Notes to Chapter 11 (Ventilation) 11th ed.

Slides

Note to Slide 2: Lung Volume Measurement

There are 4 primary lung volumes:
1. Tidal Volume (VT) the amount of air inhaled and exhaled during a normal, resting breath.
2. Inspiratory Reserve Volume (IRV) the additional amount of air that can be inhaled at the end of a tidal
inspiration.
3. Expiratory Reserve Volume (ERV) the additional amount of air that can be exhaled at the end of a
tidal exhalation.
4. Residual Volume (RV) the amount of air left in the lungs after a forceful (maximal) exhalation.
There are 4 primary lung capacities:
(Lung capacities consist of two or more lung volumes added together)
1. Vital Capacity (VC) the maximum amount of air that can be moved in or out of the lungs in a single
respiratory cycle. Usually a deep inspiration to TLC followed by a maximal exhalation to RV. The
formula is: VC = ERV + VT+ IRV.
2. Inspiratory Capacity (IC) the additional amount of air that can be inhaled from the end of a tidal
exhalation. The formula is: IC = VT + IRV.
3. Functional Residual Capacity (FRC) the amount of air left in the lung after a tidal exhalation. The
formula is: FRC = ERV + RV.
4. Total Lung Capacity (TLC) the total amount of air in the lungs after a maximal inhalation. The formula
is: TLC = IRV + VT + ERV + RV
Clinical Practice Notes:
• The figure on the Slide shows a conventional water sealed spirometer.
- Spirometers can only measure lung volumes that can be exhaled.
- Since the residual volume (RV) can’t be exhaled, spirometers cannot measure TLC and FRC.
- These capacities are measured with other devices and techniques.
• The “Minimal volume” on the spirogram represents the amount of air that would be left in the lungs if
they were removed from the thorax during an autopsy. One of the autopsy procedures is to remove the
lungs and see if they float in water. If the lungs sink one possible cause of death has been identified.

Obstructive Pulmonary Impairment:

• Obstructive lung diseases, such as asthma and emphysema (COPD) are characterized by reduced
expiratory flow rates, especially the Forced Expiratory Volume in 1 second (FEV1) measurement.
• In obstructive diseases the total lung capacity (TLC). is normal or even increased, this is especially true
in advanced COPD.
• It is important to remember four facts about asthma:
1. Asthma is an obstructive disease.
2. The condition is usually chronic.
3. However, the signs and symptoms are episodic (they come and go) while with COPD the signs
and symptoms are continuously present.
4. Therefore, we should reserve the term COPD for chronic bronchitis and emphysema.
• The symptoms and functional limitations of chronic obstructive pulmonary disease are caused by
pathological processes in the airways (asthma) and in the airways and the lung parenchyma (COPD).
1
 1. These processes lead to airflow obstruction, increased work of breathing (WOB), and gas
exchange abnormalities.
2. Over time, the processes can cause pulmonary hypertension, cor pulmonale, and left ventricular
dysfunction.
3. All of this will severely limit the patient’s exercise tolerance and ability to perform the activities
of daily living (ADL).
Restrictive Pulmonary Impairment:
• Restrictive lung diseases are characterized by reduced TLC and other lung volumes, while expiratory
airflow and airway resistance are usually normal.
• The many disorders that cause reduction of lung volumes (pulmonary restriction) may be divided into 2
groups based on the anatomical structures affected:
1. The first group is intrinsic lung diseases or diseases of the lung parenchyma (aka diffuse
parenchymal lung disease).
• Disorders of the pulmonary interstitium (interstitial lung disease), cause inflammation
and scarring of the lung tissue or result in filling of the air spaces with exudate and
cellular debris (pneumonitis).
• Restrictive impairments include idiopathic fibrotic diseases, connective-tissue diseases,
drug-induced lung disease, and primary diseases of the lungs including sarcoidosis.
• Sarcoidosis is an autoimmune disease that causes granulomas (masses
of inflammatory cells) to accumulate in the body, most commonly the
lungs, lymph nodes, eyes and skin.
2. The second group includes the extrinsic disorders (aka extra-pulmonary diseases).
• The chest wall, the pleura, and the respiratory muscles make up the respiratory pump or
chest bellows.
• If these structures do not function normally, ventilation will be abnormal.
• The mnemonic "PAINT" has been used to help remember the causes of restrictive lung
disease:
• Pleural, for example: trapped lung, pleural scarring, large pleural effusions,
chronic empyema, asbestosis.
• Trapped lung occurs when part of a bacterially infected lobe and
visceral pleura 'fix' the affected lung in a partially collapsed position.
• Alveolar, for example:
• Interstitial,
• Neuromuscular, and
• Thoracic cage abnormalities.
• Common assessment findings include: Dry (non-productive) cough, shortness of breath,
and the presence of ground glass opacities on chest x-ray.
• If restrictive disorders are complicated by parenchymal lung disease, gas transfer across
the A/C membrane may be reduced.
• This will most often be seen by severe arterial desaturation (reduced SaO2) after
exercise such as the six minute walk test.
- .
Note to Slide 3:
• The primary function of the respiratory system is the continuous exchange of gases between the
lung parenchyma (the A/C membrane) and the atmosphere.
• Carbon dioxide (CO2) is continuously produced by the body’s cells and must be continuously
removed and excreted into the atmosphere.

2
 • At the same time, oxygen (O2) is continuously being used by the cells, and a constant supply
must be absorbed from the atmosphere.
• Ventilation is the term for the mechanical process of gas exchange between the lungs and the
atmosphere.
• Respiration is the term for the complex cellular processes of producing ATP in the
mitochondria.

Note to Slide 4: Breathing Pressures

• Text, pg. 227, uses the symbol ∆Pressure to indicate the force generated by the respiratory muscles or
the mechanical ventilator during inspiration.
• Figure 11-1 uses the symbol ∆PMUIS to indicate the pressure generated by the respiratory muscles during
spontaneous inspiration.
• Table 11-2 uses the symbol ∆PMUIS to indicate what he calls the global muscle pressure difference.
Both the Figure and the Table are referring to the muscle energy needed for spontaneous inspiration.

