Embolism – fatty, airy, pulmonary, gas and embolism of arteries and vessels

Each type of embolism has its own causes.

Atrial fibrillation and other heart rhythm disturbances;

Aneurysm of the left ventricle;

Diseases of the venous system of the pelvis and limbs (thrombophlebitis, varicose veins, post-thrombophlebitis syndrome);

Large operations on the pelvic organs, abdomen and limbs;

With air embolism:

Traumatic damage to large veins;

Gross violations of the technique of intravenous manipulation;

Surgical interventions in gynecology with a violation of the technique of their implementation, abortion and difficult birth.

With fat embolism:

Massive limb injuries;

Intravenous administration of banned fat-containing drugs;

The causes of embolism are various. Blood clots along the walls of the left ventricle occur when the heart muscle is damaged. This is characteristic of aneurysm of the heart, an extensive myocardial infarction. In a large circle of blood circulation, embolism of arteries occurs when a blood clot moves from the heart to the periphery, causes thrombosis in the extremities, in the mesentery of the intestine, splenic, renal and cerebral vessels.

Pathogenesis and morphogenesis of diseases. The concept of “symptoms” and “syndromes”, their clinical significance

Sudden pain behind the sternum or in one of the half of the chest;

Drop in blood pressure (90/50 and below);

Shortness of breath and shortness of breath (over 20);

Tachycardia (more than 100) and heart rhythm disturbances;

Severe general weakness;

Cough and hemoptysis (join later).

Lack of coordination of movements;

Movement disorders such as paresis and paralysis;

Severe burning pain in the abdomen;

Bloody fluid stool;

Tachycardia and lowering blood pressure;

Lack of rumbling and intestinal motility;

Pain in the projection of the affected kidney;

Red color of urine;

Oliguria (the amount of urine is below normal).

Sudden pain at the site of localization of the embolus, which then spreads to the entire limb;

Pallor of limb skin;

Cooling of the affected segment and its numbness;

The impossibility of active and passive movements;

Signs of gangrene (bubbles with dark fluid, black spots).

(pathos – disease, genesis – development) – teaching
about the general laws of development,
course and outcome of diseases. Pathogenesis
reflects the nature of damage at different
vital levels and mechanisms
compensatory adaptive reactions
with the development of the disease.

pathogenesis considering system
protective processes aimed at
recovery of disturbed processes
and stopping the disease, called
sanogenesis (sanis – health, genesis –
development). Sanogenesis, like pre-disease,
is not an established concept,
some pathologists (school S. M. Pavlenko)
assign him the role of a paired to pathogenesis
categories with their many

(morphos – form, genesis – development) considers
the dynamics of structural disorders in organs
and systems with the development of the disease. FROM
over time, including under
a variety of treatment methods
there is a gradual change in patho
and morphogenesis of the disease – terms change
currents, outcomes, percentage of complications and
etc. This process is called pathomorphism.

pathomorphosis is clearly seen in the example
infectious diseases under the influence
systematic (in population) application

body unity (interdependence
and the relationship of violation processes
structures and functions) – one of the main
provisions of nosology. In accordance with
this in pathology is not isolated
“Functional” or “structural”
defects, but always present them
system. In this sense, morphogenesis is much
it’s more logical to consider the paired category
to pathogenesis than sanogenesis.

category is the relationship of local
and general
with the development of the disease. Illness is always
general process in the body however
set of local manifestations and
makes up all its originality.

it should be noted the category of reversibility.
When it comes to returning to a loved one
condition (e.g., recovery
after illness) such processes are convenient
call reversible, and those where return
not happening – irreversible. Category
may apply not only to the body
in general, but to specific it
morphofunctional features.

and non-specific
in the development of the disease also go side by side.
The more general pattern is revealed
with the disease, the less it is specific
and is present with many others

causative disease
factor develops consistent
complex of processes determining
specificity, the essence of the disease, its uniqueness.
Such a complex is called leading
link of pathogenesis.

the development of the disease is often a sequence
processes locked in the so-called
“Vicious circles” when subsequent
changes lead to increased primary

pathogenesis distinguish the following levels

– a sign of illness.

symptoms: subjective and objective.
To objective
include: patient examination, palpation,
percussion (percussion) and auscultation
(listening). Subjective
symptoms are sensation
the patient. This is a reflection in the mind.
patient pathological changes in
the body.

