ventilation_class_notes - Carteret Community College

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Ventilation
Ventilation is the process that exchanges gases between the external
environment and the alveoli of the lungs. Through ventilation, oxygen is carried to
the alveoli from the environment, and carbon dioxide is carried away from the
alveoli. Other, inert gases also move in and out of the lungs with oxygen and
carbon dioxide.
Understanding ventilation is essential for respiratory care practitioners, who need
to understand the following three key areas.



How the excursion of the diaphragm changes the intra-alveolar and
intrapleural pressures
Lung characteristics (static and dynamic)
Normal and abnormal ventilatory patterns
PRESSURE DIFFERENCES ACROSS THE LUNGS
Key Facts:
 Gas will always travel from an area of higher pressure to an area of lower
pressure
 All pressures are expressed in mm Hg
In order to understand the pressure characteristics of the lungs, you need to
know the following four definitions and formulas:


Driving pressure
o The pressure difference between two points in a tube or vessel,
and thus the force moving gas or fluid through a tube or vessel
o Calculation: Driving Pressure = (P1-P2)
o Example: If P1 = 20 mmHg, and P2 = 5 mmHg, then 20 mmHg - 5
mmHg = 15 mmHg
Transairway pressure
o The difference between the mouth pressure and the alveolar
pressure.
o Calculation: Pta = (Pm - Palv)
o Examples:
 Inspiration: 760 - 757 = 3 mmHg
 Gas moves into the lungs
 Expiration: 760 - 763 = -3 mmHg
 Gas moves out of the lungs

Transpulmonary pressure
o The difference between alveolar pressure and pleural pressure.
o Calculation: Ptp = (Palv - Ppl)
o
Examples:
 Inspiration: 760 - 755 = 5 mmHg
 Expiration: 763 - 758 = 5 mmHg
 The Ppl is always subatmospheric but is less negative during
expiration as compared with inspiration (758 vs. 755)

Transthoracic pressure
o The difference between the alveolar pressure and the body surface
pressure.
o Calculation: Ptt = (Palv - Pbs)
o Examples:
 Inspiration: 757 - 760 = -3 mmHg
 Gas moves into the lungs
 Expiration: 763 - 760 = 3 mmHg
 Gas moves out of the lungs
THE ROLE OF THE DIAPHRAGM IN VENTILATION
The flow of gas in and out of the lungs is caused by airway pressure changes,
which are created by the actions of the diaphragm.



During inspiration, the diaphragm contracts and moves downward.
Thoracic volume increases, and intrapleural and intra-alveolar pressures
decrease. Intra-alveolar pressure is less than barometric pressure,
allowing gas to move from the atmosphere down the tracheobronchial tree
across this pressure gradient until the two pressures are in equilibrium.
This point is known as end-inspiration.
During expiration, the diaphragm relaxes and moves upward. Thoracic
volume decreases, and intrapleural and intra-alveolar pressures increase.
Intra-alveolar pressure is greater than the barometric pressure, allowing
gas to move out of the lungs across this pressure gradient until the intraalveolar pressure and the barometric pressure are, once again, in
equilibrium, known as end-expiration.
During normal inspiration and expiration, the intrapleural pressure is
always less than the barometric pressure.
The following graphic shows the effect of the diaphragm on lung pressures and
gas flow.

At rest, the normal excursion of the diaphragm is about 1.5 cm and the
normal intrapleural pressure change is about 2-4 mmHg (3-6 cmH2O)
o mmHg x 1.5 = cmH2O

Deep inspiration
o the diaphragm may move 6-10 cm (2-4 in), which can cause the
average Ppl to drop as low as -50 cm H2O below Pb

Forced expiration
o the Ppl may raise 70-100 cmH2O above Pb
POSITIVE PRESSURE VENTILATION
Positive pressure ventilation significantly affects the normal interaction between
the diaphragm and lung pressures.
When a patient receives positive pressure ventilation, during inhalation, the
patient’s intra-alveolar pressure rises above atmospheric pressure as gas is
pushed into the lung by the machine. As positive pressure increases in the
alveoli during inspiration, the intrapleural pressure also increases, gradually
reaching about 30 cm H20 above its normal resting level (which is normally below
atmospheric pressure).
During exhalation, the intra-alveolar pressure decreases toward atmospheric
pressure. The intrapleural pressure also decreases to its resting level (below
atmospheric pressure). At end-expiration, the intra-alveolar pressure is in
equilibrium with atmospheric pressure, and intrapleural pressure is held at its
resting level.
STATIC CHARACTERISTICS OF THE LUNGS





