Lung mechanichs-1.pptx

Lung mechanichs
STATICS & DYNAMICS
BY DR.Mohammad albeetar

Agenda
• *Muscles of Respiration * Elastic Properties of the Lung
• *Pressure-Volume Curve *Compliance &Surf ace Tension
• *Regional Differences in V *Airway Closure
• *Chest Wall elasticity * Airway Resistance
• *Air flow Through Tubes *Measurement Airway Resistance
• *P During the Breathing cycle *Chief Site of Airway Resistance
• *Factors Determining Airway Resistance
• *Dynamic Compression on Airways* Causes of Uneven Ventilation
• *Tissue Resistance *Work of Breathing
12/23/2022 PRESENTATION TITLE 2

Muscles of Respiration
• INSPIRATION :-
• The most important muscle of inspiration is the diaphragm. It is
supplied by 2 phrenic nerves from cervical segments 3, 4, and 5
• When it contracts”shortens”the abdominal contents are forced
downward and forward, and the vertical dimension of the chest cavity
is increased. So increase in abdominal pressure and intrapleural
pressure will decrease
• In addition, the rib margins are lifted and moved out, causing an
increase in the transverse diameter of the thorax .
• .

• In normal tidal breathing,the level of the diaphragm moves about 1-2
cm
• Paradoxical movement inphrenic nerve palsy,cane be detected upon
asking the pt to sniff , it diaphragm will contract upward

• The external intercostal muscles connect adjacent ribs and slope
downwards and forward. When they contract, the ribs are pulled
upward and forward, causing an increase in both the lateral and the
antero-posterior diameters of the thorax. The lateral dimension
increases because of the “bucket-handle” movement of the ribs.
• The accessory muscles of inspiration include the scalene muscles,
which elevate the first two ribs, and the sternomastoids, which raise
the sternum.

• EXPIRATION :-
• This is passive during quiet breathing. The lung and chest wall are
elastic and tend to return to their equilibrium positions after being
actively expanded during inspiration.
• The most important muscles of expiration are abdominal wall
muscles (rectus abdominis, internal and external oblique muscles,
transversus abdominis) and Internal intercostal muscle.

Pressure-Volume behavior of the lungs
• Experiment:
*lung inside a jar ,and we able to decrease the pressure inside the jar
by a vacuum pump, and pressure measurement
* the lung cannulated and connected to spirometer

P= pressure C=compliance,
R= resistance V=voulme
• The pressure inside the lung is atmospheric ,i.e zero
• The P is measured with respect to atmosphere if we say the P is
negative we mean that its below atmospheric P
• Even without inflation of the lung there is a small volume (the
minimal volume)
• Turn on the pump and reduce the pressure in the jar to -5cm/h2o ane
measure the lung volume, then decrease the P to -10 cm/h2o and
measure the V ,and so on . down to -30cm/h2o{inspiratory limb} then
we go with the pressure back to zero( expiratory limb)
• Then we plotted the measurements in both inspiration and expiration

Observation on the curve
• non-linear
The p needed to inflate the lung follow a non-linear values, where the
lung became stiff and less compliant at large volumes, this area
represent the force inspiration P-V association where we need higher
pressure for a small volume change
{not like the curve of length-tension of a coiled spring,where the strain
is proportional to the stress”hookes law)
• Hysterisis :
the lung behavior path during expiration lag behind the inspiration

Pv: intra-alveolar P,,, Pp: intrapleural P
• At a given lung volume, the P difference between the lung and
surrounding( the transpulmonary pressure) will be the same, i.e if we
close the canula and change the jar Pp{the Pv inside the lung will
change in the same difference ,whether the Pp was negative or
postive
• In human body we don’t measure the intrapleural-pressure,instead
we measure the esophagus pressure hich is also around the lung in
mediastinum

Compliance of the lung “C”
• Change in volume/change in pressure C=V/P
• In normal lung, the baseline before inspiration is at FRC{functional
residual capacity = RV+FEV
• If we start at FRC ,Pp= -5, and increase the Pp by 1 cm/h2o,the
change in volume will be 200 ml/cm h2o, which is about the normal
compliance of the lung at FRC

