VENTILATION

Supplement to Text, Chapter 11

You must study BOTH the chapter and this supplement

RTT 100
Professor Michael Nazzaro

The symbols used in the chapter were covered in

the Medical Terminology Slides, and the
Physical Principals that were covered in Chapter 6.

1
 Background: Lung Volume Measurement

Figure above: Schematic diagram of a water seal

respirometer (spirometer).
• The patient breaths in and out from a dome filled
with air.
• The dome is connected to a pen that records a
tracing on graph paper attached to a drum called
a kymograph.
•The kymograph rotates at a known sped to allow
flow rates to be calculated..
• As the patient inhales and exhales, the dome
moves up and down in step with the volume of air
breathed in and out
Spirometric tracing of normal, resting (“quiet”)
• The pen traces a series of curves on the breathing. NOTE the Minimal Lung Volume.
kymograph paper (Figure at right).
• Breathing volumes and flow rates can be Reference: Note, Text pg. 415 (Fig. 20-10),
calculated from the kymograph curves. Medical Terminology Slide 46 & its Note, 2
 Ventilation: Introduction
Spontaneous ventilation (breathing) is one of the simplest processes in nature, however some writers can
make it very complicated and confusing. One way to confuse is to constantly switch between units of
pressure, especially switching from cmH2O to mmHg, and using + and – signs for the direction of airflow.
• Spontaneous ventilation is a cyclic process consisting of an inspiration followed by an expiration.
• The amount of air moved in and out of the lungs during each respiratory cycle (breath) is called the Tidal
Volume (VT).
– Breathing is called tidal because the air flows in and out regularly, like the ocean tides.
– The vital capacity (VC) and its subdivisions provide the pulmonary reserve for increasing ventilation
when necessary, i.e. exercise or illness..
• Spontaneous ventilation occurs when respiratory muscle contraction expands the thorax and produces
pressure gradients (differences) between atmospheric (ambient) pressure and alveolar pressure.
• Remember that ambient pressure at sea level is 760 mmHg, 0 PSIG, 1033.6 cmH2O, etc.
–At rest (both at end inspiration and end expiration), alveolar pressure (PA) is 0 (ambient).
–To get air to flow into the lungs, alveolar pressure (PA) has to be lower than ambient.
–To get air to flow out of the lungs, PA has to be greater than ambient.
• Alveolar pressures change in response to changes in pressure in the pleural cavity (PPL).
• In other words, during breathing pleural pressures vary a couple of cmH2O or mmHg around ambient.
–The normal contractile forces of the lung pull the visceral pleural layer inward.
–The normal outward springing of the rib cage pulls the parietal pleural layer outward.
• These opposing pulls slightly separate the plural layers, and Boyle’s law tells us that PPL will be slightly
negative in relation to ambient pressure.
– At rest (end expiration), PAO is 0 and PPL is about -5 cmH2O (or 5 cmH2O subambient).
• This resting subambient pleural pressure is responsible for maintaining the FRC.
• In normal, healthy individuals the respiratory system is able to quickly adapt the level of ventilation to the
changing levels of CO2 production and O2 consumption encountered at rest and during exercise.
– This adaptation allows the respiratory system to meet the body’s needs with the lowest expenditure of
energy (work).
• In disease, breathing may become inadequate to meet the body’s needs:
– The work of breathing may increase significantly, the respiratory muscles may loose strength, or both
conditions may occur simultaneously.
• Dyspnea is the subjective (perceived by the subject) sensation of difficult breathing.
– Respiratory care modalities reduce the work of breathing and to restore ventilation and gas exchange.
– In complete respiratory failure, mechanical ventilation is used to take over the entire breathing
workload.
Reference: Note, Text pg. 226, 227 (Table 11-1), 229 (Fig. 11-2), 240 (Fig. 11-15) 3
 Ventilation Mechanics: Breathing Pressures
• Since pulmonary anatomic structure was covered in Ch. 9, Ch. 11 simply describes the airways, alveoli,
pleural space, and chest wall in terms of pressures and pressure gradients, as the captions on the figure
show.
• The respiratory system can be described as a simple mechanical air pump, some writers even refer to it as the
chest bellows.
• A very simplified schematic diagram (Fig. 11-1, and table 11-1, pg. 227) presents the pump as a single flow
conducting tube (all of the conducting airways) connected to a single elastic compartment (all the alveoli)
surrounded by another elastic compartment (the chest wall and the pleural cavity).
• The pressures and, more importantly, the pressure gradients, (differences) between any two points in the
diagram represent the force (push or pull) that draws air into or drives air out of the alveoli.
• The author’s terminology can be confusing and represents his personal views.
–The Slides and Notes will try to use the more widely accepted set of terms for the pressures and
pressure gradients of breathing:

Four measurable pressures are significant for spontaneous breathing:

1. (PAO or PM) Mouth Pressure. The pressure at the Airway Opening (mouth and
nose or artificial airway). During spontaneous breathing at sea level, PAO is the
ambient pressure (760 mmHg or 0 PSIG).
2. (PBS) Body Surface Pressure is also ambient or atmospheric pressure (PATM).
3. (PPL) Intrapleural Pressure. The pressure within the pleural cavity.
• PPL is produced by the opposing pull of the lung and chest wall. At rest, PPL
ranges from –3 to –6 cmH2O (Fig. 11-2 uses -5 cmH2O). •∆PMUS muscle pressure
4. (PA or PALV) (alveolar or intrapulmonary pressure). At the end of expiration flow difference, the muscle
has stopped and the glottis is open. pressure applied to the
elastic structures of the
• Pressure in the airway (from the mouth to the alveoli) is equal to atmospheric
chest wall to produce the
(0 PSIG). pressure gradients for
• If the pressure was higher or lower, air would be flowing in or out. spontaneous breathing.

Reference: Note, pg. 227 (Table 11-1), 238 (Fig. 11-12, 11-13), 997 (Fig. 45-14). 4
Clinical Measurement: Measuring Lung Pressures
• During resting spontaneous breathing the glottis remains open throughout inspiration and
expiration.
• Under static (no flow) conditions the PAO, PALV, and PBS remain ambient (760 mmHg or 0
PSIG).
• The inward recoil of the lungs (elastic recoil) and the outward recoil of the rib cage slightly
separate the pleural layers.
• This separation produces the sub-ambient intrapleural pressure (Ppl) at rest.
• As the respiratory muscles (diaphragm and external Intercostals) contract during inspiration,
the rib cage expands and the thoracic cavity volume increases (remember Boyle).
• The expanding rib cage pulls the parietal pleural layer away from the visceral layer
increasing the sub-ambient pleural pressure.
• Increased subambient pleural pressure is transmitted (reflects) across the alveolar walls and
reduces pressure in the alveoli.
• This produces the transalveolar (∆PTA) gradient: PTA = PA – PPL
• The transairway (∆PTAW ) gradient increases at the same time:: PTAW = PAO – PA
• Changes in pleural pressure control alveolar pressure and those changes control airflow in
and out of the lungs.
• In clinical practice, the transpulmonary is the most important gradient is the PTP = PAO - PPL

