Egan's chpt. 11 ventilation1 pp

Learning Objectives
• Describe the physiologic functions provided by
ventilation.
• Describe the pressure gradients responsible for gas
flow, diffusion, and lung inflation.
• Identify the forces that oppose gas movement into
and out of the lungs.
• Describe how surface tension contributes to lung
recoil.
Copyright © 2017 Elsevier Inc. All Rights Reserved. 2

Learning Objectives
• Describe how lung, chest wall, and total compliance
are related.
• State the factors that affect resistance to breathing.
• Describe how various lung diseases affect the work
of breathing.
• State why ventilation is not evenly distributed
throughout the lung.

Learning Objectives
• Describe how the time constants affect alveolar
filling and emptying.
• Identify the factors that affect alveolar ventilation.
• State how to calculate alveolar ventilation, dead
space, and the VD/VT ratio.

Introduction to Ventilation
• Ventilation is the process of moving gas (usually air) in
and out of the lungs
• Ventilation is to be distinguished from respiration, which
refers to the physiologic processes of oxygen use at the
cellular level
• In health: Ventilation is regulated to meet the body’s needs under
a wide range of conditions
• In disease: This process can be markedly disrupted and often
result in inadequate ventilation and /or increased work of
breathing

Mechanics of Ventilation
• Cycles of ventilation: inspiration and expiration
• Tidal volume (VT): volume of gas moving in and out
of the respiratory tract during inspiration or
expiration
• The Vt refreshes the gas present in the lung,
removing CO2, and supplying O2 TO MEET METABOLIC
NEEDS

Pressure Differences During
Breathing
• Gases move due to pressure gradients
• Produced by thoracic expansion/contraction
• Do to elastic properties of airways, alveoli, and chest wall
• Transrespiratory pressure (PTR)
• Everything that exists between pressure measured at airway opening (PAO) and
pressure measured at body surface (PBS)
• PTR = PAO – PBS
• Equation follows direction of flow
• PAO is higher than PBS
• Components of transrespiratory pressure include:
• Airway, lungs, and chest wall
• This gradient causes gas flow in and out of lungs

Breathing

Breathing
• Transairway pressure (PTAW)
• PTAW = PAO– PA
• Whatever exists between pressure measured at airway opening and pressure
measured in alveoli of lungs
• Transalveolar pressure (PTA)
• PTA = PA– Ppl
• Whatever exists between pressure measured in model alveolus and pressure
measured in pleural space (Ppl).
• Trans-chestwall pressure (PTCW)
• Chest wall exists between pressure measured in pleural space and pressure on
body surface
• PTCW = Ppl – PBS

Breathing
• Transpulmonary pressure difference (PTP)
• Pulmonary system (airways and alveolar region), defined:
• PTP = PAO – Ppl
• Pressures must be measured to derive mechanical properties of
pulmonary system
• Under either static or dynamic (breathing) conditions
• Note, some confusion arises from:
• PTA = PAO – Ppl but only under static conditions
• Considered a special case of PTP = PAO – Ppl
• Static conditions can be imposed during mechanical ventilation
• Through use of inspiratory hold maneuver

Breathing
• Transthoracic pressure difference (PTT)
• PTT = PA – PBS
• Causes gas to flow into and out of alveoli during
breathing
• Beginning of inspiration in spontaneous breathing
subject, PA is subatmospheric compared to PAO
• Causes air to flow into alveoli
• Beginning of exhalation is opposite
• PA is higher than PAO
• Causing air to flow out of the airway

Breathing
• At end of resting exhalation, Ppl, is normally 5
cm H2O; PA = zero, there is no gas flow
• PTP is also approximately 5 cm H2O in resting
state
• This positive end expiratory PTP maintains lung
at its resting volume (i.e., functional residual
capacity, FRC)

Breathing
• Inspiration begins
• When muscular effort expands the thorax
• Thoracic expansion causes a decrease in Ppl
• Causes positive change on expiratory PTP and PTA,
which induces flow into lungs
• Inspiratory flow is proportional to (+) change in
transairway pressure difference
• The higher the change in PTA, the higher the flow
• Ppl continues to decrease until the end of inspiration

