Local muscle relaxants. Muscle relaxants. Combinations requiring special attention

solution for intravenous administration 100 mg/1 ml: vial. 2 ml or 5 ml 10 pcs. Reg. No.: LSR-003970/10

Clinical and pharmacological group:

Antidote for muscle relaxants

Release form, composition and packaging

Solution for intravenous administration transparent, colorless to light yellow.

Excipients: hydrochloric acid - q.s. to pH 7.5, sodium hydroxide - q.s. up to pH 7.5, water for injection - up to 1 ml.

2 ml - colorless glass bottles (10) - cardboard packs.
5 ml - colorless glass bottles (10) - cardboard packs.

Description of the active components of the drug " Braydan ®»

pharmachologic effect

Selective antidote for the muscle relaxants rocuronium bromide and vecuronium bromide. Sugammadex is a modified gamma-cyclodextrin, which is a compound that selectively binds rocuronium bromide and vecuronium bromide. It forms a complex with them in the blood plasma, which leads to a decrease in the concentration of the muscle relaxant that binds to nicotinic receptors at the neuromuscular synapse. This results in reversal of the neuromuscular blockade caused by rocuronium bromide or vecuronium bromide.

There was a clear dependence of the effect on the dose of sugammadex, which was administered at different periods of time and at different depths of neuromuscular conduction block. Sugammadex was administered in doses of 0.5 to 16 mg/kg both after a single administration of rocuronium bromide in doses of 0.6, 0.9, 1 and 1.2 mg/kg, or after administration of vecuronium bromide in a dose of 0.1 mg/kg, and after administration of maintenance doses of these muscle relaxants .

Sugammadex can be used at various times after administration of rocuronium bromide or vecuronium bromide.

Kidney failure. In two open clinical studies compared the effectiveness and safety of sugammadex in patients with renal failure severe or not, undergoing surgery. In one study, sugammadex was administered to reverse blockade caused by rocuronium bromide in the presence of 1-2 post-tetanic responses (4 mg/kg; n =68); in another study, sugammadex was administered at the onset of the second response in a four-shock (T2) mode (2 mg/kg; n=30). Recovery of neuromuscular conduction after blockade was not significantly longer in patients with severe renal failure compared to patients without renal failure. There were no cases of residual neuromuscular blockade or its resumption in patients with severe renal failure in these studies.

Effect on QT interval c. In three clinical studies of sugammadex used alone or in combination with rocuronium bromide or vecuronium bromide, or in combination with propofol or sevoflurane, no clinically significant QT prolongation was observed.

Indications

- elimination of neuromuscular blockade caused by rocuronium bromide or vecuronium bromide;

— elimination of neuromuscular blockade caused by rocuronium bromide in children over 2 years of age and adolescents in standard clinical situations.

Dosage regimen

Sugammadex should only be administered by or under the direction of an anesthesiologist. To monitor the degree of neuromuscular blockade and restoration of neuromuscular conduction, it is recommended to use an appropriate monitoring method. According to generally accepted practice, it is also recommended to monitor neuromuscular conduction in postoperative period for adverse events, including resumption of neuromuscular blockade. If, within 6 hours after administration of sugammadex, drugs are prescribed parenterally that can lead to the development drug interactions according to the type of displacement, it is necessary to monitor neuromuscular conduction for signs of resumption of neuromuscular blockade.

Adults

Sugammadex is used to reverse neuromuscular blockade of varying depth caused by rocuronium bromide or vecuronium bromide.

Elimination of neuromuscular blockade in standard clinical situations (residual blockade of neuromuscular conduction)

Sugammadex at a dose of 4 mg/kg is recommended to be administered when the restoration of neuromuscular conduction has reached the level of 1-2 post-tetanic contractions (in the post-tetanic counting mode (PTS)) after blockade caused by rocuronium bromide or vecuronium bromide. Average time to full recovery neuromuscular conduction (restoration of the ratio of the amplitudes of the fourth and first responses in the four-discharge stimulation mode (T4/T1) to 0.9) is approximately 3 minutes. Sugammadex at a dose of 2 mg/kg is recommended to be administered when spontaneous recovery of neuromuscular conduction after blockade induced by rocuronium bromide or vecuronium bromide has achieved at least 2 responses in the TOF mode. The average time until the T4/T1 ratio is restored to 0.9 is about 2 minutes.

When using sugammadex in recommended doses to restore neuromuscular conduction in standard clinical situations, more fast recovery T4/T1 ratios of up to 0.9 occur when neuromuscular blockade is caused by rocuronium bromide versus vecuronium bromide.

Emergency relief of neuromuscular blockade caused by rocuronium bromide

If there is a need for immediate restoration of neuromuscular conduction during blockade caused by rocuronium bromide, the recommended dose of sugammadex is 16 mg/kg.

When sugammadex is administered at a dose of 16 mg/kg 3 minutes after administration of a bolus dose of 1.2 mg/kg rocuronium bromide, the average time to restore the T4/T1 ratio to 0.9 is about 1.5 minutes.

Re-administration of sugammadex

In exceptional situations during recurarization in the postoperative period, after administration of sugammadex at a dose of 2 mg/kg or 4 mg/kg, the recommended repeat dose of sugammadex is 4 mg/kg. After administration of a repeated dose of sugammadex, it is necessary to monitor neuromuscular conduction until complete restoration of neuromuscular function.

Use of the drug in special groups patients

U patients with mild to moderate renal impairment (creatinine clearance 30-80 ml/min) the drug should be used in doses recommended for adult patients without impaired renal function. The use of sugammadex is not recommended in patients with severe renal impairment, including patients who are on program hemodialysis (HD<30 мл/мин) . Studies in severe renal impairment have not provided sufficient safety data to recommend the use of sugammadex in this group of patients.

At liver dysfunction Recommended doses of the drug remain the same as in adult patients, since sugammadex is excreted primarily by the kidneys. Due to insufficient data on the use of sugammadex in patients with severe liver failure and in cases where liver failure is accompanied by coagulopathy, it is recommended to use sugammadex with extreme caution.

