Steal syndrome angina pectoris. Introduction

4.6. Steal syndrome

In the broadest sense of the word, “steal” syndrome is understood as this type of side effect when a drug that improves the functional state of an organ causes a parallel deterioration in the functional state of other organs or systems of the body. Most often, the “steal” syndrome is observed at the level of the circulatory bloodstream in cases where expansion under the influence of vasodilators of some vascular areas and, consequently, improvement of blood flow in them, leads to deterioration of blood flow in other adjacent vascular areas. This particular type of side effect of drugs can be considered using the example of coronary “steal” syndrome.

Coronary steal syndrome develops in cases where two branches of the coronary artery arising from the same main vessel, for example, from the left coronary artery, have different degrees of stenosis (narrowing). In this case, one of the branches is slightly affected by atherosclerosis and retains the ability to expand or contract in response to changes in the myocardial oxygen demand. The other branch is significantly affected by the atherosclerotic process and therefore is constantly expanded to the maximum, even with low myocardial oxygen demand. In this situation, prescribing to the patient any arterial vasodilator, for example, dipyridamole, can cause a deterioration in the nutrition of that area of the myocardium that is supplied with blood by the coronary artery affected by atherosclerosis, i.e. provoke an attack of angina (Fig. 10).

Rice. 10. Scheme of development of coronary “steal” syndrome: A, B, A", I" -Diameters of the coronary artery

A branch of the coronary artery affected by atherosclerosis A expanded as much as possible in order to ensure adequate blood supply to the area of the myocardium irrigated by it (see Fig. 10, A). After the administration of a coronary agent, i.e. With a drug that dilates the coronary arteries, for example, dipyridamole, the coronary vessels dilate and, therefore, the volumetric velocity of coronary blood flow through them increases. However, the vessel A was previously already maximally expanded (diameter A equal to diameter L"). The vessel located nearby expands (diameter B less than diameter B"), resulting in the volumetric velocity of blood flow in the vessel B" increases, and in the vessel A", according to the laws of hydrodynamics, it decreases significantly. In this case, a situation is possible when the direction of blood through the vessel A" will change and it will begin to flow into the vessel B"(see Fig. 10, 6).

4.7. Rebound syndrome

“Rebound” syndrome is a type of side effect of a drug when, for some reason, the effect of the drug is reversed. For example, the osmotic diuretic drug urea, due to an increase in osmotic pressure, causes the transition of fluid from edematous tissues into the bloodstream, sharply increases blood circulation volume (BCV), which entails an increase in blood flow in the glomeruli of the kidneys and, as a result, greater filtration of urine. However, urea can accumulate in the tissues of the body, increase the osmotic pressure in them and, ultimately, cause the reverse transfer of fluid from the circulatory bed into the tissues, i.e. do not reduce, but increase their swelling.

4.8. Drug addiction

Drug dependence is understood as a type of side effect of drugs, which is characterized by a pathological need to take drugs, usually psychotropic ones, in order to avoid withdrawal syndrome or mental disorders that occur when taking these drugs abruptly. There are mental and physical drug dependence.

Under mental dependence understand the patient’s condition, characterized by an unmotivated need to take any drug, often psychotropic, in order to prevent mental discomfort due to stopping the drug, but not accompanied by the development of abstinence.

Physical dependence is a patient’s condition characterized by the development of abstinence syndrome due to discontinuation of a drug or after the administration of its antagonist. Under withdrawal or withdrawal syndrome understand the patient’s condition that occurs after stopping the use of any psychotropic drug and is characterized by anxiety, depression, loss of appetite, cramping abdominal pain, headache, trembling, sweating, lacrimation, sneezing, goose bumps, increased body temperature, etc. .

4.9. Drug resistance

Drug resistance is a condition in which there is no effect from taking a drug, which cannot be overcome by increasing the dose and persists even when a dose of the drug is prescribed that always causes side effects. The mechanism of this phenomenon is not always clear; it is possible that it is based not on the patient’s body’s resistance to any drug, but on a decrease in individual sensitivity to the drug, due to the genetic or functional characteristics of a particular patient.

4.10. Paramedicinal effects of drugs

The paramedicinal effect of drugs is not due to their pharmacological properties, but to the emotional, psychogenic reaction of the patient to a particular drug.

For example, the patient has been taking a calcium ion antagonist for a long time nifedipine, produced by AWD (Germany) under the name "Corinthard". At the pharmacy where he usually bought this drug, the drug produced by AWD was not available, and

The patient was offered nifedipine called "adalat" produced by Bayer (Germany). However, taking Adalat caused the patient severe dizziness, weakness, etc. In this case, we can talk not about the own side effects of nifedipine, but about a paramedicinal, psychogenic reaction that arose in the patient subconsciously due to the reluctance to exchange Corinfar for a similar drug.

CHAPTER 5 DRUG INTERACTIONS

IN In practical health care conditions, doctors very often have to deal with a situation where the same patient has to prescribe several drugs at the same time. This is largely due to two fundamental reasons.

L Currently, no one doubts that effective therapy for many diseases can only be achieved with the combined use of drugs. (For example, hypertension, bronchial asthma, gastric ulcer, rheumatoid arthritis and many, many others.)

2. Due to the increasing life expectancy of the population, the number of patients suffering from comorbid pathology, which includes two, three or more diseases, is constantly increasing, which, accordingly, requires the prescription of several drugs simultaneously and/or sequentially.

The simultaneous prescription of several drugs to one patient is called polypharmacy. Naturally, polypharmacy can be rational, i.e. useful for the patient, and vice versa, harm him.

As a rule, in practical conditions, the prescription of several drugs simultaneously for the treatment of one specific disease has 3 main goals:

increasing the effectiveness of therapy;

reducing the toxicity of drugs by reducing the doses of combined drugs;

prevention and correction of side effects of drugs.

At the same time, combined drugs can affect both the same parts of the pathological process and different parts of the pathogenesis.

produces a high level of antiarrhythmic effect (66-92% of patients). Moreover, this high effect is achieved in most patients when using drugs in doses reduced by 50%. It should be noted that during monotherapy (therapy with one drug), for example, supraventricular extrasystole, disopyramide at the usual dose was active in 11% of patients, and ethmozin - in 13%, and with monotherapy at half the dose, a positive effect could not be achieved in any from patients.

In addition to influencing one link of the pathological process, a combination of drugs is very often used to correct different links of the same pathological process. For example, in the treatment of hypertension, a combination of calcium channel blockers and diuretics may be used. Calcium channel blockers have powerful vasodilating (vasodilating) properties, mainly in relation to peripheral arterioles, reducing their tone and, thereby, helping to reduce blood pressure. Most diuretics lower blood pressure by increasing the excretion (removal) of Na + ions in the urine, reducing blood volume and extracellular fluid, and reducing cardiac output, i.e. two different groups of drugs, acting on different parts of the pathogenesis of hypertension, enhance the effectiveness of antihypertensive therapy.

An example of combining drugs to prevent side effects is the prescription of nystatin to prevent the development of candidiasis (fungal infections of the mucous membranes) during long-term treatment with antibiotics of the penicillin, tetracycline, neomycin, etc. group, or the prescription of drugs containing K + ions to prevent the development of hypokalemia during treatment with cardiac glycosides in patients with heart failure.

Knowledge of the theoretical and practical aspects of the interaction of drugs with each other is necessary for every practical medical worker, since, on the one hand, they allow, through a rational combination of drugs, to enhance the effect of the therapy, and on the other hand, to avoid complications that arise when using irrational combinations of drugs, as a result of which their side effects increase, including death.

So, drug interaction is understood as a change in the pharmacological effect of one or more drugs when used simultaneously or sequentially. The result of such interaction may be an increase in pharmacological effects, i.e. the combined drugs are synergists, or a decrease in the pharmacological effect, i.e. interacting drugs are antagonists.

Temporary improvement can be obtained by reducing myocardial oxygen demand with medications ( β-blockers) or by improving coronary blood flow ( nitrates, calcium antagonists). However, repeated ischemic episodes may occur.

The only real way to treat hibernating myocardium is timely revascularization, performed before the development of irreversible morphological changes in the myocardium.

Fixed and dynamic obstruction of the coronary arteries

Fixed Coronary obstruction causes a permanent decrease in blood flow, usually corresponding to the degree of atherosclerotic narrowing of the coronary arteries. Clinical manifestations of myocardial ischemia in patients with fixed coronary obstruction, as a rule, develop when the coronary artery narrows in excess of 70%.

Dynamic obstruction is associated: (1) with increased tone and spasm of the coronary artery, (2) thrombus formation. The addition of a dynamic component of obstruction leads to episodes of ischemia even with hemodynamically insignificant narrowing of the coronary artery.

To characterize the severity of coronary obstruction, not only the degree of narrowing of the coronary arteries at rest, but also the severity of the decrease in coronary reserve is of great importance. Coronary reserve refers to the ability of the coronary vessels to dilate and, as a result, increase blood flow when the load on the heart increases.

