Elina_Physiology_Lung Mechanics_Lung Volumes And Their Measurement

Front 1

Tidal volume (VT):

Back 1

Tidal volume (VT): Amount of air that enters or leaves the lung in a single respiratory cycle
(500 mL).

Front 2

Functional residual capacity (FRC):

Back 2

Functional residual capacity (FRC): Volume of gas in the lungs at the end of a passive expiration;
the neutral or equilibrium point for the respiratory system (2,700 ml.).

Front 3

Inspiratory capacity (IC):

Back 3

Inspiratory capacity (IC): Maximal volume of gas that can be inspired from FRC (4,000
mL).

Front 4

Inspiratory reserve volume (IRV):

Back 4

Inspiratory reserve volume (IRV): Additional amount of air that can be inhaled after a normal
inspiration (3,500 mL).

Front 5

Expiratory reserve volume (ERV):

Back 5

Expiratory reserve volume (ERV):Additional volume that can be expired after a normal expiration
(1,500 roll.

Front 6

Residual volume (RV):

Back 6

Residual volume (RV):Amount of air in the lung after a maximal expiration (1,200 mL).

Front 7

Vital capacity (Ve):

Back 7

Vital capacity (Ve): Maximal volume that can be expired after a maximal inspiration (5,500mL).

Front 8

Total lung capacity (TLC):

Back 8

Total lung capacity (TLC): Amount of air in the lung after a maximal inspiration (6,700 mL).

Front 9

Что измеряют при помрщи спирометрии?

Back 9

A spirometer can measure only changes in lung volume

Front 10

Two common indirect methods измерить TLC and FRC are:

Back 10

Two common indirect methods are:
1. Helium dilution
2_ Plethysmography

Front 11

Total ventilation=minute volume = minute ventilation это?

Back 11

Total ventilation =minute volume = minute ventilation. It is the total volume of air moved in or out (usually the volume expired) of the lungs per minute.

Front 12

.как вычислить Total ventilation?

Back 12

VE.= VT X f

VE. = total ventilation
VT = tidal volume
f :: respiratory rate

Front 13

Normal resting values would be; VT =

Back 13

500 mL

Front 14

Dead Space

Back 14

Regions of the respiratopr system that contain air but are not exchanging 02 and CO2 will
blood

Front 15

Какие виды Dead Space?

Back 15

Anatomic dead space
Alveolar dead space
Physiologic dead space

Front 16

Anatomic dead space

Back 16

Anatomic dead space includes the conducting.zone, which ends at the level s
the terminal bronchioles. Significant gas exchange (02 and CO2) with the blood occurs onl
in the alveoli.

Front 17

Какой объем Anatomic dead space?

Back 17

The size of the anatomic dead space in mL is approximately equal to a person's weight i
pounds. Thus a 150-lb individual has an anatomic dead space of 150 rnl.,

Front 18

Composition of theanatomic dead space and the respiratory zone

Back 18

.The respiratory ZOne is a veryconstant environment. Under resting conditions, rhythmic ventil;
tion introduces a Small volume into a much larger respiratory zone. Thus, the partial pressure I
gases in the alveolar compartment changes very little during normal rhythmic ventilation.

Front 19

Composition at the End of Expiration (Before Inspiration)

Back 19

At the end of an expiration, the anatomic dead space is filled with air that originated in the alvec
or respiratory zone. Thus, the composition of the air in the entire respiratory system is the sao
at this static point in the respiratory cycle.. This also means that a sample of expired gas tab
near the end of expiration (end tidal air) is representative of the respiratory zone.

Front 20

Composition at the End of Inspiration (Before Expiration)

Back 20

The first 150 mL of any inspiration fills the dead space with room air, and the first 150 mL to
reach the alveoli consists of dead space air (same composition as alveolar gas). The last 150
ml, of inspired air remains in the dead space. This can be considered dead-space ventilation.
Beyond 150 ml., room air is added to the respiratory zone. This also means that after the first
ISO mL through the remainder of inspiration, the dead space contains humidified room air.

