To suppress internal anxiety, agitation and irritability, doctors prescribe sedatives. A sedative effect - what is it? Simply put, these are drugs that calm the nervous system. They allow you to overcome neuroses and other disorders that worsen the quality of life and negatively affect your mood.

What drugs have a sedative effect?

The action of sedatives is aimed at stimulating the calm activity of the nervous system and attenuating the excitation of impulses in the brain.

Such tools perform important functions for a person:

• Promotes early sleep and deep uninterrupted healthy sleep.
• Reduce internal anxiety.
• Regulate the functioning of the central nervous system.
• Contribute to the strengthening of the properties of certain drugs (painkillers and sleeping pills).

For the most part, sedatives do not cause side effects, addiction and do not have a negative impact on the work of internal organs and systems. The advantage of these agents is that they are well tolerated by almost everyone who takes them. It is in view of this positive effect, how does a sedative affect a person, that it is often used in therapy for the elderly and pregnant women.

It is forbidden to take drugs with a sedative effect to people who, during their course intake, continue to work with dangerous goods, mechanisms, and are engaged in activities related to driving.

Sedatives may have a slight effect on the functioning of the musculoskeletal system. Otherwise, doctors prefer these sedative drugs, even if there are other drugs with a strong effect in modern pharmacology.

When should sedatives be taken?

Tablets with a sedative effect today are presented in a large assortment in pharmacies. When should you seek their help? The nervous system of a healthy person should be in a state of balance. Under the influence of negative internal or external factors, it is disturbed, and a person becomes emotionally quick-tempered, cannot control himself and even sometimes be aware of his actions.

To establish a balance of such disorders, sedative substances are prescribed. They improve the quality of life of both the patient himself and his close circle. Various factors can provoke neurosis, stress, or feelings similar to these states.

These include:

1. Problems at work or school.
2. Passing exams or reports.
3. Conflict in the family or at work / study.
4. Overwork and insomnia.

In most cases, a mild sedative, which can be purchased at a pharmacy without a prescription, helps. In more complex and serious situations, the appointment of a potent drug with the desired sedative effect is done by a qualified specialist.

Classification of sedative drugs

In addition to the fact that drugs with a sedative effect are strong and light, they are also divided according to the nature of their origin.

When classifying, the following main groups of funds are distinguished:

1. Bromides containing potassium and sodium.
2. Herbal medicines.
3. Combined phytopreparations.

The active component of the first category of sedatives is the anion of bromine. The main form of release of such funds: solutions and mixtures. This was done in order to reduce their irritating effect on the gastrointestinal tract.

The work of bromides is aimed at activating the processes of inhibition of impulses in the cerebral cortex. A large dose of such a sedative drug can cause convulsions, and a toxic one (causing pathological changes in the body) provokes a coma. These sedatives are excreted mainly through the kidneys within 12 days, exactly the same amount of time their action continues.

Herbal sedatives are based on valerian, peony, motherwort and passionflower. They relax the body, allow you to achieve peace of mind and tranquility. Such medicines are produced in the form of tablets, capsules, alcohol tinctures, dry raw materials in disposable sachets or general packaging. It does not affect their strength.

Combined sedative drugs are those in which there is simultaneously a complex of active active ingredients. Their effect on the body is stronger than other anti-anxiety drugs.

When and how to take bromides?

Bromides are synthetic sedatives that are prescribed at the initial stage of hypertension, from insomnia, with hysteria and neuroses.

Indications for the use of these sedatives may also be complex therapy in the treatment of epilepsy.

It is necessary to use these drugs with a sedative effect according to the following scheme:

• Inside and before meals.
• Dosage is not more than 1 gram per single dose.
• Multiplicity of daily dosages - 3-4 times.

IMPORTANT! To minimize side effects from taking bromides will allow regular bowel cleansing, rinsing the mouth, water procedures. To enhance the effect of the properties of the drug should be limited to the consumption of table salt.

The dosage in each case is selected individually for the patient and depends on the reasons for the appointment. After the first dose of such a sedative, the result will not be noticeable. The medicine has a cumulative effect, so you can feel its effect after at least 3-4 days. The total duration of the course with bromine is 2-3 weeks.

Bromides with a potassium compound, which have a sedative effect, can also be produced in the form of powder and tablets. A liquid form of release with various dosages is used mainly for use in children. Drops are mixed with any fruit syrup and given to the child. To reduce the irritating effect of bromides on the intestines, the doctor may additionally prescribe reparants (substances that stimulate the regeneration of the gastric membrane).

Plant-based sedatives: indications and course of treatment

Herbal medicines in their properties and action can be compared with the simultaneous intake of caffeine and bromide.

The main indications for the use of these sedatives are:

• Insomnia.
• Hysteria.
• Neurosis.
• Arrhythmia in a mild form.
• Cardioneurosis.

Also, preparations based on a plant with a calming effect are actively used in the complex therapy of angina pectoris or hypertension. The established dosage of sedative drugs depends on the age of the patient and the severity of his condition. The effect of the sedative action becomes noticeable within a few minutes after ingestion.

The course of application depends on the plant on the basis of which the medicine is made:

1. On valerian: the duration of the course does not exceed 10 days. 3-5 doses are allowed per day.
2. On motherwort: 3-4 doses during the day, 30-50 drops at a time. The medicine should be taken before meals. For brewing dry raw materials, 1 tbsp is enough.
3. On a medicinal peony: the course of treatment is about 20-30 days. A single dosage of 30-40 drops 3-4 times a day.
4. On passionflower (passion flower): taken no more than 4 times a day. In the form of release in tablets - 1 or 2 pieces, in syrup - 5-10 ml.

If there are contraindications or personal intolerance to any herbal sedative medicine, you should stop taking it.

The choice of sedatives is large enough to find an analogue suitable for sedative action. Valerian-based preparations can enhance the properties of sleeping pills, tranquilizers or antipsychotics taken.

List of sedatives

To relieve psychomotor agitation, the patient may be prescribed sedatives, the action of which is much more effective and faster. This mechanism of work became possible due to the content in their composition of several plant sedates at once.

The list of such sedative drugs includes:

Corvalol based on valerian and mint. It also contains alcohol and phenobarbital.

