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Ch. 7 Mechanics of Breathing
Muscles of Respiration
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Inspiration
o Nutshell: external intercostals & diaphragm contract resulting in an increase in SA  increase in Vol,
resulting in a decrease in pressure in the intrapleural space (-8 mm Hg), that negative pressure
transferred to the alveoli (-1 mm Hg), thus creating a negative pressure gradient which draws air in
from the mouth/nose where pressure is 0, to the alveoli
Diaphragm
o Most important muscle of inspiration
o Supplied by phrenic nerve ( via Cervical nerves 3,4,5)
o Has most tension upon exhalation giving it greater force of contraction (lengthened  starling force)
o Contraction leads to increased vertical dimension of thoracic cavity
o Simultaneously, the external intercostals contract increasing surface area of chest wall (bernoulli’s
principle increase SA decrease force on chest wall, thus increasing the pressure from the inside against
the pleural cavity further establishing a negative pressure gradient)
o Paradoxical movement -- If the diaphragm is paralyzed – it moves up instead of down
External Intercostals
o Connect adjacent ribs and slope downward and forward
o Contraction leads to the ribs being pulled upward and forward, and they rotate on an axis joining the
tubercle and head of rib
 Contraction leads to increase in both the lateral and anterioposterior diameters of the thorax
(bucket-handle, and pump handle)
o Supplied by intercostals nerves that exit the spinal cord (thoracic and some lumbar)
o Paralysis does not completely eliminate inspiration d/t force of diaphragm contraction
o i.e. a lesion in the spinal cord below cervical nerve 5 – person is still capable of independent respiration
Accessory muscles of inspiration
o Include the scalene, pectoralis major and sternocleidomastoid muscles – serves to further elevate the
sternum
 Tripod position – leaning forward with arms on knees (i.e. post exercise) allows the pectoralis
major to serve as an accessory inspiratory muscle
 Nasal flaring also involves muscles but does fairly little compared to the previous muscles
Expiration
o Passive during resting breathing
o Elastic recoil of lung is primary “restoring force” for equilibrium position
o During exercise and voluntary hyperventilation – expi becomes active
 Active expiration
 Uses abdominal muscles (rectus & transverse abdominus and external obliques) and the
internal intercostals
 When these muscles contract intra-abdominal pressure is raised which then raises the
diaphragm upward  pushing air out of the lungs (note: increasing the pleural pressure
does not subsequently increase flow of air out of the alveoli because you increase
pressure on the alveoli as well as the airway)
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Internal intercostals
o Pull the ribs downward and inward  decreasing thoracic volume
Respiratory Muscles Summary
o Inspiration is active; expiration is passive during rest
o Diaphragm is the most important muscle of inspiration; it is supplied by phrenic nerves which originate
high in the cervical region
o Other muscles include the intercostals, abdominal muscles, and accessory muscles
Elastic Properties of the Lung
Pressure – Volume Curve
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Intrapleural pressure forms an airtight seal with only a few ml of fluid
Intrapleural pressure: -8 mm Hg at apex, -3 mm Hg at base
Hysterisis
o Important point: the lungs have a greater volume if that volume is reached upon expiration than if that
volume is reached upon inspiration
o When the lung is inflated with air, the two curves become separated; the inflation curve is shifted to the
right of the deflation curve
o Separation of the deflation and inflation curves is termed hysteresis
o Why? (thanks to Schwarzstein)
 Surfactant enters into the liquid surface layer after the initiation of inhalation and begin to
reduce surface tension
 Thus, the initial part of the inflation curve is relatively flat; b/c surface tension is high and
compliance is low
 As the density of surfactant in the surface layer increases, surface tension decreases and
compliance increases; the slope of the curve becomes steeper
 Eventually, as the volume of the alveolus continues to increase, surfactant density remains
constant and the elastic recoil forces of the lung become the primary explanation for the
changes in compliance
 At high lung volumes (inspi) the elastic recoil of the lung increases, compliance decreases and
the slope of the curve begins to flatten
 During deflation (expi) the density of surfactant rapidly increases, thus surface tension
decreases, and the initial portions of the deflation curve are relatively flat
 In essence, alveolar pressure decreases, but b/c of a simultaneous decrease in surface
tension  little change in volume occurs
 Surfactant thus has a greater effect on compliance of the lung during exhalation than during
inhalation
 At the end of exhalation, even w/ surfactant present, some alveoli collapse (esp. at bases) where
transpulmonary pressure becomes negative (refer to earlier summary for explanation of
transpulmonary/transmural pressure)
 Critical opening pressure – the greater delta P necessary to re-open collapsed alveoli
 Stress relaxation – when one inflates the lung at a higher volume for several seconds, the elastic
recoil forces appear to diminish slightly
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Stress recovery – after deflation of the lung, the recoil forces increase
Stress adaptation = stress recovery & stress relaxation
 Plays a minor role in hysteresis
Pressure-Volume Curve of the Lung
o Nonlinear with the lung becoming stiffer at high volumes
o Shows hysteresis b/t inflation and deflation
o Compliance is the slope: delta V / delta P
o Behavior depends on both structural proteins (collagen, elastin) and surface tension
Compliance
o A measure of stiffness of a closed container such as a balloon; the change in volume that occurs in the
object divided by the change in pressure across the wall of the object.
