Therapy Cardio Answers Eng

1.
Инфаркт миокарда: роль неинвазивных и инвазивных методов

в диагностике и лечении инфаркта миокарда.
1. Myocardial infarction: the role of non-invasive and invasive
methods in the diagnosis and treatment of myocardial infarction.
Non-specific clinical and laboratory signs of AMI are:
1. Body temperature rise (from subfebrile numbers to 38.5–39°C).
2. Leukocytosis, not exceeding usually 12-15 x 109/l.
3. A small stick-nuclear shift of the blood formula to the left.
4. Increase in ESR.
The most sensitive and specific marker of necrosis of cardiomyocytes is

an increase in the concentration of troponins I and T.the level of cardiac
troponins begins to exceed the upper limit of normal after 2-6 hours
after anginous attack and remains high for 1-2 weeks from the
beginning of a heart attack. Very sensitive, but malespecific marker of
necrosis is the concentration of myoglobin in the blood. Its increase is
observed in 2-4 hours after anginous attack and persists for 24-48 hours
after it.
Changes in the activity of some enzymes in AMI
Enzyme Start increasing the activity of the h Peak of increased activity,

hours Return to normal, day
MV-fraction KFK 4-6 12-18 2-3
CFC 6-12 24 3-4
LDG 8-10 48-72 8-14

LDG1 8-10 24-84 10-12
ASAT 4-12 24-36 4-7
ECG diagnosis of myocardial infarction.
Violation of coronary circulation in THEM leads to the formation of

three zones of pathological changes:
1. Necrosis zone-pathological q wave (lasting more than 30 MS) and a

sharp decrease in the amplitude of the R wave or QS complex.
2. Area of ischemic damage — the offset segment RS–T is higher (if

transmural MI) or lower contour (in the upper subendocardialnah the
damage to the heart muscle).
3. A zone of ischemia — “coronary” (equilateral pointed) T wave

(positive at the upper subendocardialnah THEM and negative — with
transmural MI).
Doppler echocardiography, when they allow:
 to identify violations of local contractility of the left ventricle;
 quantitatively assess systolic and diastolic LV function;
 to identify the signs of LV remodeling (dilatation of the cavity of the

ventricle, change in LV geometry, etc.);
 to identify echocardiographic parameters of LV aneurysm;
 to assess the condition of the valve apparatus and the presence of

relative mitral valve insufficiency or a flaw in the HDL;
 to assess the level of pressure in the AIRCRAFT and to identify signs of

pulmonary hypertension;
 identify the morphological changes in the pericardium and the
presence of fluid in the pericardial cavity;
 detect the presence of intracardiac blood clots;
 to evaluate the morphological and functional changes of the main and

peripheral arteries and veins.
The use of the technique of myocardial scintigraphy with technetium is

shown for the verification of myocardial infarction mainly in cases
where there are significant difficulties in the interpretation of ECG
changes, due to the presence of a blockade of the legs of a bundle of
GIS, paroxysmal cardiac arrhythmias or signs of a previous myocardial
infarction. As a diagnostic tool is also used MSCT of the heart and
vascular program. The" gold standard " of diagnosis is coronary
angiography (with the possibility of myocardial revascularization).
2. Атипичные формы начала инфаркта миокарда: клиника,

диагностика, дифференциальный диагноз.
2. Atypical forms of myocardial infarction: clinic, diagnosis, differential

diagnosis.
There are several clinical variants of the beginning of IT:
 pain (angina), I (status anginosus)
 asthmatic variant (status asthmaticus);
 abdominal variant (status abdominalis);
 arrhythmic variant;
 cerebrovascular option;
 oligosymptomatic (asymptomatic) start THEM.
Asthma is the result of early development of acute left ventricular

failure (OLIN) with the main clinical manifestation in the form of
pulmonary edema. In this case, a typical pain syndrome (status
anginosus) is either completely absent or less pronounced. The
development of OLIN associated with the sudden decrease in the mass
of contractile myocardium. OLIN occurs in the form of three clinical
variants that are consecutive stages of a single pathological process:
1. Heart asthma occurs as a result of interstitial pulmonary edema.

Characteristic paroxysmal coming choking, the position of orthopnea,
increase or appearance in the posterior parts of the lungs wet non-
intervertebral small bubbly wheezing.
2. Alveolar pulmonary edema is characterized by the release of plasma

and red blood cells in the lumen of the alveoli, and then – the
respiratory tract, foaming protein transudate. It is characterized by a
sudden onset of asphyxiation, bubbling breath, sticky cold sweat, foamy
bloody (pink) sputum, large bubbly wet wheezing over the entire
surface of the lungs.
3. Cardiogenic shock is an extreme degree of left ventricular failure,

when a sudden sharp decrease in cardiac output is accompanied by a
pronounced and often irreversible violation of peripheral blood
circulation and a progressive decrease in blood PRESSURE. Cardiogenic
shock is often combined with alveolar pulmonary edema. Mortality
reaches 65-90%.
Arrhythmic variant of MI is the development of cardiac rhythm and

conduction disorders in the first minutes and hours of MI, causing
severe hemodynamic disorders and arrhythmia death, provided that
there is no anginous pain.
Life-threatening arrhythmias, which are the direct causes of death,

include: ventricular fibrillation (FJ); asystole; ventricular tachycardia
(GH); AB-blockade of the III degree.
To arrhythmias, aggravating heart failure and causing hypoperfusion of

vital organs include: pronounced bradycardia (heart rate < 50 per
minute); expressed sinus tachycardia (heart rate > 100 per minute);
paroxysms of flutter and atrial fibrillation; paroxysms of
supraventricular tachycardia.
The harbingers of life-threatening cardiac arrhythmias include: short

paroxysms (”runs") of ventricular tachycardia; AV-blockade of II degree
II type according to Mobitz; progressive intraventricular blockades;
frequent, paired, early, polymorphic (polytopic) FE.
The abdominal variant of the beginning IS characterized by the

development of the clinical picture of the "acute abdomen" with the
most frequent localization of pain in the epigastric region in
combination with symptoms of peritoneal tension or without them,
which requires the elimination of acute pathology of the abdominal
organs and abdominal vessels even in the case of a confirmed diagnosis
of AMI.
The cerebrovascular clinical variant of the beginning of IT is

characterized by manifestations of neurological deficiency in the
patient without a typical anginal pain syndrome.
It is characterized by the appearance of pain syndrome in the left half

of the chest or behind the sternum, not reaching the degree of severity
of a typical anginal status, combined with increased fatigue, malaise,
instability of vascular tone, etc.in some cases, clinical manifestations of
THEM may be completely absent. They can go unnoticed by the patient
and his environment if the onset is asymptomatic and asymptomatic. In
this case, failure to provide timely medical care in the early and
subsequent stages of development is fraught with the development of
severe, life-threatening early and late complications, death or disability
of the patient. A more favorable scenario is possible, when the signs of
the patient's later are detected accidentally during a planned medical
examination of the patient without clinical evidence of damage to the
cardiovascular system.
3. Лечение инфаркта миокарда неосложнённого течения.

Неотложная помощь при ангинозном статусе.
3. Treatment of myocardial infarction uncomplicated course.

Emergency care in angina status.
Treatment of uncomplicated myocardial infarction with q wave
The main strategic goals of treatment of patients in the prehospital and

hospital stages are:
1. Early myocardial reperfusion or coronary revascularization, as well as

prevention of further thrombosis.
2. Limiting the focus of necrosis and periinfarction ischemic area by

hemodynamic and metabolic unloading of the heart.
3. Prevention or early elimination of complications.
4. Physical and psychological rehabilitation of patients.

All patients with suspected emerging Q-wave, i.e. patients with acute
coronary syndrome and persistent elevation of the RS–T segment,
should be immediately hospitalized in the intensive care unit of
specialized cardiac departments.
The purpose of therapy is:
 pain relief (analgesia);
 thrombolytic therapy (including indications and contraindications);
 antithrombotic and antiplatelet therapy;
 oxygenotherapy;
 the use of anti-ischemic drugs;
 application of ACE inhibitors and receptor antagonists to angiotensin

II
Basic therapy, which is carried out in all patients includes THE following
groups of drugs:
A classic means of relieving pain in patients with IT is the use of narcotic

analgesics. Morphine also has a pronounced vagotonic effect, causes
sinus bradycardia and hypotension, reduces the amount of preload and
myocardial oxygen demand, has a pronounced sedative effect.
Oxygenotherapy is indicated for all patients with IT.
A prerequisite for the management of patients IS the appointment of

dual antiplatelet therapy.
Low-molecular heparins and unfractionated heparin are used as

anticoagulant therapy.
Antiishemic drugs (b-adrenoblokatory and nitrates) are widely used in
the treatment of patients WITH mi with a tooth Q. Due to the effective
hemodynamic unloading of the heart, they contribute to limiting the
size of THEM, first of all, the size of the periinfarction zone.
ACE inhibitors are used in patients with acute MI and patients with
postinfarction cardiosclerosis to prevent the progression of LV
dysfunction.
Also, metabolic drugs are used in therapy.
The basis for thrombolytic therapy is clinical data, as well as a marked

rise in the RS–T segment on the ECG, registered in a newly admitted
patient with heart pain. As a rule, at this moment there is no
pathological tooth q.
Absolute contraindications to reperfusion therapy: before suffering a

hemorrhagic stroke or stroke of unknown etiology; ischemic stroke
transferred within last 3 months; brain tumor, primary and metastases;
suspected aortic dissection; signs of bleeding or hemorrhagic diathesis
(excluding menses), significant closed head trauma in past 3 months;
change in the structure of cerebral vessels such as arteriovenous
malformation, arterial aneurysm.
Thrombolysis is carried out no later than 12 hours from the onset of the
disease.
Coronary angiography with the possibility of myocardial

revascularization.
4. Лечение инфаркта миокарда. Неотложная помощь при
кардиогенном шоке. Алгоритм действия врача.
4. Treatment of myocardial infarction. Emergency care for cardiogenic

shock. The algorithm of the doctor.
The main strategic goals of treatment of patients with AMI at the

prehospital and hospital stages are:


Basic therapy, which is carried out in all patients with MI with q wave,
regardless of the presence or absence of certain complications, includes
the following activities:
 thrombolytic therapy (naturally, taking into account individual

indications and contraindications);

 oxygenotherapy;
 application of ACE inhibitors and angiotensin receptor antagonists
When cardiogenic shock should be guided by the following algorithm:
5. Лечение инфаркта миокарда. Неотложная помощь при

сердечной астме и отеке легких. Алгоритм действия врача.
5. Treatment of myocardial infarction. Emergency care in cardiac
asthma and pulmonary edema. The algorithm of the doctor.
The main strategic goals of treatment of patients with AMI at the

prehospital and hospital stages are:

Basic therapy, which is carried out in all patients with MI with q wave,
regardless of the presence or absence of certain complications, includes
the following activities:
 thrombolytic therapy (naturally, taking into account individual

indications and contraindications);
 oxygenotherapy;
 application of ACE inhibitors and angiotensin receptor antagonists
In heart asthma and pulmonary edema, the following algorithm should

be followed:
6. Перикардиты: этиология, патогенез и классификация. Клиника,
этапы диагностики и дифференциальный диагноз острого
перикардита. Определение и диагностика тампонады сердца.
Лечение острого перикардита. Показания к перикардиоцентезу,
техника выполнения.
6. Pericarditis: etiology, pathogenesis and classification. Clinic, stages

of diagnosis and differential diagnosis of acute pericarditis.
Determination and diagnosis of cardiac tamponade. Treatment of
acute pericarditis. Indications for pericardiocentesis, technique.
Pericarditis (pericarditis) - infectious or non-infectious inflammation of

the serous membrane of the heart. Pericarditis occurs in many diseases
of the internal organs, being either a complication, or one of the clinical
manifestations of the disease.
Clinical classification
Acute pericarditis (less than 6 weeks)
1. Fibrinous
2. Effusion (or hemorrhagic)
B. Subacute pericarditis (6 weeks to 6 months)
1. Constrictive
2. Constrictive-effusion
B. Chronic pericarditis (more than 6 months)
1. Constrictive
2. Effusion
3. Adhesive (non-restrictive)
Etiological classification
A. Infectious pericarditis
B. non-Infectious pericarditis
V. Pericarditis, probably related to hypersensitivity or autoimmunity