Novo-passit

Persen

Valocormide based on valerian, lily of the valley, sodium bromide, menthol and belladonna.

This is an incomplete list of the names of such drugs. They differ in component composition, price and strength of action. These sedative drugs have found wide application in modern medicine.

What is glycine and how is it used?

Glycine refers to amino acids that are actively involved in many processes occurring in the human body. It refers to drugs with a sedative effect. Its advantage lies in the ease of penetration into almost all tissues and body fluids, without problems it reaches the brain.

This medicine has the following effect:

1. Improves metabolic processes of the central nervous system.
2. Eliminates depressive moods.
3. Removes irritability.
4. Promotes fast sleep.
5. Improves blood supply to the brain.

The sedation of this drug has been tested for years. It is actively prescribed to suppress hyperactive actions, with neurosis, psycho-emotional overstrain, sleep problems and decreased mental activity. It is used in complex therapy for recovery from craniocerebral injuries, encephalopathy and ischemic stroke. These sedatives affect the tone of the sympathetic nervous system.

IMPORTANT! It is forbidden to take glycine in case of personal intolerance to the medicinal component.

Release form of glycine - tablets. The maximum daily dosage of a sedative is 0.3 grams. It should be divided in equal parts into 2-3 daily doses. The duration of the course is not more than 1 month. To be effective, the tablets should be sucked under the tongue until they disappear completely.

Side effects of sedatives

Drugs that have a sedative effect on the human body can sometimes cause side effects when taken. Their list of such drugs is quite wide, but not fully understood.

Therefore, when prescribing sedatives, their use should be taken with all seriousness. You must be in constant contact with your doctor in order to identify developing pathologies in time. In each case, their action can be completely different.

Common side effects are:

• Decreased concentration and attention.
• Increased lethargy and apathy.
• Drowsiness.
• Decreased speed of mental activity.
• Slowdown of motor reactions.
• Constipation or indigestion.
• Dry mouth.
• Headache.

In most cases, taking sedatives does not distract a person from the daily routine of life, allows him to fully control himself, be aware of his actions and go to work. They drink medicines at night, which practically does not affect daily activity.

Simultaneous reception of antisedatives and sedatives is not allowed.

Who prescribes sedatives?

Having figured out what this sedative effect is, you should know who to contact for the appointment of such drugs. You can get a prescription for strong sedatives that are otherwise not sold in pharmacies by contacting a psychiatrist or psychotherapist. Their specificity is work with diseases of the psyche, nervous breakdown and disorders. It is within the competence of these medical professionals to determine the severity of the manifestation of the symptoms of the disease and prescribe drugs with a sedative effect to treat it.

For mild disorders, you can seek help from a psychologist. In addition to psychological help, he can advise drugs with a slight sedative effect. This specialist does not make appointments, since he does not belong to medical workers. And this means that his appointments are advisory in nature.

The price of sedatives

The price of sedative bromides varies from 20 rubles to 300. The cost depends on the volume of the purchased package and the strength of the drug.

In conclusion about sedative drugs

Drugs capable of sedating the nervous system have recently found wide application. This is due to a rather "nervous situation" in modern society, as well as safety and the almost absence of contraindications for sedatives. They rarely cause side effects, which means that they are well tolerated by almost all patients, including children.

The most popular in the appointment are sedatives of plant origin, as well as glycine. Their action is quite mild, therefore, they are not used as an independent method of treatment for serious disorders, but they are an important component of complex therapy.

Important! Self-medication with the use of sedative drugs is unacceptable. Appointments must be made by a specialist.

The rapid and complete elimination of the pain syndrome, leading to an increase in sympathetic activity, and painful subjective is the most important component of the early treatment of MI.

If an anginal attack does not subside within a few minutes after the cessation of the provoking factor (exercise) or if it develops at rest, the patient should take nitroglycerin at a dose of 0.4-0.5 mg in the form of tablets under the tongue or aerosol (spray). If the symptoms do not disappear after 5 minutes, and the drug is well tolerated, it is recommended to use it again. If chest pain or discomfort, regarded as its equivalent, persists for 5 minutes after repeated administration of nitroglycerin, it is necessary to immediately call the EMS and take nitroglycerin again. An exception can be made only for cases where the relief of an anginal attack in a given patient usually requires taking several doses of nitroglycerin and provided that the severity and duration of the pain syndrome have not changed.

Persistence of an anginal attack after the use of short-acting nitrates is an indication for the administration of narcotic analgesics. They should be entered only in/in. The drug of choice is morphine (except for documented cases of hypersensitivity to the drug). In addition to anesthesia, morphine helps to reduce fear, excitement, reduces sympathetic activity, increases the tone of the vagus nerve, reduces the work of breathing, causes expansion of peripheral arteries and veins (the latter is especially important for pulmonary edema). The dose required for adequate pain relief depends on individual sensitivity, age, body size. Before use, 10 mg of morphine hydrochloride or sulfate is diluted with at least 10 ml of 0.9% sodium chloride solution or distilled water. Initially, 2-4 mg of the drug should be injected intravenously. If necessary, the introduction is repeated every 5-15 minutes at 2-4 mg until pain is relieved or side effects occur that do not allow increasing the dose.

When using morphine, the following complications are possible:

severe arterial hypotension; eliminated in a horizontal position in combination with raising the legs (if there is no pulmonary edema). If this is not enough, a 0.9% sodium chloride solution or other plasma expanders are injected intravenously. In rare cases, pressor drugs;

Severe bradycardia in combination with arterial hypotension; eliminated by atropine (in / in 0.5-1.0 mg);

· nausea, vomiting; eliminated by phenothiazine derivatives, in particular, metoclopramide (in / in 5-10 mg);

Pronounced respiratory depression eliminated by naloxone (in / in 0.1-0.2 mg, if necessary, again every 15 minutes), but this also reduces the analgesic effect of the drug.

Opiates can weaken intestinal motility and lead to constipation. Drugs in this group reduce the tone of the bladder and make it difficult to urinate, especially in men with prostatic hypertrophy.

Drugs should not be used to prevent the complications of narcotic analgesics.