• Specific compliance : used in comparative physiology ,for ex: human
lung vs mouse lung
• Compliance increase with age
• Compliance increased IF Volume increased, human lungis more
compliant than mouse lung, adult lung is more compliant than
pediatric lung; ..
• conditions with low C of the lung : fibrosis, pulmonary edema, chronic
unventilated lung esp with low volume will ends in atelectasis
• conditions with high compliance : emphysema and aging lung

• What causes the elasticity of the lung “the P-V behavior”:
*Tissues inside the lung {elastin and collagen},mainly due to
geometrical change in fibers, NYLON-stocking elasticity behavior, rather
than the elasticity of the fibers themselves
*Another mechanism that increase elasticity is the surface tension

Surface Tension
*Measurement of force/unit length “dynes/cm h2o”
*attractive forces acting across 1 cm of imaginary line between
adjacent molecules ,ex: air bubble/ballone
*Can be predicted from LaPlace's law of circles/curved surfaces
P =4T/r r=radius T= surface tension
*Small r will increase the P, small alveoli P greater than large alveoli

• Why the small alveoli doesn’t blow the large one , surfactant
*Discovery of surfactant, evidence of the presence of low surface
tension led to surfactant discovery
*2 evidences of low surface tension of the lung:
1-saline filled lung easier to inflate than air filled lung, more compliant
+ less hysteresis{saline abolishes the lung surface tension}
2-stability of air bubbles from lung –wash foam{low surface tension}

SURFACTANT
• Phospholipid DPPC DiPalmitoylPhosphatidylCholine, synthesized in
the lung from blood fatty acids extaction or from fatty acids
synthesized in the lung,that’s why if embolus blocks the blood
perfusion the surfactant quantity will decrease in affected area
• Formed late in pregnancy,starts between 24-28 weeks of pregnancy,
Premature babies develops respiratory distress
• From type 2 alveolar cells

Observations:
*pure saline Surface Tension around 70dynes/cm h2o,regardless of the
area of its surface , no hysteresis
*adding a detergent reduced the surface tension around 30 regardless
of the surface area , no hysteresis
*adding lung wash, reduced the surface tension with hysteresis,surface
tension changes greatly with surface area, it falls to extremely low
values when area is small, {actually the surfactant surface tension itself
is difficult to measure coz its very low},that why small alveoli doen’t
collapse and blow the larger alveoli

Mechanism of work of surfactant
• Dppc has 2 sides, hydrophilic and hydrophobic ,they arranges in a way
that their intermolecular repulsive forces opposes the attractive
forces of the surface
• If the surface area is small the surfactant molecules willbe crowded
will increase effect
• Surfactant: *decrease surface tension, which increases the
compliance, which decrease the work of breathing
*prevent collapse and increase the stability of the lung
*keeps the alveoli dry, by decreasing the hydrostatic pressure ,which
will decrease the transudate from capillary and oedema

Regional difference in ventilation
• Pp around the base of the lung is greater {less negative} than Pp
around the apex coz of the lung weight
• Pv inside the lung = atmospheric P = zero
• Expanding pressure = Pv – Pp =
• At the apex : Pv-Pp = 0 –(-10)= 10 cm/h2o
• At the Base : Pv-Pp = 0*{-2} = 4 cm/h2o

• another mechanism that increase the stability of alveoli :
• Alveoli surrounded by other alveoli and they support each other, if
tendency to collapse increased,the expanding pressure from
surrounding parechymaincreases “ inter-dependence”

Regional difference in ventilation
• Pp around the base of the lung is greater {less negative} than Pp
around the apex coz of the lung weight
• Pv inside the lung = atmospheric P = zero
• Expanding pressure = Pv – Pp =
• At the apex : Pv-Pp = 0 –(-10)= 10 cm/h2o
• At the Base : Pv-Pp = 0*{-2} = 4 cm/h2o

• So at the Base: expanding pressure is less than at the apex , this will
cause less RV at the base, and will increase the expansion during
inspiration more than at the apex
• In other words, Ventilation at the base is greater than ventilation at
the apex
• In disease where Pp increases {pneumothorax,effusion..} collapse,no
ventilation esp if Pp became +ve
• At FRC ,the steep part of the curve
• At RV, Pp is positive after forceful expiration, there will be no
ventilation until Pp became negative