The clinic of acute pericarditis is characterized by a triad of large
symptoms: pain syndrome, fever, pericardial friction noise.
If you suspect acute pericarditis in step 1: medical history (underlying

disease, the dose of isoniazid, anticancer agents, procainamide,
gidralazina), physical examination, ECG diagnosis, x-ray examination of
the UCP, Echocardiography, General blood test, creatinine.
Biopsy l/node appropriate for lymphadenopathy, detection of

infiltration in her lungs, and bronchoscopy or lung CT scan and PCR
(Mycobacterium tubes).
The second stage is pericardiocentesis. When separating the sheets of

the pericardium less than 1 cm, this procedure is not the procedure of
choice. It is necessary for the confirmation of tuberculous, purulent or
cancer of the nature of the exudate.
The third stage is a biopsy, carried out during pericardioscopy in the

case of repeated formation of exudate in a significant amount after a
recent puncture. The optimum combination of biopsy with the
installation of drainage.
Treatment of acute pericarditis
It is always preferable to strictly bed or half-bed before the relief of

pain and fever, i.e. a few days. Prevention of deep vein thrombosis is
mandatory.
Drug therapy:
1. NSAIDs – until the disappearance of all forms (class 1B):
1. ibuprofen 300-800 mg / day, every 6-8 hours;

2. aspirin 500-1000 mg every 6 hours;
3. Indomethacin CAN not be due to the effect on coronary blood flow.
2. Gastroprotectia from the beginning of treatment recommend to all

professionals.
3. Anti-relapse treatment – colchicine 0.5 mg 2 times a day (or as

monotherapy if nevernosti NSAIDs)
Corticosteroids: 1-1. 5 mg/kg weight (average dose 60-90 mg / day) for

at least 1 month. The period of excretion from GCS therapy is not less
than 3 months. Indications: severe condition; severe circulatory failure;
severe respiratory failure; excluded tuberculous or purulent process.
If it was not possible to stabilize the patient's condition, the possibility

of joining the therapy of cytostatics: azathioprine 75-100 mg/day or
cyclophosphamide 200 mg.
Cardiac tamponade is a complication of exudative pericarditis, in which

the pressure in the pericardium increases by so much, which creates a
significant obstacle to the flow of blood into the ventricles and causes a
violation of their diastolic filling. Cardiac tamponade is an indication for
pericardiocentesis.
Pericardiocentesis (pericardial puncture). A pericardial puncture is the

introduction of a catheter into the pericardial cavity to remove fluid
from the cavity.
Technique of execution:
processing the surgical field with an antiseptic solution. Wear sterile

gloves;
- to cover the operating field with sterile diapers, leaving open the
xiphoid process and the area around it for 2 cm;
- prepare the needle by attaching a syringe to it;
- determine the puncture site. Most often, this point is located at 0.5
cm to the left and below the xiphoid process;
- insert the needle under the fragile to the skin 30 degrees in the
direction to the left mid-clavicle line;
- pushing the needle forward, constantly pull the piston;
- once the liquid or air is obtained, remove the needle from the
catheter. Remove the necessary amount of air or liquid, sufficient to
reduce the pericardial stress;
— if the catheter needs to be left in the pericardial cavity, secure it with

a patch and connect it to the drainage system.
7. Перикардиты: этиология, патогенез и классификация. Клиника,

этапы диагностики и дифференциальный диагноз хронического
перикардита. Лечение хронического перикардита. Показания к
хирургическому лечению.
7. Pericarditis: etiology, pathogenesis and classification. Clinic, stages
of diagnosis and differential diagnosis of chronic pericarditis.
Treatment of chronic pericarditis. Indications for surgical treatment.
Pericarditis (pericarditis) - infectious or non-infectious inflammation of

the serous membrane of the heart. Pericarditis occurs in many diseases
of the internal organs, being either a complication, or one of the clinical
manifestations of the disease.
Clinical classification
Acute pericarditis (less than 6 weeks)
1. Fibrinous
2. Effusion (or hemorrhagic)
B. Subacute pericarditis (6 weeks to 6 months)
1. Constrictive
2. Constrictive-effusion
B. Chronic pericarditis (more than 6 months)
1. Constrictive
2. Effusion
3. Adhesive (non-restrictive)
Etiological classification
A. Infectious pericarditis
B. non-Infectious pericarditis
V. Pericarditis, probably related to hypersensitivity or autoimmunity
There are three stages of chronic constrictive pericarditis: initial,

expressed and dystrophic. In stage I venous pressure increases only
after loading, there is no venous stagnation. Stage II is characterized by
severe venous hypertension, the appearance of ascites. Signs of stage
III are hypoproteinemia, peripheral edema, trophic ulcers.
The differential diagnosis is carried out with acute heart expansion,
pulmonary embolism, right ventricular myocardial infarction,
hydrothorax, chronic obstructive pulmonary disease and restrictive
cardiomyopathy. The best way to distinguish compressive pericarditis
from restrictive cardiomyopathy is to analyze respiratory changes in
combination with or without preload changes with Doppler EchoCG
and/or tissue Doppler. Physical signs, ECG, chest x-ray, computed
tomography and magnetic resonance, determination of hemodynamic
parameters and endomyocardial biopsy can also be useful.
The standard of instrumental diagnosis: stage 1-Echocardiography, MRI,

CT; stage 2 – catheterization of the right ventricle, myocardial biopsy
(changes are typical only for restrictive cardiomyopathy).
Treatment: diuretics, pericardectomy. Outcomes of pericardectomy:

mortality 10%, cure 50%, persistent low cardiac output 10-30%.
Drug therapy:
1. NSAIDs – until the disappearance of all forms (class 1B):
1. ibuprofen 300-800 mg / day, every 6-8 hours;
2. aspirin 500-1000 mg every 6 hours;
3. Indomethacin CAN not be due to the effect on coronary blood flow.
2. Gastroprotectia from the beginning of treatment recommend to all

professionals.
3. Anti-relapse treatment – colchicine 0.5 mg 2 times a day (or as

monotherapy if nevernosti NSAIDs)
Corticosteroids: 1-1. 5 mg/kg weight (average dose 60-90 mg / day) for
at least 1 month. The period of excretion from GCS therapy is not less
than 3 months. Indications: severe condition; severe circulatory failure;
severe respiratory failure; excluded tuberculous or purulent process.
The main methods of surgical treatment for pericarditis are:
pericardectomy, pericardiocentesis.
Pericardectomy involves the removal of the outer leaf of the

pericardium (heart bag). The main indication for the operation is
constrictive pericarditis. There are no absolute contraindications to the
operation. Relative contraindications are respiratory failure, blood
clotting disorders, chronic diseases in the acute stage.
8. Экстрасистолия: определение, этиология, патогенез,

классификация, клиника, диагностика, лечение.
8. Extrasystole: definition, etiology, pathogenesis, classification, clinic,

diagnosis, treatment.
Extrasystole is a premature contraction of the whole heart or any of its

Department under the influence of an ectopic impulse.
Etiologies produce functional extrasystoles (in individuals with a healthy

heart), organic beats (heart diseases, when exposed to toxic agents),
mechanical beats (when the mechanical irritation of the myocardium,
endo - or myocardial electrode implanted pacemaker, fold
atrioventrikulyarnogo valve the syndrome of prolapse of the valves
acrobatically).
The pathogenesis of extrasystole is based on the mechanism of re-entry
(re-entry), increased oscillatory activity of cell membranes,
asynchronous repolarization of individual myocardial sites.
Classification of arrhythmia
* Localization - atrial, AV-compound, ventricular.
• At the time of appearance in diastole-early, medium, late.
* Frequency – rare (less than 5 in 1 min), medium (6 to 15 in 1 min) and

frequent (more than 15 in 1 min).
* Density-single and steam.
• Frequency – sporadic and algorithmically (bigeminy, trigeminy,

quadrigemina).
* Emanating from one (monotopic) or from different ectopic foci

(polytopic).
Clinical picture: a feeling of shock or push in the chest, fading in the

heart. These symptoms can be accompanied by aching pain behind the
sternum, dizziness, weakness, fear and lack of air.
In the diagnosis of extrasystole, an important role belongs to ECG, daily

ECG monitoring (CM ECG).
Atrial extrasystoles on the ECG are characterized by the presence of

premature extrasystoles wave R. the Interval PQ can be normal,
shortened or lengthened. The QPS complex is not changed in most
cases. More often there is an incomplete compensatory pause.
Beats from atrioventrikulyarnogo connections are of three types:

1. from the middle part of the AV compound-with simultaneous
excitation of the Atria and ventricles (ECG no scar P, QRs complex is not
changed),
2. with premature excitation of the Atria - from the upper part of the
AV-connection (on the ECG, the negative prong P is at a short distance
before the unchanged QRS complex),
3. with premature excitation of the ventricles – from the lower part of

the AV-compound (on the ECG, the negative p tooth is behind the
unchanged QRS complex).
Nodal extrasystoles may be accompanied as incomplete,
and a full compensatory pause. The QRS complex can
to be aberrant, as in the case of auricular extrasystoles.
Ventricular extrasystoles on ECG are characterized by the absence of

extrasystolic wave P, the broadening of the QRS complex more than 0.1
seconds and the presence of a full compensatory pause.
In the choice of tactics for the treatment of extrasystole, it is necessary

to take into account the etiological factor, the source of extrasystole, as
well as the number during the day. All 4 groups of antiarrhythmic drugs
(sodium channel blockers, beta-adrenoblockers, potassium channel
blockers, calcium channel blockers) can be used in the treatment.
9. Фибрилляция и трепетание предсердий: определение,

