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MINISTRY OF HEALTH OF REPUBLIC OF UZBEKISTAN
TASHKENT MEDICAL ACADEMY
DEPARTMENT OF TRAINING GENERAL PRACTITIONERS
WITH ENDOCRINOLOGY
LECTURE TOPIC:
«DIFFERENTIAL DIAGNOSIS OF NONCORONARY PAINS IN
THE CHEST. DIFFERENTIAL DIAGNOSIS. TACTICS OF GENERAL
PRACTITIONER »
(for the students of medical-pedagogical faculty)
TASHKENT – 2013
MINISTRY OF HEALTH OF REPUBLIC OF UZBEKISTAN
TASHKENT MEDICAL ACADEMY
DEPARTMENT OF TRAINING GENERAL PRACTITIONERS
WITH ENDOCRINOLOGY
«APPROVED»
Dean of medicalprofessor
pedagogical faculty,
Zufarov P.S.
___________________
____ _____________ 2013 y
LECTURE TOPIC:
«DIFFERENTIAL DIAGNOSIS OF NONCORONARY PAINS IN
THE CHEST. DIFFERENTIAL DIAGNOSIS. TACTICS OF GENERAL
PRACTITIONER »
(for the students of medical-pedagogical faculty)
LECTURER: professor Gadaev A.G.
TASHKENT – 2013
TECHNOLOGY OF THE EDUCATION
Amount student
Time - 2 hours
Form of the scholastic
occupation
Lecture - a visualization
Plan to lectures
1.
Anatomical construction of heart, circles
blood current
2.
Main diseases, being accompanied with non
coronary pain in thorax, threatening lifes sick
3.
Heart diseases, being accompanied pain in
thorax (aneurysm, perikarditis, cаrdiomiopatys)
4.
Diseases of belly intestine tract, being
accompanied pain in thorax esophagitis, other
pathology of the gullet) diagnostics diseases being
accompanied with pain in thorax
5.
Diseases of the nervious system, being
accompanied pain in thorax
6.
The diagnostics of the diseases, being
accompanied pain in thorax.
Principles of the treatment, preventive
maintenances and dispanserisation sick with non
coronary pain of the thorax
Purpose of the scholastic occupation: acquaint student with этиологией,
патогенезом of the diseases, being accompanied non coronary pain in thorax, train
principle of the diagnostics, treatments, preventive maintenances and
dispanserisation of the diseases, being accompanied non coronary pain in thorax
The Pedagogical problems
1. Consolidate and deepen
knowledge’s a student about
disease, being accompanied
non coronary pain in thorax
2. Teach student it is correct
to install diagnosis in
accordance with modern
categorization of the diseases
3. Train student to skill to
differentiate diseases, being
accompanied non coronary
The results of the scholastic process:
the general practitioner must know:
1.
Diseases, being accompanied pain in thorax,
threatening lifes
2.
Principles of the differential diagnostics of
the diseases, being accompanied non coronary pain
in thorax
3.
Tactician of conduct, principles of the
treatment sick non coronary pain in thorax
4. Principles of the undertaking the preventive
maintenance and dispanserisation sick with non
pain in thorax
4. Acquaint student with
particularity of the current of
the diseases, being
accompanied pain in thorax,
rendering urgent help,
tactician squall
5. Train student to conduct
sick with non coronary pain
in thorax, treatment and this
coronary pain in thorax
Methods of teaching
Text to lectures, video film, questions, technology
"yes-no"
Form of the education
Lazer projector, visual material, special technical
equipment, show thematic sick
Facilities of the education
Group
Conditions of the
undertaking the scholastic
process
Auditorium
PRODUCTION CHART TO LECTURES
Stages, time
Activity
Teacher
1. Tells about subject of the
1 stage
Introductory part lectures, her purposes and plan
(5 mines)
Students
1.
Listen
2 stages
Actualization
(increasing to
value ) of the
knowledges
(20 mines)
2.1. In purpose of increasing to
actualizations (increasing to value)
of the knowledge’s student will
assign the questions:
1. Enumerate diseases, which can
be accompanied pain in thorax
2. Enumerate diseases being
accompanied pain in thorax,
threatening lifes sick
3. Enumerate reasons, bring about
arising the pains in thorax
4. Enumerate groups a preparation,
using for treatment of the diseases,
being accompanied non coronary
pain in thorax
2.1. Answer givenned
questions
2.2 Study slide 1
Conducts questioning
2.2. Showing on screen, offers to
get acquainted the student with
purpose and problem to lectures.
Slide 1, 2
3 stages
Main part
(information) (55
mines)
2.3. Study slide 2
3.1. Introduces the student with
3.1. Together analyse
lecture material, value of the
heard lecture material,
subject and principle of the shaping will assign questions
intelegent cultural personality, in
particular squall-teacher.
In purpose of increasing to
actualizations of the knowledges
conducts quick questioning a
student:
1.
On 1 point of the plan to
lectures: tell anatomical
construction a heart, circles blood
current
2.
On 2 points of the plan to
lectures: enumerate main
diseases,being accompanied non
coronary pain in thorax,
threatenning lifes sick
3.
On 3 points of the plan to
lectures: heart diseases, being
accompanied pain in thorax
(aneurysm, perikardits,
cardiomiopatys)
4.
On 4 points of the plan to
lectures: diseases of belly
intestine tract, being accompanied
pain in thorax (esophagits, other
pathology of the gullet)
5.
On 5 points of the plan to
lectures: diseases of the nervious
system, being accompanied pain in
thorax
Main moments write in
copy-book
6.
On 6 points of the plan to
lectures: diagnostics of the diseases
being accompanied with pain in
thorax
7.
On 7 points of the plan to
lectures: principles of the
treatment, preventive maintenances
and dispanserisation sick with non
coronary pain of the thorax.
Sopping for important moment of
the lectures offers to write main
positions in copy-book
4 stages
final (10 mines)
4.1. Will Assign questions:
1. Enumerate most often meeting
diseases, being accompanied non
coronary pain in thorax
2. enumerate diseases being
accompanied non coronary pain in
thorax, threatenning lifes sick
3. Tell main key moments of the
clinical current of the different
diseases being accompanied non
4.1. Answer questions
4.2. Listen, write
coronary pain in thorax
4.Назовите cardinal principles of
the treatment, preventive
maintenances and rehabilitations
sick with non coronary pain in
thorax
4.2. Gives task for independent
work student: pathology
supporting-motor device, being
accompanied with non coronary
pain in thorax
In practice, general practitioner often deal with different situations,
accompanied by pains in the chest, which often require a doctor's quick, efficient
care to patients. What should be the assistance in various specific situations
depends on what kind of pathology in the patient - whether it threatens the life of
the patient? What factor cause these pains? In this chapter we discuss some
diseases that are accompanied by chest pain with noncoronary character. First,
eliminate the most dangerous diseases that threaten the patient's life.
 Myocardial infarction
 Spontaneous pneumothorax
 PATE
 Dissecting aortic aneurysm
Only removing them, we should look for other causes of chest pain.