Elderly patients: after administration of sugammadex in the presence of 2 responses in TOF stimulation mode against the background of blockade caused by rocuronium bromide, the total time for restoration of neuromuscular conduction (T4/T1 ratio up to 0.9) in adult patients (18-64 years) averages 2.2 minutes, in for elderly patients (65-74 years) - 2.6 minutes and for elderly patients (75 years or more) - 3.6 minutes. Despite the fact that the recovery time for neuromuscular conduction in elderly patients is slightly longer, the recommended doses of sugammadex are the same as for adult patients of the usual age group.

U obese patients The dose of sugammadex should be calculated based on actual body weight. The recommended dosages suggested for adult patients should be followed.

Children

Data on the use of sugammadex in children are limited. It is possible to administer the drug to eliminate the neuromuscular blockade caused by rocuronium bromide when 2 responses appear in the TOF stimulation mode.

For eliminating neuromuscular blockade caused by rocuronium bromide, in everyday practice children and adolescents aged 2 to 17 years It is recommended to administer sugammadex at a dose of 2 mg/kg (if there are 2 responses in TOF stimulation mode).

Other situations of neuromuscular conduction restoration encountered in standard practice have not been studied, so the use of sugammadex in these cases is not recommended until further data are available.

Acute restoration of neuromuscular conduction with the administration of sugammadex in children over 2 years of age and adolescents has not been studied, and therefore in these situations the use of the drug is not recommended until further data are available.

The drug can be diluted to improve dosing accuracy in children.

Rules for administering the drug

Sugammadex is administered intravenously as a single bolus injection over 10 seconds directly into a vein or into a system for intravenous administration.

If sugammadex is administered through a single infusion system with other drugs, it is necessary to thoroughly flush the system (for example, with a 0.9% sodium chloride solution) between the administration of the drug Braydan ® and drugs that are incompatible with it, as well as if compatibility has not been established.

Sugammadex can be administered in one system for intravenous administration along with the following infusion solutions: 0.9% (9 mg/ml) sodium chloride solution; 5% (50 mg/ml) dextrose solution; 0.45% (4.5 mg/ml) sodium chloride solution with 2.5%
(25 mg/ml) dextrose solution; Ringer's solution with lactic acid; Ringer's solution; 5% (50 mg/ml) dextrose solution in 0.9% (9 mg/ml) sodium chloride solution. For use in children, the drug Braidan ® can be diluted with 0.9% (9 mg/ml) sodium chloride solution to a concentration of 10 mg/ml.

Side effect

Most often (≥1/100 to< 1/10): осложнения анестезии.

The following adverse reactions have been associated with the use of sugammadex.

Complications during anesthesia

The appearance of motor activity, coughing during anesthesia or during surgery itself, which reflects the restoration of neuromuscular function.

Unintentional retention of consciousness during anesthesia

In some cases, patients receiving sugammadex have experienced unintentional restoration of consciousness during anesthesia. However, an association with the administration of sugammadex was considered unlikely.

The recurrence rate of blockade, as assessed by neuromuscular conduction monitoring, was 2% following sugammadex administration. However, this frequency was noted in cases where a suboptimal dose of sugammadex was administered (less than 2 mg/kg).

Hypersensitivity reactions after using sugammadex, incl. and anaphylactic, were observed in several people, incl. from volunteers. During clinical studies in patients undergoing surgical treatment, these reactions were rare, and data on the frequency of such reactions after the drug was marketed are not available.

Clinical manifestations of hypersensitivity reactions have ranged from isolated cutaneous reactions to serious systemic reactions (i.e., anaphylaxis, anaphylactic shock) and have been reported in patients who have not previously received sugammadex.

Symptoms accompanying these reactions may include redness, urticaria, erythematous rash, a sharp decrease in blood pressure, tachycardia, swelling of the tongue and larynx. Severe hypersensitivity reactions can be fatal.

Information about healthy volunteers

When using sugammadex, hypersensitivity reactions were observed, incl. anaphylactic. In a study in healthy volunteers (placebo, n=150; 4 mg/kg, n=148; 16 mg/kg, n=150), hypersensitivity reactions were observed in the 16 mg/kg group and rarely in the 4 mg/kg or placebo group.

This study also noted a dose-dependent pattern of dysgeusia, nausea, and skin erythema.

Patients with lung diseases

When caring for patients with a history of pulmonary complications, the physician should always be aware of the possibility of developing bronchospasm.

Contraindications

- severe renal failure (CK< 30 мл/мин);

- severe liver failure;

- pregnancy;

- period of breastfeeding;

- children under 2 years of age;

- hypersensitivity to the components of the drug.

Pregnancy and lactation

The excretion of sugammadex in milk in women during lactation has not been studied, but based on data from preclinical studies, this possibility cannot be excluded. Oral absorption of cyclodextrins is low and has no effect on the baby following administration of a bolus dose of sugammadex to a nursing mother. However, sugammadex should be used with caution in women during breastfeeding.

special instructions

Monitoring respiratory function during restoration of neuromuscular conduction

It is necessary to carry out mechanical ventilation until adequate spontaneous breathing is fully restored after elimination of the neuromuscular blockade. Even if complete restoration of neuromuscular conduction has occurred, others medications, which were used in the peri- and postoperative periods, may depress respiratory function, and therefore prolonged mechanical ventilation may be required.

If neuromuscular blockade develops again after extubation, it is necessary to ensure adequate ventilation in a timely manner.

Resumption of neuromuscular blockade

Re-development of neuromuscular blockade was observed mainly in cases where suboptimal (insufficient) doses of the drug were administered. In order to prevent the resumption of neuromuscular blockade, doses lower than recommended should not be used.

Time intervals at which muscle relaxants can be reintroduced after restoration of neuromuscular conduction with sugammadex

Repeated administration of rocuronium bromide or vecuronium bromide after use of sugammadex (up to 4 mg/kg) is possible at the following intervals:

Based on the pharmacokinetic model, the time interval at which 0.6 mg/kg rocuronium bromide or 0.1 mg/kg vecuronium bromide can be reintroduced after administration of sugammadex to patients with mild to moderate renal impairment should be 24 hours. If a shorter interval is required time to resume neuromuscular blockade, the dose of rocuronium bromide should be 1.2 mg/kg.