The development of dynamic obstruction in atherosclerotic lesions of the coronary vessels is caused by impaired reactivity of the coronary arteries and activation of thrombogenic mechanisms. These processes are facilitated by systemic endothelial dysfunction, which occurs, for example, with hyperhomocysteinemia, diabetes mellitus, dyslipoproteinemia and other diseases.

Impaired reactivity of coronary arteries affected by atherosclerosis is caused by the following mechanisms:

Reduced formation of vasodilators;

Reduced bioavailability of vasodilators;

Damage to smooth muscle cells of the coronary vessels.

Increased thrombogenicity in atherosclerotic damage to the coronary arteries and ischemia is explained by the following factors:

Increased formation of thrombogenic factors (tissue thromboplastin, plasminogen activator inhibitor, von Willebrand factor, etc.);

Reducing the formation of atrombogenic factors (antithrombin III, proteins C and S, prostacyclin, NO, tissue plasminogen activator, etc.).

The significance of dynamic obstruction increases with endothelial damage and destabilization of the atherosclerotic plaque, which leads to platelet activation, the development of local spasm and acute thrombotic occlusive complications, in particular acute coronary syndrome.

Thus, atherosclerotic damage to the coronary vessels, in addition to a mechanical reduction in the lumen of the vessel (fixed obstruction), can be the cause of dynamic obstruction.

The phenomenon of stealing

The phenomenon of coronary steal consists of a sharp decrease in coronary blood flow in the myocardial zone, supplied with blood from a partially or completely obstructed coronary artery with an increase in the number of vasodilators, as well as with physical activity.

The steal phenomenon occurs as a result of blood flow redistribution and can form either within the basin of one epicardial artery (intracoronary steal), or between the blood supply basins of different coronary arteries in the presence of collateral blood flow between them (intercoronary steal).

With intracoronary steal at rest, there is a compensatory maximum expansion of the arteries of the subendocardial layer with a loss of their sensitivity to vasodilators, while the arteries of the epicardial (outer) layer still retain the ability to expand under the influence of vasodilators. With physical exertion or the predominance of humoral vasodilators, rapid expansion of the epicardial arteries occurs. This leads to a decrease in resistance in the segment “poststenotic area - epicardial arterioles” and a redistribution of blood flow in favor of the epicardium with depletion of the subendocardial blood supply.

Rice. 1.9. Mechanism of intracoronary steal phenomenon

(according to Gewirtz N., 2009).

For intercoronary steal phenomenon a “donor” section of the heart is distinguished, which receives blood from a normal artery, and an “acceptor” section, which lies in the vascularization zone of the stenotic artery. At rest, the “donor” region supplies blood to the “acceptor” region due to collaterals. Under these conditions, the arterioles of the “acceptor” region are in a state of submaximal dilatation and are practically insensitive to vasodilators, and the arteries of the “donor” region fully retain the ability to dilate. The occurrence of a vasodilator stimulus leads to dilation of the arterioles of the “donor” region and a redistribution of blood flow in its favor, which causes ischemia of the acceptor region. The more developed the collaterals between the normal and ischemic parts of the heart, the greater the likelihood of intercoronary steal.

Rice. 1.9. The mechanism of the intercoronary steal phenomenon

Acute coronary syndrome: symptoms and treatment

Acute coronary syndrome - main symptoms:

Nausea
Vomit
Fainting
Lack of air
Chest pain
Confusion
Spread of pain to other areas
Pale skin
Cold sweat
Fluctuations in blood pressure
Excitement
Fear of death

Acute coronary syndrome is a pathological process in which the natural blood supply to the myocardium through the coronary arteries is disrupted or completely stopped. In this case, oxygen does not reach the heart muscle in a certain area, which can lead not only to a heart attack, but also to death.

The term "ACS" is used by clinicians to refer to certain heart conditions, including myocardial infarction and unstable angina. This is due to the fact that the etiology of these diseases is coronary insufficiency syndrome. In this condition, the patient requires emergency medical care. In this case, we are talking not only about the development of complications, but also a high risk of death.

Etiology

The main cause of acute coronary syndrome is damage to the coronary arteries by atherosclerosis.

In addition, the following possible factors in the development of this process are identified:

severe stress, nervous tension;
vasospasm;
narrowing of the lumen of the vessel;
mechanical damage to the organ;
complications after surgery;
coronary artery embolism;
inflammation of the coronary artery;
congenital pathologies of the cardiovascular system.

Separately, it is necessary to highlight factors that predispose to the development of this syndrome:

overweight, obesity;
smoking, drug use;
almost complete lack of physical activity;
imbalance of fats in the blood;
alcoholism;
genetic predisposition to cardiovascular pathologies;
increased blood clotting;
frequent stress, constant nervous tension;
high blood pressure;
diabetes mellitus;
taking certain medications that lead to a decrease in pressure in the coronary arteries (coronary steal syndrome).

ACS is one of the most life-threatening conditions for humans. In this case, not only emergency medical care is required, but also urgent resuscitation measures. The slightest delay or incorrect first aid actions can lead to death.

Pathogenesis

Due to thrombosis of the coronary vessels, which is provoked by a certain etiological factor, biologically active substances begin to be released from platelets - thromboxane, histamine, thromboglobulin. These compounds have a vasoconstrictor effect, which leads to a deterioration or complete cessation of blood supply to the myocardium. This pathological process can be aggravated by adrenaline and calcium electrolytes. At the same time, the anticoagulant system is blocked, which leads to the production of enzymes that destroy cells in the necrosis zone. If the development of the pathological process is not stopped at this stage, then the affected tissue will transform into a scar, which will not take part in the contraction of the heart.

The mechanisms of development of acute coronary syndrome will depend on the degree of thrombus or plaque occlusion of the coronary artery. The following stages are distinguished:

with a partial decrease in blood supply, attacks of angina may occur periodically;
with complete overlap, areas of dystrophy appear, which later transform into necrosis, which will lead to a heart attack;
sudden pathological changes lead to ventricular fibrillation and, as a consequence, clinical death.

It is also necessary to understand that a high risk of death is present at any stage of the development of ACS.

Classification

Based on the modern classification, the following clinical forms of ACS are distinguished:

acute coronary syndrome with ST segment elevation - the patient has typical ischemic pain in the chest, reperfusion therapy is required;
acute coronary syndrome without ST segment elevation – changes typical for ischemic disease, attacks of angina, are noted. Thrombolysis is not required;
myocardial infarction diagnosed by changes in enzymes;
unstable angina.

Forms of acute coronary syndrome are used only for diagnostic purposes.

Symptoms

The first and most characteristic sign of the disease is acute chest pain. The pain syndrome can be paroxysmal in nature and radiate to the shoulder or arm. With angina pectoris, the pain will be squeezing or burning in nature and short-lived. In case of myocardial infarction, the intensity of this symptom can lead to painful shock, so immediate hospitalization is required.

In addition, the following symptoms may be present in the clinical picture:

cold sweating;
unstable blood pressure;
excited state;
confusion;
panic fear of death;
fainting;
pale skin;
the patient feels a lack of oxygen.

In some cases, symptoms may be accompanied by nausea and vomiting.

With such a clinical picture, the patient needs to urgently provide first aid and call emergency medical care. Under no circumstances should the patient be left alone, especially if there is nausea with vomiting and loss of consciousness.

Diagnostics

The main method for diagnosing acute coronary syndrome is electrocardiography, which must be done as soon as possible after the onset of a painful attack.

A full diagnostic program is carried out only after the patient’s condition has been stabilized. Be sure to notify the doctor about what medications were given to the patient as first aid.

The standard program of laboratory and instrumental examinations includes the following:

general blood and urine analysis;
biochemical blood test - the level of cholesterol, sugar and triglycerides is determined;
coagulogram - to determine the level of blood clotting;
ECG is a mandatory method of instrumental diagnostics for ACS;
echocardiography;
coronary angiography - to determine the location and degree of narrowing of the coronary artery.

Treatment

The therapy program for patients with acute coronary syndrome is selected individually, depending on the severity of the pathological process; hospitalization and strict bed rest are required.

The patient’s condition may require measures to provide emergency first aid, which include the following:

provide the patient with complete rest and access to fresh air;
put a nitroglycerin tablet under your tongue;
Call emergency medical services and report your symptoms.

Treatment of acute coronary syndrome in a hospital may include the following therapeutic measures:

oxygen inhalation;
administration of medications.

As part of drug therapy, the doctor may prescribe the following drugs:

narcotic or non-narcotic painkillers;
anti-ischemic;
beta blockers;
calcium antagonists;
nitrates;
disaggregants;
statins;
fibrinolytics.

In some cases, conservative treatment is not enough or is not appropriate at all. In such cases, the following surgical intervention is performed:

stenting of the coronary arteries - a special catheter is passed to the site of narrowing, after which the lumen is expanded using a special balloon, and a stent is installed at the site of narrowing;
coronary artery bypass grafting - the affected areas of the coronary arteries are replaced with shunts.