Regional differences in ventilation at RV
will result in n
• At RV, Pp is positive after forceful expiration, there will be no
ventilation until Pp became negative
• All Pp will increase and became less negative {coz of lower lung
volume and then lower elastic recoil of the lung} , and this will cause
no ventilation at the Base at RV, but the Apex now in the steep part in
the curve
• Direct evidence of this regional difference,size of the alveoli

Why RV can’t be expelled with forceful
expiration?
• Because with forceful expiration,even so that Pp will became *ve, the
airway closure or collapse will prevent expelling of RV
• In practice: the compressed part of the lung, respiratory bronchioles
will close first, thus trapping of gas in the distal alveoli,
• this closure occurs only at very low lung volumes at RV in young
subjects,but in elderly subjects,with apparently normal lung, the
closure will present at larger volumes at FRC, coz of decrease elastic
recoil with aging, causing higher Pp compression effect,resulting in
intermittent ventilation at the lower most lung regions, decrease gas
exchange

Chest wall elasticity
• Chest wallis elastic and change its volume with Pp changes , ex:
pneumothorax, the collapsed lung will be pulled inward ,the chest
wall pulled outward

• Relaxation pressure of the lung alone {i.e airway pressure is zero}is at
RV
• Relaxation pressure of the chest wall alone {airway pressure is zero} at
75% of VC
• Actual relaxation point of both chest wall-lung is at FRC

Air flows through the tubes
• 3 types:
1-Laminar flow: low flow rate , stream parallel to the wall
2-Transitional flow: intermediate flow rate with eddy formation zt
branches
3-Turbulent flow ;high flow rate,

Laminar flow
• In a straight circular tubes, the volume flow rate is
F= Pπr*4/ 8nl = Poiseuille equation
P=driving pressure between alveolar and airway
r= radius n= viscosity l=length
FLOW resistance R= P/F =8nl/πr*4 ,so if r halved the R will increase 16
folds, but if l doubled the R will increase by double, R can be measure
by Pmouth-Palveoli/flow rate
Viscosity of the gas not density, so viscous gas flow will be laminar
Velocity profile : high axial flow low Re

Turbulent Flow
• The flow is turbulent not parallel to walls
• P = Kf*2 k is a constant,pressure is proportional to flow square
• Viscosity of the gas became relatively unimportant, but increase in
density of the gas will increase the pressure drop
• No high axial flow
• High Re above 2000,high velocity, large diamter

• Re = Reynold number = 2rvd/n
Re will determine the flow type,
if viscous gas =low Re =laminar flow
If dense gas = high Re = turbulent flow
Law density gas such as helium tend to produce less turbulent, used in
diving helium-o2 mixture to decrease work of breathing

Quick summary for part one lung mechanics
*Muscles of breathing
*pressure-volume curve is not linear,and shows hysteresis picture,unlike the spring,at a given lung volume, the
P difference(transpulmonary pressure}will be the same, Pv & Pp values changes With the same difference
• compliance C=V/P around 200 ml/cm h2o which increases with age and increasing volume { Human>
mouse,emphysema} mainly due to geometrical change in fibers, NYLON-stocking elasticity behavior, rather
than the elasticity of the fibers themselves and suface tension & surfactant, LaPlace's law of circles/curved
surfaces P =4T/r , small alveoli P greater than large alveoli P
• Regional diff in ventilation picture,At FRC ,the steep part of the curve ,base ventilation >apex Where At RV,
Pp is positive after forceful expiration, there will be no ventilation until Pp became negative so the apex
ventilation>base, Direct evidence of this regional difference,size of the alveoli picture
• Why RV can’t be expelled with forceful expiration?airway closure picture.Relaxation pressure-volumes curve
• 3 types of flow picture Poiseuille law to detect the flow-volume pictures,if r halved the R will increase 16
folds, but if l doubled the R will increase by double,Re = Reynold number = 2rvd/n Re will determine the flow
type,
• if viscous gas =low Re =laminar flow ,,If dense gas = high Re = turbulent flow

type,

than the elasticity of the fibers the mselves and suface tension & surfactant, LaPlace's law of circles/curved
type,

type,

In practice, the flow types:
• Because of complicated airway system the application of those
priciplles is difficult ,
• Most of the flow is transitional
• Laminar flow can occur in terminal bronchioles where Re is low
around 1
• Turbulent flow may occur in trachea with forceful expiration esp in
exercise
• P1-P2 = driving pressure