этиология, патогенез, классификация, клиника, диагностика,
лечение.
9. Atrial fibrillation and flutter: definition, etiology, pathogenesis,
classification, clinic, diagnosis, treatment.
Flickering (atrial fibrillation) is a very frequent, but not regular (erratic)
activity of the Atria.
Atrial flutter (AF) is a very frequent, but regular activity of the Atria.
Causes of AF and TP: heart disease (cardiosclerosis, cardiomyopathy,

heart disease, coronary artery disease, hypertension); idiopathic;
thyrotoxicosis; dysfunction of the autonomic nervous system.
Electrophysiological mechanism of FP and TP-re-entry
The main forms of FP:
1. FP first identified.
2. Paroxysmal-the duration of the attack of AF up to 7 days, is stopped

independently or medicamentally.
3. Persistent AF-the duration of the AF episode is more than 7 days,

while a medical or electric cardioversion is necessary to restore the
rhythm.
4. Permanent (permanent) - the duration of AF more than 1 year, in

which drug recovery or electroimpulse therapy was not carried out, or
was ineffective and the doctor considers it possible to preserve the
arrhythmia.
ECG signs of AF: absence of p wave in all leads, presence of random

waves f of different shape and amplitude with frequency 350-700 per
minute, wrong rhythm of QRS complexes
ECG signs of TP:atrial waves F of the correct sawtooth form, similar to

each other, rhythmic (not always) with a frequency of 200-400 per
minute, in most cases, the correct ventricular rhythm, the presence of
unchanged QRS complexes, each of which is preceded by a certain,
more often constant, number of atrial waves F (2:1, 3: 1, etc.).
There are 2 types of atrial flutter.
1 type (right-atrial) - activation of the Atria with a frequency of 240-339

in 1 min, the same sawtooth waveform F, easily stopped by electrical
stimulation.
2 type (operation and levopredserdnoy) with a frequency of from 340

to 430 in 1 min intervals F-F change is not interrupted by the
stimulation.
The frequency of the ventricular contractions of release:

tahisistolicescie (CSG more than 90 per minute); normostenichesky (CSI
60-90 per minute) and it's bradycardic (CSI less than 60 per minute)
form.
Clinical picture: tachysystole palpitations,
weakness, shortness of breath, fatigue, cardiovascular insufficiency

increases. In bradyarrhythmia: dizziness, attacks of loss of
consciousness. If normalthey often there are no complaints.
Treatment of atrial flutter and flicker — treatment of the arrhythmia

and prevention of thromboembolic complications (taking into account
the CHA2DS2-VASc scale). There are 2 ways to treat arrhythmia:
* restoration and maintenance of sinus rhythm;
* ventricular rate control while maintaining AF.
To restore sinus rhythm in paroxysms of flicker and flutter - propanorm

and amiodarone. To stop the arrhythmia can be used procainamide
(intravenous 50-100 mg/min to effect). Less frequently used
intravenous administration of isoptin in a dose of 5-10 mg or obzidan at
a dose of 5 mg. With the rapid increase of signs of heart failure are
shown electropulse therapy in the hospital.
With the duration of paroxysm of AF and TP more than 48 hours, due to

the high risk of normalization of thromboembolism, the restoration of
the sinus rhythm should be postponed for 3 weeks of anticoagulant
therapy, during this period, measures to reduce the frequency of
ventricular contractions: digoxin, β-blockers Sa-blockers (verapamil,
diltiazem), amiodarone.
If the duration of paroxysm is more than 7 days, EIT is preferable.
• Treatment of atrial flutter type 1 – radiofrequency catheter ablation

of macro-re-entry in the right atrium in the area of the isthmus
cavotricuspid by applying linear damage
* Treatment of atrial flutter type 2 is carried out by analogy with the

treatment of atrial fibrillation.
• To maintain sinus rhythm in patients with FP BB, flecainide,

propafenone and sotalol. Amiodarone and dofetilide are
recommended as alternative therapies. It is not recommended to use
quinidine, procainamide.
* To reduce the frequency of ventricular contractions mainly
take β-blockers or isoptin. In case of their insufficient
the effectiveness of add cardiac glycosides: digoxin, tselanid at a dose

of 0.125-0.75 mg per day.
Non-drug treatments for atrial fibrillation (AF).
1. Transvenous radiofrequency modification of AV conduction (i.e., the

restriction of conduction of atrial impulses to the ventricles).
2. Transvenous radiofrequency ablation of AV compound with EX

implantation in VVI(R) mode.
3. Transvenous ablation of re-entry in the Atria and/or the foci of

ectopic activity (according to the type of operations "corridor",
"labyrinth"). This procedure is highly effective, but very difficult
technically and time-consuming.
Cardiac pacing is indicated for Bradi and Tahi-Bradi AF (i.e., the

syndrome sick sinus and AV blockade).
10. Синдромы предвозбуждения желудочков (Вольфа-

Паркинсона-Уайта): этиология, патогенез, клиника, диагностика,
лечение.
10. Syndromes of ventricular preexcitation (wolf-Parkinson-white):
etiology, pathogenesis, clinic, diagnosis, treatment.
WPW syndrome is caused by the congenital presence of additional

conductive pathways (ADP) connecting the Atria and ventricles
bypassing the AV node (Kent beam).
There is a phenomenon of WPW (asymptomatic, does not require

treatment) and the manifestation of WPW syndrome. Some patients
may not have clinical manifestations. The main manifestation of wolf-
Parkinson-white - arrhythmia syndrome. Often there are paroxysmal
tachyarrhythmias: supraventricular reciprocal, atrial fibrillation, atrial
flutter. Quite often the syndrome occurs in diseases of the heart -
Ebstein anomaly, hypertrophic cardiomyopathy, ASD, mitral valve
prolapse. WPW syndrome is differentiated from AV-nodal tachycardia
by the value of the RP' interval on the intracardiac or transesophageal
endogram. In WPW it is more than 100 MS.
In WPW syndrome, isolated:
• paroxysmal reciprocal AV Autodromo tachycardia (anterograde

impulses conducted through the AV node, retrograde through DFS),
* paroxysmal reciprocal AB antidromic tachycardia (anterograde –

through DPP, retrograde – through AB node).
Diagnostics. EKG, SMACH, electrophysiological study.
ECG-indications: Short P — R interval (P — Q) is less than 0.12 s. the Δ

Wave. Its appearance is due to the "drain" is the contraction of the
ventricles. Expansion of QRS complex more than 0.1 s due to the wave
Δ. Tachyarrhythmias: orthodromy and antidrama supraventricular
tachycardia, fibrillation and atrial flutter.
Treatment. To prevent attacks of tachycardia with the syndrome WPW:

amiodarone, sotalol, disopyramide. With the appearance on the
background of WPW syndrome with paroxysmal supraventricular
tachycardia applies adenosinfosfatom intravenously. In the event of
atrial fibrillation against the background of WPW syndrome, it is
urgently necessary to conduct EIT. In the future, it is recommended to
carry out the destruction of additional conducting paths.
Indications for surgical treatment of wolf-Parkinson-white syndrome

are: the presence of frequent attacks of atrial fibrillation,
tachyarrhythmia attacks with hemodynamic disorders, the preservation
of tachyarrhythmia attacks during antiarrhythmic therapy, a situation
where long-term drug therapy is undesirable (young age, planned
pregnancy).
Planned treatment of WPW syndrome-catheter radiofrequency

ablation of DPP. Preventive antiarrhythmic therapy in reciprocal
tachycardia is carried out only with contraindications or refusal of the
patient from radiofrequency ablation.
11. Фибрилляция желудочков и асистолия: клиника,

диагностика, лечение.
11. Ventricular fibrillation and asystole: clinic, diagnosis, treatment.
Ventricular flicker (fibrillation) is a frequent and erratic activity of the

ventricles, the most common cause of sudden death. There are
primary, secondary and late ventricular fibrillation.
Causes: IHD, cardiomyopathy, heart disease, idiopathic.
Clinical picture. With this violation of the heart rhythm, blood flow
stops immediately. Paroxysm of FJ leads to syncope, a Morgana-edams-
Stokes attack, and in the case of permanent – to clinical death.
Heartbeat disappears, heart sounds are not heard, blood PRESSURE is
not determined, the skin is pale with a bluish tint.
Within 20-40 seconds, the patient loses consciousness, seizures may

appear, pupils expand, breathing becomes noisy and frequent.
On ECG: continuously varying in shape, duration, height and
the direction of the wave with frequency 150-300 on 1 minute.
Treatment:
1. With ventricular fibrillation and the inability to immediately
defibrillation to strike with his fist in the precordial area and start
cardiopulmonary resuscitation.
2. The defibrillation is sequentially with increasing power-200 and then

360 joules.
3. Central or peripheral vein catheterization.
4. Adrenaline 1 mg IV every 3-5 min of cardiopulmonary resuscitation.
5. Heart massage and ventilator 1 min, defibrillation 360 j and

consistent administration of drugs in/in:
* Lidocaine 1.5 mg/kg.
* Repeat the injection of lidocaine.
* Procainamide 1 g •
* Propafenone 280 mg.
* Monitor vital signs.
The effectiveness of these measures depends on
the length of time they are started and the opportunities
conducting electrical defibrillation of the heart.
Program of treatment of asystole (cardiac arrest):
 if the rhythm is not known and FJ is possible, defibrillation is

performed;
 if asystole is diagnosed:
1) installation of I/o accesses;
2) epinephrine 1:10 000 – 0,5-1 mg (I / o bolus);
3) tracheal intubation, if possible in the first minutes;
4) atropine-1 mg / bolus (repeat every 5 minutes);
5) the purpose of sodium bicarbonate;
6) temporary EX.
12. Пароксизмальная тахикардия (суправентрикулярная,

желудочковая): этиология, патогенез, клиника, диагностика,
купирование приступа.
12. Paroxysmal tachycardia (supraventricular, ventricular): etiology,
pathogenesis, clinic, diagnosis, relief of the attack.
Paroxysmal tachycardia-a sudden, most often
a sharp increase in cardiac activity, usually in excess of 140 beats per

minute with a sudden start and end. The pulses originate from the
center located outside the sinus node.
Causes: disorders of the autonomic nervous system, excessive use of

strong coffee, tea. Organic cardiac disease, hypertension, WPW
syndrome, ovarian dysfunction and other disharmonize, reflexes from
internal organs, electrolyte imbalance, overdose of antiarrhythmic
drugs.
Types of paroxysmal tachycardia: supraventricular (atrial,

atrioventricular), ventricular.
Clinic paroxysmal tachycardia: palpitations, dizziness, until syncope,
restlessness. Often sets the rhythm of the gallop, disappearing after
cessation of the attack.
Supraventricular paroxysmal tachycardia:
Atrial tachycardia:
1) deformed wave P (more often positive in II standard lead);
2) oscillating rhythm frequency 150-300 in 1 min.;
3) the absence in most cases of deformation of the ventricular complex;
4) the presence of progressive shortening of R-R intervals
after the attack ("warm").
Tachycardia of atrioventrikulyarnogo connection:
Akhshay with atrial tachycardia if the ECG is not clearly traced the teeth
of R. Sometimes the retrograde conduction to the Atria is accompanied
by the appearance of a negative P in II, III and aVF leads.
ECG ventricular tachycardia:
1) QRS is expanded and deformed
2) R-R are shortened, equal to
3) P (if visible) has a natural frequency, is not associated with QRS, is

superimposed on various sections of QRS in the form of notches (better
visible in II and V1)
Treatment supraventricular tachycardias.
When unstable hemodynamics is used for the relief electric pulse tach.
Against the background of stable hemodynamics and clear
consciousness of the patient, the relief of paroxysmal supraventricular
tachycardia begins with "vagal" samples. In the absence of the effect of
reflex techniques requires the use of antiarrhythmic means (starting
with the/adenosine or ATP, interrupting the circle of "re-entry"). In the
absence of the effect of adenosine, it is advisable to use calcium
antagonist verapamil (isoptin). Verapamil should be used only for
rhythm disturbances with a" narrow " QRS complex. Alternative
verapamil can serve as procainamide (procainamide). It is also possible
to use β-blockers (propranolol) and cardiac glycosides (digoxin).
For relief of ventricular paroxysmal tachycardia, antiarrhythmic

substances and electric cardioversion are used. The priority drugs are
lidocaine, trimecaine. In the absence of effective use of procainamide
intravenously, while monitoring ECG and BP. Possible intravenous
application of obsidan to 5 mg. In cases of low blood pressure use
electrical cardioversion.
In ventricular tachycardia, the drugs of choice for preventive therapy

are β-blockers and amiodarone. An alternative to medical treatment is
implantation of a cardioverter-defibrillator. Class 1 drugs in the
presence of IHD for long-term antiarrhythmic therapy are not
recommended. Planned treatment includes radiofrequency catheter
ablation of abnormal focus of pacemecer activity or (in case of failure of
the operation or refusal of the patient) selection of cupping (with rare
paroxysms) or preventive antiarrhythmic therapy.
13. Электроимпульсная терапия при нарушениях сердечного
ритма: показания, техника проведения.
13. Electroimpulse therapy in cardiac arrhythmias: indications,
technique.
Electroimpulse therapy (EIT) is the treatment of cardiac arrhythmias

with an electric pulse. EIT is carried out on emergency and planned
indications. The methods of emergency EIT therapy include
defibrillation, cardioversion).
The electrical cardioversion is the application of an electric discharge

synchronized with the R wave on the ECG under short-term intravenous
anesthesia.
Indications for electrical cardioversion: supraventricular tachycardia,

atrial flutter, atrial fibrillation with frequent ventricular response
accompanied by symptoms and rapidly progressive heart failure,
hypotension, ECG signs of acute myocardial ischemia in the absence of
an immediate response to the use of pharmacological agents. Before
performing cardioversion necessary to ensure patient medication sleep.
Immediate EC is indicated for patients with paroxysm of AF and high