Such medical measures make it possible to prevent the development of myocardial infarction from ACS.

In addition, the patient must follow general recommendations:

strict bed rest until stable improvement;
complete elimination of stress, strong emotional experiences, nervous tension;
exclusion of physical activity;
as the condition improves, daily walks in the fresh air;
exclusion from the diet of fatty, spicy, too salty and other heavy foods;
complete exclusion of alcoholic beverages and smoking.

You need to understand that acute coronary syndrome, if the doctor’s recommendations are not followed, can lead to serious complications at any time, and the risk of death in case of relapse always remains.

Separately, diet therapy for ACS should be highlighted, which implies the following:

limiting the consumption of animal products;
the amount of salt should be limited to 6 grams per day;
exclusion of overly spicy, seasoned dishes.

It should be noted that compliance with this diet is necessary constantly, both during the treatment period and as a preventative measure.

Possible complications

Acute coronary insufficiency syndrome can lead to the following:

heart rhythm disturbance in any form;
development of acute heart failure, which can lead to death;
inflammation of the pericardium;
aortic aneurysm.

It should also be understood that even with timely medical measures, there remains a high risk of developing the above complications. Therefore, such a patient should be systematically examined by a cardiologist and strictly follow all his recommendations.

Prevention

You can prevent the development of cardiovascular diseases if you follow the following doctor’s recommendations in practice:

complete cessation of smoking, moderate consumption of alcoholic beverages;
proper nutrition;
moderate physical activity;
daily walks in the fresh air;
elimination of psycho-emotional stress;
control of blood pressure indicators;
control blood cholesterol levels.

In addition, we should not forget about the importance of a preventive examination by specialized medical specialists and compliance with all doctor’s recommendations regarding the prevention of ailments that can lead to acute coronary insufficiency syndrome.

If you think that you have Acute Coronary Syndrome and the symptoms characteristic of this disease, then doctors can help you: a cardiologist, a therapist.

We also suggest using our online disease diagnostic service, which selects probable diseases based on the entered symptoms.

The death of a section of the heart muscle, leading to the formation of coronary artery thrombosis, is called myocardial infarction. This process leads to the disruption of blood circulation in this area. Myocardial infarction is predominantly fatal because the main heart artery is blocked. If, at the first sign, appropriate measures are not taken to hospitalize the patient, then death is 99.9% guaranteed.

Vegetovascular dystonia (VSD) is a disease that involves the entire body in the pathological process. Most often, the peripheral nerves, as well as the cardiovascular system, receive negative effects from the autonomic nervous system. The disease must be treated without fail, since in its advanced form it will have serious consequences on all organs. In addition, medical care will help the patient get rid of the unpleasant manifestations of the disease. In the international classification of diseases ICD-10, VSD is coded G24.

Transient ischemic attack (TIA) is cerebral circulatory failure due to vascular disorders, heart disease and low blood pressure. It is more common in people suffering from osteochondrosis of the cervical spine, cardiac and vascular pathology. A feature of a transient ischemic attack is the complete restoration of all lost functions within 24 hours.

Pneumothorax of the lung is a dangerous pathology in which air penetrates where physiologically it should not be - into the pleural cavity. This condition is becoming more common these days. The injured person needs to begin providing emergency care as soon as possible, since pneumothorax can be fatal.

Incarcerated hernia is the most common and most dangerous complication that can develop during the formation of a hernial sac of any location. Pathology develops regardless of a person’s age category. The main factor leading to pinching is an increase in intra-abdominal pressure or sudden lifting of weights. However, a large number of other pathological and physiological sources may also contribute to this.

With the help of exercise and abstinence, most people can do without medicine.

Symptoms and treatment of human diseases

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Treatment of myocardial hibernation

Temporary improvement can be obtained by reducing myocardial oxygen demand with drugs (β-blockers) or by improving coronary blood flow (nitrates, calcium antagonists). However, repeated ischemic episodes may occur.

The only real way to treat hibernating myocardium is timely revascularization, performed before the development of irreversible morphological changes in the myocardium.

Fixed and dynamic obstruction of the coronary arteries

Fixed coronary obstruction causes a permanent decrease in blood flow, usually corresponding to the degree of atherosclerotic narrowing of the coronary arteries. Clinical manifestations of myocardial ischemia in patients with fixed coronary obstruction, as a rule, develop when the coronary artery narrows in excess of 70%.

Dynamic obstruction is associated: (1) with increased tone and spasm of the coronary artery, (2) thrombus formation. The addition of a dynamic component of obstruction leads to episodes of ischemia even with hemodynamically insignificant narrowing of the coronary artery.

Impaired reactivity of coronary arteries affected by atherosclerosis is caused by the following mechanisms:

Reduced formation of vasodilators;

Reduced bioavailability of vasodilators;

Damage to smooth muscle cells of the coronary vessels.

Increased thrombogenicity in atherosclerotic damage to the coronary arteries and ischemia is explained by the following factors:

Increased formation of thrombogenic factors (tissue thromboplastin, plasminogen activator inhibitor, von Willebrand factor, etc.);

Reducing the formation of atrombogenic factors (antithrombin III, proteins C and S, prostacyclin, NO, tissue plasminogen activator, etc.).

The significance of dynamic obstruction increases with endothelial damage and destabilization of the atherosclerotic plaque, which leads to platelet activation, the development of local spasm and acute thrombotic occlusive complications, in particular acute coronary syndrome.

Thus, atherosclerotic damage to the coronary vessels, in addition to a mechanical reduction in the lumen of the vessel (fixed obstruction), can be the cause of dynamic obstruction.

The phenomenon of stealing

Rice. 1.9. Mechanism of intracoronary steal phenomenon

(according to Gewirtz N., 2009).

With the intercoronary steal phenomenon, a “donor” section of the heart is distinguished, which receives blood from a normal artery, and a “acceptor” section, which lies in the vascularization zone of the stenotic artery. At rest, the “donor” region supplies blood to the “acceptor” region due to collaterals. Under these conditions, the arterioles of the “acceptor” region are in a state of submaximal dilatation and are practically insensitive to vasodilators, and the arteries of the “donor” region fully retain the ability to dilate. The occurrence of a vasodilator stimulus leads to dilation of the arterioles of the “donor” region and a redistribution of blood flow in its favor, which causes ischemia of the acceptor region. The more developed the collaterals between the normal and ischemic parts of the heart, the greater the likelihood of intercoronary steal.

Rice. 1.9. The mechanism of the intercoronary steal phenomenon

(according to Gewirtz N., 2009).

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The phenomenon of intercoronary steal is characterized by the following signs. During the period of physical activity, most of the blood goes “where it is easier,” that is, outside the zones of narrowing of the coronary arteries, and blood flow in the arteries affected (by stenosis or spasm) decreases. The phenomenon of intercoronary “steal” develops. In patients with ST during FN, there is (as a result of vasodilation) an increase in blood flow in the unaffected coronary arteries, which is accompanied by a decrease in it in the affected area and the development of myocardial ischemia distal to the areas of stenosis. Dipyridamole in large doses can enhance the manifestations of this phenomenon (coronary artery disease is not treated with dipyridamole, but it is used to improve blood circulation).

Less significant reasons for the development of an attack of angina are hypotension, CHF, shortening of diastole due to tachyarrhythmia, hemodynamically ineffective bradycardia

Reasons that increase myocardial oxygen consumption: activation of the SAS (increased release of norepinephrine from the endings of adrenergic nerves) in response to psychoemotional or physical stress (for example, mental stress or anger can significantly increase adrenergic tone and blood pressure, reduce vagal activity), excessive metabolic needs caused by tachycardia of any origin, thyrotoxicosis or infection with high fever, cold air - due to increased peripheral vascular resistance, the load on the myocardium increases, which is necessary to maintain adequate perfusion, disruption of the receptor and regulatory apparatus of the heart.

Reasons that intensify the work of the myocardium: disruption of the regulatory apparatus of the heart, arrhythmias, hypertension, high end-diastolic pressure (EDP) in the LV, severe LVH (aortic stenosis), LV dilatation, increased tension in its wall

Reasons that reduce oxygen supply: anemia (the heart increases contractions to compensate for the decrease in blood volume, usually changes in the ST-T interval occur when the hemoglobin (Hb) concentration decreases to 70 g/l and below), aortic stenosis or insufficiency, impaired Hb function, hypoxemia (pneumonia, chronic obstructive pulmonary disease - COPD, sleep apnea syndrome), pulmonary hypertension (PH) and interstitial pulmonary fibrosis

As a result of the combination of all these factors, myocardial ischemia is formed, which is clinically manifested as stable angina or unstable angina.

NS is included in the concept of acute coronary syndrome (ACS). This is not a diagnosis, but a primary assessment of the situation when meeting a patient, when there is a group of symptoms that allows one to suspect MI or NS or SCD

The pathophysiology of acute coronary syndrome involves a complex process - plaque rupture, activation and aggregation of platelets in the damaged area, leading to the development of thrombosis, endothelial dysfunction and coronary artery spasm.