Reference: Note, Text pg. 227-29, 231 & Fig.11-5

5
 Physics of Breathing:: The Equation of Motion
We don’t use the Equation of Motion (EOM) to calculate any numbers, it is a conceptual tool to explain
that pressure (energy) must be generated to overcome the resistances to breathing.
• The EOM for the Respiratory System is the mathematical expression of how much energy (pressure) the
respiratory muscles or the ventilator must produce to overcome the both the frictional resistance of the
airways and the elastic resistance of the lung and chest wall.
– The EOM is useful as a tool to help understand the relationships between all the factors: pressure,
resistance, compliance, elastance, and flow that determine ventilation.
• The Text uses a simplified version of the EOM derived from the classic EOM:
volume + (Resistance X Flow)
Pressure = compliance
• Pressure is the amount of energy needed to move air into the alveoli.
• Volume is the amount of air that is moved into the alveoli with each breath.
• Compliance (C) is a measure of how much pressure is required to increase
the volume (expand) the lung, calculated as ∆ (change) in volume / ∆ in pressure.
• Elastance (E) is the reciprocal of compliance, calculated as 1 over compliance.
• Resistance is calculated with Ohm’s Law: R= ∆ pressure or Poiseuille’s Law: R= fluid viscosity x tube
4
length
flow tube radius
• Flow is look
A brief the volume changeEOM
at the Classic per unit
mayofmake
time (as
the in liters affecting
factors per minute ormovement
gas milliliters per second).
a little easier to understand:

• The classic form of the EOM is simply: P = PEL + PRES

• P (or PMUS) is the total muscle energy needed to produce the pressure gradient required to move air into the resistive/elastic
pulmonary system (Table 10-2 calls it the Global muscle pressure difference).
- If the patient was getting positive pressure ventilation, the pressure would just be labeled P, not P MUS.
• Pel is the portion of the pressure (energy) that is stored in the elastic fibers of the alveoli (a shorthand expression for the
pulmonary interstitial matrix) and the chest wall. Pel doesn’t help to expand the lung, but it is available to power expiration.
• Pres is the pressure dissipated (used up) to overcome airway frictional resistance (RAW).

The Classic EOM tells us several things about breathing:

1. Pressure is the force needed to overcome all of the different resistances (load) in the respiratory system.
2. If Pel (alveolar elastic resistance or elastance) increases, more muscle pressure will be needed to inflate the lungs.
3. If Pres (airway frictional resistance) increases, more muscle pressure will also be needed to inflate the lungs.
4. If the patient is on a mechanical ventilator and P (the pressure the ventilator must generate) changes, the cause is most likely
changes in Pel and/or Pres. (compliance and/or resistance).

Reference: Note, Text pg. 227 & Table 11-2 6

 Spontaneous Ventilation: Pressure Gradients
• In order for ventilation to occur pressure gradients must be created between the lungs and the atmosphere.
– Respiratory pressures are usually reported in centimeters of water (cmH2O).
– They are usually referenced to the average atmospheric pressure at sea level (760 mmHg or 0 PSIG).
• A pressure below ambient that is generated by the respiratory muscles is actually a subambient pressure.
• The text (Table 11-2) lists seven pressure gradients that can be assessed during ventilation:
1. The Transrespiratory (PTR) is the gradient between the airway opening (mouth) and the body surface.1
• The PTR gradient is what causes air to flow in and out of the lungs during breathing.
The remaining six gradients are subdivisions of the transrespiratory gradient.
2. The Transairway (PTAW) is the gradient between the airway opening and the alveoli.2
3. The Transpulmonary (PTP) is the gradient between the airways and the alveoli (PAO – PPL).
• The Text (pg. 228) definition for this gradient is an example of the author’s unique terminology.
• Most writers define the PTP as the difference between alveolar and pleural pressure (PA - PPL).
• Changes in PTP produce the pressure for spontaneous inhalation followed by expiration.
4. The Transalveolar (PTA) is the difference between alveolar pressure and pressure in the pleural space.
• This gradient results from the opposing forces that pull the pleural layers apart.
• The PTP is responsible for maintaining the FRC at the end of spontaneous expiration
5. The Transthoracic (PTT) is the gradient between the alveolar pressure and the body surface; the
pressure across the chest wall.
• The PTT gradient represents the muscle force necessary to expand or contract both the lungs and the chest wall.
• Remember, the airway opening is on the body surface, so P bs and Pao are the same: ambient pressure.
6. The Trans-Chest Wall (PTCW) is the pressure difference between the pleural space and the body surface.
• It may be assessed in some disease states to account for the effect of chest wall stiffness..
7. The Global Muscle Pressure Difference (PMUS) is used in the equation of motion to assesses the
muscle force used for spontaneous inspiration.

1 The author’s statement that for inspiration, PAO is higher than PBS, only applies to positive pressure ventilation.
2 During spontaneous inspiration, PAO is lower than PBS, and it is higher during expiration.

Reference: Note, Text pg. 228 (Table 11-2), 1018-19 & Figs. 46-1 & 46-2 7
 Ventilation Mechanics: Pressure, Volume, Flow
• A calm, systematic 1. At the end of inspiration, intrapleural
assessment of Fig.11-2 pressure (Ppl) is about subambient 8 (– 8
(below) reveals that it cmH2O,) and alveolar pressure (PA) is
compares pleural pressure zero. The pressure gradient between the
(red), alveolar pressure mouth and the lungs (Pl or Ptp) is
(blue), airway flow (green), therefore 8 cmH2O:
and airway volume (purple). • Pl = PA - Ppl = 0 – (– 8) = 8 cmH2O. (Text
– The graph shows Ppl says 10 cmH2O).
returning to zero at the end – The – 8 cmH20 Ppl means that the
of expiration (the figure is
incorrect), text on pg. 228 respiratory muscles are holding the
is correct). thorax expanded with enough force to
• The vertical (Y) axis measures generate an 8 cmH2O difference
pressure and flow. between the mouth and the pleural
− Negative and positive space.
values for flow indicate the – Muscle energy has lowered alveolar
direction of movement (in pressure about 1 cmH2O below ambient
or out) of the air flow. and about 500 ml of air has flowed into
• Negative values for pressure the lungs. Alveolar volume is now FRC
are subambient. + 500 ml.
• All values in the figure have 2. At the end of expiration, alveolar pressure
been multiplied by 10. is again 0 and pleural pressure is back to
• The Text labels expiratory its resting level of –5 cmH2O. The
flow as NEGATIVE (pg.228). gradient between the mouth and pleura is:
• Pl = PA - Ppl = 0 - (-5) = 5 cmH2O.
– The respiratory muscles have relaxed
Volu and 500 ml of air has flowed out of the
me lungs.
– Alveolar volume has returned to FRC.
Flo – Alveolar pressure and flow have
w returned to zero (ambient).
PA • During forced inspiration the diaphragm will move – Pleural pressure has returned to its
LV to its maximum downward excursion and Ppl can resting level of about subambient 5
get as low as – 50 cmH20, producing signs (– 5 cmH20).
PP including pulsus paradoxus and retractions.
L • During forced expirations Ppl can increase to + 50 3. During the breath, the Ppl has moved
or even as high as +100 cmH20, producing signs across a range of 3 cmH2O, from -5 to-8
produced including reduced cardiac output and and back to -5 cmH2O.
syncope.

