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Файл:Pathophysiology of breathing and cardiovascular pathology. Educational and methodological manual
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Topic 1. Cardiac pathophysiology
pulmonary artery. Low filling pulse, coincides with heart rate —
114 per minute. BP 90/60 mm Hg. On the liver side — hepatomegaly, Kurlov dimensions: 12—11—8 cm. Spleen not enlarged.
Swelling to the lower third of the lower legs.
Results of additional examination:
Complete blood count: WBC — 11
4.3
band — 11
23
12
× 10
/L; Eosinophils — 2 %, Basophils — 1 %, Neutrophils
%, Neutrophils segmented — 56 %; Lymphocytes —
%; Monocytes — 7 %; ESR — 47mm/h.
9
× 10
/L; RBC —
Urinalysis: Protein — 0.033 g, Leukocytes — 12, RBC — 5,
Epithelial cells — 12 in field of view.
Biochemical blood test: C-reactive protein (+), ALT — 214 U/L,
AST — 142 U/L. The troponin blood test is negative.
X-ray examination of the chest organs: dilation of the boundaries of the heart, congestion in the lungs.
ECG — sinus tachycardia up to 130 per minute, signs of left
ventricular hypertrophy with overload, negative tooth in thoracic
leads.
Questions:
1. Presumptive diagnosis.
2. What studies are needed to verify the diagnosis?
Answers:
1. Preliminary diagnosis: Acute myocarditis of viral-bacterial
etiology. Complication of CHF 2 B, CHF 3.
2. Additional studies:
— EchoCG, renal ultrasound. Liver ultrasound;
— Urine according to Nechiporenko;
— Blood biochemistry: bilirubin, transaminases over time
(AsaT, AlaT), blood glucose, lipidogram, protein fractions study,
blood creatinine;
— Hepatitis B virus markers, C;
— If myocardial biopsy with histological examination is necessary.
Comment: clinical data — acute, clear association with viral
infection, lack of antibiotic effect, clinical signs of heart failure,
21
Pathophysiology of breathing and cardiovascular pathology
inflammatory blood reaction and C — reactive protein (+), elevated
transaminases, changes in the heart and lungs according to X-ray
and ECG (sinus tachycardia, negative T teeth) indicate severe myocardial damage and CHF. Increased levels of AST and ALT, dysprotenemia in the blood (decrease in the ratio of albumin/globulin),
changes according to EchoCG (decrease in EF, dilation of cavities,
etc.) make it possible to reliably verify the diagnosis.
Clinical case №
8
Patient N., 55 years old, a teacher, was taken by ambulance to
the reception department with complaints of intense pressing pains
behind the sternum with irradiation in the left shoulder, lasting for
1.5 hours, not relieved by nitroglycerin, for cardiac interruptions,
sharp general weakness, cold sticky sweat.
History: the day before I worked too hard physically in the
country. For 4—5 years, she notes attacks of compressive pain behind the sternum during fast walking, lasting 3—5 minutes, passing at rest and from taking nitroglycerin.
Objectively: the condition is severe, the skin is pale, acrocyanosis, the palms are wet. Pulse 96 per minute, irregular. BP —
90/60 mm Hg. The boundaries of the heart are widened to the left
by 1.5 cm. Tones are deaf, arrhythmic. In the lungs, vesicular
breathing. The abdomen is soft, painless. The liver is not palpable.
Laboratory and instrumental data:
ECG: The rhythm is sinus, incorrect. HR 115 per minute,
polytope extrasystoles. Left ventricular hypertrophy. S-T segment
down from isoline, deep negative T wave in I, II, AVL, V3-V6 thoracic leads
12
× 10
Complete blood count: RBC — 4.3
Neutrophils band — 4
phocytes — 23
%, Monocytes — 7 %, ESR — 10 mm/h.
%, Neutrophils segmented — 66 %, Lym-
, WBC — 9.2 × 109,
Troponin test at admission — negative.
Blood chemistry: CRP (+), CPK 2.4 mmol/hl, AST 24 U/l,
ALT 16 U/l.