Rupture of a lipid-rich atherosclerotic plaque is a common initial sign of unstable angina, MI with and without ST-interval elevation. Plaque rupture leads to the deposition of platelets at the site, and then the coagulation cascade and thrombus formation are initiated. Factors causing plaque instability include activation of lymphocytes and macrophages and increased inflammation. Chlamydia infection (pneumonia) plays a role. Plaque rupture causes the appearance of clinical symptoms, but does not always lead to the development of MI

Thrombus formation is initially associated with contact of circulating platelets with plaque contents, which leads to platelet adhesion and aggregation and ultimately to thrombus formation. Activation of platelets stimulates a change in the conformation of the glycoprotein receptor IIb/IIIa on their surface, which promotes further activation and aggregation of platelets. The effect of this will be a significant increase in thrombin production, causing further expansion and stabilization of the clot.

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■ vertebrobasilar insufficiency (in approximately 66% of cases; transient ischemic attacks in approximately 1/3 of patients, symptoms of ischemia of the upper limb - in approximately 55%);

■ ischemia of the upper limb;

■ symptoms of distal digital embolism (no more than 3 - 5% of cases);

■ coronary-mammary-subclavian steal syndrome (does not exceed 0.5%);

■ according to the literature, about 20% of patients with damage to the subclavian artery do not have clinical symptoms.

Vertebrobasilar insufficiency is clinically manifested by one of the following symptoms or a combination of them: dizziness, headaches, instability when walking or standing, cochleovestibular syndrome, drop attacks, visual disturbances, etc. With pathology of the subclavian artery, vertebrobasilar insufficiency occurs, as a rule, with the development of steel syndrome: with proximal occlusion or critical stenosis of the subclavian artery before the vertebral artery departs from it, as a result of a decrease in blood pressure (BP) in the distal bed of the subclavian artery, blood flows from the contralateral vertebral artery artery along the ipsilateral vertebral artery into the subclavian artery distal to the site of stenosis, that is, to the detriment of the brain, blood flows from it to the arm.

1 - stage of compensation: there is increased sensitivity to cold, chilliness, paresthesia, and a feeling of numbness;

2 - stage of subcompensation: symptoms of ischemia in the fingers, hands and forearm muscles during physical activity - pain, weakness, coldness, numbness, fatigue;

3 - stage of decompensation: symptoms of ischemia at rest with pain, constant numbness and coldness, muscle wasting, decreased muscle strength;

4 - stage of ulcerative-necrotic changes: swelling, cyanosis, severe pain, impaired trophism, ulcers, necrosis and gangrene.

Stages 3 and 4 of ischemia of the upper limb in chronic atherosclerotic occlusion of the subclavian artery occur quite rarely; this is explained by the well-developed collateral circulation of the upper limb.

■ complete vertebral-subclavian steal syndrome;

■ collateral blood flow in the distal portion of the subclavian artery;

■ retrograde blood flow through the vertebral artery;

■ positive test of reactive hyperemia.

Stenosis of the first segment of the subclavian artery is characterized by:

■ transitional vertebral-subclavian steal syndrome - main-line altered blood flow in the distal section of the subclavian artery, systolic reversal of blood flow through the vertebral artery;

■ blood flow through the vertebral artery is shifted below the isoline to approximately 1/3;

■ during decompression, the blood flow curve through the vertebral artery “sits” on the isoline.

Unconditional confirmation of the presence of steel syndrome is the results of X-ray contrast angiography (digital subtraction arteriography), which remains the “gold standard” for visualizing the lumen of the vascular bed. The vast majority of authors, despite advances in the development of non-invasive methods, consider angiography to be a mandatory and unconditional condition for a high-quality diagnosis and determination of treatment tactics. During X-ray contrast angiography, when a contrast agent is injected into the contralateral (healthy) RCA, the affected RCA is filled through the vertebral artery system.

Literature: 1. article “Surgical treatment of vertebral-subclavian steal syndrome” by V.L. Shchipakin, S.V. Protsky, A.O. Chechetkin, S.I. Skrylev, L.P. Metelkina, N.V. Dobzhansky; journal “Nervous Diseases” No. 2 / 2006; 2. article “Surgical treatment of atherosclerotic lesions of the subclavian artery” by prof. Doctor of Medical Sciences Yanushko V.A., Ph.D. Turlyuk D.V., Isachkin D.V., Mikhnevich V.B (Republican Scientific and Practical Center “Cardiology”, Minsk, Belarus); 3. article “Surgical correction of cerebral blood flow steal syndromes in stenotic lesions of the branches of the aortic arch” P.V. Galkin 1, G.I. Antonov 2, G.E. Mitroshin 2, S.A. Terekhin 2, Yu.A. Bobkov 2 (1 - Clinical Hospital No. 119 of the Federal Medical and Biological Agency of Russia, and the Central Military Clinical Hospital named after A.A. Vishnevsky of the Ministry of Defense of the Russian Federation); article published in the journal “Surgery” No. 7, 2009; 4. article “Reconstruction of the brachiocephalic basin in case of steel syndrome” by A.D. Aslanov, A.K. Zhigunov, A.G. Kugotov, O.E. Logvina, L.N. Ishak, A.T. Edigov (Department of Hospital Surgery, Kabardino-Balkarian State University; Republican Clinical Hospital, Department of Vascular Surgery, Nalchik) Kardio -serdečno-sosud hir 2012; 3: 86; 5. abstract of the dissertation “Diagnostics and surgical treatment of occlusions of the first segment of the subclavian arteries” Stenyaev Yuri Afanasyevich, Moscow, 2003; 6. article “Vertebrobasilar insufficiency” S. Volkov 1, S. Verbitskaya 2 (1 - A.V. Vishnevsky Institute of Surgery of the Russian Academy of Medical Sciences, 2 - Polyclinic No. 151, Moscow); published in the magazine: “DOCTOR”; No. 5; 2011; pp. 73-76.; ru.wikipedia.org.

read also the article “Spinal-subclavian steal syndrome” by A.V. Zavaruev, Federal State Budgetary Educational Institution of Higher Education "Amur State Medical Academy of the Ministry of Health", Blagoveshchensk, Russia (Journal of Neurology and Psychiatry, No. 1, 2017) [read]

“CLINICAL PHARMACOLOGY Approved by the Ministry of Education of the Russian Federation as a textbook for students of medical schools and colleges UDC 615 BBK 52.8J K 85 Reviewers: ...”

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An increase in drug reabsorption may also play an important role in the development of toxic effects. Therefore, reducing the reabsorption of drugs during an overdose is a way to combat intoxication. For example, in case of poisoning with acetylsalicylic acid, the urine becomes acidic, as a result of which the molecules of acetylsalicylic acid are in non-ionized form and are easily reabsorbed, i.e. their excretion decreases. In this case, alkalinization of urine by administering sodium bicarbonate to the patient causes the acetylsalicylic acid molecules to become more ionized, i.e. less soluble in fats and, as a consequence, will be less reabsorbed, which will entail increased excretion of acetylsalicylic acid by the kidneys.

Excretion of drugs by the liver. Drugs metabolized by the liver can be excreted in the bile into the intestine. In this case, part of the drug is eliminated in the feces, and part of the drug is reabsorbed into the blood plasma as a result of deconjugation under the influence of intestinal enzymes. This phenomenon is called gastrointestinal or enterohepatic circulation. The ability of the liver to excrete drugs with bile can also be used for therapeutic purposes.

For example, for inflammatory diseases of the biliary tract, antibiotics are prescribed that are excreted by the liver unchanged (for example, tetracycline, erythromycin), which leads to a sharp increase in their concentration in the bile and the implementation of local antimicrobial action.

Excretion of drugs by the lungs. Mainly gaseous drugs (inhalation anesthetics) and ethyl alcohol are excreted from the body through the lungs. Excretion of ethanol (ethyl alcohol) by the lungs is of great practical importance, since the ethanol content in exhaled air is directly proportional to its content in the blood.

Drugs can also be excreted from the body through sweat, tear fluid, saliva, vaginal secretions, etc. However, from a practical point of view, these ways of removing drugs from the body are not of significant importance.

A special place is occupied by the excretion of drugs with the milk of a nursing mother. This is due to the fact that the drugs in milk, once they enter the body of a newborn, can have a wide variety of effects on him, including damaging ones (this issue will be discussed in detail later - see page 83).

CHAPTER 4 INCIDENTAL

EFFECT OF MEDICINES

It has now become obvious that drugs used in the treatment of various diseases can themselves cause the development of severe pathological conditions. According to statistical data, drugs exhibit their harmful effects in 10-20% of outpatients and in 25-50% of patients undergoing intensive care. Moreover, in 0.5% of cases, these harmful effects of drugs are life-threatening, and in 0.2% of patients they lead to death.

In accordance with the currently accepted definition by the World Health Organization (WHO), a side effect of a drug includes “any reaction to a drug that is harmful or undesirable for the body, which occurs when it is used for the treatment, diagnosis and prevention of diseases.”