Repeated administration of rocuronium bromide or vecuronium bromide after immediate resolution of neuromuscular blockade (16 mg/kg sugammadex)

In rare cases where immediate relief of neuromuscular block is necessary, the recommended period of time for repeated administration of muscle relaxants is 24 hours.

If there is a need for neuromuscular blockade before this time has elapsed, non-steroidal muscle relaxants should be used.

The onset of action of a depolarizing muscle relaxant may be slower than expected due to the fact that a significant portion of postsynaptic nicotinic receptors may still be occupied by the muscle relaxant.

Renal dysfunction

Interactions due to prolonged exposure to rocuronium bromide or vecuronium bromide

In the instructions for use of rocuronium bromide or vecuronium bromide, you should pay attention to the list of drugs that potentiate neuromuscular blockade. If neuromuscular blockade recurs, mechanical ventilation and reintroduction of sugammadex may be required.

Complications of anesthesia

When restoration of neuromuscular conduction was carried out intentionally during anesthesia, signs of superficial anesthesia (movement, coughing, grimacing) were occasionally observed.

If neuromuscular blockade is reversed during anesthesia, additional doses of anesthetics and/or opioids may be required.

Liver dysfunction

Sugammadex is not metabolized in the liver, so studies have not been conducted in patients with impaired liver function. When using the drug in patients with severe liver dysfunction, special caution should be used. If liver failure is accompanied by coagulopathy, see special instructions for the effect on homeostasis.

Use of sugammadex in conditions intensive care

The use of sugammadex in patients receiving rocuronium bromide or vecuronium bromide in the intensive care unit has not been studied.

Use of sugammadex to reverse neuromuscular blockade caused by other muscle relaxants (not rocuronium bromide or vecuronium bromide)

Sugammadex should not be used to reverse neuromuscular blockade caused by muscle relaxants such as suxamethonium or benzylisoquinoline compounds.

Sugammadex should not be used to reverse neuromuscular blockade caused by other steroidal muscle relaxants as there are no data on efficacy and safety for such use. There is only limited data on the reversal of neuromuscular blockade caused by pancuronium bromide, but insufficient data does not allow us to recommend sugammadex for restoring neuromuscular conduction when using this muscle relaxant.

Slow recovery

In conditions associated with prolongation of circulation time (cardiovascular diseases, old age, renal and liver failure), the recovery time of neuromuscular conduction may increase.

Hypersensitivity reactions

The physician should be alert to possible hypersensitivity reactions and should take the necessary precautions.

Patients on a sodium-controlled diet

Each ml of solution contains 9.7 mg of sodium. A sodium dose of 23 mg can be considered sodium-free. If more than 2.4 ml of solution needs to be administered, this should be taken into account in patients on a sodium-restricted diet.

Effect on hemostasis

In vitro experiments showed an additional increase in aPTT and prothrombin time when sugammadex was used with indirect anticoagulants, unfractionated heparin, low molecular weight heparins, rivaroxaban and dabigatran. In studies in volunteers, doses of sugammadex 4 and 16 mg/kg caused a prolongation of mean maximum aPTT values ​​by 17% and 22%, respectively, and prothrombin time (MHO) values ​​by 11-22%, respectively. This limited prolongation of aPTT and prothrombin time (MHO) was short-term (≤30 min).

To date, no clinically significant effect of sugammadex (as monotherapy or in combination with these anticoagulants) on the frequency of peri- or postoperative bleeding has been identified.

Given the short-term nature of the limited increase in aPTT and prothrombin time caused by sugammadex (as monotherapy or in combination with the above anticoagulants), it is unlikely that sugammadex increases the risk of bleeding. Since there is currently no information on the use of sugammadex in patients with coagulopathies, their coagulation parameters should be carefully monitored in accordance with standard clinical practice.

After diluting sugammadex with infusion solutions, the physical and chemical stability of the drug is maintained for 48 hours at temperatures from 2° to 25°C. When opening a bottle containing sugammadex, it is necessary to strictly observe the rules of asepsis. Administration of the drug must be started without delay. If sugammadex is used in a delayed manner, then compliance with the time and storage conditions before its use is the responsibility of the physician. If the dilution was made under uncontrolled and unvalidated aseptic conditions, the storage time of the diluted solution should not exceed 24 hours at a temperature of 2° to 8°C.

Any remaining contents of infusion line bottles following administration of sugammadex should be disposed of in accordance with local regulations.

Impact on the ability to drive vehicles and operate machinery

Potentially hazardous activities that require high speed psychomotor reactions, such as driving a car or operating machinery, should be avoided.

Overdose

To date, there has been one report of an accidental overdose of the drug at a dose of 40 mg/kg. There were no significant side effects. Sugammadex good tolerated in doses up to 96 mg/kg with the absence of any side effects, dose-related or not.

Treatment: It is possible to remove sugammadex from the bloodstream by hemodialysis using a high fluid permeability filter, but not a low fluid permeability filter. Based on clinical studies, after a 3-6 hour hemodialysis session with a high fluid permeability filter, the plasma concentration of sugammadex is reduced by approximately 70%.

Drug interactions

Toremifene

Introduction fusidic acid

Hormonal contraceptives.

Physical incompatibility

Conditions for dispensing from pharmacies

The drug is available with a prescription.

Storage conditions and periods

The drug should be stored out of the reach of children, protected from light, at a temperature of 2° to 8°C. Do not freeze. Shelf life - 3 years.

Drug interactions

Interaction by binding type (hormonal contraceptives)

Due to the administration of sugammadex, the effectiveness of some drugs may be reduced due to a decrease in their (free) plasma concentration. In such a situation, it is necessary to either reintroduce the drug in question or prescribe a therapeutically equivalent drug (preferably of a different chemical class).

Interaction due to displacement of the muscle relaxant from the complex with sugammadex

Due to the administration of certain drugs after the use of sugammadex, theoretically, rocuronium bromide and vecuronium bromide may be displaced from the complex with sugammadex, resulting in a resumption of neuromuscular blockade. In such cases, it is necessary to resume the use of mechanical ventilation. Infusion administration of a drug that has led to the displacement of rocuronium bromide or vecuronium bromide from the complex with sugammadex should be discontinued. If interaction is expected to develop according to the type of repression after parenteral administration another drug (which was administered within 6 hours after the use of sugammadex), it is necessary to constantly monitor the level of neuromuscular conduction to identify signs of resumption of blockade. Displacement-type interactions are possible after administration of the following drugs: toremifene, flucloxacillin and fusidic acid.

