Download Myocardial infarction with Q waves

MINISTRY OF HEALTH OF UZBEKISTAN
CENTRE FOR MEDICAL EDUCATION
Tashkent Medical Academy
"Approved"
Head of main department
science and education
Ministry of Health
Republic of Uzbekistan
S. E. Atakhanov
___________________________
“____”________________ 2011 y.
Protocol number
MYOCARDIAL INFARCTION
(Educational tools for students of IV courses
and professors of medical schools)
Tashkent - 2011
Compiled by:
Juraeva E.R. - Associate Professor and Faculty Hospital Therapy Faculty of Medicine,
and Internal disease and preventive health care department.
Ziyaeva F.K. - Assistant Professor of Faculty and Hospital medical care Department of
Internal Medicine and Health prevention department.
G.T. Bekenova - Assistant Professor of Faculty and Hospital medical care Department of
Internal Medicine and Health prevention department.
Reviewers:
. Yakubov A.V - Department of Clinical Pharmacology, TMA, prof.
Zohidova M.Z. - Department for the preparation of a general practitioner of the Tashkent
Institute of Postgraduate Education, prof.
Educational tools considered and approved at a meeting of ICC TMA (Minutes № _____
"_____"_____ 2011).
DNC Chairman, Professor
M. Sh.Karimov
Training manuals approved by the Academic Council of TMA and recommended for
publication (Minutes № _____ "_____"_____ 2011.).
Scientific Secretary
Prof. G.S. Rahimbaeva
Theme : myocardial infarction
1 Venue lessons, equipment
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Cardiology, coronary care and general cardiorheumatology therapy department of laboratory and
instrumental diagnostics, training rooms.
Blood samples, clinical and biochemical tests, immunological studies, x-ray, ECG, PCG, EhoKS,
training-control tests, case patients, handout.
TV-video, overhet, multimedia, tables, slides, information and computer software.
2. Duration of training
Time to light the subject, 270 minutes
3. Session Purpose:
Education students etiology, pathogenesis, clinical symptomatology, laboratory and instrumental
diagnosis and rational therapy, prevention of complications, rehabilitation.
The purpose of education - the development and consolidation of theoretical knowledge.
The educational goal - the formation of a physician in training relevant international standards of
interest to the profession, a sense of responsibility, raising interest in expanding their knowledge, the
formation of a deontological level of education, the formation of caution in the implementation of
practical work, clarity and responsibility.
Developmental goal - the formation of students' independent thinking and debate, critical thinking
in students (clinical, hygienic).
Tasks
1. Definition of myocardial infarction
1. The etiology of myocardial infarction
2. The pathogenesis of myocardial infarction.
3. The clinical picture of acute myocardial infarction: subjective data, a general inspection of the data
palpation, percussion and auscultation, the conclusion of laboratory and instrumental methods of
research.
4. Differential diagnosis of acute myocardial infarction.
5. Basic principles of treatment and rehabilitation of myocardial infarction.
6. Course and prognosis of myocardial infarction.
The student should know:
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etiology of myocardial infarction
pathogenesis of myocardial infarction
hospital myocardial infarction
methods of diagnosing myocardial infarction
basic principles of treatment
The student should be able to:
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Gather medical history, patient complaints, conduct an overall inspection, palpation, percussion and
auscultation
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Make a plan examination of the patient
Interpret laboratory data rates
Interpret ECG
To substantiate the clinical diagnosis by steps
Write a prescription for drugs and to explain their mechanism of action, side effects
4. Motivation
Currently, the study of myocardial infarction is of great importance because it is one of the most
common causes of death and disability in the population and can lead to life-threatening
complications of the patient.
5. Interdisciplinary communication and internal disciplinary
Interdisciplinary communication:
Myocardial infarction
Integrate with the following items:
I.
1.
2.
3.
4.
5.
6.
II.
Vertically
Normal anatomy
Normal physiology
Histology
Morbid anatomy
Physiopathology
Propaedeutics of Internal Medicine
Horizontal
1. Teaching surgery
2. Radiology
Normal anatomy
The human heart - is a muscular pump divided into four chambers. The two upper chambers called
atria and two lower - the ventricles.
These two types of heart chambers perform different functions: the atria collect blood coming into
the heart and push it into the ventricles and the ventricles eject blood from the heart into the arteries
through which it enters into all parts of the body.
The two atria are separated by septal and two ventricle - interventricular septum. Atrium and
ventricle on each side of the heart are connected atrioventricular orifice. This hole opens and closes
the atrioventricular valve. The left atrioventricular valve is also known as mitral valve, and the right
atrioventricular valve as tricuspid valve.
The valves act as gates, giving the ability of blood to pass from one chamber of the heart to another
and from the heart chambers in the associated blood vessels. The heart valves are as follows:
tricuspid, pulmonary (pulmonary trunk), bicuspid (also known as mitral) and aortaly.
Tricuspid valve.
Tricuspid valve is located between the right atrium and right ventricle. When you open this valve
moves blood from the right atrium into the right ventricle. Tricuspid valve prevents blood from
flowing back into the atrium, closing during ventricular contraction The very name of this valve
indicates that it consists of three wings.
The pulmonary valve
With a closed tricuspid valve blood in the right ventricle is the only way out in the pulmonary trunk.
Pulmonary trunk divides into right and left pulmonary arteries, which are respectively the left and
right lung. Log in pulmonary trunk is closed pulmonary valve. Pulmonary valve has three leaflets that
open at the time of reduction of the right ventricle and closed at the time of relaxation. Pulmonary
valve allows blood to get out of the right ventricle into the pulmonary artery, but prevents blood from
flowing back from pulmonary artery into the right ventricle.
Bicuspid valve (mitral valve)
Bicuspid or mitral valve regulates blood flow from the left atrium into the left ventricle. As with
tricuspid valve, butterfly valve is closed at the time of contraction of the left ventricle. Mitral valve
has two flaps.
Normal physiology
Function automatic. Automatism function - is the heart's ability to generate electrical impulses in
the absence of external stimuli.
Conductivity function. The function of conductivity - the ability for the excitation of fibers of the
conducting system of the heart and the contractile myocardium.
The function of excitability. Excitability function - the ability of cells of the heart conduction
system and myocardial contractile excited by external electric pulses.
Contractility. Contractility is the ability of the heart muscle to contract in response to stimulation.
This function has basically the contractile myocardium.
As a result of successive contraction and relaxation of different parts of the heart by most - the heart
pumping function. Histology
The structure of the myocardium. In light microscopy shows branching filaments consisting of
cardiomyocytes. In the center of each kernel is cardiomyocytes.
The structure of the cardiomyocytes (data of electron microscopy). We see a number of parallel
myofibrils, consisting of segments - the sarcomeres.
The structure of the sarcomere. The location of fibers on the cross-section of the sarcomere. In the
center of the disc A (Zone M) is the only thick filament (myosin), in its peripheral regions - and the
thick and thin filaments (actin), each thick filament surrounded by six thin. In the drive I have only
thin filaments.
Histology
The structure of the myocardium. In light microscopy shows branching filaments consisting of
cardiomyocytes. In the center of each kernel is cardiomyocytes.
The structure of the cardiomyocytes (data of electron microscopy). We see a number of parallel
myofibrils, consisting of segments - the sarcomeres.
The structure of the sarcomere. The location of fibers on the cross-section of the sarcomere. In
the center of the disc A (Zone M) is the only thick filament (myosin), in its peripheral regions - and
the thick and thin filaments (actin), each thick filament surrounded by six thin. In the drive I have
only thin filaments.
INFARCTION
fibers
The arrows indicate the intercalated discs
Purkinje fibers in the myocardium
Hematoxylin and eosin
1-purkinje
2-endocardium
3 - myocardium
Purkinje fibers in the myocardium
Hematoxylin and eosin
1-purkinje
2-endocardium
3 - myocardium
Purkinje fibers in the myocardium
Hematoxylin and eosin
1-purkinje
2-endocardium
3 - myocardium
fibers
Stained with iron hematoxylin
fibers
Morbid anatomy
Myocardial infarction (MI) - is ischemic necrosis of cardiac muscle, which develops as a result of
acute failure of coronary circulation.
The earliest morphological changes in the cardiac muscle in the developing myocardial infarction
can be detected only by using electron microscopy. Within 15-20 minutes after coronary occlusion
exhibit swelling of mitochondria and depletion of glycogen. 60 min after cessation of coronary
blood flow revealed irreversible ischemic cell damage in the form of the collapse of the chromatin
of nuclei and marked contracture of sarcomeres. When using light microscopy, the first change in
the focus of MI detected only after 12-18 hours of onset of infarction.There has been expansion of
capillaries, swelling of muscle fibers. After 24 h revealed the fragmentation of muscle fibers and
infiltration of polymorphonuclear leukocytes.
Macroscopically, the picture begins to identify myocardial infarction only after 18-24 hours of
onset. Foci of necrosis and appears pale hydropic, and 48 h zone of necrosis becomes gray tint and
becomes flabby. In the uncomplicated process of forming scar ends in about 6 weeks from the start
of MI.