From a practical point of view, it is necessary to distinguish between the side (toxic) effect of a drug and the side (concomitant) effect of a drug. The term “side effect of a drug” always refers to the harmful effect of a drug on the patient’s body. For example, the calcium channel blocker nifedipine causes swelling of the lower extremities in many patients; class III antiarrhythmic amiodarone causes pigment deposition in the cornea of the eye; The centrally acting antihypertensive drug methyldopa causes orthostatic hypotension in most patients in the first week of use. A side (concomitant) effect of a drug is understood as a spectrum of pharmacological effects of a drug that do not harm the health of patients, but are “useless” in the treatment of this particular pathology. For example, the spectrum of pharmacological activity of acetylsalicylic acid includes its anti-inflammatory (the drug was created as a non-steroidal anti-inflammatory and antipyretic agent) and anti-aggregation properties. Currently, acetylsalicylic acid is widely used as an antiplatelet agent for the prevention of thrombotic complications in patients with coronary artery disease and the prevention of transient cerebrovascular accidents. The anti-inflammatory and antipyretic properties included in the spectrum of its pharmacological activity are harmless but also useless for this category of patients.

In principle, side effects are divided into two main groups:

1. A side effect of a drug, noted in most patients when the dose of the drug is increased and associated with exceeding the usually known pharmacological effect.

Such adverse reactions include orthostatic hypotension, characteristic of many drugs (hypotensive - apressin, clonidine, pentamine, etc., antiarrhythmics - novocaine-amide, neuroleptic aminazine, etc.), hypoglycemia (sharp drop in blood sugar, for example, after use non-selective (3-blocker propranolol), hypokalemia (a sharp decrease in the level of potassium in the blood, for example, when taking thiazide or loop diuretics), arrhythmogenicity (i.e. the ability to cause or increase cardiac arrhythmias) in many antiarrhythmic drugs, etc. .

2. Side effects of drugs that are not related to their known pharmacological action.

This group of adverse reactions of drugs consists of: immunologically determined side effects (see details on page 51) and genetically determined adverse reactions. For example:

in patients suffering from the genetically determined disease von Willebrand disease (angiohemophilia - a hereditary disease characterized by a sharp increase in bleeding time due to a reduced level of blood clotting factor VIII in the body), even the administration of small doses of acetylsalicylic acid can cause massive bleeding;

Prescribing the antimicrobial drug primaquine to patients with a genetically determined deficiency of the enzyme glucose-6-phosphodehydrogenase, which plays an important role in the metabolism of carbohydrates (including in red blood cells), can lead to the development of a hemolytic crisis (massive breakdown of red blood cells in the bloodstream).

This type of side effect of drugs is called idiosyncrasy.

Idiosyncrasy, as a rule, is caused by congenital enzymopathy (absence or impaired activity of any enzymes). However, idiosyncrasy can also be acquired. In this case, enzymopathy develops as a result of previous or existing diseases.

Another classification of side effects of drugs is based on their pharmacokinetic characteristics:

side effects of drugs that occur at their therapeutic concentrations in the blood plasma (bronchial spasm when using non-selective (3-blockers);

side effects of drugs that occur at toxic concentrations in the blood plasma, i.e., with an overdose of drugs;

a side effect of drugs that is not related to their concentration in the blood plasma (dysbacteriosis, i.e. qualitative and quantitative disturbances of the natural intestinal microflora caused by long-term use of antibiotics).

However, for practical medical workers, the most convenient classification of side effects of drugs is based on the pathogenetic principle:

side effects of drugs associated with their pharmacological properties;

toxic complications caused by relative and absolute overdose of drugs;

side effects of drugs caused by increased tissue sensitivity (idiosyncrasy, allergic reactions);

side effects of drugs caused by the peculiarities of the functional state of the body;

withdrawal syndrome;

"steal" syndrome;

rebound syndrome;

drug addiction;

drug resistance;

paramedicinal side effects of drugs.

4.1. Side effects of drugs associated with their pharmacological properties This type of side effect is understood as a pharmacological effect that develops when taking drugs in therapeutic doses and is caused by their influence on the same type of receptors located in various organs and tissues of the body, or on other types of receptors and/ or specialized areas of receptive tissues of target organs. This type of side effect of drugs is quite widespread. For example:

The non-selective β- and β2-adrenergic blocker propranolol, by blocking β-adrenergic receptors of the heart muscle, reduces the frequency and strength of heart contractions.

This effect of the drug has found its application in the treatment of patients with coronary artery disease and arterial hypertension. At the same time, the drug also blocks β2-adrenergic receptors located in the bronchi, causing an increase in the tone of their smooth muscles, which in patients with broncho-obstructive syndrome can provoke bronchospasm, i.e. propranolol in moderate therapeutic doses, influencing the 3-adrenergic receptors of the heart and lungs, on the one hand, has a positive effect in ischemic heart disease, and on the other hand, a harmful side effect, manifested by a worsening of the broncho-obstructive syndrome;

The drug nifedipine, by blocking slow calcium channels in vascular smooth muscle cells, mainly arterioles, lowers blood pressure, i.e. forms a therapeutic hypotensive effect, and at the same time has a similar effect on intestinal smooth muscle cells, promoting the development of constipation, i.e. has side, harmful effects on the body.

Another example of a side effect of drugs associated with their pharmacological properties. The cardiotonic (increasing force of heart contractions) effect of cardiac glycosides used in the treatment of heart failure is associated with their ability to block the membrane K+-, Ia+-ATPase of contractile cardiomyocytes (muscle cells of the heart). Blockade of membrane ATPase of vascular smooth muscle cells by cardiac glycosides leads to their contraction and, thereby, to an increase in total peripheral resistance, i.e.

a harmful side effect of the drug is realized, since an increase in total peripheral resistance increases the afterload on the heart muscle.

4.2. Toxic complications caused by relative and absolute overdose of drugs As a rule, the development of the toxic (damaging) effect of a drug is based on an excessive increase in its concentration. in blood plasma and/or organs and tissues of the body.

Such a damaging effect of drugs, on the one hand, can be caused by an overdose, i.e. taking an excessive amount of the drug, and on the other hand, a violation of its pharmacokinetics (decreased binding to protein and, as a consequence, an increase in the content of its active fraction in the blood plasma;

slowdown of biotransformation; decreased renal excretion, etc.).

The toxic effect of drugs can be divided into both general and local, and organ-specific (neuro-, nephro-, hepato-, ototoxicity, etc.).

The local toxic effect of drugs can manifest itself, for example, in the form of an abscess at the site of intramuscular injection of a 40% glucose solution or in the form of phlebitis (inflammation of the vein wall) at the site of intravenous administration of the cytostatic drug emhibin.

A general (generalized, systemic) side effect of a drug is characterized by a systemic manifestation of the damaging (harmful) effect of the drug. For example, orthostatic hypotension after the administration of the ganglion blocker pentamine or severe hypotension after the administration of the class I antiarrhythmic procainamide. A systemic toxic effect may include inhibition of hematopoiesis during treatment with cytostatics. Quite often, toxic effects occur in drugs that have a small therapeutic breadth and are treated for a long time (for example, class I antiarrhythmics - quinidine, novocainamide, allapinine, etc.; cardiac glycosides, etc.).

Drugs prescribed in therapeutic doses, but capable of cumulating (accumulating) in the body, for example, cardiac glycosides (digoxin, Celanide, etc.), can also exhibit a general toxic effect.

The general toxic effect of a drug can also be caused by a violation of the functional state of the organ through which it is excreted from the body. In these cases, the drug prescribed in a therapeutic dose will gradually accumulate in the body, resulting in its concentration exceeding the therapeutic one. For example, if the metabolic function of the liver is impaired, lipophilic drugs accumulate in the body (hypnotics, tranquilizers, indirect anticoagulants, etc.), and if the excretory function of the kidneys is impaired, drugs excreted in the urine accumulate in the body (for example, cardiac glycosides - strophanthin and corglycone).

A number of drugs have an organ-specific effect, i.e. a toxic effect realized in any specific organ.

Neurotoxic (damaging tissue of the nervous system) effect. For example, the antimicrobial drug from the fluoroquinolone group, lomefloxacin, causes insomnia, dizziness, and headache; An antibiotic from the tetracycline group, minocycline, causes vestibular disorders, dizziness, and ataxia.

Another example of a neurotoxic effect is the CNS-damaging effect of the local anesthetic novocaine and the class I antiarrhythmic drug novocainamide, which is similar in chemical structure. When administered intravenously, dizziness, paresthesia (unpleasant sensations, often in the extremities, manifested by numbness, tingling, burning, “crawling”, etc.), motor agitation, etc. may develop.

The antibiotic for treating tuberculosis patients, cycloserine, can even cause the development of psychoses, hallucinations, and pseudoepileptic seizures.