Reference: Note, Text, pg. 227-28 (Tables 11-1 & 2), 229 & Fig. 11-2, 1019 & Fig. 46-2. 8
 Clinical Measurement: RR, VT, & BCT
• The respiratory rate for a healthy, Each breath is a cycle of two events: Inspiration
average adult awake and at rest (i.e. followed by Expiration.
not actively exercising) is anywhere • Each cycle takes a certain amount of time.
from 12-20 breaths/minute. • That time can be called by several names:
– Note that a very wide range of – Breath Cycle Time (BCT).
accepted “normal” rates exist.
– Total Cycle Time (TCT).
• Tidal volume is defined as the volume
of air inhaled and exhaled in one • It is often necessary to calculate breathing times:
normal breath. – How long is the BCT?
• Normal resting adults are estimated to – How long is Inspiratory Time (TI)
have an average VT of about 6.3 ml/kg – How long is Expiratory Time (TE)
with a range of about 5-7 ml/kg of ideal • The first step is to calculate BCT:
(predicted) body weight.
– This gives the textbook VT of 500 ml BCT equals the number of
for the average healthy adult at rest. seconds in a minute (60) divided
• The ratio between Inspiratory Time by the respiratory rate or
(TI) and Expiratory Time (TE) for a frequency (abbreviated RR or f).
normal resting adult is usually stated
as 1:2 (the I from the I:E is always 1) Breathing frequency (RR) determines the BCT:
– Normally, expiration lasts about • If the RR is 12/min. the BCT would be 60/12 = 5
twice as long as spontaneous sec./breath.
inspiration.
– That means that if the I:E is 1:2, TE • If the RR was 16/min. the BCT would be 60/16 =
will be twice as long as inspiratory 3.75 sec./breath.
time. • If the RR was 19/min. the BCT would be 60/19 =
– Various disease processes will alter 3.157 ≈ 3.20 sec./breath.
the I:E ratio.
Reference: Note, Text pg. 242, 1184. 9
 Clinical Measurement: Inspiratory Expiratory Ratio
• The Breath Cycle Time (BCT) is the amount of time available to complete each phase of the breathing cycle.
• The BCT is divided into an Inspiratory Time period (TI) and an Expiratory Time period (TE)
• The Inspiratory to Expiratory Ratio (I:E) expresses the relationship between TI and TE.
–The I:E for a normal person at rest is usually stated as 1:2 (the I from the I:E ratio is always 1).
–An I:E of 1:2 means that normally, expiration takes twice as long as inspiration, (can you explain why?)
• Various disease processes will alter the I:E (can you describe how two disease processes will do this?).
• If the BCT and the I:E ratio are known, TI and
TE can be calculated using the formula below.
TI TE
TI = Inspiratory Time
BCT x I
TI = I + E BCT = Breath Cycle Time
Breath Cycle Time (BCT) with a normal I:E of 1:2 I = The I from the I:E Ratio
E = The E from the I:E Ratio

Calculate TI and TE for a patient with a RR of 12/min. and an I:E of 1:2 • There is a short period of no
flow between the end of the
• BCT = 60/12 = 5 sec./breath. expiration and the start of the
• I:E = 1:2 next inspiration.
• TI = 5 sec. x 1/ (1+2) - That period is called the
• TI = 5/3 = 1.66 ≈ 1.7 sec. End Expiratory Pause
• TE = BCT – TI = 5 sec. – 1.7 sec. = 3.3 sec. (EEP).
- The EEP is about 25% of
TE, so it can be estimated
• Obstructive pulmonary disorders increase TE by multiplying TE by 0.25.
– Either because elastic recoil energy is reduced or airway • In the example at left, the EEP
resistance is increased (or more usually, because of both). would be about 3.3 sec. x 0.25
• Restrictive pulmonary disorders decrease TE = 0.825 sec. ≈ 0.8 sec.
– Either because elastic recoil energy has increased or alveolar • Knowing the duration of the
filling volume has decreased (or more usually, because of both). EEP is useful in calculating the
FIO2 delivered by low flow O2
devices.
Reference: Text pg. 402 & Fig. 20-1 10
 VENTILATION

RTT 100
Professor Michael Nazzaro
Supplement to Text Chapter 11
You must study BOTH the Chapter and this supplement

Forces Opposing Lung Inflation

Reference: Text pg. 229-235

11
 Ventilation: Forces Opposing Lung Inflation
Resistance is defined as any force that opposes movement. In order to improve understanding of
the forces that resist lung expansion, most writers group resistances into two broad categories:
Forces that produce elastic resistance, and forces that produce frictional resistance.
1.Elastic resistance1 (elastance) forces include:
– The elastic recoil of the lung (primarily the elastic and collagen fibers of the airway and the
alveolar interstitium). Note that “alveolar elastic recoil” is shorthand for interstitial elasticity.
– The elastic recoil of the chest wall (flexible cartilages and rib-sternum-vertebra articulations).
– Alveolar surface tension (produced by the gas/liquid interface and modulated by pulmonary
surfactant).
2.Frictional resistance2 forces include:
– Friction between the moving gas and airway walls (about 80% of total frictional resistance).
– Internal fluid friction (viscosity) of the gas itself (not usually a problem in normal individuals
breathing air).
– Lung tissue resistance (about 20% of the total resistance to inflation) is a complex and
controversial subject. It can be simplified to the statement that as the lung tissues expand
and contract during inspiration and expiration, they have to move over each other and this
movement generates frictional resistance.
Resistances in the normal lung are so well balanced by the available muscle energy that
we usually aren’t even aware that we are breathing.
– Awareness of breathing most often occurs when resistance and energy become unbalanced
and we have to expend more energy than usual to breathe.
• Such conditions produce the clinical symptom of dyspnea.
1 Hooke’s Law states: In an Elastic Structure, Stretch is Proportional to Stress). Elastance is a measure of the
resistance to stretch. Compliance is a measure of the amount of force (stress) need to overcome elastance.
2 Poiseuille’s Law states: Fluid flowing through a tube looses pressure as energy is converted to heat while

overcoming frictional resistance.

Reference: Note, Text, pg. 229-35. 12
 Opposing Ventilation: Elastance & Surface Tension

Lung Volume % TLC

AirAirfilled Saline
filled
lung
lung filled lung
Air filled
lung
Pressure around the lung (cmH2O)
• (Fig. 10-4 pg. 229) shows an excised lung in a sealed bell jar (Left).
• The bell jar is connected to a vacuum pump and a pressure manometer; the lung is connected to a spirometer.
• As air is pumped out of the bell jar pressure around the lung decreases, simulating spontaneous inspiration.
• As air is allowed to return to the bell jar pressure around the lung increases, simulating expiration.
- The volume of air flowing in and out of the lung is recorded on the spirometer
- Pressure changes are made in discrete steps (dots) while lung volumes are recorded.
- Each dot on the curve is called a specific compliance. Note that as volume approaches TLC the curve flattens out.
- Volumes and pressures are then plotted on a graph to give inflation and deflation compliance curves (center left).
• When the lung is air filled, the inflation (right curve) and deflation (left curve) plots are not the same:
- At any given pressure, lung volume is slightly higher during deflation than the volume during inflation.
- The difference in compliance between inspiration and expiration is called hysteresis*.
• The presence of hysteresis in the lung shows that another force besides elastic recoil must be at work during deflation
of the air filled lung. Of course, that force is surface tension.
• This is proved when a saline filled lung is placed in the bell jar and inflation/deflation curves are plotted (center right).
- Inflation and deflation curves for the saline filled lung are virtually identical with almost no hysteresis, this is because
surface tension is not present since there is no air in the lung to create a liquid/gas interface.
- The inflation/deflation curves for the air filled lung are actually an inspiratory/expiratory loop (a common pulmonary
function testing procedure). The loops in the two center figures include extremes of lung deflation and inflation.
• Most normal, resting breathing occurs around the VT and displays much less hysteresis (inset far right). This is explained
because the P/V (compliance) curve is steepest (the most expansion for the least pressure) at normal lung volumes.
Reference: Note, *In elastic structures such as the lung, hysteresis occurs when it takes some amount of time for the inhaled
Text, pg. 227, 229, volume to leave the lung after the inspiratory muscle force stops being exerted.
231, 1161 13
 Clinical Measurement: Compliance & Elastance
• When assessing pulmonary mechanics, elastic resistance (elastance), is the factor that
determines the amount of pressure needed to inflate the lungs.
– Elastance and compliance are reciprocals: each divided into 1 equals the other.
∆Volume (liters) __ ∆Pressure 1 1
C= ∆Pressure (cmH2O) E= ∆Volume C= E E= C