Pressure & Flows during Breathing Cycle

*a subject is breathing into a spirometer {volume}normal TV
*Flow meter { with wire screen in the airway , laminar flow coz of the
wire screen,}flow rate
*Ballone in the esophagus to estimate Pp
*Alveolar pressure from body box Plethysmograph or calculated
During inspiration : Pp decreases, Pv decreases, flow increases and
reaches its maximum value in mid inspiration and mid expiration

• Diaphram contraction ,increase intrapleural space, decrease PV to
intiate flow from mouth{without difference no flow wil be detected}
& Pp decreases coz of not only Pp decrease{the interrupted line}but
an additional fall in Pp caused by the fall in Pv , vertical distance is
the same of alveolar pressure
In normal lung, P difference of only 1 cm is enough to initiate a flow
But in OLD the P difference needs to be larger coz of increase
resistance , to initiate flow

Factors determining airway resistance
• Which airway in the lungs contripute to most airway resistance?
• It was thought that small airways contribute to most of resistance coz
of R proportional to r*4 on Poiseuille equation, but in practice it’s the
medium sized airways ,why?
• After direct measurements of the pressure drop along the bronchial
tree its found that medium sized bronchioles is the primary site of
resistance, more than small sized airways although its narrower, they
are numerous around 50000, less than 20% of pressure drop happens
in small airways,{ the sum of R}

• This fact is important, because it will make the detection of
abnormally rising small airway resistance difficult, so considerable
small airway disease can be present before medical investigation can
detect it
• Resistance has inverse relationship with lung volume, and so small
airways at very low lung volumes{at the buttom} will close with high
Resistance, and that’s why in OLD pt often breath at high volumes
because with increase TV,R decreased

Continue ..factors affecting the R
Bronchial smooth muscles :
• Sympathetic activation causes airway dilatation, as do epinephrine
• Parasympathetic activation: bronchoconstriction
• Broncho-constriction may occur by reflex from irritants-stimulation of
receptor in trachea and large airways
• Co2 decrease R by direct action on bronchial smooth muscles
• Histamine causes smooth muscles constriction

Density & viscosity of the inspired gas
During diving the increase in pressure causes increase in resistance coz
this increase in P will increase the density of the gas, hence the use of
helium-o2 mixture
The fact that changes in density rather than viscosity have such an
influence on R is evidence that flow isnot purely laminar in medium
sized airways

In obstructive lung diseases
• High R
• Abnormally low alveolar pressure during inspiration and abnormally
high during expiration, because when R increases , the driving P
between the mouth and alveoli must increase to maintain the flow
• How does hyperinflation affect airway resistance during
exacerbation? Hyperinflation increases lung volume which in turn will
decrease R, but inspite of that ,the airway R still higher than normal
• Overinflation :high lung volumes .decrease compliance, stiff lung

Dynamic compression of airway

• 3 patterns of breathing patterns,
A ; forceful inspiration and expiration>>high Flow rate
B ;starts with slow expiration then accelerates
C ; submaximal flow
Notice that all have the same path at the end with the same flow rate,,
i.e something is limiting the flow, flow here is effort-independent

Isovolumic pressure-flow curve

• Each curve represent The sum of series of pressures at a given volume
for the same subject
• Notice that : at high volume the flow rate continue to increase with
increasing effort even at the ends of curve,but at low and middle
volumes the curve became effort –independent at the ends, why?
• Because of airway closure