Hepatotoxic (damaging liver tissue) effect. For example, lincosamide antibiotics (lincomycin and clindamycin) cause jaundice with an increase in the level of hepatic transaminases in the blood plasma, indicating damage to the liver tissue.

Nephrotoxic (damaging kidney tissue) action develops due to the fact that most drugs secreted by the kidneys can cause damage to kidney tissue due to direct contact with them. The development of so-called drug nephropathy can be caused by drugs such as aminoglycoside antibiotics (amikacin, gentamicin, kanamycin), a drug containing gold (crisanol), bismuth salts (bijoquinol and bismoverol), etc.

Ototoxic (damaging to hearing organs) effect. For example, long-term use of aminoglycoside antibiotics can lead to hearing loss, including the development of irreversible deafness.

Most cytostatic drugs have a hematotoxic (inhibitory) effect, since in addition to their effect on tumor cells, they usually have an inhibitory effect on the hematopoietic system (bone marrow).

Damage to the organs of vision. For example, the class III antiarrhythmic amiodarone, which contains iodine in its chemical structure, can cause microdetachment of the retina, optic neuritis, and the cornea of the eye may acquire a bluish tint.

Special types of organotoxic effects of drugs include mutagenic (damaging the chromosomal apparatus of male and female germ cells, as well as the fetus). Drugs that have a mutagenic effect, as a rule, are not widely used in the clinic due to their ability to cause chromosomal aberrations (deviations from the normal chromosome structure), i.e. the ability to have a potentially damaging effect on the fetus. Typically, therapy with mutagenic drugs is carried out only for health reasons - for the treatment of cancer patients with cytostatics or suppressing the immune system with immunosuppressants in order to prevent tissue incompatibility reactions during organ and tissue transplantation, etc. In these cases, patients must be warned about the possibility of a mutagenic effect of the drug and a minimum period of time during which they should refrain from conceiving children must be specified. For example, patients taking the immunosuppressant azathioprim are advised to abstain from conceiving children for 3 months for men and for one year after stopping the drug. Cytostatic drugs especially often cause chromosomal aberrations in both therapeutic and toxic doses.

If the number of mutagenic drugs in the clinic is insignificant, then the number of drugs that have a damaging effect on the fetus is quite large and, unfortunately, this type of side effect of drugs cannot always be identified at the preclinical stage of drug study. For example, widespread use in the early 1960s of GT. The sleeping pill thalidomide led to the fact that about 7,000 children were born in Germany and England with congenital pathology of the limbs. Only after the congress of gynecologists in the city.

Kiel (Germany) managed to find out that the basis of this pathology is the damaging effect of thalidomide on the fetus.

The complexity of this issue also lies in the fact that up to 60-80% of pregnant women during pregnancy often take drugs without consulting a doctor, i.e. self-medicate.

Depending on the timing of pregnancy, there are 3 types of damaging effects of drugs on the fetus: embryotoxic (0-3 weeks.

after fertilization); teratogenic (4-10 weeks after fertilization); fetotoxic (10-36 weeks after fertilization).

The features of the damaging effect of drugs on the fetus will be discussed in detail below (see page 85).

Also, oncogenicity is classified as a special type of drug toxicity.

Oncogenicity is the ability of a drug to cause malignant neoplasms. If such a side effect is detected in a drug, it is immediately prohibited from clinical use.

4.3. Side effects of drugs caused by increased tissue sensitivity Idiosyncrasy is a congenital hypersensitivity to drugs, usually caused by hereditary (genetic) enzymopathies (discussed in detail - p. 46).

Allergic reactions. If idiosyncrasy develops after the first dose of a drug, then an allergic reaction to the drug always occurs only after taking it again, that is, in cases where the patient’s body was previously sensitized to it. In other words, an allergic reaction to a drug is understood as this type of interaction of a drug or its metabolite with the human body, as a result of which a pathological process develops upon repeated administration of the drug.

Since most drugs have a relatively small molecular weight, they cannot be considered as complete antigens (substances with a fairly large molecular weight - proteins, peptides, polysaccharides, etc.), but are incomplete antigens - haptens. Drugs become a complete antigen only after they enter the patient’s body and form a complex with proteins.

There are 4 main types of allergic reactions involving drugs.

The first type of allergic reaction of the body to drugs is reagin (or immediate allergic reactions - anaphylaxis). This type of allergic reaction develops in cases where drugs that first enter the body sensitize tissues and become fixed on mast cells. In this case, immunoglobulin E (IgE) acts as an antibody, which interacts with mast cell receptors. When taking the same drugs again, immunoglobulin E stimulates the release of so-called allergy mediators - histamine, bradykinin, prostaglandins, serotonin, etc. The result of a sharp release of allergy mediators into the blood is a decrease in blood pressure, increased capillary permeability, tissue swelling, etc. up to the development of anaphylactic shock. Allergic reactions of the reagin type can be caused by various vaccines, serums, antibiotics of the penicillin group, local anesthetic novocaine, etc.

The second type of allergic reaction of the body to drugs - a cytotoxic reaction - develops when the drug, having first entered the body, forms antigenic complexes with proteins located on the membrane of blood cells.

The resulting complexes are perceived by the body as foreign proteins and specific antibodies are produced to them.

When taking drugs repeatedly, antibodies interact with antigenic complexes located on the membrane of blood cells, resulting in the development of an immune cytotoxic reaction. In cases where an immune cytotoxic reaction occurs on the platelet membrane, thrombocytopenia develops (a decrease in the number of platelets in the blood plasma), and if the reaction occurs on the erythrocyte membrane, hemolytic anemia develops, etc.

A cytotoxic allergic reaction can be caused by penicillin and cephalosporin antibiotics, class I antiarrhythmic quinidine, the centrally acting antihypertensive drug methyldopa, non-steroidal anti-inflammatory drugs from the salicylates group, etc.

The third type of allergic reaction of the body to drugs - the formation of toxic immune complexes - develops in cases where the drug, having first entered the body, causes the formation of toxic immune complexes with the participation of immunoglobulins M and G (IgM, IgG), the largest part of which is formed in endothelial cells vessels. When drugs re-enter the body, damage to the vascular wall occurs due to the release of biologically active substances (bradykinin, histamine, etc.). Lymphocytes are attracted to the reaction zone and an inflammatory process develops. Clinically, this manifests itself as vasculitis, alveolitis, nephritis, etc. This type of allergic reaction includes serum sickness, which is manifested by fever, joint pain, swollen lymph nodes, and itchy skin rash. The disease develops gradually and reaches its maximum by 8-10 days from the moment of re-taking the drug.

The fourth type of allergic reaction of the body to drugs - a delayed-type allergic reaction - develops 24-48 hours after the drug is re-administered. When a drug enters the patient’s body for the first time, it causes the appearance of antigen-specific receptors on T-lymphocytes. Upon repeated admission, drug molecules interact with sensitized T-lymphocytes, resulting in the release of biologically active substances - lymphokinins, for example, interleukin-2, which have a damaging effect on tissue. This type of allergic reaction usually develops with the transdermal method of using drugs, for example, the Mantoux and Pirquet tests (allergy tests for the diagnosis of tuberculosis).

According to the intensity of clinical manifestations, allergic reactions of the body to drugs are divided into fatal, severe, moderate and mild forms.

Fatal allergic reactions, for example, include allergic shock.

An example of severe allergic reactions is, for example, the development of Morgagni-Adams-Stokes syndrome - a reversible sudden loss of consciousness, accompanied by convulsions, pallor, followed by cyanosis, respiratory failure, and severe hypotension. This syndrome can develop as a result of an allergic reaction to the class I antiarrhythmic drug quinidine.

A moderate reaction is, for example, an attack of bronchial asthma in response to repeated intake of the non-steroidal anti-inflammatory drug acetylsalicylic acid, the so-called “aspirin” asthma.

Naturally, severe and moderate manifestations of an allergic reaction to drugs require immediate discontinuation of the drug and special desensitizing therapy.

Mild forms of an allergic reaction, as a rule, do not require special desensitizing therapy and quickly disappear when the drug that caused the allergy is discontinued.

In addition, allergic reactions to drugs are divided according to the time of their occurrence: into acute - they occur instantly or within several hours from the moment of repeated administration of the drug (for example, anaphylactic shock); subacute - occur within a few hours or the first 2 days from the moment of repeated administration of drugs (for example, thrombocytopenia); delayed or delayed type (for example, serum sickness).

It should also be remembered that it is also possible to develop a cross-allergy to drugs, i.e. in cases where the patient is allergic to some drug, for example, the sulfonamide drug sulfapyridazine, then an allergic reaction may develop upon the first dose of the sulfonamide drug sulfadimethoxine, which is close to it in chemical structure.

4.4. Side effects of drugs caused by changes in the functional state of the body This type of side effect of drugs can occur in patients suffering from diseases of any organs when drugs are prescribed in average therapeutic doses.