Other methods of pain relief have also been proposed, in particular, the combination of the narcotic analgesic fentanyl with the neuroleptic droperidol (dehydrobenzoperidol). The initial dose of fentanyl, as a rule, is 0.05-0.1 mg, droperidol 2.5-10 mg (depending on the level of blood pressure). If necessary, drugs are administered repeatedly at lower doses.

Reducing the pain syndrome is facilitated by the rapid restoration of the patency of the CA, the blood supply to the MI zone, the elimination of hypoxemia, the use of nitrates and b-blockers.

To reduce fear, it is usually sufficient to create a calm environment and administer a narcotic analgesic. With severe arousal, tranquilizers may be required (for example, intravenous diazepam 2.5-10 mg). Important for the emotional comfort of the patient is the appropriate style of behavior of the staff, explanation of the diagnosis, prognosis and treatment plan.

In patients with persistent anxiety and impaired behavior, as well as withdrawal symptoms from nicotine dependence, it is reasonable to use tranquilizers (minimal doses of benzodiazepine derivatives for a limited period of time). For severe symptoms associated with nicotine withdrawal, replacement therapy may be required. In case of agitation and delirium, intravenous administration of haloperidol is quite effective and safe. Altered perception, especially after administration of a fibrinolytic, is suspicious for intracranial hemorrhage, which should be ruled out prior to sedation.

Anxiety and depression that persist despite the psychological support of medical staff and communication with visitors may require specialist advice and specific medication.

Oxygen therapy

Breathing oxygen through nasal catheters at a rate of 2-8 l / min is indicated for arterial hypoxemia (arterial oxygen saturation less than 95%), acute heart failure. In severe HF, pulmonary edema, or mechanical complications of STEMI, severe hypoxemia may require various means of respiratory support, including tracheal intubation with mechanical ventilation, to correct severe hypoxemia.

There is no convincing evidence of benefit from oxygen administration in patients with uncomplicated STEMI.

organic nitrates

Organic nitrates - primarily nitroglycerin - a means of reducing myocardial ischemia. Nitroglycerin is a powerful vasodilator. Therefore, it can be used to eliminate or reduce the severity of myocardial ischemia, reduce elevated blood pressure and treat heart failure. With persistent myocardial ischemia (repeated anginal attacks), hypertension or congestive heart failure, nitrate infusion can be extended to 24-48 hours or more. There is no convincing evidence to support the use of nitrates in uncomplicated STEMI.

Nitroglycerin acts quickly and effectively when taken orally (standard tablets of 0.4 mg under the tongue with an interval of 5 minutes). An aerosol (spray) of nitroglycerin can also be used at the same dose and at the same intervals. However, an intravenous infusion should be established as soon as possible, because. it is with this method of administration that it is easier to choose an individual dosage of the drug. The criterion for an adequately selected rate of administration (dosage) is the level of SBP, which can be reduced by 10-15% in normotonic patients and by 25-30% in persons with hypertension, but not lower than 100 mm Hg. Art. The usual initial rate of drug administration is 10 µg/min. If it is ineffective, the infusion rate is increased by 10-15 mcg / min every 5-10 minutes until the desired effect is achieved.

Decreased SBP<90-95 мм рт. ст., развитие бради- или тахикардии свидетельствует о передозировке. В этом случае введение нитроглицерина следует приостановить. Т.к. период полужизни препарата короток, АД, как правило, восстанавливается в течение 10-15 мин. Если этого не происходит, следует предпринять стандартные мероприятия по увеличению притока крови к сердцу (приподнять нижние конечности; в более упорных случаях возможно в/в введение 0,9% раствора хлорида натрия, других плазмоэкспандеров и даже прессорных аминов).Если артериальная гипотензия препятствует применению надлежащих доз b-адреноблокаторов или ИАПФ, от применения нитратов можно отказаться.

With prolonged infusion, tolerance to nitroglycerin may develop. The most realistic way to combat it is to increase the rate of administration. If it is not possible to achieve the target level of blood pressure reduction, even by increasing the infusion rate to 200 mcg / min, the administration of the drug should be abandoned.

Contraindications for nitrates in STEMI: arterial hypotension (SBP<90-95 мм рт. ст.); выраженная индуцированная брадикардия (ЧСС <50 уд/мин) или тахикардия (ЧСС >100 beats / min in patients without severe pulmonary congestion), RV myocardial infarction, taking phosphodiesterase V inhibitors in the previous 48 hours.

Antiplatelet agents

ASK. ASA has a proven positive effect on mortality and recurrent myocardial infarction, starting from the early stages of the disease. Therefore, all patients with suspected STEMI who have no contraindications and have not regularly taken ASA in the previous few days should take a tablet containing 250 mg of the active substance as soon as possible. The drug is absorbed faster when chewed. From the next day, an unlimited long (lifelong) intake of ASA inside at a dose of 75-100 mg 1 time / day is shown. Enteric-coated ASA tablets have a slow onset of action and are therefore not suitable for the early treatment of STEMI (if only these are available, the tablet must be chewed). The ability of buffered or enteric-coated ASA tablets to reduce gastrointestinal bleeding has not been proven. If it is impossible to take ASA orally, it is possible to administer it intravenously, while taking into account the pharmacological characteristics of the drug with this method of administration, a dose of 80-150 mg may be sufficient.

ASA should be used with caution in liver disease, it is contraindicated in allergy or intolerance, exacerbation of gastric or duodenal ulcer, ongoing serious bleeding, hemorrhagic diathesis.

Blockers P2Y 12 platelet receptor to adenosine diphosphate. In all patients without contraindications, regardless of reperfusion therapy (except when urgent CABG is necessary), P2Y 12 receptor blockers should be used in addition to ASA.

Clopidogrel. The action of clopidogrel develops slowly. For an accelerated manifestation of the effect, it is advisable to start treatment as early as possible with a loading dose. The usual loading dose is 300 mg; for planned primary PCI, it should be increased to 600 mg. The justification for using a loading dose in people over 75 years of age who are not expected to undergo primary PCI has not been established (the recommended value of the first dose of clopidogrel in these cases is 75 mg). Obviously, in patients not receiving reperfusion treatment, a loading dose of 300 mg can be used, although there are no clinical data to support this opinion. Maintenance dose of clopidogrel - 75 mg 1 time / day. After primary PCI with stenting, clopidogrel 150 mg once a day can be considered to reduce the incidence of adverse outcomes and prevent stent thrombosis on days 2-7, but this approach is associated with an increased risk of major bleeding.

