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Файл:Pathophysiology of breathing and cardiovascular pathology. Educational and methodological manual
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Topic 2. Vascular pathophysiology
Answer: In this case, the patient developed acute vascular failure by the type of syncope. This is the mildest form of acute vascular failure associated with the development of short-term cerebral
mal blood. The reasons are diverse, one of them is strong excitement, which was the case in this case. Differential diagnostic signs
that distinguish syncope from collapse in this case are — developed loss of consciousness, which is associated with a sharp violation of the blood supply to the brain, not a very pronounced drop in
BP. A drop in BP, a weak and rare pulse, as well as a decrease in respiratory movements are due to a violation of the blood supply to the
brain, including subcortical centers — vasomotor and respiratory.
Clinical case №
4
Patient S., 47 years old, trolleybus driver, presents complaints
of headaches, dizziness, nausea. For the past two years, headaches
have periodically bothered. A year ago, an increase in blood pressure was recorded. Pulse — 84 beats/min, the boundaries of the
heart were not changed. Blood pressure —160/80 mm Hg, electrocardiogram unchanged. Urinalysis unchanged.
Question: Characterize the state of vascular tone and justify
the pathogenesis of developing changes.
Answer: based on the patient's complaints, history and objective examination, it is possible to conclude that he has hypertension. Hypertension is confirmed by increased BP, characteristic
complaints. The lack of data on somatic pathology does not suggest the presence of symptomatic hypertension. And the indication
of professional employment (hard work of the driver) additionally
confirms the development of essential hypertension in this case.
Clinical case №
5
Patient A., 43 years old. Three years ago, for the first time, blood
pressure sharply increased, seizure-like headaches appeared. The
41
Pathophysiology of breathing and cardiovascular pathology
heart border was shifted to the left by 1 cm, pulse — 82 beats/min,
blood pressure — 145/90 mm Hg. With a quick turn of the head,
blood pressure rises to 200/120 mm Hg. Urinalysis is normal. Carotid angiography revealed a narrowing of the left carotid artery.
Question: Characterize the state of vascular tone and substantiate the pathogenesis of developing changes.
Answer: The patient has arterial hypertension, as indicated by
increased BP. Data from an objective study of the patient (sharp
increase in BP during head rotation, angiography) indicate narrowing of the carotid artery. The lack of data indicating the presence of
pathology on the part of other organs and systems regulating BP
allows us to conclude on the development of angiogenic hypertension in this case.
Clinical case №
6
Patient K., 50 years old, architect, entered the cardiology department with complaints of severe headaches in the occipital region of a pulsating nature, accompanied by nausea, single vomiting, dizziness, the appearance of a "net" in front of the eyes.
History: Headaches are noted for many years, more often in
the morning or after psycho-emotional tension. I did not seek medical help. The last attack of headaches arose suddenly against the
background of satisfactory well-being. Before that he was on a
business trip, worked hard.
Objective: Moderate condition. The patient is somewhat excited, frightened. The skin is clean, high humidity, hyperemia of the
face and neck is noted. Vesicular breathing in the lungs, no wheezing. Respiratory Rate 18 per minute. Pulse — tense, frequent — 92
in 1 min. BP — on the right hand — 195/100 mm Hg., on the left —
200/100 mm Hg. The borders of the heart м the left — 1.5 cm outward from the left midclavicular line. The heart tones are sonorous,
rhythmic, the accent of P tone on the aorta. HR — 92 in 1 min. The
abdomen is soft, painless. The liver was not enlarged. Pasternatsky's symptom is negative. There are no edema.
42
Topic 2. Vascular pathophysiology
Laboratory and instrumental data:
12
× 10
Complete blood count: Hb — 132 g/L, RBC — 4.5
9
× 10
WBC — 6.0
70
%, Lymphocytes — 24 %, Monocytes — 5 %, ESR — 8 mm/h.
/l, CPU — 0.9; Eosinophil — 1 %, Neutrophils —
/l,
Blood glucose — 4.5 mmol/l.
Urinalysis: ud. weight — 1018, no protein, no sugar, white
blood cells — 1—3 in view.
X-ray examination: left ventricular hypertrophy. Lungs without
pathology.
ECG: the electrical axis of the heart deflected to the left, HR
78 per minute. Signs of left ventricular hypertrophy with systolic
overload. Troponin test negative
Questions:
1. Make a preliminary diagnosis.
2. What is your screening plan?
Answer:
1. Preliminary diagnosis: Stage II hypertension. Risk 4 (very
high). Hypertensive crisis types 1.