CHD with unstable hemodynamics: acute myocardial infarction; arterial
hypotension; angina; heart failure; arrhythmogenic shock; pulmonary
edema.
1.The energy of the first category when using the synchronized

defibrillator – 120 j, if you are using is not synchronized – up to 200
joules.
2. When the first discharge is ineffective, the energy power is increased
by 100 J each time, to a maximum of (360 or 400 j)
3. The interval between two consecutive digits is not less than 1

minute.
Indications for defibrillation: ventricular fibrillation. At the heart of

defibrillation is the transmission through the chest of a short (0.01
seconds) single discharge of a high voltage electric current, which
results in a one-time depolarization of the "critical" number of
cardiomyocytes, after which the sinus rhythm is restored.
To reduce the electrical resistance of the chest, the electrodes are

lubricated with pastes, gels, or put a gauze moistened with 0.9% NaCl
under them; the electrodes are tightly pressed to the chest. One
electrode is placed to the right of the sternum under the clavicle, the
second – at the level of the left nipple (the center of the electrode – on
the left mid-axillary line). It is also possible to place one electrode on
the front over the heart area, and the second in the back.
Defibrillation is carried out with increasing discharge energy, starting

with 200 j. Perform it on exhalation with a minimum time interval
between discharges necessary to monitor the effectiveness.
14. Атриовентрикулярная блокада: этиология, патогенез,

14. Atrioventricular blockade: etiology, pathogenesis, classification,
clinic, diagnosis, treatment.
Atrioventricular (AB) blockade occurs due to disruption of the electrical

pulse from the Atria to the ventricles through the AV-connection.
The causes of conduction disturbances through the AV compound may
be ischemic heart disease, myocarditis, heart defects, electrolyte
balance disorders or damage to the atrioventricular node during
surgical procedures. In some cases, the AV blockade is hereditary.
Classification of AV-blockade:
* I degree (slowing of the pulse from the Atria to the ventricles through
the AV node);
* II degree (slowing the pulse from the Atria to the ventricles through
the AV node with the periodic development of a complete blockade
with loss of ventricular contractions);
* III degree (complete absence of the pulse from the Atria to the
ventricles through the AV node with a reduction of the ventricles due to
the appearance of the 2nd or 3rd order rhythm driver).
Separately isolated artificially created AV-blockade. There are also

proximal (only AB-node) and distal (with damage to the GIS-Purkinje
system) AV-blockade. Distal AV blockades are prognostically less
favorable.
Clinical manifestations in AV blockade depend on the etiology of the

underlying disease and the degree of heart rate reduction.
* In the case of AV blockade of the I degree, the state of health may not
change, less often there are feelings of a rare rhythm or heart failure.
Auscultation can detect the attenuation of sound I and incremental
atrial tone. This type of blockade does not require special treatment.
* In case of AV-blockade of the II degree, if the loss of complexes occurs

rarely and only one ventricular complex falls out, patients may feel
nothing. Sometimes there are moments of cardiac arrest, in which
there may be attacks of severe weakness, dizziness with darkening in
the eyes, premonitory or syncopal States. Clinical symptoms increase
with the loss of several consecutive ventricular complexes.
* AV-blockade of the III degree in all patients is accompanied by a

deterioration of hemodynamic parameters due to a decrease in
myocardial contractility and a decrease in the ventricular ejection
fraction. This is manifested by the deterioration of blood supply to all
organs and primarily to the brain, heart and others. The patients had
attacks of Morgagni-Edems-Stokes, and in some cases sudden death.
Electrocardiographic signs of AV blockade of I degree:
* p-R (Q) interval lengthening more than 0.21 seconds at normal

frequency and more than 0.22 seconds at sinus bradycardia;
• increase in range is due to the elongation of the segment from the

end of R until the-beginning of the R-wave or Q. the norm of AV-delay
and the segment R—R (Q) is 0.07 seconds.
Electrocardiographic signs of AV blockade of the II degree:
• Type I or type I is characterized by Mobetta periodicals Samoilov-

Wenkebach: gradual prolongation of the interval R-R (Q) during each
cardiac cycle; loss of the QRS complex that occurs after the longest R-R
(Q), and then again recorded the normal interval R-R (Q). In the
absence of QRs complex loss, the same pattern is observed when the
normal duration of this interval is restored after the longest p-R (Q)
interval;
• Type II, or type of Mobitz II: deposition of the QRS complex with a
normal duration of interval R-R (Q). Constant increase in the interval P-
R (Q), i.e. the degree I AB-blockade, in combination with the loss of the
QRS complex. Sometimes recorded rhythmic loss QRS in the ratio of 2:
1,3: 1,4: 1, etc.
Electrocardiographic signs of AV blockade of III degree (complete

transverse heart blockade):
* termination of the pulses from the Atria to the ventricles (Atria are
excited and reduced in its rhythm with a frequency of 60-80 beats /
min, and the ventricles – 30-60 beats / min);
* changes in the form and magnitude of ventricular complexes QRS

compared with the sinus rhythm, existed previously, as sources of
excitation of the ventricles are AV-compound or conducting system of
the ventricles, which are designated as ectopic centers of automatism II
or III order;
• in individual complexes P is superimposed on the segment ST and T of

the QRST complex, deforming them;
* there is no relationship between P and the subsequent QRTS

complex, and the p-p intervals are always smaller and remain constant,
and R-R is greater than p-P and may be different in magnitude.
In the vast majority of cases, with the appearance of an AV blockade of

the III degree, temporary transvenous electrostimulation of the heart is
carried out, and then constant-with the installation of an artificial
rhythm driver working on demand.
15. Нарушения внутрижелудочковой проводимости: этиология,
патогенез, классификация, клиника, диагностика, лечение.
15. Disorders of intraventricular conduction: etiology, pathogenesis,
Intraventricular blockades occur in violation of the propagation of the

pulse from the sinus node and Atria to the ventricles due to the
absence or delay of one of the legs of the bundle of GIS. One ventricle is
activated through the interventricular septum later than the other by
about 0.04-0.06 seconds. Therefore, the ventricular complex becomes
wide (more than 0.12 seconds) and deformed. The most frequent are
the blockade of the right or left legs of the bundle of GIS.
ECG-signs of a complete blockade of the right leg of a bunch of GIS:
• extension of the QRS complex to 0.12 seconds or more;
* splitting of the QRS complex in the form of m – rsR, rsR', RSR', RR'
forms and increased time of internal deviation in the V1 ,V2, V3R, aVR
leads for more than 0.06 seconds;
* deep, serrated tooth S with a duration of more than 0.04 seconds in

leads I, V5, V6, sometimes in leads II, aVL. Leads I and II have
predominantly positive QRs complex, in which R > S;
* downward displacement of the ST segment and negative t wave in

V1 ,V2, V3R leads, possibly in III and aVF leads;
* the electrical axis of the heart often occupies an indifferent position,

or there is a slight deviation to the right or left.
ECG-signs of a complete blockade of the left leg of a bunch of GIS:
• extension of the QRS complex to 0.12 seconds or more;

* wide and split tooth R (missing teeth Q and S) in the form of a wide
letter " L " in the I-lead, increased time of internal deviation to 0.08
seconds and more in the leads I, V5, V6, aVL;
• expanded and serrated prong S or QS complex in leads opposite V1,

V2, and sometimes in leads III and aVF;
* downward displacement of the segment ST with negative asymmetric

wave T in the leads V5, V6, I, aVL. Shifted upward, the ST segment with
high asymmetric T in leads V1, V2, and sometimes in leads III and aVF;
* in the vast majority of cases, there is a horizontal position of the

electric axis of the heart (forms I, aVL leads correspond to V5, V6) or a
pathological deviation of the axis to the left. Treatment of
intraventricular blockages is aimed at treatment of the underlying
disease.
16.Синдром слабости синусового узла: этиология, патогенез,

16. Sinus node weakness syndrome: etiology, pathogenesis,
Sinus node weakness syndrome (SSS) is a rhythm disturbance caused by

the weakening or termination of the Sino – atrial node automatism
function. With SSS, the formation and conduction of a pulse from the
sinus node to the Atria is disturbed, which is manifested by a decrease
in the heart rhythm (bradycardia) and accompanying ectopic
arrhythmias. In patients with sinus node weakness syndrome, a sudden
cardiac arrest may occur.
The sinus node is powered by a separate artery, extending generally

from a.coronaris dextra. The cause of sinus node fibrosis can be
myocarditis, infiltrative lesions (hemochromatosis, amyloidosis). In
addition, SSS can be observed in cardiomyopathy (dilated,
hypertrophic). In some cases, the primary disease is not found and
then talk about idiopathic SSS.
Symptoms of SSS
* Persistent bradycardia less than 60 per minute
* Transient sinoauricular blockade. Here may develop periodicals

Samoilov-Wakenbake, periodicals 2: 1 and persistent sinoaurikuliarnaya
blockade. Transient sinoauricular blockade may be accompanied by
darkening of the eyes, syncopal conditions, fainting, which requires
mandatory therapy.
* Tachy Brady syndrome. There is the appearance of paroxysmal

tachycardia (atrial fibrillation, nodal tachycardia). This can lead to a long
pre-automatic pause of more than 2 seconds when the rhythm is
restored. Patients experience hypoxia of the brain. This form has been
going on for years.
* Bradysystolic form of atrial fibrillation. These patients often

additionally revealed a violation of AV conduction.
Diagnosis of SSS
* ECG monitoring for 24-72 hours.
* Atropine test: 1-1. 5 ml of atropine is administered and an ECG is

recorded at intervals of 3-5 minutes. With SSS heart rate does not
exceed 90 per minute.
• Electrophysiological study (EPS).

