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Файл:Pathophysiology of breathing and cardiovascular pathology. Educational and methodological manual
.pdf
IMMANUEL KANT BALTIC FEDERAL UNIVERSITY
E. V. Kirienkova, M. A. Vulf, R. M. Tursunov, L. S. Litvinova
PATHOPHYSIOLOGY OF BREATHING
AND CARDIOVASCULAR PATHOLOGY
Educational and methodological manual
Immanuel Kant Baltic Federal University Press
2024
1
UDK 616-092;616.1;616.2
BBK 52.5
K431
Reviewers
Dr hab. Svetlana Zamorina, Senior Research Fellow,
Laboratory of Cellular Immunology and Nanobiotechnology,
Institute of Ecology and Genetics of Microorganisms,
Ural Branch of the Russian Academy of Sciences;
Dr hab. Olga Urazova, Professor, Head of the Department
of Pathophysiology, Siberian State Medical University,
operating under the auspices of the Ministry of Health of Russia;
Corresponding Member of the Russian Academy of Sciences
This educational and methodological manual was prepared based on the results obtained within the framework of the Russian Science Foundation project
(№
23-15-00061; topics 1 and 2) and the State assignment (№ FZWM-2024-0012).
Kirienkova, E. V.
K431 Pathophysiology of breathing and cardiovascular pathology : edu-
cational and methodological manual / E.
R.
M. Tursunov, L. S. Litvinova. — Kaliningrad : Immanuel Kant
V. Kirienkova, M. A. Vulf,
Baltic Federal University Press, 2024. — 97 p.
ISBN 978-5-9971-0928-8
Systematizes the basic knowledge in the field of pathophysiology of the
respiratory and cardiovascular system.
The manual deals with the etiology and pathogenetic factors of the
development of respiratory and cardiac insufficiency as well as the mechanisms
of the development of clinical symptoms and pathogenetic therapeutic approaches.
Developed in accordance with the work program of the discipline "Pathophysiology, Clinical Pathophysiology" and is intended for students of medical
universities and students of the Faculty of Continuing Education, postgraduate
students, residents, research physicians and students of biological faculties.
UDK 616-092;616.1;616.2
BBK 52.5
ISBN 978-5-9971-0928-8 © IKBFU, 2024
© Kirienkova E.
Tursunov R.
V., Vulf M. A.,
M., Litvinova L. S., 2024
2
.
.
.
CONTENT
Topic 1. Cardiac pathophysiology ..........................................................4
Topic 2. Vascular pathophysiology ........................................................
Topic 3. Pathophysiology of external respiration ..................................
Topic 4. Pathophysiology of internal respiration. Hypoxia ...................
31
47
82
3
Topic 1
CARDIAC PATHOPHYSIOLOGY
Training objectives:
The result of the development of any form of heart pathology is
the formation of heart failure (Fig. 1—3). In this regard, the main
focus of the lesson will be on the study of the general patterns and
mechanisms of its occurrence, the analysis of the etiology and
pathogenesis of the most common types of cardiac pathology —
coronary heart disease and arrhythmias (Fig. 4). Pathophysiological analysis of situational problems will allow you to learn how to
correctly formulate a conclusion about the possible causes and
mechanisms of development of certain types of heart pathology.
As a result of studying the topic, students must:
— have an idea of the main typical types of cardiac pathology
and their manifestations;
— know the causes leading to the development of heart failure,
the main mechanisms underlying its development, the role of individual organs and systems in the formation of heart failure, the
main compensatory mechanisms on the part of the heart itself and
other organs that restrain its development, the main types of arrhythmias, their manifestations, general patterns and mechanisms
of their development;
— be able to correctly interpret the main clinical and laboratory, as well as experimental data in order to determine certain types
of heart pathology. According to the results of electrocardiography,
be able to determine the main types of heart rhythm disturbance —
automatism, excitability, conductivity;
— have the skill of pathophysiological analysis of clinical situations indicating the pathology of cardiac activity, formulate a conclusion on the possible causes and mechanisms of the development
of pathological processes in the heart, differentiate certain types of
heart pathology.
4
5
Fig. 1. Dynamics of development and therapy of heart failure
5
Fig. 2. Heart failure
6
6
7
Fig. 3. Pathogenesis of heart failure at the cellular level
7
Pathophysiology of breathing and cardiovascular pathology
Fig. 4. Myocardial ischemia
Biochemical markers of myocardial necrosis (MN)
In myocardial necrosis, the contents of the dead cell enter the
general bloodstream and can be determined in blood samples. The
choice of myocardial necrosis markers is determined by their diagnostic value, primarily sensitivity and specificity (Fig. 5, 6).
1. Cardiac troponins I and T have the highest specificity and
sensitivity.
2. Sensitivity to creatine phosphokinase is sufficient for the diagnosis of large-onset MI, as is usually the case with IMpST. Creatine kinase (CK) is a heterogeneous enzyme whose molecule con-
8
Topic 1. Cardiac pathophysiology
sists of two subunits B and M. Combinations of these subunits
form three different isoenzymes: MM — contained in skeletal
muscles, BB — in the brain and CF — hybrid — in the heart muscle. Normally, the content of QC isoenzymes in blood serum is:
QC — MM — 94—96
%, QC-MB — 4—6 %, QC-BB is absent or
detected in the trace amount. The advantage of CF CPK is an earlier increase in blood to a diagnostically significant level than in troponins.
Fig. 5. Pathogenesis of clinical symptoms in heart failure
3. Fatty acid binding protein (FABP) 2 enters the blood early.
Such a biochemical marker of myocardial necrosis can be detected
as early as 2 hours from the onset of the attack, and in some cases
earlier.
9
Pathophysiology of breathing and cardiovascular pathology
Fig. 6. Pathogenesis of the development of metabolic disorders
in cardiomyocytes
4. In myocardial infarction, AST is one of the early markers of
damage to the heart muscle (increases in 93—98
% of patients
within 2—20 norms), but its specificity is not high. Serum ACT
10
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