Physiopathology
The emergence of ischemia of the heart muscle leads to profound disturbances in the metabolism of
myocardial cells and the vascular system of the heart. As a result of the termination or significant
limitation of coronary blood flow develop hypoxia, which disturbs the synthesis of ATP in
mitochondria. At the same cardiomyocytes contractile function rapidly decreases. A significant
limitation of coronary blood flow with fatty acids and glucose, which are the main energy substrate
cells, activates anaerobic glycolysis (breakdown of glycogen). Moreover, glycogen is metabolized
to lactate, only that the shortage of oxygen does not oxidize further. The concentration of lactate
and other unoxidized products in cardiac muscle and coronary sinus blood increases, and in the
myocardium is a shift of pH in the acidic side (acidosis), which contributes to further reduction in
electrical activity and myocardial contractility. ATP deficiency leads to the discovery of potassium
channel cell K + ions out into the extracellular medium, thus reducing the transmembrane resting
potential and excitability of cardiomyocytes. At the same time decreases the rate of growth TMPD,
total duration, as well as the speed of the electric pulse. Characteristically, the extent of these
violations in some parts of the ischemic myocardium is different. Therefore, during ischemia, the
conditions for the occurrence of severe inhomogeneity of electrophysiological properties of heart
muscle that underlies many cardiac arrhythmias. As a result of ischemia, also violated the reverse
transport of Ca2 + in the sarcoplasmic reticulum and extracellular environment. Concentration Ca2
+ in the cell grows and develops so-called "ischemic contracture" cardiomyocytes, leading to
disruption of diastolic relaxation. Significant inhibition of K +-Na + pump, resulting from
deficiency of ATP, is also accompanied by an increased concentration of Na + ions in the cell and,
accordingly, its swelling. As a result of a myocardial infarction is a violation of diastolic and
systolic left ventricular function, and begin the complex process of remodeling it.
Change the transmembrane action
potential (TMPD) in the zone of ischemic
damage.
Left ventricular remodeling in transmural myocardial infarction. a
- the impact of intragastric pressure on cyto lytic necrotizing area
of heart muscle (the 2nd day of MI), b - increase the area of heart
disease, thinning of the walls in the area of necrosis and dilatation
of the left ventricle.
Propaedeutics of Internal Medicine
During transmural myocardial infarction (heart attack with a tooth Q) are usually distinguished five
periods:
1) prodrome, 2) acute and 3) sharp, and 4) subacute and 5) postinfarction period.
On examination, is not rare skin pallor, cold extremities and severe sweating. In most cases,
cyanosis is defined lips pronounced cyanosis, orthopnea position, combined with the wet. finely
rattling in the bottom of the lungs and increased frequency of respiratory movements indicate the
presence of acute left ventricular failure.
Palpation of the heart: palpation of the heart, there may be local tenderness in the left beforecardiac
area.
Auscultation of the heart during myocardial infarction: the weakening of the first tone and muted at
the apex, the weakening of the second tone, the accent on the second tone of pulmonary artery,
sinus tachycardia. Blood pressure in the first minutes and hours of MI may increase. With the
development of acute vascular insufficiency of blood pressure is reduced, mainly due to systolic
BP.
Dynamics of electrocardiogram changes in acute (a-e), subacute (g) and scar (s) stages of
myocardial infarction.
Radiology
Chest X-ray. In patients with myocardial infarction with a tooth Q, hospitalized in the department
cardiac intensive care, chest X-ray is usually performed on special indications, namely, to timely
diagnosis of interstitial pulmonary edema and other complications of the disease (pneumonia,
pulmonary infarction, hydrothorax or effusion pericardial), radiological findings are described in
the relevant chapters of the manual. The study is conducted using special portable x-ray machines
directly in cardiac intensive care office with the patient lying on his back.
Myocardial scintigraphy 99mTs-pyrophosphate (technetium) is used to visualize the foci of
myocardial infarction, since this is a radioactive substance is selectively accumulated in necrotic
tissue of the heart muscle in the event that persists in the affected area for at least 10-40% of blood
flow (including collateral) necessary for the delivery of technetium to the foci of necrosis.
Scintigram record in three Standard projections at 90 min after intravenous injection of an
indicator. This time is necessary to cleanse the blood of the indicator due to its absorption of bone
and necrotic tissue. Analysis of the scintigram performed after the procedure, the accumulation of
pulses and procedures for background subtraction. Hotbed of acute myocardial infarction detected
by this technique after 24 h of onset. In the ordinary course of myocardial necrosis hearth rendered
up to 8-10 days of illness. If technetium continues to accumulate in heart muscle in 2 to 3 weeks
from the onset, it indicates a slowing down of reparative processes, protracted course of
myocardial postinfarction aneurysm or development.
Two-dimensional echocardiograms recorded in patients with postinfarction cardiosclerosis a - akinesia of
interventricular septum, b - posteriodiaphragmal (lower) segment of the left ventricle
Scintigram myocardial 99m Tc-pyrophosphate, recorded in a patient with posterolateral diaphragmatic (lower) with
myocardial infarction with a tooth Q. Notably the accumulation of technetium in posterolateral diaphragmatic (lower)
segment of LV (light areas scintigram))
Surgery
Coronary revascularization
In the absence of the effect of drug therapy and maintaining signs of recurrent myocardial ischemia
is shown holding a coronary revascularization: percutaneous transluminal coronary angioplasty
(PTCA) or coronary artery bypass grafting (CABG). The main indications for the emergency
coronary revascularization, are features that characterize a high risk of myocardial infarction and
death:
1Repeated episodes of myocardial ischemia (recurrent pain and / or negative dynamic segment of
the RS-T).
2. Elevated serum troponins or CK-MB.
3. Hemodynamic instability (hypotension or progressive heart failure).
4.Threatening arrhythmias (ventricular tachycardia or recurrent episodes of ventricular fibrillation).
5. Early post-infarction angina.
Internal disciplinary communication:
Acquired in the course of training know-how can be applied in the study subjects: cardiology,
pulmonology, gastroenterology.
6. Content of classes
1. Theoretical part
Myocardial infarction (MI) - is ischemic necrosis of cardiac muscle, which develops as a result of
acute failure of coronary circulation .In the Russian Federation annually infarction occurs in 0.20.6% of men aged 40 to 59 years (NA Mazur). In men, the older age group (60-64 g) of MI
incidence is even higher, reaching 1.7% per year. Women get sick infarction in 2.5-5 times less
likely to men, especially in young and middle age, that is usually associated with the later (about 10
years) the development of their atherosclerosis. After menopause (age 55-60 years) the difference in
incidence between men and women is significantly reduced. Modern classification of MI provides
for his division:
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magnitude and depth of lesions of the heart muscle;
the nature of the disease;
Localization of MI;
on the stage of disease;
by the presence of complications of MI.
1. The magnitude and depth of lesions of the heart muscle and differentiate transmural infarction
notransmural .When transmural MI (myocardial infarction with a tooth Q) captures the focus of
necrosis, or the entire thickness of cardiac muscle from subendocardial to subepicardial layers of
the myocardium, or a large part of that is reflected on the surface ECG as the formation of a
pathological Q wave or QS complex in several ECG leads . Hence the synonym of transmural
myocardial infarction - "myocardial infarction with a tooth Q". Typically, such damage to the heart
muscle is extensive enough and focus of necrosis extended to two or more segments of the left
ventricle (macrofocal MI).
When notransmural MI (myocardial infarction without tooth Q) captures only the focus of necrosis
subendocardial or intramural divisions left ventricle and is not accompanied by pathological
changes of the complex QRS ("wave myocardial infarction without Q"). For a long time in the
Soviet literature to describe without Q-wave myocardial infarction using the term " small focal
them." Indeed, in most cases without Q-wave myocardial infarction is much smaller in extent than
transmural infarction, but often there are cases of extensive subendocardial infarction that span
multiple segments of LV, but only affecting the subendocardial layers of myocardium.
2. By the nature of the disease are distinguished primary, recurrent and recurrent MI. Primary MI
diagnosed in the absence of anamnestic and instrumental signs of myocardial infarction in the past
IM. Repeated diagnosed in cases where the patient, in whom there is documented information of
past myocardial infarction, there are credible signs of new foci of necrosis, often forming a pool of
other satellites in extend beyond 28 days from the date of the previous infarction. For recurrent
myocardial infarction clinical laboratory and instrumental signs of the formation of new foci of
necrosis appear in a period of 72 hours (3 days) until 28 days after myocardial infarction, before the
end of its basic processes of scarring.
Transmural (with a tooth Q) and notransmural (without tooth Q) myocardial infarction
(Figure).
3. To localize them to allocate:
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anterioseptal (anteriopartition); anterior apical;
anterolateral;
anteriobazalis (high-front);
common anterior (septal, apical and lateral);
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posteriodiaphragmal (lower);
posterolateral;
posteriobazal;
common background;
Right ventricular infarction.
MI is more often localized in the left ventricle, hitting him front, back, side walls and / or the
interventricular septum (MZHP), which depends on the location of the critical stenosis or occlusion
of a spacecraft. Poor circulation to the LAD LCA can lead to myocardial infarction anteriopartition
area, tops and much rarer - posteriodiaphragmal (lower) wall of the left ventricle. Cessation of
blood flow in LCA impact assessment is accompanied by the anteriobazal, lateral or posteriobazal
infarction (occlusion distal RH LCA). When blood circulation in the basin of PKA may develop
posterolateral diaphragmatic (with the defeat of the proximal PCA) or posteriobazal infarction
(occlusion distal PKA). Isolated right ventricular infarction is relatively rare. There is often a
combination of its various localizations.
4.By stage of the disease are distinguished:
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acute period - up to 2 hours from the start of it;
acute period - up to 10 days from the start of MI;
subacute period - from 10 days before the end of 4-8 weeks;
postinfarction period - usually after 4-8 weeks.
The division of a heart attack on stage. The explanation in the text
Sometimes singled out the so-called prodromal period ("preinfarction angina"), which
corresponds to a certain extent, the notion of unstable angina, myocardial infarction complicated
by development.