– Since they are static properties, measurements are only valid when assessed during periods
of no flow so that pressure needed to overcome frictional resistance is not added.
•Elastance can not be measured directly, it is assessed indirectly as the reciprocal of
compliance which can be effectively measured with an esophageal balloon (Slide 12).
– For that reason, most writers find it more effective to concentrate on the lung or pulmonary
compliance (CL), the chest wall or thoracic compliance (CCW ), and the total compliance (CT)
• Total compliance (CT) is the sum of the lung and chest wall compliances (CL + CCW).
– The text calls the sum of CL and CCW the compliance of the respiratory system (CRS).
• CRS is the same as what other writers call total compliance (CT). CL x CCW
–The text offers a formula for calculating CRS (pg. 230) CRS = CL + CCW
• The only problem is that chest wall compliance cannot be directly measured, it must be
1
calculated after Cl and CRS (CT) are known. C1 – C1 = C ERS = EL + ECW
T L CW
• The other problem is that total compliance is determined by measuring delivered volumes at
various inspiratory pressures on anesthetized patients on mechanical ventilators.
• It should be obvious that the numbers found in textbooks for normal lung and chest wall
compliance are essentially lab values that are not determined for individual patients on a case by
case basis.
• Clinicians routinely measure static lung compliance on patients receiving mechanical ventilation.
• These measurements provide important immediate clinical information on patients’ lung
compliance.
Reference: Note, Text pg. 228-230, 235-7 14
 Ventilation: Lung -Thorax (Chest Wall) Forces
Fig. A: If the lungs are removed from
the thorax (or if air is allowed to enter
the pleural space) the lung’s natural
tendency will be to contract to a small,
almost airless mass, below residual
volume to minimal volume.
Fig. B: The chest after the lungs were
removed and the apex left open to the
atmosphere. The natural tendency of
the thorax will be to expand outward to
a larger size.
Fig. C: In the normal intact thorax the
pleural layers couple the outward pull
of the chest wall with the inward pull of
the lungs. This controls the changes in
pleural pressure and causes air
movement in and out of the lungs.
•The lung-thorax system is often described as
two sets of springs pulling in opposite • The normal collapsing forces of the
directions (above). lung (elastic recoil and surface
•The lung spring tends to contract inward and tension) exert about – 4 to – 5
the chest wall spring tends to expand outward. mmHg of inward pressure.
•Recoil is the term used for both the inward •Therefore intrapleural pressure
movement of the elastic lung and the outward (Ppl) must be at least – 4 to – 5
movement of the chest wall. mmHg (pulling in the opposite
•The figure above shows a section of the left direction) to counteract lung recoil
chest wall, pleura, and lung with the lung is at and maintain the FRC.
rest (FRC), therefore: • The normal expanding forces (the
– Palv = 0 outward springing of the ribs and the
– Patm (also body surface and airway FRC) balance the lung’s elastic
opening) = 0 recoil force and account for the
– Lung elastic recoil = +5 cmH2O (inward) subambient PPL at rest.
– Thorax elastic recoil = – 5 cmH2O (outward) • This balance makes Palv 760
– Ppl = – 5 cmH2O mmHg or Zero PSIG when the lung
volume is at FRC.
Note: The figure (above left) uses cmH2O. text Fig. 10-7 and above use mmHg. Some Reference: Note,
figures don’t use any units. The units don’t matter for illustrative purposes to make Text pg. 231-2, 1042-5
comparisons as long as they are consistent within each figure. (1 cmH2O ≈ 0.7 mmHg).
15
 Pulmonary Compliance: Normal vs. Pathological CL
• Changing the pressure around the lung by changing the pleural pressure produces the ∆P for spontaneous breathing.
• Lung compliance (CL) is a measure of the amount of volume change (∆V) obtained for each unit of pressure applied.
•∆V is caused by moving air into the lung; lung volume means lung size (determined by how much air is in the lung).
• CL expresses the ratio between volume and distending pressure; the Volume /Pressure curves graph this relationship.
– The flat portions of the curves show lower compliance because increasing P produces little or no increase in V.
– The steep portions of the curves show higher compliance because increasing P produces a corresponding increase in V.
• . The emphysema lung is
V/P curve of the normal lung characterized by loss of elastic
tissue which reduces elastance.
- The lung has high compliance
(large V increase at low P).
- It produces a steep curve shifted
to the left of normal.
• Emphysema also reduces the
energy for exhalation leading to air
trapping, an obstructive condition.
• The fibrotic lung is characterized by
an increase in the forces that tend
• In the normal lung alveoli at the apex to close (collapse) the alveoli.
are pulled open by gravity - These can include interstitial
fibrosis, but it can also result from
– Since they are already partially pulmonary edema, pleural
inflated they can’t get much bigger effusion, pneumonia, or any
so their compliance is low (they are condition that reduces alveolar
on the flat part of the curve).
expansion
• Alveoli at the lung bases are - It produces a much flatter curve
compressed by gravity. that is shifted to the right of
– But they are also on a steep part of normal (small V increase at each
the V/P curve so they expand well level of P).
during inspiration.
Reference: Note, Text pg. • Fibrotic changes increase elastance
• Alveoli in the Mid-Airway zone are on 232 Fig. 11-6 B, pg. 238 Fig.
the steepest part of the V/P curve and and produce pulmonary restriction
they have the highest compliance. 11-12 & 11-13.
16
Work of Breathing: Integrating Pressure & Volume
Work of breathing is quantified by integrating the curves for volume and pressure.
•Figure 11-11: If the lung is inflated slowly with pauses to measure pressure, inflation is
essentially static, and the V/P curve only measures the work done to overcome elastic
resistance (solid line AB). The slope of AB is the static compliance of the lung. The triangular
area under the curve ABD (labeled 1) represents the total elastic work of breathing.
•During normal airflow (dynamic conditions) a curve ABC, is produced. The extra length of
the curve represents the added resistance of friction during inspiratory and expiratory flow.
The semi-lunar area under the curve (labeled 2) represents the inspiratory muscle work
needed to overcome airway and tissue frictional resistance.
• The total resistance to breathing is the sum of Area 1 + Area 2.
•At points A and B (end expiration) flow stops, frictional resistance is not present, and the
curves merge with the static V.P line.
•Figure 11-12: Compares the area under the curve for healthy subjects to those with
restrictive and obstructive breathing patterns. WOB is much higher in the presence of lung
disease, but it is distributed differently according to the nature of the impairment.
•(A) In healthy subjects, WOB is determined by the breathing pattern. Large VT increase
elastic work. Rapid rates (at high inspiratory flows) increase resistive work.
•(B) In restriction, the size of the area under the curve is much greater, because the slope of
the static (CL) line is shallower than normal. Inspiratory work is hardest.
•(C) In obstruction the area represented by frictional resistive work is large because frictional
resistance during expiration is very high. The expiratory curve actually bulges to the left
showing positive pleural pressure during expiration.