Acute dissecting aortic aneurysm. Aneurysm - this is a local sacciform bulging
wall of the aorta, or diffuse enlargement of the entire aorta in more than 2-fold
compared with the norm. The main causes: atherosclerosis, trauma, Marfan
syndrome, syphilis, cystic medionekroz. Acute delamination - the most frequent of
emergency conditions associated with disease of the aorta. This is more common in
men. Clinicaldelamination occurs by sudden disintegration intense pain in the chest
or in the back radiating to the course of the aorta. Characteristic for pain is
undulating course, which indicates a further exfoliating aorta. In this context,
location and irradiation of pain is changed. Status of patients is severe, resembling
shock, but the blood pressure initially elevated (high blood pressure is one of the
main reasons for separation of the aorta). In the propagation of delamination, may
be developed gemiperikards with cardiac tamponade, aortic insufficiency due to
aortic valve detachment, ischemia of various organs. Often there is an asymmetry
of pulse and blood pressure at the upper and lower extremities. The diagnosis is
confirmed by dynamic radiography (expanding shadow of the aorta, double loop),
computed tomography, magnetic resonance imaging, echocardiography, Doppler,
aortography. High diagnostic value by splitting the thoracic has transesophageal
echocardiography. Sensitivity and specificity is 90%.
Forms of flow separation of the aorta: acute - hours, subacute - days (rarely 2-4
weeks), and chronic - months. Without treatment, the first 2 weeks 70% of patients
die, 50% of the survivors die within a year. The most common cause of death aortic rupture.
Surgical treatment - emergency aortic replacement.Medication is shown
immediately before the operation, and in cases of suspected acute peel. In case of
high blood pressure, there is assigned beta-blockers, first intravenously and then
inside. Further, it is needed sodium nitroprusside. In normal blood
pressure,monotherapy of beta-blockers is conducted to reduce the contractility of
the left ventricle.
Cardiomyopathy (ILC) - a group of diseases of the heart muscle with unknown
etiology. They are referred to as primary or idiopathic, cardiomyopathies. The
secondary cardiomyopathy includes diseases, where etiology is known. This
myocardial damage is in systemic diseases, alcohol poisoning, with heart diseases
and other pathological conditions. There are three primary forms of
cardiomyopathy: dilated, hypertrophic and restrictive. Presumably causal role for
various damaging factors: toxic, metabolic, infectious. There are indications of
immune disorders in dilated Commission and the hereditary nature of the disease
in hypertrophic ILC with autosomal dominant inheritance.
Dilated cardiomyopathy (DCM) - a disease characterized by an increase in heart
size, systolic dysfunction and congestive heart failure. The clinical picture.
Symptoms usually develop gradually. Sometimes the disease progresses over
months and even years without symptoms, but with dilation of the left ventricle,
and is found in the X-ray or echocardiogram. The first symptoms - fatigue and
weakness, shortness of breath and then joined, initially with exertion, and in later
cases - cardiac asthma, orthopnea. Peripheral edema and hepatomegaly - late and
optional features.Very often cardialgia and much less-angina. A significant part of
the clinical picture is occupied by thromboembolic complications that develop as a
result of the separation of intracardiac thrombus, and the veins of the lower
extremities. Sudden thromboembolism in the pulmonary artery can be the first
symptom of dilated and the ILC. On examination - cold skin, alternating pulse,
systolic and pulse pressure, expanding the boundaries of the heart often left, left
ventricular pulse, and in later cases - right ventricle. Auscultation - a systolic
murmur due to mitral or - to a lesser extent - tricuspid regurgitation, gallop rhythm,
heart rhythm disturbances. In marked dilatation of the left ventricle and a
significant decrease in ejection fraction, prognosis is unfavorable. The diagnosis is
made on the basis of chest X-ray, ECG, echocardiography, radionuclide
ventriculography, coronary angiography and myocardial biopsy. When X-rays,
there is determined by the increase of the left ventricle, often cardiomegaly. There
are revealed signs of venous congestion in the lungs, interstitial and alveolar
edema, even, pleural effusion. On ECG - sinus tachycardia, sometimes various
atrial and ventricular arrhythmias, and intraventricular and atrioventricular
conduction.There can be detected abnormal tooth Q, reflecting extensive
noncoronary myocardial fibrosis, and ST-segment changes and T wave. In
Echocardiography, there are increase in left ventricular with rise in end-diastolic
and end-systolic volumes, lower ejection fraction, mitral and tricuspid
regurgitation. A characteristic is diffuse myocardial damage. Radionuclide
ventriculography confirms diffuse hypokinesia wall infarction, increased volume
of the heart, low ejection fraction, coronary angiography revealed normal blood
vessels, it is necessary for patients with an abnormal Q wave on the
electrocardiogram in the differential diagnosis of myocardial infarction. In the
study of biopsy material is defined extensive interstitial and perivascular fibrosis,
sometimes foci of calcifications. However, the specific diagnostic features, unique
to dilated Commission, are absent.
Treatment. Drug treatment is aimed at fightingagainsy heart disease. Basic
principles are not different from the treatment of heart failure of any cause and
they control sodium and water in the body, reducing preload and afterload,
improving the pumping function of the heart. Patients are advised to limit physical
activity and reduce the consumption of salt. Because of the risk of pulmonary and
systemic embolism in patients with dilated cardiomyopathy with parietal thrombus
in the left ventricle, as well as atrial fibrillation and reduced ejection fraction
(<20%), there should be applied anticoagulation therapy such as warfarin starting
dose of 10 mg / day under the constant control of prothrombin time. For the
treatment of cardiac arrhythmias in DCM, it is best to use the correction of
hypoxia, electrolyte disorders and acid-base balance (potassium supplements,
antioxidants) and to carry out the fight against heart shortage. The use of
antiarrhythmic drugs in patients with DCM did not increase life expectancy,
although in recent years there are reports about beneficial effect in usingpjselective adrenergic blockers (such as metoprolol, loglresora) or p-antagonist with
vasodilating properties (bucindolol or carvedilol). In addition to the antiarrhythmic
action, they improve hemodynamic function. In carvedilol, there is also revealed
antiaptoz effect. In cases of sustained ventricular tachycardia, and episode of
syncope or sudden death, there is shown setting of automatic implantable
defibrillator. If heart failure refractory to medical therapy, you need to decide on
the heart transplant.
Hypertrophic cardiomyopathy - a disease of the myocardium characterized by
asymmetric or symmetric hypertrophy of the left ventricle with mandatory
involvement in the process of hypertrophic interventricular septum.The clinical
picture. The disease is more common in young age. Symtoms are variable: from
asymptomatic to severe clinical symptoms and sudden death. In asymptomatic
forms with prerequisite to a detailed examination of patients, there is detected
sudden systolic heart murmur or ECG changes. Particularly attention is paid to the
patients who have a family history of hypertrophic Commission or sudden death.
One of the most common symptoms - various cardialgiae: from rare stabbing pain
to typical angina. The latter is a consequence of the relative coronary insufficiency
due to the mismatch of muscle perfusion and, depending on the degree of
hypertrophy, or mechanical compression of the coronary arteries of the
hypertrophied myocardium, as well as the diastolic filling of intramural vessels due
to violation of myocardial relaxation. Second is due to frequency of occurrence of
a sign - arrhythmic syndrome (30 to 70%). Extremely wide range of arrhythmias:
these violations of atrioventricular conduction, and ventricular arrhythmias of
various grades, including ventricular tachycardia and supraventricular arrhythmias,
including atrial, although the last of the disease is not typical. Accordingly, a high
frequency of arrhythmias and palpitations disruptions of the heart - a common
complaint of patients with hypertrophic ILC. One of the main symptoms are
fainting. Their occurrence is associated with both episodes of arrhythmia
(paroxysmal
ventricular
and
supraventricular
tachycardia,
complete
atrioventricular block), and the syndrome of small output. The frequency of
syncope and presyncope varies considerably - from single to multiple daily over a
lifetime. Less frequently in patients with hypertrophic Commission, there are
found signs of heart failure. Of these, most often cited dyspnea, while swelling and
enlargement of the liver are very rare. On examination revealed enlargement of the
heart, though not always considered to be a typical attenuation I tone at the top and
the presence of systolic murmurs of different nature and intensity, often to the left
edge of the sternum, in the III-IV intercostal space. It is associated with obstruction
of the outflow tract of the left ventricle due to hypertrophy of the upper third of the
interventricular septum with anterosystolic movement of the anterior leaflet of the
mitral valve and mezosystolic cover of aortic valve. The diagnosis of hypertrophic
Commission is verified using electrocardiography, echocardiography, chest X-ray.