Clinically significant pharmacodynamic interactions with other drugs can be expected:

- for toremifene, flucloxacillin and fusidic acid, displacement-type interactions cannot be excluded (clinically significant binding-type interactions are not expected);

- for hormonal contraceptives, the possibility of interaction by binding type cannot be excluded (clinically significant interaction by displacement type is not expected).

Interactions Potentially Affecting the Efficacy of Sugammadex

Toremifene, which has a relatively high binding constant and relatively high plasma concentrations, is capable of displacing vecuronium bromide or rocuronium bromide from the complex with sugammadex to some extent. Therefore, recovery of the T4/T1 ratio to 0.9 may be delayed in patients who received toremifene on the day of surgery.

Introduction fusidic acid in the preoperative period may lead to some delay in the recovery of the TOF (T4/T1) ratio to 0.9. However, in the postoperative period, the development of recurarization is not expected, since the rate of infusion of fusidic acid is more than several hours, and its accumulation in the blood is more than 2-3 days.

Interactions potentially affecting the effectiveness of other drugs

Hormonal contraceptives. The interaction between sugammadex (4 mg/kg) and progesterone may result in a decrease in progestogen exposure (34% AUC), which is similar to the decrease observed when the daily dose of an oral contraceptive is taken 12 hours later than usual, which in turn may lead to a decrease effectiveness of contraception. For estrogens, a reduced effect can also be expected. Therefore, a bolus dose of sugammadex is considered equivalent to one missed daily dose of oral hormonal contraceptives (combined or progestogen-only). If an oral contraceptive was taken on the day you took Sugammedx, you should refer to the section of the instructions for use of oral contraceptives that describes what to do if you miss a dose.

When using hormonal contraceptives that have a route of administration other than oral, the patient should use an additional non-hormonal contraceptive method for the next 7 days and refer to the instructions for use of this contraceptive for information.

Effect on laboratory parameters

In general, sugammadex has no effect on laboratory tests with the possible exception of the serum progesterone quantitation test.

Pharmaceutical incompatibility

The drug Braydan ® should not be mixed with other drugs and solutions except those recommended. If Braydan ® is administered through a single infusion line with other drugs, it must be flushed (for example, with 0.9% sodium chloride solution) between the use of Braydan ® and other drugs.

Physical incompatibility sugammadexa was observed with verapamil, ondansetron and ranitidine.

All antidepolarizing muscle relaxants have a structure resembling a double acetylcholine molecule, which is incorporated into a rigid ring structure. That is why, anti-depolarizing muscle relaxants in 1951 Bovet proposed to call it pachykurare (from the Greek. pachys- thick). The distance between the cationic nitrogen centers in the molecules of antidepolarizing muscle relaxants should be 1.00.1 nm.

MD: Antidepolarizing muscle relaxants penetrate the neuromuscular synapse and block the active centers of HH-cholinergic receptors, preventing them from interacting with acetylcholine. As a result, acetylcholine, which is released during the action potential, is not able to activate the receptors and trigger muscle contraction. The blockade of HH-cholinergic receptors is competitive in nature, i.e. when the level of acetylcholine increases, it can displace the muscle relaxant from its connection with the receptor and muscle excitability is restored.

Scheme 7. Mechanism of action of muscle relaxants. Normally, acetylcholine occupies the active site H M -cholinergic receptor opens a channel for sodium ions and ensures the generation of an action potential.

Antidepolarizing muscle relaxant tubocurarine occupies H M -cholinergic receptor and blocks the gate of the sodium channel in the closed state. Acetylcholine is not able to activate the receptor and open the gate. The action potential does not develop.

Depolarizing muscle relaxant succinylcholine, binding to H M -cholinergic receptor, fixes it in the open state and causes the development of a long-term potential, during which the muscle goes into a refractory state and no longer responds to nerve impulses with contractions.

At higher concentrations, anti-depolarizing muscle relaxants can directly block the sodium channel itself, establishing van der Waals bonds with its proteins with their hydrophobic radicals. This type of blockade is non-competitive in nature and acetylcholine, even in high concentrations, is not able to displace the muscle relaxant from its connection with the receptor channels.

Ultimately, the administration of muscle relaxants of this group leads to the occurrence of “flaccid” (peripheral) paralysis. Paralysis skeletal muscles occurs only if at least 80% of the receptors are blocked.

Atracurium (Atracuriumbesylate, Tracrium) Like tubocurarine, it is a benzoisoquinoline derivative; it is sometimes classified as a third generation muscle relaxant 3.

FC: The atracurium molecule has 2 ammonium cationic centers separated by a chain of 11 carbon atoms. Due to its high polarity, atracurium is not absorbed and is administered only intravenously. A distinctive feature of atracurium is its unique elimination mechanism. Atracurium undergoes hydrolysis in blood plasma in 2 ways:

Elimination Hofmann- This is a non-enzymatic hydrolysis that occurs spontaneously and its rate depends only on body temperature and tissue pH. When body temperature decreases from 37°C to 23°C, the half-life of atracurium increases 2.5 times (from 19 minutes to 49 minutes). This metabolic pathway produces laudanosine and benzoisoquinoline monoacrylate. The electrophilic monoacrylate molecule may undergo secondary elimination Hofmann, releasing the diacrylate. Both mono- and diacrylate are cytotoxic poisons that can alkylate nucleophilic molecules of cell membrane proteins. However, this effect appears only if the dose of atracurium exceeds the usual myoparalytic dose by 1,600 times. Laudanosine is eliminated from the body very slowly, mainly by the liver (half-life 115-150 min). It is able to penetrate the BBB and, in high concentrations (6 and 10 μg/ml, respectively), cause a drop in blood pressure and seizures. Typically, when using myoparalytic doses of atracurium, the level of laudanosine is only 0.3-0.6 μg/ml, but with prolonged administration it can increase to 5.5 μg/ml.