•Fig 11-13: Shows how changing respiratory rate and inspired volume effects WOB.
•For any given level of alveolar ventilation (𝐕A ) there is an optimal breathing pattern that
produced the lowest WOB.
•Normal subjects breathe at rates of 10-15/minute. At these rates the combined elastic and
flow resistive work load is lowest.
•Patients with restrictive impairments (increased elastance) find the lowest WOB at high
rates with low volumes.
•Patients with obstructive patterns (increased compliance) find the lowest WOB at low rates
with high volumes.
Reference: Note, Text pg. 237-38 17
 Ventilation: Lung & Chest Wall Compliance • A calm, systematic assessment of Figure 11-7 shows
normal lung AND chest wall (thoracic) compliances both
separately and combined. The arrows (vectors) on the
lung figures show the direction and relative strength of
lung and chest wall recoil forces at different lung
volumes. Volumes are expressed as percentages of
Vital Capacity (VC) and Total Lung Capacity (TLC).
• The relaxation curves were plotted from lung volumes at
various airway pressures (inset picture). with the airway
opening tightly closed and the respiratory muscles
relaxed. Note the steep slope of the lung curve (blue)
and the sigmoidal slope of the thorax curve (red) and
the combined lung-thorax curve (purple).
• The lung curve is steepest at FRC. Muscle force needed
for a breath that starts at FRC is aided by the outward
force of chest wall recoil.
The lung figure pressures (in cmH2O) should be read
on a line across the three curves at each lung volume
(like line a-b).

• (A) is the lung after a forceful expiration of the ERV to FRC, leaving a volume of air in the lungs that is only slightly above RV.
The volume of air left in the lungs is only about 20% of the VC.
– At this low volume there is not much air for the elastic alveoli to compress, so lung recoil (inward or collapsing) pressure is
only about + 3 to +4 mmHg. The lung vector (arrow) is short, indicating this low level of lung recoil pressure.
– At low lung volume, the thorax is compressed, and the thorax vector is long, indicating an outward recoil (pull) of about -10
mmHg. This outward thoracic recoil helps power inspiration.
• (B) is the lung at end of a normal expiration to FRC is normally between 40-50% of VC (text, pg. 233 uses 40%).
– The pressure of the outward pulling thorax point a (-5 mmHg) and the inward pulling lung point b (+5 mmHg) balance each
other and alveolar pressure is zero (which means 760 mmHg or ambient).
– The point of balance between lung and thorax recoil pressures determines the volume of the lung at FRC.
• (C) is the lung after a deep inspiration with the lungs inflated to about 70% of TLC (pg. 233).
– The more inspiration stretches the lung, the more forcefully it tries to recoil, and the more subambient the pleural pressure
will become. Thoracic recoil is zero (the chest wall’s natural resting level) and the lung’s elastic recoil force is available for
exhalation without opposition from thoracic outward recoil.
• (D) is the lung after a maximal inspiration to TLC with the alveoli and chest wall stretched nearly to their limits.
– Lung and chest wall recoil pressures are both high (lung is higher) and are exerting an inward pressure against further lung
expansion. These high pressures reduce compliance and aid expiration.

Reference, Note 18
 Opposing Ventilation: Airway Resistance
• Airway resistance (RAW) accounts for about 80% of the frictional resistance to lung inflation.
∆P
• RAW is defined as the ratio of driving pressure to airflow. RAW = (∆P = Palv- Pao )
V
• RAW is difficult to measure in a spontaneous breathing subject:
– Palv– Pao the pressure drop across the airway, is measured in a body plethysmograph.
– V (flow) is usually measured with a pneumotachometer.
– Most RAW measurements cited in texts are done on patients on mechanical ventilators.
cmH2O
• ∆P is measured in cmH2O and V is measured in Liters/second, therefore: RAW =
L/sec
• Textbooks state that RAW for a normal, healthy adult ranges from about 0.5 to 2.5
cmH2O/L/sec.*
– In order to get a normal, resting inspiratory airflow of 1L/second, the subject must lower his alveolar
pressure about 0.5 to 2.5 cmH2O below atmospheric (subambient).
• The pattern of airflow; laminar, turbulent, or transitional (tracheobronchial), also affects the
amount of driving pressure needed move air through the airway.
– (Text, Table11-3) uses Reynold’s equation to compare the driving pressure needed to move air at
specific flow rates with laminar versus turbulent flow:
– Driving pressures for the same flow rate are greatly increased (squared) when flow is turbulent.
∆P
• With laminar flow, the pressure needed is directly related to flow: RAW=
V
∆P
• With turbulent flow the pressure needed is directly related to the square of the flow: RAW = 2
V
• Poiseuille’s equation demonstrates the relationship between airway diameter and resistance to
V
flow: ∆P= 4
r
• If airway diameter is reduced by ½, the driving pressure will have to increase by a factor of 16
to maintain the same flow rate.
Small reductions in airway lumen diameter, especially in the large airways, greatly
increase RAW.
*Other texts state normal RAW as 0.5 – 1.5 and Reference: Note, Text pg. 233-4, 238 &
0.6 – 2.4 cmH2O/L/sec. Just so you know. Figs. 11-12 & 11-13.
19
 Ventilation: Distribution of Airway Resistance
• The human airway is a complex network of branching
tubes that become narrower, shorter, and more
numerous as they penetrate deeper into the lungs.
• Starting with the trachea, the airways undergo
dichotomous branching until the alveoli (usually cited
as generation 23) are reached.
• All of these branchings produce two main physical
results beyond the level of the terminal bronchioles:
1.The velocity of inspired air decreases and flow
becomes much less turbulent.
2.When flow changes from convective (bulk flow) to
diffusional flow, turbulence and airway resistance
essentially disappear.
• A number of factors influence RAW including lung
volume and bronchial smooth muscle tone.
• The figure shows the distribution of airway – As the thorax expands during inspiration, airway
resistances across the airway generations from caliber (diameter) also increases.
the mouth (airway opening) to the alveoli. – The increased transpulmonary pressure gradient
• About 80% of the RAW occurs in the nose, the during inspiration aids in this bronchial dilation.
mouth, and the large airways (the trachea, •On expiration the chest (and the airways) are
bronchi, and bronchioles larger than 4 mm in compressed.
diameter).
- The nose is the site of highest resistance in •This explains why wheezing (rhonchi) is most often
the adult airway heard during expiration.
- The medium sized bronchi (larger than 4 mm – Bronchial smooth muscle tone is controlled by the
in diameter) provide most of the resistance. autonomic nervous system (and some local factors
• About 20% of the RAW occurs in the airways that in the bronchi themselves).
are less than 2 mm in diameter. – Substances including histamine, acetylcholine, and
• Resistance decreases as the airways get prostaglandins cause bronchial smooth muscle
smaller,
• There is almost no resistance to flow around contraction.
generation 20 (alveolar ducts) and beyond.
Reference: Note, Text pg. 224 & Table 11-3 20
Exhalation: Transmural Pressure & the Equal Pressure Point
• Transmural (Ptm ) is the pressure across the walls of tubes. It is the ratio of pressure
inside (which acts to distend the tube) to pressure outside (which tends to collapse
the tube).
-Transmural pressure = Distending Pressure minus Collapsing Pressure.
• Ptm gradients are especially important in tubes such as small airways and capillaries
that lack intrinsic structural support elements like cartilage and connective tissue.
The airway transmural pressure gradient is determined by the following elements:
1.Pleural pressures normally remain subambient during quiet breathing,
2.Airway (and alveolar) pressure varies slightly around zero (ambient) during quiet
breathing.
3.As air flows out of the lung during exhalation, the driving pressure decreases
(remember P1 – P2 ?).
- This pressure drop occurs because of frictional resistance and reduced alveolar
gas volume which lowers alveolar recoil pressure.
Small airways are like
this “soggy” soda straw. A careful appraisal of Fig 11-10 reveals the following:
If too high a flow rate is • The picture compares a forced exhalation (arrows under the diaphragm) between a
attempted, the EPP will normal lung (left) and an emphysema lung (right).
be reached quickly and • Downstream means in the direction of flow (toward the mouth in expiration).
dynamic compression
will result. A slow, gentle • Upstream means closer to the source of flow (small airways and alveoli in expiration)
flow rate may prevent • Elastic recoil pressure in the normal alveoli is +10.cmH2O.
the EPP from being • Pleural pressure (outside the lung) during forced exhalation rises to + 20 cmH2O
reached. - The driving pressure for exhalation flow is 20+10 = + 30 cmH2O.
• As air flows out of the alveoli (downstream) pressure in the airway decreases.
• When pressure inside equals pressure outside the airway, the Equal Pressure Point
(EPP) is reached.
• The Ppl (pressure around) the emphysema lung also rises to +20 cmH2O.
• But elastic recoil pressure in the emphysema alveoli is only +5 cmH2O.
- The driving pressure for exhalation flow is 20 + 5= +25 cmH2O.
- An excessively high expiratory flow rate will cause the EPP and dynamic
compression (early airway closure) to occur further upstream.
- Upstream airway closure will worsen air trapping.
- Slow exhalation through pursed lips (resistance) maintains exhalation driving
pressure at a level above Ppl for a longer time maintaining effort dependent flow.