Front 21

Alveolar dead space

Back 21

Alveolar dead space
Alveoli containing air but without blood flow in the surrounding capillaries.

Front 22

Physiologic dead space

Back 22

Physiologic dead space
This is the total dead space in the lung system (anatomic dead space plus alveolar dead space).

Front 23

Alveolar Ventilation

Back 23

Alveolar ventilation represents the room air delivered to the respiratory zone per minute. The
first 150 mL of each inspiration comes from the anatomic dead space and does not contribute
to alveolar ventilation.

Front 24

Alveolar Ventilation
VA=

Back 24

VA= (VT-Vd)X f

VA = alveolar ventilation
VT ;;: tidal volume
V0 = dead space
f = respiratory rate

Front 25

The alveolar ventilation per inspiration is

Back 25

The alveolar ventilation per inspiration is 350 ml.,

Front 26

Increases in the Depth of Breathing

Back 26

There will be equal increases in total and alveolar ventilation per breath, since dead space volume
is constant.
If the depth of breathing increases from a depth of 500 mL to a depth of 700 mL, the increase
in total and alveolar ventilation would be 200 mL

Front 27

Increases in the Rate of Breathing

Back 27

Increases in the Rate of Breathing
There will be a greater increase in total ventilation than in alveolar ventilation, because the
increased rate causes increased ventilation of dead space and alveoli.
For every additional inspiration with a tidal volume of 500 mL, total ventilation would
increase 500 rnl., but alveolar ventilation would increase by only 350 mL (assuming dead space
is 150 mL).

Front 28

Muscles of Respiration
Inspiration

Back 28

The major muscle of inspiration is the diaphragm. Contraction of the diaphragm enlarges the
vertical dimensions of the chest. Also utilized are the muscles of the chest walL Contraction of
these muscles causes the ribs to rise and thus increases the anterior-posterior dimensions of
the chest

Front 29

Muscles of Respiration
Expiration

Back 29

Expiration
Under resting conditions, expiration is normally a passive process; i.e., it is due to the relaxation of
the muscles of inspiration. When it is active, the muscles of the abdominal wall can be considered
the main muscles of expiration. The contraction forces the diaphragm up into the chest.
Included would be external oblique, rectus abdominal, internal oblique, and transverse abdominal
muscles.

Front 30

In respiratory physiology, they are usually given as ern H20.
1 cm H20 =

Back 30

Units ofpressure
In respiratory physiology, they are usually given as ern H20.
1 cm H20 = 0.74 mrn Hg (I mrn Hg = 1.36cm H20)

Front 31

the two main forces acting on
the lung:

Back 31

lung recoil and intrapleural pressure.

Front 32

Lung Recoil

Back 32

• Represents forces that develop in the wall of the lung as the lung expands.
• As the lung enlarges, recoil increases; as the lung gets smaller, recoil decreases.
• Recoil, as a force, always acts to collapse the lung.

Front 33

Intrapleural Pressure

Back 33

• Represents the pressure in the thin film of fluid between the lung and the chest wall.
Subatmospheric pressures (-) act as a force to expand the lung, and positive pressures
(+) act as a force to collapse the lung.
During normal restful breathing, intrapleural pressure is always subatmospheric (or
negative) and thus acts as a force to expand the lung.
When intrapleural pressure is a greater force than lung recoil. the lungs expand.
When the recoil force is greater than that created by intrapleural pressure, lung volume
will be decreasing.
~en the force of recoil and intrapleural pressure are equal and opposite, a static state
exists, and lung size will be constant.

Front 34

MECHANICS UNDER RESTING CONDNONS
Before Inspiration

Back 34

The glottis is open, and all respiratory muscles are relaxed (FRC). This is the neutral or equilibrium
point of the respiratory system (Figure VII-I-4). Intrapleural pressure is negative at FRC
because the inward elastic recoil of the lungs is opposed by the outward-directed recoil of the
chest wall. The intrapleural force and recoil force are equal and opposite, and because no air is
flowing through the open glottis, alveolar pressure must be zero.Byconvention, the atmospheric
pressure is set to equal zero.