If you need to specify the extent of myocardial damage and coronary artery
catheterization, there is performed heart and coronary angiography, Doppler
ultrasound and biopsy endomiokarda. The presence of pathological Q waves in the
ECG is a characteristic feature of hypertrophic ILC. Usually it is defined in II, III,
aVF and left precordial leads, while not growing R wave in the right precordial
leads. In some patients, pathologic Q wave detects from the right precordial leads,
and the ventricular complex may be in the form QS - these changes are most
characteristic of asymmetric septal hypertrophy. A typical ECG sign of apical
hypertrophic forms of ILC are giant negative T waves in the precordial leads.
Rhythm and conduction disturbances, described earlier, may not be available on a
standard ECG, but are usually identified by its daily monitoring. Echocardiography
- the main method of diagnosis of hypertrophic ILC. Thickening of the
interventricular septum in its various departments of more than 13 mm in
combination with its hypokinesia (range of motion of less than 3 mm) is
considered a classic sign. There is also haracteristic of anterosystolic movement
anterior mitral valve and partially cover mezosystolic aortic valve, a decrease in
left ventricular diastole. X-ray of the heart reveals the typical signs of left
ventricular hypertrophy, sometimes - signs of increased left atrium. But some
patients radiograph is different from normal. Cardiac catheterization and coronary
angiography help to clarify the nature and extent of violations of intracardiac
hemodynamics (determine the pressure gradient between the left ventricle and the
aorta, the increase in end-diastolic pressure in the left ventricle) and the coronary
circulation. With the same purpose, there can be used radioisotope methods of
research. Doppler (color Doppler scan) allows non-invasive way to get enough
accurate information about the state of intracardiac hemodynamics. In biopsy
endomiokarda, there are investigated five morphological characters: a) short fibers,
interspersed with connective tissue, and b) a large ugly core, c) fibrosis d) with the
disappearance of the degenerating muscle myofibrils, and e) a chaotic arrangement
of muscle fibers with a twist.
Classification. According to the localization of hypertrophy, there are the
following morphological variants of hypertrophic Commission: 1. Idiopathic
hypertrophic stenosis subaortalny the disproportionate hypertrophy of the
interventricular septum, outflow tract obstruction of the left ventricular endocardial
thickening under the aortic valve thickening and paradoxical motion of the anterior
leaflet of the mitral valve to the septum in systole. 2. Asymmetric septal
hypertrophy without changing the portal and the mitral valve and without outflow
tract obstruction of the left ventricle.
3. Apical Hypertrophic Commission with restricted zone of apical hypertrophy.
4. Symmetrical with concentric hypertrophic Commission of left ventricular
hypertrophy. Differential diagnosis is conducted with ischemic heart disease,
valvular aortic stenosis, pulmonary stenosis, ventricular septal defect, mitral
insufficiency, and in the beginning of the disease - and neuro dystonia. The use of
these research methods eliminates the above mentioned diseases. Treatment of
patients with hypertrophic Commission aims to reduce the symptoms of the
cardiovascular system with medical therapy, and in the case of resistance,
surgeryisindicated. Among medication, p-blockers and verapamil are most widely
used in the treatment of hypertrophic Commission. Their appointment is necessary
at the stage of clinical manifestations (pain, arrhythmia, shortness of breath), and in
asymptomatic because of their actions on retention of disease progression by
reducing the intraventricular pressure gradient and improve diastolic ventricular
function. Preparations are shown in normal doses, propranolol to 120-160 mg /
day, verapamil to 240-480 mg / day. There is possibility of selective p-blockers.
Patients with dangerous arrhythmias justify the appointment of amiodarone.
Nitrates should be avoided because of the danger and vasodilators increase
obstruction of the left ventricle. Patients with atrial fibrillation should
anticoagulant therapy, and it must be continued from the date of registration of the
arrhythmias (aspirin or warfarin). Surgical treatment in the form of a partial muscle
resection in the basal part of the interventricular septum (myotomy-miektomiya) is
recommended in patients with severe clinical manifestations and in the outflow
tract gradient greater than 50 mm Hg. Art., and if drug therapy is no longer having
the desired effect.
Restrictive cardiomyopathy - a disease characterized by diastolic dysfunction of
the heart as a result of morphological changes of the endocardium, and
subendokarda infarction. The dimensions of the heart is usually not enlarged, and
sometimes reduced. Endomyocardial fibrosis and fibroplastic eosinophil parietal
endocarditis of Leffler, previously denoted as independent entities that are now
seen as the different stages of the same disease. Sometimes there is the name
"endomyocardial disease." Primary for the disease is pronounced eosinophilia
(sometimes called leukemia), reaching 36 to 75%. Regardless of the cause of
eosinophilia in the development of heart disease, there are allocated three stages:
necrotizing, thrombotic, fibrotic. As a result, developing a dramatic thickening and
endocardial ventricular cavity obliteration by fibrous tissue and thrombotic masses.
Often both ventricles are affected (in 50-70% of cases), but occurs isolated lesion
of the right or of the left ventricle with approximately equal frequency. The clinical
picture. The main symptoms of the disease are associated with heart failure,
arrhythmias and embolism. The first signs of the disease are non-specific
weakness, shortness of breath, decreased exercise tolerance. Pain in the heart is
relatively rare. In the future, the clinical manifestations are determined with right
or left ventricular failure, but even when lesions of the left and right heart
combined, right ventricle symptoms usually predominate. Often there is a recurrent
ascites, hepatomegaly (sometimes without peripheral edema), pronounced cyanosis
of the face, swelling of the neck veins. Regardless of the prevalence of disease,
there is revealed pericardial effusion, often fluid in the pleural cavity. Accordingly,
heart tones are muted, usually tachycardia, low blood pressure. Often auscultated
mitral insufficiency, gallop rhythm.Thromboembolic pneumonia, a frequent
complication of restrictive Commission. Electrocardiography, chest X-rays,
echocardiography, angiocardiography, cardiac catheterization and endocardial
biopsy, blood tests - methods used to confirm the diagnosis of restrictive
Commission. According to the ECG, there is revealed a low voltage QRS and T,
especially with pericardial effusion, various arrhythmias, conduction block. In
right ventricular endomyocardial fibrosis, 75% of patients had pathologic Q waves
in leads V1-V2, negative - T-segment ST, sometimes high pravopredserdnye teeth
R. During fluoroscopy in patients with right ventricular fibrosis determined marked
increase in the right atrium and ventricle, reducing the blood supply pulmonary
circulation, pericardial effusion in patients with left ventricular - increased left
atrial stasis in the pulmonary circulation. Both forms near the top and in the
outflow tract is sometimes revealed a linear calcification. Echocardiography
reveals thickening of the endocardium, obliteration of the ventricular cavity,
paradoxical movement of septum, pericardial effusion, often a diastolic opening of
the pulmonary valve. Angiocardiography supports resizing, uneven contours of the
ventricles, obliteration of the cardiac apex, increased outflow tract, reduced cardiac
output. Application of endocardial biopsy justified in the differential diagnosis of
sarcoidosis, myocarditis, cardiac amyloidosis. In the analysis of CROP, there is
registered anemia, eosinophilia varying degrees. Differential diagnosis is
conducted withwithkonstrictpericarditis, pericardial any etiology, atrial myxoma,
sarcoidosis, myocarditis, cardiac amyloidosis, and other types of idiopathic
cardiomyopathy. In contrast to hypertrophic and dilated restrictive KMP, KMP is
not peculiar to cardiomegaly, heart size is usually small and characteristic
obliteration of the cavities of the ventricles in the apical region. Most often, it
should be distinguished from constrictive pericarditis. Presence indications of a
history of tuberculosis, trauma (including surgeries on the heart), pericarditis, and
prior systemic diseases that may involve in the process of the pericardium, makes
the most likely diagnosis of constrictive pericarditis. Treatment. Effective
treatment of restrictive Commission does not exist yet. It is justified to carefully
use diuretics in cases of stagnation in the small and large circulation and digoxin in
the case of reduction of left ventricle. Drugs with positive inotropic action
isineffective, and vasodilators should be used with great caution in order to avoid
the deterioration of the ventricular filling due to excessive loss of preload. To
maintain adequate cardiac output during the Commission's restrictive, there is a
necessity of high ventricular filling pressure. Conclusive evidence of this
pathology calcium channel does not exist yet, though they may be able to increase
the stretch in ventricular diastole.