Note to Slide 5: Measuring Lung Pressures

On pg. 228, the author states that “What may be confusing is that there are other definitions of Transpulmonary
pressure in the literature.”
• In my opinion, the author is confused and is needlessly spreading his confusion.
• Trans anything means across, so transpulmonary means across the lung.
• By the same token, transpulmonary and transrespiratory are essentially interchangeable terms that mean
across the lung and across the respiratory system.
• Lung and Respiratory System are just different terms for all the tissue structures between the
airway opening and the alveoli.
• Also, the transairway pressure gradient is just the difference in pressure across the airway, from the
opening to the alveolar ducts.
In spontaneous breathing, inspiratory pressure gradients are produced by muscle effort that reduces first pleural
pressure and then alveolar pressure below ambient.
In positive pressure breathing (mechanical, machine, ventilator – pick the term you like best) the pressure
gradient to move air into the lung is produced when the machine compresses a volume of gas and pushes it into
the patient’s lungs through an artificial airway.

Clinical Practice Note

• Increased pressure in the abdominal cavity restricts diaphragmatic excursion (movement) and limits
ventilation.
• Causes of increased abdominal pressure include:
• Large abdominal tumors.
• Severe obesity (sometimes complicated by acute overeating).
• Third trimester pregnancy.
• Diaphragmatic hernias.
• Large abdominal ascites.
• Abdominal pressure can be measured with a swallowed esophageal catheter.
Some mechanical ventilators include an input port) for monitoring abdominal pressure with the swallowed
catheter.
3
 Alveolar Pressure (Palv) is measured with an integrated volume
and flow monitor.
• A healthy subject inhales a known volume of air then holds the
breath with the glottis open.
- At this point the pressure in the lungs equals only the elastic
recoil pressure of the lungs because the respiratory muscles
are expending energy to hold the chest wall fixed in an
expanded position.
• The subject then seals the mouthpiece tightly, pinches the nostrils
shut, and relaxes the respiratory muscles.
• The pressure at this point is the relaxation pressure.
- It equals only the elastic recoil pressure of the chest wall
because the sealed mouth and nose trap air in the lungs.
- The trapped air generates a pressure equal to the lung’s elastic
recoil pressure, cancelling lung recoil out of the measurement.

Pleural Pressure (Ppl) is measured with an esophageal

balloon catheter:
• Pleural pressures are not measured directly in humans (too
difficult & traumatic).
• They are approximated by having the patient swallow an
esophageal balloon which remains in the esophagus between
the lungs.
• The flexible esophagus responds to pressure changes in the
thoracic cavity and transmits them to air in the balloon which is
connected to a pressure transducer.
Transdiaphragmatic Pressure (Pdi) is measured with
esophageal and gastric balloon catheters:
• Pdi is used to measure of diaphragmatic strength and excursion.
• It is measured by having the patient swallow a double
esophageal balloon catheter.
- One catheter remains in the esophagus above the
diaphragm (intrathoracic Pdi or Ppl)
- The other catheter goes into the stomach below the cardiac
sphincter (gastric Pga).
• Diaphragmatic contraction lowers thoracic pressure and
increases abdominal pressure.
• Transdiaphragmatic pressure is calculated as: Pdi = Pga - Ppl

Note to Slide 6: The Equation of Motion

• Breathing is a type of work in which energy in the form of pressure is exerted to overcome resistance in
order to move air.
• The heartbeat is exactly the same type of work, except that it is bold not air that is being moved.
• Breathing is a cyclical process: inspiration followed by expiration.
• The cycle repeats continuously as long as the body is alive.
• Air moves in and out of the lungs in response to pressure gradients.
• In spontaneous breathing those gradients are produced by the action of the respiratory muscles.
• With mechanical ventilation the gradient for inspiration is produced by the ventilator.
• A spontaneous breath starts when the respiratory muscles begin to contract and the thoracic cavity
begins to expand.

4
 • Rib cage expansion pulls the parietal pleural layer outward while lung’s elastic recoil pulls the
visceral layer inward.
• As a result, pressure in the pleural space (Ppl) becomes more subambient.
• The subambient Ppl reflects across the alveolar capillary (A/C) membrane and alveolar pressure (PA)
begins to become subambient.
• This produces a pressure gradient between the airway and the atmosphere and air begins to flow down
that gradient into the lungs.
• Writers can make the name used for this pressure gradient confusing, for example:
• The text calls the difference between the pressure at the airway opening and pressure at the body
surface (PAO ─ PBS) the transrespiratory pressure gradient (PTR).
• While it is obvious that the airway opening is at the body surface, the statement is correct for
spontaneous inspiration because the subambient PPL reflects across the A/C membrane and
lowers pressure throughout the airway all the way up to the airway opening.
– The text’s statement is clearer if we understand that PAO means inside the
airway opening.
• The text also lists additional gradients: The transairway (Ptaw) gradient, the transpulmonary
gradient (Ptp), the transalveolar (PTA) pressure gradient, the transthorachc (PTT) gradient, and the
global muscle pressure difference (Pmus).
• It is clear that each of these gradients carries some of the responsibility for moving air
during breathing.
• The significance of these additional gradients is that if the pressures that make them up can be
measured, they may reveal information about the condition of the different parts or subdivisions
of the respiratory structures shown in the model in Fig. 11-1.
• During normal spontaneous breathing, the glottis remains open and pressure at the body surface and
outside the airway opening remain ambient.
Physiology Note:
• Voluntary glottic closure near the end of expiration produces a “grunt.”
• End expiratory grunting is NOT a normal finding.
• Premature infants often perform this maneuver to help prevent alveolar collapse.
• Grunting is defined as:
• Abnormal, short, deep, hoarse sounds in exhalation that often accompany severe chest pain.
• The grunt occurs because the glottis briefly closes and stops the flow of air, halting the
movement of the lungs and their surrounding or supporting structures.
• Grunting is most often heard in a person who has pneumonia, pulmonary edema, or fractured or
bruised ribs.
• In neonates with respiratory problems including atelectasis, grunting generally occurs
throughout expiration as the baby forcefully exhales against a partially closed glottis.
• It appears to be a self-administered form of peak end expiratory pressure (PEEP); by
maintaining a high alveolar pressure atelectasis is reduced and ventilation and gas exchange are
improved.
Physics Note:
• In biological systems (living bodies), mechanical work occurs when a force is applied to a structure that
results in movement.
• The amount of work is calculated as the product of the force applied and the distance moved:
• Work = Force x Distance
• In spontaneous ventilation:
• The Force is the pressure generated by the respiratory muscles.
• The Distance is the Tidal Volume (VT).