Breathing
• Beginning of expiration
• Thoracic recoil causes Ppl to start to rise
• Thus, transpulmonary pressure difference starts to decrease
• PTP is decreasing; opposite of inspiration
• So flow is in opposite (negative) direction
• Driving force for expiratory flow is energy stored in combined elastances of lungs and
chest wall
• Pleural pressures: always negative (subatmospheric) during
normal inspiration and exhalation
• During forced inspiration (big downward movement of
diaphragm), pleural pressure can drop up to –50 cm H2O

Breathing
Pmus = 0
= (Elastance × Volume) + (Resistance × Flow)
• Rearranging the formula, we get:
(Elastance  Volume) = − (Resistance  Flow)
= Resistance  (− Flow)
• Flow is negative (indicating expiration)
• The driving force for expiratory flow is the energy stored in the
combined elastances of lungs and chest wall

Pressure Differences During Breathing

Forces Opposing Lung Inflation
• Lungs have tendency to recoil inward, while chest
wall has tendency to move outwards
• Those opposing forces keep lung at its resting volumes
(FRC)

• Elastic opposition to ventilation
• Elastic and collagen fibers provide resistance to lung stretch
• Application of pressure causes stretch
• Greater pressure causes greater stretch until maximum
inflation is reached
• Deflation is passive recoil; less force is required to maintain
same volume
• During deflation, lung volume at any given pressure is slightly
greater than during inflation.
• Difference between inflation and deflation curves is hysteresis

• Hysteresis indicates factors other than simple elastic
tissue forces are present
• Major factor, especially in sick lungs: opening of
collapsed alveoli during inspiration that tend to stay
open during expiration until very low lung volumes
are reached

• Chest wall elastance and lung elastance are
connected in a series:
• Have same flow and change in volume but do not
have same pressure differences
• Elastance of respiratory system (ERS) = sum of lung
(pulmonary) elastance (EL) and chest wall elastance
(ECW)
• Applies to both natural and artificial airways (ETT)

Surface Tension Forces
• Hysteresis partly caused by surface tension
• Surface tension opposes lung inflation
• If surface tension is removed, hysteresis becomes very small
• Lung recoil occurs due to tissue elasticity and surface tension
• Pulmonary surfactant reduces lung surface tension
• Produced in alveolar type II pneumocytes
• Surfactant stabilizes alveoli by preventing collapse
• When surface area decreases, ability of pulmonary surfactant to
lower surface tension increases

Surface Tension Forces (Cont.)

Lung Compliance
• CL defined as change in volume (ΔV) per unit of change in
pressure (ΔP) difference across structure or
CL = ΔV L (normal 0.2 L/cm H2O)
ΔP cm H2O
• Pulmonary pathology alters CL
• Emphysema , obstructive lung disease, increases CL (loss elastic
tissue, lungs more distensible)
• Large changes in volume for small pressure changes
• Fibrosis, restrictive lung disease, decreases CL (↑ elastic tissue)
• Smaller volume change for any change in pressure
• Stiffer lungs, usually with reduced volume

Lung Compliance

Relationship Between
Chest Wall and Lung
• Lungs and chest wall recoil in opposite
directions
• Compliance in both is ~0.2 L/cm H2O
• Each oppose other, resulting in system compliance
of ~0.1 L/cm H2O
• FRC established at resting lung level where
tendency of chest wall to expand equals that of
lungs to collapse
• Occurs at ~40% TLC

Relationship Between
Chest Wall and Lung (Cont.)

Frictional Resistance to
Ventilation
• Tissue viscous resistance (~20% of the total resistance to lung inflation )
• Frictional forces during displacement of lungs, ribs, diaphragm, and abdominal
organs
• Airway resistance (~80% of of the frictional resistance to ventilation)
• Gas flow causes frictional resistance
Airway radius exponential effect (r4) on resistance
• Artificial airway size or bronchospasm
• Resistance is highest at nose (50% of total resistance) falls to ~20% of total
resistance at small airways
• Resistance in nonventilated patients is measured in pulmonary function
laboratory

Frictional Resistance to Ventilation
(Cont.)