Alcoholic cardiomyopathy develops in years of regular alcohol abuse. In the
event of a so-called "beer" heart decisive in the defeat of the myocardium is
contained in beer cobalt with clinical symptoms differ from those in alcoholic heart
disease. In chronic alcoholism, occurs cardiac at the subcellular level, intracellular
transport of calcium is disturbed, which leads to disruption of relaxation
myocardium. Clinical painting at an early stage of alcoholic cardiomyopathy is
manifested with tachycardia, arrhythmia, sometimes withatrial fibrillation. There
may be listened can rhythm of gallop. Identified and other signs of chronic
alcoholism - hand tremors, severe sweating. In the later period, there was an
increase in heart size, symptoms of cardiac decompensation. On ECG decreased or
negative prong T. Treatment is aimed at the complete exclusion of alcoholic
beverages, taking vitamins and other products that will improve myocardial
metabolism. In heart failure, there are used cardiac glycosides, diuretics,
antiarrhythmic agents. If severe heart failure is absent, there is appointed a small
dose of p-blockers. Other forms of secondary cardiomyopathy in infectious and
parasitic diseases, amyloidosis, etc. are discussed in the relevant chapters.
Myocardiodystrophy - noncoronary group and non-rheumatic diseases
infarction, characterized by impaired metabolism in the heart muscle and certain
structural changes that occur under the influence of noncardiac causes. Among
them, according to V. X. Vasilenko (1983) and NR Paleeva (1991), myocardial in
anemia, malnutrition and obesity, vitamin deficiency, kidney damage and liver
damage, violation of certain types of metabolic diseases, endocrine system
diseases, intoxication, physical stress, infections . Pathophysiological mechanism
is the development of energy deficit in adaptive hyperactivity infarction, designed
to maintain an adequate level of functioning of the cardiovascular system in a
situation of long-acting noncardiac causes. As a result, myocardial damage occurs
and the picture of myocardial is developed. Changes that occur in the heart muscle,
are nonspecific. When extracardiac factor actions are eliminated, changes in the
heart muscle are reversible. In the development of myocardial dystrophy, there are
distinguished three stages. The first stage is peculiar adaptive hyperfunction
infarction, usually with hyperkinetic circulation option arising due to dysfunction
of regulatory systems, increasing the effects of the sympathoadrenal and
suppressing effects of parasympathetic nervous system. Stage II is characterized by
the formation of the exchange-structural changes, leading to cardiac dysfunction.
Stage III develops severe pathological changes in metabolism, structure and
function of the heart muscle, accompanied by heart failure and heart rhythm
disturbances. The clinical picture in accordance with the phasing of the
development of myocardial dystrophy to a certain extent depends on its stage. In
the early stages of cardiac complaints myocardiodystrophy character may be
absent. Fatigue, decreased performance, poor exercise tolerance can be regarded as
a manifestation of the underlying disease. Most often, patients note cardialgiae
localized in the apex of the heart, long-term, no clear association with physical
activity at the time of its execution, persists even after taking nitroglycerin. At the
same time, both physical and emotional overload often provoke false angina in
these patients, but often - after a while. Sometimes the pain can be unreasonable. In
addition, many patients concerned about short of breath, dizziness, palpitations. In
stage II-III of myocardiodystrophy, may appear edema, dyspnea at rest, cardiac
arrhythmias and conduction. An objective examination in the early development of
myocardial dystrophy, there is determined attenuation / ton over the top of the
heart, a short systolic murmur, and tachycardia. Later there may be generated
rhythm of gallop due to pathological III tone, often found rhythm and conduction
disturbances (arrhythmias, atrial fibrillation, intraventricular and atrioventricular
block); there is lack of blood circulation. Defining clinical manifestations are based
on those extracardiac pathologies that led to the development of myocardial
dystrophy. Thus, in myxedema,the size of the heart can significantly increase, the
movement of its walls with the sluggish and slow, very early in thyrotoxicosis may
develop atrial fibrillation, with symptoms of anemia can be simulated valvular
heart disease - can be auscultated systolic murmur typical of mitral, tricuspid and
aortic valves, with disovarialnyh diseases often patients complain of "tides", hot
flashes, sweating, paresthesia in the extremities, etc. In the ECG often detected
reduction and flattening of the T wave, particularly marked in the right precordial
leads (V,3), rarely in Left. Sometimes shifted segment ST, disturbed
intraventricular conduction. If such changes are installed on the ECG for diagnosis
performed pharmacological tests (potassium, obzidanovaya). In the event of such
changes in intracellular potassium deficiency ingesting 6.4 g of potassium chloride
can normalize the ECG. In excess effects of catecholamine on myocardium, there
is a possibility of normalization of the ECG for 1 - 1.5 h after administration of 6080 mg obzidan (Inderal, inderal). In cases where the depletion of norepinephrine in
the sympathetic nerve endings of the heart, ECG can be restored after
administration of p-agonists izadrina. However, it should be noted that these
pharmacological tests do not need to be exaggerated. Only the combination of
clinical, instrumental methods and dynamical examination can allow a diagnosis of
myocardial dystrophy. Treatment should be directed towards the main process that
caused degenerative changes in the myocardium. In addition to this, oral drug
therapy that affects the metabolism in the heart muscle (Riboxin, mildronat,
safinor, vitamins Vit. Etc.) normalizing electrolyte balance (drugs potassium,
magnesium), which improves the microcirculation (dipyridamole, Teonikol,
aspirin), acting on catecholamine Balance (Inderal, obzidan, Inderal).
Simultaneously, there is conducted antiarrhythmic therapy, the treatment of heart
failure.
