Lung Volume Measurement: Notes To Chapter 11 (Ventilation) 11 Ed. Slides
Lung Volume Measurement: Notes To Chapter 11 (Ventilation) 11 Ed. Slides
Lung Volume Measurement: Notes To Chapter 11 (Ventilation) 11 Ed. Slides
Slides
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• 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.
• 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.
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• 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).
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• 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.
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
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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).
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─ 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. EXPIRATION
• The inspiratory muscles contract, and thoracic TIME 2–4 SEC:
volume increases. • Respiratory muscles relax during expiration
- Increased volume lowers alveolar pressure - Lung and thoracic volumes decrease.
about 1 mm Hg below atmospheric • Air pressure in the lungs increases to about 1 mm
pressure (point A2), Hg above atmospheric pressure (point A4).
- Air flows into the alveoli (point C1 to point • Alveolar pressure is now higher than atmospheric
C2). pressure, so air flow direction reverses and air
- Since thoracic volume changes faster than flows out of the lungs.
air can flow in, alveolar pressure reaches TIME 4 SEC:
its lowest value about halfway through • At the end of expiration alveolar pressure is again
inspiration (point A2). equal to atmospheric pressure and air flow stops
• As air continues to flow into the alveoli, (point A5).
pressure increases until the thoracic cage stops - Lung volume reaches its minimum for the
expanding, just before the end of inspiration. breath cycle (point C3).
- Air flow continues for a fraction of a • At this point, the breath cycle has ended and after
second longer, until alveolar pressure the EEP the body is ready to begin another cycle
equalizes with atmospheric pressure (point with the next breath.
A3). - The pressure differences shown in the figure
• At the end of inspiration, lung volume is at its apply to quiet breathing.
maximum for the breath cycle (point C2), and - During exercise or forced heavy breathing,
alveolar pressure is equal to atmospheric these values become proportionately larger.
pressure.
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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.
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• 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.
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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.
Terminology Note:
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• 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.
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Note to Slide 14: Compliance & Elastance
Increasing alveolar volumes
• 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.
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• 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).
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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.
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Note to Slide 18: Lung & Chest Wall Compliance
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.
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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)
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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.
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Note to Slide 30: Ventilation Efficiency
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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.
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