Is a collection of closely related
symptoms reflecting certain
pathological changes in systems and
tissues. For example: edema syndrome (edema,
ascites ascites, pallor or cyanosis
skin); bronchospastic (choking,
cough, wheezing during auscultation); syndrome
shock (weakness, skin moisture, filiform
pulse, low blood pressure).

What is embolism?

Embolism is a pathology, exclusively, of the arterial vascular bed, which is based on the overlap of its lumen at a certain level with a partial or complete cessation of blood flow caused by factors unrelated to the pathology of the affected vessel. Emboli are called those substances of the internal environment of the body or the environment that block the vascular lumen. It means that:

Embolism is caused by the ingress or migration of emboli into the arteries of the large or small circle of blood circulation from other parts of the vascular bed;

Emboli can have a different nature: blood clots, blood clots, detached atherosclerotic plaques, fat cells and oily solutions, air;

Arterial and venous vessels of any localization, as well as the heart, can become sources of emboli;

The diameter of the embolus determines the caliber of the artery that it blocks;

It is impossible to predict which pool of the arterial vascular bed the embolus will enter.

The pathogenesis of embolism can take place in three ways:

The source of emboli are arterial vessels. In this case, the pool in which the breakdown occurred is affected. In this case, a thrombus or atherosclerotic plaque, breaking away from its place in a vessel of large diameter, becomes an embolus and migrates to smaller vessels in the basin of its branching;

Venous vessels are the source of emboli. Their role may be blood clots, air, fat cells. Their migration is a little more complicated, since they first enter the veins into the heart, from where they are ejected in any direction (brain, limbs, intestines, kidneys, etc.);

The source of emboli is the heart. These are, as a rule, small blood clots that form against the background of arrhythmias. After they come off from the usual place of localization, they migrate to any arterial vessels.

Embolism is always an acute condition requiring urgent measures. The entry of emboli into arterial vessels leads to a cessation of blood flow. This is fraught with the occurrence of ischemia, which can turn into gangrene or organ infarction (within 6-12 hours). This feature distinguishes it from arterial thrombosis, which is a chronic process that compensates for lost blood flow due to collateral (additional) vessels.

The embolus classification is based on the type of embolus and its final localization after the cessation of migration. The main types of embolism are shown in the table.

Type of embolism by origin of embolus

Type of embolism according to the location of the embolus

Thromboembolism (thrombi of arteries, veins and heart act as an embolus)

Carotid artery thromboembolism and their branches;

Thromboembolism of the subclavian arteries and its branches (upper limbs);

Thromboembolism of the visceral branches of the aorta (mesenteric and renal arteries);

Thromboembolism of the iliac, femoral arteries and their branches (lower extremities);

Combined multiple lesions of the arterial bed in several pools.

Air and gas embolism (emboli are formed when air enters the veins or from vesicles of blood gases)

Fat embolism (emboli are fat cells or substances)

From the table it becomes obvious that regardless of the nature of the embolus, any of the arterial vessels can be its final location.

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Fat embolism

Fat embolism occurs as a result of the penetration of drops of fat from molten or destroyed fat cells in the body into the venous bed. This is possible with massive injuries (injuries to the bones and soft tissues of the limbs, pancreatic necrosis). Another source of fat embolism may be intravenous fat solutions that are not intended for this route of administration.

Once in the bloodstream, drops of fat are not able to dissolve in the blood. Their spacing throughout the arterial bed leads to the accumulation of fatty particles in certain places. If there are more of them than the diameter of the vessel, this leads to signs of impaired blood flow. As a rule, fat embolism is relatively not difficult, as it affects small vessels.

It is an overlap of the lumen of arterial vessels with air or gas bubbles. This is possible with damage to large veins, especially in the neck. If such a wound is not closed in time, and the vein is squeezed, this can result in suction of air into its lumen, which with a blood stream enters the heart and spreads throughout the arterial pools.

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Gas embolism occurs without impaired vascular integrity. Its origin is responsible for sudden changes in atmospheric pressure. This is possible with scuba divers and is called decompression sickness. If a diver quickly rises from great depths, the gas mixture inhaled by him does not have time to digest as quickly as it did at high depths. As a result, undissolved air bubbles that block small arterial vessels throughout the body.