Pericarditis - inflammation of the pericardium sheets (epicardium and
pericardium) that occurs as a complication of various diseases and is very rare for a
separate disease. Currently, the main causes of pericarditis - connective tissue
diseases, tuberculosis, bacterial and viral infections, postperikardiotomny
syndrome associated with cardiac surgery, pericarditis with neoplastic processes,
postinfarction, uremic. In 3-10% of cases, pericarditis found at autopsy, according
to various authors. The frequency of pericarditis, detected clinically, is much less,
since it occurs almost asymptomatic in many patients. The clinical picture.
Pericardial disease usually occurs in one of three clinical forms: acute dry or
swampy, swampy and chronic constrictive. At the beginning of the inflammatory
process Pericarditis usually happens because DRY fibrin deposits in the exposed
epicardium. The most important feature of it - chest pain, usually sharp, stabbing,
but it can be a dull, oppressive. The pain is worse with deep breathing, coughing,
turning the torso in the supine position and the left side is facilitated in a sitting
position, and when you lean forward. It is not made easier and is not stopped
taking nitroglycerin. The pain often radiates to the left supraclavicular region, neck
and shoulders. The pain in most cases precedes fever (a characteristic feature of the
differential diagnosis of a myocardial infarction), weakness, fatigue, myalgia.
Pericardial rub - the most important objective sign of illness. Often, it is
determined only by careful listening, pressing the stethoscope on the chest and the
patient lying on his stomach, if the patient is based on the elbows and knees, in a
deep breath, or if the patient leans forward. Pericardial friction is often transient
and may disappear in a few hours after the occurrence. Sometimes pericarditis is
accompanied by extrasystoles, atrial fibrillation and other arrhythmias.
Pericardial effusion appears almost simultaneously with the deposition of fibrin,
but in the beginning, because of severe absorptive capacity of the pericardium, it is
insignificant and often accumulates gradually. Normally, heart bag contains about
25-35 ml of fluid; accumulated effusion reduces pain in the heart and leads to
shortness of breath, tachycardia, and increase in jugular veins without falling down
on the breath, cyanosis, and sometimes temporary disturbance of consciousness.
Area of cardiac dullness is increased; apical impulse in most cases is not defined,
the tones become deafer, pericardial rub vanishes. Increasing the number of
exudate can lead to cardiac tamponade and the emergence of a paradoxical pulse
(pulse amplitude reduction or complete disappearance on his breath); it is best felt
in a carotid or femoral artery. Grow pale skin, cyanosis of the lips, nose, and ears;
there is a swelling of the face and neck ("collar Stokes"). Sometimes, there are
developed preferential overflow veins and swelling of one and one-hand, mostly
left hand, due to compression of innominate vein fluid in the upper sinuses
pericardium. Further increases and becomes harrow liver, especially the left lobe.
Ascites formation and swelling in the legs and lower back. The hallmark of
pericarditis that congestion in the lungs,is usually absent. The final stage of the
progression of acute pericarditis can be constrictive pericarditis, but often it is
developing and initially differing dramatic thickening and seal heart shirt. This
leads to a decrease in elasticity of the heart and fill it with cameras followed
congested peripheral veins. Stagnation in the systemic circulation - the main
clinical symptom of constrictive (adhesive) pericarditis. Patients complain about
shortness of breath, fatigue, weakness, rapid expansion of the neck veins. There is
revealed enlargement of the liver with ascites and peripheral edema. Venous
pressure sharply increases (usually more than 250 mm of water. Cent.). Muffled
heart sounds are often heard extra tone after 0,1-0,12 II after a tone, sometimes
systolic click, splitting / / tone due to the early closure of the aortic valve with a
decrease of systolic ejection. Usually, there is determined paradoxical pulse,
characteristic tachycardia, aggravated by the slightest load. Squeezes pericarditis is
characterized by triad Beck: high venous pressure, ascites, a small quiet heart.
Chronic constrictive pericarditis occurs with a gradual progression of heart failure.
In the development of chronic constrictive pericarditis, there are 3 stages: initial,
intense and dystrophic. In the initial stage, there is marked weakness, shortness of
breath when walking, venous pressure rises after much pressure. Appearance of
ascites is typical for the stage of pronounced symptoms. Syndrome is also
characterized by a combination of hypertension in the system and the superior vena
cava syndrome of hepatic and portal circulation, the ratio of which, in contrast to
cases of pericardial tamponade is independent on patient's body. Dystrophic stage
is characterized by the development of hypoproteinemia. At this stage of the
process, along with ascites and pleural effusion, there is produced edema in the
lower extremities, genitals, on the body, face, hands. This is facilitated by
hypoproteinemia. In the diagnosis of pericarditis, ECG study plays an important
role. On the ECG with dry pericarditis, there is found concordant ST segment
position in 2 or 3 standard leads, especially in lead II and V2_6, no significant
changes of the complex ORS. Subacute effects on ST segment returns to the
contour with the emergence of a slight negative T wave.When the effusion occurs,
voltage of complex QRSdecreases. In cases of constrictive pericarditis, it reduces
more, often there is formed deep and wide tooth Q. Changes of repolarization,
frequent signs of stress of the left atrium and atrial fibrillation are typical
Echocardiographicallyis detected at an early stage pericardial thickening or a
small amount of fluid in the pericardial cavity. In effusion pericarditis, there is
clearly defined extra fluid, quantity can be installed. Constrictive pericarditis
characterized by obtaining two separate echo signals corresponding to the visceral
and parietal pericardium sheets of paper, restricting the movement of the rear wall
of the left ventricle. Radiographically there is established increase in the heart
shadow, changing its contours (smoothing of the waist), a weakening heart beating,
and congestive expansion of root vessels. In cases of constrictive pericarditis, heart
size normal or reduced, only the left atriumslightly increases. A typical feature pericardial calcification, sharp weakening or absence of pulsation of the heart.
Pericardiocentesis not only confirm the presence of effusion of heart shirts, but
also to determine its nature, to distinguish pericarditis from hydropericardium
(transudate), Hilo and hemopericardium, a detailed cytological study of fluid, put
bacteriological, immunological and biochemical tests. Classification. According to
etiologic classification, there are distinguished three groups of pericarditis: 1.
