Download Disturbancies of external ventilation

Disturbances of external
ventilation
Prof. J. Hanáček, M.D., Ph.D.
Respiration - movement of oxygen from atmosphere to the cells and
return of carbon dioxide from cells to the environment
External respiration : movement of air from atmosphere to
the lung and from the lung to atmosphere
1. lung ventilation
2. distribution of air in lung
3. diffusion of gases across the A– c membrane
4. perfusion of lung by blood
5. distribution of blood in lung
6. ventilation - perfusion ratio
Internal respiration - refers to the intracellular chemical reactions in which
oxygen and substrates are used and carbon dioxide and other
metabolites are produced
The lecture is devoted to external respiration – to its disturbances
Any disease of respiratory system (RS), diseases of other body
systems and organs of men, may lead to changes of components of
external respiration
Lung ventilation (LV) is able to compensate partially or totally the
disturbances of air distribution, diffusion of gases and perfusion blood
in lungs
!! Renew your knowledge on anatomy, histology and
physiology of respiratory system
VD
VT
VL
VA
VD
VA
V
tot
Lung ventilation and mechanisms involved
in its disturbances
LV - movement of air in and out of the lungs
The main role of LV is to provide required O2 and CO2
concentration in the alveoli
Alveolar unit
- it is outlined as spherical structure containing gas (alveolar volume = VA)
connected to the outside air by a tube (dead space volume = VD)
- gas exchange between the blood and air takes place in
the acinus, mainly in alveolar space, not in dead space
Lung volume (VL) : VA + VD = VL
Lung dead space ( VD) :
• anatomical dead space (VD,an)
• alveolar dead space (VD,A)
• functional dead space (VDf): volume of that part of the
respiratory tract and alveoli which is not involved in the
exchange of gases between the blood and inhaled air
Total ventilation (respiratory output, Vtot.): the air volume flowing to
or from the lung per unit of time (respiratory rate X tidal volume)
Alveolar ventilation (VA): the portion of Vtot which flows into the
alveolar space
Dead space ventilation (VD): the portion of Vtot which does not
contribute to alveolar gas replacement
Note !
a) Intensity of alveolar ventilation is reflected by PO2 and PCO2
in alveolar space
b) The intensity of alveolar wash out is determined by the ratio
of VA/VA
A low value indicates low intensity of alveolar
gas replacement  alveoli are underventilated
c) The intensity of alveolar wash out is determined also by t
he ratio of VD to VA
A high value indicates bad alveolar
ventilation  alveoli are underventilated
Ad b) Changes in total alveolar volume may be due to:
- increase (growth of the lung, exercise?) or decrease number of
alveolar units (pneumonia, edema, senescence, lobectomy,
pneumonectomy)
- increase (emphysema) or decrease of the size of the alveolar units
(pneumonia, edema, pulmonary fibrosis)
With respect to alveolar ventilation, the following
terminology is used
1. normoventilation - VA corresponds (is matched), to the metabolic
rate of tissue of the whole body  normocapnia
of the arterial blood
2. hypoventilation - VA is low in proportion to the metabolic
rate  hypercapnia of the a. blood
3. hyperventilation - VA is high in proportion to the metabolic
rate  hypocapnia of the a. blood
Alveolar hypoventilation is very important and very frequent
cosequence of respiratory diseases
What basic machanisms are involved in development of alveolar
hypoventilation ?
a) VA normal, VA is decreased (e.g. respiratory center inhibition,
airway obstruction…)
b) VA is increased, VA is normal (e.g. emphysema pulmonum )
c) VA and VA are normal, but VD is increased (e.g. ventilated but not
perfused alveoli)
! Try to deduce from presented scheme the pathological events
which can be involved in onset of alveolar hyperventilation !