2. Additional examination plan: ECG over time, EchoCG, lipidogram, blood creatinine, daily blood pressure monitoring, consultation with an ophthalmologist, neurologist. To confirm hypertensive encephalopathy — CT.
Comment: hypertensive crisis uncomplicated type 1, clinically
characterized by a triad of signs: headache, dizziness, nausea
(vomiting) combined with a sudden increase in BP to high digits.
Additional research methods reveal the main sign: left ventricular
hypertrophy, indicating hypertension, and the condition of the fundus vessels — on the development of hypertensive retinopathy.
The neurologist determines the indications for CT.
Clinical case №
7
Patient K., 58 years old, chief engineer of the plant, entered the
cardiology department with complaints of severe headaches in the
43
Pathophysiology of breathing and cardiovascular pathology
occipital region of a pulsating nature, accompanied by nausea, single vomiting, dizziness. At the same time, compressive pain behind
the sternum and shortness of breath arose.
History: Headaches are noted for many years, more often in
the morning or after psycho-emotional tension. I did not seek medical help. During the last month, pain behind the sternum appeared
during physical activity, which passed at rest. This condition arose
suddenly against the background of nervous overvoltage. Before
that, I was at a meeting where an accident at work was discussed.
Objective: Moderate condition. The patient is somewhat excited, moans of pain. The skin is clean, high humidity, hyperemia of
the face and neck is noted. In the lungs vesicular breathing, a small
number of wet wheezing in the lower parts. NPV 24 per minute.
Pulse — tense, frequent — 92 in 1 min. BP — on the hand —
195/100 mm Hg, on the left — 200/100 mm Hg. The borders of the
heart are left — 2 cm outward from the left midclavicular line.
Heart tones are deaf, rhythmic, P tone accent on the aorta. HR —
92 in 1 min. The abdomen is soft, painless. The liver is not palpable. Pasternatsky's symptom is negative. The lower limbs are pastose.
Laboratory and instrumental data:
Complete blood count: Hb — 142 g/L, RBC — 4.8
WBC —9.0
band — 5
Monocytes — 5
9
× 10
/L, CPU — 0.9; Eosinophil — 0 %, Neutrophils
%, Neutrophils segment 68 %, Lymphocytes — 26 %,
%, ESR — 6 mm/h.
× 10
12
/L,
Blood glucose: 4.5 mmol/l.
Urinalysis: ud. weight — 1018, protein — 0.066, no sugar,
white blood cells — 1—3, red blood cells — 8 in view.
ECG: Head axis deflected to the left, HR 78 per minute. Signs
of left ventricular hypertrophy with systolic overload. The S-T segment rises above the isolinia in the leads of the 2,3 AVF.
Questions:
1. Make a preliminary diagnosis.
2. What is the survey plan?
44
Topic 2. Vascular pathophysiology
Answer:
1. Preliminary diagnosis: Stage III hypertension. Hypertensive
crisis complicated type 2. Acute coronary syndrome: myocardial
infarction of the lower wall, acute stage. Complication: CHF 2 "A".
2. Follow-up study plan: troponin test, lipidogram, blood biochemistry: creatinine, glucose, bilirubin, blood transaminases, coagulogram and blood coagulation, daily ECG monitoring in an intensive care unit, consultation with an ophthalmologist, neurologist.
After stabilization of EchoCG, CT or MRI.
Comment: hypertensive crisis complicated by type 2, develops
against the background of a sudden increase in BP to high numbers, is accompanied by acute damage to the target organs, in this
case, the development of ACS (acute coronary syndrome). To verify the diagnosis, a troponin test is required. Due to the fact that the
ECG has an upward elevation of the S-T segment from the Purdy
arc isoline in the leads of 2.3, AVF can be assumed to develop a
large-onset myocardial infarction of the lower wall in the acute
phase. It is necessary to predict the appearance of a pathological Q
wave on the ECG in the coming hours, which is evidence of the
development of large-onset MI. This situation dictates the need for
urgent measures to treat hypertensive crisis and acute myocardial
infarction in a specialized cardiology department.
References
1. Тема 5. Патофизиология сосудов // Патофизиология органов и
систем. Клиническая патофизиология : учебно-методическое пособие / под ред. Л.
DTIJGU.
2. Foëx P., Sear J.
Continuing Education in Anaesthesia Critical Care & Pain. 2004. Vol. 4,
3. P. 71—75.
№
3. Williams B., Mancia G., Spiering W. et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension // Eur Heart J. 2018.