Pericarditis from exposure to the infectious agent organism (bacteria, tuberculosis,
rheumatism, viral and rickettsial, fungal, protozoal for invasion). 2. Aseptic
pericarditis: allergic, with connective tissue diseases (systemic lupus
erythematosus, rheumatoid arthritis), trauma, autoimmune (postinfarction,
postcommissurotomy, etc.), with blood diseases, cancer, metabolic disorders deep
(uremic, gouty). Differential diagnosis is conducted with acute myocardial
infarction, pneumonia, pleurisy, pulmonary embolism, dissecting aneurysm of the
aorta, restrictive cardiomyopathy, liver cirrhosis, tricuspid valve stenosis, mitral
stenosis, vena cava syndrome isrhnsymediastinal tumors. Treatment is conducted
strictly differentiation depending on the etiology of the disease and its forms. With
infectious pericarditis, there are appointed antibiotics including tolerability and
sensitivity of the microflora. In the treatment of tuberculous pericarditis, there is
usually used a combination of three drugs: rifampin - 600 mg, isoniazid and
ethambutol -300 - 50 mg / kg of body weight daily. In cases of dry or exudative
pericarditis with unknown etiology and no active inflammatory lesions, antibiotic
therapy is usually not assigned. If a purulent pericarditis or cardiac shirt hit due to
sepsis, purulent center or pneumonia, antibiotics are shown always. In this case,
antibiotics should enter into the cavity of the heart shirts as possible after
extraction through the catheter and washing effusion cavity. Treatment of allergic,
autoimmune and recurrent pericarditis begins with the appointment of nonhormonal anti-inflammatory and antihistamine (voltaren, diclofenac, indomethacin,
plaquenil, diphenhydramine, suprastin). If there is no effect, then there is shown
steroid hormones, and in some cases, immunosuppressive drugs (azathioprine,
colchicine). When pericarditis associated with rheumatic diseases, systemic lupus
erythematosus, steroid use is justified in the very early stages of development. The
same approach is also used for post-MI pericarditis (Dressler's syndrome). First,
there are appointed non-steroidal anti-inflammatory drugs such as aspirin, 650 mg
orally every 6-8 hours, or indomethacin 25-50 mg orally every 4-8 hours, in cases
of severe clinical manifestations applied prednisolone 1 mg / kg / day by mouth
with a gradual decrease dose. In cases of acute pericarditis in the initial stages
macrofocal myocardial infarction should be prescribed only by aspirin. The use of
other
non-steroidal
anti-inflammatory
drugs
or
glyukokortikoidngh
contraindicated, as they can slow scar formation and increase the probability of
rupture of the myocardium. Anticoagulants in heart attack pericarditis as much as
possible should be avoided because of the danger of hemorrhagic pericarditis with
subsequent cardiac tamponade. In case of the neoplastic nature of pericarditis and
detection of cancer cells effusion into the cavity, there is reintroduced cytostatics,
preferably tyhiotepa (50 mg). In dialysis pericarditis, the number of hemodialysis
increases to 6-7 weeks. If this is not successful, or there are signs of cardiac
tamponade, there will be showed perikardektomiya or pericardial drainage. In
cases compressing pericarditis patients should be kept under constant surveillance
from retrying echocardiography to assess the effectiveness of anti-inflammatory
treatment. If the volume of pericardial effusion is reduced and symptoms of cardiac
tamponade disappear, then pericardiocentesis is required. If such a resolution of the
disease does not occur, there are indications in the removal of fluid from the
pericardial cavity. In constrictive pericarditis, there is performed surgery, the
amount of which is determined by the prevalence of compressing the capsule, the
degree of proliferation of connective tissue, the severity of calcium deposits. Most
often, the task of surgeon is to free the surgeon from compressing the capsule from
the left ventricle. During the liberation of the heart from the right ventricle, there
may occur pulmonary edema intraoperative deaths. Increased surgery dramatically
increases the risk of injury walled heart and large veins. For the symptomatic
treatment of pericarditis, there are appointed cardiac glycosides, diuretics,
angiotensin-converting enzyme.
Pleurisy - an infectious or aseptic inflammation of various etiologies in pleura,
accompanied by the formation on the surface fibrinous overlays and (or) the
accumulation of fluid in the pleural cavity (serous, purulent, hemorrhagic,
hileznogo etc.) exudate. Pleurisy may be primary and secondary. Pleurisy is
considered primary in cases where the local inflammatory process and the related
general reaction of the body are the main symptoms of the disease. The vast
majority of pleurisy is a secondary process and occurs in the presence of
inflammatory processes in the adjacent (tuberculosis, pneumonia, mediastinitis,
liver abscess, subdiaphragmatic abscess, paranephritis, pancreatitis, etc.) or remote
(osteomyelitis, otitis media, sinusitis, etc.) bodies and tissues. Depending on the
presence or absence of effusion pleurisy, it is divided into dry (fibrinous) and
effusion (exudative). Adhesions and scars in the pleural space are often referred to
as an adhesive, ossificans pleurisy. However, it’s proper to consider them as an
outcome of inflammation. Free pleural effusion occurs in the absence of adhesions
between the sheets of the visceral and parietal pleura and can be located typically
and atypically. Encysted pleurisy occurs in the presence of adhesions between the
pleural leaves. Their location is very diverse. Clinical presentation and diagnosis.
Symptomatic dry pleurisy usually begins with a sudden pain in one or the other
side of the chest, fever and cough. There are common phenomena - fatigue,
malaise, loss of appetite, night sweats, chills. On examination, while observing the
patient, attention is drawn to his posture, facial expressions and character of
breathing. Thus, a patient with unilateral pleurisy spares the affected side: restricts
breathing movements, prefers a prone position on the patient side, motionless,
hand presses the affected side while sitting or standing.
Auscultation over the area of dry pleurisy, there can be listened weakened
breathing and pleural friction rub, a different timbre and duration, localized or
diffuse. Pleural friction rub, at first, is very soft, then gets rougher character, like
the creaking of new skin or rough scrapes. The clinical picture of exudative
(effusion) pleurisy usually depends on the disease, a complication which it came.
In symptomatic pleural effusion, typical complaints of patients are shortness of
breath, a feeling of heaviness in the chest and coughing. With the accumulation of
exudate breathlessness and a feeling of heaviness in the chest expands, although a
strict dependence of the complaints the amount of fluid in the pleural cavity is not
marked. On examination, the patient`s typical forced position can be observed lying on the sick side. For very large effusions or phenomena of respiratory and
heart failure, patients take semi-sitting position. Respiratory excursions patient side
of the chest is limited (chest on the affected side behind when breathing). The
increased pressure of accumulated fluid in the pleural cavity increases the amount
of the relevant part of the chest, and also leads to bulging and expanding the
intercostal spaces. If the number of pleural exceeds 300-500 ml, then on the
affected side there are marked and deadened sound (with massive effusions chupoy
pike), weakening or disappearance of voice trembling and breathing noises.
Blunting area has a curved upper boundary (line Damuazo). In left-sided
pleurisy,space Traube disappears. Often decisive diagnostic method is pleural
puncture. There is evaluate the appearance of the pleural fluid, its cellular
composition, performed biochemical and biological research. On X-ray
examination in dry pleurisy, there is revealed only limited mobility of the
diaphragm on the affected side, and later there is a slight darkening of diffuse
pulmonary field due to pleural adhesions, Mooring. X-ray mapping of pleural
effusion depends on the quantity, condition pleural cavity (eg, adhesions, Mooring,
etc.) and position of the body the patient (vertical or horizontal). The x-ray light is
determined by the darkening of a small to a total depending on the size of effusion.
Very great diagnostic importance is thoracoscopy with pleural biopsy, which
reveals tuberculous pleurisy or tumor origin.
Treatment. Treatment of pleurisy should be comprehensive and aimed primarily
at eliminating the main process leading to its development. Symptomatic treatment
is aimed at pain relief, faster resorption of fibrin, preventing the formation of
extensive adhesions and is moored in the pleural cavity. Risk of transformation of
serous fluid in purulent or encysted necessitates regular pleural puncture (1-2 w),
with its maximum evacuation. This tactic works best anatomical and functional
outcomes as lung completely crushes and does not develop obliteration. In purulent
exudate, pleurisy is evacuated; the cavity is drained and washed with antiseptic
solutions, and there are introduced intrapleural antibiotics. In intoxication,
dyspnea, disorders of the heart, there are used intravenously plasma-substituting
solutions, inhalation of oxygen, cardiac glycosides. In order to reduce pain
(especially in patients with dry pleurisy), there can be used banks, mustard, dry
heat, hot compress with tight bandaging the lower parts of the chest, smearing the
affected side of iodine tincture in a grid. As resorption of fluid, after the
disappearance of pain, normalization of body temperature and erythrocyte
sedimentation rate, and the patient should exercise therapy sessions including
breathing exercises to prevent pleural adhesions. In the absence of
contraindications, there are performed physiotherapy (Solux, inductothermy,
electrophoresis) and spa (local motels, Southern Coast of Crimea, the Black Sea
coast, etc.) treatment.