Pulmonary embolism

One of the most frequent and formidable embolism is pulmonary embolism. In most cases, it is represented by thromboembolism. Regardless of the specific nature of the embolus, the manifestations of the disease with vascular lesions of a certain diameter will be identical. On this basis, pulmonary embolism is classified as follows:

Embolism of the central trunk of the pulmonary artery;

Embolism of large branches of the pulmonary artery;

Embolism of small branches of the pulmonary artery.

The first form of the disease is considered the most formidable condition. This is due to the possibility of reflex cardiac arrest at the time of embolism as a result of the pulmonary coronary reflex. This is possible only with thromboembolism, when large blood clots become emboli and are fixed at the mouth of the pulmonary artery.

Air and fat embolism lead to the defeat of only small branches of the pulmonary artery and do not cause severe manifestations. The exception is cases of massive ejection of small blood clots with a constant new ejection from the heart. The defeat of large branches of the pulmonary artery often results in death due to the development of acute cardiopulmonary failure or pulmonary infarction.

Thromboembolic lesions of the arteries of the brain, intestines and kidneys are considered its most dangerous types. In all cases of damage to large main vessels, necrosis of the corresponding organ occurs within a short time (kidney infarction, intestinal gangrene, brain stroke). This will lead to either profound disability or death.

Embolism of the peripheral arteries of the extremities is much easier. Usually, they are easy to diagnose, since such conditions occur very acutely and are accompanied by a vivid clinical picture. Timely surgery, prevents severe consequences. Otherwise, gangrene of the limb occurs.

Since embolism is an acute disease, its treatment requires urgent measures. The sooner they are provided, the better the prognosis for the patient. Differentiated therapeutic tactics are given in the table.

The complex of therapeutic measures

Emergency surgery – thromboembolectomy. It is indicated in the early stages after the onset of the disease (preferably up to 6 hours). It is performed on all arteries of large and medium caliber, including the arteries of the intestine and brain. In the pulmonary and renal arteries, thromboembolectomy is practically not performed due to technical difficulties and the severity of the patient’s condition (high operational risk). On the extremities, the intervention is performed under local anesthesia and is not difficult. The main criterion for its feasibility is the lack of limb contracture. During the intervention, thromboembolas are removed from the arteries using a special Fogarty probe;

Emergency fibrinolysis. The most common type of treatment is the inability to perform thromboembolectomy. Its focus is the dissolution of thromboembolism. For these purposes, pharmacokinase, alteplase, arikstra are used;

Anticoagulant therapy – blood thinning. It is best to use regular heparin, which is later replaced by its analogues (fraxiparin, clexane);

Improving the rheological properties of blood and metabolic therapy for affected tissues (rheosorbilact, refortan, trental, actovegin, corvitin, metamax, ascorbic acid);

Symptomatic events. They are aimed at maintaining the basic parameters of homeostasis – hemodynamic parameters and respiration. For this, cardiac glycosides (strophanthin, korglikon), glucocorticoid hormones (prednisone, dexamethasone), diuretics (furosemide), nitrates (nitro-mic, isoket), aminophylline, oxygen instillation, cerebroprotectors (ceraxone, piracetam) are introduced;

After stopping the critical condition, an adequate amount of nutrition (including parenteral) is prescribed, antibiotic prophylaxis of complications of an infectious nature, stress ulcers and bleeding;

Give the lower end of the body an elevated position. At the same time, the head drops slightly;

If a central venous catheter is installed, try to aspirate the air with a syringe;

With progressive worsening of the condition, it is recommended that patients be transferred to artificial lung ventilation and resuscitation;

Hyperbaric chamber treatment and hyperbaric oxygenation;

Stabilization of hemodynamic parameters and infusion therapy.

Stabilization of vital parameters in case of their violation (mechanical ventilation, resuscitation measures);

Instillation of an oxygen mixture;

Drugs that contribute to the dissolution of fat emboli (essentiale, lipostabil, decholine);

Glucocorticoid hormones (dexamethasone, hydrocortisone, prednisone);

Anticoagulants (heparin, clexane);

Cardiac glycosides and other symptomatic drugs, depending on the prevailing clinical picture.

Preventive measures are divided into several sections.

taking anticoagulants (aspirin, cardiomagnyl, warfarin);

Monitoring of blood coagulation indicators (APTT, PTI INR), especially in people at risk for thromboembolic complications;

Timely and adequate treatment of heart rhythm disturbances;

Elimination of venous pathology of the lower extremities;

Installation of cava filters in people at risk;

Elastic compression of the legs and prophylactic doses of anticoagulants in people at risk who have surgery;

Dosed physical and mental stress.