With the simultaneous use of ASA and clopidogrel before CABG and other major surgical interventions, clopidogrel should be discontinued 5-7 days in advance, unless the risk of refusing urgent intervention outweighs the risk of increased blood loss.

Clopidogrel can be used instead of ASA when its use is not possible due to allergies or severe gastrointestinal disorders in response to taking the drug.

When using clopidogrel in a number of patients, the degree of inhibition of the functional activity of platelets is lower than desired, which is associated with an increased risk of thrombotic complications (primarily stent thrombosis). The feasibility of identifying such patients through genetic testing or platelet aggregation testing, and the role of adjusting treatment based on the results of such testing (in particular, switching to ticagrelor or prasugrel) continue to be refined.

Ticagrelor. Ticagrelor is indicated only for planned primary PCI. See section 9.10 for details. Switching to ticagrelor (loading dose) is also possible in patients receiving clopidogrel. Taking ticagrelor does not preclude the use of GP IIb/IIIa blockers during PCI.

With the simultaneous use of ASA and ticagrelor before CABG and other major surgical interventions, ticagrelor should be discontinued 5-7 days in advance, unless the risk of refusing urgent intervention outweighs the risk of increased blood loss.

Prasugrel. Currently, there are data on the use of prasugrel only after preliminary CAG, PCI with stenting (primary or performed at least 24 hours after administration of a fibrin-specific thrombolytic and 48 hours after administration of streptokinase). Details are set out in section 9.10. The use of prasugrel in patients receiving clopidogrel, as well as pre-hospital initiation of the drug, have not been studied. The use of prasugrel does not preclude the use of GP IIb/IIIa blockers during PCI.

With the simultaneous use of ASA and prasugrel before CABG and other major surgical interventions, prasugrel should be discontinued 7 days in advance, unless the risk of refusing urgent intervention outweighs the risk of increased blood loss.

GP IIb/IIIa platelet blockers. GP IIb/IIIa platelet blockers are used in patients with STEMI only for PCI. See section 9.10 for details.

The use of GP IIb/IIIa platelet blockers is associated with an increased risk of major bleeding; thrombocytopenia may also occur. The level of Hb, Ht and the number of platelets should be determined initially, after 2, 6, 12, 24 hours from the start of the drug administration. With a decrease in the number of platelets<100000 в мм 3 может потребоваться отмена антитромботической терапии, <50000 в мм 3 – инфузия тромбоцитарной массы.

Parenteral administration of anticoagulants

Parenteral anticoagulants should be used in all patients with STEMI who have no contraindications. The choice of drug and the duration of its administration is determined by the approach to reperfusion treatment and the risk of clinically significant bleeding. In all cases, it is necessary to ensure proper continuity of treatment, avoiding unnecessary change of drugs.

NFG. In STEMI, UFH is used during PCI, during TLT, for the prevention and treatment of arterial or venous thrombosis and TE.

During PCI, UFH is administered as IV boluses to maintain certain ABC values ​​(Appendix 12).

As an accompaniment of TLT, UFH is used for 24-48 hours. At the same time, 60 IU / kg of the drug is initially administered intravenously (but not more than 4000 IU) and a constant intravenous infusion is started at an initial rate of 12 IU / kg / h (but no more than 1000 IU/h). Subsequently, the dose of UFH is selected, focusing on the APTT values, which should be in the range of 50-70 seconds or exceed the upper limit of the norm for the laboratory of a particular medical institution by 1.5-2 times. To reduce the risk of serious bleeding, at the beginning of treatment it is important to monitor the APTT quite often (after 3, 6, 12 and 24 hours after the start of the drug administration). This short-term use of UFH is inferior in efficacy to longer-term subcutaneous administration of enoxaparin and is currently used mainly in patients with severe renal insufficiency, a high risk of bleeding.

The same doses are used for the prevention of cardioembolic complications and the treatment of arterial or venous thrombosis and TE. The need for this arises in the presence of a thrombus in the LV cavity, with previous episodes of peripheral arterial TE, AF / AFL, mechanical and, in some cases, biological prosthetic heart valves (if the patient does not continue to take vitamin K antagonists). If long-term use of anticoagulants is needed, an oral vitamin K antagonist should be switched to an oral vitamin K antagonist in the coming days (Appendix 13).

If it is necessary to prevent venous thrombosis and TE, a dose of 5000 IU 2-3 times / day is recommended, which is administered during hospitalization until the end of bed rest (if there is no need to use higher doses of anticoagulants for other indications).

NMG. Enoxaparin is used to treat STEMI.

Primary PCI can be performed after an IV bolus of enoxaparin at a dose of 0.5 mg/kg. In terms of efficiency and safety, this approach is at least as good as the use of UFH.

In TLT, long-term (up to 8 days or shorter with early discharge from the hospital or successful PCI) s / c administration of enoxaparin, the dose of which is selected taking into account age and kidney function, is most effective (Appendix 12). Long-term use of enoxaparin in TLT has been studied in patients with blood creatinine levels<2,5 мг/дл (220 мкмоль/л) для мужчин и <2,0 мг/дл (177 мкмоль/л) для женщин. Если во время лечения эноксапарином возникает необходимость в ЧКВ, процедуру можно осуществлять без дополнительного введения других антикоагулянтов: в пределах 8 ч после подкожной инъекции при ЧКВ дополнительных антикоагулянтов не вводить не следует; в пределах 8-12 ч после подкожной инъекции или если была сделана только одна подкожная инъекция эноксапарина – перед процедурой необходимо ввести в/в болюсом 0,3 мг/кг. Устройство для введения катетеров может быть удалено из бедренной артерии через 6-8 ч после последней п/к инъекции эноксапарина и через 4 ч после в/в введения препарата.

The same doses of enoxaparin are used for the prevention of cardioembolic complications and the treatment of arterial or venous thrombosis and TE (indications are similar to UFH).

