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Respiratory obstruction

This can be:   

Intrathoracic or extrathoracic

Variable or fixed

Flow-volume curve can be used to identify whether a variable obstruction is intrathoracic or extrathoracic. It cannot identify fixed intrathoracic or extrathoracic.

In variable intrathoracic obstruction, the inspiratory flow-volume curve is less affected than the
expiratory flow-volume curve. In variable extrathoracic, obstruction. The expiratory flow-volume curve is less affected than the inspiratory flow-volume curve.



Expiratory flow-volume curve

Inspiratory flow-volume curve


                                    (Fixed obstruction)



                           (Variable Extrathoracic obstruction)



                                        (Variable intrathoracic obstruction)                                                                   


A.  Compliance

This is defined as the change in volume for a unit change in pressure.It denotes stretchibility and is inverse of elasticity.


A plot of the change in volume with a change in pressure is the volume-pressure curve or the relaxation-pressure curve. When the relaxation – pressure curve is plotted for the total respiratory system (i.e. taking into account the interaction between the recoil of the lungs and recoil of the chest) the volume of the gas in lungs when the pressure is zero is called the relaxation volume. The relaxation volume equals the functional residual capacity.

Types of compliance measurements

  1. Static compliance : This is the measurement made without taking into account the effect of the different phases of respiration. Lungs : 220 ml/cm of H2O   Lungs+Thorax : 130 ml/cm of H2O  
  2. Dynamic compliance : Compliance measurement during the difference phases of respiratory
  3. Specific compliance (Independent of lung volume) =    Compliance FRC

Factors affecting compliance

  1. Lung volume :  Smaller the lungs, smaller is the compliance. Therefore, specific compliance measurement normalizes the effect of lung size on compliance.
  2. For a given lung size, the compliance becomes less at extremes of lung volume.
  3. Compliance is more during deflation than during inflation
  4. If surface tension is more, compliance is less
  5. Compliance at Apex is less than that at Base of lungs.
  6. Compliance measured with saline is more than compliance measured with air.


Condition in which compliance is affected

  1. Compliance decreased: Pulmonary congestion, pulmonary fibrosis etc.
  2. Compliance increased:  Emphysema, old age



Alveolar surface tension

This is exerted by the film of fluid that lives the alveoli; this surface tension is less at lower lung volumes (this is due to the effect of surfactant)




1. The surface tension in alveoli is produced due to air-fluid interphase. Surfactant is made up of PHOSPHOLIPID- DI-PALMITOIL-PHOPHATIDYL-CHOLINE (DPPC)  + two major proteins having molecular weights of 32,000 and 10,000, fibrin etc.


2. It is secreted by TYPE II ALVEOLAR EPITHELIAL CELLS (type II pneumocytes) . It reduces surface tension in alveoli by not dissolving uniformly in the fluid lining the alveolar surface.


3. Instead, part of the molecule dissolves, while the remainder spreads over the surface of the water in the alveoli, thereby breaking the structure of water present inside the alveoli.


4. When the lung volume is less, the alveoli are smaller and therefore the concentration Eg. surfactant per unit area is more so more active during expiration.


5. Stability of alveoli of alveoli is mainly the function of surfactant which prevents their collapse under Surface tension.


6. Main functions:

a. It increases the Compliance

b. Reduces work of breathing

c. Prevents collapse of alveoli at end of expiration : law of Laplace(P=2T/r)

d. Prevents pulmonary edema by keeping the alveoli dry

e. Alveolar size regulation: As the alveoli increase in size, the surfactant becomes more spread out over the surface of the liquid. This increases surface tension effectively slowing the rate of increase of the alveoli. This also helps all alveoli in the lungs expand at the same rate.


7. It has high concentration in the fetal lungs at 20 weeks of gestation . However, it does not reach the surface of the lung until 28-38 weeks when it is present in amniotic fluid.  .Maximum secretion occurs at 34 weeks


8. When the lung volume is less, the alveoli are smaller and therefore the concentration Eg. surfactant per unit area is more. Consequently, the surface tension is less at lower lung volumes.

Work of breathing

Normal. 0.5 kg/m/min. 2 types

  1. Elastic work (65%)

a. Tissue elasticity (1/3rd)

b. Surface tension elasticity (2/3rd)

  1. Non-elastic work (35%)

a.  Viscous resistance (7%)

b. Airway resistance (28%)

  1. The work of breathing can be calculated from the relaxation – pressure curve.
  2. The work of breathing for the lung alone is more than that for the total respiratory system. Since the airway resistance becomes more during turbulent flow, the work of breathing is more during turbulent flow than during laminar flow.
  3. The work of breathing is increased in conditions such as emphysema, asthma, congestive heart failure

Hysteresis loop


If there were no frictional resistance due to airway and viscous resistance, the relaxation – pressure curve would be a straight line. However, because of the frictional resistance, any change in volume which is expected because of change in pressure does not happen immediately but happens after a time delay. This causes the relaxation – pressure curve to take a curved shape (instead of a straight line). This is called hysteresis.