Conducting acute antiarrhythmic therapy in the syndrome of
bradicardia very dangerous because of the possibility asystole and
death of the patient. Installation of pacemaker is the only reliable
method of treatment of sinus node weakness syndrome.
17.Синдром Морганьи-Эдемса-Стокса: этиология, патогенез,

классификация, клиника, диагностика и лечение. Показания к
временной и постоянной электрокардиостимуляции
17. Syndrome of Morgagni-Edems-Stokes equations: etiology,
pathogenesis, classification, clinic, diagnostics and treatment.
Indications for temporary and permanent pacing
Syndrome of Morgagni-Edems-Stokes is manifested by attacks of loss of

consciousness with rapid development of severe cerebral ischemia due
to a significant reduction in cardiac output in patients with cardiac
arrhythmias (asystole, flutter and fibrillation of ventricles).
There are three pathogenic forms blink-Edems-Stokes: bradycardias,

tahiaritmicheskoy and mixed forms.
Clinical manifestations of the syndrome of Morgagni-Edems-Stokes,

depending on the duration of life-threatening cardiac arrhythmias:
* Within 3-5 seconds. Sudden onset of lightheadedness (lipoliticescoe)

status: marked weakness, dark circles front of your eyes, slow speech,
loss of coordination, indifference to surroundings, and disorientation,
increasing noise or ringing in the ears and head, nausea, vomiting,
paleness, decreased blood pressure, heart rhythm disorders.
• For 10-20 seconds. Fainting (syncopal state): loss of consciousness,

pale skin, cyanosis of the lips, acrocyanosis, falling blood PRESSURE,
decreased muscle tone, the patient lies still, can occur clonic twitching
of the face and body, weakened, almost invisible breathing, heart
rhythm disorders.
• Within 20-40 seconds. There is a profound swoon: progressive

hemodynamic disorder, remain, respiratory disorders appear
generalized epileptiform convulsions, can be biting tongue, involuntary
urination and defecation, and cardiac arrhythmias.
• For 1-5 min. a Condition of clinical death: periodic breathing, such as

Cheyne-Stokes with increase in period apnea, bubbling breath, as with
increasing pulmonary edema, intense cyanosis, often the entire top half
of the body, heart sounds deaf, sparse rhythm, periods of asystole,
alternating with periods of arrhythmia, heart rate and blood pressure
not determined, dilated pupils, reduced and disappear corneal reflexes
cardiac arrhythmia.
* After 5-10 minutes. Comatose state or biological death: periodic

breathing, such as the Chaine-Stokes, with an increase in the period of
apnea, bubbling breath, as with increasing pulmonary edema, intense
cyanosis, cardiac tones are deaf, rare rhythm, periods of asystole,
alternating with periods of arrhythmia, pulse and blood PRESSURE are
not determined, pupils are enlarged, root reflexes are reduced and
disappear, heart rhythm disorders.
Attack Morgagni-Edems-Stokes can be docked in all phases of

emergency resuscitation. The treatment strategy is determined by the
type of cardiac arrhythmia.
Indications for temporary EX: patients with complete AV blockade in

acute myocardial infarction (regardless of its location and at any width
of the QRS complex).
Indications for constant EX:
- sinus node dysfunction syndrome. Central to the solution of a

question about installing a pacemaker is the presence of severe
bradycardia accompanied by clinical signs of decreased cerebral blood
flow (e.g., fainting).
-atrio-ventricular blockade II–III degrees, accompanied by severe

bradycardia and attacks of Morgagni-Edems-Stokes.
18. Классификация АГ. Основные принципы дифференциальной

диагностики гипертонической болезни и симптоматических АГ.
18. Classification of AG. Basic principles of differential diagnosis of

hypertension and symptomatic hypertension.
Arterial hypertension (AH) is a persistent increase in blood pressure

(systolic blood pressure > 140 mm Hg. article and/or diastolic blood
pressure > 90 mm Hg. art.), registered at least 2 medical examinations,
each of which blood PRESSURE is measured at least twice.
Depending on the etiology, all cases of hypertension are divided into

two groups:
1. Primary (essential) hypertension.
2. Secondary (symptomatic) AG
a. Nephrogenic (renal)
i. Renovascular (atherosclerosis, dysplasia of renal vessels, vasculitis,

thrombosis, aneurysm of the renal artery, tumors that compress the
renal vessels)
II. Rinofaringitis (chronic pyelonephritis, glomerulonephritis,
amyloidosis, nephrosclerosis, hydronephrosis, systemic lupus
erythematosus, polycystic kidney disease)
b. Hemodynamic (due to the lesion of the great vessels and the heart):
aortosclerosis, coarctation of the aorta, aortic valve insufficiency,
nonspecific aortoarteritis
c. Endocrine
I. adrenal (pheochromocytoma, Connes syndrome, adrenal cortex

hyperplasia)
II. thyroid (hypothyroidism, thyrotoxicosis) and parathyroid
III. pituitary (acromegaly, Cushing's disease)
iv. climacteric
d. Neurogenic (caused by diseases and lesions of the Central nervous

system): trauma, brain tumors, meningitis, encephalitis, stroke.
e. Medicinal (against the background of taking mineral and

glucocorticoids, progesterone and estrogen-containing contraceptives,
levothyroxine, salts of heavy metals, non-steroidal anti-inflammatory
drugs, etc.)
Essential (primary) hypertension include those cases where it is

impossible to establish a connection between the increase in blood
PRESSURE and a particular organ or endocrine pathology that precedes
the occurrence of hypertension.
Symptomatic hypertension-secondary hypertension, arising from the

defeat of organs and systems that regulate blood PRESSURE. They are
not an independent disease. They are considered only as one of the
manifestations of another pathology.
The causes and mechanisms of symptomatic hypertension are either

known or can be established. The elimination of an etiological or
leading pathogenetic factor often leads to normalization or to a
noticeable decrease in blood PRESSURE.
19. Почечные АГ: классификация, этиология, патогенез, клиника,

диагностика, дифференциальная диагностика, лечение.
19. Renal AH: classification, etiology, pathogenesis, clinic, diagnosis,

differential diagnosis, treatment.
Renal arterial hypertension (AH) is divided into 2 groups:
1. Renovascular (atherosclerosis, dysplasia of kidney diseases, systemic

vasculitis, thrombosis, aneurysm of the renal artery, tumors that
compress the renal vessels)
2. Rinofaringitis (chronic pyelonephritis, glomerulonephritis,

amyloidosis, nephrosclerosis, hydronephrosis, systemic lupus
erythematosus, polycystic kidney disease)
Renovascular hypertension is caused by stenosis of the main renal

artery. The most common causes are atherosclerosis and fibromuscular
dysplasia.
Atherosclerotic stenosis-mainly in older streets, more often in men,

especially in smokers. In 30-50% of patients have bilateral involvement.
Patients have signs of generalized atherosclerotic process.
Fibromuscular dysplasia is more common in women 20-30 years and is
less severe than atherosclerotic lesions. The most typical type of vessel,
reminiscent of beads. In 30% of cases, both renal arteries are involved
in the process.
The pathogenesis of renovascular hypertension is based on renin

hyperproduction due to kidney ischemia and associated activation of
angiotensin and aldosterone.
For clinical picture characterized by acute onset with sudden increase in

blood pressure; a severe, predominantly diastolic hypertension; pulse
pressure is reduced, the tendency to orthostatic hypotension; acute
episode of lower back pain, including that associated with trauma,
hematuria or embolism of peripheral arteries in history; no cases of
essential hypertension in the family; vascular systolic or less, systolo-
diastolic murmur in the umbilical region (in the projection of divergence
from the aorta, renal artery), which may radiate to the flank and back.
Diagnosis: 1) indirect signs of kidney ischemia (excretory urography,

radionuclide renography); 2) the level of renin secretion; 3) narrowing
of the renal artery (selective radiopaque angiography).
Treatment: revascularization (transluminal balloon angioplasty or

surgery) and drug therapy, which includes drugs that reduce the
secretion of renin (beta-blockers, a-methyldof) and the formation of
angiotensin II (ACE inhibitors). Not effective spironolactone and
saluretics.
Renourishment in the pathogenesis of hypertension include: 1) loss of

depressor function of kidneys due to a decrease in the formation in
them of prostaglandins A2, E2, and kinins; 2) increase in circulating
plasma due to the violation of renal excretory function; 3) activation of
the renin-angiotensin-aldosterone system due to vascular lesions and
secondary especially with the development of renal scarring.
Chronic glomerulonephritis-more often in young people, the

predominant increase in diastolic blood PRESSURE, the stability of
hypertension, the absence of crises, changes in urinary sediment in the
form of urinary syndrome with a predominance of red blood cells and
cylindrical.
Chronic pyelonephritis is an intermittent character of increased blood

PRESSURE in the early stages of the disease associated with
exacerbations of the disease. High levels of diastolic blood PRESSURE.
In the history – obstructive urinary tract, recurrent uroinfection,
congenital anomalies of the kidneys.
AH in polycystic kidney disease is associated with their ischemia due to

cystic degeneration, nephrosclerosis or the addition of infection
(secondary pyelonephritis). In this case, the kidneys are significantly
increased in size, with an instrumental examination, multiple cysts are
detected.
The Genesis of hypertension in diabetes is due to: 1) diabetic

nephrosclerosis; 2) concomitant essential hypertension; 3) isolated
systolic hypertension due to atherosclerosis of the aorta; 4)
renovascular hypertension of atherosclerotic etiology; 5) accompanying
diabetes chronic pyelonephritis. Persistent proteinuria in diabetic
nephrosclerosis. Hypertensive crises are not characteristic. With the
development of a wrinkled kidney, severe hypertension and chronic
renal failure (CKD) are established.
Treatment of hypertension in acute glomerulonephritis-normalization
of circulating plasma (limitation of liquid, salt and furosemide). In
chronic kidney disease tactics depend on the presence of CPN. In its
absence, a combination of 2-3 drugs is recommended-saluretic, neuro-
and myotropic drug (vasodilator), ACE inhibitors. In CPN avoid excessive
restriction of salt and taking saluretics, as well as reducing diastolic
blood PRESSURE below 100 mm Hg.V. Combine 3 drugs: furosemide,
beta-blocker (or a-methyldopa) and hydralazine (or prazosin, or calcium
channel blocker, or ACE inhibitor). In terminal chronic renal failure,
ultrafiltration and hemodialysis are used.
20. Эндокринные артериальные гипертензии: классификация,

этиология, патогенез, клиника, диагностика, дифференциальная
20. Endocrine hypertension: classification, etiology, pathogenesis,

clinic, diagnosis, differential diagnosis, treatment.
Endocrine AH include: adrenal diseases (pheochromocytoma, icenko-

Cushing's syndrome, Connes syndrome); thyroid (Hypo-and
hyperthyroidism); hyperparathyroidism; pituitary (acromegaly,
Cushing's disease); climacteric; obesity.
Cushing's syndrome-the presence of a cortisol-secreting tumor