If it is necessary to prevent venous thrombosis and TE, a dose of enoxaparin 40 mg 1 time / day is recommended, which is administered during hospitalization until the end of bed rest (if there is no need to use higher doses of anticoagulants for other indications). Other LMWHs, dalteparin and nadroparin, can be used in the prevention of venous thrombosis and TE (Appendix 12).

An important advantage of LMWH over UFH is the ease of administration and the absence of the need for regular coagulological monitoring when using high (therapeutic) doses.

Fondaparinux sodium. Fondaparinux sodium is a synthetic pentasaccharide, a selective antagonist of activated coagulation factor X.

For TLT, long-term (up to 8 days or shorter in case of early discharge from the hospital or successful PCI) s.c. injections of fondaparinux, the first dose of which is given as an i.v. bolus, are most effective (Appendix 12). Evidence for the benefit of fondaparinux has been obtained with streptokinase and in cases where no reperfusion treatment is given. This approach to treatment has been studied in patients with blood creatinine levels.<3,0 мг/дл (265 мкмоль/л) и характеризуется низкой частотой геморрагических осложнений. Так же, как и при использовании НМГ, при лечении фондапаринуксом нет необходимости в регулярном коагулологическом контроле. В отличие от гепарина фондапаринукс не взаимодействует с кровяными пластинками и практически не вызывает тромбоцитопению. По большинству показаний вводится в дозе 2,5 мг 1 раз/сут п/к вне зависимости от МТ; противопоказан при клиренсе креатинина <20 мл/мин.

To prevent thrombotic complications during PCI in patients receiving fondaparinux, it is recommended to administer standard doses of UFH intravenously during the procedure (Appendix 12).

Fondaparinux can be used for the prevention and treatment of venous thrombosis and TE of the vessels of the pulmonary circulation (in the treatment of deep vein thrombosis and PE, higher doses of the drug, selected according to MT, should be used).

Bivalirudin. Bivalirudin is a direct selective thrombin antagonist. It has a very short half-life (average 25 minutes). Used for primary PCI. See section 9.10 for details.

Bivalirudin may also be used in patients with heparin-induced immune thrombocytopenia. Its use does not imply coagulation control; in case of renal insufficiency, the dose should be reduced (in severe cases, bivalirudin is contraindicated).

Complications when using parenteral anticoagulants. The most common complication of anticoagulant use is bleeding. Therefore, during treatment, it is necessary to actively look for signs of bleeding, determine the composition of red blood (including platelets) and Ht. With hemorrhagic complications, it is usually sufficient to stop the administration of the anticoagulant, however, in the case of severe bleeding, it may be necessary to neutralize the effect of the administered drug. The anticoagulant effect of UFH is eliminated by protamine sulfate (1 mg of protamine sulfate to neutralize 1 mg or 133 IU of the drug); protamine sulfate neutralizes no more than 60% of LMWH activity. There is no antidote for fondaparinux and bivalirudin. With severe anemia (Hb<75 г/л), усугублении ишемии миокарда, нарушениях гемодинамики требуется переливание эритроцитарной массы и свежезамороженной плазмы. Для выбора дозы и выявления противопоказаний к использованию НМГ, фондапаринукса и бивалирудина необходимо учитывать функцию почек. Клиренс креатинина (или скорость клубочковой фильтрации) следует определить в начале их использования и в дальнейшем регулярно переоценивать.

UFH and LMWH can cause immune thrombocytopenia. This is a dangerous complication. With a decrease in the number of platelets in the blood<100000 в мм 3 или более чем наполовину от исходного, введение гепарина следует прекратить. В большинстве случаев после этого количество тромбоцитов постепенно нормализуется. Если выраженная тромбоцитопения приводит к тяжелым геморрагическим осложнениям, возможно введение тромбоцитарной массы.

Oral anticoagulants.Vitamin K antagonists. If STEMI develops while taking a vitamin K antagonist and an INR value of ≥2, parenteral anticoagulants should be avoided. At the same time, PCI and TLT can be performed against the background of maintaining therapeutic INR values; for PCI, access through the radial artery is preferable. If the INR does not reach 1.5 at the start of treatment, the usual doses of parenteral anticoagulants can be used.

If vitamin K antagonists were not used prior to the development of STEMI, in patients with indications for long-term use of anticoagulants, dose titration should begin without delay, against the background of ongoing parenteral administration of anticoagulants (rules for switching from parenteral anticoagulants to vitamin K antagonists are set out in Appendix 13).

New oral anticoagulants. Experience in the treatment of STEMI while taking apixaban, dabigatran etexilate or rivaroxaban has not yet been accumulated.

It seems that when using these drugs, primary PCI by access through the radial artery is preferable. At the same time, it is reasonable to use standard doses of parenteral anticoagulants with a possible preference for bivalirudin (the shortest-acting drug, the i.v. infusion of which can be stopped after the end of the procedure). If only thrombolytic therapy is available, when deciding on the possibility of its implementation, it is worth considering the values ​​of indicators characterizing the content and activity of a new anticoagulant in the blood (thrombin time in dilution, ecarin clotting time or APTT for dabigatran etexilate; prothrombin time for apixaban and rivaroxaban), which should not be higher than the VGN. In this case (as in the absence of reperfusion treatment), the start of additional administration of parenteral anticoagulants should be delayed until the effect of new oral anticoagulants disappears (at least 12 hours after the last dose and longer in the presence of renal failure, especially when taking dabigatran etexilate).

8.6. β-adrenergic receptor blockers

Blockers of β-adrenergic receptors (β-blockers) in the acute period of STEMI, by reducing myocardial oxygen demand and improving coronary blood flow, help reduce myocardial ischemia, limit the size of ischemic damage and, as a result, reduce mortality, the frequency of recurrent MI, life-threatening arrhythmias , including VF, and according to some data, the frequency of heart ruptures. The effects of β-blockers are best studied in patients who did not receive reperfusion treatment; to a lesser extent this applies to TLT. In the early stages of STEMI, the choice of an acceptable dose of the drug is of paramount importance, which should not be too high if there is a risk of complications (primarily in the presence of HF).

