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Файл:Pathophysiology of breathing and cardiovascular pathology. Educational and methodological manual
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Topic 3. Pathophysiology of external respiration
2. Obstructive type of impaired respiratory function.
3. The presence of suffocation attacks accompanied by the appearance of whistling wheezing; generalized reversible bronchial
obstruction (according to PFT); the presence of eosinophils in sputum, as well as the absence of other diseases that have similar clinical symptoms, in addition, a aggravated allergic history, blood eosinophilia indicate bronchial asthma.
4. Bronchial asthma, severe course in the exacerbation phase.
Pulmonary emphysema. Respiratory Failure II.
5. Specify the underlying pathogenesis links.
I. Alveolar ventilation disorder. Bronchial, restrictive type.
III. Perfusion disorder. Blood bypass.
VI. Combination of pathogenetic factors.
References
1. Тема 6. Патофизиология внешнего дыхания // Патофизиология
органов и систем. Клиническая патофизиология : учебно-методическое пособие / под ред. Л.
С. 89—114. EDN EOFWYI.
2. John B.
W. Respiratory pathophysiology. M., 2008.
3. Propaedeutics of internal diseases: Collection of clinical problems /
ed. by A.
V. Tkacheva, G. N. Tarasova. Rostov o/D, 2016.
4. Litvitsky P. F. Clinical pathophysiology. M., 2017.
5. Pulmonology. Clinical guidelines / ed. by A. G. Chuchalina. M.,
2008.
6. Pathophysiology / ed. by V.
zova. M., 2015. Vol. 1.
7. Pathophysiology / ed. by V.
Vol. 2.
С. Литвиновой. Калининград, 2023.
V. Novitsky, E. D. Goldberg, O. I. Ura-
V. Novitsky, O. I. Urazova. M., 2018.
81
Pathophysiology of breathing and cardiovascular pathology
Topic 4
PATHOPHYSIOLOGY OF INTERNAL RESPIRATION. HYPOXIA
Training objectives:
Assimilate the classifications of hypoxia, study the causes and
mechanism of development of each individual type of hypoxia, the
main compensatory mechanisms that arise in response to hypoxia,
as well as the main changes in the body in hypoxia.
As a result of studying the topic, students must:
— have an idea of internal breathing and processes of its components, of types of hypoxia and patterns of their development, of
protective and adaptive reactions developing in response to hypoxia, of the damaging effect of hypoxia on the body;
— know the main causes and consequences of disruption of
oxygen and carbon dioxide transport by blood, the causes and
mechanism of development of certain types of hypoxia, their characteristic and distinctive features, types and mechanism of development of protective and adaptive reactions developing in response
to hypoxia, the main disorders of metabolism and functions of organs and systems;
— be able to correctly interpret the main clinical and laboratory, as well as experimental data in order to determine certain types
of hypoxia;
— have the skill of pathophysiological analysis of clinical situations indicating the development of various forms of hypoxia,
formulate a conclusion on the possible causes and mechanisms of
their development, differentiation of certain types of hypoxia.
Hypoxia is a typical pathological process characterized by a
decrease in oxygen content in the blood (hypoxemia) and tissues,
the development of a complex of secondary nonspecific metabolic
and functional disorders, as well as an adaptation reaction.
82
Topic 4. Pathophysiology of internal respiration. Hypoxia
The first classification of hypoxic states was proposed by Barcroft (1925), and then supplemented and improved by I. R. Petrov
(1949). The classification of I. R. Petrov is used in our time. According to this classification, hypoxia of exogenous and endogenous origin are distinguished (Fig. 20, 21).
Fig. 20. Classification of hypoxia
83
Pathophysiology of breathing and cardiovascular pathology
Fig. 21. Changes in a cell during hypoxia
Exogenous types of hypoxia
1. Hypobaric exogenous hypoxia:
GEF— Reduced Air PO2.
MLP — hypoxemia.
Compensation — tachycardia, shortness of breath.
84
Topic 4. Pathophysiology of internal respiration. Hypoxia
Consequences — hypocapnia, gas alkalosis, hypotension.
The consequence of hypocapnia is a spasm of the cerebral
arterioles and heart. Shift of oxyhemoglobin dissociation curve to
the left (Table 2, 3).
2. Normobaric exogenous hypoxia:
GEF — reduced air PO2, increased air P
MLP — hypoxemia (↓PaO2), hypercapnia (↑Pa
CO2
.
).
CO2
Compensation — tachycardia, shortness of breath.
Consequences — hypoxemia and hypercapnia, gas acidosis.
Shift of oxyhemoglobin dissociation curve to the right (Fig. 22,
Table 2, 3).