5
 • Please think about the equation of motion in terms of pathological increases in resistance and
decreases in muscle and recoil strength.
• Remember that oxygen is essential to the production of the ATP needed for muscle contraction.
• Consider the O2 cost of breathing, especially in COPD.

Math Notes to the Equation of Motion:

• The equation of motion describes the interactions between the source of energy for breathing (i.e. the
respiratory muscles or the ventilator); the patient’s pulmonary mechanics (i.e. lung and chest wall
compliance and airway resistance).wall compliance. The classic equation of motion is really a simple
statement:
P (t) = PEL (t) +PRES (t)
t indicates the time the pressure is applied (i.e. during inspiration and expiration).
• Any pressure (P) applied to the system is either stored as elastic pressure (Pel) or dissipated as resistive
pressure (Pres):
• The text’s simplified equation of motion for the respiratory system (pg. 227) simply adds the resistances
of elastance and airway frictional resistance.
• The elastic resistance (PEL) of the lung and chest wall is the result of compliance and tidal volume:
PEL = VT / CL
• The non-elastic or frictional resistance (PRES) is the result of flow (V dot) and airway resistance:
PRES = V x R
• This may be clarified by studying pg. 238, Fig. 11-13.
Basic mechanisms:
In a spontaneously breathing subject, the pressure generated by the respiratory muscles (P or more precisely,
PMUS) during inspiration is dissipated (used up) to overcome both the elastic and resistive forces opposing
respiratory system inflation, as described by the equation of motion for the respiratory system:
Pmus = (Rrs × VI) + (Ers × V)
Where:
• Ers is the elastance of the respiratory system,
• Rrs is resistance of the respiratory system,
• VI is inspiratory flow rate.
• V is volume of the respiratory system above functional residual capacity (FRC).
It should be obvious from the equation of motion that if the muscle force available is lower than the load,
the result will be respiratory failure.

Terminology Note:
• Ohm’s Law helps us understand the equation of motion:
• Ohm’s Law expresses the relationship between voltage, Resistance, and current in an electrical
circuit.
• In electricity voltage is analogous to pressure and current is analogous to flow.
• Ohm’s formula for Resistance is: R = Voltage/Current.
• The analogous formula for breathing is: Voltage drop (which is V1 – V2) divided by Flow:
• R = (V1 – V2) / Flow

6
Classic respiratory mechanics is based on Newtonian physics as expressed in the equation of motion. The
respiratory system is considered to be a resistive and elastic element in series. Any pressure (P) applied to it is
either stored as elastic pressure (Pel) or dissipated as resistive pressure (Pres):
P (t) =Pel (t) +Pres (t)
where t indicates a particular time
Note to Slide 7: Pressure Gradients
• NOTE that the order in which the gradients are presented in the text on pg. 228 is different than
the order in Table 11-2.
• It may seem as if the author set out to make pg. 228 as confusing as possible.
• But buried within the confusion there are some useable facts:
• Figure 11-1 shows that the airways and lungs can be easily described as one big resistive tube
(airway) ending in one big compliant-elastic balloon (alveoli) contained within another compliant-
elastic structure (the pleural membranes).
• Spontaneous breathing, particularly inhalation, requires that the respiratory muscles create a
gradient between the atmosphere and the alveoli.
• Examining the pressures needed for the various subdivisions of these gradients can indicate the
condition of the structures responsible for the gradient:
- Normal of high airway resistance:
- Normal, high, or low lung and chest wall compliance.
- Normal or low respiratory muscle strength.
• Spontaneous ventilation (breathing) occurs due to pressure gradients (differences) between
atmospheric (ambient) pressure and alveolar pressure.
• Alveolar pressures change in response to changes in pressure in the pleural cavity (aka the pleural space)
called pleural pressure changes.
- Remember that in order for air to flow into or out of the lungs, alveolar pressure has to be
lower or higher than ambient.
• Airway pressures below 760 mmHg are subambient.
• Subambient pressures are often incorrectly called negative pressures.
The error is almost universal, so it is OK, as long as YOU know what is correct.
• Note that some writers prefer to describe PPL and PALV in mmHg.
• This is because alveolar and pleural pressures vary slightly above and below atmospheric and
atmospheric pressure is usually described in mmHg.
• Don’t let this confuse you:
• 760 mmHg ≈ 559 cmH2O.
• To convert from one set of units to the other, just multiply by a conversion factor:
• MmHg = cmH2O x 0.7355
• cmH2O = mmHg x 1.36
Pressure Differences Shown on Page 228 of the text:
The author has developed a unique set of terms and values for breathing pressures and gradients.
Please note the following:
• The prefix Trans means across.
• The text uses the root Respiratory for the entire respiratory system, including the airways, lungs,
pleura, and the chest wall.
• The text also uses the root Pulmonary for the airways and the alveolar region of the lung).
 Transrespiratory Pressure gradient; abbreviated PTR or PRS and symbolized ∆PTR.
─ PTR is the pressure difference between the atmosphere (the airway opening and the body surface) and the
alveoli.
─ The text defines PTR as the difference between pressure at the airway opening and the body surface (PAO
– PBS).
7
 ─ Fig. 11-2 on pg. 228 and Slide 5 show that this is essentially a correct statement for the following
reasons:
1. Airway pressure and alveolar pressure are the same during breathing.
2. As pleural pressure decreases alveolar and airway pressures also decrease.
3. Pressure at the proximal end of the airway, the airway opening, will also be lower than ambient.
4. The statement “for inspiration, PAO is higher than PBS” is only correct for positive pressure
ventilation, NOT for spontaneous breathing.
• Pleural pressure is measured indirectly by a swallowed balloon tipped catheter that remains in the
esophagus between the lungs.
• Transdiaphragmatic pressure (Pdi) is measured with two esophageal balloons, one remains above the
diaphragm and the other below the diaphragm.
Note to Slide 8: Pressure, Volume, and Flow