H
Y
P
O
V
E
N
T
I
L
A
T
I
O
N
Physiologic
VE
VI
VA
H
Y
P
E
R
V
E
N
T
I
L
A
T
I
O
N
VA
VA 
VA 
VD
VA 
VD 
Pathological processes involved in disturbances
of alveolar ventilation
Alveolar hypoventilation
I. Extrapulmonary causes
A. Central nervous system dysfunction
1. Drug induced inhibition of respiratory centres
2. Infection processes (e.g. bulbar polio etc.)
3. Trauma
4. Idiopathic depression of the respiratory
centre (Ondines curse)
Ondine
B. Peripheral nervous system
1. Guillain - Barré syndrome – Acute inflammatory demyelinating
polyradiculoneuropathy
2.
Different forms of polyneuritis
3.
Poliomyelitis
4.
Trauma (spinal cord, phrenic nervs damage etc.)
C. Primary or secondary myopathy
1. Myasthenia gravis
2. Adverse reactions to curare
3. Other forms of myopathy
(myositis, myalgia, respiratory muscles fatique)
D. Metabolic causes
1. Metabolic alkalosis
2. Hypothyroidism
E. Chest wall
1. Kyphoscoliosis
2. Obesity
3. Trauma, surgery
II. Pulmonary (airway) causes
A. Obstruction of central airways
– e.g. obstructive sleep apnoea sy
B. Obstruction of peripheral airways
1. Inflammation of the airway mucosa
2. Hyperplasia of the mucous glands and goblet cells
3. Contraction of smooth muscles - bronchospasm
4. Loss of elasticity of airway wall and lung tissue,
airway remodelation
C. Lung parenchyma
1. Emphysema
2. Post – inflammatory (postinjury) fibrosis
3. Interstitial infiltration or fibrosis
4. Intra alveolar processes – pneumonia, alveolar edema....
D. Vascular
1. Pulmonary congestion
2. Pulmonary hypertension
E. Pleural
1. Pleural effusions, inflammations
2. Pleural scaring
3. Pneumothorax, hydrothorax...
Alveolar volumes
and gravity
Different alveolar volume
depends on different
transpulmonary pressure and
Elasticity curve of
alveolar unit
Regional differences
in alveolar
ventilation
Elasticity curve of
the alveolar unit
Distribution of air in lungs and mechanisms
involved in its disturbances
- Distribution of alveolar volume - depends on mechanical
characteristics and the force (transpulmonaly pressure) exerted on
different part of lungs and different alveolar units (inflammation, fibrosis,
emphysema, gravity, degree of lung inflation, breathing phase) during
breathing
- It is clear that under pathological conditions the alveolar volume
distribution is profoundly disturbed, is unequal
- Distribution of alveolar ventilation - depends on the same factors as
distribution of alveolar volume, and is unequal, too
Changes in alveolar volume distribution and in alveolar
ventilation distribution may lead to 4 possible situations
a) Equal distribution of volume and ventilation-VA and VA are of the
same magnitude in all alveoli  equal distribution of the VA/VA ratio
(ideal situation)
b) Distribution of VA and VA in the lung is unequal, but they have
the same proportion in the same compartment
Note !Equality of the VA/VA ratio in each alveolar unit of the lung is
more important for the gas exchange than equality in total
magnitude of the mentioned separate components
in the lungs
c) Unequal distribution of ventilation ( VA1 VA2 ) is accompanied
by equal distribution of volume (VA1= VA2)
Common situation - even under normal condition there are regional
differences in the VA/VA ratio as a result of the effect
of gravity on the lung
- some alveolar units – small amount - may be
sligtly hypo- or hyperventilated under these conditions
d) Unequal distribution of volume (VA1 VA2) accompanied by equal
distribution of ventilation (VA1= VA2)
This type of unequality is not common (some-large amount of alveolar unit may
be hypoventilated, other hyperventilated)
Disturbances of alveolar volume and alveolar ventilation distribution may be space
and time dependent. Very often can be seen unequal and asynchronous
ventilation
A
B
VA
1
1
2
VA
VA1= VA2
VA
2
VA1< VA2
VA1= VA2
VA1/VA1 = VA2/VA2
VA1< VA2
VA1/VA1 = VA2/VA2
C
D
1
2
2
1
VA1= VA2
VA1< VA2
VA1< VA2
VA1= VA2
VA1/VA1 < VA2/VA2
VA1/VA1 > VA2/VA2
1. Differences in regional flow resistance in airways as a cause
of unequal and asynchronous ventilation