It is impossible to know in advance about embolism, however, the probability of occurrence should always be expected with appropriate surgical interventions and therapy of heart diseases. Therefore, to prevent embolism, drugs that reduce blood coagulation are prescribed, they require curing of carious teeth and other foci of chronic infection before a planned operation.

Embolism is treated in four main areas:

  • maximum preservation of ischemic organ;
  • anti-shock measures;
  • removal of the embolus and restoration of patency of the vessel;
  • prevention of sepsis through the use of antibiotics.

Removal of parietal thrombi, sources of embolism, in peripheral veins

Most often, events are equated with resuscitation. The patient is transferred to artificial respiration, large doses of Fibrinolysin, Heparin are introduced to dissolve the thrombus, fluids that normalize the properties of blood (Reopoliglyukin), drugs to activate collaterals, hormonal drugs.

Catheterization of large vessels and the heart is possible only in specialized clinics, it will be successful if applied in a few minutes after an embolism.

One of the latest developments for the prevention of embolism is the installation of special filters in large vessels that do not pass emboli into vital arteries.

To avoid embolism in the future, you need to deal with the prevention of diseases and maintaining health now.

The fate of the clogged vessel and the consequences

Arterial embolism contributes to narrowing or complete obstruction of the vessel. The consequence is a malnutrition of the body receiving blood along this branch. At the site of blockage of the vessel, the blood flow slows down, this helps the formation of a secondary thrombus. The viability of the affected organ depends on the speed of formation of the network of collaterals, additional vessels bypassing the blocked. With good opportunities, they develop in a few hours and completely replace the lost blood supply.

For this, the following matters:

  • the ability of the heart to eject blood under high pressure to open the auxiliary vessels and increase blood flow;
  • properties of the vessels themselves to eliminate spasm.

With heart diseases with chronic or acute heart failure, severe atherosclerosis, such results can not be expected.

Embolism Prevention

Compliance with the rules of smooth ascent from high depths by divers;

Correct and fast treatment of wounds with damage to venous vessels;

The correct laying of women on the operating table during gynecological operations, thorough and quick dressing of damaged veins;

Strict adherence to the technique of intravenous injection;

Prevention of fat embolism:

Fast and persistent immobilization of a damaged limb;

Early surgical interventions or other methods of reposition, leading to stabilization of bone fragments;

Compliance with the rules of intravenous administration of drugs.

Article author: Volkov Dmitry Sergeevich | K.M. surgeon, phlebologist

Education: Moscow State University of Medicine and Dentistry (1996). In 2003, he received a diploma from the educational and scientific medical center for managing the affairs of the President of the Russian Federation.

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Pathogenesis and morphogenesis of diseases. The concept of “symptoms” and “syndromes”, their clinical significance

blood circulation is shared:

liver vein;

the vascular system is smaller
vessels, arterioles and venules;

channel – blood and lymph circulation in

two types of violation
blood circulation:

– occurs during a load;

– manifests itself in a state of physical

Clinical and morphological
manifestations of circulatory disorders:

skin integument;

circulatory disorders:

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heart function;

(violation of vascular tone);

both of the above functions.

Manifestations of the disease depend on the diameter of the vessel and the organ or part of the body that is fed from it. A sign of embolism of an limb artery is acute pain. The mechanism of pain is considered to be overstretching of the artery wall at the site of thrombus insertion and irritation of nerve fibers. Spasm of the vessel occurs reflexively. At night the pain intensifies.

On palpation, you can feel the absence of a pulse below the site of thrombosis. The skin of the limb turns white, it becomes cold to the touch. Cyanotic spots appear at your fingertips. There is a decrease in skin sensitivity.

Gangrene of the foot after embolism of the shin vessel

After 6 – 8 hours from the moment of embolism, provided that the blood supply is completely stopped, symptoms of tissue necrosis (gangrene) appear. In this case, the pain becomes very intense. Dry gangrene usually develops.

With fat embolism

Clinical manifestations occur 1 to 2 days after an injury, surgery or other critical condition. There are two types of embolism:

  • pulmonary – occurs in 60% of all cases, the patient suddenly has suffocation, blue face, cough with hemoptysis, pulmonary edema is possible;
  • cerebral – sudden loss of consciousness or loss of orientation, agitation, delirium, convulsions.
  • At the same time, signs of acute heart failure appear: a drop in blood pressure, tachycardia, and rhythm disturbance.