• During forceful expiration :
the Pp became larger than airway P , transpulmonary = 11 difference ,
causing closure of the airway, here at the collapsed airway the airway P
increases and became the same as Pp = 30 cm h2o,
At this point the Pv – AIRWAY p = 8; i.e the driving pressure causng the
flow , and even if we exhale with more effort, the Pp will increase but
stays equal to P airway , Pv will also raise with the same value, the
driving pressure will stay the same, and that’s why its effort
independent, its resemble the starling resistor effect
This is a very important mechanism in pts with lung disease

factors exaggerate this flow-limiting mechanism.
• Any increase in resistance o the peripheral airways because that
magnifies the pressure drop along them and thus decreases the
intrabronchial pressure during expiration (19 cm water in D).
• Another is a low lung volume because that reduces the driving
pressure (alveolar-intrapleural).This driving pressure is also reduced if
recoil pressure is reduced, as in emphysema.
• Also in this disease, radial traction on the airways is reduced, and they
are compressed more readily.
• while this type of flow limitation is seen only during forced expiration
in normal subjects, it may occur during the expirations of normal
breathing in patients with severe lung disease.
12/23/2022 100

• There at least 3 factors where patients with COPD tends to exaggerate
this mechanism ,resulting in lower flow rate
1-compression point{equal pressure point}will move distally toward
the alveoli{because of the COPD-induced increased airway resistance,
which will increase the rate of pressure loss along the airway}so
decrease airway pressure>decrease in driving P, decrease flow rate
2-decrease elastic recoil > increase C> decrease airway P> decrease
flow rate
3-loss of radial-traction of the airway >less stable>>risk for collapse

DYNAMIC compression of airways
• Limits air flow in normal subjects during forced expiration.
• May occur in diseased lungs at relatively low expiratory flow
rates,thus reducing exercise ability.
• During dynamic compression, flow is determined by alveolar
pressure minus pleural pressure (not mouth pressure) and is there-
fore independent of effort.
• Is exaggerated in some lung diseases by reduced lung elastic recoil
and loss of radial traction on airways.

• Tissue resistance : R from sliding of tissues , less than 20% of total R
• In PFT: information about airway resistance in patients with lung
disease : either obstructive or restrictive pattern
• Restrictive :both FVC & FEV1 will decrease
• Obstructive : the decrease in FEV1 much more than FVC,low ratio
• FEF 25-75% average flow rate measured over the middle half of
expiration ,generally its reduced when FEV1 decrease,but it can
decrease with normal FEV1

Work of breathing
• Difficult to be Measured as Pressure * Volume
• Its the energy needed to extend the lung
• Why patients with stiff lung tend to take small rapid breaths?and why
patients with severe lung disease breath slowly??
Because by doing so ,work of breating decreases
So what is a normal work of breathing? And how RR ,C affect that?

• In inspiration, the intrapleural pressure follows the curve ABC, and
the work done on the lung is given by the area 0ABCD0.
• O this, the trapezoid 0AECD0 represents the work required to
overcome the elastic forces, and the hatched area ABCEA represents
the work overcoming viscous (airway and tissue) resistance

• the presence of airway resistance, the Pp needs to fall more in
negative values, this are will indicate the additional work done on the
lung, the path will be 0ABCD0
• some patient will not increase the ventilation because the o2 gain
from this = o2 used in hyperventilation
• In expiration : if no resistance the path will be CEA ,but if there is
resistance the path will be CFA, which is already in the trapezoid area
,i.e no more work needed to be done in expiration even with elevated
resistance

Total work of breathing
• the total work can be calculated by measuring the O2 cost of
breathing and assuming a figure or the effciency as given by
• Efficiency Useful work /Total energy expended or {O cost} *100%
• The effciency is believed to be about 5% to 10%. The O2 cost of quiet
breathing is extremely small, being less than 5% o the total resting O2
consumption.
• With voluntary hyperventilation, it is possible to increase this to 30%.
In patients with obstructive lung disease, the O2 cost of breathing
may limit their exercise ability

Causes of uneven ventilation
compliance,resistance,respiratory rate
• A- in normal lung C& R: the lung expands largely and rapidly before
expiration starts
• B- in conditions with low C and normal airway R: the lung volume change is
small and rapid
• C-if normal C & high R: the lung volume change is slow and small before
exhalation starts
• D- in high RR : smaller volume
• E-incomplete diffusion: in abnormally dilated respiratory bronchioles will
result in unequal gas distribution in the acinus
remember that the dominant mechanism of ventilation beyond respiratory
bronchioles is by diffusion,

Is this VOLUME CONTROL OR PRESSURE CONTROL??