Ventilation – perfusion ratio

Normal value for entire lung is 0.8. But at Base it is 0.6 and apex 1.3

  1. Ventilation per unit lung volume decreases from base to the apex (low due to low compliance)
  2. Perfusion decreases from base (more due to gravity)  to the apex
  3. The ventilation – perfusion ratio increases from base to apex
  4. Both Ventilation & perfusion are maximum at base but ratio is less because perfusion is more than ventilation and at apex reverse is true.
  5. As a result of less gas exchange there is wasted ventilation occurring at apex also called Alveolar dead space & pO2 is also maximum, that’s why TB of apex is more common.

2. Dead space            

  1. Since gaseous exchange in the respiratory system occurs only in the terminal portions of the airways, the gas that occupies the rest of the respiratory system is not available for gas exchange with pulmonary capillary blood this volume is called as anatomic dead space (150ml) Q.
  2. When alveolar dead space (i.e.all the air in the alveoli that is not participating in gas exchange) is included in the total measurement of dead space, this is called the physiologic dead spaceQ i.e Anatomic dead space plus alveolar dead space
  3. In a normal person, the anatomic and physiologic dead spaces are nearly equal because all alveoli are functional in the normal lung. Q
  4. Normally, physiologic dead space = anatomic dead space = 150 mL.

3. Dead space is decreased in:

  1. Females
  2. Children
  3. supine position
  4. neck fully flexed  with depressed chin
  5. low lung volumes
  6. Expiration
  7. Tracheostomy & endotracheal intubationQ (Artificial airway)

4. Dead space increased by:

  1. Males
  2. Old age
  3. Inspiration
  4. Artificial airway  with tubeQ (increased mechanical DS due to tube volume)
  5. standing positionQ (due to hypoperfusion of apical alveoli)
  6. emphysema Q
  7. gneck extension Q
  8. Ipratropium (Bronchodilation)

5. Diffusion Capacity of Lung

Definition: The diffusion capacity of the lung (DL)is defined as the volume of gas diffusing across the respiratory membrane in 1 minute when the pressure gradient is 1 mmHg.

Where k is proportionality constant
A = Area of the membrane
S = Solubility of the gas
W = molecular weight of the gas
D = thickness of the membrane


Diffusion capacity of carbon monoxide (DLCO) is taken as an index of diffusion capacity as it has a very high affinity for Hb as a result it is 0% dissolved in blood, Hence PaCO remains zero allowing 100% CO diffusion. DLO2 is never measured directly, it is expressed with DLCO as the index.
Toxicity of CO is limited to its diffusion d/t (AIIMS Nov 09)
A. The binding capacity of CO to HB with high avidity
B. CO does not diffused across the alveolar capillary membrane
C.  Decreased permeability across alveoli-blood membranes
D. Decreased diffusion across blood-brain barrier.
A The binding capacity of CO to HB with high avidity
6. Factors affecting DLCO
A. Decrease DLCO is decreased in any condition which affects the effective alveolar surface area i.e Diffusion across respiratory membrane:
  1. Hindrance in the alveolar wall. e.g. fibrosis, alveolitis, vasculitis
  2. Decrease of total lung area, e.g. Restrictive lung disease.
  3. Uneven spread of air in lungs, e.g. emphysema.
  4. Pulmonary embolism
  5. Cardiac insufficiency
  6. Pulmonary hypertension
  7. Bleomycin (upon administration of more than 200 units)
  8. Anemia-due to decrease in blood volume However, many modern devices compensates for the hemoglobin value of the patient (taken by blood test), and excludes it as a factor in the DLCO interpretation.
7. Factors that can increase the DLCO include polycythaemia, asthma (can also have normal DLCO) and increased pulmonary blood volume as occurs in exercise or congestive heart failure. Other factors are left-to-right pulmonary shunting that occurs in left heart failure, alveolar hemorrhage, and smoking within 24 hours of the test.
DLO2 = 25 mL/ min / mm Hg
DLCO2 is 20 times DLO2
Conditions in which DL is affected
  1. Perfusion limited Gas exchange: (Perfusion dependent; free flow across membrane)
    when the gas passing through equilibrates early in the course through the capillary. now the only way to increase diffusion is to increase the blood flow through the capillary. eg: O2 at rest is exchanged by perfusion limited mechanism .
  2. Diffusion limited Gas exchange (Not dependent on perfusion; diffusion across membrane is hampered),the gas in the blood and alveoli does not equilibrate even after reaching the end of the capillary. The partial pressure gradient is present even after passage thru the capillaries. eg: Carbon Monoxide & in case of restrictive lung disease , the thickening of the alveolar membrane does not allow proper diffusion across it.
  1. Lung Volumes, Capacities and Dead Space
Spirometry : Measures all volumes and capacities except those involving measurement of residual volume; Therefore, it cannot measure residual volume, functional residual capacity and total lung capacity
  1. Respiratory Volumes
    1. Tidal volume (TV) - normal volume moving in/out (0.5 L)
    2. Inspiratory reserve volume (IRV) - volume inhaled AFTER normal tidal volume when asked to take deepest possible breath (2.1-3.2 L)
    3. Expiratory reserve volume (ERV) - volume exhaled AFTER normal tidal volume when asked to force out all air possible (1.0-2.0 L)
    4. Residual volume (RV) - air that remains in lungs even after totally forced exhalation (1.2 L)
    5. Closing volume (CV) the lung volume above the residual volume of which the airways in the lower, dependent parts of the lung begin to close off because of lesser transmural pressure in these areas. This phenomenon is called as Dynamic Compression of airways). If CV> FRC collapse of lungs takes place example RDS due to increased Surface tension.
  2. Respiratory Capacities: Sum of 2 or more volumes
    1. Inspiratory capacity (IC) = TV + IRV (MAXIMUM volume of air that can be inhaled) 3-4 L
    2. Functional residual capacity (FRC) = ERV + RV (measured by Helium dilution method, nitrogen washout method & Plethysmography) 2.5 L. Also called relaxation volume as recoil of chest wall is balanced by lung recoil at this volume.
    3. Vital capacity (VC) = TV + IRV + ERV (max. insp. followed by max exp.) 4.8 L in Males & 3.2 Females.
    4. Total lung capacity (TLC) = TV + IRV + ERV + RV (the SUM of all volumes; about 6.0 L).Depends on lung compliance if compliance is more so is the TLC eg. emphysema