o C = delta V / delta P
o Higher compliance = more flexible, less rigid
 Emphysema – causes increase in compliance
 Aging and asthma also increase compliance
o Lower compliance = less flexible, more rigid
 Unventilated regions in the lungs increase in compliance
 Fibrosis – causes decrease in compliance
 Increased pulmonary artery pressure resulting in engorgement
Normal range of lung compliance 200 ml h2o
o Compliance of lung depends on size
o Elastin and collagen surround the alveolar walls and bronchi
 Increased volume of the lung thereby increase the compliance and the transmural pressure
within the airways and bv’s
 Mesh stocking analogy (bv’s and airways are tethered to the lung)
Surface Tension (alveolus as a bubble)
o a bubble consists of a pherical film of liquid soap surrounding a gas, there are:
 gas-liquid & air-liquid interactions
 interactions give rise to surface tension
 Surface tension = the force with which a surface contracts per unit length of surface and has the
units (dynes/cm (squared))
o a bubble within liquid – surrounded by equal pressure
 because of equal surrounding force – no net movement
o a bubble at the surface – exposed to both air and liquid forces
 uneven forces act upon the bubble (i.e. lateral strongest, less on surface)
 uneven pressure results in net force toward the center of the bubble
 net effect: bubble contracts and strength of that contraction = surface tension
o Surface tension allows a leaf to float on water
Law of laplace: P = 2T/r
 Bubbles with a small radius have greater pressure than bubbles with a large radius
 As the radius of the bubble decreases it requires an increasing pressure in the bubble to offset
the surface tension and prevent collapsing
 i.e. Surfactant: reduces surface tension and therefore prevents collapse of the bubble (i.e.
alveoli)
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Surfactant
o Helps keep the alveoli dry
o Reduces the surface tension of the alveolar lining layer
o First thing inspired air comes into contact with
o Produced by type II alveolar epithelial cells
 Generally at week 20-23 during Canalicular embryonic period
o Contains dipalmitoyl phosphatidylcholine
o Absence results in reduced lung compliance, alveolar atelectasis, and tendency to pulmonary edema
Lungs display interdependence
o Refer to link:
 http://www.medicalexplorer.org/resp_phys1/index.php?ch=4&fig=9
 http://www.medicalexplorer.org/resp_phys1/index.php?ch=2&fig=10
Cause of regional differences in ventilation
o Alveoli at apex:
 decreased compliance
 start at greater initial volume: thus less change upon inhalation
 lung is easier to inflate at lower initial volume
 decreased blood flow d/t gravity
 More negative intrapleural pressure (-8 mm Hg)
 Greater PAO2 (wasted ventilation)
o Alveoli at base
 Increased compliance
 Start at lower initial volume: thus greater change upon inhalation
 Increased blood flow (hyperperfuse / wasted blood flow)
 Lower PAO2
 Less negative intrapleural pressure (-3 mm Hg)
o Lung at VERY LOW VOLUMES
 Apex ( increase in pressure from -8 to -3)
 Base ( increase in pressure from -3 to +3)
 Due to positive pressure in base, subsequent positive transmural pressure results in lower
airways and they collapse
 Normal distribution of ventilation is inverted, the upper regions ventilating better than the
lower regions
o Airway Closure
 Compressed region of lung does not have all of its gases expelled
 During expi, region of respiratory bronchioles close first, this trapping air in the alveoli distal to
the closure (at pt. where transmural pressure becomes negative = pt. of collapse)
 Old people – airway closure occurs in lowermost regions
 Schwarzstein says: decreased compliance, and increased resistance in primary
conducting airways
 West says: decreased elastic recoil, and decreased intrapleural pressure
 Seen in chronic lung disease
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Elastic Properties of Chest wall
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Resting potential of chest wall is outward
Resting potential of lungs is inward
Thus if pneumothorax occurs: lungs recoil, and chest expands
o i.e. if air is introduced to the intrapleural space resulting in + pressure
outward force of chest wall is countered by the inward recoil of the lungs thus little work is required for normal
breathing
FRC: where the outward force of chest is equal to the inward force of lungs
o Note the airway pressure (x-axis) in fig 7-11, is replaced by transmural pressure (in schwarzstein)
o Thus above FRC (inspi) a positive transmural pressure is maintained
o The chest wall line drawn to the right of “airway pressure” is where the thorax is hyper-extended and
therefore above it’s resting capacity to expand and subsequently becomes an inward (restoring force)