Static Versus Dynamic Mechanics
• Resistance and compliance can be evaluated under static
or dynamic conditions
• Static implies flow throughout respiratory system has
ceased and all ventilatory muscle activity is absent
• Static conditions can be imposed with an inspiratory pause
when patient is sedated and being mechanically ventilated
• Dynamic is when flow of airway opening = 0
• Useful for lung protective ventilation strategies in patients w/
acute lung injury and acute respiratory distress syndrome

Static Versus Dynamic Mechanics
• Due to different time constants, mechanics estimated
during static conditions will yield different values than
when evaluated during dynamic conditions
• This due to multiple compartment system when flow is zero at
airway opening, there may still be flow between compartments
(pendelluft)
• Result: dynamic mechanics become dependent on
respiratory frequency
• Typically, both compliance and resistance decrease as
frequency increases

Mechanics of Exhalation
• Airway size is determined by structural support and
transmural pressure
• Pressure difference between inside and outside airway wall
• Support comes from cartilage and traction from
surrounding tissues
• Small airways lack cartilage, thus they are more subject to
collapse

Mechanics of Exhalation
• During quiet breathing, Ptm is negative, maintaining
airway’s patency
• Equal pressure point (EPP): pressure inside airway =
pressure outside, downstream airway compression
occurs
• May result in airway collapse
• Dynamic compression of the airways (narrowing of the
airways owing to an increase in surrounding pressures)
• Responsible for the characteristic flow patterns observed in
forced expiratory tests of pulmonary function

Mechanics of Exhalation (Cont.)

Work of Breathing (WOB)
• Respiratory muscles perform work
• Resting inhalation requires work
• Resting exhalation is passive
• Forced exhalation requires work
• Pulmonary disease can dramatically increase WOB
• Restrictive disease work is greater due to elastic tissue recoil
• Obstructive disease work is greater due to increased
resistance

Work of Breathing (WOB)
• Mechanical
• Work done on an object is result of force (F) exerted
on object and distance (x) it is moved
• W = force  distance
• Work muscles do to inflate pulmonary system is
defined as transpulmonary pressure (PTP )
• Work done by a ventilator to inflate respiratory system
is defined as transrespiratory system pressure (PTR)
• Pressure-volume curve is used for setting optimal
PEEP

Pathology’s Affect on WOB
A: Normal
B: Restrictive disease: slope of the volume-pressure
curve is less, showing increased elastic work
C: Obstructive disease: Frictional resistance
increases dramatically, noted as bulging inspired
and expired curves 39

Pathology’s Affect on WOB

Metabolic Impact of
Increased WOB
• Respiratory muscles consume O2 to perform work
• O2 cost of breathing (OCB) is indirect measurement of
WOB
• Normal OCB <5% of oxygen consumption
• In disease, OCB may increase dramatically and may > 30%
• Limits exercise tolerance
• Impacts ability to wean from mechanical ventilation
• In shock, intubation and mechanical ventilation may be
indicated to decrease excess oxygen consumption of
respiratory muscles
• Preserves oxygen delivery for vital organs

Distribution of Ventilation
• In healthy lungs, neither ventilation (V) or perfusion (Q)
are distributed evenly
• Result: uneven ventilation to perfusion ratio
• V/Q ratio of 0.8
• In upright lung, ventilation and perfusion (V/Q) are
matched best at bases (dependent area)
• Apical alveoli are larger but harder to ventilate compared to
those at bases
• Gravity pulls more blood to bases
• In local disease, place good lung down for better V/Q
matching

Regional Factors Affecting
• Regional factors interact with gravity:
• Thoracic expansion
• Shape of lungs and muscle action causes greater
expansion at bases, so more gas flow
• Transpulmonary pressure gradients: Directly related
to Ppl, closest alveoli most affected
• Apical Ppl −10 cm H2O, while at bases –2.5
• Alveoli at apices have larger resting volume than at
bases

Local Factors Affecting
• CL and Raw influence local distribution of ventilation
• Time constants: time required for local alveolar filling
and emptying
• Time constant (units of time) = R  C
• Time constant (TC) always equals time necessary for lungs
to fill or empty by 63%
• For each time constant , inspiratory or expiratory, lung
volume changes by 63%
• After 2 time constants, lung volume has changed 86%
• In ventilator pressure control modes, inspiratory time must
be set to at least 3 time constants long to deliver 95% of
volume
• For any mode, expiratory time must be set to at least 3 time
constants for lungs to passively empty by 95%