INSPIRATION
TIME 0: End Expiratory Pause:
• During the EEP (the brief pause between
breaths) alveolar pressure is equal to
atmospheric pressure 0 mm Hg (point A1).
- When pressures are equal, there is no air
flow.
TIME 0–2 SEC: Inspiration.
• The inspiratory muscles contract, and thoracic
volume increases.
- Increased volume lowers alveolar pressure
about 1 mm Hg below atmospheric
pressure (point A2),
- Air flows into the alveoli (point C1 to point
C2).
- Since thoracic volume changes faster than
air can flow in, alveolar pressure reaches
its lowest value about halfway through
inspiration (point A2).
• As air continues to flow into the alveoli,
pressure increases until the thoracic cage stops
expanding, just before the end of inspiration.
- Air flow continues for a fraction of a
second longer, until alveolar pressure
equalizes with atmospheric pressure (point
A3).
• At the end of inspiration, lung volume is at its
maximum for the breath cycle (point C2), and
alveolar pressure is equal to atmospheric
pressure.
EXPIRATION
TIME 2–4 SEC:
• Respiratory muscles relax during expiration
- Lung and thoracic volumes decrease.
• Air pressure in the lungs increases to about 1 mm
Hg above atmospheric pressure (point A4).
• Alveolar pressure is now higher than atmospheric
pressure, so air flow direction reverses and air
flows out of the lungs.
TIME 4 SEC:
• At the end of expiration alveolar pressure is again
equal to atmospheric pressure and air flow stops
(point A5).
- Lung volume reaches its minimum for the
breath cycle (point C3).
• At this point, the breath cycle has ended and after
the EEP the body is ready to begin another cycle
with the next breath.
- The pressure differences shown in the figure
apply to quiet breathing.
- During exercise or forced heavy breathing,
these values become proportionately larger.

8
Note to Slide 9: RR, VT, & BCT
Physiology Note:
• Normal breathing values are based on the basal Energy Expenditure (BEE) which is more commonly
called the Basal Metabolic Rate (BMR).
• The BMR measures the rate at which a healthy, resting, awake adult breaks down nutrients to release
energy.
• The BMR measures the minimum amount of energy that must be produced to sustain life,
wakefulness and a normal body temperature in a comfortably warm environment.
• The conditions under which the BMR is assessed:
• The subject who has had a good night's rest and has fasted for 12 to 18 hours before the test.
• The subject has been physically, mentally, and emotionally at rest for at least 30 minutes; is lying
down, and is trying not to move any muscles.
• The subject is in a neutral thermal environment where metabolic rate is not influenced by the
ambient temperature.

Note to Slide 12: Forces Opposing Lung Inflation

Pulmonary Surface Tension:
• The resistance to inspiration (lung & chest wall expansion) exerted by the respiratory system is known
as elastance.
• Elastance of the respiratory system is the sum of elastance of the lungs and the elastance of the
chest wall.
• Since chest wall elastance normally remains relatively constant, the system’s resistance
to expansion mainly results from variations in the lung elastance.
• which depends on:
• Elastic recoil forces exerted by elastin fibers in the pulmonary interstitium.
• Forces due to the surface tension occurring at the air-interstitial fluid interface.
(Elastance forces are also responsible for the energy to expel air during expiration)
Laplace's Law applied to the Alveoli:
• According to Laplace’s law, alveolar surface tension for a particular alveolar radius must be opposed by
an appropriate transmural pressure to prevent collapse.
• This is the transpulmonary pressure.
• If the only fluid lining the alveoli was just alveolar lung liquid, the transmural pressure needed for lung
inflation would be enormous.
• However, surface tension is significantly reduced by the pulmonary surfactant secreted by
alveolar type II cells.
• When an air-fluid interface is curved (as in a bubble), the net force exerted by the surface tension would
be acting inwards, creating a large collapsing force.
• To counteract this force, a positive air pressure would have to be exerted inside the bubble or a negative
pressure would have to be exerted outside the bubble.
• According to Laplace’s Law:
• The transmural pressure (PT) required to keep such a bubble inflated is directly proportional to
the surface tension (T) at the air/liquid interface and is inversely proportionate to the radius (r) of
the bubble (Text, pg. 109).
• The relationship is: Pt = 2T/r.
Pulmonary Surfactant:
(Ch. 9 Slides and Notes)

9
 • Surfactant is a mixture of about 40% dipalmatoilphosphatidylcholine, about 40% other phospholipids,
about 5% surfactant associated proteins, and about 5% other minor compounds including cholesterol.
• Surfactant is secreted by the type II alveolar epithelial cells in response to beta adrenergic stimulation.
• Surfactant synthesis is increased by corticosteroids.
• If a mother is at risk of delivering a baby prematurely, administering steroids to the mother may
improve the baby’s lung function at birth.
• Surfactant is a detergent; it lines the air-liquid interface of the alveoli converting it into an air-surfactant
interface.
• This conversion allows surfactant to serve three functions in the lung:
• Reduces surface tension
• Maintains alveolar stability
• Reduces capillary ultra-filtration which helps to prevent pulmonary edema.
1. Reduction of Surface Tension Example:
• Without surfactant, the interstitial fluid lining the alveoli has a surface tension of about 70 dynes per cm.
• It would take a transmural pressure of 28 cm H2O to keep a surfactant free alveolus with a radius of
50µm expanded.
• Pulmonary surfactant reduces alveolar surface tension by approximately one sixth to 12 dynes per cm at
FRC.
• The surface tension reduction means that the transmural pressure required to expand the alveoli with
surfactant is only to 5 cm H2O.
2. Maintaining Alveolar Stability:
• As the alveoli get smaller (contract) during exhalation, surfactant’s surface tension reduction increases.
• This is because the thickness of the surfactant layer increases since it is covering a smaller
alveolar surface area.
• Remember that the alveoli do not all have the same radius, therefore:
• According to Laplace’s law, the smaller radius alveoli should empty into the larger radius alveoli.
• But, since the lining of surfactant becomes thicker in smaller alveoli; the reduction in surface
tension is also greater in smaller alveoli.
• This means that surfactant equalizes the intra-alveolar pressure in the smaller with the larger
alveoli.
• This prevents the smaller alveoli from emptying.
• The honeycomb-like arrangement of the alveoli also provides radial traction the help prevent the
small alveoli from collapsing.
3. Reduction of Ultra-Filtration:
(Ch. 9 Slides & Notes)
• Surfactant doesn’t just lower alveolar surface tension, it also helps to prevent pulmonary edema.
• The blood perfusing the dense alveolar capillary network, like all capillary beds, is subjected to the
Starling’s forces:
• The filtration of fluid across the capillary wall into the interstitium depends on the hydrostatic
and osmotic pressure gradients across the capillary wall.
• Without surfactant the transpulmonary pressure would have to be -28 cm H2O to expand the
alveoli.
• This would lead to a net pressure gradient acting outwards.
• Since surfactant reduces alveolar surface tension it also reduces the required transpulmonary
pressure.
• This produces a net pressure gradient that acts inwards maintaining the alveolar interstitium
relatively dry.