Diseases of the esophagus - achalasia (undisclosed) cardio (kardiospazm,
hiatospazm, functional obstruction cardio of esophagus) is a violation of the motor
function of smooth muscle of the esophagus, where it becomes hypertensive lower
sphincter, does not relax during swallowing and esophageal peristalsis replaced his
abnormal contractions. AK - a relatively rare disease, its rate is 7 deaths per 100
thousand population. The etiology is not established. It is believed that the cause of
the disease are the psycho-emotional disorders and stress, prolonged use of cold
(ice) drinks and ice cream. Pathogenesis.On the base of AK, there is a violation of
the innervation of the smooth muscle wall of the esophagus and the lower
esophageal sphincter, which will stop the disclosure of physiological cardia in
swallowing, increased tone and motility of the esophagus and the delay of food in
it. The clinical picture. The main features of CA are dysphagia, regurgitation and
chest pain when swallowing. Dysphagia initially episodic, in severe cases is
observed at every meal, especially dry or poorly chewed, increases in sea. To
facilitate the passage of food, patients drink water or milk; take a deep breath,
arching body back, which helpsin some cases. Regurgitation appears with stuck in
the esophagus, saliva, mucus, and food residues arising in the torso, with a packed
esophagus or at night while you sleep. Nocturnal regurgitation of food into the
mouth with its flowing into the airways is accompanied by symptoms of "nocturnal
cough", "wet pads", "night vomiting," etc. Often, there are developed aspiration
pneumonia and bronchitis. Patient has chest pain when swallowing or eating out.
They disappear after regurgitation or passage of food into the stomach. A complete
picture of the AK is a chronic progressive dysphagia and weight loss in a few
months or years. Diagnosis.In X-ray, there is not determined air in the stomach.
Levels of air and fluid in the patient standing show a delay of food in the
esophagus. If barium is swallowed, there is expansion of the esophagus, and in
severe cases the esophagus looks like the sigmoid colon. Peristalsis in the lower
two thirds of the esophagus is abnormal, its terminal part steadfastly coracoid
narrowed and presented with not weakening lower esophageal sphincter. Reception
of table 1-2., nitroglycerin relaxes the esophageal sphincter and the content goes to
the stomach. With the help of manometry, defined normal or increased pressure in
the lower esophageal sphincter, and it is not relaxed on swallowing. In endoscopic
esophageal cavity, tehre is found extensive evidence of chronic esophagitis
(congestion, edema, erosion, excessive bleeding). This method eliminates the
cancer of the esophagus. Complications: recurrent aspiration pneumonia and
chronic bronchitis.
Treatment. Drug treatment is to receive sedatives, nitrates (nitroglycerin,
sustak, nitrong, nitro poppy nitrosorbid, izoket, Erin, and others), anticholinergics
(gastrotsepin, metatsin, platifillin etc.) and calcium antagonists (nifedipine - on 1020 mg sublingually 20 minutes before a meal). Also, there can beappled Buscopan
(1 tablet 3 times a day), nonabsorbable antacids (fosfalgagel, Maalox, almagel
etc.). In failure of conservative treatment, it is resorted to cardiodiosis. With
experienced specialist, this method is effective in about 85% of cases. Possible
complications include perforation of the esophagus cardiodiosis and bleeding.
A hiatal hernia is the displacement after hiatal in the posterior mediastinum of
some abdominal organs (usually the cardia of the stomach). In frequency, it takes
third place after peptic ulcer and cholecystitis. It’s found in womedslightly more
often than men. Etiology and pathogenesis. In the formation of hernias is
characterized by a sharp increase in the value of intra-abdominal pressure,
congenital hypoplasia of the connective tissue structures, reinforcing the
esophagus, or degenerative changes in the elderly, the shortening of the esophagus,
the fall muscle tone, loss of fatty tissue under the diaphragm, kyphosis of the spine,
and others differ axial ( sliding) hernia, in which the chest cavity out abdominal
segment of the esophagus and cardia, and paraesophageal (more rare) when the
abdominal segment of the esophagus and cardia remain below the diaphragm and
into the chest out of the stomach or other abdominal organs. The clinical picture is
determined by the symptoms of failure cardia and reflux oesophagitis: worry
belching, regurgitation of gastric contents, heartburn (especially torso or lying
down, sagging in vertical position); frequent dysphagia, aerophagia, fast saturation
during meals, persistent hiccups, vomiting mixed with blood, iron deficiency
anemia. There may be experienced shortness of breath, palpitations, angina reflex.
Paraesophageal hernias often asymptomatic or may be accompanied by pain in the
epigastric region and the denial. Complications: bleeding of varying intensity,
causing anemia; erosion and ulcers, scars the esophagus, denial (especially
paraesophageal hernia), aspiration pulmonary complications, arrhythmia and other
diagnosis. Hernia in most cases allows revealing radiography in the horizontal
position of the patient, with straining. With the help of esophagoscopy, there are
revealed axial hernia and associated esophagitis. The reduction of pressure in the
lower esophageal sphincter, identified during esophagotomokymography is
considered. Treatment is mainly conservative. There are appointed a sparing diet
within the extended table number 1, a binding agent (bismuth nitrate by 0.25-0.5 g
2-3 times a day, silver nitrate (0.12 g - 200 ml) 1 tbsp. Spoon 3 times a day for 15
minutes before eating) and antacids (almagel 1-2 teaspoons 3-4 times a day 30
minutes before meals vikalin on the table 1-2. 3 times a day 1 hour after meals
Crushed as in 1/2 cup warm water; magnesium oxide by 0.5-1 g 3-4 times a day 1
hour after meals, etc.). If necessary, there are applied antispasmodics (no-spa on
the table 1-2. 2-3 times a day, papaverine, 0.04 g 2-3 times a day) and
anticholinergics (atropine sulfate and 1 table. 2-3 times a day before food platifillin
1 table. 2-3 times a day before meals, metatsin to 0.002-0.005 g 2-3 times a day).
Upon accession of serious complications, there is conducted a surgical treatment,
which downgrades the hernial sac into the abdominal cavity, fixing the cardia and
fundoplication. It is not recommended to work which is related to the bend of the
trunk and abdominal tension. Should be slept with the head of the bed elevated (23 pads), mainly on the right side.
Esophageal cancer (RP) is the 5th place among all cancers in men. This tumor
is with uneven rate in different countries and regions. Especially the highfrequency band it covers is Central Asia, Kazakhstan, Yakutia. In European
countries, Poland is relatively rare: Men - 6, Women - 2 per 100 thousand
populations. Etiology. Drinking alcoholic beverages, too hot or spicy foods,
smoking, poor diet, and a small amount in the diet of fresh fruits and vegetables are
the predisposing factors of this cancer. Chronic esophagitis, esophageal polyps,
cicatricial stricture, achalasia cardia, Plammsra Vinson syndrome (deficiency of
iron in the body) have an important role.