Enzymatic hydrolysis. It is carried out by pseudocholinesterase and is a minor metabolic pathway. In patients with a genetic defect of pseudocholinesterase, the effect of atracurium is not prolonged.

FE: After administration of atracurium, complete muscle paralysis develops within 2-4 minutes, but lasts only 20-40 minutes. With an increase in the dose of atracurium, no prolongation of muscle relaxation is observed, only a deepening of the degree of paralysis occurs.

The sequence of development of paralysis is similar to that when using tubocurarine. Atracurium does not affect the autonomic ganglia, so it does not cause significant changes in blood pressure, heart rate, central venous pressure or cardiac output. When using high doses, due to muscle relaxation of the muscle masses of the lower extremities, 1.0-1.5 liters of blood may be deposited in the veins, which will lead to a slight decrease in blood pressure.

Features of application. To create muscle relaxation, doses of 0.3-0.5 mg/kg intravenously are used. Typically, a double injection technique is used: first, atracurium is administered at a test dose of 0.08 mg/kg, and then, after 3 minutes, the administration is repeated at a dose of 0.42 mg/kg. Children are somewhat less sensitive to atracurium and their myoparalytic dose is 0.6 mg/kg.

NE: In high doses, atracurium can cause histamine release from mast cells, so it is not recommended for use in patients with a history of allergic reactions.

Atracurium has mutagenic activity. Experiments on animals have proven its embryotoxic and teratogenic effects (visceral and skeletal abnormalities). This effect is believed to be due to choquinoline monoacrylate.

Since the end of the action of atracurium does not depend on the work of plasma, liver and kidney enzymes, it can be used in persons with impaired excretory function of these organs, as well as in cases of enzymopathies.

FV: 1% solution in ampoules of 2.5 and 5 ml. It should be remembered that the solution loses about 6% of activity per year if stored at a temperature of 5°C. If the storage temperature rises to 25°C, then the loss of activity reaches 5% per month. If atracurium solutions are stored at room temperature, they should be used within 14 days.

Pipecuronium (Pipecuroniibromidi, Arduanum) It is an aminosteroid compound. Refers to second generation muscle relaxants.

FK: Pipecuronium molecules also contain 2 ionized nitrogen atoms, so it is not absorbed from the gastrointestinal tract and must be administered exclusively intravenously.

Pipecuronium is metabolized in the liver, producing 3-deacetyl, 17-hydroxy and 1,17-dihydroxy metabolites. 3-deacetyl-pipecuronium has a muscle relaxant effect, which is 40-50% of the effect of pipecuronium itself. Excretion of pipecuronium is carried out mainly by the kidneys (60%). Due to this double elimination, no dose adjustment is required with a single injection of pipecuronium, but with repeated administrations it is necessary to reduce the dose of the drug in patients with chronic renal failure.

FE: The muscle relaxant effect develops at a moderate speed, but persists for an extremely long time (60-120 minutes). Unlike muscle relaxants of the benzoisoquinoline structure, pipecuronium contributes very little to the liberation of histamine. Pipecuronium does not affect the autonomic ganglia and M-cholinergic receptors of the myocardium, so it does not cause changes in hemodynamic parameters (BP, heart rate, cardiac output).

Features of application. Pipecuronium is prescribed in doses of 70-80 mcg/kg; if it is necessary to prolong the effect, pipecuronium is re-administered in doses equal to ⅓ of the original.

NE: When using pipecuronium in high doses, hypotension may develop due to the fact that due to relaxation of the muscles of the lower extremities, 1.0-1.5 liters of blood can be deposited in the vessels and lead to a decrease in the volume of circulating blood.

Like all steroids, pipecuronium slightly increases blood clotting.

FV: powder in ampoules of 4 mg.

Indications for the use of muscle relaxants with antidepolarizing action:

To relax the muscles of the larynx and pharynx during intubation during mechanical ventilation or inhalation anesthesia. For this purpose, fast but short-acting muscle relaxants (atracurium) are used.

When performing operations on the thoracic and abdominal organs, the administration of muscle relaxants allows one to achieve muscle relaxation with a lesser depth of anesthesia (narcotics themselves are capable of creating muscle relaxation, but it occurs at a level of anesthesia close to toxic; if a muscle relaxant is prescribed, the dose of the narcotic may be significantly reduced).

Relief of convulsive syndrome in tetanus, status epilepticus, electroconvulsive therapy.

All depolarizing muscle relaxants have a flexible linear structure with clearly formed two acetylcholine fragments. The distance between their cationic heads is 1.00.1 nm. Bovet called these remedies leptocurare (from the Greek. leptos– thin, delicate).

Succinylcholine (Succinylcholine, Dythylin, Listenon, Suxamethoniiiodide) MD: When introduced into the body, succinylcholine is quickly taken up by muscle fibers in quantities 20 times greater than antidepolarizing muscle relaxants. It binds to the active center of the NM-cholinergic receptor and causes its long-term activation. Under the influence of activated cholinergic receptors, Na + channels of the muscle fiber open, depolarization of its membrane develops, and initial muscle contraction occurs.

Succinylcholine, however, is not able to quickly dissociate from the receptors and they remain in a state of prolonged activation, maintaining membrane depolarization. Depolarization causes the gradual closing of the inactivation gates of Na + channels and they become inactive. The muscle relaxes and stops responding to nerve impulses. Flaccid paralysis occurs.

In human muscles, as well as in fast skeletal muscles In cats, only the depolarizing effect of succinylcholine is usually observed, which is called phase I of the depolarization block. However, in the slow skeletal muscles of cats and humans, when administered together with halogenated narcotic gases, the so-called. II phase of depolarizing block 4.

The development of this phase is associated with the following mechanism. Gradually, due to the opening of K + channels and the release of potassium ions from the cell, its membrane is repolarized and the sensitivity of sodium channels is restored. However, acetylcholine, which is released during the passage of a nerve impulse, is still unable to cause activation of the receptors, since they remain bound to succinylcholine, which shields their active site. That. in this phase, succinylcholine behaves as a typical antidepolarizing muscle relaxant and maintains a state of flaccid muscle paralysis.