The benefit of β-blockers is the higher, the earlier therapy is started and the faster their action is manifested. Therefore, the initial dose may be administered intravenously, especially in patients with hypertension, persistent ischemia, tachycardia in the absence of signs of heart failure, followed by a transition to taking oral drugs. With intravenous administration of the drug, it is possible to select an individual dose more accurately and faster, the sufficiency of which is usually judged by the desired heart rate. It should not be lower than 44-46 beats per 1 minute at night at rest. In randomized, controlled trials in the early stages of MI, atenolol and metoprolol have been studied in more detail, with sufficiently long-term use - carvedilol, metoprolol and propranolol (Appendix 12). However, there is reason to believe that a beneficial effect in MI is characteristic of all drugs of this class, with the exception of those with internal sympathomimetic activity.

The usual doses of β-blockers are given in Appendix 12. It contains indicative doses that may be less or slightly higher than those indicated, depending on the effect achieved. During the administration of drugs, blood pressure, ECG, symptoms of heart failure (dyspnea, moist rales in the lungs) and bronchospasm should be monitored.

The most rapid effect can be achieved with the on / in the introduction of esmolol, a significant advantage of which is a short half-life.

Absolute contraindications to the use of β-blockers in STEMI: cardiogenic shock, severe obstructive pulmonary disease in the acute stage, AV block II-III stage. in patients without a functioning artificial pacemaker, allergies. Relative contraindications: clinical manifestations of HF, evidence of low cardiac output, SBP<100 мм рт. ст., ЧСС <60 ударов в 1 мин, удлинение интервала PQ>0.24 sec, history of obstructive pulmonary disease, risk factors for cardiogenic shock. In patients with a significant violation of LV contractility, treatment should begin with minimal doses of β-blockers. In the presence of persistent tachycardia, it is advisable to perform echocardiography before starting the use of β-blockers.

If there are contraindications to β-blockers in the early stages of STEMI, the possibility of prescribing them should be regularly reassessed. It is reasonable to start dose titration of drugs for oral administration 24-48 hours after the disappearance of severe bradycardia, arterial hypotension, severe heart failure, AV blockade.

With an overdose of β-blockers, β-adrenergic agonists, for example, i.v. infusion of isoproterenol (1-5 μg / min), give a quick positive result.

RAAS inhibitors

ACE inhibitor are widely used both in the acute period of STEMI and after discharge from the hospital. In addition to the prevention of LV remodeling, they have a wide spectrum of action and reduce mortality. ACE inhibitors are especially effective in the most severe patients with extensive myocardial necrosis, reduced LV contractility (EF ≤40%), symptoms of heart failure, diabetes. A positive effect on mortality is observed from the very beginning of MI and increases with continued use of ACE inhibitors.

ACE inhibitors should be used from the first day of the disease. Given that many patients with STEMI are relatively unstable in the first hours of hemodynamics, it is recommended to start treatment with minimal doses. For the most commonly used early disease, captopril, the starting dose is 6.25 mg. If this dosage does not cause an undesirable decrease in blood pressure (for normotonic SBP<100 мм рт. ст.), через 2 ч доза может быть удвоена и затем доведена до оптимальной, не вызывающей выраженного снижения CАД. ИАПФ оказывают положительный эффект на фоне любой сопутствующей терапии, в т.ч. АСК. Общий принцип лечения – постепенно увеличивать (титровать) дозу до рекомендуемой (целевой), которая по данным клинических исследований обеспечивает положительное влияние на прогноз, а если это невозможно, до максимально переносимой (Приложение 12). Наиболее частое осложнение при использовании иАПФ – артериальная гипотензия. В случаях выраженного снижения АД на фоне лечения следует исключить наличие гиповолемии, уменьшить дозу сопутствующих препаратов, а если это не помогает или нежелательно, снизить дозу иАПФ. При САД <100 мм рт. ст. иАПФ следует временно отменить, а после восстановления АД возобновить прием, уменьшив дозу препарата. В процессе лечения иАПФ необходимо контролировать содержание креатинина и калия в крови, особенно у больных со сниженной функцией почек.

Contraindications for the use of ACE inhibitors: SBP<100 мм рт. ст., выраженная почечная недостаточность, гиперкалиемия, двусторонний стеноз почечных артерий, беременность, индивидуальная непереносимость.

Angiotensin II receptor blockers(valsartan). Experience with angiotensin II receptor blockers in STEMI is much less than with ACE inhibitors. According to available data, in STEMI complicated by a decrease in LV contractility (EF ≤40%) and / or signs of heart failure, valsartan has an effect comparable to that of an ACE inhibitor. The initial dose of valsartan is 20 mg / day; with good tolerance, the dose of the drug is gradually increased up to 160 mg 2 times a day. Considering that neither angiotensin II receptor blocker monotherapy nor their combination with an ACE inhibitor has any apparent advantages over ACE inhibitor monotherapy, the use of angiotensin II receptor blockers is limited to cases where patients with STEMI with reduced LV contractility or hypertension have ACE intolerance.

Aldosterone antagonists. The use of eplerenone in addition to optimal medical therapy, including b-blockers and ACE inhibitors, is indicated for patients with an EF ≤40% in combination with signs of heart failure or diabetes. In most cases, dose titration can begin on day 3-14 of the disease, provided that the level of creatinine in the blood in men was<2,5 мг/дл (220 мкмоль/л), <2,0 мг/дл (177 мкмоль/л) у женщин, а уровень калия в крови <5 ммоль/л. Альтернативой эплеренону может быть спиронолактон.

VF prevention

There are no reliable symptoms - precursors of VF. At the same time, given the high probability of its development in the first hours of the disease, it is desirable to have a universal method of prevention, at least in the initial period. The previously widespread tactics of prophylactic administration of lidocaine in almost all patients diagnosed with MI did not justify itself: despite a decrease in the number of cases of primary VF, overall mortality did not decrease, but increased due to side effects of the drug.

The early use of b-blockers contributes to a decrease in the frequency of primary VF. It is also advisable to maintain the concentration of potassium in the blood in the range of 4.0±0.5 mmol/l, magnesium >1 mmol/l. Electrolyte disturbances in the blood, in particular a decrease in the concentration of potassium, are so common in STEMI that intravenous infusion of potassium salt preparations is an almost universal measure in the initial period of the disease. However, the introduction of potassium salts is recommended to appoint after clarifying the content of electrolytes in the blood.