10
 Surfactant also helps to protect the lungs from infection:
• We know that pulmonary surfactant reduces alveolar surface tension and helps to maintain alveolar
stability during breathing.
• But surfactant is also an important part of the lung’s immune system.
• Remember that pulmonary surfactant is 90% lipids and 10% protein.
• There are four surfactant proteins: SP-A, SP-B, SP-C, and SP-D.
• Of these proteins, SP-A and SPD bind to pathogens and damage pathogen cell membranes.
• They also aid phagocytosis by alveolar macrophages through a process called opsonization (Greek
“make ready to eat”).
• SP-A and SP-D also help control the activation or deactivation of inflammatory responses by alveolar
macrophages.

Note to Slide 13: Elastance & Surface Tension

Note that in the small inset picture on the far right figure on Slide 13:
PA is alveolar pressure. PIP is intrapleural pressure.
• The expiratory limb of the pressure/volume (P/V) curve does NOT follow the inspiratory limb.
• Physiologists call the difference between the inspiratory and expiratory P/V curves hysteresis.
• Also note that as the tidal volume increases, the loop widens; why is this happening?
• For any particular volume, the pressure on the expiratory curve is less than that on the inspiratory curve.
• This is because the elastic recoil force on expiration is always less than the distending pressure
gradient used to inflate the lung.
• This is a manifestation of energy loss during exhalation.
• Energy loss is a property that is common to all elastic structures that obey Hooke's law.
• If we slowly inflate a lung, and then simply leave it inflated (prevent exhalation), the pressure in the
lung will drop to about 70 to 80% of the initial value.
• The compliance calculated from this "final" (or plateau pressure) is the static compliance.
• The compliance calculated using the higher (peak inspiratory) pressure is the dynamic compliance.
• Dynamic compliance will always be lower than the static compliance because it includes the
pressure needed to overcome airway resistance.
• Exhalation is slower than inhalation for a number of reasons including:
• Less pressure available for exhalation.
• Collapse of small airways at the equal pressure point (EPP).
Some scholarly explanations for lung hysteresis:
• The lung appears to demonstrate a "memory" of its recent volume history:
• If the lung is ventilated at low-volumes for a period of time its compliance will decrease.
• The reduction can be reversed by taking one or more deep breaths (sighs).
• In addition to elastic hysteresis, the lung has other time-dependent behaviors exhibited by elastic
structures.
• Causes for time-dependent lung elasticity may include:
• The phenomenon of stress relaxation commonly seen in elastic materials when stretched.
• Redistribution of air between alveolar units with different time constants.
• Changes in the distribution and activity of surfactant with changes in lung volume, especially
during positive pressure ventilation (see Pilbeam, Ch. 16).

Terminology Note:
11
 • Hysteresis is a term from mechanical and electrical engineering.
• The term flux is also from engineering.
• Physiologists often use engineering terms to describe physiological processes.
– Hysteresis represents the history dependence (aka memory) of physical systems, for example:
• If you push on something, it will yield (deform).
• If it does not spring back completely when you release pressure it is exhibiting hysteresis.
The term is most commonly applied to magnetic materials, but it happens in lots of other systems, including
elastic structures such as the lung.
• The elastic resistance of the lungs (pulmonary elastance, EL) and the elastic resistance of the chest wall
(ECW) act like resistors connected in series (Text, p. 233). Also see the Rule of Thumb on pg. 233.
• The total resistance of resistors in series is simply the sum of each resistor.
• Energy (PMUS) must overcome both the resistance of the lungs (EL) and the resistance of the chest wall
(ECW) to inhale.
The chapter uses the term hysteresis at least 4 times without every trying to define it, so here goes:
• Hysteresis is a term from mechanical and electrical engineering, just like the term flux.
• Physiologists often use engineering terms to describe physiological processes.
• Hysteresis represent the history dependence (aka memory) of physical systems.
If you push on something, it will yield: when you release, does it spring back completely?
• If it doesn't, it is exhibiting hysteresis.
• The term is most commonly applied to magnetic materials, but it happens in lots of other systems,
including elastic structures such as the lung.

 While the hysteresis curve at left is for magnetic materials,

NOT the lung, it is very similar to the curve for the lung in
the Text Fig. 11-5.
 The hysteresis loop shows the relationship between the
induced magnetic flux density (B) and the magnetizing
force (H).
 A magnetic material that has never been previously
magnetized or has been thoroughly demagnetized will follow
the dashed line as the magnetizing force H is increased.
 The magnetizing force is analogous to inflation and deflation
pressures shown in the Text Fig. 11-5.

Normal compliance values:

• In healthy adults, the compliance of the lungs and chest wall are approximately equal at 0.2 L/cm H2O.
• However, because the lungs are contained within the thorax, the two systems act as springs pulling
against each other.
• This reduces the compliance of the system to approximately half that of the individual components, or
0.1 L/cm H2O.
• Impedance to ventilation by the movement of gas through the airways is meant by the term airway
resistance.