o To the left of the 0 line is a negative transmural pressure, thus below FRC the transmural pressure
becomes negative ( how collapse can occur )
 Collapse is prevented by the cartilage in the main airways and the gradient of airflow (i.e. as
pressure becomes positive it is still less positive than the pressure at the mouth  thus air flows
from alveoli to the mouth and the cartilage prevents collapse in the airway)
Relaxation Pressure-Volume Curve
o Elastic properties of both the lung and chest wall determine their combined volume
o At FRC, the inward pull of the lung is balanced by the outward spring of the chest wall
o Lung retracts at all volumes above minimal volume
o Chest wall tends to expand at volumes up to about 75% of vital capacity
Airway Resistance
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Similar to V=IR; Q = delta P x R
o or delta P = Q/R
Turbulent flow
o Flow is proportional to Velocity squared
o Long tube of conducting airways serves to increase flow
o Greatest resistance is in the Conducting airways  thus highest velocity
 Turbulent flow results
Laminar Flow
o Flow is directly proportional to velocity
o Flow is linear with the highest velocity in the center of the tube, and molecules around the edges
encounter friction reducing velocity
o As air reaches the alveoli (branches are in parallel, thus surface area is drastically increased and the flow
essentially goes to zero)
o Furthermore, since each subsequent bronchiole division is wider and shorter in length, velocity is further
decreased
o flow becomes laminar allowing diffusion to occur
o velocity profile – air in center is twice as fast as velocity near edges of tube
Reynolds number (Re)
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Increased Reynolds number = likelihood of turbulent flow
Re is directly proportional to: velocity, radius, and viscosity
 And inversely proportional to density
 i.e. why heliox (He + O2) is given to people with laryngeal spasm  decreased density of helium
compared to nitrogen allows oxygen velocity to reach the alveoli in spite of increased resistance
in trachea
o Re > 2000 = turbulent flow
Laminar and Turbulent Flow
o In laminar flow, resistance is determined by the 4th power of the radius
o In laminar flow, the velocity profile shows a central spike of velocity
o Turbulent flow is most likely to occur at high Reynolds numbers, that is when inertial forces dominate
over viscous forces
Measurement of Airway Resistance
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Pressure difference b/t the alveoli and the mouth divided by flow rate
R = delta P / Q
Again, resistance is highest in the conducting airways
Pressures During the Breathing Cycle
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Mouth = 0 mm Hg
Intrapleural pressure = -5 mm Hg (avg.)
Alveoli = -1 mm Hg
As one inspires, the intrapleural pressure moves towards -8 mm Hg (decreases) d/t increased volume of thoracic
cavity
o Negative pressure is transferred to the alveoli as they expand
o Pressure gradient between mouth and alveoli drives air into the lungs
As one expires, the intrapleural pressure is less negative (-3 mm Hg)
o Pressure in the alveoli becomes positive (+1 mm Hg)
o Pressure at mouth is still 0
o So air follows the gradient from the alveoli to the mouth
o Increased Velocity occurs d/t:
 Drop in pressure as air passes through the increased resistance results in increased velocity
(bernoulli’s principle)
 i.e. lake  river  stream (w/ rapids)
 total cross sectional area diminishes  increased velocity
 change from laminar to turbulent flow decreases pressure more (work is done)—heat is
produced
 Note: flow doesn’t change, only the velocity changes
o http://www.medicalexplorer.org/resp_phys1/index.php?ch=4&fig=3&s=24
o http://www.medicalexplorer.org/resp_phys1/index.php?ch=3&fig=10
Chief site of airway resistance
o Greatest pressure drop occurs in medium-sized bronchi (5th division)
o Silent zone – peripheral airways
 Contribute very little to resistance
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Early detection of disease – can be present before usual measurement of airway resistance can
detect an abnormality
Factors determining Airway Resistance
o Bronchi are supported by radial traction
o Conductance vs. Resistance = linear relationship
 Conductance = ease through which air passes
 Resistance = difficulty through which air must overcome to pass
o As lung volume is reduced, airway resistance rises rapidly
o Contraction of bronchial SM – narrows the airways and increases airway resistance
 i.e. d/t irritants such as smoke
 innervated by Vagus nerve
 Beta 2 agonists – albuterol  bronchodilators
 Rx. For asthma
 Parasympathetic activity – causes bronchoconstriction