(adenoma, adenocarcinoma) of one of the adrenal glands or with long-
term treatment with glucocorticosteroids (exogenous syndrome).
The disease Itsenko-Kushinga – bilateral diffuse hyperplasia of the

cortical substance of the adrenal glands with increased production of
cortisol under the influence of excessive production of ACTH by the
anterior lobe of the pituitary gland or (rarely) corticotropin-releasing
hormone by the hypothalamus.
The pathogenesis of AG: 1) increased synthesis of angiotensin I; 2)

increased reactivity of blood vessels in relation to noradrenalinu and
other Pressor substances; 3) retention of sodium and water kidneys
with increasing DTP under the influence of excess cortisol and
mineralocorticoids.
Hypertension often soft, wears systolo-diastolic in nature and takes

place without crises.
Clinical manifestations: centripetal obesity, moon face, muscle

weakness and muscle atrophy, crimson striae, acne, hypertrichosis,
virilization, hirsutism.
Diagnosis: polycythemia, leukocytosis, decreased glucose tolerance,

moderate hypokalemia, increased excretion of 17-oxycetosteroids and
17-ketosteroids in the urine per day, ACTH levels in the blood,
dexamethasone test. Hypercorticism of pituitary origin is also
characterized by an increase in the blood content of ACTH in the basal
conditions and the suppression of its secretion after taking 1 mg of
dexamethasone.
The diagnosis uses CT of the adrenal glands with contrast, MRI of the
adrenal glands, CT and NMR of the Turkish saddle.
Radical treatment of the disease-surgical (removal of the tumor of the

pituitary or adrenal gland), according to the indications – replacement
therapy.
Primary hyperaldosteronism (Conn's syndrome) due to hypersecretion
of aldosterone by the adenoma or cancer of the cortical substance of
the adrenal glands. Aldosterone increases sodium reabsorption and
increases potassium and hydrogen secretion. The cause of
hypertension is an increase in the reactivity of arterioles to Pressor
effects. AG is in the nature of objektiviem.
More often women younger than 40 years. AG is usually mild or

moderate, systolic-diastolic, postural arterial hypotension may be
observed. Characterized by the absence of edema. Signs of
hypokalemia (muscle weakness, paresthesia, polyuria and polydipsia).
Diagnosis: detection of elevated levels of aldosterone in the blood and

daily urine in combination with reduced plasma renin activity;
computed tomography and nuclear magnetic resonance of the adrenal
glands.
In adenoma treatment of choice is economical resection of the adrenal

gland with the removal of the tumor.
Pheochromocytoma is a tumor consisting of chromaffin cells and

producing significant amounts of catecholamines – adrenaline and
noradrenaline. In 90% of cases pheochromocytoma is localized in the
brain layer of the adrenal glands, in 10% – non-renal localization (nerve
plexus of the abdominal cavity, along the thoracic and abdominal aorta,
kidney gates, bladder).
Pathogenesis of AH: tumor release of a significant amount of

catecholamines, to a sharp increase in the total peripheral resistance of
blood vessels. With the simultaneous activation of the renin-
angiotensin-aldosterone system, the course of the hypertensive
syndrome becomes severe, malignant AG can develop.
Forms of clinical course: asymptomatic, latent (blood PRESSURE

increases very rarely); with a crisis increase in blood PRESSURE against
the background of its normal level in the intercritic period; with mild
hypertensive crises against the background of constantly increased
blood PRESSURE.
Hypertensive crisis in pheochromocytoma develops suddenly, without

precursors. Provoke crisis mechanical irritation of the tumor (palpation
of the abdomen), hyperventilation, the use of alcoholic beverages,
foods containing tyramine, taking drugs with pronounced vasodilating
properties. Clinical picture of the crisis: pallor, acrocyanosis, sweating
(sometimes profuse), body tremor, tachycardia, may be a violation of
vision and hearing, fever, leukocytosis and hyperglycemia. The crisis
stops suddenly, its duration varies from several seconds to several days.
Diagnosis: determination of the concentration of normetanephrine and

metanephrine; examination of blood and urine during an attack with
the definition of leukocytosis, the level of glycemia and presence of
glycosuria; CT adrenal with contrast); sample, provoking the crisis
(palpation of abdomen, cold test, test with histamine).
Treatment-surgical removal of the tumor. Hypertensive crisis cropped

rapid intravenous injection of 5-10 mg of phentolamine.
Hypothyroidism-reduced function of the thyroid gland. A characteristic

feature of hypothyroidism is high diastolic blood PRESSURE, as well as a
decrease in heart rate and cardiac output.
Hyperthyroidism-increased thyroid function. Hyperthyroidism is
characterized by increased heart rate and cardiac output, mainly
isolated systolic hypertension with low (normal) diastolic blood
PRESSURE.
21. Гемодинамические артериальные гипертензии:

классификация, этиология, патогенез, клиника, диагностика,
дифференциальная диагностика, лечение.
21. Hemodynamic arterial hypertension: classification, etiology,

pathogenesis, clinic, diagnosis, differential diagnosis, treatment.
Hemodynamic (cardiovascular) hypertension can develop when an

isolated lesion of the heart (myocardium, conduction system, valvular)
or vessels (coarctation of the aorta, pulseless disease, or syndrome,
Takasi). This increases mainly systolic blood pressure.
Coarctation of the aorta is a congenital disease associated with

thickening of the muscle layer in the area of the aortic isthmus. There is
a redistribution of blood-a sharp overflow of blood vessels above the
narrowing and insufficient blood filling of the vessels below the
narrowing. The main symptoms of the disease are manifested by the
period of puberty. Subjectively marked headache, feeling of fever or
high tide to the head, nosebleeds. Objectively: hypertrophy of the
upper half of the trunk and hypotrophy of the lower; hyperemic face;
pulse on the radial artery full, tense; cold feet, weakened pulse on the
legs; to the left of the sternum rough systolic murmur; apical impulse
greatly enhanced; HELL on the brachial artery high, feet – low;
radiographs of usurate edges; the main method of diagnosis –
aortography. Patients with aortic coarctation are subject to surgical
treatment.
Takasi disease (Takayasu), nonspecific aortoarteritis. The causes of the
disease are not reliably determined. Her debut is associated with
exposure to infectious and allergic agents and autoimmune aggression.
The disease is more common in young women. The clinical course
depends on the level of damage to the aorta (arc, thoracic or
abdominal aorta) or pulmonary artery with its branches. Characteristic
features are asymmetry or lack of pulse on the brachial arteries,
difference in blood PRESSURE on different limbs, aortic noise,
angiographic changes – narrowing or occlusion of the aorta and its
branches. Treatment of Takayasu disease is carried out by
corticosteroids, cerebrovascular complications are frequent.
AG in aortic insufficiency (congenital or acquired) is associated with the

flow of blood from the aorta, leading to an increase in cardiac output
and cardiac output, resulting in hypertension acquires a systolic
character. Diastolic blood PRESSURE is reduced, and the pulse pressure
increases. Low diastolic blood PRESSURE and insufficient blood filling of
the coronary arteries due to diastolic regurgitation of blood in the left
ventricle are the cause of heart pain. Medical and surgical treatment
(aortic valve prosthetics).
Systolic hypertension in complete atrioventricular blockade is caused by

an increase in the shock volume of blood due to an increase in blood
filling of the left ventricle during prolonged diastolic pauses. The
diagnosis is made when registering on an electrocardiogram of a
complete transverse blockade of the heart. Treatment: placement of a
pacemaker.
AG in atherosclerotic aortic lesions of the aorta is most characteristic of

older age groups. The cause of hypertension may be a violation of
blood supply and hypoxia of the brain centers involved in the regulation
of blood PRESSURE, a decrease in the number and changes in the
functional properties of Baro - and chemoreceptors of the aortic arch
and synocarotide zone due to atherosclerotic lesions, a decrease in
elasticity and loss of aorta "damping" properties, especially in the
common severe atherosclerotic process, accompanied by calcification
of the vascular wall.
With atherosclerotic hypertension increases systolic and pulse

pressure, diastolic pressure changes slightly. On radiographs recorded
detailed, condensed, expanded and elongated aorta, calcification is
sometimes found her. In atherosclerotic hypertension, hypertrophy of
the left ventricle is less common and is much less pronounced than in
hypertension.
22. Гипертонический криз. Определение, классификация.

Оказание неотложной помощи.
22. Hypertensive crisis. Definition, classification. Aid.
Hypertensive crisis – ha) - a sudden increase in blood PRESSURE in

patients with hypertension (AH), accompanied by disorders of the
autonomic nervous system and increased disorders of the brain,
coronary and renal blood circulation.
Hypertensive crises are divided into uncomplicated and complicated.
Uncomplicated ha often occurs in the early stages of the disease,

characterized by the absence of target organ damage. These crises are
also called "hypertensive crisis type I" or "hyperkinetic crises". They are
mainly associated with the activation of the sympathetic-adrenal
system and the release of catecholamines into the blood, mainly
adrenaline. In the clinical picture, vegetative disorders predominate, as
well as symptoms associated with a sudden increase in blood
PRESSURE, crises develop violently, but are relatively short (no more
than 2-3 hours) and are easily stopped by antihypertensive agents.
Complicated GK often develops in the late stages of the disease and is

characterized, in addition to a significant increase in blood pressure, the
development of hypertensive encephalopathy or other cardiovascular
complications (haemorrhagic or ischemic stroke, subarachnoid
hemorrhage, cerebral edema, dissecting aortic aneurysm, acute left
ventricular failure, myocardial infarction, or unstable angina, eclampsia,
acute renal failure, hematuria, severe retinopathy).
GK, complicated hypertensive encephalopat also called "hypertensive

crisis type II" or "hypokinetic crises".
Emergency therapy for uncomplicated (adrenal) ha should be started

with tablets:
* captopril 0.025 g (ACE inhibitor) - under the tongue;
• 0.01 g of nifedipine (a blocker of slow calcium channels) – under the

tongue;
* propranolol 0.01 g (nonselective β-blocker), 10-40 mg orally;
Parenteral therapy is prescribed only in the case of insufficient effect

from taking antihypertensive drugs inside or the development of
certain complications of ha.
Emergency therapy for complicated ha depends on the type of

complication.
GK, complicated by onmc. Often, the increase in blood PRESSURE is
compensatory and is aimed at improving the blood supply to the
damaged areas of the brain, while the blood PRESSURE is reduced
slowly. Captopril 25 mg under the tongue or enalaprilat-1.25 mg in 1
ml, in / slowly for 10 minutes, magnesium sulfate 25% -10.0 ml in / in,
Actovegin 5.0 ml, Semax 1% solution – 2-3 drops in each nasal passage.
Therapy is also aimed at maintaining the vital functions of the body.
Ha, complicated by acute hypertensive encephalopathy. There is the

dilatation and increased permeability of blood vessels, which lead to
swelling of the brain. Clinical signs: intense headache, dizziness, nausea,
vomiting, vision impairment (swelling of the optic nerve, retinal
hemorrhage). In the neurological status note unstable emotional
background, disinhibition, excitement, sometimes confusion,
psychomotor stun or disorientation. Later, focal symptoms, coma may
develop. With a decrease in blood PRESSURE there is a rapid recovery
of brain function. Drugs of choice for reducing blood PRESSURE are
enalaprilat 0,625-1,25 mg/V, magnesium sulfate 10 ml of 25% solution
b / V, with convulsive syndrome-diazepam 2 ml of 0.5% solution b/V.
Ha complicated by acute coronary syndrome. Against the background

of high blood PRESSURE numbers can develop acute myocardial
ischemia. The clinic consists of symptoms of ha and anginous attack. On
ECG-signs of acute ischemia, myocardial infarction, acute blockade of
the leg of the bundle of GIS. Treatment is aimed at relieving pain,
improving myocardial nutrition and reducing blood PRESSURE:
* nitroglycerin sublingual in tablets, aerosol or spray, or intravenously