When prescribing cardiac glycosides in moderate therapeutic doses to patients with acute myocardial infarction, the development of severe cardiac arrhythmias may occur due to the positive inotropic effect caused by these drugs, i.e.

strengthening the contractile function of the myocardium, which entails an increase in the heart’s need for oxygen, worsening the condition of the ischemic focus, etc. At the same time, the same patient, before the development of a heart attack, could take cardiac glycosides in average therapeutic doses without developing any side effects.

If a patient has a prostate adenoma, if he is prescribed in moderate therapeutic doses a drug that has an M-anticholinergic (atropine-like) effect, for example, the class I antiarrhythmic disopyramide, acute urinary retention may develop due to the drug reducing the tone of the smooth muscles of the bladder and increasing the tone of the sphincters bladder. In patients who do not suffer from prostate adenoma, the development of acute urinary retention is unlikely when disopyramide is used in moderate therapeutic doses. Acute urinary retention in patients with prostate adenoma can also be caused by narcotic analgesics (for example, morphine), which cause an increase in the tone of the bladder sphincter.

There are a lot of similar examples, but the greatest clinical significance is the violation of the pharmacodynamics and pharmacokinetics of drugs when they are prescribed in average therapeutic doses to patients suffering from liver and kidney disease. In patients with this type of disease, both the metabolic rate and the rate of elimination from the body of a wide variety of drugs may be impaired, as a result of which their concentration in the blood plasma increases and their toxic effect is realized. Therefore, for this category of patients, drug doses are selected strictly individually.

For example, in patients with reduced renal excretory function, the dose of drugs eliminated (excreted) by the kidneys is selected strictly depending on the amount of renal clearance. Currently, for drugs excreted by the kidneys, the annotations provide a dosage calculation for patients with impaired renal excretory function. For example, when prescribing the antiviral drug acyclovir to patients of this kind, it is always dosed as follows: when creatinine clearance (CC) is more than 50 ml/min, it is prescribed at 5 mg/kg every 8 hours, when CC decreases to 25-50 ml/min - 5 mg/kg every 12 hours, with CC 10-25 ml/min - 5 mg/kg every 24 hours, and with CC below 10 ml/min - 2.5 mg/kg every 24 hours immediately after hemodialysis .

4.5. Drug withdrawal syndrome

In patients who, as a rule, take certain drugs for a long time (antihypertensive drugs of central action, for example, clonidine, (3-blockers - propranolol, indirect anticoagulants - neodicoumarin, antianginal drugs from the group of organic nitrates and others), sudden cessation of their use may lead to This will lead to a sharp deterioration in their condition. For example, if you suddenly stop taking the antihypertensive drug clonidine, a hypertensive crisis may develop (for details on methods of prevention and side effects of drugs, see page 242).

4.6. Steal syndrome

Coronary steal syndrome develops when two branches of the coronary artery arising from the same main vessel, for example, the left coronary artery, have different degrees of stenosis (narrowing). In this case, one of the branches is slightly affected by atherosclerosis and retains the ability to expand or contract in response to changes in the myocardial oxygen demand. The other branch is significantly affected by the atherosclerotic process and therefore is constantly expanded to the maximum, even with low myocardial oxygen demand. In this situation, prescribing to the patient any arterial vasodilator, for example, dipyridamole, can cause a deterioration in the nutrition of that area of the myocardium that is supplied with blood by the coronary artery affected by atherosclerosis, i.e. provoke an attack of angina (Fig. 10).

Rice. 10. Scheme of development of coronary “steal” syndrome:

A, B, A", Z" - Diameters of the coronary artery The branch of the coronary artery A affected by atherosclerosis is maximally expanded in order to ensure adequate blood supply to the area of the myocardium irrigated by it (see Fig. 10, a).

After the administration of a coronary agent, i.e. With a drug that dilates the coronary arteries, for example, dipyridamole, the coronary vessels dilate and, therefore, the volumetric velocity of coronary blood flow through them increases. However, vessel A had already been maximally expanded (diameter A is equal to diameter L"). The vessel located nearby expands (diameter B is less than diameter B"), as a result of which the volumetric flow rate of blood flow in vessel B increases, and in vessel A ", according to the laws of hydrodynamics, decreases significantly. In this case, a situation is possible when the direction of blood through vessel A" changes and it begins to flow into vessel B" (see Fig. 10, 6).

4.7. Rebound syndrome

4.8. Drug dependence Drug dependence is understood as a type of side effect of drugs, which is characterized by a pathological need to take drugs, usually psychotropic ones, in order to avoid withdrawal syndrome or mental disorders that occur when taking these drugs abruptly. There are mental and physical drug dependence.

Mental dependence is understood as a patient’s condition characterized by an unmotivated need to take any drug, often psychotropic, in order to prevent mental discomfort due to stopping the drug, but not accompanied by the development of abstinence.

Physical dependence is a patient’s condition characterized by the development of abstinence syndrome due to cessation of taking a drug or after the administration of its antagonist. Abstinence or withdrawal syndrome is understood as the patient's condition that occurs after stopping the use of any psychotropic drug and is characterized by anxiety, depression, loss of appetite, cramping abdominal pain, headache, trembling, sweating, lacrimation, sneezing, goose bumps, fever bodies, etc.

4.9. Drug resistance Drug resistance is a condition in which there is no effect from taking a drug, which cannot be overcome by increasing the dose and persists even when a dose of the drug is prescribed that always causes side effects. The mechanism of this phenomenon is not always clear; it is possible that it is based not on the patient’s body’s resistance to any drug, but on a decrease in individual sensitivity to the drug, due to the genetic or functional characteristics of a particular patient.

4.10. Paramedicinal effect of drugs The paramedicinal effect of drugs is not due to their pharmacological properties, but to the emotional, psychogenic reaction of the patient to a particular drug.

For example, the patient took the calcium ion antagonist nifedipine, manufactured by AWD (Germany) under the name “Corinfar,” for a long time. At the pharmacy where he usually bought this drug, the drug produced by AWD was not available, and the patient was offered nifedipine under the name “adalat”, produced by Bayer (Germany). However, taking Adalat caused the patient severe dizziness, weakness, etc. In this case, we can talk not about the own side effects of nifedipine, but about a paramedicinal, psychogenic reaction that arose in the patient subconsciously due to the reluctance to exchange Corinfar for a similar drug.

CHAPTER 5 INTERACTION

MEDICINES

In practical healthcare settings, doctors very often have to deal with a situation where the same patient has to prescribe several drugs at the same time. This is largely due to two fundamental reasons.

2. Due to the increasing life expectancy of the population, the number of patients suffering from concomitant pathology, which includes two, three or more diseases, is constantly increasing, which, accordingly, requires the prescription of several drugs simultaneously and/or sequentially.

The simultaneous prescription of several drugs to one patient is called polypharmacy. Naturally, polypharmacy can be rational, i.e. useful for the patient, and vice versa, harm him.

As a rule, in practical conditions, the prescription of several drugs simultaneously for the treatment of one specific disease has 3 main goals:

increasing the effectiveness of therapy;

reducing the toxicity of drugs by reducing the doses of combined drugs;

prevention and correction of side effects of drugs.

At the same time, combined drugs can affect both the same parts of the pathological process and different parts of the pathogenesis.

For example, a combination of two antiarrhythmics ethmosin and disopyramide, which belong to class IA antiarrhythmic drugs, i.e. drugs that have similar mechanisms of action and realize their pharmacological effects at the level of the same link in the pathogenesis of cardiac arrhythmias provide a high level of antiarrhythmic effect (66-92% of patients). Moreover, this high effect is achieved in most patients when using drugs in doses reduced by 50%. It should be noted that during monotherapy (therapy with one drug), for example, supraventricular extrasystole, disopyramide at the usual dose was active in 11% of patients, and ethmozin - in 13%, and with monotherapy at half the dose, a positive effect could not be achieved in any from patients.

Calcium channel blockers have powerful vasodilating (vasodilating) properties, mainly in relation to peripheral arterioles, reducing their tone and thereby helping to lower blood pressure. Most diuretics lower blood pressure by increasing the excretion (removal) of Na+ ions in the urine, reducing blood volume and extracellular fluid, and reducing cardiac output, i.e. two different groups of drugs, acting on different parts of the pathogenesis of hypertension, enhance the effectiveness of antihypertensive therapy.

An example of combining drugs to prevent side effects is the prescription of nystatin to prevent the development of candidiasis (fungal infections of the mucous membranes) during long-term treatment with antibiotics such as penicillin, tetracycline, neomycin, etc., or the prescription of drugs containing K+ ions to prevent the development of hypokalemia during treatment with cardiac glycosides in patients with heart failure.

Synergism is a type of drug interaction in which the pharmacological effect or side effect of one or more drugs is enhanced.

There are 4 types of drug synergy:

sensitization or sensitizing effect of drugs;

additive effect of drugs;

summation of effect;

potentiation of the effect.