(In previous figure – part A)
- Raw 1 (airway resistance in compartment 1) is higher than Raw 2
-
If C1 (compliance in compartment 1) is the same as in C2 – ventilation of
compartment 2 is higher than in compartment 1. Compartment 1 ventilation also
legs in time behind compartment 2, i.e. besides inequality there is also
asynchrony of ventilation
- Inequality and asynchrony increase with rate of breathing because airway
resistance in the place of airway stenosis increases with rate of breathing. This
situation can occur in obstructive types of lung diseases (asynchronous and
uneven alveolar ventilation)
- Slow, deep breathing is thus favourable in cases of obstructive type of
lung diseases
2. Differences in the elasticity of the lung distribution as a cause
of unequal and asynchronous ventilation (In figure – part B)
-  CL( decreased lung compliance) not equally distributed over the whole lung
leads to asynchronous and uneven alveolar ventilation
- C1is lower than C2 (because, e.g. fibrosis in compartment 1), ventilation of
compartment 1 is lower than compartment 2, and besides inequality there is
asynchrony: the ventilation of the diseased part of alveolar units precedes
that of the normal parts of lung
- The opposite of what happens in obstructive lung disease, in cases of disturbances
of elasticity, the limiting factor for alveolar ventilation is not the rate of
breathing but the breathing volume. In these conditions, shallow, rapid
breathing is more effective
A
RC1 > RC2
VA1/VA1 < VA2/VA2
VA
Raw
2
1
VA1
VT
B
CL
2
1
VA2
RC1 < RC2
VA1/VA1 < VA2/VA2
2
2
1
 time
1
Pathological processes involved in disturbances in
distribution of air in the lung
I. Extrapulmonary causes
A. Peripheral nervous system
1. Polyneuritis in one - side of the chest
2. Trauma influencing nervous system in one side of
the body (one-side phrenic nerve damage ....)
B. One - side primary and secondary myopathy
C. Kyphoscoliosis, trauma or surgery of one - side of the chest
II. Pulmonary causes :
A. Unevenly distributed obstruction of the peripheral bronchi
1. Inflammation of airway mucosa
2. Hyperplasia of the mucous glands and goblet cells
3. Bronchospasm
4. Loss of elasticity of airway wall, airway remodelation
B. Uneven distribution of lung parenchyma damage
1. Emphysema
2. Post - inflammatory fibrosis
3. Intersticial infiltration or fibrosis
4. Intra alveolar processes - pneumonia
C. Vascular changes unevenly distributed :
1. Pulmonary congestion
2. Pulmonary edema
D. Pleural changes unevenly distributed
1. Pleural effusions, inflammations
2. Pleural scaring
3. Pneumothorax
Diffusion of gases across the A –c membrane
and its disturbances
Diffusion of gases in the lung is a passive process
Components of alveolar - capillary diffusion
1. Membrane factor - transport of gases across the membrane
is determined by the following factors :
a) alveolar-capillary gas pressure gradient
b) solubility and molecular weight of the gases
c) thickness, surface area and
composition of the A-c membrane
}
represented by diffusion
coefficient
2. Blood factor - binding of gases to the haemoglobin is determined by:
a) rate at which the gas combines with haemoglobin
b) capillary blood volume
c) venous - capillary gas pressure gradient
3. Circulatory factor - the transport of the dissolved gases with the
circulation depends on the following factors :
a) capacitance coefficient
b) blood flow in the alveolar capillaries
c) arterial- venous gas pressure gradient
Lung diffusion capacity = Lung transfer factor = amount of gas
(in mmol) diffused across the alveolar – capillary membrane during
1 min at the pressure difference 1 kPa
Transfer coefficient = transfer factor per 1l of VA
a) Alveolar - capillary transport of carbon dioxide and its
disturbances
- Carbon dioxide - diffuses very easy across alveolar - capillary
membrane because of high solubility of CO2
- Limiting factor in CO2 exchange is thus blood factor, and
circulatory factor is also important
- Under normal conditions at rest there is no measurable Pco2
gradient between the alveolar gas and the gas at the venular end