12
Note to Slide 14: Compliance & Elastance
Increasing alveolar volumes

 The pulmonary compliance diagram

shows that decreases in pleural pressure
(PPL) are reflected into the alveoli.
 Subambient PPL cause air to flow into the
alveoli.
 The compliance curve has a steep slope
during which slight changes in PPL
produce large changes in alveolar
volume.
 The curve flattens out when the elastic
lungs reach their limit of expansion.
 Note that this figure can also represent
positive pressure ventilation, where
pressure is delivered directly to the
alveoli by the ventilator.

• The elastic resistance of the lungs (pulmonary elastance, EL) and the elastic resistance of the chest wall
(ECW) act like resistors connected in series (Text, p. 233). Also see the Rule of Thumb on pg. 233.
• The total resistance of resistors in series is simply the sum of each resistor.
• Energy (Pmus) must overcome both the resistance of the lungs (EL) and the resistance of the chest wall
(ECW) to inhale.
Normal compliance values:
• In healthy adults, the compliance of the lungs and chest wall are approximately equal at 0.2 L/cm H2O.
• However, because the lungs are contained within the thorax, the two systems act as springs pulling
against each other.
• This reduces the compliance of the system to approximately half that of the individual components, or
0.1 L/cm H2O.
• Impedance to ventilation by the movement of gas through the airways is meant by the term airway
resistance.

Note to Slide 15: Thorax (Chest Wall) Forces

• The Rule of Thumb (Text, pg. 231) correctly states that in terms of the pressures they exert, the lung and
chest wall pull in opposite directions against each other.
• This opposite pulling makes the two elastic springs behave like resistors connected in parallel.
The total resistance of resistors in parallel is the reciprocal of the individual resistances.

Note to Slide 16: Normal vs. Pathological CL

• Compliance of the lung appears to decrease as breathing frequency (RR) increases.
• This phenomenon is called frequency dependence of compliance.

13
 • Compliance measured during breathing is dynamic as it includes pressure changes created by resistance
to airflow.
• Since dynamic compliance decreases as the respiratory rate increases, some lung units must
have abnormal time constants.
• Any stimulus to increase ventilation, such as exercise, may redistribute inspired gas.
• Severe mismatching of ventilation and perfusion can result in hypoxemia, severely limiting an
individual’s ability to perform activities of daily living (ADL).
• In addition the increased breathing frequency and decreased dynamic compliance may result in
significant increases in oxygen consumption (V dot O2).

Note to Slide 17 Integrating Pressure & Volume

Ventilatory Muscle Work:
• The amount of work the ventilatory muscles perform is determined by:
• Minute ventilation (VE)
• Air way Resistance and Lung Compliance (Time constant)
• VE and TC together determine both ventilatory muscle efficiency and the breathing pattern the patient
will adopt.
Figure 10-12 C (Text, pg. 238) shows the increased WOB in patients with obstructive disease.
• Obstruction increases compliance and decreases elastance.
• Fig 11-13 C shows that in obstruction frictional resistive work increases.
• Clinically, airway resistance is usually assessed by measuring peak expiratory flow rates (PEFR).
• PEFR below predicted is considered evidence of increased airway resistance (RAW).
• Thought Question: Has airway resistance really increased, or might another factor be at
work?

Another view of Fig. 11-11

14
 Clinical Practice Note:
Patients adopt a breathing pattern that provides adequate alveolar ventilation with the lowest amount of work.
Figure 10-12 shows this for patients with restrictive and obstructive impairments, but it applies to normal
subjects as well.
• What might cause a patient to suddenly adopt a rapid-shallow breathing pattern?
• If you saw a patient breathing slowly and fairly deeply, what do you think might be the cause?
Respiratory muscle fatigue often complicates primary pulmonary disease. Muscles generate force by
contracting. A weak muscle is unable to contract with an adequate amount of force. The terms muscle weakness
and muscle fatigue both refer to muscles with inadequate contractile ability, but the terms refer to different
causes of weakness:
• Muscle weakness means that a rested muscle has a reduced ability to produce force
• Skeletal muscle weakness most often results from neuromuscular or systemic disease conditions.
• Muscle fatigue means that an actively working muscle is experiencing a reduction in its ability to
produce contractile force (getting tired).
• Fatigue can be reversed by resting the muscle.
• If the fatigued muscle is the diaphragm, the only way to rest it is to mechanically ventilate the
patient.
• Overt diaphragmatic fatigue is defined as the diaphragm’s inability to maintain an adequate
contraction force throughout inspiration.
• Diaphragmatic fatigue can be assessed by measuring the transdiaphragmatic pressure gradient (Pdi).
• Pdi is measured by having the patient swallow a tube with an esophageal and a gastric balloon.
• The Pdi during quiet breathing and the Pdi max during energetic breathing make the Pdi/Pdi max
ratio.
• The Pdi/Pdi max ratio increases when elastance and Raw increase. It decreases when muscle
weakness is present.
• Obviously, this test can’t be performed on a debilitated, acute or chronically ill patient.
• The clinical sign of overt diaphragmatic fatigue is abdominal paradox, which is easy to see and
doesn’t require an invasive procedure.
• Another clinical tool is the frequency to tidal volume ratio (f/VT). F (in breaths per minute) is
counted and VT (in liters) measured with a spirometer.
• The test is also called the rapid, shallow breathing index. It predicts the likelihood of a patient
being able to breathe adequately without needing mechanical ventilatory support.
• An f/VT ratio >100 is associated with a 95% probability of developing ventilatory failure.

15
Note to Slide 18: Lung & Chest Wall Compliance

Here is another view of the effect of the opposing

lung and chest wall forces. The thickness of the
arrows shows the relative strength of the forces at
different lung volumes:
 D: At FRC (the end of a normal, resting
expiration) the forces are in balance and the next
inspiration requires very little muscle force.
 E: At RV (the end of a maximal expiration) chest
wall forces are strongest and aid chest expansion
for the next inspiration.
 F: As lung volume increases above the normal
tidal volume level, lung elastic forces are stronger
than chest wall forces and aid in expiration.
 G & H: As lung volume increases, first to about
70% of TLC and then to TLC, the lung elastic
forces become much stronger than chest wall
forces and greatly help expiration.
o That is how we blow up balloons and blow
whistles.

Interpreting Figure 11-7:

• At the beginning of the breath, the tendency of the chest wall to expand facilitates (aids) lung expansion.
• When lung volume nears 70% of the VC, the chest wall reaches its natural resting level.