Static refers to the study of matter at rest and the forces resulting in or
maintaining equilibrium.
The lungs have a natural tendency to recoil inward - collapse
The chest wall has a natural tendency to move outward - expand
The lungs are at their resting volume when the inward recoil force of the
lungs is equal to the outward force of the chest wall
FRC: the volume remaining in the lungs when the recoil pressure of the
lungs and the outward pressure of the chest wall equilibrate during normal
quiet breathing.
There are two major forces in the lungs that cause an inflated lung to recoil
inward:
1. the elastic properties of the lungs
2. the surface tension produced by the layer of fluid that lines the alveoli
Elastic Properties of the Lungs
 How readily the elastic force of the lungs accepts a volume of inspired air
is known as lung compliance
o the ease in which the lung distends and fills

Compliance determines how many units of air (liters or milliliters) the
lungs can accommodate for each centimeter of transpulmonary pressure
change (cm H2O).
 Example: if a person generates a negative intrapleural pressure of 5 cm
H2O during inspiration and the lungs accept a new volume of 0.5 L of gas,
the CL of the lungs would be expressed as:
CL =


V (L)
=
0.5 L
= 0.1 L/cm H2O
P (cmH2O)
5 cm H2O
The change in driving pressure can be either:
o negative (during spontaneous breathing)
 drop in Palv to -5 cmH2O
o positive (during mechanical ventilation)
 increase in Pm to 5 cmH2O
o compliance is always expressed as a positive number
At rest, the average lung compliance for each lung is about 0.1 L/cm H 2O.
o 100 mL of air is delivered into the lungs per 1 cm H2O pressure
change
o When lung compliance increases, the lungs accept a greater
volume of gas per unit of pressure change (i.e. 120 mL).

o When lung compliance decreases, as occurs with many lung
diseases, the lungs accept a smaller volume of gas per unit of
pressure change (i.e. 80 mL)
CL also decreases as the alveoli approach their filling capacity.
o The elastic force of the alveoli steadily increases as the lungs
expand which lowers the ability of the lungs to accept more gas.
This volume/pressure relationship is shown in the following graphic.
Hooke’s Law
 Hooke’s Law helps explain compliance by describing elastance, the
natural ability of matter to respond to force and to return to its original
shape after force is no longer exerted.
 Elastance is the opposite of compliance. Lungs with high compliance have
low elastance, and lungs with low compliance have high elastance.
o Formula: ∆P/∆V
 Hooke’s Law states that elastic bodies respond to force in a predictable
and measurable way.
o When an elastic body is acted on by 1 unit of force, the elastic body
will stretch one unit of length.
o When acted on by 2 units of force, it will stretch 2 units of length,
etc.
o When the force goes beyond the elastic limit of the substance, the
ability of the length to increase stops.
o If the force continues to rise, the elastic substance will break.
 When applied to the lungs, volume is substituted for length, and pressure
is substituted for force.
o Volume varies directly with pressure until the elastic limit of the lung
unit is reached. At this point little or no volume occurs. If the
pressure continues to rise, the lung unit will rupture.
o Hooke’s Law helps explain why hazards such as pneumothorax
(resulting from the rupture of alveolar sacs) can occur with the
increased pressure of mechanical ventilation.
SURFACE TENSION AND ITS EFFECT ON LUNG EXPANSION
In order to understand how the liquid that lines the inner surface of the alveoli
can affect lung expansion, an understanding of the following is essential:
1. surface tension
2. Laplace’s Law
3. the role of pulmonary surfactant
Surface Tension
 Surface tension is the attraction between gas and liquid molecules.
 Surface tension is measured in dynes per centimeter
o One dyne/cm is the force necessary to cause a tear 1 cm long in
the surface layer of a liquid
 the liquid inside the interior alveolar surface can exert more
than 70 dynes/cm