Vol. 39, №
С. Литвиновой. Калининград, 2023. С. 77—88. EDN
W. Hypertension: pathophysiology and treatment //
33. P. 3021—3104.
45
Pathophysiology of breathing and cardiovascular pathology
4. Pathophysiology / ed. by V.
V. Novitsky, E. D. Goldberg, O. I. Ura-
zova. M., 2015. Vol. 1.
5. Pathophysiology / ed. by V.
V. Novitsky, O. I. Urazova. M., 2018.
Vol. 2.
6. Porth C., Grossman S. Porth’s pathophysiology concepts of altered
health states. Lippincott, 2013.
7. Copstead L.
8. Tkachev A.
E., Banasik J. Pathophysiology. Saunders, 2012.
V., Tarasova G. N., Bogatyrev V. G. et al. Propaedeutics
of internal diseases. Collection of clinical problems. Rostov o/D : Publishing House of RostGMU, 2016. 115 p.
46
Topic 3. Pathophysiology of external respiration
Topic 3
PATHOPHYSIOLOGY OF EXTERNAL RESPIRATION
Training objectives:
Learn modern ideas about the types, etiology, pathogenesis,
manifestations, principles of diagnosis of respiratory failure.
As a result of studying the topic, students must:
— be aware of the underlying causes, mechanisms and mani-
festations of respiratory disorders;
— to know the main pathogenetic factors, which play an important role in the development of diseases of the apparatus of external breathing;
— be able to solve typical situational problems on the topic of
the lesson.
Key points in the physiology of external respiration:
• Approximately one-third of each inhalation occurs in areas of
the lungs that do not take part in gas exchange. The common (physiological) dead space includes the anatomical dead space of the
bronchial tree and the dead space of the non-transfused alveoli.
• Alveolar ventilation can be severely impaired in people with
small respiratory volume or an increase in dead space. When the
respiratory volume is slightly larger than the dead space, increasing
the respiratory rate is ineffective in restoring minute alveolar ventilation.
• For air to enter the lungs, the respiratory muscles generate
negative intrapleural pressure, which causes air to enter due to the
pressure gradient between atmospheric pressure (zero pressure)
and alveolar pressure (negative pressure).
• The airways and lung tissue resist inhalation. Resistance is
provided by the airways, elastic fibers in the lungs, and the surface
tension force of the alveoli. The degree of resistance can be estimated by measuring total lung volume.
47
Pathophysiology of breathing and cardiovascular pathology
• Airway resistance is primarily determined by airway diameter. Narrowing the airways significantly increases airway resistance. Parasympathetic stimulation of the airways leads to their
narrowing; sympathetic (β2) stimulation leads to dilation.
• Elastic fibers in the lungs stretch during inhalation and then
contract passively to allow exhalation. Breaking down elastic fibers increases lung extensibility; excessive fiber production (fibrosis) reduces lung elasticity.
• High surface tension in the alveoli causes surfaces to stick together, causing lung ventilation to decrease. Surfactants reduce
surface tension. Lack of surfactant makes it difficult for the lungs
to stretch (reduced stretch ability).
• The medulla oblongata and bridge contain neurons that integrate information from chemoreceptors, proprioceptors and stretching receptors. Respiratory neurons of the medulla oblongata initiate
inhalation. Neurons in the respiratory center of the medulla oblongata primarily affect the rate and depth of respiration.
• Central chemoreceptors located in the brain respond to changes in pH and P
. Peripheral chemoreceptors are located in the
CO2
aorta and carotid arteries and respond to changes in arterial pH,
, and PO2. An increase in P
P
CO2
or a decrease in pH or PO2 stimu-
CO2
lates alveolar ventilation (Fig. 12, 13).
Pathophysiology of external respiration
The main criterion of Respiratory failure (RF) is a change in
the gas composition of arterial blood:
• hypoxemia;
• hypercapnia (gas acidosis);
• less often hypocapnia (gas alkalosis).
General pathogenesis of RF:
I. Alveolar ventilation disorder.
II. Diffusion disorder.
III. Perfusion disorder. Blood bypass.
48
Topic 3. Pathophysiology of external respiration
IV. Disorders of ventilation-perfusion ratio.
V. Dysregulation of respiration.
VI. Combination of pathogenetic factors.
Fig. 12. Chemoreceptors
49
Pathophysiology of breathing and cardiovascular pathology
Fig. 13. Chemoreflex
I. Alveolar ventilation disorder
Alveolar hypoventilation is a decrease in the amount of air
coming from the external environment to the alveoli per unit time
50
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