22
Topic 1. Cardiac pathophysiology
Questions:
1. Make a preliminary diagnosis.
2. Draw up a follow-up plan.
Answer:
1. Preliminary diagnosis: CHD, Acute coronary syndrome. Dif-
ferentiate between unstable angina and myocardial infarction.
2. Additional examination plan: complete blood count over
time, ECG over time, blood clotting, repeat blood test for troponins, blood glucose, chest X-ray, EchoCG, Holter-ECG. Consider
the need for coronarography.
Comment: clinical picture (long-term pain behind the sternum,
not relieved by nitroglycerin, ECG changes indicating subendocardial myocardial injury indicate the development of ACS with the
possible development of myocardial infarction. In the first hours,
the troponin test is negative, which does not exclude myocardial
infarction. Troponin test should be repeated after 6 hours and ECG
dynamics. To clarify the diagnosis and determine the parameters of
the functional state of the myocardium, while stabilizing the state,
it is advisable to conduct EchoCG. In the presence of a specialized
cardiac surgery department, coronary imaging is performed in order to determine the indications for endovascular surgical treatment.
Clinical case №
9
Patient Ch., 61, artist, complained of paroxysmal pain behind
the sternum and in the left half of the chest, irradiating into the
hands, which arise during physical exertion, passing at rest for
3—4 minutes. Nitrates were not taken.
History: since childhood, he was registered with a rheumatologist with a diagnosis: rheumatism with mitral heart disease. Heart
pains began to bother 2 years ago with physical activity.
Objectively: The condition is satisfactory. Skin and mucous
membranes of normal color. In the lungs, vesicular breathing. The
23
Pathophysiology of breathing and cardiovascular pathology
boundaries of relative dullness of the heart are expanded to the left
by 1.5 cm. Heart tones are muted, rhythmic. HR — 76 per minute.
BP 105/60 mm Hg.
Additional studies: ECG at rest — sinus rhythm with a heart
rate of 70 per minute. There are no ischemic signs. Clinical analysis of blood and urine without pathology. Blood cholesterol
5.79 mmol/L.
On EchoCG: myocardial hypertrophy was not detected, contractile function was normal (EF — 60
%), mitral valve insuffi-
ciency 1 st.
Questions:
1. Make a preliminary diagnosis.
2. Make a follow-up plan to verify the diagnosis.
Answer:
1. Preliminary diagnosis: IDC, tension angina 2—3 FC.
2. Additional studies required:
Bicycle ergometry, if the difficulties are Holter-ECG, lipidogram, blood glucose. If necessary, coronarography.
Comment: According to the clinical picture, there is latent coronary insufficiency, which can be verified by dosed exercise on the
ECG using Veloergometry or Holter-ECG, which will identify ischemic signs that are not detected at rest. Lipidogram and glucose
determination will make it possible to clarify the severity of atherosclerosis and exclude the severity of CHD with diabetes mellitus.
Severe angina 3—4 Class, especially if the therapy is ineffective,
coronary angina and endovascular surgical treatment.
Clinical case №
10
Patient V., 58 years old, an engineer, was taken to the admission department of the hospital with complaints of frequent erratic
heartbeat, accompanied by weakness, unpleasant sensations in the
heart area that arose 2 hours ago while working in a summer cottage, shortness of breath, mixed nature, when climbing the stairs,
rapid fatigue.
24
Topic 1. Cardiac pathophysiology
History: Over the past year, notes a heartbeat sensation, more
often during the load. These episodes were transient and took place
on their own at rest. When analyzing the outpatient card over the
past 2 years, a repeatedly increased cholesterol content was noted
(7.6 mmol/L — low-density lipoproteins prevail). On the ECG
filmed a month ago: the rhythm is sinus, correct. Left atrial and left
ventricular hypertrophy.
Objective: moderate condition, acrocyanosis of the lips, hypersthenic type of addition. In the lungs, breathing is vesicular, in
the lower parts there is a small number of silent moist wheezing.
RR (respiratory rate) 22 per minute. The left border of the heart is
along the midclavicular line. BP — 150/100 mm Hg. The pulse on
the radial arteries is arrhythmic, the frequency is 102 per minute.