Fig. 11-10, Text pg. 236 Reference, Note, Text pg. 235-36 21
 Mechanics of Exhalation: Radial Traction
• Airway caliber in non-cartilaginous airways is maintained by at least two addition factors :
1.The anatomic support of adjacent tissues; often referred to as radial traction or tethering.
2.The transmural pressure across the airway walls.
• Small airways, starting with the bronchioles, lack both the cartilage and peribronchial connective tissue
sheaths that support the larger airways.
• These airways need the external anatomic support provided by their connection to the surrounding lung
parenchymal tissues to maintain patency.
– The lung parenchyma consists of tens of thousands of closely packed, cohesive functional units (primary
lobules or acini) and the interstitial fluid (a gel-like matrix).
– These structures are affected by the recoil of the chest wall (through the pleural membranes) which tends
to pull the visceral pleura away from the parietal pleural layer.
– The outward pull of the parietal layer puts traction on the visceral layer, and that traction is transmitted to
the lung.
– The spheroid shape of the alveoli means that the traction applied to them operates in a radial pattern.
• Conditions that damage alveolar tissue disrupt radial traction and predispose to airway collapse (pg. 238).
(A): Extra alveolar blood vessel mechanically tethered to
adjacent alveoli and connective tissue.
• As lung volume increases the diameter of these vessels
increases.
(B): Alveoli are mechanically tethered adjacent alveoli.
• Alveolar radial traction is important in preventing atelectasis
in units that are only partially inflated.
(C): Small, non-cartilaginous airways are mechanically tethered
to adjacent alveoli and connective tissue.
• The diameter of small airways increases and their RAW
decreases as the lung expands during inspiration.
NOTE: Structures at the pleural surface (blood vessels, airways,
and alveoli) are not surrounded by supporting tissues, so radial
traction does not exist for the tissues in contact with the pleura.
However, pleural pressure provides support to these structures.
Radial traction in a section of lung parenchyma Reference, Text pg. 235, 237. 22
 Ventilation: Work of Breathing (WOB)
• Physicists describe workas the application of energy to overcome resistance and cause movement. The
equation is: Work = Force x Distance Moved (in the Direction of the force).
• In respiratory physiology, work is done by the respiratory muscles that supply the energy (in the form of
pressure) to move air in the direction of the force (in or out) against the resistances of the lung and chest
wall. The equation is: WOB = ∆P x ∆V.
Applied to the pulmonary system, ∆P is the force, and ∆V is the distance moved.
• Work of Breathing (WOB) can be divided into two broad categories:
1.Mechanical work which is the energy expended to overcome frictional and elastic resistances
– It is almost impossible to measure WOB in a spontaneously breathing subject.
– Professors have induced medical students (healthy volunteers) to enter a whole body negative
pressure ventilator (an Iron Lung) and become completely relaxed (anesthetized).
– Most of what we know about WOB in healthy subjects comes from these experiments.
• Mechanical work is further subdivided into Elastic and Resistive compartments.
2.Metabolic work of breathing (the oxygen cost of breathing) is the amount of energy expended by the
respiratory muscles to move air.
– The rate of oxygen uptake (consumption), the VO2, at rest and at different levels of ventilation is
measured by monitoring the O2 levels in inhaled and exhaled air.
– If breathing is the only work the subject is performing, the difference between the VO2 at rest and
the VO2 during energetic breathing will reflect the oxygen cost of breathing.
– Healthy subjects’ respiratory muscles consume O2 at a rate of 0.5 – 1 ml/L of increased ventilation
(ventilation above resting VT). This is still less than 5% of the body’s total O2 consumption.
– At extremely high levels of ventilation (above 120 L/min) the oxygen cost of breathing increases
greatly in healthy individuals. This is one of the factors that limits athletic performance.
• Are patients with lung disease able to achieve high levels of ventilation? Why?
– In patients with pulmonary disease, the oxygen cost of breathing can become so high that the
patient’s exercise tolerance is severely reduced.
Reference: Note, Text pg. 236-39 23
 Work of Breathing: Oxygen Cost of Breathing
• The oxygen cost of breathing is the amount of O2
consumed by the respiratory muscles themselves.
• In healthy individuals, this is about 0.5 to 1 ml of O2 for
every liter total ventilation (the VE).
• This represents less than 5% of the body’s total O2
consumption (VO2).
• During vigorous exercise, when VE is >100 L/min (Text
uses120 L/min), the oxygen cost of breathing will
increase tremendously because all the respiratory
muscles (both primary and accessory) are working at or
near maximum (generating higher pressure equals doing
more work).
– At some point the cardiopulmonary system will be
unable to deliver sufficient O2 to all the muscles.
– This is a major limiting factor in human performance.
• In advanced COPD, when the primary muscle of
ventilation (the diaphragm) is either working at a reduced
• Measuring VO2 in an exercise physiology lab. level or not working at all:
• Healthy, athletic subjects perform vigorous exercise • The burden of breathing falls to the much less
to determine their limits of performance and efficient accessory muscles.
endurance. • At the same time, the efficiency of the damaged lungs
• The Pdi/Pdi Max ratio is another useful test in this in extracting oxygen from the air is reduced.
setting. • In these cases, the oxygen cost of breathing can rise
• Obviously these tests are impossible for patients to as much as 10 ml O2 per Liter of ventilation.
like the Guy in the Chair. • Rather like making the minimum payment on a large
balance-high interest credit card, a no-win situation.
𝐕O2 • Fig. 11-14 compares the oxygen cost of breathing (respiratory muscle VO2) to minute
ventilation (VE) for normal subjects and patients with COPD (emphysema).
• The normal curve is flat over the range of VE seen at rest and during moderate exercise.
• Oxygen cost only begins to increase at exercise levels requiring VE approaching 60L/m.
• In COPD the oxygen cost of breathing is high at rest and rises steeply with even low levels of
exercise.
Reference: Text pg. 239 & Mini-Clini, 242, 483, 1166-67 24
 Ventilation: Distribution of Ventilation 1
Air inhaled with every breath is not distributed uniformly, even in normal lungs. In disease, especially
COPD, the distribution of ventilation is often so uneven as to be a major cause of morbidity and
mortality. A number of reasons for this maldistribution exist, including the force of gravity, the thoracic
shape, and the movement of the diaphragm; but all the causes produce three simple results:
1. Uneven resistances to airflow in different parts of the lung.
2. Uneven compliances in different lung regions.
3. Uneven distending pressures applied to different areas of the lung.
• Alveoli generally have similar volume capacities (size limits) and similar pressure/volume (elastic)
characteristics. Alveolar pressure is atmospheric (0 PSIG) everywhere in the lung during inspiration.
• So far, pleural pressure has been presented as if it were uniformly -5 cmH2O at FRC throughout the
lung, but that is not the case. The -5 cmH2O figure actually represents the average pleural pressure at
the middle level of the lung.
• The adult lung is about 30 cm long from apex to base. The lung’s weight pulls down on the apical
segments and presses the basal segments against the diaphragm.
– This makes the resting Ppl at the lung apices closer to -10 cmH2O and Ppl at the lung bases nearer to
-2.5 cmH2O.
– Ppl increases (gets less subambient) by about 0.25 cmH2O for every cm downward from the apices
to the bases.
• The transpulmonary pressure gradient (Ptp) at the lung apices is high: (0) - (-10) = 10 cmH2O.
– This gives the apical alveoli a large resting volume but little room to expand during inspiration so
their compliance is low and that puts them on a flat part of the V/P curve.
• The Ptp at the bases is low: (0) - (-2.50) = 2.5 cmH2O.
– This gives the basal alveoli a small resting volume but a larger change in volume per unit of Ppl
change and puts them on a steep part of the V/P curve.
– The phenomenon of small resting volume with large ventilation also applies to dependent lung
areas when the patient is placed in the supine and lateral positions.