Front 35

MECHANICS UNDER RESTING CONDmONS
During Inspiration

Back 35

1. Inspiration is induced by the contraction of the diaphragm and some accessory muscles
that expand the chest wall. The net result is to make intrapleural pressure more negative.
The greater the contraction, the greater the change in intrapleural pressure and the larger
the force trying to expand the lung.
2. The expansion of the lung causes the gases in the alveoli to expand, creating a slightly
negative alveolar pressure, This causes air to flow into the lung.

Front 36

MECHANICS UNDER RESTING CONDmONS
End of Inspiration

Back 36

End of Inspiration
1. The lung expands until the recoil force increases to equal intrapleural pressure. Once the
forces are again equal and opposite, the lung is at its new larger volume.
2. The inflowing air returns alveolar pressure toward zero, and when it reaches zero, airflow
stops. Under resting conditions, about 500 mL of air flows into the lung system in order
to return alveolar pressure back to zero.

Front 37

MECHANICS UNDER RESTING CONDmONS
Expiration

Back 37

Expiration
L Expiration under resting conditions is produced simply by the relaxation of the muscles
of inspiration.
2. Relaxation ofthe muscles of inspiration causes intrapleural pressure to return to -5 cm H2O.
3. Lung deflation begins and continues until the recoil force decreases to again equal intrapleural
pressure. Once this occurs, the lung system is back to FRe.
4. Deflation of the lung compresses the gases in the alveoli, creating a slightly positive alveolar
pressure. This causes air to flow out of the lungs.
5. The outflowing air returns alveolar pressure toward zero, and when it reaches zero, airflow
stops.

Front 38

Intrapleural pressure during a normal respiratory cycle

Back 38

Under resting conditions, it is always a subatrnosphere pressure.

Front 39

Intraalveolar pressure during anormal respiratory cycle

Back 39

Intraalveolar pressure is slightly negative during inspiration and slightly positive during expiration.
By convention, total atmospheric pressure = O.

Front 40

EFFECTS OF INTRAPLEURAL PRESSURE ON PULMONARY BLOOD
FLOW AND VOLUME
Inspiration

Back 40

• Intrapleural pressure becomes more negative (decreases).
• Systemic venous return and right ventricular output are increased.
• An increase in the output of the right ventricle will delay the closing of the pulmonic
valves and may result in a splitting of the second heart sound.
Pulmonary vessels expand, and the volume of blood in the pulmonary circuit increases.
• Venous returns to the left heart, and the output of the left ventricle is decreased,
causing decreased systemic arterial pressure.
• Expansion of the right atrium and the ensuing drop in blood pressure cause 11 reflex
increase in heart rate (sinus arrhythmia),

Front 41

EFFECTS OF INTRAPLEURAL PRESSURE ON PULMONARY BLOOD
FLOW AND VOLUME
Expiration

Back 41

Intrapleural pressure becomes more positive (increases).
• Systemic venous return and output of the right ventricle are decreased.
Pulmonary vessels are compressed, and the volume of blood in the pulmonary circuit is
decreased.
• The return of blood and output of the left ventricle are increased, causing increased
systemic arterial pressure.
The right atrium is compressed, and the blood pressure is increased, causing a reflex
decrease in heart rate,
AValsalva maneuver will also increase intrapleural pressure and central venous pressure
and decrease venous return.

Front 42

POSITIVE~PRESSURERESPIRATION

Back 42

Assisted Control Mode Ventilation (ACMV
Positive End-Expiratory Pressure (PEEP}

Front 43

Assisted Control Mode Ventilation (ACMV)

Back 43

Assisted Control Mode Ventilation (ACMV)
Inspiratory cycle initiated by patient or automatically if no signal is detected within a specified
time window.