The end of the action of succinylcholine is associated with its hydrolysis under the influence of cholinesterase (pseudocholinesterase plays the main role in hydrolysis).

FC: The succinylcholine molecule contains 2 quaternary nitrogen atoms, so it penetrates extremely poorly through histohematic barriers, does not enter the central nervous system and is used only in the form of intravenous infusion or injection to create muscle relaxation.

The metabolism of succinylcholine occurs in the blood plasma due to hydrolysis by pseudocholinesterase into 2 molecules of choline, acetate and succinate. The rate of hydrolysis does not depend on liver and kidney function, so succinylcholine can be used in patients with chronic liver and kidney diseases.

FE: The myoparalytic effect of succinylcholine develops within 30-60 seconds after administration and lasts only 10-15 minutes. Immediately after administration, short-term muscle twitching (fasciculations) may be observed, followed by paralysis. But, at the same time, the nature of the development of paralysis differs from that with the introduction of antidepolarizing muscle relaxants. The muscles of the neck and limbs are the first to be turned off, then paralysis affects the muscles of the face, chewing and oculomotor muscles (however, these muscle groups are never completely paralyzed), and the muscles of the pharynx. The muscles of the torso are turned off last.

Respiratory muscles are extremely resistant to the action of succinylcholine (its range of myoparalytic action is 1:1,000) and are blocked only when toxic doses of the drug are used.

Table 7. Comparative characteristics of depolarizing and anti-depolarizing blocks.

Parameter	Anti-depolarizing block (tubocurarine)	Depolarizing block (succinylcholine)
Type of paralysis		Fasciculations progressing to flaccid paralysis
Species sensitivity	Rats > rabbits > cats	Cats > rabbits > rats
Effect on the muscle fiber membrane	Increasing the depolarization threshold	Depolarization
Effect on isolated skeletal muscle	Absent	Muscle contracture
Administration of neostigmine	Eliminates a block	Does not affect the block
Temperature reduction	Reduces block	Strengthens the block
The effect of cathodic current on the muscle	Reduces block	Strengthens the block
The order of development of paralysis	Fingers, eyes → limbs → neck, face → torso → respiratory muscles	Neck, limbs → face, jaws, eyes, pharynx → torso → → → respiratory muscles

Features of application. Succinylcholine is most often used for tracheal intubation and reduction of hip or shoulder dislocation (since in these areas large muscle mass prevents bone traction). However, it should be remembered that succinylcholine is not suitable for performing reduction in comminuted fractures, because in this case, the initial muscle twitching can cause displacement of fragments and injury to the neurovascular bundles.

Typically, succinylcholine is administered at a dose of 1.5-2.0 mg/kg.

NE: Succinylcholine is a histamine liberator and its administration can provoke a release of histamine, leading to bronchospasm. This effect can be prevented by first injecting an H1-blocker (antihistamine) - diphenhydramine (diphenhydramine).

Muscle fasciculations caused by succinylcholine lead to microtrauma of skeletal fibers, which is accompanied by nagging pain in muscles, appearing after 10-12 hours. This effect can be prevented by preliminary administration of 5-10 mg of diazepam, which reduces muscle tone.

Long-term depolarization of skeletal muscles leads to the opening potassium channels and the release of potassium ions from the muscle fiber in an attempt to repolarize it. The loss of potassium is so significant that it can cause clinically significant hyperkalemia with muscle weakness, block-type heart rhythm disturbances (especially in people taking cardiac glycosides).

Succinylcholine is able to stimulate the autonomic ganglia. This may lead to an increase blood pressure. In addition, it increases the tone of the external muscles of the eye and somewhat compresses the eyeball, so it is not used in ophthalmology, as well as in patients with traumatic injuries to the eyeball.

Sometimes, when using succinylcholine, idiosyncrasy develops, which can manifest itself in two conditions:

Abnormal prolongation of the myoparalytic action of succinylcholine to 3-5 hours. This effect is associated with hereditary deficiency of pseudocholinesterase (occurs with a frequency of 1: 8,000-9,000). To eliminate the effect of succinylcholine, such patients should be given pseudocholinesterase or transfused with ≥500 ml of donor blood (it also contains pseudocholinesterase).

Malignant hyperthermia. Occurs with a frequency of 1:15,000 in children and 1:100,000 in adults. The likelihood of development increases when succinylcholine is used concomitantly with halogenated anesthetic gases. It is believed that the development of this syndrome is associated with a hereditary defect in the structure of T-tubules of muscle fibers. Under the influence of succinylcholine, a massive release of calcium ions occurs from the T-tubules of the sarcoplasmic reticulum and this leads to stimulation of bioenergetic processes in the muscles and increased contractile thermogenesis. Symptoms of malignant hyperthermia are characterized by:

Hyperthermia (temperature increases by 0.5°C every 15 minutes);

Rigidity of skeletal muscles instead of the expected relaxation;

Tachycardia over 140 beats per minute with transition to arrhythmia and acute heart failure;

Metabolic and respiratory acidosis (increased formation of lactate and CO 2);

Hyperkalemia;

DIC syndrome.

Help with the development of malignant hyperthermia consists of intravenous administration of dantrolene (a drug that interferes with the release of calcium from the sarcoplasmic reticulum), inhalation of 100% oxygen, elimination of hyperthermia (the patient is covered with ice, gastric lavage is performed and Bladder ice-cold physiological solution, physiological solution cooled to 4°C is injected intravenously in a volume of 500-1000 ml). Activities continue until body temperature drops below 38°C. To eliminate hyperkalemia, 20-40 units of insulin are administered intravenously in 40-60 ml of 40% glucose.

FV: powder in ampoules of 100, 250 and 500 mg, 2% solution in ampoules of 5 and 10 ml.

Muscle relaxant antagonists

In case of overdose of antidepolarizing muscle relaxants or the need to urgently stop their myoparalytic effect, anticholinesterase drugs are used. They block cholinesterase, as a result of which the hydrolysis of acetylcholine stops and its concentration in the synapse increases. Excess acetylcholine can displace the muscle relaxant from its connection with the receptor and restore conductivity. Usually they resort to intravenous administration of 0.5-2.0 ml of a 0.05% solution of neostigmine. Since neostigmine increases the level of acetylcholine both in neuromuscular synapses and in M-cholinergic synapses of internal organs, in order to avoid the unwanted M-cholinomimetic effect of neostigmine, 0.5-1.0 mg of atropine is administered to the patient before using it.