Fig. 22. Exogenous causes of hypoxia development
85
Table 2
Characteristics of the different types of hypoxia
Compensa-
Skin
AB
Venous
Composition
Arterial Blood Gas
Arterial
tion
tion
colora-
2
on O
difference
blood
2
Curve HbO
and Dissociation
blood
HR, BOC
RR, CO,
(↑RC, VC,
(↑HHb)
Cyanosis
N, trend
towards ↓
2
2,
РО
% HbO
hypocapnia,
Hypoxemia, dyspnea,
gas alkalosis, left shift
2
O2
P
% HbO
EP)
of the curve
RR, CO,
Cyanosis
N,
2
РО
Hypoxemia, dyspnea,
2
РО
EP)
HR, BOC
(↑RC, VC,
RR, CO,
(↑HHb)
trend
Cyanosis
N
towards ↓
2
% HbO
2
РО
hypocapnia,
the curve to the left
Hypoxemia, hyper-
gas. alkalosis, shifting
2
% HbO
2
РО
HR, KEC
trend to↑
2
% HbO
capnia, gas. acidosis,
right shift of the curve
2
% HbO
RR (±),
Cyanosis
N
2
РО
Hypoxemia, hyper-
2
РО
BOC
H R, CO,
trend to↑
2
% HbO
capnia, gas. acidosis,
right shift of the curve
2
% HbO
atm
P
in the air
Aetiology
2
(mountains)
O
Ratm = N
in the air
2
O
in the air
Ratm = N
O
2
Hypoventila-
tion (RMV,
DO, etc.)
Type
Pathophysiology of breathing and cardiovascular pathology
of hypoxia
1. Exogenous
hypobaric
86
2. Exogenous
normobaric in
an open space
3. Exogenous
normobaric in
a confined spa-
ce
4. Respiratory
hypoxia
86
87
BOC,
RR,
HR (±)
anosis
Acrocy-
2
Topic 4. Pathophysiology of internal respiration. Hypoxia
% HbO
velocity,
↑ in blood
blood flow
(with a in
uti-
2
↑ in O
contact time
with tissues,
HR
RR, CO,
dice
or jaun-
N Paleness
= N
2
= N
2
lization)
РО
% HbO
but the total
volume of
2
O
right
—
Crimson
Dissocia-
or brown
2
tion HbO
left
No hypoxemia
=
2
= N
% HbO
(±) —
2
PO
in case of
Shift the curve to the
Hypoxemia, acidosis,
=
2
= N
2
monary
in the pul-
stagnation
circulation
РО
= N
% HbO
but the to-
tal volume
Shift the curve to the
2
2
= N
2
of
РО
%HbO
AboutO
(CO Hb,
—
No
cyanosis
=
2
= N
О2
% HbO
No hypoxemia Р
=
2
= N
% HbO
= N
2
РО
MetHb)
ciency
(CO, BP)
cular insuffi-
5. Circulatory Cardiac, vas-
Erythro-
cytes, Hb,
6. Hemic (ane-
mic)
BOC
Erythrocytes
7. Hemic
norma,
(SON b,
b-formers,
CO, MetH
MetHb)
BOC
Impaired
8. Tissue (his-
tissue
starvation
respiration,
totoxic) and
substrate
87
p
N
N
d
b
d
N
m
—
—
—
—
—
—
—
—
t
y
N
N
NNN
tion
Compensa-
End of Table 2
tion
Skin
colora-
2
AB
on O
HR, BOC
RR, CO,
o cya-
nosis
45
,
2
Table 3
loo
% of he-
O
mmHg
Voltage
77 35
2
O
moglobin
saturation
Venous
16 70
,
2
O
vol.%
Content
difference
5,5 12
sues, vol.%
blood to tis-
100 4,0
mmHg
Venous
=
2
2
РО
blood
% HbO
2
from
2
O
Transition of
,
2
Voltage O
Pathophysiology of breathing and cardiovascular pathology
88
Arterial Blood Gas
Composition
and Dissociation
Aetiology Arterial blood
Type
of hypoxia
o hypoxemia
Curve HbO
= N
2
РО
hysical
9. Physiologi-
= N
2
% HbO
activity
cal (overload)
Arterial bloo
% of he-
moglobin
98 80
2
O
saturation
20,5 96
, vol.%
2
Content
O
20,5 16,5
Changes in blood gas composition in different types of hypoxia
Oxygen
capacity,
%
N N N N
)
or
Type of hypoxia
17,4
or
Hypoxic (exogeno-
us + respira
Hemic
Circulatory (stag-
nant) N N N N
Tissue (histotoxic)
Note: N — norm; — decrease; — increase.
88
Topic 4. Pathophysiology of internal respiration. Hypoxia
Endogenous types of hypoxia
1. Respiratory hypoxia.
GEF — respiratory failure.
MLP — ↓RaO2 and ↑Ra SO2.
Compensation — tachycardia, shortness of breath.
Consequences — ↓pH and ↓SaO2; ↓PvO2 and ↓SvO2.
Shift of oxyhemoglobin dissociation curve to the right (Fig. 23,
24).
Fig. 23. Mechanisms of compensation in acute hypoxia
89
Pathophysiology of breathing and cardiovascular pathology
Fig. 24. Dissociation of hemoglobin
2. Circulatory hypoxia.
GEF — hypovolemia, heart failure, decreased vascular wall
tone, microcirculation disorders, oxygen diffusion disorders from
capillary blood to cells.
MLP — ↓PvO2.
Compensation — ↑AVD (arterio-venous difference) by O2.
Consequences — ↓pH, ↓Sv
(Fig. 23—25).
O2
1. Hemic anemic.
GEF is anemia.
MLP — ↓blood oxygen capacity: ↓VaO2 at the rate of PaO2.
Compensation — ↑AVD (arteriovenous difference) by O2 due
to tissue acidosis.
Consequences — ↓pH, ↓VvO2, ↓PvO2 (Fig. 24).
90
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