The most common complications of MI include:
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acute left ventricular failure (pulmonary edema);
cardiogenic shock;
ventricular and supraventricular arrhythmias;
conduction abnormalities (CA-blockade, AV block, bundle-branch block, block);
acute left ventricular aneurysm;
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external and internal discontinuities infarction, cardiac tamponade;
aseptic pericarditis (epistenocarditic);
thromboembolism.
Aetiology and Pathogenesis
The main cause of myocardial infarction is atherosclerosis SC (95%). It should also be borne in
mind that infrequently (no more than 5% of patients), myocardial infarction may result from
embolism of the SC (infective endocarditis , intraventricular blood clots), birth defects and other
coronary lesions KA (koronariity in systemic lupus erythematosus, rheumatoid arthritis ,
rheumatoid arthritis), etc. However, in these cases they are not regarded as a clinical form of
coronary artery disease, and as a complication of one of these diseases.
In most cases, termination or a sharp restriction of coronary blood flow occurs as a result of
thrombosis of the spacecraft, which usually develops in the "complicated" plaque, which is thinned
capsule damaged (tear, ulceration, exposure of the lipid core plaque). This contributes to platelet
activation and plasma coagulation factors and tissue thromboplastins collagen. Initially formed
platelet "white" parietal thrombus. At the same time in this area is allocated a number of
biologically active substances with potent vasoconstrictor effect (endothelin, serotonin, thrombin,
antithrombin A2.The result is a pronounced spasm of the stenotic spacecraft, further limiting blood
flow to the coronary artery. In addition, small platelet aggregates may embolize to the coronary
vessels microcirculatory level, which further limits coronary blood flow. Gradually increase the size
of the thrombus and the wall, if it does not happen spontaneously lysis due to natural activation of
the fibrinolytic system of its own, or not performed thrombolytic therapy, clot completely occluding
the vessel lumen and evolving transmural myocardial infarction (heart attack with a tooth Q). In
cases where for various reasons, complete occlusion of the spacecraft does not occur or a
spontaneous clot lysis may develop subendocardial or mural myocardial infarction (heart attack
without tooth Q). The latter may develop and complete occlusion of the SC, if well developed
collaterals. The consequences of myocardial infarction. As a result of a myocardial infarction is a
violation of diastolic and systolic left ventricular function, and begin the complex process of
remodeling it. At the same time there are significant changes in the functional state of other organs
and systems.
The clinical picture of "uncomplicated" myocardial infarction with Q waves
During transmural myocardial infarction (heart attack with a tooth Q) decided to allocate five
periods: 1) prodrome, 2) acute and 3) sharp, and 4) subacute and 5) postinfarction period. The
clinical picture of each of them consists of:
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typical clinical manifestations of uncomplicated myocardial infarction;
clinical symptoms of multiple complications.
Prodrome (preinfarction angina)
Most patients with MI with a tooth Q (70-80%) the formation of thrombotic occlusions total can
range from 2 to 18 days. At this time the coronary circulation is characterized by extreme volatility,
which is reflected in the clinical picture of disease, resembling, as a rule, one of the options for
unstable angina:
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first emerged angina (unstable and rapidly progressive course);
progressive angina;
spontaneous anginal attacks pain at rest (including Prinzmetal's variant angina).
Acute period
Acute transmural myocardial infarction period - this time from the onset of clinical and / or
instrumental (ECG) signs of acute myocardial ischemia prior to the formation of foci of necrosis (23 h). During this period, morphological changes in the cardiac muscle more reversible, and timely
application of thrombolytic agents may be possible to restore coronary blood flow and prevent the
formation of myocardial necrosis.
The first clinical manifestation of myocardial infarction associated with the completion of
thrombotic occlusion of the full SC or a sudden its development (in the absence of patient
symptoms prodromal period). There are several clinical variants of early myocardial infarction:
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pain (anginal) version of the start (status anginosus);
asthmatic option (status asthmaticus);
abdominal option (status abdominalis);
arrhythmic variant;
cerebrovascular option;
oligosymptomatic (asymptomatic) myocardial infarction beginning.
Complaints
Bout of intense pain in the heart is the most characteristic clinical sign of early myocardial
infarction. The pain is localized in the chest, often spreading to the entire region before cardiac left
and right of the sternum, and even epigastric region. In most cases, pain radiating to left arm, left
shoulder blade, neck, at least - in interscapulum, the lower jaw in both hands, etc.
The intensity and nature of pain is usually distinguished from an attack of angina pectoris:
myocardial infarction patients describe it as unusually severe, painful, "cruel" pain squeezing,
crushing, or burning Expander nature, often accompanied by fear of death. The pain occurs
suddenly, quickly reaching the maximum intensity. It is not docked with nitroglycerin sublingually
or isosorbide dinitrate. Often the pain just stopped by after the application of narcotic analgesics
("marginal" or "morphine" pain). The duration of pain, in typical cases is 40-60 minutes, sometimes
persisting hours and days, justifying its name - status anginosus.
Sometimes, perhaps as a "wave-like change in pain intensity: 20-30 minutes after the limit of
strength," morphines "pain comes short (10-15 minutes), pain relief, after which she resumed with
renewed vigor.
It should be remembered that the pain they sometimes can pass on their own, even if the patient had
not received appropriate medical care.
Much less pain when they may be less intense and prolonged. In these cases, pain can be quite
"tolerant" of their duration does not exceed 15-20-30 minutes, sometimes pain can cut short after
taking several tablets of nitroglycerin.
Most patients with transmural infarction occurrence of intense pain attack is accompanied by signs
of a painful shock. Patients complain of a sudden appeared a sharp weakness, dizziness, sweating
expressed, heart rate (tachycardia), cold extremities. There is apathy and weakness, and in some
cases, even a short blackout. There is a decrease in blood pressure.
Described clinical signs indicate the occurrence of acute vascular insufficiency, which develops,
usually at an altitude of pain. As a result of reflex dilatation of the abdominal cavity and the skeletal
muscle of blood is deposited in these vascular areas, reducing blood flow to the heart, developing
hypovolemia, reduced blood pressure and cerebral hypoperfusion.
This clinical picture of acute circulatory failure is very similar to the initial clinical manifestation of
true cardiogenic shock due to a sharp fall in cardiac output. However, in contrast, signs of reflex
painful shock short-lived, quickly, within a few minutes, go alone or with the use of drugs that
increase the vascular tone.
Shortness of breath. Subjective manifestations of acute left ventricular failure are observed more
than half of patients transmural myocardial infarction, including patients with pain (anginal) option
infarction. Against the background of continued pain after the attack, or relieve the feeling of lack
of air, breathing discomfort, shortness of breath, which intensified in the horizontal position of a
patient with a low headboard. These symptoms are associated with rapidly evolving against a
background of severe myocardial ischemia, diastolic and systolic LV dysfunction, improvement of
CRT in the ventricle, the average pressure in the LP and the veins of the pulmonary circulation and
venous congestion in the lungs.
It should be emphasized that the development of more severe manifestations of acute left
ventricular failure (cardiac asthma or alveolar pulmonary edema) in acute myocardial infarction
period pain is not typical. An exception is the option early asthmatic MI, which is regarded as a
complicated course of myocardial infarction and is considered by us in the section "Complications
of myocardial infarction."
Arrhythmias. Most patients with transmural infarction (90%) as a monitor observation can reveal a
variety of arrhythmias and conduction, including emerging in the earliest period of the disease.
Most of them are accompanied by complaints of patients on heart rate and disruptions of the heart.
A detailed description of certain types of arrhythmias is shown below (see: "Complications of
myocardial infarction").
History. In the history of the vast majority of patients with acute myocardial infarction there are
indications of clinical manifestations of coronary heart disease (angina or rest), as well as the
presence of certain risk factors for aggravating heart attack (AH, LLA, smoking, diabetes, obesity,
family history etc.). Details should ask the patient or relatives about the period immediately
preceding the development of myocardial infarction (prodromal stage), and the factors trigger the
development of myocardial infarction (excessive exercise, psycho-emotional stress, infections, etc.).
Physical examination. The purpose of physical examination of patients with MI is not so much a
diagnosis of MI, which is confirmed in the main data laboratory and ECG studies, assessment of
how the functional state of the cardiovascular system and timely diagnosis of severe complications
infarction. Inspection. With the general examination in the first minute or 1-1.5 h, the last of the
onset of the disease, attention is drawn to marked agitation and restlessness of patients experiencing
at this time of pain. They are trying to change position, sometimes even walking around the room,
sit in a chair, lie on the bed in search of provisions to relieve the suffering. This feature is
characteristic of patients with MI, distinguishes them from patients with angina who, during the
pain attack as if frozen in place. After the relief of pain stimulation in patients with developing
myocardial infarction, usually takes place. The exceptions are cases of progressive left ventricular
failure, accompanied by suddenly appearing and rapidly increasing dyspnea and suffocation. On
examination, often marked pallor of the skin, cold extremities and severe sweating, indicating the
possible development of acute circulatory failure (short-term reflex painful shock) or the initial
clinical manifestation of true cardiogenic shock. In most cases, cyanosis is determined by the lips.