 this can easily cause complete alveolar collapse
Surface tension is a property of the fluid and is constant for any specific
fluid
Laplace’s Law
Describes how the distending pressure of a liquid bubble is influenced by:
1. the surface tension of the bubble
2. the size of the bubble itself
If there is one liquid - gas interface (bubble in liquid), then
P = 2ST
r
P = pressure difference
ST = surface tension
r = radius of the liquid sphere (cm)
2 = factor
If there is two liquid - gas interfaces (soap bubble on end of a tube), then
P = 4ST
r
P = pressure difference
ST = surface tension
r = radius of the liquid sphere (cm)
4 = factor
Laplace’s Law shows that the distending pressure of a liquid sphere is:
1. directly proportional to the surface tension of the liquid
a. As the surface tension of a liquid bubble increases, the distending
pressure needed to hold the bubble open increases
2. inversely proportional to the radius of the sphere
a. When the radius of a liquid bubble increases, the pressure
necessary to keep the bubble open decreases

When 2 different size bubbles, having the same surface tension, are in
direct communication, the greater pressure in the smaller bubble will
cause it to empty into the larger bubble.

Surface tension is the same in both the small and large bubble; it's the
distending pressures that change.
Laplace's Law Applied to the Alveolar Fluid Lining



On the inner surface of the alveoli is fluid that can resist lung expansion.
Since the liquid film that lines the alveoli resembles a bubble, a high
transpulmonary pressure must be generated to keep the small alveoli
open.
This collapsing tendency is offset by pulmonary surfactant which
significantly lowers surface tension
How Pulmonary Surfactant Regulates Alveolar Surface Tension



Pulmonary surfactant is a complex substance made of phospholipids
(90%) and proteins (10%) that is produced by the alveolar type II cells.
o Pulmonary surfactant works to lower surface tension at the alveolar
gas-liquid interface.
The primary chemical is DPPC (dipalmitoyl phosphatidylcholine), a unique
molecule with water-soluble and water-insoluble ends that allow it to
bridge the interface and promote gas-liquid interchange by lowering the
surface tension there.
The DPPC molecule at the alveolar gas-liquid interface causes surface
tension to decrease in proportion to its ratio to alveolar surface area
o when the alveolus decreases in size (expiration), the proportion of
surfactant to alveolar surface area increases, increasing the
physiologic effect of the pulmonary surfactant
o when the alveolus increases in size (inspiration), the amount of
surfactant to alveolar surface area decreases
 the number of surfactant molecules doesn't change when the
size of the alveolus changes
 this is not significant because the distending pressure
decreases as the radius of the alveolus increases

In the absence of pulmonary surfactant, the alveolar lining fluid behaves
according to Laplace’s law:
o High intrapleural pressure is needed to keep the alveoli open.
o Lack of sufficient offsetting pressure can result in the collapse of
the alveoli, which is called atelectasis.
o In order to keep the alveoli open in situations of low surfactant, the
patient experiences a significant increase in the work of breathing.
Causes of Pulmonary Surfactant Deficiency
GENERAL CAUSES
Acidosis
Hypoxia
Hyperoxia
Atelectasis
Pulmonary vascular congestion
SPECIFIC CAUSES
Adult respiratory distress syndrome (ARDS)
Infant respiratory distress syndrome (IRDS)
Pulmonary edema
Pulmonary embolism
Pneumonia
Excessive pulmonary lavage or hydration
Drowning
Extracorporeal oxygenation (ECMO)
DYNAMIC CHARACTERISTICS OF THE LUNGS
In terms of the lungs, dynamic refers to the movement of gas in and out of the
lungs, as well as the pressure changes needed to move the gas. To understand
the lungs’ dynamic characteristics, you need to understand Poiseuille’s law for
flow and pressure, as well as the airway resistance equation.
Poiseuille’s Law Arranged for Flow
During normal inspiration and expiration, the bronchial airways lengthen and
shorten, respectively. These changes really don’t make much difference during
normal breathing, but with certain respiratory disorders, such as asthma and
emphysema, flow and pressure can be impacted significantly.
The equation:
V= ∆Pr4π
8l n
Poiseuille’s equation states that flow is directly proportional to pressure (P) and
the radius (r4) of the vessel or tube. Flow is also inversely proportional to tube
length (l) and viscosity (n) of the gas or fluid. Thus, flow will decrease when
pressure and tube radius decrease. Flow will also decrease in response to
increased tube length and increased viscosity.
As anyone with asthma knows, flow is profoundly affected (shown as a power of
4 in the equation) by the radius of the tube or vessel. For example, if pressure
remains constant, reducing the radius of a tube by half reduces the gas flow to
1/16 of the original flow.
Similarly, decreasing a tube radius by 16 percent decreases the gas flow to onehalf of the original rate.
Poiseuille’s Law Arranged for Pressure
The equation:
P= V8l n
r4π
Poiseuille’s law arranged for pressure states that pressure is directly proportional
to flow, tube length, and viscosity, and it is inversely proportional to tube radius.
Thus, pressure decreases in response to decreased flow rate, tube length, and
viscosity, while it increases in response to a decreased tube radius. Pressure is
also profoundly affected by the tube radius.
If the radius of a bronchial tube with a driving pressure of 1 cm H2O is reduced in
size by half due to swelling, then the driving pressure through the bronchial tube
has to increase 16 times (16 cm H2O) to maintain the same flow rate.
Similarly, decreasing a tube radius by 16 percent requires a pressure of twice its
original level to maintain the same flow.
Poiseuille’s Law Rearranged to Simple Proportionalities
Poiseuille’s law rearranged to simple proportionalities simply states that flow
diminishes during exhalation because the bronchial airway radius decreases.
However, the actual change in flow in normal exhalation is minimal. If gas flow is
to remain constant during exhalation, the driving pressure must increase to
maintain a constant gas flow. Again, during normal exhalation, this is not a factor,
but in people with respiratory disorders such as emphysema, the flow reductions
and transthoracic pressure increases may be significant.
AIRWAY RESISTANCE
Airway resistance is the pressure difference between the mouth and the alveoli
(transairway pressure), divided by the flow rate. Airway resistance is measured in
centimeters of water per liter per second. Normal airway resistance in adults is
about 0.5 to 1.5 cm H2O/L/sec. Patients with chronic obstructive pulmonary
disease (COPD) and infants have much higher airway resistance.
Air moves through the bronchial airways in two ways:


Laminar flow is a streamlined gas flow
o the gas molecules move through the tubes in a pattern parallel to
the sides of the bronchial tubes
o It occurs at low flow rates and low pressure gradients.
Turbulent flow is a random gas flow
o The gas encounters resistance from the tubes and from other
molecules.
o It occurs at high flow rates and high pressure gradients.
TIME CONSTANTS
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


Time constant is product of airway resistance and lung compliance.
It is the time (in seconds) needed to inflate a lung region to 60 percent of
its capacity.
If all variables are constant and the airway resistance in a lung region
doubles, time constant will double as well.
If lung compliance is reduced by half, time constant will also be halved, as
will the lung region’s capacity to fill.
DYNAMIC COMPLIANCE
How readily a lung fills with gas during a specific time period is called dynamic
compliance. Dynamic compliance differs from static compliance in that dynamic
compliance is determined during a period of actual gas flow; static compliance is
determined during a period of no gas flow.
In healthy lungs, the dynamic compliance is roughly equal to static compliance at
all breathing frequencies.
VENTILATORY PATTERNS
The Normal Ventilatory Pattern
The ventilatory pattern consists of:
1. Tidal volume
a. the volume of air that normally moves into and out of the lungs in
one quiet breath
b. Normal value: 7-9 mL/kg (3-4mL/lb) of ideal body weight
c. Ideal Body Weight (lbs)
i. Male: 106+6(H-60)
ii. Female: 105+5(H-60)
1. H=height in inches
2. Ventilatory rate
a. the number of breaths per minute
b. Normal value: 10-20 bpm
3. Relationship between inhalation and exhalation (I:E Ratio)
a. Normally considered 1:2
b. The actual gas flow is 1:1 but “2” includes pause at end expiration
c. Three equal phases:
i. inspiratory phase
ii. expiratory phase
iii. pause at end-expiration
Alveolar Ventilation versus Dead Space Ventilation