When sensitization occurs as a result of the use of several drugs that have different, often heterogeneous, mechanisms of action, the pharmacological effect of only one of the drugs included in the combination is enhanced. For example, the therapeutic effect of a polarizing mixture used in the clinic of acute myocardial infarction (500 ml of 5% glucose solution, 6 units of insulin, 1.5 g of potassium chloride and 2.5 g of magnesium sulfate is based on this principle. In the absence of potassium chloride and magnesium sulfate, they can be replaced with 20 ml of panangin solution). The mechanism of action of this combination is based on the ability of glucose and insulin to enhance the transmembrane flow of K+ ions into the heart cell, which makes it possible to prevent or stop cardiac arrhythmias.

Another example of the sensitizing effect of drugs may be an increase in the concentration of iron ions in the blood plasma when ascorbic acid (vitamin C) is co-administered with drugs containing iron.

This type of drug interaction is expressed by the formula 0 + 1 = 1.5.

The additive effect of a drug is a type of interaction in which the pharmacological effect of a combination of drugs is greater than the effect of each individual drug included in the combination, but less than the mathematical sum of their effect. For example, the therapeutic effect of the joint administration of the adrenal stimulant salbutamol and the phosphodiesterase inhibitor theophylline to patients suffering from bronchial asthma. Salbutamol and theophylline have bronchodilator properties, i.e. bronchodilator effect. Let us assume that the administration of salbutamol alone expands the lumen of the bronchi by 23%, and theophylline by 18%. When drugs are prescribed together, the lumen of the bronchi expands by 35%, i.e. the therapeutic effect of the combination is greater than the effect of each individual drug, but less than the mathematical sum of their individual effects (23% + 18% = 41%).

This type of drug interaction is expressed by the formula 1 + 1 = 1.75.

As a result of the summation of drug effects, the pharmacological effect of a drug combination is equal to the mathematical sum of the pharmacological effects of each of the jointly prescribed drugs. For example, the joint administration of two diuretics ethacrynic acid and furosemide (belonging to the “loop” group

diuretics, i.e. having a similar mechanism of action) in patients with heart failure leads to the summation of their diuretic effect.

This type of interaction is expressed by the formula 1 + 1=2.

Potentiation of the effect of a drug is a type of interaction in which the pharmacological effect of a combination of drugs is greater than the mathematical sum of the pharmacological effects of each individual drug prescribed together. For example, the hypertensive effect in shock from the administration of a combination of the glucocorticosteroid prednisolone and the α-adrenergic agonist norepinephrine, or the bronchodilator effect from the administration of a combination of the same prednisolone and the phosphodiesterase inhibitor aminophylline in status asthmaticus.

This type of drug interaction is expressed by the formula 1 + 1 = 3.

In drug antagonism, as a result of the combined use of several drugs, the pharmacological effect of one or more drugs included in this combination is weakened or blocked. For example, when organic nitrates and 3-adrenergic receptor blockers are jointly prescribed for the treatment of coronary artery disease, the latter, by blocking Pj-receptors of the heart, prevent the development of reflex tachycardia caused by nitroglycerin preparations.

This type of interaction is expressed by the formula 1 + 1 = 0.5.

Naturally, both synergism and antagonism of drugs can lead not only to optimization of the therapeutic effect, but also have an undesirable, harmful effect on the patient’s body.

For example, when combining aminoglycoside antibiotics and loop diuretics (furosemide, ethacrynic acid), their ototoxic side effects are mutually enhanced; with the combined use of tetracycline antibiotics and aminoglycoside antibiotics, pharmacological antagonism develops, as a result of which their antimicrobial activity is leveled.

The interaction of drugs with each other is based on 4 main mechanisms that determine the main types of their interaction:

pharmaceutical or physicochemical interaction;

pharmacodynamic interaction;

physiological interaction;

pharmacokinetic interaction.

5.1. Peculiarities of pharmaceutical drug interactions This type of drug interaction refers to the physico-chemical processes that occur during the combined use of drugs before their introduction into the patient’s body (in a syringe, dropper, etc.) and/or at the injection site, or in the lumen of the gastrointestinal tract and etc. This situation develops when drugs that enter into a simple chemical interaction are used in combination. For example:

It is known that cardiac glycosides precipitate in the presence of tannins in the solution. Adding hawthorn extract containing tannins to drops containing tincture of lily of the valley and motherwort leads to precipitation of cardiac glycosides of lily of the valley;

When a solution of the phosphodiesterase inhibitor aminophylline with the antihistamine diphenhydramine or aminophylline and the cardiac glycoside strophanthin is mixed in one syringe, a white suspension is formed - “milk”. This is due to the fact that the pH of the aminophylline solution is 9.0-9.7, the pH of the solution of diphenhydramine and strophanthin is 5.0-5.7, i.e. one solution is alkaline and the other is acidic. Due to a simple chemical interaction of drugs, a neutralization reaction occurs, as a result of which the mixed drugs lose their pharmacological activity.

The same reactions can occur in the lumen of the gastrointestinal tract when drugs are co-administered per os. In this case, drugs can enter into simple chemical interactions not only with each other, but also with food and/or digestive juices, although the latter can be attributed to the features of pharmacokinetic interactions of drugs (see below). This happens when, in the lumen of the gastrointestinal tract, one of the combined drugs enters into a physicochemical interaction with another, as a result of which it loses its pharmacological activity. For example:

anti-sclerotic (antilipidemic) drug cholestyramine, being an ion-exchange resin in its mechanism of action, when jointly prescribed with drugs such as indirect anticoagulants (neodicoumarin, phenylin, etc.), cardiac glycosides (digoxin, digitoxin), non-steroidal anti-inflammatory drugs (butadione, acetylsalicylic acid acid, etc.) due to the release of C1~ ions, converts them into insoluble, inactive compounds;

the effectiveness of therapy with indirect anticoagulants (neodicoumarin, phenylin, etc.) largely depends on the composition of the food:

If the diet includes a large amount of ingredients containing vitamin K (leafy vegetables - cabbage, spinach, etc.), then due to antagonism with vitamin K, the anticoagulants will lose their activity.

5.2. Features of pharmacodynamic interaction of drugs As mentioned above (see page 19), most drugs realize their pharmacological effects at the receptor level.

This is where their pharmacological interaction occurs. Currently, there are 4 main types of pharmacological interactions of drugs at the receptor level:

competition of drugs for binding to the receptor;

changes in the kinetics of drug binding at the receptor level;

interaction of drugs at the level of mediators;

change in receptor sensitivity under the influence of a combination of drugs.

Competition of drugs for binding to the receptor. Compete, i.e. drugs of both unidirectional action (agonist-agonist; antagonist-antagonist) and opposite action (agonist-antagonist) can fight for communication with the receptor. The competitiveness of drugs in relation to the receptor mainly depends on the degree of their affinity for it. Competition between drugs for binding to the receptor can have both positive therapeutic significance and be extremely dangerous for the patient’s body. For example: to treat an overdose of M-cholinergic receptors, which are agonists of cholinergic receptors, atropine is usually used, a blocker of cholinergic receptors, which, due to its greater affinity for cholinergic receptors, displaces cholinomimetics and thereby stops their action, i.e. has a positive therapeutic effect.

However, the prescription of the same atropine as an antispasmodic (for example, for renal colic) to patients receiving the Mcholinomimetic pilocarpine for the treatment of glaucoma may be accompanied by a sharp increase in intraocular pressure and, as a consequence, vision loss. This is based on 2 mechanisms:

greater affinity for the M-cholinergic receptor of the antagonist atropine than the agonist pilocarpine, and the ability of pilocarpine to increase the sensitivity of M-cholinergic receptors.

Changes in drug kinetics at the receptor level. This type of drug interaction implies a change in the processes of local transport of another by one drug or a change in its distribution at the site of action (in the biophase). As a rule, these processes occur in the area of receptors specific to these drugs and are directly determined by the peculiarities of their mechanism of action.

For example, a change in the pharmacological activity of the sympatholytic octadine against the background of the prescription of tricyclic antidepressants (for example, imipramine). The mechanism of action of octadin is based on its ability to deplete norepinephrine reserves in adrenergic synapses and thereby reduce high blood pressure.

Octadine can penetrate adrenergic synapses only with the help of a specific transport system. Tricyclic antidepressants, by blocking the activity of enzymes that ensure the penetration of octadine into adrenergic synapses, prevent the implementation of its hypotensive effect.

Interaction of drugs at the mediator level. As is well known, mediators are biologically active substances secreted by nerve endings and transmitting a nerve impulse (signal) at the synapse from the presynaptic to the postsynaptic ending. There are three main types of effects of drug combinations on mediators:

Type I - blockade by one drug of subsequent stages of action of another drug at the level of one biological process. For example, when the central α2-adrenergic receptor stimulant methyldopa and the ganglion blocker pentamine are co-administered, a consistent blockade of the process of blood pressure regulation occurs. Methyldopa, by stimulating central α2-adrenoreactive receptors, activates inhibitory processes in the central nervous system, leading to a decrease in sympathetic stimulation to the vessels, and pentamine, by blocking impulse transmission in the sympathetic ganglia, also reduces sympathetic impulses to the vessels.

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