Severe cyanosis, orthopnea position, combined with moist finely rattling in the bottom of the lungs
and increased frequency of respiratory movements indicate the presence of acute left ventricular
failure. Palpation and percussion of the heart. On palpation of the heart, there may be local
tenderness in the left before cardiac area. When percussion is no noticeable increase in LV cavity
acute illness can not be identified. The exceptions are patients with previous myocardial diseases
that are accompanied by dilatation of LV (hypertension, atherosclerotic and postinfarction cardio,
etc.). Auscultation of the heart. In acutest period of MI in patients can identify several auscultatory
phenomena: 1. Weakening and muted tones on top of I associated with a decrease in contractility of
the ischemic left ventricular. 2. 2. Weakening II tone due to deceleration of early left ventricular
diastolic relaxation and reduction of pressure in the aorta. When the pressure in the pulmonary
artery, caused venous congestion in the pulmonary circulation, determined tone accent II on the
pulmonary artery. Finally, some patients with myocardial infarction and severe atherosclerotic
aortic seal can listen to the tone accent II aorte.3. Sinus tachycardia, which in the first 2-3 hours
after the start of IM suggests, rather, not the presence of heart failure, and marked activation of the
CAC, taking place against the backdrop of painful stress. 4. 4. Sinus bradycardia, sometimes
detected in patients with myocardial infarction is associated, on the contrary, with a predominance
of parasympathetic nervous system activity and the inhibition of CA-node automaticity, which is
especially often observed in the field of left ventricular infarction posterolateral diaphragmatic. In
addition, in more rare cases, bradycardia may be due to blockade of the SA-or AV-block II and
even III degree.
Arterial pulse and blood pressure. Blood pressure in the first minutes and hours of MI may increase,
which is often associated with elevated CAC increased concentration of catecholamines in the
blood, appearing as a result of the pain and emotional stress. With the development of acute
vascular insufficiency of blood pressure is reduced, mainly due to systolic BP. Simultaneously, a
decrease of filling, tension and magnitude of arterial pulse, as well as its acceleration.
Acute period.
Acute myocardial infarction period corresponds to the time of formation of foci of necrosis and the
emergence of the so-called reabsorbision necrotic syndrome associated with a common reaction to
the absorption (resorption) of necrotic masses in the blood. During this period also begins the
complex process of LV remodeling is accompanied by a violation of the functional state of the
cardiovascular system. In uncomplicated acute myocardial infarction during the period usually lasts
about 7-10 days.
Complaint. Pain in the heart. In the absence of complications, pain in the heart of this period
usually does not occur. Preservation of pain for a few days of illness onset may indicate a further
distribution of thrombotic process in the coronary system and expanding the zone of ischemic
damage of the heart muscle or of involvement in the pathological process of the pericardium.
Fever. At the 2-3rd day of illness the body temperature up to 37,2-38 ° C and above, which is one
of the first clinical signs of necrotic resorption syndrome. Fever usually persists for 3-4 days, rarely
about 1 week. More prolonged increase in body temperature may indicate the development of
complications of myocardial infarction: pneumonia, thrombotic endocarditis, pulmonary infarction,
etc.
Shortness of breath and other signs of left ventricular failure frequently observed in acute
transmural myocardial infarction, suggesting left ventricular dysfunction. Feeling short of breath,
tachycardia, small for a short time can be detected even in cases that are considered in general as for
uncomplicated heart attack. In more severe cases may develop interstitial or alveolar pulmonary
edema, which is regard as a very serious complication of MI (details - see: "Complications of
myocardial infarction").
Arrhythmias. In the acute stage of the disease remains a high risk of a variety of arrhythmias and
conduction, including paroxysmal ventricular tachycardia and ventricular fibrillation. When
uncomplicated myocardial infarction patients can be kept moderately severe sinus tachycardia or
bradycardia, isolated extrasystoles.
Physical examination.
Examination. Uncomplicated acute period of MI, usually not accompanied by any specific
changes, detectable by the general inspection. In the study of the cardiovascular system during this
period may reveal a slight decrease in systolic blood pressure.Often reveals a moderate sinus
tachycardia due to heart failure or related to the presence of fever. For percussion of the heart may
reveal a slight shift to the left the left border of the relative dullness, which may indicate the
beginning of LV remodeling, its dilation and reduced contractility. Auscultation of the heart I
relaxed tone, sometimes significantly, due to a sharp decrease in left ventricular contractility,
dilatation of its occurrence or relative insufficiency of mitral valve damage as a result of papillary
muscle. In the latter case, the weakening of the tone I often combined with systolic noise at the top,
under way at the left armpit. Approximately one third of patients with MI in the acute stage can
hear protodiastolic or presystolic gallop rhythm. Protodiastolic gallop rhythm due to the appearance
of abnormal heart tones III shows the progressive fall of left ventricular contractility and volume
overload. Diagnostic value of auscultatory phenomenon increases with the presence of other signs
of left ventricular failure (dyspnoea, cyanosis, wheezes in the lungs, etc.). Sometimes the apex of
the heart can hear presystolic gallop rhythm associated with the appearance of abnormal heart tones
IV, due to increasing end- diastolic pressure in the left ventricular diastolic stiffness, and severe
ischemic myocardium. 2-4 days of the disease on auscultation can hear the noise of friction
pericardium due to involvement in the disease process leaves the pericardium (aseptic pericarditis),
which is seen as a complication of myocardial infarction). Finally, in more rare cases, may appear at
the top of the beat, coupled with the weakening of tone I caused the defeat of the papillary muscles
and the relative development of mitral valve insufficiency. Maximum noise is determined at the top.
The noise carried in the left armpit.
Subacute period
In the subacute stage of MI gradually formed connective tissue scar, which replaces the necrotic
masses. Work is also continuing the process of LV remodeling. The duration of subacute period
varies widely and depends primarily on the volume of foci of necrosis, infarction of the surrounding
state, not involved in the necrotic process, the degree of development of collaterals, the presence of
concomitant diseases and complications of MI. Typically, the duration of subacute period is 4-6
weeks. In general, the subacute period are relatively more relaxed and favorable, than the two
previous periods. The condition of patients gradually stabilized. In uncomplicated disease course
pain in my heart and life-threatening severe arrhythmias (ventricular tachycardia and ventricular
fibrillation Paroxysmal) are absent. Decreases the incidence of arrhythmias, sinus tachycardia and
other arrhythmias. In patients with evidence of AV block I or II that have developed in the acute
stage, often restored atrioventricular conduction. Reduced manifestations of heart failure (shortness
of breath, tachycardia), if they occurred in the acute period.In other cases, with extensive damage to
the heart muscle symptoms of congestive heart failure may progress, especially against the
background mode is activated patient. At the same time grows short of breath, tachycardia, edema
appear on the legs, increases the liver, stored moist wheezes in the lower lungs, etc. In most cases in
the subacute stage of a tendency to normalization of blood pressure, although sometimes the level
of systolic blood pressure is lower than before the onset of MI. Auscultation is usually kept muted
tone I at the top, but protodiastolic and presystolic gallop rhythm are heard less often. In patients
with relative insufficiency of the mitral valve due to valvular dysfunction (papillary muscle)
continues to listen systolic murmur at the apex. Pericardial friction noise is absent.
Postinfarction period
In the immediate postinfarction period in the rumen increased amount of collagen and ends with his
seal (consolidation of the scar). At the same time continuing the formation of a number of
compensatory mechanisms aimed at maintaining the hemodynamics at the proper level
(hyperfunction and hypertrophy of the intact myocardium, moderate dilatation of the LV,
contributing, according to Starling mechanism, a slight increase in cardiac output, etc.). The clinical
picture of postinfarction period is affected by many factors:
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postinfarction scar size;
functional state of the surrounding myocardium;
of compensatory mechanisms of cardiac activity;
rate of progression of coronary atherosclerosis, etc.
In the near term post-infarction angina may resumeIf during this period there are
frequent anginal attacks occurring in a patient with the slightest exertion, psychoemotional stress or at rest, it is regarded as one of the options for unstable angina (an
early post-infarction angina) requiring emergency treatment. The second group of
subjective symptoms observed in some patients in the postinfarction period is associated
with progression of chronic heart failure (shortness of breath, tachycardia, leg swelling,
increasing weakness, fatigue, etc.). Finally, in the postinfarction period remains an increased
risk of occurrence of various arrhythmias and conduction. These objective study conducted
in the postinfarction period, often support some degree of hemodynamic instability (wheezes
in the lungs, edema, liver enlargement, cyanosis, ventricular dilation, etc.).
Features of the clinical picture of myocardial infarction without Q wave
The clinical picture of myocardial infarction without wave Q (no transmural) is broadly
consistent with the above clinical manifestations of acute coronary syndromes. Since the
basis of no transmural MI in most cases is the development of "complicated" plaque wall
thrombus and appearance of the heart muscle area and expressed relatively a long-term
ischemia, the main clinical manifestation of MI without Q-wave is pain. In most cases, are
characterized by pain, prolonged rest angina (lasting more than 20-30 minutes), poorly
stoped nitroglycerin. As a rule, anginal attacks do not reach the intensity characteristic of an
emerging transmural infarction with a tooth Q, and more like the rest angina, characteristic
of patients with NA. Sometimes retrosternal pain may be accompanied by sharp attacking
weakness, sweating, shortness of breath, transient arrhythmias and conduction and / or a
sudden drop in blood pressure. Less commonly, infarction without Q wave manifests less
intense but more frequent bouts of angina, a rapid decrease in exercise tolerance, etc more
reminiscent of progressive symptoms of the National Assembly. In all these cases the lack
of persistent elevation RS-T on the background causes pain attacks carried out a differential
diagnosis between HC and myocardial infarction without tooth Q. Physical examination
usually provides little new information to confirm the diagnosis no transmural MI, except
for transient significant weakening of the fundamental tone heart and the appearance of
additional tones (III or IV) during the occurrence of anginal attack. Sometimes you can
detect transient arrhythmias, and various changes in blood pressure. Thus, the analysis of
clinical data in most cases, suggesting the development of coronary heart disease in a patient
with acute coronary syndrome, but in order to confirm or refute the presence of myocardial
infarction without tooth Q, should be targeted lab tests.