8.9. Metabolic Therapy and Blood Glucose Control

The introduction of "polarizing mixtures" containing glucose, potassium and insulin did not justify itself in the same way as the use of antioxidants.

The preferred approach to blood glucose control in patients with diabetes and/or hyperglycemia in STEMI remains unclear. The current recommendation for early STEMI is to maintain blood glucose levels ≤11 mmol/L (200 mg/dL), which may require IV insulin infusion in some cases. It is important to avoid hypoglycemia (blood glucose levels<5 ммоль/л или 90 мг/дл). В последующем следует индивидуализировать лечение, подбирая сочетание инсулина, его аналогов и гипогликемических препаратов для приема внутрь, обеспечивающее наилучший контроль гликемии. У больных с тяжелой СН (III-IV ФК по NYHA) не следует использовать производные тиазолидиндиона, способные вызвать задержку жидкости, устойчивую к мочегонным.

In the presence of hyperglycemia in early STEMI in patients without previously diagnosed DM, fasting blood glucose, HbA1c, should be measured, and if the result is questionable, a glucose tolerance test should be performed, preferably at least 4 days after hospitalization.

Magnesium salts

The use of magnesium salts in patients without a decrease in its content in the blood and paroxysms of VT of the "pirouette" type is not justified.

In the presence of pronounced psychomotor agitation, the main task is to stop it.

For this purpose, against the background of physical retention, the patient is injected intravenously with 2-4 ml of 0.5% solution of sibazon.

Approximately in 70-80% of cases this dose is sufficient.

If after 5-10 minutes there is no relief of excitation, it is allowed to re-administer this drug in the amount of half the dose from the original.

You can use chlorpromazine or tizercin (25-50 mg), but when prescribing them, you need to remember about a possible decrease in blood pressure.

A good effect is achieved when neuroleptics are combined with desensitizing drugs (diphenhydramine, suprastin, etc.).

A good effect is the use of 0.5-1.0 ml of 0.5% solution of haloperidol.

The main goal of subsequent sedative therapy is to prevent possible excitation and induce a long, up to 16-18 hours, sleep.

Maintenance doses of sedative drugs and the frequency of their administration are selected individually.

Therapy with nootropic drugs.

Simultaneously with sedative drugs, nootropics are prescribed, which normalize metabolic processes in the brain.

Detoxification therapy the main disease is produced according to the indications and methods set out in chapter 13. ENDOGENOUS INTOXICATION SYNDROME and chapter 16. ACUTE POISONING.

relief of dehydration, the elimination of metabolic shifts and disturbances in water and electrolyte balance is carried out according to the generally accepted rules of infusion therapy under the control of hourly diuresis and CVP (see Chapter 3. WATER-ELECTROLYTE METABOLISM and Chapter 4. ACID-ALKALINE STATE).

As infusion media, solutions of colloids, crystalloids, low molecular weight dextrans, a polarizing mixture, soda are used, and the patient is also given plenty of fluids.

Detoxification is carried out using hemodez and the method of forced diuresis.

The duration of infusion therapy is different.

In severe delirium, it lasts from 12 to 48-60 hours.

The indication for stopping infusion therapy is the elimination of signs of dehydration, the normalization of the somatic state and sleep.

Symptomatic therapy

1. Elimination of hemodynamic shifts.

2. Prevention or elimination of impaired renal and hepatic function (see Chapter 12. ACUTE RENAL AND LIVER FAILURE).

3. Treatment of intercurrent diseases.

4. In the treatment of patients with alcoholic delirium, special attention is paid to the state of the cardiovascular system, since the most common cause of their death is acute cardiovascular insufficiency. Treatment and prevention of this pathology are carried out according to the rules set out in Chapter 7. EMERGENCY CONDITIONS IN DISEASES OF THE CARDIOVASCULAR SYSTEM.

hospitalization issues.

The presence of an uncomplicated delirious state in an inpatient is not an indication for hospitalization in a psychiatric hospital.

In the presence of a complicated delirious condition, the issue of hospitalization is decided on an individual basis, depending on the severity and nature of the underlying somatic disease and the conclusion of a psychiatrist.

If alcoholic delirium occurs at home - urgent hospitalization in a psychiatric hospital using physical restraint of the patient; when this pathology occurs in somatic patients in a hospital setting (for example, in the early postoperative period), treatment is usually carried out on the spot in cooperation with a psychiatrist.

23.3.2. Oneiroid state (oneiroid)

Oneiroid- dream-like, dream-like obscuration of consciousness with impaired orientation and self-awareness, with fantastic experiences and visions that form a certain plot and form a single whole (space flights, adventures, etc.), in which the patient feels himself to be an active participant.

Epidemiology. True oneiroid often culminates in the development of an attack of recurrent schizophrenia, and is less common in other diseases.

clinical picture.

At the first stages of development of oneiroid, there are sleep disorders, then appears staging nonsense: it seems to the patient that everything around him is specially arranged and it is for him that the scenes are played out.

At this time, the patient has dual orientation: he is simultaneously in the real and fantasy world, partly understanding this.

The patient experiences colorful fantasies: visits other worlds, maybe in heaven or hell, is the liberator of all mankind, controls the movement of the planets, etc., but his behavior does not correspond to his experiences: he is detached from the environment in a stupor-like or sub-stuporous state, with open eyes and a fixed gaze fixed into the distance (the eyes may also be closed); silent or senselessly pathetically excited, facial expressions frozen, tense or enthusiastic.

Sometimes there is waxy flexibility, and some patients may walk with a "charmed smile".

The dreamlike state may be associated with signs of delirium, verbal hallucinosis, or acute paranoid.

Unlike delirium, with oneiroid, not suggestibility is observed, but (more often) negativism, there is no wakefulness symptom typical of delirium (A. A. Portnov, D. D. Fedotov, 1967).

The main signs of oneiroid are detachment from the outside world, fantastic delusional experiences, double orientation, the exclusivity of one's own personality and the discrepancy between the experiences and behavior of the patient.

Upon exiting the oneiroid, partial memories are revealed, more complete and consistent - about subjective phenomena-400

i x and insufficient, or completely lost - about real events.

