
plasma > interstitial fluid > cytosol
> mitochondria
– For PCO2 – mitochondria > cytosol
> interstitial fluid > blood plasma >
alveoli
16
Q
Surface Area for Diffusion
A
- Respiratory membrane
– Large surface area, extensive
branching & clusters of alveoli
– Thin membrane, single layer of
epithelial cells, single layer of
endothelial cells, fused basement
membranes
17
Q
Factors that Create Gas Diffusion
A
- Molecular basis of gas diffusion
– Net movement follows a pressure gradient - Diffusion barriers
– Exchange of O2 and CO2 in the lung takes
place in 3 separate phases (air, solid, and
liquid), each involving diffusion
– A fluid lining, alveolar membrane, an
epithelial basement membrane, interstitium,
a capillary basement membrane, capillary
endothelial membrane, plasma, and RBC
cell membrane - Only dissolved gas in fluid accounts for
partial P of that gas
18
Q
COPD – Definition
A
- (Global Initiative for Chronic Obstructive Lung Disease,
GOLD) – a disease state characterized by airflow limitation
that:
– is not fully reversible
– is usually progressive
– is associated with an abnormal chronic inflammatory response
of the lungs to noxious particles or gases - A disease state characterized by the presence of airflow
obstruction due to chronic bronchitis and/or emphysema; the
airflow obstruction is generally progressive, may be
accompanied by airflow hyperactivity, and may be viewed as
partially reversible, characterized by chronically poor airflow
and typically worsened over time
19
Q
COPD – Prevalence
A
- The only one out of the top 10 causes of death with increasing prevalence
– Prevalence increases with age - Increase more marked in women
- Worldwide, COPD affects 329 million people (~ 5% of the population). In 2012, it killed >3 million people
- Worldwide, the number of deaths is projected to increase due to higher smoking rates and an aging population
- Resulted in an estimated economic cost of $2.1 trillion in 2012
20
Q
Principle of Physical Examination
A
- Physical exam cannot diagnose early disease
- Airflow obstruction
– Wheezing (why?) when theres obstruction , airflow going in and out become turbulent rather than laminay, causing more energy
– Prolongation of forced expiratory time (inspiration vs. expiration) expiration takes longer time to get air out bc after inspired air into lung, enough alveolar space is compressed of bronchiole, diameter is too narrow, further compressed by air, prolongation of forced expiratory time - Lung hyperinflation
– Low diaphragmatic position
– Increased resonance to percussion (why?) there will be some emphysema and air gets trapped in lung without surrounding alveolar wall, there’s less resistance of alveolar wall
– Decreased intensity of heart and breath sounds (why?) it’s blocked by air, can’t be transmitted by solid tissue - Severe disease
– Pursed-lip breathing (why?) air flow more stable, to get air into and out easier
– Use of accessory respiratory muscles (why?) expiration is more difficult because of airway limitation/obstruction. accessory muscle needed to help get air into and out of lung to breathe
– Retraction of intercostal space (why?) contraction is harder, vacuum space causes negative pressure so even the muscle is retracted, so intercostal space