of alveolar capillary
- In pathological conditions a small alveolar end-capillary gradient of CO2
can occur (pCO2 in capillary blood). This indicates a serious disturbance
of alveolar-capillary diffusion or very rapid perfusion of the blood in A-c
bed
- Even in normal circumstences there is a small A-c CO2 gradient during
physical activity
- In lung function disturbances this gradient increases with intensity
of exertion
A
CO2 exchange
PA CO2
PV CO2
Er
KPa mmHg
6
45
PC´ CO2
KPa mmHg
PV CO2
6
- disturbance
rest state
B
45
excercise
C
norm 5,4
PA CO2
40
0,8s
PC´ CO2
5,4
40
0,4s
b) Alveolar - capillary transport of oxygen and its
disturbances
- Diffusion of O2 across the A-c membrane is limiting factor because of
relatively bad solubility of O2 in fluids
- Other limiting factors in O2 exchange are blood factor and circulating
factor
- Neither at rest nor during work there is an oxygen gradient
between the alveolar gas (A) and the end - capillary blood (c)
in healthy persons
B) The normal alveolar - arterial gradient in O2 is almost entirely
the result of venous mixing or of unequal ventilation - perfusion
ratios
B) During work, the inequality in ventilation-perfusion ratio diminishes
C) In various lung function changes the A-c trasport of O2 is disturbed,
bringing about an abnormally large oxygen gradient between the alveoli
and the end-capillary blood
D) Under hypoxic conditions the alveolar tension of O2 is low O2 flows
across the membrane more slowly and the rate at which O2 combines to
Hb is than too low for equilibrium to be created between the alveolar
gas and the capillary blood before the blood leaves the pulmonary
capillaries
A
PA O2
PV O2
KPa mmHg
100
12
B
4
12
norm -
PC´ O2 ~ PA O2
rest state
- disturbance
40
100
PV O2
KPa mmHg
12
100
D
0,8 s
PC´ O2
exercise
40
PV O2
0,4 s
PA O2
PC´ O2
PC´ O2 ~ PA O2
C
4
PC´ O2
hypoxia
4
40
0,8 s
PV O2
Pathological processes involved in disturbances
of A – c gas transport
A. Normal A-c membrane is uniform in structure
The major portion of A-c surface is effectively involved in gas exchange
B. The increase in pulmonary blood flow – e.g. physical exertion:
- number of functioning capillaries  effective surface area of A-c
membrane  transfer factor and coefficient
C. Pathological processes in the A-c membrane (inflammation,
fibrosis, edema, embolism): the gas transfer properties are reduced
and distributed unequally. The transfer factor and coefficient are
abnormally low
D. Local loss of function of the lung tissue (atelectasis, tumours,
inflammation, resection): the effective alveolar surface is small, where as
transfer in the remaining normal alveoli may not be disturbed  transfer
factor is decreased, transfer coefficient in undamaged lung tissue
is usually normal
E. Obstruction in the pulmonary circulation (e.g. stenosis of mitral
valve): the blood volume per alveolus increases, filling of the
capillaries is greater and hitherto closed capillaries will open. This is
associated with a decrease in pulmonary blood flow   transfer
factor and transfer coefficient
F. In emphysema :
 effective A-c surface area   transfer factor
 transfer coefficient
G. Abnormal haemoglobin (Hb) molecule
(e.g. methaemoglobin) or abnormal quantity of Hb (anemia,
polycythemia) influence the A-c gas transfer
H. Thickening of A-c membrane ( quantity of intersticial fluid,
interstitial alveolar fibrosis, primary pulmonary hypertension) 
 disturbances of gas transfer
I. Pulmonary edema:  distance for gas diffusion   gas transfer 
 transfer factor and transfer coefficient
A
B
C
D
E
F
G
H
I
Perfusion of lung by blood and its disturbances
Pulmonary circulation - low pressure system (BP is about
(functional)
1/5 - 1/7 of that in systemic circulation)
- the most important function of the pulmonary
circulation is the exchange of gases
Nutritional pulmonary circulation - bronchial arteries - high pressure
system. Capillaries of functional pulmonary circulation anastomose with
nutritional ones. For more information on pulmonary circulation look at
textbook of physiology !