25
Reference: Note, Text pg. 239-41
 Ventilation: Distribution of Ventilation 2
• In the upright lung, basal alveoli are closer to the diaphragm and are exposed to a greater range of
diaphragmatic excursion (the lower thorax expands about 50% more than the upper chest).
• The higher (less subambient) Ppl at the bases also exerts more transmural pressure on the small
airways (Fig. 11-15), predisposing them to collapse, especially at low lung volumes (near RV).
– This means that patients breathing shallowly (as in obesity, post operative pain, post anesthesia
depression, etc.) may actually have poorer ventilation in their bases because of early airway closure
during exhalation and consequent air trapping.
• Pleural pressure is not evenly transmitted across the lung because some of the pressure (energy) is lost
overcoming tissue viscous resistance.
– For this reason alveoli at the lung periphery (closer to the pleura), get higher distending pressures
than alveoli deeper in the lung.
• Local differences in alveolar compliance will affect the filling and emptying (ventilation) of lung
segments. These differences will effect the Time Constants of lung regions.
– Alveoli with high compliance take longer to fill because they can accommodate a larger volume, but
they also have less elastance and therefore empty more slowly.
– Alveoli with low compliance fill more quickly because they can only hold a smaller volume, but their
high elastance lets them empty more quickly.
• Local differences in airway resistance also affects emptying and filling of lung areas.
– RAW determines the magnitude of the pressure drop across the airway.
– Pressure used up overcoming RAW is not available to overcome elastance and expand alveolar
volume.
• The size (caliber) of the airway can be effected by a number of factors, including:
– Causes of local obstruction such as secretions or irritation.
– Local airway compression may be caused by body posture or by compression of small airways during
exhalation (Fig. 11-15).
Reference: Text pg. 240 26
 Ventilation: Distribution of Ventilation 3
• Figure 10-18 graphs the difference in Ppl between the top
and the bottom of the lung.
•The reason for the difference is the effect of gravity (the
weight of the lung) which pulls on the visceral pleura at the
apices and compresses it at the bases.
•These effects make Ppl at the apices lower (more
subambient) and Ppl at the bases higher (less subambient).
•The Transpulmonary Pressure Gradient (∆PTP), the pressure
difference between the alveoli and the pleural space, is the
alveolar distending pressure.
•Alveolar distending pressure at the apices is about four times
as high as it is at the lung bases.

• Medical student volunteers inhaled radioactive

133xenon gas and performed a breath hold while
standing in front of a battery of radiation counters.
-Xenon gas is relatively insoluble in plasma, so
inhalation produces a high instantaneous reading
from well ventilated alveoli.
- Xenon readings indicate that ventilation was
distributed into three “zones” in the upright lung:
- Ventilation per unit volume is greatest at the lower
zone (lung bases), lower in the middle zone, and
lowest in the upper zone (lung apices). This
distribution resulted from the force of gravity on the
upright lung.

Reference: Text pg. 240 & Rule of Thumb.

27
 Ventilation: Dead Space vs Alveolar Space
• The figure (upper right) shows that all the lung parenchyma (alveoli) are
located distal to the airway opening.
– That means that all of the conducting airways are proximal to the
acini; the lung parenchyma.
• The conducting airways constitute the anatomic deadspace (VDanat or
just VD).
– Assessment of alveolar dead space requires an accurate
measurement of the anatomic dead space (VDanat).
• The figure (middle right) gives an idea of the huge number of airways
that make up the VD of the human lung.
• Clearly, the volume of the anatomic VD cannot be measured directly.
• The anatomic VD stated in most texts is derived from calculations using
Fowler’s equal area method.
– Fowler’s technique results in an estimated VD of 1 ml/lb (2.2 ml/kg)
of predicted (aka ideal) body weight.
• All of the methods, Fowler’s, as well as the methods of Hatch,
Cummings, and Bowes, use capnograms and elaborate mathematical
calculations to determine VD from exhaled CO2.
• The figure (lower right) shows a normal capnographic curve of exhaled
CO2 from an intubated subject
– The portion of the curve from beginning of expiration to point A
(called phase I) represents deadspace gas that contains virtually no
CO2. Phase I is used to calculate anatomic VD.
– The curve from point A to pint B (phase II) shows a rapid rise in
CO2 as alveolar gas rich in CO2 mixes with dead space gas.
– The slope from point B to C (phase III) shows a plateau indicating
that exhaled gas is mostly coming from ventilated and perfused
alveoli.
– End expiration, point C, represents end-tidal gas and the PCO2 at
this point is called end tidal CO2, abbreviated PetCO2.
– The rapid drop in exhaled CO2 at end expiration indicates that no
more CO2 is being exhaled and inhalation of fresh air has started.
– The difference between the PaCO2 and the PetCO2 is very small in
normal individuals The difference increases in various disease
states.
Reference: Note, Text pg. 243, 244 & Table 11-4. 28
 Ventilation: Dead Space vs Alveolar Ventilation
Read the numbers in the little green
circles. The numbered bullets in this
box describe what is happening in the
picture.
1. Is the END OF AN INSPIRATION:
• A VT of 500 ml (ambient air with
a PO2 160 mmHg) has been
inhaled.
• The lungs now contain the 2200
ml FRC + the 500 ml VT = 2700
ml.
• Of the 500 mL VT, 150 ml
remains in the anatomic VD
(Vdanat).
2. Is EXPIRATION:
• The 500 ml VT is exhaled.
•The first 150 ml exhaled is
ambient air from the VD.
•The next 350 ml exhaled is
alveolar gas.
•The lungs now contain the 2200
ml FRC.
3. Is the END OF EXPIRATION:
• The lungs contain 2200 ml FRC.
• The VD contains 150 ml of
alveolar gas (stale air).
4. Is the START OF THE NEXT
NSPIRATION:
•Inhale a 500 ml VT (ambient air).
•The first 150 ml of the VT is stale
air from the VD.
•350 ml of fresh air reaches the
alveoli.
•150 ml of fresh air remains in the
VD.
Alveolar and anatomic dead space ventilation in a normal subject with 150 mL of
VDANAT. Reference: Text pg. 243 29
 Ventilation: Efficiency
• Ventilation is the mechanical process of moving gas (usually air) between the atmosphere and
the alveoli in order to meet the body’s needs for O2 uptake and CO2 removal.
• Ventilation can be spontaneous (breathing) or artificial (mechanical ventilation).
• For survival, ventilation must maintain normal concentrations of O2 and CO2 in alveolar gas.
– (Diffusion maintains normal partial pressures of O2 and CO2 in capillary blood).
• Ventilation is measured per minute as Minute Ventilation (VE),1 the amount of air moved in and
out of the airways and alveoli in one minute: VE = Tidal Volume x Respiratory Rate. (VT x RR)
– In healthy individuals, VE is controlled by the central chemoreceptors responding to the level
of CO2 in the blood.
– CO2 production and therefore PaCO2 depends on body size and the rate of metabolic
activity. VE normally ranges from 5 to 10 L/m in healthy adults at rest
• VE is not the amount of air that reaches the alveolar/capillary (A/C) membrane because it does
not include the volume of air in the anatomic dead space (VD).
– (VD ≈ 1 ml /lb or 2.2 ml/kg of PBW) For example, a150 lb patient’s VD ≈ 150 ml.
– Dead space ventilation (VD ) is “wasted.” The equation is: VD= VD x RR.
• The amount of air that reaches the gas exchange surface in the lung is called the Alveolar
Minute Ventilation (VA). The equation is: VA = VT - VD
If our 150 Lb. patient has a VT of 500 ml and a RR of 12 his VE = 500 ml x 12 = 6000 ml (6 L).
His VD(wasted ventilation) = 150 ml x 12 = 1800 ml (1.8 L).
His VA (effective ventilation) = (500 ml – 150 ml) x 12 = 350 mL x 12 = 4200 ml (4.2 L).
If his VT becomes 250 mL and he doubles his RR to 24, his VE still = 250 x 24 = 6000 ml (6 L).
But his VD(wasted ventilation) will increase: 150 ml x 24 = 3600 ml (3.6 L).
And his VA (effective ventilation) will drop: (250 ml -150 ml) = 100 ml x 24 = 2400 ml (2.4 L)