Pathogenesis. Strong alcoholic drinks, hot food and drink injure esophageal
mucosa, facilitates contact with her carcinogens. Chronic esophagitis creates the
conditions for the implementation of the carcinogenic action of agents contained in
tobacco smoke, and entering with food and water. Polyp of the esophagus is a real
danger of transition to cancer. Scarring of the esophagus alarms in terms of their
malignant transformation.Pathology.Poland - almost always the primary and
located in areas of physiological restrictions.90% of cases presented with
squamous cell carcinoma and 10% - adenocarcinoma. Metastasis occurs in 50% of
cases and occurs with current lymph. The clinical picture. In patients, there is
progressed dysphagia and they lose weight. Dysphagia starts when taking tight,
then semi-liquid food. In the propagation of tumor tissue, there occursper
esophageal pain in the chest. Bleeding from the tumor is usually small, but can
sometimes be significant. Because of the discomfort in swallowing, patients
restrict his diet and lose weight. In the case of tumor invasion into surrounding
tissue, pain becomes with agonizing character and is particularly disturbs the
patient at night. When involved in the pathological process of recurrent nerve,
there is arisen hoarseness, and with lesions of the trachea and bronchi, there are
painful cough, shortness of breath, aspiration pneumonia and lung abscess. In the
propagation of the tumor in the supraclavicular region it may be determined by
enlarged lymph nodes, and with lesions of the liver - an increase. Diagnosis.
Patients with persistent dysphagia and (or) a decrease in body weight in a short
time should be carefully examined. Esophagographyis most important for
diagnosis: the expansion of the lumen of the esophagus may occur early in the
disease. Ulceration of tumor formation must be distinguished from peptic ulcers in
the esophagus lined with columnar epithelium. Any ulcers localized outside this
zone, suspicious at the ER. In all cases of suspected RP, there is underwent
endoscopy. Multiple biopsies and cytology help in the diagnosis. Computed
tomography is needed to identify the tumor spreaded to the mediastinal area and
about intra-aortic lymph nodes. Changes in the blood are characterized by
indicators of anemia, thrombocytosis, elevated erythrocyte sedimentation rate.
Bloodis determined in the stool. Treatment is carried out by oncologists. There are
used surgical, radiation, drug and combined methods. Prognosis in most cases is
poor. Prevention consists of smoking cessation, alcohol and hot tea, nutrition, early
detection and treatment of precancerous lesions.
Esophagitis - inflammation of the esophageal mucosa of various etiologies.
There are acute and chronic esophagitis (reflux esophagitis).
Acute esophagitis. Etiology. Acute esophagitis can be a consequence of the
mucous membrane of the esophagus various damaging factors (thermal, chemical,
mechanical), acute inflammatory diseases of the mouth cavity, gastrointestinal
tract, infectious diseases (typhoid fever, influenza, diphtheria), allergic reactions.
Pathology. Depending on the intensity of the lesions vary Bluetongue, edematous,
erosive, pseudomembranous, hemorrhagic, exfoliative, and necrotic abscess forms.
The lesion may be focal or diffuse. The clinical picture. Mild forms are
asymptomatic. In more severe forms, there are marked burning sensation in the
chest while eating, pain along the esophagus, worse when swallowing, drooling,
belching, regurgitation. In erosive and hemorrhagic forms, it is possible
hematemesis, melena, with exfoliative - fever. For abscess and necrotizing
esophagitis is characterized by intense pain, vomiting, and severe general
condition. Complications.There is possibility of bleeding, perforation,
mediastinitis, stricture.
Diagnosis.There is recorded medical history, the results of esophagoscopy congestion, erosion, ulceration, and necrosis. Prognosis depends on the nature and
extent of lesions, associated complications. When abscess and necrotic forms poor. Treatment.Cold drinks are applied, 0.25% solution of novocaine in, vegetable
oil (200 ml) anestezin (2 g) 1 tbsp. spoonful every hour. Pain syndrome is removed




with subcutaneous injection of 1-2 ml of 1% solution of morphine. In order to
prevent possible esophageal spasm, there made subcutaneously 1 ml of 0.1%
solution of atropine and 2 mL of 2% solution of papaverine. Prophylactic
antibiotics in massive doses are started. It is recommended hungry 1-2da.
Subsequently, there is appointed diet number 1a, 16, 1, in severe cases - parenteral
nutrition. In the case of exposure of strong alkalis or acids, stomach is washed with
a weak solution of soda or acetic or citric acid. In all cases, we treat the underlying
disease and athogenetic factors of esophagitisare eliminated.
Osteoporosis of the spine. For that, the most important are: - few children and
childless women - women with fragile body shape, early menopause, prolonged
use of corticosteroids, other diseases (hyperthyroidism, Cushing's disease or
syndrome, type I diabetes, liver disease and kidney disease), low body mass index
<19 kg/m2. Awkwardness and discomfort in the spine. Slightly and middle
incentive pain in the chest and spine. The pain intensifiesduring prolonged sitting,
standing, walking.
Spondylartropatiya.Characterized by a combination of chest pain with uveitis
and arthralgia (including history).
• age at onset 40 years
• slow, gradual increase in pain
• duration of pain more than 3 months
• morning stiffness
• reduction in pain after exercise and during movement
Chest pain also occurs in lesions of bone and rib structures of the chest:
Tietze's syndrome
Costosternal syndrome (against bronchitis, kostosternalnayahondrodiniya)
The front edge syndrome
Ksifoidalgiya
Chest pain at the spinal cord tumors
Sudden pain or increases gradually
Bilateral or unilateral pain
Pain is reduced when driving, often occurs at night
Sensory disorders in the area of root innervation.
Herpes zoster.
Shingles (herpes zoster) - sporadic disease that occurs as a result of activation of
latent varicella-zoster virus.
Characterized by inflammation of the posterior roots of the spinal cord and spinal
ganglia. In most cases, the disease begins acutely. The body temperature can rise to
38-39 ° C, and its rise accompanies general toxic reactions (headache, malaise,
chilling). In the area of innervation of one or more spinal ganglia, there appears
skin rash characteristic with pain and other subjective sensations. Characterized by
burning, fit-sided chest pain, which intensifies at night and often accompanies by
emotional reactions.
The appearance of erythematous papules and vesicles surrounded by flushing rim
Psychogenic chest pain.It is a frequent variant of pain, which consists in the fact
that the phenomenon of pain, as the leading in the clinical picture of the disease at
some point, exists at the same time in the structure of the various affective and
autonomic disorders.
Psychogenic chest pain usually is localized in the zone apex, precordium and the
region of the left nipple.
The most common psychogenic pain in the chest marked with:
- Disturbingly hypochondriacal disorders
- phobic.
- Disturbingly panic disorder
- Depression
The basic criteria of psychogenic pain: prevalence of multiple and prolonged pain.
Regardless of the absence or presence of organic causes of pain complaints of the
patient is much higher than those that are possible for theseorganic remains. The
existence of a temporary connection between the problem and
psychogenicdevelopment or increase pain of a temporary connection between the
problem and the development of psychogenic or increase pain may be aching,
stabbing, pressing, squeezing, burning or throbbing pain. There may be aching,
stabbing, pressing, squeezing, burning or throbbing pain. Continuous.It coincides
with periods of fatigue and great emotional stress. There's also a short-term
pain,which is not associated with physical activity.
List of the literature
1. Jeffrey Bender, Kerry Russell, Lynda Rosenfeld, Sabeen Chaudry-Oxford
American Handbook of Cardiology, 2011
2. A.Zaza An introduction to cardiac electrophysiology
3.ABC of Interventional Cardiology - Ever D. Grech, 2004
4. Cardiovascular Disease in the Elderly - Wilbert S.Aronow, Jerome L.Fleg,
5.www.vidal.ru /кардиология
6.medlistok.com./infarct.asp
7.health. mail.ru /disease/infarct/
8.мedportal.ru>…>кардиолоия
9.www.it-med.ru/library/p/heart1.htm