You can read more about fat embolism in this article.

The scheme of damage to the cerebral arteries

Pulmonary embolism is a complication of not only heart disease, but also surgical interventions. After surgery, it develops unexpectedly during the patient’s recovery period against the background of a general improvement, even before discharge from the hospital. Statistics determine up to 6% of this postoperative complication. The frequency directly depends on the duration of the operation.

With heart diseases (acute myocardial infarction, aneurysm, malformations, atrial fibrillation), an embolism in the pulmonary artery is possible. The largest vessel is not always clogged. Most often, the embolus enters the narrower artery of the lower lobe of the right lung. With the defeat of the main vessel, a lethal outcome occurs. Clinical symptoms do not have time to develop, but when examining the deceased, they pay attention to the sharp redness of the upper parts of the body.

If the embolus is localized in small branches, it causes pulmonary infarction. The patient complains of a sharp sudden pain in the side, shortness of breath, cough, sometimes with hemoptysis. Following a heart attack, pneumonia develops, pleurisy.

Three groups of symptoms can be distinguished:

  • neurovascular – anxiety, fear, pain in the heart, palpitations, decreased blood pressure;
  • pulmonary – pains in the side, hemoptysis, cough, shortness of breath;
  • general – fever, yellowness of the skin and sclera, leukocytosis in a blood test.

Embolism of the abdominal aorta is more common with rheumatic heart disease. The embolus is located on the branching of the aorta and leads to subsequent secondary thrombosis. The main symptoms are sudden pain in the legs, their blanching and cooling, the disappearance of pulsation in the arteries of the foot. Pain is given to the perineum, lower abdomen, sacrum.

The effects of embolism can be paralysis and numbness of the legs. The patient is in a state of shock. Gangrene develops rapidly. If smaller arteries are affected, patients complain of weakness in the legs, lameness and pain when walking. In men, an erectile dysfunction occurs.

Renal artery embolism leads to kidney infarction. Patients note sharp lower back pain in the absence of dysuric phenomena (pain during urination, frequent urges). Two days later, blood appears in the urine. Possible increase in blood pressure. In severe cases, pain throughout the abdomen, bloating, vomiting, stool and urine retention.

Impaired blood circulation. Types, general characteristics, development mechanisms and clinical manifestations, values ​​for the body

Axon provides
not only carrying out arousal, but also
transport of various substances from the body
neuron to the nerve endings and back.
These are the substances necessary for exercise.
synaptic activity (neurotransmitters,
neuromodulators, synthesis enzymes
neurotransmitters, etc.), and substances
providing trophic and regeneration

Axonal transport (axotok)
carried out with the help of neurofilaments,
and contractile proteins. Violation
Axotoka can occur: a) upon destruction
microtubules and neurofilaments (under
exposure to colchicine, vinblastine and
other); b) with a lack of energy for
contractile protein contraction and
change in Ca2 concentration
(with ischemia, hypoxia, exposure
cyanides, dinitrophenol, etc.);

axonal transport lead to disruption
trophic neurosis as proximal as
and the distal axon, causing
development of dystrophic changes
neurons and tissues innervated by them, and
also a violation of synaptic processes
(education and isolation of neurotransmitters).

Diagnostic Issues

Diagnosis of embolism is difficult because it is limited in time. Pathological changes develop suddenly and very quickly lead to irreversible conditions. It matters the patient’s questioning about past illnesses, examination and checking the pulse on the limbs.

Information about starting thrombosis can give:

  • blood coagulation test;
  • set of signs on the ECG;
  • chest x-ray;
  • ultrasound examination of large veins and abdominal organs.

Vascular angiography is performed according to clinical indications in large vascular centers and specialized departments.

Possible catheterization of the cavities of the heart.

The general etiology of the disease. The concept of risk factors. Heredity and pathology

The total
etiology of the disease.
Is a doctrine of causes and conditions
the occurrence of diseases and pathological

diseases that can be easily identified
(for example, a skull injury leads to
disease – concussion).

disease is a pathological factor,
causing the disease.

the disease has its cause.

there are exogenous and endogenous.

about risk factors.
Risk Factors
Are factors that increase the likelihood
the occurrence of a disease.

disease risk

and pathology.
There are gene diseases

By autosomal
recessive type – transmitted by
inheritance and boys and girls – outside
gender dependence (phenylketonuria,
butterfly wings).