Dynamic Lung Volumes & Capacities

  1. Forced vital capacity (FVC) - total volume exhaled after forceful exhalation of a deep breath
  2. FEV1 amount of air expired in 1st second normal value 80%, FEV2 - 95%, FEV3 – 100%
  3. Minute respiratory volume (MRV) or PV - total volume flowing in & out in 1 minute (resting rate = 6 L per
  4. Maximum Breathing Capacity (MBC) – Maximum air that can be moved in or out of the lungs per minute.90-170 Litre/min   


Peak Expiratory Flow

This is the speed of the air moving out of your lungs at the beginning of the expiration, measured in liters per second. It is effort dependent (on strength of expiratory muscles) 5-15 L/sec


Forced Expiratory Flow 25–75%

This is the average flow (or speed) of air coming out of the lung during the middle portion of the expiration. It is effort independent and depends on the small airway resistance. Very sensitive indicator for bronchial asthma.3-5L/sec



Obstructive lung disease

Restrictive lung disease

Residual volume






Total lung capacity

Normal to increase


Diffusion capacity

 Normal  (exceptemphysema)


Vital capacity



FEF 25-75%



FEV1/FVC (Most Imp)


Normal to increase


  1. Pulmonary plethysmographs are commonly used to measure the functional residual capacity (FRC) of the lungs—the volume in the lungs when the muscles of respiration are relaxed—and total lung capacity.
  2. In a traditional plethysmograph, the test subject is placed inside a sealed chamber the size of a small telephone booth with a single mouthpiece. At the end of normal expiration, the mouthpiece is closed. The patient is then asked to make an inspiratory effort. As the patient tries to inhale, the lungs expand, decreasing pressure within the lungs and increasing lung volume. This, in turn, increases the pressure within the box since it is a closed system and the volume of the box compartment has decreased to accommodate the new volume of the subject. And during forceful expiration the lung pressure increases and chamber pressure decreases as thorax occupies less volume inside the chamber i.e decompression of chamber.mcq 2011 AIPG
  3. Boyle's Law is used to calculate the unknown volume within the lungs. First, the change in volume of the chest is computed. The initial pressure and volume of the box are set equal to the known pressure after expansion times the unknown new volume. Once the new volume is found, the new volume minus the original volume is the change in volume in the box and also the change in volume in the chest. With this information, Boyle's Law is used again to determine the original volume of gas: the initial volume (unknown) times the initial pressure is equal to the final volume times the final pressure.
  4. The difference between full and empty lungs can be used to assess diseases and airway passage restrictions. An obstructive disease will show increased FRC because some airways do not empty normally, while a restrictive disease will show decreased FRC. Body plethysmography is particularly appropriate for patients who have air spaces which do not communicate with the bronchial tree; in such patients gas dilution would give an incorrectly low reading.
  5. Obstructive lung disease  include : Asthma, Bronchiectasis, chronic bronchitis & Emphysema (COPD), Bronchiolitis, Cystic fibrosis
  6. Restrictive lung disease include:
    1. Interstitial lung diseases (the most common of which are sarcoidosis, rheumatoid lung, scleroderma lung, the pneumoconioses, histocytosis X, lymphangitic carcinomatosis, and idiopathic pulmonary fibrosis)
    2. Chest wall deformities (kyphoscoliosis, Ankylosing spondylitis, thoracoplasty)
    3. Pleural fibrosis
    4. Alveolar-filling disease (alveolar proteinosis, alveolar cell carcinoma, des­quamative interstitial pneumonia, and alveolar microlithiasis)
    5. Neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis,GB syndrome, Diaphragmatic palsy)

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