Laboratory diagnosis of myocardial infarction
Laboratory confirmation of acute myocardial infarction based on the identification of: 1)
nonspecific indicator of tissue necrosis and inflammatory reaction of the myocardium, 2)
hyperenzymemy and 3) increase in blood myoglobin and troponin.
Nonspecific reaction to the occurrence of acute myocardial infarction is associated primarily with
the disintegration of muscle fibers, breakdown products of protein absorption into the bloodstream
and local aseptic inflammation of the heart muscle, mainly in developing peryinfarct zone. The
main clinical and laboratory signs of reflecting these processes are: increased body temperature
(from subfebrile figures to 38,5-39 ° C), leukocytosis, usually not exceeding 12-15 x 109 / l.,
Aneozinofiliya, a small stab shift of the blood to the left, increasing the ESR. Markers of
myocardial necrosis: Troponin. The most sensitive and specific marker of myocardial necrosis is an
increased concentration of troponin I and T included, as is known in the troposphere myosin
complex contractile myocardium. Normally cardio-specific troponins in blood are not detected or
the concentration is less than the most minimal values established separately for each clinical
laboratory. Cardiomyocyte necrosis is accompanied by a relatively rapid and significant increase in
the concentration of troponin I and T levels are starting to exceed the upper limit of normal within
2-6 hours after anginal attack and remains high for 1-2 weeks from onset of infarction. Myoglobin.
Very sensitive, but few specific marker of necrosis is the concentration of myoglobin in the blood.
His rise is observed 2-4 hours after anginal attack and persists for 24-48 hours afterwards. The yield
of myoglobin from heart muscle and increase its concentration in the blood occurs before the
formation of foci of necrosis, etc expressed at the stage of ischemic heart muscle. You should also
remember that increasing the concentration of myoglobin in the blood may be due to other causes
(other than a heart attack): Disease and injury of skeletal muscles, a lot of physical stress,
alcoholism, renal insufficiency. Unfortunately, not all clinics are now able to determine the
concentration of troponin laboratory and myoglobin in the blood. Therefore, in practice retains its
value determination of other, less sensitive and specific, markers of myocardial necrosis The most
valuable of them for the diagnosis of acute myocardial infarction is to determine the activity of
several enzymes in serum:
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CK (K FA), especially its MB-fraction (CF to PC);
lactate dehydrogenase (LDH) and its isoenzyme 1 (LDG1);
aspartate aminotransferase (AST).
Creatine kinase (K FA) and its MB fraction to the FC. More specific laboratory test is to identify
acute myocardial infarction MW fraction to FC (CF to PC). Its activity begins to increase after 4-6
h, reaching a peak after 12-18 hours and returned to their original numbers after 48-72 hours from
the start of anginal attack. Of particular importance is the dynamics of enzyme activity: reliable
signs of acute myocardial infarction considered to increase the activity of CF FC by 25% in two
samples taken from the 4-hour intervals, or a gradual increase in enzyme activity over 24 hours is
informative to the increased activity of CF FC 10 - 13 IU / liter. Activity common to FC in MI
undergoing a similar trend: the end of the first day of the enzyme level in the 3-20 times higher than
normal, but after 3-4 days of onset of the disease returned to baseline values. In contrast, the
increased activity of MB fraction to FC, contained mainly in the myocardium, specific for heart
muscle damage, primarily for acute myocardial infarction. MB-fraction to FC does not respond to
damage of skeletal muscle, brain and thyroid gland. However, be aware that any cardiac
intervention including coronary angiography, catheterization of heart cavities and electro-therapy,
usually accompanied by a brief rise of activity-MB fraction to the FC. In the literature there are also
indications of the possibility of increasing the level of CF to FC with severe paroxysmal
tachycardia, myocarditis, and long strokes of rest, assessed as a manifestation of unstable angina.
Lactate dehydrogenase (LDH). The activity of this enzyme in acute myocardial infarction is
growing more slowly than the CK and CF to CF, and remains elevated for longer. Peak activity
occurs usually 2-3 days from onset of infarction, and return to its original level - only 8-14 days.
Should be remembered that the total LDH activity also increased in liver disease, shock, congestive
heart failure, hemolysis and megaloblastic anemia , pulmonary embolism, myocarditis, an
inflammation of any localization, coronary angiography, cardioversion, heavy physical exertion and
and so on. In this regard LDG1 isoenzyme more specific for heart disease, in particular for acute
myocardial infarction, although it is also present not only in heart muscle but also in other organs
and tissues, including red blood cells. Aspartate aminotransferase (AST) is also an enzyme with a
relatively fast peak of the upcoming increase in activity (24-36 h of the onset of infarction). After 47 days the concentration of AST returned to baseline levels. Changes in the activity and AST is not
specific for acute myocardial infarction: the level of AST with ALT levels increased in many
pathological conditions, including liver diseases. Yet it must be remembered that in patients with
lesions of the liver parenchyma to a greater extent increases the activity of ALT, and heart diseases
- AST. In the MI ratio Rytis (the ratio of AST / ALT) greater than 1.33, and for diseases of the liver
- less than 1.33. Given the specific characteristics of leaching of various enzymes of foci of necrosis
and duration of their presence in the serum, should keep a few principles of enzymatic diagnosis of
acute myocardial infarction.
Electrocardiography
Myocardial infarction with Q waves
According to the ideas Bayley, violation of the coronary circulation during myocardial
infarction leads to the formation of three zones of the lesions: necrosis around the site are
areas of ischemic damage and ischemia. In the leads, the active electrode which is located
directly above the area of MI, each of these areas is involved in the formation of these ECG
changes.
1. The zone of necrosis - pathological tooth Q (lasting more than 30 ms) and a sharp
decrease in the amplitude of R wave or complex QS.
2. The zone of ischemic damage - offset RS-T segment above (transmural infarction) or
lower contour (with subendocardial lesions of the heart muscle).
3. The zone of ischemia - "coronary" (equilateral and spiky), T wave (high positive in
subendocardial MI and negative - with transmural infarction).
Acute stage (up to 2 hours from the start of IM) is recorded on the ECG-segment RS-T above
isoline (transmural ischemic injury). RS-T segment with merges with a positive T wave, forming
the so-called monophasic curve that resembles the shape of TM PD.
The acute stage is characterized by rapid, within 1 - 2 days, formation of a pathological Q wave or
QS complex and reduced wave amplitude R, which indicates the formation and expansion of the
zone of necrosis. At the same time for several days stored offset RS-T segment above the contour
and merges with it at first positive and then negative spike T. A few days later RS-T segment is
close to contour lines and by the end of 1st week or the beginning of the 2nd week of illness is
isoelectric that indicates a decrease in the zone of ischemic damage. Negative coronary T wave
abruptly deepens and becomes symmetrical and sharp (re-inversion of T wave).
Three zones of pathological changes in heart
muscle in acute myocardial infarction (from
Bayley) and their reflection on the ECG (Figure)
In the subacute stage of MI registers or pathological Q prong set QS (necrosis) and a negative
coronary T wave (ischemia), whose amplitude, ranging from 20 to 25-days of myocardial
infarction, is gradually reduced. RS-T segment is located on the contour. Scar stage of MI is
characterized by persistence over many years of pathological Q wave or QS complex and the
presence of negative, positive or smoothed the T wave. Depending on the localization of myocardial
infarction and prevalence of these changes are found in different ECG leads.
ECG anteriorseptal myocardial infarction with the transition to the top of A and anterolateral
myocardial infarction-B
ECG in advanced anterior myocardial infarction-A and anterior basal (high anterior)
myocardial infarction: a - the usual arrangement of thoracic electrodes (myocardial
infarction not detected), b - by placing electrodes on the two edges of the above (recorded
typical symptoms of myocardial infarction)-B
ECG during acute posterolateral diaphragmatic (lower) myocardial infarction. In leads I, aVL, V1V4 recorded reciprocal ECG changes.
Direct and reciprocal ECG signs of myocardial infarction with Q waves of different localization
Localization of infarction
Leads that show signs of myocardial infarction
Direct evidence:
Reciprocal
features:
pathological Q (QS);
depression RS-T;
elevation RS-T;
high positive T;
negative coronary T
higher R (at the rear
MI)
Myocardial infarction left ventricular anterior wall
anterior septal
V1 - V3
anterior apical
V3, V4
The front side
I, aVL, V5, V6
Anterior basal (high-front)
V24 - V26 and / or V34 - V36
Common front
I, aVL, V1 - V6
III, aVF, II
Myocardial infarction left ventricular posterior wall
Posterolateral diaphragmatic III, aVF, II
(lower)
posterior basal
V7 - V9
V1 - V3
Rear side
V5, V6, III, aVF
Common background
III, aVF, II, V5, V6, V7 — V9 III, aVF, II, V1 — V3 V1 - V3
V5, V6, V7 - V9
Myocardial infarction without Q wave
Myocardial infarction without Q wave characterized by the development of cardiac muscle
necrosis notransmural, localized subendocardial or intramural. In contrast, transmural infarction,
these foci of necrosis does not violate the propagation of waves of depolarization of the heart, so
the abnormal tooth Q or QS complex are absent. Significant violations are detected only during
the formation of RS-T segment and during the final phase of ventricular repolarization (T wave).