(under constant blood PRESSURE and heart rate control);
• morphine (narcotic analgesic) – 1 ml of 1% solution in/in divided by 4
to 10 ml every 5 to 15 min until the elimination of pain and shortness of
breath either before the emergence of side effects (vomiting,
hypotension, respiratory depression);
* propranolol (non-selective β-adrenoblocker) - in / slowly

administered 1 ml of 0.1% solution under the control of blood
PRESSURE, heart rate, ECG.
When reaching 160/100 mm Hg.assigned article anticoagulants and

antiplatelet agents required in the treatment of coronary artery
disease.
Ha, complicated by acute left ventricular failure. Develops stagnation

and increased pressure in the vessels of the small circle of blood
circulation, which leads to pulmonary edema. Clinical picture: position
of orthopnea, severe respiratory dyspnea,cyanosis of the skin. In
auscultation of the lungs – wet, finely bubbly rales on both sides.
Treatment is aimed at relief of pulmonary edema and decrease in blood
pressure. All patients should be given a sitting position with their limbs
lowered down, if possible, start oxygen inhalation, give nitroglycerin in
tablets or spray. For optimum blood pressure reduction is in/with the
introduction of enalaprilat 0,625-1,25 mg is Further added furosemide
1% solution in ampoules of 2 ml (20-100 mg). When the expanded lung
oedema often assigned morphine with the purpose of sedation, relief
of anginal pain, reducing shortness of breath. Contraindication to
morphine-respiration rate more than 40 per minute (overexcitation of
the respiratory center). The introduction of morphine in this situation
can cause respiratory arrest.
23. Миокардиты: определение, этиология, патогенез,
классификация, клиника, диагностика, дифференциальная
23. Myocarditis: definition, etiology, pathogenesis, classification,
clinic, diagnosis, differential diagnosis, treatment.
Myocarditis is a defeat of the heart muscle of predominantly

inflammatory nature, caused by the influence of infection, parasitic or
protozoal invasion, chemical and physical factors mediated through the
immune mechanisms, as well as occurs in allergic and immune diseases.
Classification
By the pathogenetic variants:
* infectious and infectious-toxic
* allergic (immunological), including infectious-allergic
* toxic-allergic
The prevalence of inflammation:
• focal
• diffuse
Adrift:
• acute
• subacute
• recurrent
• latent
• chronic
According to the clinical variant:
• oligosymptomatic
• pseudoternary
* decompensation
• arrhythmic
* pseudo-valve
• thromboembolic
• mixed
Clinical picture. Manifestations of myocarditis develop 1-2 weeks after

the onset of infection. Aching, stabbing pain in the heart without
intoxication, are not removed with nitrates, but with local use of
NSAIDs in the form of ointments and, especially, in combination with
indomethacin, gradually subside. There are also a weakness, weakness.
In some patients-the phenomenon of heart failure: shortness of breath,
swelling on the legs, most of the pulse more than 100 minutes.
Objectively: tachycardia, extrasystole, lowering blood PRESSURE.

Deafness I tones, soft systolic murmur, occupying 1/2 or more of the
systole. Pendulum rhythm shows large diffuse changes of myocardium.
Split tones, the appearance of III and IV tones, gallop rhythm. Fever,
often low-grade fever.
Instrumental diagnosis of myocarditis
1. The ECG can be repolarization changes, tachycardia, arrhythmia.

2. Radiological, echocardiographic, scintigraphic signs of cardiomegaly.
3. Subantimicrobial biopsy, and sometimes coronary angiography and

ventriculography is used in special cases to confirm the diagnosis.
The differential diagnosis is carried out with neurocirculatory dystonia,

ischemic heart disease, thyrotoxicosis, rheumatic heart disease,
osteochondrosis.
Treatment. Bed rest up to 3 weeks. According to the indications-

antibacterial and antiviral therapy. Desensitizing agents can be used as
an auxiliary therapy. In severe myocarditis of non – viral etiology-
glucocorticoids. Means to improve metabolism in the myocardium
(vitamins B1, B6, Riboxin, Mexico, Neoton, etc.) after elimination of the
pathogen.
24. Этиология, патогенез и классификация первичных КМП.

Дилатационная кардомиопатия. Клиника, диагностика,
особенности течения, лечение.
24. Etiology, pathogenesis and classification of primary MMR. Dilated

cardiomyopathy. Clinic, diagnosis, features of the course, treatment.
Cardiomyopathies (CMP) are diseases of the myocardium of unknown

etiology resulting in dysfunction of the heart.
According to the etiological principle, primary and secondary CMPS are

distinguished. Primary KMP-genetically determined lesions of the heart
muscle (associated with mutations in the genes of structural proteins of
cardiomyocytes), mixed (dilated, restrictive), acquired (inflammatory,
peripartal, arrhythmogenic KMP). Secondary ILC associated with diffuse
involvement of the myocardium.
There are 4 groups of primary CPM: dilated, hypertrophic, restrictive,
arrhythmogenic right ventricular dysplasia.
Dilated cardiomyopathy (dkmp) is more common in men, especially in

the age of 30-50 years. In the Genesis of dkmp is important genetic
predisposition; the impact of exogenous factors (Coxsackie viruses,
hepatitis C, herpes, cytomegalovirus, alcohol); autoimmune disorders.
At the heart of the formation of dkmp is the primary damage and death
of cardiomyocytes.
DCM is clinically manifested with three main syndromes:
1. Systolic CHF (left ventricular or biventricular).
2. Frequent occurrence of arrhythmias and conduction (ventricular

arrhythmias, atrial fibrillation, AV blockade and blockade of the legs of
the bundle of GIS).
3. Thromboembolic complications (pulmonary embolism and embolism

of the arteries of the systemic circulation).
Characterized by rapid and steady progression of the disease and signs

of decompensation, as well as refractory to traditional treatment of
CHF. Sometimes patients note pain in the heart, different from the
typical attacks of angina. Sudden death in dkmp can occur as a result of
fibrillation, asystole or thromboembolism in the pulmonary trunk or
brain vessels.
At General examination, signs of heart failure are detected. The apical

push is strengthened, spilled and shifted to the left and down.
Epigastric pulsation can often be detected. Expansion of borders of
relative cardiac dullness by percussion. Absolute dullness of the heart is
usually expanded by dilation of the right ventricle. Auscultation of the I
tone at the apex is weakened. The protodiastolic rhythm of the gallop
at the top. Characteristic systolic murmurs at the top and at the point
of listening to the tricuspid valve.
On the ECG signs of LV hypertrophy and PL, sometimes in combination

with hypertrophy of the pancreas, depression of segment RS-T in the
left chest leads; signs of blockade of the left bundle branch block; atrial
fibrillation or other arrhythmias; lengthening of the interval QT.
Echo: significant LV dilatation with normal or reduced thickness of its

walls and reduced EF (below 30-20%). Expansion of other chambers of
the heart is often noted. As a rule, total hypokinesia of the walls of the
LV develops. Often visualized intracardiac mural thrombi.
X – ray examination-signs of cardiomegaly; smoothness of the contours

of the left heart; spherical heart shape; signs of venous and arterial
pulmonary hypertension and the expansion of the roots of the lungs.
Coronary angiography and ventriculography are used for differential

diagnosis of dkmp and IBS.
Endomyocardial biopsy allows to detect intensive fields of interstitial

and perivascular fibrosis with minimal necrosis and cell infiltration.
Treatment of DCM:
Limitation of physical activity, consumption of salt. ACE inhibitors are

the first choice in the treatment of patients with dkmp at all stages of
the disease. β-blockers are indicated in patients with persistent sinus
tachycardia, as well as in patients with atrial fibrillation. Diuretics are
used in the presence of stagnation of blood in the lungs and/or in a
large circle of blood circulation. Nitrates contribute to the deposition of
blood in the venous bed of a large circle of blood circulation, reduce the
amount of preload and signs of stagnation of blood in the lungs. Cardiac
glycosides are indicated in patients with a constant form of atrial
fibrillation.
The use of antiaggregants is indicated in all patients with dkmp,

because in 30% of cases the course of the disease is complicated by
intracardiac thrombosis and the development of thromboembolism.
Patients with dkmp with atrial fibrillation shows the appointment of
indirect anticoagulants (warfarin).
Indications for heart transplantation surgery are: rapid progression of

heart failure and the lack of effect of the therapy; the occurrence of
life-threatening heart rhythm disorders; high risk of thromboembolic
complications.
The use of artificial left ventricle can be considered in the framework of

pre-transplantation preparation of patients with dkmp. The use of a
mesh frame made of organic polymers in dkmp provides an
improvement in the quality of life of patients, but does not have a
positive effect on the prognosis.
Two-chamber cardiac electrostimulation with an implantable

pacemaker such as DDD in some cases can improve intracardiac
hemodynamics by increasing the systolic function of the ventricles and
prevent the development of some complications of the disease.
25. Этиология, патогенез и классификация первичных
кардиомипатий. Гипертрофическая КМП. Клиника, диагностика,
25. Etiology, pathogenesis and classification of primary

cardiomyopathy. Hypertrophic cardiomyopathy. Clinic, diagnosis,
features of the course, treatment.



Hypertrophic cardiomyopathy (hcmp) is a primary myocardial lesion

characterized by severe hypertrophy of the left ventricular (LV)
myocardium (less often the right ventricle), normal or reduced size of
the LV cavity, a significant violation of the diastolic function of the
ventricle and the frequent occurrence of cardiac arrhythmias.
Distinguish between asymmetrical and symmetrical forms of HCM. For

the symmetrical form of hcmp is characterized by almost the same
thickening of the anterior, posterior walls of the LV and interventricular
septum (MWP) – concentric hypertrophy of the LV. Most often there is
an asymmetric form with predominant hypertrophy of the upper,
middle or lower third of the MW. The thickness of the IVS can reach 50-
60 mm. In some cases of hypertrophy of the IVS combined with the
increased muscle mass of the anterior or anterolateral wall of the LV
during the normal thickness of the rear wall. In some cases, the
predominant hypertrophy of the apex (the apical form of HCM). In an
asymmetric (or total) defeat of the IVS with the obstruction of the
output tract of the left ventricle is talking about idiopathic subvalvular
subaortic (muscle) stenosis.
Heart weight increases sharply, reaching in some cases 800-1000g. The

LV cavity is usually narrowed. Increased rigidity of hypertrophied
muscle leads to diastolic dysfunction.
The incidence of gkmp is 2-5 people per 100 thousand population or 2-

3 cases per 1000 young people (20-35 years). Hypertrophic KMP is
inherited by autosomal dominant type (50% of cases) or occurs
sporadically.
It may be asymptomatic. The first clinical manifestation of the disease

may be sudden death (more often – children and adolescents, often
during or after physical activity). Clinical manifestations of the disease
are most often characterized by shortness of breath, symptoms of
angina, fatigue, syncopal or presyncopal conditions.
In obstructive form there are symptoms of muscular subaortic stenosis:

chest pain, dizzy spells with a tendency to unconscious States,
pristupoobraznaya night breathlessness, double or triple apical
impulse, loud systolic murmur in the III-IV intercostal spaces at the left
edge of the sternum, is not performed in the carotid arteries with a
maximum at mid-systole, sometimes combined with a systolic murmur
of regurgitation, caused "papillary" mitral regurgitation. Frequent
arrhythmias and violation of intracardiac conduction. The progression
of hypertrophy can lead to the development of heart failure.
On ECG – signs of hypertrophy of the left ventricle and widening of the

Q-wave in many leads (II, III, aVF, V4-6). On the daily monitoring of ECG
recorded rhythm disturbances (atrial and ventricular). Radiography of
the chest cavity-a slight or moderate increase in the contour of the
heart or without deviations.
The main method of diagnosis of HCM is echocardiography. In patients

with obstruction, a systolic movement forward of the mitral valve
leaflet is detected. Radionuclide scintigraphy with thallium-201 scans
and blood volume allow you to visualize the size and orientation seem
to be.
Histological examination of the myocardium reveals disoriented chaotic

location of cardiomyocytes, myocardial fibrosis in the form of diffuse or
focal development of connective tissue in the heart muscle.
In the treatment of hcmp used β-blockers (reduce the severity of

angina and syncope, protect the patient from sudden death). Effective
combination of cordarone with β-blockers. Calcium channel blockers
reduce the diastolic pressure in the LV.
Surgical myotomy / myoectomy of hypertrophied septum can lead to

long-term symptomatic improvement, but high mortality, reaching
10%, makes use of this operation only in patients with severe disease
and a high degree of obstruction, resistant to drug therapy.
It is necessary to avoid the appointment of digitalis, diuretics, nitrates,

β-adrenergic agonists, nifedipine, especially in the presence of a
pressure gradient in the outflow from the left ventricle.
The natural course of hypertrophic cardiomyopathy is very variable,
many patients ' health improves or stabilizes over time. However, it is
possible to develop atrial fibrillation, endocarditis, left ventricular
dilation and dysfunction with the disappearance of the pressure
gradient and, consequently, symptoms of the disease.
26. Этиология, патогенез и классификация первичных

кардиомипатий. Гипертрофическая КМП. Клиника, диагностика,
26. Etiology, pathogenesis and classification of primary

cardiomyopathy. Hypertrophic cardiomyopathy. Clinic, diagnosis,
features of the course, treatment.