Front 44

Positive End-Expiratory Pressure (PEEP}

Back 44

Positive End-Expiratory Pressure (PEEP}
Volume cycled rather than pressure or timed cycled is the most common.
In some cases, the opening of the lung to the pleural space may function as a valve allowing the
air to enter the pleural space but not to leave.
Strong inspiratory efforts promote the entry of air into the pleural space, but during expiration,
the valve doses and positive pressures are created in the chest cavity. Ventilation decreases but
the positive pressures also decrease venous return and cardiac output.
Controlled mode-machine-triggered
Assist mode-inspiratory cycle initiated by the patient
CPAP-continuous airway pressure in spontaneous breathing patients
PEEP {positive end-expiratory pressurej-s-positive pressure is applied at the end of the expiratory
cycle to decrease alveolar collapse. Small alveoli have a strong tendency to collapse,
creating regions of atelectasis. The largeralveoli are also better ventilated, and supplementary
oxygen is more effective at maintaining a normal arterial P02, One downside to positive pressure
ventilation and accentuated by PEEP is a decrease in venous return and cardiac output.
Positive pressure ventilation and the addition of PEEP are illusrrated below.

Front 45

PNEUMOTHORAX

Back 45

• Intrapleural pressure increases from a mean at -5 em H20 to equal atmospheric pressure.
Lung recoil decreases to zero as the lung collapses.
• Chest wall expands. At FRC, the chest wall is under a slight tension directed outward.
It is this tendency for the chest wall to spring out and the opposed force of recoil that
creates the intrapleural pressure of -5 cm H20.

Front 46

Tension pneumothorax

Back 46

Tension pneumothorax most commonly develops in patients on a positive-pressure ventilator,

Front 47

Lung compliance is

Back 47

Lung compliance is the change in lung volume (tidal volume) divided by the change in surrounding
pressure. This is stated in the following formula:
dV
Compliance = dP

Front 48

Increased Lung compliance means Reduced Lung compliance means

Back 48

Increased compliance means more air will flow for a given change in pressure.
Reduced compliance means less air will flow for a given change in pressure.

Front 49

Increased lung compliance also occurs with

Back 49

Increased lung compliance occurs with aging and with a saline-filled lung.

Front 50

Components of lung Recoil

Back 50

Lung recoil has two components:
1. The tissue itself, more specifically, the collagen and elastin fibers of the lung.
The larger the lung, the greater the stretch of the tissue and the greater the recoil force.
2. The surface tension forces in the fluid lining the alveoli. Surface tension forces are created
whenever there is a liquid-air interface (Figure VII-I-II).
Surface tension forces tend to reduce the area of the surface and generate a pressure. In the
alveoli, they act to collapse the alveoli; therefore, these forces contribute to lung recoil.
Surface tension forces are the greatest component of lung recoil.
The relationship between the surface tension and the pressure inside a bubble is given by
the law of LaPlace.

p= Tr
p= pressure
T= tension
r == radius

Front 51

If wall tension is the same in two bubbles, the smaller bubble will have

Back 51

If wall tension is the same in two bubbles, the smaller bubble will have the greater pressure.
it follows that small alveoli tend to be
unstable. They have a great tendency to empty into larger alveoli and collapse (creating regions
of atelectasis) Collapsed alveoli are difficult to reinflate.

Front 52

Surfactant has three main functions:

Back 52

1. It lowers surface tension forces in the alveoli. In other words, surfactant lowers lung recoil
and increases compliance.
2. It lowers surface tension forces more in small alveoli than in large alveoli. This promotes
stability among alveoli of different sizes by decreasing the tendency of small alveoli to
collapse (decreases the tendency to develop atelectasis).
3. It reduces capillary filtration forces and thus reduces the tendency to develop pulmonary
edema. A negative intrathoracic pressure is a force promoting capillary filtration. Low
recoil means an intrapleural pressure closer to atmospheric, and under these conditions
it is not a significant force promoting filtration.