In order to inspire (inhale) to a lung volume greater than about 70% of TLC, the inspiratory muscles have to
overcome the recoil (elastance) of both the lung and the chest wall.
• Patients with low compliant “stiff lungs”, have increased elastic work of breathing.
• Moving large tidal volumes against increased elastance increases work of breathing.
• Patients with (stiff) lungs usually adopt a rapid and shallow breathing pattern, examples:
─ Acute pulmonary edema compresses the lungs.
─ The air trapping in COPD produces intrinsic PEEP (aka PEEPi), which increases the threshold
load the patient must overcome to inhale the next breath.
Note to Slide 19: Airway Resistance
• When changing from quiet breathing (resting) to energetic breathing (exercise), healthy subjects adjust
their tidal volumes and breathing frequencies to minimize the work of breathing.
• Similar adjustments occur in individuals who have lung disease (Figure 11-12); examples:
─ Acute bronchospasm found in bronchitis and asthma reduces airway lumen and increases
airway resistance.
─ The chronic bronchitis that is often a feature of COPD also increases the resistive load on the
respiratory muscles.

16
Note to Slide 20: Distribution of Airway Resistance

The table above compares the driving pressures needed to maintain inspiratory flow rates when flow is laminar
and when it is turbulent.
The “turbulent” column at right of the table shows that when flow is turbulent it requires much more pressure
(energy) to maintain the same rate of flow as when it is laminar (Ch. 6 Text & Slides)

Note to Slide 21: Equal Pressure Point

• During normal, quiet breathing the pleural pressure remains subambient. It ranges from about -5 to -10
cmH20.
• Subambient pleural pressure keeps the transmural pressure gradient around the airways negative
throughout both inspiration and expiration.
– The negative transmural pressure gradient helps to support the small airways and keep them open
during exhalation.
• During exhalation, pressure inside the airways diminishes as air flows downstream from the alveoli
toward the mouth.
• At some point along the airway, the pressure inside equals the pressure outside (in the pleural space).
– This point is referred to as the Equal Pressure Point (EPP).
Equal Pressure Point:
• Downstream from the EPP (toward the airway opening), pleural pressure exceeds the airway pressure.
• The resulting positive transmural pressure gradient causes airway compression and can lead to actual
collapse. Airway compression increases expiratory airway resistance and limits flow.
• At the EPP, greater expiratory effort only increases pleural pressure, further restricting flow.
• In airways of healthy subjects, the EPP occurs only with forced exhalation and at low lung volumes.
Effort Dependent Flow:
• In spontaneous breathing, all inspiratory air flow is effort dependent because it requires muscle energy
(Pmus).
Effort Independent Flow:
• During the first 30% of the forced vital capacity (FVC) pulmonary function test, the maximum peak
expiratory flow rate (PEFR) depends on the amount of muscle effort exerted by the subject.
• The more effort the patient exerts, the higher the PEFR and FEF200-1200 values will be.
• This is because the air being expired during this part of the FVC maneuver comes from the large
airways which are supported by cartilage.
• The flow rate of the remaining 70% of FVC is called effort-independent (or non-dependent flow).
• The more muscle effort the subject exerts, the lower the expiratory flow rate will be.
• This is because the air being expired comes from the non-cartilaginous airways which lack the
support the large airways have.
17
 • Increased muscle contraction causes dynamic compression of the walls of the small airways.
• Dynamic compression produces an equal pressure point airway closure (Text, pg. 236. Fig. 11-
10).
• The effect of dynamic compression is very pronounced in patients with COPD.

Note to Slide 23: Work of Breathing

The work of breathing is done to overcome elastic and resistive forces during inhalation.
In normal individuals about 2/3 of the WOB is used to overcome elastic resistive forces, about 1/3 to overcome
frictional resistive forces and about 5 to 7% to overcome viscous tissue resistance.
• There are three types of work in breathing:

Compliance Airway Resistance Tissue Resistance

Work Work Work
Work done to Work done to Work done to
overcome lung overcome airway overcome tissue
elastic recoil. resistance, mostly in Viscous Resistance
the large airways.
In normal, resting In normal, resting In normal, resting
breathing this is breathing this is breathing this is
about 65% of the about 28-30% of the about 5-7% of the
work of breathing work of breathing work of breathing

Notes to Slide 25: Distribution of Ventilation 1

Text pg. 240 & Rule of Thumb talk about the effect of gravity on distribution of ventilation and V/Q matching
in the upright lung. Remember that anatomical positional terminology allows clinicians to describe body parts
and structures in relation to each other from a common point of reference. Think about what upright means in
the context of this terminology:
• When the thorax is perpendicular to the surface of the earth (standing or sitting), the lungs are upright.
• In that posture the lung apices are superior (at the highest point) and the bases are inferior (at the lowest
point).
• The effect of gravity on alveolar size and blood distribution in the upright lung is obvious.
• When the subject is supine, the apices are still at the top of the lungs, and the bases are still at the bottom,
but the anterior portions of the lung are superior, and the posterior portions are inferior.
• Prone positioning reverses the superior-inferior relationship.
• Gravity compresses the inferior alveoli and directs more blood flow to the inferior capillaries.
• In terms of distribution of ventilation and V/Q matching, it is important to remember superior and inferior
as well as apices and bases.
• In an adult-sized lung (approximately 30 cm from apex to base), pleural pressure at the apex is
approximately –10 cm H2O.
• At the base, pleural pressure is only about –2.5 cm H2O.
• Because of these differences, the transpulmonary pressure gradient at the top of the upright lung is
greater than it is at the bottom.