Regional lung perfusion and gravity
With regard to the alveolar vessels (not extra alveolar vessels) West has
created a model in which the lung is divided into 4 zones:
Zona 1: Pericapillary pressure (Ppc) exceeds the pressure in the pulmonary
artery and vein. Ppc is slighthy smaller than the alveolar
(atmospheric) pressure. Blood flow across this zone is low or absent
Zona 2: Pulmonary arterial pressure (Ppa) is greater than the Ppc, which in
turn is greater than the venous blood pressure. Blood flow is
determined by difference between Ppa-Ppc. The intracapillary and
pericapillary pressures are almost the same. Blood flow is present
Zona 3: Ppc is below the arterial and venous pressure and the blood flow is
determined by the arterial - venous pressure gradient. This results
in greater capillary filling (capillary distension) and increased blood
flow through capillaries.
Blood flow is there the highest comparing with other zones
of the lung
Zona 4 : Try to explain the mechanisms influence
the blood flow across this zone !
Pathological processes involved in disturbances
of blood perfusion across the lung
A change in lung perfusion is the result of a change in the degree
of filling and/or the number of capillaries involved in the perfusion
A. Normal perfusion in a sitting position at rest: perfusion of basal
parts of the lung is considerable, while apical zone is perfused,
but little
B. Increased perfusion during work: apical zone is perfused and
regional differences are still present but in lower intensity. Intensity of
regional blood flow differences depends on intensity of exercise
C. Greatly increased perfusion: caused by heavy work or severe cardiac
left - right shunt. Regional differences
in blood flow are not present
D. Decreased perfusion: caused by pulmonary hypotension or other
causes leading to reduced cardiac output (e.g.
embolisation to pulmonary artery)
E. A reduced capillary bed: due to destruction of capillaries
(inflammation, degeneration, vascular
obstruction, emphysema, tumours )  totally
unequal perfusion
F. Capillary blockage: is caused by obstruction of venous return (e.g. left
heart failure)
A
B
C
D
E
F
Alveolar ventilation - perfusion ratios
and their disturbances
Ventilation - perfusion ratio
Normal gas exchange between alveoli and capillary blood is possible if
certain alveolar ventilation and certain blood flow through alveolar capillary
is present. In normal circumstances there is a continuous distribution
VA/QC ratios ( ventilation-perfusion) from zero (shunt circulation) to
infinity ( dead space ventilation), in which by far the majority of lung
units are in the region of VA/QC = 0.8, the extremes only being
represented to a very small extent
Under pathological conditions this distribution deviates considerably
from the norm, and a large proportion of the lung units have
abnormally high or low VA/Q c values
The continuous distribution of VA/QC throughout the lung under
pathological conditions is often simplified to a model in which the lung
consists of two or three areas with different VA/QC ratios and
areas with dead space ventilation and with shunt circulation
(Fig. 10)
The extent of VA is shown by the length of the ventilation arrow and
that of alveolar perfusion by the thickness of the perfusion arrow.
The absence of ventilation and perfusion is presented without arrows.