Duration - up to several weeks.

Urgent care similar to the treatment of delirium.

Hospitalization Issues in a psychiatric hospital are decided on an individual basis, depending on the severity and nature of the underlying disease.

amentia

Amentia (amental state of personality)- a form of clouding of consciousness, characterized by a loss of the ability to synthesize, with phenomena of incoherent speech, a violation of all types of orientation, including awareness of one's own personality, impaired motor skills and confusion.

Epidemiology. Amentia can occur against the background of a long-term, debilitating illness, with extreme somatic and mental exhaustion, lasting for a long time, up to several months.

Symptoms amentias are manifested in the impossibility in general to catch the connection between objects and phenomena.

The incoherence of all types of mental activity and speech is characteristic.

It becomes incoherent, meaningless and consists of separate words, sounds, interjections, often pronounced by the patient repeatedly with different volumes.

Motor excitation is limited to the limits of the bed: the patients bend, rotate, shudder, throw the limbs to the sides.

Separate motor reactions (the patient touches something, pushes away, grabs) and the corresponding facial expressions indicate the presence of hallucinatory-delusional experiences that are fragmentary.

Motor activity can be replaced by stupor.

There is no speech contact.

From individual statements, it is sometimes possible to conclude that these patients have an affect of bewilderment and helplessness, symptoms that are constantly encountered with confusion.

The main signs of amentia are gross disorientation in time, place and self, the impossibility of contact, motor speech anxiety against the background of the progression of the underlying disease with rapid weight loss against the background of the patient's refusal to take water and food.

Amenia ends with deep asthenia with complete amnesia of what has been transferred.

Urgent care similar to help with delirium (see above section 23.3.1. delirious syndrome) but more intense, and after the relief of psychomotor arousal, additional emphasis is placed on complete parenteral nutrition.

Hospitalization in a psychiatric hospital, as a rule, due to the severity of the somatic condition, is not performed.

Treatment in a specialized hospital in collaboration with a psychiatrist.

Table of contents of the subject "Stunning. Stupefaction. Delirium. Oneiric.":
1. Clouding of consciousness. Delirium. Delirious syndrome. Epidemiology of delirium. delirium symptoms. Delirious symptoms.
2. Sopor. Coma. Moderate coma (coma I, one). Coma deep (coma II, two). Terminal coma (coma III, three).
3. Clouding of consciousness. Delirium. Delirious syndrome. Epidemiology of delirium. delirium symptoms. Delirious symptoms.
4. Clinic (signs) of delirium syndrome (deliry). The first stage (phase) of delirium. Emergency (first) aid during the first phase of delirium.
5. Clinic (signs) of the second, third stage (phase) of delirium. The second, third stage (phase) of delirium. Emergency (first) care during the second, third phase of delirium.
6. Occupational delirium. Mumbling (mumbling) delirium. Alcoholic delirium (delirium tremens).
7. Clinic (signs) of alcoholic delirium. stages of delirium. Infectious delirium. delirium prevention.
8. Emergency (first) aid for delirium. Drug therapy for psychomotor agitation. Calming psychotherapy. Antipsychotic (sedative) therapy for delirium.
9. Symptomatic therapy for delirium. Questions of hospitalization at a delirium. When to hospitalize if the patient has delirium?
10. Oneiroid. Oneiroid state. Epidemiology of oneiroid. Clinic (signs) of oneiroid. Emergency (first) aid for oneiroid.

Emergency (first) aid for delirium. Drug therapy for psychomotor agitation. Calming psychotherapy. Antipsychotic (sedative) therapy for delirium.

Undoubtedly pathogenetically substantiated treatment of delirium of any etiology is detoxification therapy (see below), but in the presence of psychomotor agitation, treatment should begin with its relief, which consists of three directions:

1. Physical patient retention.

2. Calming psychotherapy.

3. Drug therapy.

physical hold produced by nurses; the patient is laid on his back and kept in this state, trying not to cause pain. When using fixing bandages, care must be taken not to pinch the blood vessels.

Calming psychotherapy is permanent. It is necessary to seek contact with the patient, explain what is happening, etc.

Drug therapy for psychomotor agitation includes the appointment of neuroleptic (sedative) and nootropic drugs, detoxification and symptomatic therapy.

Antipsychotic (sedative) therapy

In the presence of pronounced psychomotor agitation the main task is its cupping. For this purpose, against the background of physical retention, the patient is injected intravenously with 2-4 ml of 0.5% solution of sibazon. Approximately in 70-80% of cases this dose is sufficient. If after 5-10 minutes there is no relief of excitation, it is allowed to re-administer this drug in the amount of half the dose from the original. You can use chlorpromazine or tizercin (25-50 mg), but when prescribing them, you need to remember about a possible decrease in blood pressure. A good effect is achieved when neuroleptics are combined with desensitizing drugs (diphenhydramine, suprastin, etc.). A good effect is the use of 0.5-1.0 ml of 0.5% solution of haloperidol. The main goal of subsequent sedative therapy is to prevent possible excitation and induce a long, up to 16-18 hours, sleep. Maintenance doses of sedative drugs and the frequency of their administration are selected individually.

Therapy with nootropic drugs. At the same time with sedatives nootropics are prescribed that normalize metabolic processes in the brain. Recommended drugs and their doses of administration - see topic Stunning.

Detoxification therapy of the underlying disease produced according to the indications and methods outlined in the topic. SYNDROME OF ENDOGENOUS INTOXICATION and the topic ACUTE POISONING.

Relief of dehydration, the elimination of metabolic shifts and disturbances in water and electrolyte balance is carried out according to the generally accepted rules of infusion therapy under the control of hourly diuresis and CVP (see the topic WATER-ELECTROLYTE METABOLISM and the topic ACID-ALKALINE STATE). As infusion media, solutions of colloids, crystalloids, low molecular weight dextrans, a polarizing mixture, soda are used, and the patient is also given plenty of fluids. Detoxification is carried out using hemodez and the method of forced diuresis. The duration of infusion therapy is different. In severe delirium, it lasts from 12 to 48-60 hours. The indication for stopping infusion therapy is the elimination of signs of dehydration, the normalization of the somatic state and sleep.

Emergency care scheme for delirium