 Sympathetic activity – bronchodilation
 Fall in PCO2 causes bronchoconstriction (don’t want CO2 you have, to escape)
Airway Resistance
o Highest in the medium-sized bronchi; low in small airways
o Decreases as lung volume rises b/c the airways are pulled open (tethered)
o Bronchial SM is controlled by the ANS; stimulation of Beta-adrenergic receptors causes
bronchodilation
o Breathing a dense gas as in diving increases resistance
Dynamic Compression of Airways
http://www.medicalexplorer.org/resp_phys1/index.php?ch=4&fig=12A
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Upon expiration – maximal flow occurs at initial expiration
It can be seen that at high lung volumes, the expiratory flow rate continues to increase with effort
Effort independent: At mid or low volumes the flow rate reaches a plateaus and can’t be increased with further
increase in intrapleural pressure
o This is because the increased pressure by the pleura affects both the alveoli and the airway
http://www.medicalexplorer.org/resp_phys1/index.php?ch=4&fig=10B
http://www.medicalexplorer.org/resp_phys1/index.php?ch=4&fig=13
Equal Pressure Point = where transmural pressure =0, collapse occurs when PTM becomes negative
Limits air flow in normal subjects during a forced expiration
May occur in diseased lungs at relatively low expiratory flow rates thus decreasing exercise ability
During dynamic compression flow is determined by alveolar pressure minus pleural pressure (not mouth
pressure)
Is exaggerated in some lung diseases by reduced lung elastic recoil and loss of radial traction on airways
May occur during normal expiration d/t disease
Forced Expiratory volume – vol. of gas that can be exhaled in 1 second at TLC
Forced Expiratory flow—avg. flow rate measured over the middle half of the expiration
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Causes of Uneven Ventilation
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Time constant = Compliance x Resistance
Largely due to the elastic recoil force of the lungs
o Diseases that alter the elastic recoil of the lungs thereby affect the time constant
A measure of how rapidly gas is moved into and out of the alveoli; provides information about the rate at which
gas is replenished within an alveolus.
Higher time constant = poorly ventilated regions of the lung
Short time constant = rapid exchange
Concept offers explanation for the shape of the flow-volume loop in pt w/ emphysema
o i.e. provide oxygen to pt. w/ emphysema
o air that exits first is from areas of lung w/ short time constant
o intermediate zone demonstrates expiratory coving
 expiratory coving – concave upward appearance in what is usually linear flow following max.
exhalation
o finally, the most diseased units will empty very slowly with low flows (seen near RV on flow-vol. loop)
Uneven diffusion w/in resp. zone
o Dilation of the of the airways in region of resp. bronchioles  increases the distance to be covered by
diffusion (i.e. leading to decreased perfusion and increased time constant)
o w/ uneven diffusion – gas is unevenly distributed w/in resp. zone b/c of uneven ventilation along the
lung units
Tissue Resistance
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Pulmonary resistance – pressure required to overcome the viscous forces within the tissues as they slide over
one another
o Different from airway resistance
o 20% of total resistance, although may increase in disease states
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Work of Breathing
http://www.medicalexplorer.org/resp_phys1/index.php?ch=4&fig=8&s=24
Work is required to move the lung and chest wall : W= P x V
Work done on the lung
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Inspi
ABC – intrapleural pressure
0ABCD0 – work done on the lung (by thorax + pleura + lungs)
0AECD0 – work to overcome elastic forces
ABCEA (hatched) – work overcoming viscous (airway & tissue) resistance
Expi
AECFA – work required to overcome airway (+tissue) resistance
 Normally = to 0AECD0, making energy stored from inspi, usable for expi; thus decreasing the
work necessary for expiration/passive respiration
Pt’s with reduced compliance (fibrosis) take small rapid breaths
Pt’s with air obstruction (increased resistance) breathe more slowly
Both serve to reduce work done by the lungs
With increased compliance:
 C lies further to the right
With increased resistance
 The curve from A to B to C is stretched to the right (i.e. more work done on inspi)
Hatched area = intrapleural pressure (fx. Of vol. as you breathe)
D = alveoli
Total Work of Breathing
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Efficiency % = [ (useful work) / Total energy expended (or O2 cost) ] x 100
Normally 5-10%
With voluntary hyperventilation  30%
With OPD – efficiency may limit exercise tolerance