The ventilation - perfusion ratios are divided into six categories :
A. VA/QC = normal (0.8) - for each litre of blood flowing through
the alveolar units the alveolar ventilation is 0.8 l
(normoventilation - Fig.10/6)
•
A normal VA/QC ratio continues when ventilation and perfusion
increase or decrease equally (proportionally) in these alveolar
units (Fig.10/1, Fig.10/11)
B. VA/QC is less then 0.8 (hypoventilation) – ventilation of alveolar
unit is smaller in comparison with the alveolar perfusion  O2 uptake
and CO2 output are decreased  abnormally high CO2 tension and
abnormally low O2 tension is present at the end - capillary
(hypoventilation)
• Such conditions occur when there is insufficient ventilation with
normal perfusion (Fig.10/7) or increased perfusion with normal
(Fig.10/2) or decreased ventilation (Fig.10/3)
• Reduction of VA is often the result of increased airflow resistance
in the airways
• Increased perfusion (QC) at rest usually indicates compensatory
hyperperfusion
C. VA/QC is high (hyperventilation) - ventilation is high in proportion
to alveolar perfusion  abnormally large quantity of oxygen and
carbon dioxide are transported  higher capillary 02 tension and low
carbon dioxide tension
• Hyperventilation occurs when perfusion is normal but ventilation
is excessive (Fig. 10/5) - result of metabolic acidosis, or when, with
normal or increased ventilation, the alveolar perfusion is
abnormally small
(Fig. 10/10, Fig. 10/9) - result of regional closure of the pulmonary
vascular bed (embolism)
D. VA/QC is zero (shunt circulation) - there is no ventilation of
alveoli which are, however, perfused (Fig. 10/4, 8, 12)
•
There is no gas exchange in these alveoli, and the blood gas values
do not alter during passage through the alveoli (alveolar shunt
circulation)
E. VA/QC is infinitely large (dead space ventilation) - there is
no blood supply to the alveoli which are, however, ventilated
(Fig. 10/13, 14, 15)
Are there in the alveolar units like this gas exchange?
F. VA and QC are both abolished - alveoli of this kind generally
have no function with regard to gas transport  e.g. collapse
of lung units
1
2
3
5
6
7
9
10
13
14
11
15
A
B
C
D
E
4
8
12
16
VA =0 QC = 0
Comparison of blood
flow and ventilation
of alveoli in different
level of lung

Development of hypoxemia due to decrease of VA/Qc
?
C
C
20
D
C
A
Vol % O2
C
B
High V´A=1 /2
1
V´A/Q´
C
V´A= /2 Low
V´A/Q´
1
Q´=1
Q´=1
10
Physiologic V´A/Q´
20
40
60
V´A=1
V´A=1
Q´=1
Q´=1
80
PaO2
100
120 mmHg
Mechanisms involved in compensation of hypercapnia
B
50
Vol % CO2
A
Low V´A=2/3
V´A/Q´
Z
C
Q´ = 1
P
V´A=11/3
25
11/3 + 2/3 = 2
High Q´=1
V´A/Q´
PhysiologicV´A/Q´
Q´=1
mmHg
V´A=1
20
V´A=1
40
60
PaCO2
Q´=1
In a German tale known as Sleep of Ondine, Ondine is a water
nymph. She was very beautiful and, like all nymphs,
immortal. However, should she fall in love with a mortal man and
bear his child, she would lose her immortality. Ondine eventually
falls in love with a handsome knight, Sir Lawrence, and they were
married. When they exchange vows, Lawrence vows to forever love
and be faithful to her. A year after their marriage, Ondine gives birth
to his child. From that moment on she begins to age. As Ondine’s
physical attractiveness diminishes, Lawrence loses interest in his
wife.
One afternoon, Ondine is walking near the stables when she hears
the familiar snoring of her husband. When she enters the stable,
she sees Lawrence lying in the arms of another woman. Ondine
points her finger at him, which he feels as if kicked, waking him up
with surprise. Ondine curses him, stating, "You swore faithfulness to
me with every waking breath, and I accepted your oath. So be it. As
long as you are awake, you shall have your breath, but should you
ever fall asleep, then that breath will be taken from you and you will
die!"