There are hereditary
dominant diseases
type – when one gene suppresses the action

There are diseases
interlocked with the floor.

diseases – when children are born with a violation
chromosomes (Down’s disease).

The basic one
hereditary pathology mechanism
are hereditary errors
information. The causes may be exogenous.
and endogenous

Dendrites and spines
create a significant area of ​​synaptic
contacts, ensure receipt
information into a neuron and play a crucial
role in implementing its transfer
and integrative activities. Degeneration
dendritic-spine apparatus is observed
with ischemia, hypoxin, various
intoxication, concussion, cranial
brain injury, electric
current, stress, Alzheimer’s disease and

4. Pathology
neuronal membranes are among the typical
pathological processes at the level
neuron (as well as any arc of a cell) carry
also damage to the membrane apparatus.
The main membrane-damaging factor
is an excess of products
free radical oxidation. is he
arises due to amplification of processes
lipid peroxidation (LPO)
membranes and (or) weakening antioxidant
(catalase, glutathione peroxidase) and
antiradical (superoxide dismutase,
α-tocopherol, ascorbic acid,
reduced glutathione, ubiquinone and
other) protection.

LPO processes
occur under the action of substances
providing direct prooxidant
action (Fe2 ions,
adrenaline, various poisons, etc.), as well as
in other pathological processes
(epilepsy, schizophrenia, and

shemia, hypoxia,
stress, neurosis, etc.).

Barrier violation
membrane properties leads to a sharp
increase in Ca2 current
and Na
in neuron and K
from a neuron. Leak To
leads to disruption of repalization processes
membranes, which may
hyperactivity of neurons is maintained
and generator activity pathologically
enhanced excitation (GPUV).

Excess Ca2
activates Ca2-dependent in the cell
proteases and phospholipases, divides
oxidative phosphorylation, etc.
In addition, damage to the outside
neuronal membrane causes exit
from a neuron of various substances, including
the number of antigens that can cause
development of an autoimmune process,
aggravating damage to a neuron.

The object of aggression products FLOOR
can be
not only the outer membrane, but also the membrane
mitochondria, which leads to energy deficiency,
Damage to the cell genome by products
FLOOR causes
violation of the synthesis of RNA and protein, which means
structural deficit. Conformational
changes in the membrane with increased LPO
the functioning of receptors for mediators,
comedians, trophogens, medicinal
drugs, etc.

5. Energy

Energy deficit in
neuron (as in any other cell)
may develop due to: a)
lack of oxygen; b) lack
substrates; c) damage to mitochondria.
In turn, the reason for the formation
the listed pathogenetic factors
may be: metabolic effect
poisons (cyanides, dinitrophenol), any shock
etiology, convulsions, trauma, violations
cerebral circulation, hypoglycemia
and etc.

energy shortages disrupt all
volatile processes in the cell,
dystrophy of the neuron secondary
structural plastic failure
and endogenous damage to a neuron,
which may end in his death.

6. Effects
hypoxia and ischemia

pathogenetic damage factors
individual neurons and the brain
hypoxemia in general (decrease
and ischemia (decreased blood supply
brain tissue due to flow restriction
blood through arterial vessels). In both
cases hypoxia develops (typical
pathological process), consequences
which are also typical.
Sequence of events presented
on pic

Improving oxygen supply to the brain
(maintaining the required level of PaO2
and cerebral perfusion pressure);

Reduced Brain Needs
in oxygen (craniocerebral
hypothermia, barbiturates, etc.
pharmacological drugs that reduce
metabolic rate
in neurons);

– maintenance
ATP concentration

– calcium blockade

– sodium blockade

– blockade of amino acids

– blockade of education

– production blockade
vasospastic substances

– blockade of education
free radicals

Svetlana Borszavich

General practitioner, cardiologist, with active work in therapy, gastroenterology, cardiology, rheumatology, immunology with allergology.
Fluent in general clinical methods for the diagnosis and treatment of heart disease, as well as electrocardiography, echocardiography, monitoring of cholera on an ECG and daily monitoring of blood pressure.
The treatment complex developed by the author significantly helps with cerebrovascular injuries and metabolic disorders in the brain and vascular diseases: hypertension and complications caused by diabetes.
The author is a member of the European Society of Therapists, a regular participant in scientific conferences and congresses in the field of cardiology and general medicine. She has repeatedly participated in a research program at a private university in Japan in the field of reconstructive medicine.