KEY CONCEPTS
• 1. Inspiration is active, but expiration during rest is passive. The most
important muscle of respiration is the diaphragm.
• 2. T he pressure-volume curve o the lung is nonlinear and shows
hysteresis. T he recoil pressure o the lung is attributable to both its
elastic tissue and the surace tension o the alveolar lining layer.
• 3. Pulmonary surfactant is a phospholipid produced by type II alveolar
epithelial cells. If the surfactant system is immature, as in some
premature babies, the lung has a low compliance and is unstable and
edematous. 4. T he chest wall is elastic like the lung but normally
tends to expand. At FRC, the inward recoil o the lung and the outward
recoil o the chest wall are balanced.

• 5. In laminar flow as exists in small airways, the resistance is inversely
proportional to the fourth power of the radius.
• 6. Lung airway resistance is reduced by increasing lung volume. If
airway smooth muscle is contracted, as in asthma, the resistance is
reduced by β2-adrenergic agonists.
• 7. Dynamic compression o the airways during a forced expiration
results in flow that is effort independent. The driving pressure is then
alveolar minus intrapleural pressure. In patients with chronic
obstructive lung disease, dynamic compression can occur during mild
exercise, thus causing severe disability.

• In acute Asthma excacerpations,What changes would you expect to see in
alveolar pressure during inspiration and expiration compared with a
normal person? The alveolar pressure will be abnormally low during
inspiration and abnormally high during expiration in order to maintain
pressure difference between the mouth and the alveoli in the sitting of
abnormal increasing in airway pressure and resistance
• How does the observed hyperinflation affect airway resistance during his
asthma exacerbation?
although the hyperinflation will increase compliance and decrease airway
resistance, coz of increased radial traction extension on airways,the airway
pressure will be higher than normal coz of airway constriction

Mechanical ventilation in COPD notes
• Any mode can be used, Clinician’ s experience is the most important
determinant o f mode selection.
• Initial ventilator settings are recommended like that; TV: 6–10 ml/kg,
FiO2: 1.0, RR: 10–14 breaths/minute, no PEEP, inspiratory flow rate:
80–100 liter/minute with square waveform.
• Monitoring the lung mechanics on ventilator graphic screen
continuously and detecting any sign o f DHI or PEEPi are very
important.

• auto-PEEP (PEEPi) & Dynamic hyperinflation(DHI) may exist before
intubation or induced by mechanical ventilation.
• The minute volume (MV) should be adjusted to pH and not t o the
PaCO2 levels.
• Clinicians should avoid over ventilation and paCO2 levels should
decreased gradually. It is important to provide lower MV (RR x tidal
volume (TV)) and higher inspiratory flow rate which has allow longer
expiratory time.

• The clinicians should be followed existing any clinical signs to avoid
the complications of DHI. The most important complications of DHI
are hypotension hemodynamic collapse, barotrauma and increased
work of breathing . Therefore, that strategies must be applied by
clinicians to reduce auto-PEEP; providing the longest expiratory phase
that is possible, reducing patient ventilatory demand and MV, and
reducing airflow resistance by bronchodilators and steroids

Barotrauma is an important risk at the COPD patients
Alveolar pressure can be detected with plateau
pressure (Pplat) and suggested Peak Inspiratory
Pressure < 50 cmH2O, Pplat < 30 cmH2O to avoid
barotrauma

• Quantifying PEEPi is a difficult and favored process. PEEPi amount o f
proportionated with degree of bronchial obstruction. Different
techniques can be used t o calculate PEEPi. Clinicians can directly
measure by occluding the expiratory port for 1–3 seconds at end
expiration or by using expiratory hold maneuver on new ventilators.
• Static PEEPi can be measured in this way only in sedatized patients
without active respiratory effort

• . The PEEPi can then calculated by subtracting the external PEEP from the
total PEEP.
• If there is spontaneous respiratory effort of the patient, dynamic PEEPi can
be determined by simultanously recording esophageal pressure and airflow
tracings.
• It is measured at end expiration as the negative deflection of esophageal
pressure to the point of zero flow.
• The dynamic PEEPi is usually measured lower than static PEEPi by reason of
different longer of time constant While PEEPi is determined extrinsic PEEP
(PEEPe) at 80% of PEEPi should be added to reduce patient triggering
effort. Ventilator trigger sensitivity must be justify minimal

Concerning the pressure-volume behavior o the lung:
• A. Compliance decreases with age.
• B. Filling an animal lung with saline decreases compliance.
• C. Removing a lobe reduces total pulmonary compliance.
• D. Absence o surfactant increases compliance.
• E. In the upright lung at FRC, or a given change in intrapleural
pressure, the alveoli near the base o the lung expand less than do
those near the apex.