18
Note to Slide 28: Dead Space vs Alveolar Space
• During quiet, spontaneous breathing about 500 mL of fresh air is inspired and expired with each breath.
• This is called the tidal volume (VT)
• Not all of the inspired VT reaches the alveoli (VA).
• About 150 mL of the VT remains in the volume of the anatomic deadspace (VDANAT).
• VDANAT consists of the upper airways (trachea and bronchi) that have no gas exchange tissue.
• The VDANAT is estimated to be about:
• 1 mL per pound of predicted body weight, or
• 2.2 mL per kilogram of predicted body weight.
• The VDANAT can be measured with the Single Breath N2 Test (called Fowler’s method or Fowler’s
equal area method).
• Most textbooks state that the VDANAT averages 150 mL for a normal, resting adult.
• Fowler’s Equal Area Method:
Fowler’s equal area method to calculate VD
• From FRC, the patient takes a deep breath of 100%
oxygen.
─ Obviously, 100% O2 contains zero nitrogen.
─ 100% oxygen fills the VDANAT with pure O2 and
reduces (dilutes) alveolar nitrogen from about
80% to about 40%
• The patient then exhales slowly through a tube
connected to a nitrogen analyzer and a gas volume
measuring spirometer.
─ The first part of exhaled air is pure dead space gas
which contains zero nitrogen (Fig. A “Start of
expiration”).
─ As alveolar gas begins to mix with dead space gas
the nitrogen begins to rise.
─ When the nitrogen concentration reaches 40% the
patient is exhaling pure alveolar gas (Fig. A
“Alveolar plateau”).
• Fowler’s curve shows both dead space gas and
alveolar gas.
• To interpret curve, a vertical line is drawn through
the curve to divide the rapidly rising nitrogen % line
into two equal areas (Fig. B dashed line, areas A
and B).
─ The point where the vertical line crosses the curve
will normally intersect with 150 mL on the X axis.
• There are several other methods to estimate the
VDANAT, you might try researching them.

Equipment dead space

must also be
considered when the
patient has an
artificial airway.

19
 Note to Slide 30: Ventilation Efficiency

As the figure shows, in obesity, the actual body

weight has no effect on the size of the lungs.
Therefore, obese body weight has NO effect on the
anatomic dead space.
• The Predicted Body Weight (aka Ideal Body
Weight) is the weight that people are expected to
have based on their age, gender, and height as
compiled in actuarial tables.
• The Metropolitan Life Insurance Company
developed the most commonly used tables in
the 1940s.
• The Met Life tables are still used.
• The PBW is used as a clinical tool for calculating
the dosages of most medications.
• In pulmonary medicine, the PBW is used for
determining lung volume and the volume of the
anatomic dead space (VDanat) in obese people.
• Excess body weight (obesity) doesn’t increase VD.
• In obese individuals, calculations of ventilator
settings must be based on PBW, NOT on actual
body weight.
Here is the PBW formula that is often used in
RTT 300:

PBW (in Kg) Males:

50 + 2.3 x (height in inches - 60) or
50 + 0.91 x (height in cm - 152.4)
PBW (in Kg) Females:
45.5 + 2.3 x (height in inches - 60) or
45.5 + 0.91 x (height in cm - 152.45)

Note to Slide 31: Dead Space Ventilation

Alveolar ventilation depends on tidal volume, dead space, and breathing rate.
For a patient with the following values:
• Respiratory rate 16/min.
• VT 625 ml.
• Anatomic dead space (VDANAT) 275 ml.
• Note that this patient’s minute exhaled volume (V dot E) is 16 breaths per minute x 275 ml per breath
which equals 10,000 ml or 10 L/min.
• Alveolar ventilation (VA) is often called the corrected volume because it subtracts anatomic dead space
volume and just counts air actually reaching the lung parenchyma (the A/C membrane).
• The alveolar ventilation is calculated as follows:
VA = 16 x (625 ml – 275 ml) = 16 x 350 = 5600 ml/min or 5.6 L/min.
Mixed venous blood:
Systemic blood returning from all the body tissues is collected and mixed in the right ventricle and the
pulmonary artery.
This blood is called Mixed Venous Blood, and it is the venous blood that is sent to the lung for gas exchange.
The different volumes of blood collected from different regions of the body are called aliquots (the term means
part of the whole).
20
 Body tissues are not all equally active:
• Some tissues, like the heart, extract a large amount of O2 and deliver a large amount of CO2 to
the venous blood.
• Others, like the kidneys, extract only a little O2 and add only a small amount of CO2.
On average, Red Blood Cells flow past (perfuse) an alveolus in about 0.75 seconds.
• In about 0.25 seconds the PVCO2 goes from 45 to 40 mmHg and the PVO2 goes from 40 to 100
mmHg.
• When the blood leaves the left ventricle it is called arterial blood and we measure its PaO2 and
PaCO2.
Three factors can reduce gas diffusion across the AC membrane:
1. Decreased alveolar/capillary surface area.
2. Decreased PIO2 or PAO2.
3. Increased AC membrane thickness.
Two factors can reduce the amount of O2 in the blood:
1. An inadequate quantity of hemoglobin.
2. A substantial amount of defective hemoglobin.

Note to Slide 32:

Time Constant is symbolized with the Greek letter tau (t) but in clinical
practice the abbreviation Tc is usually used.
Time constants express exponential processes.
• In exponential processes, the rate of change is not linear.
In pulmonary medicine (as well as in science engineering) 1 TC is defined
as the time it takes to get 63% of the volume in or out of a system, leaving
37% of the volume to be moved.
• That means that the next TC will move 63% of the remaining 37%
and so on.
• The system will never completely fill or empty.
The analogy to a full bath tub emptying applies to the lung as well.
• In the bath tub, the pressure of water flowing out is directly related
to the pressure generated by the volume of water in the tub.
• As the water volume decreases the pressure (and outward flow of
water) will also decrease exponentially. If evaporation is
discounted, the tub will never fully empty.

21
Calculate TC for a patient with the following values:
VT = 500 ml
RAW is “normal” (2.5 cm H2O/L/second)
CL = is “normal” (0.2 L/cm H2O)
Tc = 2.5 cm H2O/L/second x 0.2 L/cm H2O
TC = 0.5 second.

Explanation:
• About 60% (0.6) of the VT will be moved during each Tc.
• After 1TC (0.5 seconds) 300 ml will have been moved: 500 x .6 = 300 ml.
• After 2TC (1.0 seconds) 120 ml will have been moved: 200 x .6 = 120 ml.
• After 3TC (1.5 seconds) 48 ml will have been moved: 80 x .6 = 48 ml.
After 3 TC 468 ml (about 94% of the 500 ml VT) will have been moved, leaving 32 ml of the 500 not delivered.

22