The pulse deficit 6 at 1 minute. The tones of the heart at the apex
have inconsistent sonority, are arrhythmic, heart rate — 112 per
minute. The abdomen is soft, painless. The liver was not enlarged.
Laboratory and instrumental data:
Complete blood count: Hb — 140 G/L, RBC — 4.5
WBC — 6.0
Neutrophils segmented — 65
tes — 8
%, Glucose — 4.5 mmol/l.
9
× 10
/l, ESR — 6 Mm/h, Neutrophils band — 2 %,
%, Lymphocytes — 25 %, Monocy-
× 10
12
/L,
Urinalysis — ud. weight — 1020, no protein, no sugar, white
blood cells — 1—2 in a field of view (FOV).
Blood chemistry: total cholesterol — 7.6 mmol/L, AST — 5 U/L,
ALT — 4 U/L, CRP — 0,
Examination of the fundus — atherosclerosis of the retinal vessels.
Questions:
1. Make a preliminary diagnosis.
2. Plan an additional survey.
Answer:
1. Preliminary diagnosis: CHD, arrhythmic variant by atrial fibrillation type (atrial fibrillation), paroxysmal form. Complication:
CHF 2 "A," CHF — NYHA PK 2.
2. Follow-up plan: daily Holter monitoring, endocrinologist
consultation, EchoCG, lipidogram.
25
Pathophysiology of breathing and cardiovascular pathology
Comment: Clinical findings reveal cardiac rhythm abnormalities that are pathogenetically associated with atherosclerosis and
CHD. For a reliable diagnosis, it is necessary to register episodes
of arrhythmia using daily monitoring of the ECG study Holter, because on a separately removed ECG, it does not detect rhythm disturbances, EchoCG in order to clarify the condition of the valve
apparatus and determine the size of the left atrium. To exclude thyroid pathology — consultation with an endocrinologist, lipidogram
to clarify the severity of atherosclerosis.
Clinical case №
11
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. NPV 18 per minute. Pulse — tense, frequent — 92/min. BP —
on the right hand — 195/100 mm Hg., on the left — 200/100 mm
Hg. The borders of the heart — 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/ min. The abdomen is soft,
painless. The liver was not enlarged. Pasternatsky's symptom is negative. There are no edema.
Laboratory and instrumental data:
12
× 10
Complete blood count: Hb — 132 g/L, RBC — 4.5
WBC — 6.0
9
× 10
, CI (color index) — 0.9; Eosinophil — 1, Neu-
/l,
26
Topic 1. Cardiac pathophysiology
trophils band — 4 %, Neutrophils segmented — 66 %, Lymphocytes — 24
%, Monocytes — 5 %, ESR — 8 Mm/H, Glucose —
4.5 mmol/l.
Urinalysis: ud. weight — 1018, no protein, no sugar, l — 1—3 in
a field of view (FOV).
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 type 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 hypertensive disease, and the condition of the vessels of the ocular day — on the development of
hypertensive retinopathy. The neurologist determines the indications for CT.
Clinical case №
12
Patient K., 57 years old, a teacher, was taken by an ambulance
with complaints of intense pressing pains behind the sternum with
irradiation to the left shoulder, lasting for 1.5 hours, not relieving
with nitroglycerin, lasting about an hour, feeling of heart failure,
sharp general weakness, cold sticky sweat.
27
Pathophysiology of breathing and cardiovascular pathology
History: the day before I worked too hard physically in the
country. History — For 4—5 years, notes attacks of compressive
pain behind the sternum during fast walking, lasting 3—5 minutes,
passing at rest and from taking nitroglycerin.
Objectively: the condition is severe, the skin is pale, acrocyanosis, the palms are wet. Pulse 96 per minute, single extrasystoles.
BP — 90/60 mm Hg. The boundaries of the heart are expanded to
the left by 1.5 cm. Tones are deaf, single extrasystoles. In the
lungs, vesicular breathing. The abdomen is soft, painless. The liver
is not palpable.