Two bubbles have the same surface tension, but bubble X has 3 times the
diameter of bubble Y. The ratio of the pressure in bubble X to that in
bubble Y is:
A. 0.3:1
B. 0.9:1
C. 1:1
D. 3:1
E. 9:1

The basal regions o the upright human lung are normally
better ventilated than are the upper regions because:
A. Airway resistance o the upper regions is higher than
that o the lower regions.
B. T here is less suractant in the upper regions.
C. The blood flow to the lower regions is higher.
D. The lower regions have a small resting volume and a
relatively large increase in volume.
E. The Pco 2 of the lower regions is relatively high.

An anesthetized patient with paralyzed respiratory muscles and normal lungs is
ventilated by positive pressure. If the anesthesiologist increases
the lung volume 2 liters above FRC and holds the lung at that volume for 5 s,
the most likely combination of pressures (in cm H 2O) is likely to be:
Mouth Alveolar Intrapleural
A. 0 0 −5
B. 0 +10 −5
C. +10 +10 −10
D. +20 +20 +5
E. +10 0 −10

When a normal subject develops a spontaneous pneumothorax
of his right lung, you would expect the following to occur:
A. Right lung contracts.
B. Chest wall on the right contracts.
C. Diaphragm on the right moves up.
D. Mediastinum moves to the right.
E. Blood ow to the right lung increases.

According to Poiseuille’s law, reducing the radius o an airway to one third will increase its
resistance how many old?
A. 1/3
B. 3
C. 9
D. 27
E. 81
Concerning air flow in the lung:
A. Flow is more likely to be turbulent in small airways than in the trachea.
B. T he lower the viscosity, the less likely is turbulence to occur.
C. In pure laminar ow, halving the radius o the airway increases its resistance eight old.
D. For inspiration to occur, mouth pressure must be less than alveolar
E. During diving, airway resistance as well the gas density will increase

The most important factor limiting flow rate during most
of a forced expiration from total lung capacity is:
A. Rate o contraction o expiratory muscles
B. Action o diaphragm
C. Constriction o bronchial smooth muscle
D. Elasticity o chest wall
E. Compression o airways
Which of the following factors increases the resistance of
the airways?
A. Increasing lung volume above FRC
B. Increased sympathetic stimulation of airway smooth muscle
C. Going to high altitude
D. Inhaling cigarette smoke
E. Breathing a mixture o 21% O2 and 79% helium (molecular weight
4)

A normal subject makes an inspiratory effort against a closed airway.
You would expect the following to occur:
A. Tension in the diaphragm decreases.
B. T he internal intercostal muscles become active.
C. Intrapleural pressure increases (becomes less negative).
D. Alveolar pressure falls more than does intrapleural pressure.
E. Pressure inside the pulmonary capillaries alls.

A 20-year-old man is asked to perform spirometry as part o a research
project. On the first attempt, he deliberately exhales with only 50%
o his maximum effort. On the second attempt, he exhales and gives
100% o his maximum effort. If you analyzed the data rom the second
attempt, which pattern of changes in peak expiratory flow and flow in
the latter part of expiration would you expect to see compared with the
first attempt?
Peak Expiratory Flow End-Expiratory Flow
A No change No change
B Decreased No change
C Increased increased
D Increased No change
E No change Increased

Pulmonary surfactant:
• A. Increases the surface tension o the alveolar lining liquid
• B. Is secreted by type I alveolar epithelial cells
• C. Is a protein
• D. Increases the work required to expand the lung
• E. Helps to prevent transudation o uid rom the capillaries into the
alveolar spaces

Lung mechanichs-1.pptx

Recommended

Recommended

More Related Content

Similar to Lung mechanichs-1.pptx

Similar to Lung mechanichs-1.pptx (20)

Recently uploaded

Recently uploaded (20)

Lung mechanichs-1.pptx