In case of overdose of depolarizing muscle relaxants, their effect does not require special drug elimination, due to rapid hydrolysis by pseudocholinesterase. In patients with pseudocholinesterase deficiency, its effect can be stopped by intravenous administration 500 ml of donor blood, which contains this enzyme.

Muscle relaxants to relieve muscle spasms, when do you resort to taking them? Many are sharp and chronic diseases musculoskeletal system are accompanied by the appearance of persistent spasms of skeletal muscles. This intensifies the existing pain syndrome and can help to consolidate the pathological positions of the affected areas of the body. In addition, spasmed muscles become dense and sometimes compress nearby neurovascular bundles. Therefore, the treatment regimen for many diseases includes muscle relaxants to cope with muscle spasms.

How do muscle relaxants work?

After a doctor's recommendation to take muscle relaxants, people often wonder what it is. Often, by mistake, people start taking antispasmodics (usually No-shpu or drotaverine) and are disappointed when they do not get the required effect.

Actually it's 2 different groups drugs.

Muscle relaxants act on striated muscles, which are designed to maintain body position and carry out voluntary and automated movements. It is also called skeletal because these muscles are attached to the bones. But antispasmodics act primarily on smooth muscle fibers, which are located in the walls of blood vessels and hollow internal organs. Therefore, the indications for these drugs are different.

Muscle relaxants are classified according to their mechanism of action. They are central and peripheral, it depends on the area of ​​application of the molecules of the active substance. Each group includes drugs of different molecular structures, which determines the characteristics of their use.

Peripheral-acting drugs are depolarizing, non-depolarizing, and mixed. They have a curare-like effect, affecting neuromuscular transmission at the level of synapses with acetylcholine receptors.

Non-depolarizing drugs have a competitive effect with respect to acetylcholine; they are also called antidepolarizing drugs. Due to the content of nitrogen atoms, peripheral muscle relaxants are water-soluble and practically do not penetrate the blood-brain barrier. They are destroyed by digestive enzymes, so they can only be administered parenterally. Drugs in this group are quite powerful, so it is necessary to strictly adhere to the dosage and monitor the function of the respiratory muscles during their use.

Central muscle relaxants act at the level of the central nervous system. They influence the formation of excitatory impulses in certain motor areas of the brain and some areas of the spinal cord. The stability of their molecules and pharmacodynamic features allow the use of many of these drugs in the form of tablets and solutions for parenteral administration. They are often prescribed for various diseases of the spine and other pathologies of the musculoskeletal system, including outpatient treatment.

Scope of application

Centrally acting muscle relaxants are included in the anesthetic protocol for various surgical interventions, since their administration facilitates tracheal intubation and allows temporary blocking of the respiratory muscles if mechanical ventilation (artificial ventilation) is necessary. They are also used in traumatology during the reposition of displaced fragments during a fracture to relax large muscle groups. Some drugs are used to relieve resistant convulsive syndrome and in the modern version of electroconvulsive therapy.

Peripheral muscle relaxants have much more wide application, which is explained not only by their ease of use, but also by their higher security profile.

The most common situations in which drugs of this group are prescribed:

• severe myofascial syndrome, including those supported by psychosomatic and neurotic causes, chronic stress;

• chronic pain syndrome of various origins, often caused by the presence of muscle spasms;

• in the presence of central paralysis (after a stroke, with multiple sclerosis, cerebral palsy).

Simply put, central muscle relaxants are often prescribed for local or radiating to the limbs and neck, and for spastic paralysis. And if there is muscle tension in the cervical region, these drugs may be an indication.

Contraindications

The use of muscle relaxants is limited by the presence of renal and liver failure, myasthenia gravis and myasthenic syndrome, Parkinson's disease, peptic ulcers, hypersensitivity to the components of the drug.

Epilepsy and convulsive syndrome other etiologies are a contraindication for the prescription of drugs in this group. But in case of intractable attacks that threaten cardiac arrest, the doctor may decide to administer muscle relaxants while simultaneously transferring the patient to mechanical ventilation. At the same time, the use of a muscle relaxant is not a way to combat seizures; it only helps to reduce spasms upper sections respiratory tract and respiratory muscles, achieve controlled breathing.

Muscle relaxants are not recommended for use by pregnant and breastfeeding women. Such drugs are prescribed only when other treatment methods are ineffective, if potential benefit for the mother there is a higher risk of complications in the child.

Side effects and overdose

The following side effects may occur with the use of muscle relaxants:

• headache, dizziness;

• general weakness;

• nausea, discomfort in a stomach;

• dry mouth;

• lowering blood pressure (mainly when using peripherally acting drugs);

• skin rash;

• anaphylactic shock;

• weakness of the muscles of the face, neck and respiratory muscles (intercostal muscles and diaphragm) - when using peripheral muscle relaxants.

Failure to comply with doctor's recommendations and unauthorized excess permissible dose is fraught with the development of an overdose, which can be life-threatening. But pronounced side effects can develop even with an average therapeutic dose of the drug. When using peripheral muscle relaxants, this may be due to acetylcholine deficiency due to congenital features or using other medications.

Strengthen the effect muscle relaxants alcohol, psychotropic drugs and medications that affect the rate of drug metabolism in the liver.

An overdose of muscle relaxants requires emergency assistance. Since there is a high risk of respiratory arrest due to inhibition of the respiratory muscles, they try to hospitalize the patient in the intensive care unit. If anti-depolarizing drugs were used, proserin or other anticholinesterase drugs. There are no antidotes for other muscle relaxants, so in all other cases, methods of blood purification, mechanical ventilation, and symptomatic therapy are used.

Main representatives

The list of centrally acting muscle relaxants most commonly used in the Russian Federation includes drugs such as Baclofen, Sirdalud, Mydocalm and their analogues.

In addition, drugs from other pharmaceutical groups with additional muscle relaxant effects can also be used - for example, tranquilizers and memantine preparations.