Laboratory and instrumental data:
Complete blood count: RBC — 4.3
Neutrophils — 70
%, Lymphocytes — 23 %, Monocytes — 7 %,
12
× 10
, WBC — 9.2 × 109,
ESR — 10 mm/h.
Blood chemistry: CRP (+), LDH — 360 U/L, CPK —
2.4 mmol/HL, AST — 24 U/L, ALT — 16 U/L.
Complete blood count on the sixth day after hospitalization: WBC — 6.0
%, Neutrophils segmented — 64 %, Lymphocytes — 24 %, Mon-
2
ocytes — 9
%, ESR — 24 mm/h.
9
× 10
, Eosinophil — 1 %, Neutrophils band —
Questions:
1. Make a preliminary diagnosis.
2. Draw up a follow-up plan.
Answer:
1. Myocardial infarction with Q wave.
2. Follow-up study plan: complete blood count over time, ECG
over time, blood count for CPK, LDH, AST, ALT, CRP, PT, blood
coagulation, urine myoglobin, chest X-ray, radioisotope diagnosis,
coronary imaging.
Clinical case №
13
Patient D., 55 years old, a teacher in high school, turned to an
appointment with a cardiologist with complaints of a feeling of
interruptions in the heart area. From the history: such sensations
28
Topic 1. Cardiac pathophysiology
are noted for about a year, however, over the past month, interruptions have become more frequent, often accompanied by weakness
and even dizziness. The appearance of interruptions is more often
associated with physical activity. It also notes periodic attacks of
compressive pain behind the sternum during fast walking, passing
at rest.
Objectively: the general condition is satisfactory, the skin is of
ordinary color and humidity. In the lungs, vesicular breathing, no
wheezing. BP — 140/95 mm Hg. Pulse — 74 per 1 minute, arrhythmic. The boundaries of the heart are unchanged. Heart tones
are somewhat muted, arrhythmic — against the background of a
regular rhythm, an extraordinary contraction or a longer interval
between cardiac contractions is periodically determined, the heart
rate is 76 per minute. The abdomen is soft, painless. The liver was
not enlarged.
Laboratory and instrumental data:
Complete blood count: Hb — 144 g/L, WBC — 6.0
Neutrophils — 67
%, Lymphocytes — 25 %, Monocytes — 8 %,
× 109/L,
ESR — 4 mm/h.
Biochemical blood count: AST — 5 U/L, ALT — 4 U/L,
CRP — 0, total cholesterol — 7.8 mmol/L (low density lipoproteins prevail).
Blood glucose: 4.5 mmol/l.
Urinalysis: ud. weight — 1020, no protein, no sugar, Neutrophils band — 1—2 a field of view.
ECG: polytopic extrasystole.
Questions:
1. Make a preliminary diagnosis.
2. Follow-Up Plan.
Answer:
1. CHD: extrasystolic rhythm disorder (probably ventricular).
2. Additional examination plan: daily Holter monitoring,
ECHO-CS, bicycle ergometry, ophthalmologist's consultation.
29
Pathophysiology of breathing and cardiovascular pathology
References
1. Тема 4. Патофизиология сердца // Патофизиология органов и
систем. Клиническая патофизиология : учебно-методическое пособие / под ред. Л.
С. Литвиновой. Калининград, 2023. С. 58—76. EDN
SMZEYG.
2. Kamyshnikov V.
S. Handbook of Clinical and Biochemical Re-
search and Laboratory Diagnostics. M., 2009.
3. Titz N.
W. Clinical Guide to Laboratory Tests. M., 2003.
4. Stein W., Bohner J., Krais J. et al. Macro creatine kinase: Determination and differentiation of two types by their activation energies //
Clin. Chem. 1982. Vol. 28. P. 19—24.
5. Pathophysiology / ed. by V.
V. Novitsky, E. D. Goldberg, O. I. Ura-
zova. M., 2015. Vol. 1.
6. Pathophysiology / ed. by V.
V. Novitsky, O. I. Urazova. M., 2018.
Vol. 2.
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8. Copstead L.
E., Banasik J. Pathophysiology. Saunders, 2012.
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