The most common ECG signs of myocardial infarction without Q wave are: 1) a shift RS-T
segment below the contour (in rare cases, possible RS-segment elevation of T), 2) a variety of
pathological changes of the T wave (usually symmetrical and sharp negative coronary T wave);
3) the emergence of these changes on the ECG after a long and intense pain attack and keep them
within 2-5 weeks. Diagnostic localization of myocardial infarction without Q wave based on the
same principles as the transmural MI.
ECG of the two patients with non-Q-wave and anterior location posterolateral diaphragmatic
Echocardiography is one of the required research methods that are used for the diagnosis of acute
myocardial infarction and assessment of hemodynamic and structural damage in this disease. The
use of two-dimensional, one-dimensional and Doppler echocardiography in MI you can:
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identify local disturbances of LV contractility;
quantify systolic and diastolic function ЛЖ ; LV;
reveal signs of LV remodeling (dilatation of the cavity ventricle, left ventricular geometry
changes, etc.);
identify echocardiographic signs of left ventricular aneurysm;
assess the condition of the valve apparatus and the presence of relative insufficiency of
mitral valve defect or MZHP;
assess the level of pressure in the aircraft and identify the signs of pulmonary hypertension;
identify morphological changes in the pericardium and the presence of fluid in the
pericardial cavity;
intracardiac thrombi detect the presence of;
assess the morphological and functional changes of main and peripheral arteries and veins.
One-dimensional echocardiograms recorded from various sites of patients with MI, which are
clearly visible signs of hypokinesia or akinesia segments of diseased left ventricle.
One-dimensional echocardiograms recorded from the left parasternal access in a healthy person (a
- scheme) and the patient postinfarction cardiosclerosis (b). visible hypokinesia septal
Two-dimensional echocardiograms recorded in patients with postinfarction cardiosclerosis a akinesia of interventricular septum, b - posterolateral diaphragmatic akinesia (lower) segment of
the left ventricle
Selective coronary angiography (CAG) in patients with acute myocardial infarction is carried out
in cases where surgery is supposed to coronary vessels - percutaneous transluminal angioplasty or
coronary artery bypass grafting. Obtained in the CAG are very important when choosing a method
of surgical correction of obstructive lesions of the SC. Because when the CAG, as a rule, make the
left ventriculography, it allows us to estimate a number of important hemodynamic parameters and
verify some of the serious complications of MI (left ventricular aneurysm, rupture MZHP, etc.). The
most common indications for emergency CAG and subsequent surgical repair in patients with acute
myocardial infarction are:
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cardiogenic shock;
severe left ventricular failure, particularly if it is combined with severe mitral insufficiency
or rupture of the interventricular septum ;
recurrent episodes of life-threatening ventricular arrhythmias (ventricular tachycardia,
ventricular fibrillation);
Early post-infarction angina.
It should be noted that in recent years in the major cardiology centers greatly expanded indications
for emergency CAG. The study is now carried out for many patients with acute myocardial
infarction hospitalized in the early stages of disease onset (4-6 h) to restore coronary blood flow or
limit the zone of necrosis by selective intracoronary administration of thrombolytic therapy or
surgical correction of blood flow in the spacecraft.
Treatment of uncomplicated myocardial infarction with Q waves
The existing system currently in the treatment of patients with MI include:
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specialized cardiac ambulance (prehospital) providing first medical care of patients with MI;
specialized branch infarction with intensive care unit or coronary care department (hospital
phase);
specialized rehabilitation centers (departments of hospitals and cardiology sanatorium);
Cardiac consultative and diagnostic centers and clinics cardiology offices (clinical
examination of patients after myocardial infarction).
The main strategic objectives of the treatment of patients in the prehospital and hospital stages are:
1. Early reperfusion of the myocardium or coronary revascularization, as well as preventing further
blood clots.
2. Limiting the focus of necrosis and coronary band periinfarction with hemodynamic and
metabolic unloading of the heart.
3. Prevention or elimination of the early complications of myocardial infarction.
4. 4. Physical and psychological rehabilitation of patients with MI.
All patients with suspected myocardial infarction with a tooth forming Q, patients with acute
coronary syndrome and persistent elevation RS-T, must be immediately hospitalized in intensive
care specialist cardiac units. Basic therapy, which is carried out in all patients with myocardial
infarction with a tooth Q, regardless of the presence or absence of certain complications, includes:
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pain relief (analgesia);
thrombolytic therapy (of course, tailored to individual indications and contraindications);
antithrombotic and antiplatelet therapy;
oxygen therapy;
the use of anti-ischemic drugs;
ACE inhibitors and angiotensin receptor antagonists II.
Pain
Relief of anginal attack is a prerequisite for all further therapeutic measures. Anginal pain retaining
supports hyperactivation of SAS, which is accompanied by tachycardia, positive inotropic effects,
increases myocardial oxygen demand and leads ultimately to an increase in infarct. In addition, SAS
background activation lowers the threshold of ventricular fibrillation, which in itself can have fatal
consequences. If there are no signs of a sharp fall in cardiac output and blood pressure (arterial
pulse filling satisfactory and acceptable numbers of blood pressure), patients are encouraged to rereception of nitroglycerin sublingual or inhalation irrigation of the oral mucosa by aerosol
nitroglycerin or isosorbide dinitrate. These simple measures should be carried out at the first contact
a patient with a doctor before ECG recording.
Morphine. The classic means of pain relief in patients with myocardial infarction is the use of
narcotic analgesics. Morphine, an agonist of opioid receptors, in addition to rapid pain relief,
reduces venous tone and, consequently, reduces the venous return of blood to the heart, the
magnitude of preload and myocardial oxygen demand. Morphine has also pronounced sedative
effect. In addition, he has a marked effect vagotonic causes sinus bradycardia and hypotension.
In patients with acute coronary syndrome, including suspected myocardial infarction, morphine is
administered intravenously at an initial dose of 2-4 mg, followed by 2-6 mg every 10-15 minutes (a
total of no more than 20-30 mg) up to pain relief or the appearance of side effects:
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nausea, vomiting, sinus bradycardia (vagotonic effects);
hypotension;
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signs of depression of the respiratory center.
Keep in mind that vagotonic side effects relatively easily eliminated by intravenous (0.5-1.0 ml) of
0.1% solution of atropine sulfate, and the signs of depression of the respiratory center - 0.1-0.2 mg
intravenous naloxone.
In the absence of effects from the use of morphine and maintaining pain showed intravenous drip
solution of nitroglycerin and / or b-blockers, which contribute, as we know, the hemodynamic
unloading of the heart and reduce myocardial oxygen demand.
Nitroglycerin (0.1% solution) is administered intravenously. Just as in the National Assembly, the
initial rate of intravenous infusion of nitroglycerin is 10 mg / min. Then it increases to 10 mcg / min
every 3-5 min until the reaction of blood pressure changes or symptoms. At the same systolic blood
pressure should be below 110 mm Hg. Art. or in a patient with hypertension - 25% below baseline.
β-blockers. Intravenous b-blockers in the acutest period they can contribute to reduction of pain
syndrome and control of areas of necrosis. b-blockers reduce contractility and myocardial oxygen
demand and weaken the influence of catecholamines on the heart, reduce heart rate, blood pressure,
increase the threshold for ventricular fibrillation and prevent supraventricular arrhythmias. It is
recommended to use cardioselective b1-blocker (metoprolol, atenolol, and others).
Should be considered contraindications to the use of b-blockers in patients with myocardial
infarction:
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signs of congestive heart failure (including wet wheezes in the lower regions of the lungs);
Heart rate below 60 bpm in minutes;
AV block II, III and I grade at P-Q (R) with more than 0.24;
systolic blood pressure below 90 mm Hg. ;
concomitant presence of asthma;
chronic obstructive bronchitis in the presence of dry wheeze in the lungs (one of the
symptoms of bronchial obstruction).
Oxygen therapy
Oxygen therapy is indicated for all patients with myocardial infarction with a tooth Q. The use of
oxygen by mask or nasal catheter increases the saturation of arterial blood oxygen (SaO2) above
90%, resulting in an increase of its diffusion in the area of ischemic myocardium surrounding intact
areas of the heart muscle, helping to reduce the size of the zone of ischemic damage (periinfarct
zone). Oxygen therapy is indicated for patients of MI at least during the first 1-2 days after
admission to the intensive care unit.
Antiplatelet drugs
Mandatory condition of patients with MI is the appointment of antiplatelet drugs. Most often
prescribe aspirin at a dose no higher than 325 mg per day. At the first contact with the patient is
recommended to chew an aspirin without membranes (250-325 mg) if this was not done before. In
the presence of contraindications to its use may use ticlopidine or clopidogrel, which are inhibitors
of ADP receptors of platelets. Effective is the combination of aspirin and clopidogrel
Heparins
Heparin is an effective indirect thrombin inhibitor, exerts its antithrombotic effect through
activation of physiological anticoagulant - antithrombin III. Appointment of heparin in acute
coronary syndrome with elevation RS-T, including myocardial infarction with a tooth at Q, is
justified primarily as a means of preventing further thrombus formation in the SC and reduces the
incidence of venous thrombosis and intraventricular wall with the subsequent development of
thromboembolic complications.
Anti-ischemic drugs
Anti-ischemic drugs are widely used in the treatment of patients with MI with a tooth Q. Thanks to
an efficient hemodynamic unloading of the heart, they help to limit the size of infarction in the first
place, the size of periinfarct zone. The latter is preserved areas of viable myocardium that directly
border zone of necrosis.
The most appropriate designation of patients with MI of two groups of drugs that have the property
to limit periinfarct zone: b-blockers and nitrates.