1 𝐕 actually means the volume of air exhaled over one minute. Exhaled air is
E Reference: Note,
easy to measure, and it obviously reflects the volume that was inhaled. Text pg. 242-46
30
 Ventilation: Dead Space (VD) Ventilation
• Calculating wasted ventilation (VD) is essential in assessing the efficiency of ventilation.
• VD is usually considered in two categories: Anatomic VD(aka VDanat) and alveolar VD.
• When the categories are assessed together the measurement is often called physiologic VD.
– As usual, you will find great variation in the terminology as you read different sources.
• The ventilation wasted in the VDanat ≈ 1 ml/Lb (2.2 ml/Kg) of Predicted Body Weight (PBW).
– VDanat can increase slightly with large inspirations because radial traction expands the
bronchi increasing their volume.
• Any gas that ventilates unperfused alveoli reduces effective ventilationand increases the VD.
• Increased VDphys is usually caused by pulmonary circulation defects. The most common is
pulmonary embolus which blocks perfusion to ventilated alveoli.
• Physiologic dead space (Vdphys) is the sum of Vdanat and Vdalv . (Vdphys = Vdanat + Vdalv).
• Minute alveolar ventilation (VA ) is best assessed as respiratory rate (fB) times physiologic dead
space: fB x (VT - Vdphys ) or simply: VA = VE - Vdphys.
• The Dead Space/Tidal Volume Ratio (VD/VT) is a measure of the amount of wasted ventilation
per breath.
• Arterial CO2 (PaCO2) and mixed expired CO2 ( PE CO2) must be known to calculate VD/VT.
–PaCO2 comes from the arterial blood gas and PECO2 is measured from a collected gas
sample or from an exhalation capnograph.
(PaCO −PECO )
• A modified version of the Bohr equation is used to calculate VD/VT: VD/VT = 2 2
PaCO2
• A patient with a normal PaCO2 of 40 mmHg and a normal PE CO2 of 28 mmHg will have a
VD/VT:
(40 −28) 12
VD/VT = = = 0.3 which means that about 30% of his ventilation is wasted.
40 40
• Normal VD/VT ranges between 0.2 to 0.4. It decreases with exercise because VT increases.

Reference: Note, Text pg. 243-45 31

 Ventilation: Pulmonary Time Constants
• When a change in pressure (∆P) is applied to a lung unit, it takes a certain
amount of time until a change in volume (∆V) occurs. This applies to both
inspiration and expiration.
• Compliance and resistance determine the rate (time) of alveolar filling and
emptying.
• The combined effects of lung compliance (CL) and airway resistance (RAW)
on a lung unit can be measured as a physical property called the unit’s time
constant (Tc).
– The ventilation Tc is simply the product of airway resistance and
pulmonary compliance, the formula is: Tc = RAW x CL.
– RAW is expressed in cmH2O/L/second, and CL is expressed in L/cmH2O.
• All the units will cancel out except time (second), so Tc is expressed in
seconds.
– For example, normal RAW is 2.5 cmH2O/L/s ec and normal CL is 0.2
L/cmH2O:
• Normal Tc will be 2.5 x 0.2 = 0.5 second.
• Lung units with high compliance and/or high resistance will have a longer
than normal Tc:
A graph of the effect of abnormal
–They have a larger inspiratory volume and their low elastance takes more CL and RAW on the time constants
time to empty. of lung units exposed to equal
• Lung units with low compliance and resistance will have a shorter than inflation pressures.
• Lung unit A has normal RAW and
normal Tc. CL so it fills and empties at a
– They have a smaller inspiratory volume and their high elastance lets normal rate and has a normal
them empty quickly. Tc.
• Lung unit B has normal RAW and
• Frequency dependence of compliance, is observed in patients with COPD reduced CL so it fills and
when the small number of lung units with relatively normal Tc’s get more empties at a faster rate and has
ventilation than abnormal units. As normal Tc units fill, their CL goes down. a low Tc.
• Dynamic compliance assesses P/V relationships during breathing. • Lung unit C has normal CL but
high RAW so it fills and empties
• Patients with abnormal Tc receiving positive pressure mechanical ventilation at a slower than normal rate and
may experience dynamic hyperinflation (air trapping) and intrinsic PEEP. has a high Tc.

Reference: Note, Text pg. 241 & Rule of Thumb, 242 & Fig. 11-16, 1001 & Fig. 45-19 32
 Ventilation: Basic Ventilator Graphics (Again)
Chapter 10 is supposed to be about spontaneous ventilation, but the author often puts concepts from
mechanical ventilation into the text. These intrusions may be a problem because the text rarely makes a clear
distinction between the spontaneous and the mechanical. One intrusion from mechanical ventilation that is
valuable are the Ventilator Waveforms (aka Graphs). Modern intensive care ventilators are microprocessor
controlled machines capable of monitoring and displaying a large amount of information about the main
parameters of mechanical ventilation: pressure, volume, flow, and time. These parameters are most often
displayed on the ventilator screen as graphs or waveforms that compare, pressure to time, volume to time,
and flow to time. Since the parameters are compared to time, the waveforms are called scalars (as opposed
to vectors that compare a parameter to direction).

Reference: Pg. 992 & Fig. 45-5.

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