Factors Affecting
• Lung unit has long time constant (TC) if CL and Raw is high
• Lung unit has short time TC if CL and Raw is low
• Effects of unequal lung TCs are different for different ventilator
modes
• e.g., Volume Control (VC) with constant inspiratory flow, compared to
Pressure Control (PC) with constant inspiratory pressure
• Units with equal R and C: both VC and PC result in equal
distribution of volume
• Units with different TCs but equal Rs: VC gives more uniform
volumetric expansion and perhaps lower risk of volutrauma than
PC
• Units with different TCs but equal Cs: PC gives more uniform
volumetric expansion and perhaps lower risk of volutrauma than
PC

Factors Affecting Distribution of
Ventilation

Efficiency of Ventilation
• Efficiency
• Lungs should have low OCB and produce little CO2
• Healthy lungs waste some gas due to:
• Anatomic dead space
• Gas left in conducting airways after inspiration
• Alveolar dead space
• Alveoli that are ventilated but have no perfusion
VE = VA –VD or VT = VA –VD

Efficiency of Ventilation
• Physiologic dead space = sum of anatomic and
alveolar dead space
• The larger the dead space, the less efficient the tidal
volume will be in eliminating CO2

Minute and Alveolar Ventilation
• Ventilation = expressed in liters per minute of
fresh gas entering the lungs
• Total volume moved in and out per minute =
Minute ventilation (VE)
• Normal VE = 5-10 L/min
• VE = fB  VT
• 6 L/min = 12 breaths/min  0.5 L (500 mL)
• VE driven by CO2 production (metabolic rate) and subject size

Minute and Alveolar Ventilation
• Alveolar Ventilation: amount of fresh gas
reaching alveoli per minute
• Determined by VT, dead space, and fB (RR)
VA = (VT – VD)  fB
• VA is always less than VE due to dead space

Dead Space Ventilation
• Physiologic dead space (VDphs) = anatomic
(VDanat) + alveolar dead space (VDalv)
• VDanat: volume in conducting airways
• 1 mL/lb of IBW (2.2 mL/kg)
• Does not participate in gas exchange because it is
rebreathed
• Recent research shows poor agreement
between individual patient’s estimated VD and
actual measured

• VD/VT can be more accurately estimated for
mechanically ventilated adult patients using
more data available at bedside
• Using measured end tidal CO2

• Alveolar dead space (VDalv): Volume of gas
ventilating unperfused alveoli
• Alveoli receive gas, but no perfusion or:
• have ventilation exceeding perfusion (high V/Q
ratios)
• excessive ventilation, more than necessary to
arterialize alveolar blood is wasted ventilation

• Usually related to defects in pulmonary circulation
• e.g., pulmonary embolism
• Blocks portion of pulmonary circulation
• Apical alveoli have minimal or no perfusion in
normal upright subject at rest, contributing to dead
space

Bohr Equation: VD/VT Ratio
• Sum of anatomic and alveolar dead space
= physiologic dead space (Vdphys )
• Measuring (Vdphys ):
• More accurately assesses alveolar ventilation
• Preferred clinical measure of ventilation
efficiency
• VDphys is expressed as ratio (VD/VT)

• Measured clinically using modified Bohr equation
• Provides an index of wasted ventilation
• If no dead space existed, then PaCO2 would equal
PeCO2
• Due to anatomic and alveolar dead space, PeCO2 is always
less than PaCO2
VD/VT
=
(PaCO2 – PeCO2)
Pa2

• Normal VD/VT ratio is 30% (range of 0.2-0.4)
• VD/VT increases with disease
• Tough to wean from mechanical ventilation if >0.6
• High FB and low VT result in high proportion of
wasted ventilation per minute (low VA)
• Most efficient breathing pattern is slow and deep
• Effective compensation for increase requires
increased VT , not increased FB

Effectiveness of Ventilation
• Ventilation is effective when CO2 is removed to
maintain normal pH
• Resting CO2 production (VCO2) = 200 mL/min
• CO2 level determined by VA and VCO2
.
PCO2 =
VCO2
VA

Egan's chpt. 11 ventilation1 pp

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