β-blockers. In the absence of β-blockers are contra-indications are encouraged to nominate all
patients with MI. The positive effect of these agents in myocardial infarction due to their negative
inotropic and chronotropic action, accompanied by a decrease in myocardial oxygen demand and
ischemia heart rate. This is to some extent makes it possible to maintain the viability of the
myocardium periinfarct zone and, thereby, limit the area of infarction. In addition, β-blockers have
the ability to raise the threshold of fibrillation, which reduces the risk of fatal cardiac arrhythmias.
Finally, the impact of β-blockers on the activity of the NAC and the RAAS is accompanied by a
slowing and LV remodeling has a significant impact on survival in the short and long periods of MI.
Nitrates are used in patients with myocardial infarction to left ventricular hemodynamic unloading
and reduced myocardial oxygen demand. The positive effect of nitrates on the value of periinfarct
zone and the reduction or relief of some symptoms of the disease (pain in the heart, shortness of
breath and other signs of left ventricular failure).
Metabolic drugs
Currently, patients are used, basically, two ways of actively influencing the metabolism of cardiac
muscle: the use of trimetazidine (preduktala) and intravenous drip of glucose-insulin-potassium
mixture.
Trimetazidine has a direct cytoprotective effect, implemented at the level of cardiomyocytes and
subcellular structures. Trimetazidine administered in the usual therapeutic dose - 1 table. 3 times a
day.
Glucose-insulin-potassium mixture (HEC) is widely used for the treatment of patients with MI. The
use of glucose-insulin-potassium mixture based on the idea that the increase in glucose delivery to
ischemic myocardium may have a protective effect by stimulating the accumulation of glycogen in
cardiomyocytes. The latter is a source of glucose during anaerobic glycolysis and thus enhances the
formation of ATP (GD Lopaschuk, 2000). It is not excluded that the introduction of glucoseinsulin-potassium mixture helps to reduce the level of circulating fatty acids, since insulin inhibits
the mobilization of free fatty acids from adipocytes.
ACE inhibitors
Recently, ACE inhibitors are increasingly used to treat patients with acute myocardial infarction
and patients with postinfarction cardiosclerosis, primarily to prevent progression of left ventricular
dysfunction.
In addition to optimizing the level of blood pressure, afterload and preload values, reducing the
production of aldosterone and, accordingly, sodium and water retention in the body, ACE inhibitors
are able to limit the adverse effects of rapid cardiac remodeling in patients with myocardial
infarction. Thus, ACE inhibitors reduce the effect of tissue angiotensin II in the processes of
hypertrophy of cardiomyocytes, interstitial fibrosis, improving endothelial function, increasing the
production of vasodilating substances and contributing to an increase in coronary flow reserve. In
addition, ACE inhibitors promote atherosclerotic plaque stabilization and reducing the frequency of
repeated acute coronary syndrome.
Thrombolytic therapy
Thrombolytic therapy is currently regarded as the primary method of restoring coronary blood flow
(reperfusion) in patients with acute coronary syndrome with persistent elevation RS-T. All drugs
currently used for thrombolysis in patients with myocardial infarction, are endogenous activators of
plasminogen. The most common ones include:
Streptokinase - indirect plasminogen activator derived from a culture of b-hemolytic streptococcus
group C. Streptokinase forms a covalent bond with the blood of plasminogen activating its
conversion to plasmin. In this regard, streptokinase, in addition to effects on fibrin clot formation,
has also expressed a systemic fibrinolytic action.
Urokinase - an enzyme that directly activates the conversion of plasminogen to plasmin. The drug is
prepared from a culture of human embryonic kidney.
Alteplaza - is a tissue plasminogen activator (tPA), which is produced mainly by endothelial cells
of blood vessels. Activation of tPA in the vascular bed occurs under the action of plasmin, trypsin,
kallikrein and activated factor X clotting. Tissue plasminogen activator, in contrast to streptokinase,
has an affinity to fibrin, so that it selectively acts on the fibrin clot, showing properties or fibrin
selectivity of fibrin specificity. This is a positive characteristic alteplaza explains the high efficacy
of the drug. It should nevertheless be borne in mind that the use of doses required for lysis of
thrombus, alteplaza affects both circulating in the blood of plasminogen, also exerting systemic
effects on fibrinolysis, although less pronounced than streptokinase. This leads to a decrease in
fibrinogen levels in the blood serum and an increased risk of bleeding (major complications of
thrombolytic therapy).
New educational technologies used in class:
Interactive game "cat in a bag"
In applying the method of "The Cat in the Bag" bag is put in a few sheets with questions on the
subject. Students take turns taking out of the bag sheets with questions and answers.
Examples asked questions on the topic:
1. The etiology of myocardial infarction
2. The pathogenesis of myocardial infarction
3. Classification of myocardial infarction
4. Clinical variants of myocardial infarction
5. The clinical course of myocardial infarction
6. Laboratory Methods of myocardial infarction
7. ECG signs of myocardial infarction
8. Differential diagnosis of acute myocardial infarction.
9. Basic principles of treatment and rehabilitation of myocardial infarction.
10. Complications of myocardial infarction.
6.2. The analytical part.
Situational problems
1. Patient M. age 62 turned to the clinic complaining of severe chest pain, feeling short of breath,
general weakness. A patient suffering from coronary heart disease for a long time. Pain started 2
hours ago, the pain does not even nausea Paulsen receive 4 tablets of nitroglycerin. OBJECTIVE:
pale skin, cold sweat, lips cyanosis, pulse 92 beats per 1min., Blood pressure 90/50 mmHg
I. Your tentative diagnosis:
A. CHD: myocardial infarction *
B. ischemic heart disease: angina FC I
V. ischemic heart disease: progressive angina
G. ischemic heart disease: angina angiospastic
D. CHD: angina FC IV
II. Necessary for the diagnosis methods:
A. Ultrasound
B. ECG *
V. X-ray
G. EhoKS
D. radioisotope scan
2. In the clinic enrolled patient complaining of pain dagger in the heart, not stoped taking
nitroglycerin, accompanied by cold sweat and feeling the fear of death. Auscultation of the heart
tones of the deaf.
I. Your tentative diagnosis:
A. CHD: myocardial infarction *
B. ischemic heart disease: angina
V. hypertension, hypertensive crisis
G. ischemic heart disease: angina angiospastic
II. What changes in the ECG:
A dome-shaped segment elevation ST *
B. negative T waves
V. ST segment on the isoelectric line, the expansion of the QRS complex
G. metabolic changes in the myocardium, the signs of left ventricular hypertrophy
D. ECG unchanged
3. Patient A., 44. Complains of chest pain compressive nature, cold sweats, general weakness.
Anamnesis: in 5 years suffer from coronary heart disease. Deterioration began this morning.
Deterioration began this morning. Repeated reception of nitroglycerin pain is not docked.
OBJECTIVE: The state of medium gravity, there is pallor of the skin. In the lungs, vesicular
breathing. Cardiac deaf. Pulse regular, intense, 80 beats per minute. BP 180/90. The ECG - sinus
rhythm in leads III, AVF ST segment above the contour lines and contour otvedeniiV3 below.
I. Your diagnosis:
A. CHD. Acute myocardial infarction anterior left ventricular wall
B. CHD. Acute myocardial infarction anterior septal area
V. CHD. Acute myocardial infarction posterior wall *
G. CHD. Acute myocardial infarction of the apical region
II. What complications can occur early in the patient?
A syndrome Dresllera
B. Cardiogenic shock *
V. Chronic aneurysm
G. postinfarction cardio
4. Patient K., aged 46. Complains of chest pain compressive nature. Of history: During the 3 years
of age suffer from hypertension. In the last 2-3 months periodically bothered squeezing chest pain
character, who with nitroglycerin pills quickly passed. Today, because of the lack of nitroglycerin
patient did not accept it. The patient was given a pill under the tongue Validol, but chest pain
persisted, and he brought the ambulance to the emergency department of a hospital. OBJECTIVE:
The state of medium gravity, skin pale and covered with cold sweat. In the lungs, vesicular
breathing. Cardiac deaf. Pulse 74 beats rhythmic min. AD140/90. The ECG - isoelectric STsegment elevation in I-II, AVL, V5, V6 leads.
I. Your diagnosis:
A. CHD. Progressive angina
B. CHD. Acute myocardial infarction posterior wall
V. CHD. Acute myocardial infarction side wall of the left ventricle *
G. CHD. Acute myocardial infarction of the anterior-septal
II. What changes in laboratory parameters are possible:
A neutrophilic leukocytosis, accelerated erythrocyte sedimentation rate, hyperenzymemia *
B. anemia, neutrophilic leukocytosis, eosinophilia.
V. leukocytosis, accelerated SOE, fibrinopenia
H. Leukopenia, anemia
7. Methods of testing practical skills and theoretical knowledge.
1. Professional examination and questioning of the patient with myocardial infarction
Purpose:
- Information necessary for diagnosis;
- Assessment of the likelihood of disease;
- The identification of other sources of information (relatives, other doctors, etc.);
- Establishing trust relationships with patients;
- Assessment of a patient's personality and his attitude to the disease (the internal picture of
disease);
- Assess the state of consciousness and mental status of the patient, his position, general appearance,
state of the external cover and some parts of the body.
Uses: survey is mandatory for all patients in mind, survey conducted in all patients.
Equipment: well-lit chambers, doctors' offices, fluorescent lighting.
Conditions of performance: the absence of unauthorized persons, confidential atmosphere.