Alveolar ventilation is the portion of the tidal volume that reaches the
alveoli and participates in gas exchange
Any gas that does not reach the alveoli is not effective and is called dead
space ventilation.
Dead space is ventilation without perfusion.
Three types of dead space:
o Anatomic dead space
 the volume of gas in the conducting airways: nose, mouth,
pharynx, larynx, lower airways, and terminal bronchioles
 Normally 1 mL / lb (2.2 mL / kg) 1kg=2.2 lbs
 because of anatomic dead space, the gas that enters the
alveoli during inspiration is actually a combination of dead
space gas and fresh gas
o Alveolar dead space
 Occurs when an alveolus is ventilated but not perfused with
pulmonary blood
 the air that enters the alveolus is not effective in terms of gas
exchange.
 This can occur when a blood clot, called a pulmonary
embolus, blocks pulmonary blood flow to a portion of the
lung.
o Physiologic dead space
 The sum of the anatomic dead space and alveolar dead
space.
 Normally, 0.2 – 0.4
Calculation for Alveolar Ventilation
Formula: VA = (VT - VD) x f
Example: If VT = 500 mL, VD = 150 mL and f = 12, then:
(500-150) x12 = 4200 mL = 4.2L
The Effect of Breathing Depth and Frequency on Alveolar Ventilation
Subject
A
B
C
VT (mL)
150
500
1000
Frequency (f)
40
12
6
VE (mL)
6000
6000
6000
VD (mL)
150* x 40 = 6000
150 x 12 = 1800
150 x 6 = 900
VA (mL)
0
4200
5100
*Individual’s ideal body weight is 150 lbs
Significance: An increased depth of breathing (tidal volume) is far more effective
than an increased rate in increasing total alveolar ventilation.
HOW NORMAL INTRAPLEURAL PRESSURE DIFFERENCES CAUSE
REGIONAL DIFFERENCES IN NORMAL LUNG VENTILATION
Regional differences in lung ventilation are caused by:
In the upright lung:
1. Intrapleural pressure is always below atmospheric pressure (Pb) during
both inspiration and expiration
2. Intrapleural pressure gradients exist from the upper lung region to the
lower lung region
3. The negative intrapleural pressure at the apex is normally greater (-7 to 10 cmH2O) than at the base (-2 to -3 cmH2O) Average: -3 to -6 cmH2O
4. Changes due to:
a. gravity
b. distribution of weight in the lungs
c. lungs are suspended at the hilum
d. lung base weighs more than the apex (increased blood flow)
5. Greater negative pressure in the upper regions causes the alveoli in those
areas to be more expanded than alveoli in the lower regions.
a. Many alveoli are close to or at their total filling capacity.
b. The compliance of alveoli in the upper regions is lower than the
compliance of alveoli in the lower regions.
c. Ventilation is much greater and more effective in the lower lung
regions.
THE EFFECT OF AIRWAY RESISTANCE AND LUNG COMPLINACE ON
VENTILATORY PATTERNS
Ventilatory patterns can change due to changes in lung compliance and airway
resistance. For example, a person may adopt a ventilation pattern based on
expenditure of energy rather than on efficiency of ventilation.
Condition
Decreased CL
Increased Raw


Frequency (f)
Increased
Decreased
Tidal Volume (VT)
Decreased
Increased
These patterns decrease the work of breathing for the individual
The pattern adopted may not be most efficient in terms of physiologic gas
exchange
OVERVIEW OF SPECIFIC VENTILATORY PATTERNS
The following are the most frequently seen ventilatory patterns.



Apnea: absence of spontaneous ventilation. Without intervention, death
follows in minutes.
Eupnea: normal, spontaneous breathing
Biot’s respiration: short episodes of rapid, uniformly deep inspirations,
followed by 10 to 30 second periods of apnea; first noted in patients with
meningitis







Hyperpnea: increased volume of breathing with or without increased
frequency
Hyperventilation: increased alveolar ventilation due to increased breathing
depth or rate; a breathing pattern resulting in an arterial carbon dioxide
level below normal. Note that a rapid rate may or may not result in
hyperventilation, depending on the underlying lung disease.
Hypopnea: decreased rate and depth of breathing
Hypoventilation: decreased alveolar ventilation due to decreased
breathing depth or rate; a breathing pattern resulting in an arterial carbon
dioxide level above normal
Tachypnea: rapid breathing rate
Cheyne-Stokes respiration: 10 to 30 seconds of apnea, followed by a
gradual increase in breathing volume and frequency, which is then
followed by a gradual decrease in breathing volume and frequency;
associated with cerebral disorders
Kussmaul’s respiration: increased breathing depth and rate; commonly
associated with diabetic ketoacidosis


Orthopnea: when a person is able to breathe most comfortably in the
upright position only
Dyspnea: difficulty in breathing that the person is aware of. Note that
unconscious people cannot have dyspnea.
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