Front 53

Respiratory Distress Syndrome (RDS)

Back 53

Infant respiratory distress syndrome (hyaline membrane disease): deficiency of surfactant
Adult respiratory distress syndrome (ARDS): acute lung injury

Front 54

Adult respiratory distress syndrome ( : acute lung injury via the following:

Back 54

• Bloodstream-Sepsis-develops from injury to the pulmonary capillary endothelium,
leading to interstitial edema and increased lymph flow. This leads to injury and
increased permeability of the alveolar epithelium and alveolar edema. The protein
seepage into the alv~oli reduces the effectivenessof surfactant. Neutrophils have been
implicated in the progressive lung injury from sepsis.
• Airway-Gastric aspirations-v-direct acut~ injury to the lung epithelium increases
permeability of the epithelium followed by edema.

Front 55

The symproms ARDS) include:

Back 55

The symproms include:
I. Increased lung recoil and decreased lung compliance.
At a given lung volume, intrapleural pressure willbe more negative.
A greater change in intrapleural pressure is required to inflate the lungs.
2. Atelectasis
There is a greater tendency for small alveoli to collapse. Once collapse occurs. it is difficult
to reinflate these alveoli.
This is illustrated in curve B in Figure VII-I-l3. Here a very negative intrapleural pressure
(inspiratory effort) is required to reinflate the alveoli.
3. Pulmonary edema
Because a deficiency of surfactant increases recoil, a more negative intrathoracic pressure
is required to maintain a given lung volume.
Very negative intrapleural pressures represent a large force promoting capillary filtration.

Front 56

AIRWAY RESISTANCE

Back 56

Radius of an Airway
1
Resistance ~ radius4
In the branching airway system of the lungs, it is the first and second bronchi that represent
most of the airway resistance.

Front 57

Parasympathetic nerve stimulation produces

Back 57

Parasympathetic nerve stimulation produces bronchoconstriction. -

Front 58

Circulating catecholamines produce

Back 58

Circulating catecholamines produce bronchodilation,

Front 59

что происходит с AIRWAY RESISTANCE во время вдоха?

Back 59

During inspiration, intrapleural pressure is decreasing, which produces greater transverse
stretch that opens the airways. Consequently, airway resistance decreases during inspiration.
The more negative the intrapleural pressure, the lower the resistance of the airways.

Front 60

PULMONARY FUNCTION TESTING

Back 60

Vital Capacity (VC)

(FEY1)

(FVC)

Front 61

(FEY1). the forced expiratory volume in 1sec is?

Back 61

During the FVCmaneuver, the volume of air exhaled in the first second
is called the forced expiratory volume in 1sec (FEY\).

Front 62

dynamic compression of the
airways is?

Back 62

Normal people can exhale only 80% of their VC in 1 second because during a forced expiration,
intrapleural pressure becomes positive and the airways are compressed. Compression of the
airways limits expiratory flow rates. This compression is called "dynamic compression of the
airways

Front 63

Obstructive pulmonary disease

Back 63

Obstructive disease is characterized by an increase in airway resistance that is measured as a
decrease in expiratory flow rates. Examples are chronic bronchitis, asthma, and emphysema

Front 64

Obstructive pattern

Back 64

Total lung capacity (TLC) is normal or larger than normal, but during amaximal forced expiration
from TLC, a smaller than normal volume is slowly expired.

Front 65

Obstructive FEV1 =
FVC

Back 65

FEV1 < 80%
FVC

Front 66

Restrictive FEV1 =
FVC

Back 66

FEV1 > 80%
FVC

Front 67

Restrictive pulmonary disease

Back 67

is characterized by an increase in elastic recoil-e-a decrease in
lung compliance-which is measured as a decrease in all lung volumes. Reduced vital capacity
with low lung volumes are the indicators of restrictivepulmonary diseases

Front 68

Restrictive pattern

Back 68

TLC is smaller than normal, but during a maximal forced expiration from TLC, the smaller volume
is expired quickly and more completely than in a normal pattern; therefore, even though
FEVr is also reduced, the FEY/FVC is often increased. However, the critical distinction is low
FVCwith low FRCand RV.