Performed steps (stages):
№
1
2
3
4
5
6
7
8
9
10
action
not fulfilled
Inquire passport data
collection complaints
Medical history of the disease
Medical history of life
Epidemiological, allergic history
An objective examination of the patient
Compilation of survey
Correct diagnosis
differential diagnosis
Treatment plan
Total:
0
0
0
0
0
0
0
0
0
0
0
Fully
implemented
correctly
5
15
20
15
5
5
5
5
20
5
100
2. Compilation of dietary recommendations and treatment programs.
Purpose: Treatment and prevention of disease complications.
№
1
2
3
4
5
action
The study of the characteristics of medical tables on
Pevsner
The right choice of dietary table in accordance with
the diagnosis
Assessment of usefulness of the diet
In accordance with the diagnosis, disease severity and
stage of the appointment of primary therapy
In accordance with the diagnosis, disease severity and
stage of the appointment of primary therapy.
not fulfilled
0
Fully
implemented
correctly
10
0
10
0
0
20
20
0
20
6
preventive measures
Total:
0
0
20
100
Tests
1. The greatest risk of fatal myocardial infarction is associated with the development of:
A pulmonary edema
B. Aneurysm
V. cardiogenic shock *
G. paroxysm of atrial fibrillation
2. The acute period of myocardial infarction on ECG is characterized by:
A high T-wave *
B. ST-segment depression
V. arcuate lifting ST interval
G. barb deep Q
3. What is the most characteristic feature of transmural myocardial infarction
A pronounced tooth Q
B. negative T waves
V. tooth formation QS *
G. R-wave amplitude decrease
4. Increased sedimentation rate in myocardial infarction is usually marked:
A. in the first hours
B. On the second day
V. 3-4 days
By the end of first week *
5. At what stage of myocardial infarction is characterized by the formation of pathologic wave Q:
A. sharpest
* B. acute
V. subacute
G. scar
6. Which of the biochemical changes in the early hours of acute myocardial infarction:
A. ALT AST *
B. thymol test
V. reduction of fibrinogen
G. increase CPK, LDH
7. By the early complications of myocardial infarction are not
A pulmonary edema
B. Cardiogenic shock
V. cardiac tamponade
Mr. Dressler's syndrome *
8. What does the symptom of scissors in myocardial infarction:
A decrease in ALT and LDH-1 increased
B. reduction of LDH-1 and increased ALT levels during the first week
V. reduction of leukocytosis and increased ESR in the first week *
G. lowering ESR, and leukocytosis growth during the first week
8. Criteria for evaluating the current control
The level of student knowledge
Progress
evaluatio
in% and the n
score
A student on the major issues and themes for students' independent
work::
Summarizes
and
makes
decisions
creative
thinking
independently
analyzed
Into
practice
Shows high activity, a creative approach to the conduct of interactive
games
Correctly solves the case studies with full justification for the answer
Understands
the
subject
matter
Knows,
says
confident
Has
a
faithful
representation
Prepares informative modern visual aids or abstracts of high quality
using data from the recent literature of 7-10 sources and the Internet.
96-100
A student on the major issues and themes on the SIW:
creative
thinking
independently
analyzed
Into
practice
Shows high activity, a creative approach to the conduct of interactive
games
Correctly solves the case studies with full justification for the answer
Understands
the
subject
matter
Knows,
says
confident
Has
a
faithful
representation
Prepares informative modern visual aids or abstracts of high quality
using data from the recent literature of 4-6 sources and the Internet.
91-95
A student on the major issues and themes on the SIW:
independently
analyzed
Into
practice
Shows high activity, a creative approach to the conduct of interactive
games
Correctly solves the case studies with full justification for the answer
Understands
the
subject
matter
Knows,
says
confident
Has
a
faithful
representation
Prepares informative modern visual aids or abstracts of high quality
using data from the recent literature of 3-5 sources and the Internet.
86-90
A student on the major issues and themes on the SIW:
Into
practice
Shows high activity, a creative approach to the conduct of interactive
games
Correctly solves the case studies with full justification for the answer
Understands
the
subject
matter
81-85
5
5
5
4
Knows,
says
confident
Has
a
faithful
representation
Prepares informative modern visual aids or abstracts of high quality
using data from the recent literature of 3-5 sources and the Internet.
A student on the major issues and themes on the SIW:
Shows high activity during the interactive games
Correctly solve situational problems, but the justification for an
incomplete answer
Understands the subject matter
Knows, says confident
Has a faithful representation
Prepares modern visual aids or abstracts using the recent literature
data of 1-2 sources.
76-80
4
A student on the major issues and themes on the SIW:
Correctly solve situational problems, but the justification for an
incomplete answer
Understands the subject matter
Knows, says confident
Has faithful representations or
A student on the major issues and themes on the CDS:
Mistakes in solving situational problems
Knows, says uncertainly
Has a faithful representation of some issues topic
Prepares informative modern visual aids or abstracts of high quality
using data from the recent literature of 7-10 sources and the Internet.
Prepares modern visual aids or abstracts of high quality using data
from the recent literature of 4-6 sources and the Internet.
71-75
4
A student on the major issues and themes on the SIW:
Understands the subject matter
Correctly solve situational problems, but can not justify a response
Knows, says confident
Has a faithful representation of some issues topic
66-70
3
61-65
A student on the major issues and themes on SIW:
Mistakes in solving situational problems
Knows, says uncertainly
Has a faithful representation of some issues topic
3
A student
on
the
major
issues
and
themes
on
SIW:
55-60
3
Knows,
Has a partial view
A student on
It
does
Do not know
says
the
major
not
issues and themes
accurately
uncertainly
on SIW:
represent
Less
55
then
2
9. Chronological map of classes.
№
Stages of the practice session
forms of
employment
Expectancy at
(minutes)
270
1.
2.
3.
Introduction by the teacher (study subjects).
10
Discussion topics practical training, testing
Poll.
students' knowledge base with new teaching explanations.
technologies, demonstration material (slides,
audio - video tapes, x-rays, EKG, etc.).
60
Conclusion of the discussion.
20
4.
The distribution of tasks for students to
perform the practical part of training.
Guidance
and
clarification
on
the
requirements for practical tasks. SelfSupervision.
50
5.
Mastering by the teacher of practical
Medical history,
exercises (case-patient Supervision).
interactive
games,
case studies.
40
6.
Interpretation
of
laboratory
and
Working
instrumental methods of investigation of the clinical
thematic patient, differential diagnosis, laboratory
treatment plan and prevention, prescription, equipment.
etc.
with
and
40
7.
Discussion of the theoretical and practical
Oral questioning,
knowledge of students, their reinforcement test,
discussion,
and assessment of the group in achieving the checking the results
goal classes.
of practical work.
30
8.
Conclusion of the teacher on the passed
Questions
lesson, evaluation of each student and the homework.
announcement of the results. Development
tasks to prepare for the next session (a
20
for
collection of questions).
10. Questions for the control of knowledge
1. The etiology of myocardial infarction
2. The pathogenesis of myocardial infarction
3. Classification of myocardial infarction
4. Clinical variants of myocardial infarction
5. The clinical course of myocardial infarction
6. Laboratory Methods of myocardial infarction
7. ECG signs of myocardial infarction
8. Differential diagnosis of acute myocardial infarction.
9. Basic principles of treatment and rehabilitation of myocardial infarction.
10. Complications of myocardial infarction.
11. Recommended Reading
Summary:
1. AI Martynov, NA Mukhin et al, "Internal Medicine" textbook in two volumes. Moscow:
GEOTAR Media, 2009. 1227str.
2. NA Mukhin, VS Moiseev, AI Martynov, "Internal Medicine"
textbook in two volumes. Moscow: GEOTAR Media, 2006. 1272str.
Optional:
1. Therapy. Allen R., MD Meyrs Moscow, Medicine GEOTAR 1997. 1024str.
2. Differential diagnosis of internal diseases. R. Helgin.,
Trans. German ed. Tareeva, MA, Medicine 1993.
3. Diagnosis and treatment of internal diseases. Guidelines for doctors in 3 volumes. Under the
general editorship. Kosarev FI M., Medicine 1991.
4. Roitberg GE, Strutynsky AV "Internal Medicine:
The cardiovascular system. " 856 p. Moscow, 2007.
5. Okorokov AN "Diagnosis of diseases of internal organs." V.6. Diagnosis of diseases of the
heart and blood vessels. Moscow, 2003, 464 pages
6. Okorokov AN "The treatment of diseases of internal organs." V.3,
kn.1. Treatment of diseases of the heart and vessels. Moscow, 2005 464 pages
Sites: www.TMA.uz., http://www.meddean.luc.edu,
http://www.embbs.com
REVIEW
for a teaching manual on integrated learning associate E.R. Juraev assistant F.K. Ziyaeva, G.T.
Bekenova on "Myocardial infarction".
Submitted by the authors of educational textbook devoted to an important topic in cardiology,
namely, myocardial infarction, which is one of the most common causes of death and disability in
the populationIn recent years, the increase in the incidence of myocardial infarction, particularly
among young and middle age. Despite the widespread reduction in hospital mortality from
myocardial infarction, overall mortality from this disease remains high, reaching 30-50% of the
total number of cases.
A teaching manual is designed for students of 4th year on the subject of Faculty Therapy, contains
basic information on the etiology, pathogenesis, classification, clinical presentation, diagnosis and
differential diagnosis, as well as the treatment of myocardial infarction. Educational tools built on
the principle of the integral. A distinctive feature of this handbook is the presence of a diagnostic
algorithm that represents the student-oriented framework for recognition of the disease. This
approach can provide substantial assistance in the preparation of general practitioners, as well as in
the formation of clinical thinking in students.
Head of the Department Clinical Pharmacology medical and medico-pedagogical TMA Faculty,
Professor A.B. Yakubov