Restrictive cardiomyopathy (RCMP) is characterized by a violation of

the diastolic filling of the left and/or right ventricle, a decrease in their
volume, as well as normal or almost normal systolic function. The walls
of the ventricle acquire a significant rigidity and prevent the filling of
the ventricular cavity.
Causes of RCMP:
1. Idiopathic restrictive cardiomyopathy (endomyocardial fibrosis,

eosinophilic endomyocardial infiltration of Leffler)
2. Secondary restrictive cardiomyopathy (hemochromatosis,

amyloidosis, sarcoidosis, scleroderma, carcinoid, glycogen accumulation
disease).
RCMP causes 25% of deaths in young patients due to cardiac pathology

among natives of Africa, South America and India.
At General examination it is necessary to identify the extracardial signs

of possible systemic diseases in which there is a RKMP. Heart sounds
can be muted, often heard III and IV tones. Unlike constrictive
pericarditis, the apical push is usually well palpated.
Diagnosis of RCMP. Blood test: an increase in the number of eosinophils

may indicate eosinophil endomyocardial infiltration. Radiography of the
chest cavity - no cardiomegaly, normal cardiac silhouette,
manifestations of pulmonary venous hypertension and stagnation, no
calcification of the pericardium. ECG: low voltage, non-specific ST and T
changes, various arrhythmias.
Echocardiography: symmetrical thickening of the walls of the heart

chambers, normal or slightly reduced ventricular volume and systolic
function, rapid early diastolic filling, slow late diastolic filling.
Cardiac catheterization: increased ventricular end-diastolic pressure,

impaired left ventricular diastolic function, normal or slightly reduced
ejection fraction.
Endomyocardial biopsy: typical eosinophilic infiltration in the
inflammatory stage, myocardial fibrosis in the later stages.
Complications of RCMP: thromboembolism, arrhythmia, cardiac

cirrhosis, progressive deterioration of cardiac function.
Treatment of RCMP. Idiopathic forms of RCMP have no specific

treatment. Symptomatic therapy: diuretics, cardiac glycosides,
vasodilators, antiarrhythmic and anticoagulant drugs according to
indications. Surgical treatment – andacademia.
Arrhythmogenic right ventricular dysplasia (ARVD) is pathology of

unknown etiology, which represents an isolated involvement of the
right ventricle. Is characterized by adipose or fibro-adipose infiltration
of the myocardium of the ventricles. Accompanied by ventricular
arrhythmias. Is characterized by late involvement of the left ventricle
with relative Intertoto partitions. The first clinical manifestations can
occur in adolescence, rarely after 40 years. Inheritance in different
families and on autosomal dominant, and on autosomal recessive type
is proved. The disease is more often registered among athletes.
Clinical manifestations of ARVD is characterized by the presence of

ventricular arrhythmias. Sudden cardiac death may be the first
manifestation of the disease. The main clinical symptoms: a feeling of
heartbeat, heart failure, fatigue, dizziness, fainting, symptoms of heart
failure, sudden stop of blood circulation.
ECG and daily ECG monitoring: persistent or unstable ventricular

tachycardia with signs of blockade of the left leg of the bundle of GIS,
frequent ventricular extrasystole, negative t teeth in V1-4 leads against
the background of sinus rhythm, broadening of the QRS complex,
incomplete blockade of the right leg of the bundle of GIS, ventricular
fibrillation, atrial tachycardia, atrial fibrillation.
Echo: dilatation, impaired contractility and the reduced ejection

fraction of the right ventricle, local aneurysm of the right ventricle. To
confirm the diagnosis using the x-ray contrast ventriculography.
Endomyocardial biopsy shows fibrotic fat infiltration of the right
ventricle.
Drug treatment is antiarrhythmic therapy for life-threatening

tachyarrhythmias. The most effective implantation of cardioverters-
defibrillators in patients with malignant ventricular arrhythmias.
The most effective is surgical treatment-heart transplantation.
27. Специфические кардиомиопатии на фоне интоксикаций,

«болезней накопления», гастроэнтерологических и эндокринных
заболеваний: клинические особенности и принципы
дифференциальной диагностики.
27. Specific cardiomyopathies against the background of intoxication,
"accumulation diseases", gastroenterological and endocrine diseases:
clinical features and principles of differential diagnosis.
At the heart of secondary cardiomyopathy, regardless of etiological

factors are dystrophic changes in cardiomyocytes.
Alcoholic cardiomyopathy
Alcohol abusers may develop a clinical picture identical to that of

dilated cardiomyopathy: significant dilation of the heart chambers,
systolic and diastolic myocardial dysfunction and the absence of severe
hypertrophy of the heart muscle, high frequency of arrhythmic and
embolic complications.
Of course, alcoholic cardiomyopathy is the main form of secondary

cardiomyopathy in the West. Cessation of alcohol consumption before
congestive heart failure may stop the progression or even reverse the
development of the disease, while primary cardiomyopathy is
characterized by a constant progression of the disease.
Alcoholic cardiomyopathy is associated with low cardiac output and

systemic vasoconstriction.
The key to the treatment of patients with alcoholic cardiomyopathy is

the absolute refusal of alcohol consumption.
Medicinal cardiomyopathy
A variety of drugs can cause acute myocardial damage, leading to

sudden onset of congestive heart failure and death, or affect the
myocardium for a long time, gradually causing damage to it.
Anthracycline derivatives, in particular doxorubicin (adriamycin), being

powerful anticancer drugs, in large doses can cause fatal heart failure.
The occurrence of heart failure contributes to a number of risk factors:
irradiation of the heart, age over 70 years, concomitant heart disease,
hypertension, the use of cyclophosphamide (cyclophosphane).
Radionuclide ventriculography can detect preclinical signs of left
ventricular dysfunction and facilitates the selection of the drug dose. In
50% of patients without clinical signs of the disease, receiving standard
doses of the drug, for many years after discontinuation of treatment
with radionuclide ventriculography can be detected dysfunction of the
left ventricle. The risk of cardiotoxicity decreases with slower
administration of the drug, as well as with the use of a specific
cardioprotector – cardioxan.
Cyclophosphamide, administered in high doses, can cause severe heart

failure or acute within 2 weeks after the start of treatment. The
characteristic histological signs are edema and myocardial necrosis. In
rare cases, patients receiving 5-fluorouracil (fluorouracil), there are pain
in the chest and electrocardiographic signs of myocardial ischemia or
heart attack.
Hemochromatosis
it should be suspected in cases where cardiomyopathy occurs on the

background of diabetes, liver cirrhosis, skin hyperpigmentation.
Phlebotomy is informative when it is performed in the early stages of
the disease. With long-term subcutaneous administration of
desferrioxyamine, the iron content in the body in cases with severe
course of the disease may decrease, but it is not clear whether this
leads to clinical improvement.
Myocardial sarcoidosis
usually accompanied by other clinical manifestations of systemic

disease, it can occur with signs of both diastolic and systolic dysfunction
of the ventricular myocardium, as infiltration of the heart with sarcoid
granulomas causes not only an increase in myocardial rigidity, but also
reduces its systolic contractile function. A variety of arrhythmias,
including atrioventricular blockade, can be registered.
Transvenous endocardial biopsy (more often right ventricle) is

increasingly used to obtain tissue samples for histological examination
and electron microscopy. This relatively simple and safe method is very
important for the diagnosis of myocardial diseases, especially
infiltrative processes such as amyloidosis, hemochromatosis,
sarcoidosis.

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1.

Инфаркт миокарда: роль неинвазивных и инвазивных методов

Non-specific clinical and laboratory signs of AMI are:

1. Body temperature rise (from subfebrile numbers to 38.5–39°C).

2. Leukocytosis, not exceeding usually 12-15 x 109/l.

3. A small stick-nuclear shift of the blood formula to the left.

The most sensitive and specific marker of necrosis of cardiomyocytes is

Changes in the activity of some enzymes in AMI

Enzyme Start increasing the activity of the h Peak of increased activity,

MV-fraction KFK 4-6 12-18 2-3

CFC 6-12 24 3-4

LDG 8-10 48-72 8-14

ASAT 4-12 24-36 4-7

ECG diagnosis of myocardial infarction.

Violation of coronary circulation in THEM leads to the formation of

1. Necrosis zone-pathological q wave (lasting more than 30 MS) and a

2. Area of ischemic damage — the offset segment RS–T is higher (if

3. A zone of ischemia — “coronary” (equilateral pointed) T wave

Doppler echocardiography, when they allow:

 to identify violations of local contractility of the left ventricle;

 quantitatively assess systolic and diastolic LV function;

 to identify the signs of LV remodeling (dilatation of the cavity of the

 to identify echocardiographic parameters of LV aneurysm;

 to assess the condition of the valve apparatus and the presence of

 to assess the level of pressure in the AIRCRAFT and to identify signs of

 detect the presence of intracardiac blood clots;

 to evaluate the morphological and functional changes of the main and

The use of the technique of myocardial scintigraphy with technetium is

2. Атипичные формы начала инфаркта миокарда: клиника,

2. Atypical forms of myocardial infarction: clinic, diagnosis, differential

There are several clinical variants of the beginning of IT:

 pain (angina), I (status anginosus)

 asthmatic variant (status asthmaticus);

 abdominal variant (status abdominalis);

Asthma is the result of early development of acute left ventricular

1. Heart asthma occurs as a result of interstitial pulmonary edema.

2. Alveolar pulmonary edema is characterized by the release of plasma

3. Cardiogenic shock is an extreme degree of left ventricular failure,

Arrhythmic variant of MI is the development of cardiac rhythm and

Life-threatening arrhythmias, which are the direct causes of death,

To arrhythmias, aggravating heart failure and causing hypoperfusion of

The harbingers of life-threatening cardiac arrhythmias include: short

The abdominal variant of the beginning IS characterized by the

The cerebrovascular clinical variant of the beginning of IT is

It is characterized by the appearance of pain syndrome in the left half

3. Лечение инфаркта миокарда неосложнённого течения.

3. Treatment of myocardial infarction uncomplicated course.

Treatment of uncomplicated myocardial infarction with q wave

The main strategic goals of treatment of patients in the prehospital and

1. Early myocardial reperfusion or coronary revascularization, as well as

2. Limiting the focus of necrosis and periinfarction ischemic area by

3. Prevention or early elimination of complications.

4. Physical and psychological rehabilitation of patients.

The purpose of therapy is:

 pain relief (analgesia);

 thrombolytic therapy (including indications and contraindications);

 antithrombotic and antiplatelet therapy;

 the use of anti-ischemic drugs;

 application of ACE inhibitors and receptor antagonists to angiotensin

A classic means of relieving pain in patients with IT is the use of narcotic

Oxygenotherapy is indicated for all patients with IT.

A prerequisite for the management of patients IS the appointment of