And in aesthetic cosmetology, Mirra muscle relaxant cream is used ( plant origin) and botulinum toxin preparations. Clinical practice and reviews show that they allow you to achieve obvious and lasting relaxation of facial muscles with increased tone.

Relaxation of muscles with the elimination of spasms of skeletal muscles makes it possible to influence one of the important mechanisms of the development of pain, improve the patient’s condition with spastic paralysis, and even increase external attractiveness. But you should not use muscle relaxants uncontrolled, because these drugs can cause serious side effects. In addition, contacting a doctor will allow you to clarify the cause of the existing symptoms and select the most appropriate comprehensive treatment regimen.

Muscle relaxants or muscle relaxants are drugs that cause striated muscles to relax.

Classification of muscle relaxants.

The generally accepted classification is in which muscle relaxants are divided into central and peripheral. The mechanism of action of these two groups differs in the level of impact on synapses. Central muscle relaxants affect the synapses of the spinal and medulla oblongata. And peripheral ones - directly to the synapses that transmit excitation to the muscle. In addition to the above groups, there is a classification that divides muscle relaxants depending on the nature of the effect.

Central muscle relaxants have not become widespread in anesthesiology practice. But peripherally acting drugs are actively used to relax skeletal muscles.

Highlight:

• depolarizing muscle relaxants;
• anti-depolarizing muscle relaxants.

There is also a classification based on duration of action:

• ultra-short - lasts 5-7 minutes;
• short - less than 20 minutes;
• medium - less than 40 minutes;
• long-acting - more than 40 minutes.

Ultra-short-acting depolarizing muscle relaxants: listenone, succinylcholine, dithiline. Short-, medium- and long-acting drugs are mainly non-depolarizing muscle relaxants. Short-acting: mivacurium. Medium-acting: atracurium, rocuronium, cisatracurium. Long-lasting: tubocurorine, orphenadrine, pipecuronium, baclofen.

Mechanism of action of muscle relaxants.

Non-depolarizing muscle relaxants are also called non-depolarizing or competitive. This name fully characterizes their mechanism of action. Non-depolarizing muscle relaxants compete with acetylcholine in the synaptic space. They are tropic to the same receptors. But acetylcholine is destroyed under the influence of cholinesterase in a matter of milliseconds. Therefore, it is unable to compete with muscle relaxants. As a result of this action, acetylcholine is not able to act on the postsynaptic membrane and cause the depolarization process. The chain of conduction of the neuromuscular impulse is interrupted. The muscle is not excited. To stop the blockade and restore conduction, anticholinesterase drugs, for example, proserin or neostigmine, must be administered. These substances will destroy cholinesterase, acetylcholine will not break down and will be able to compete with muscle relaxants. Preference will be given to natural ligands.

The mechanism of action of depolarizing muscle relaxants is to create a persistent depolarizing effect that lasts about 6 hours. The depolarized postsynaptic membrane is unable to receive and conduct nerve impulses, and the signal transmission chain to the muscle is interrupted. In this situation, the use of anticholinesterase drugs as an antidote will be erroneous, since accumulating acetylcholine will cause additional depolarization and increase neuromuscular blockade. Depolarizing relaxants are mainly ultra-short-acting.

Sometimes muscle relaxants combine the actions of depolarizing and competitive groups. The mechanism of this phenomenon is unknown. It is assumed that anti-depolarizing muscle relaxants have an aftereffect in which the muscle membrane acquires persistent depolarization and becomes insensitive for some time. As a rule, these are longer-acting drugs

Use of muscle relaxants.

The first muscle relaxants were alkaloids of certain plants, or curare. Then they appeared synthetic analogues. It is not entirely correct to call all muscle relaxants curare-like substances, since the mechanism of action of some synthetic drugs differs from that of alkaloids.

The main area of ​​application of muscle relaxants has become anesthesiology. Currently clinical practice can't do without them. The invention of these substances made it possible to make a huge leap in the field of anesthesiology. Muscle relaxants made it possible to reduce the depth of anesthesia, better control the functioning of body systems, and created conditions for the introduction of endotracheal anesthesia. For most operations, the main condition is good relaxation striated muscles.

The effect of muscle relaxants on the functioning of body systems depends on the selectivity of the effect on receptors. The more selective the drug, the fewer side effects it causes from organs.

The following muscle relaxants are used in anesthesiology: succinylcholine, dithiline, listenone, mivacurium, cisatracurium, rocuronium, atracurium, tubocurarine, mivacurium, pipecuronium and others.

In addition to anesthesiology, muscle relaxants have found use in traumatology and orthopedics to relax muscles during the reduction of dislocations and fractures, as well as in the treatment of diseases of the back and ligaments.

Side effects of relaxers.

From the outside of cardio-vascular system muscle relaxants can cause increased heart rate and increased blood pressure. Succinylcholine has a dual effect. If the dose is small, it causes bradycardia and hypotension; if it is large, it causes the opposite effects.

Depolarizing-type relaxants may cause hyperkalemia if the patient's potassium levels are initially elevated. This phenomenon occurs in patients with burns, major injuries, intestinal obstruction, tetanus.

In the postoperative period, undesirable effects include prolonged muscle weakness and pain. This is explained by the persisting depolarization. Long-term restoration of respiratory function can be associated both with the action of muscle relaxants and with hyperventilation, obstruction respiratory tract or an overdose of decurarizing drugs (neostigmine).

Succinylcholine can increase pressure in the ventricles of the brain, inside the eye, in cranium. Therefore, its use in relevant operations is limited.

Depolarizing muscle relaxants in combination with drugs for general anesthesia may cause a malignant increase in body temperature. This is a life-threatening condition that is difficult to treat.

Basic names of drugs and their doses.

Tubocurarine. The dose of tubocurarine used for anesthesia is 0.5-0.6 mg/kg. The drug should be administered slowly over 3 minutes. During surgery, maintenance doses of 0.05 mg/kg are administered in fractional increments. This substance is a natural alkaloid of curare. Tends to decrease pressure, in large doses causes significant hypotension. The antidote for Tubocurarine is Prozerin.

Ditilin. This drug is a depolarizing type relaxant. Has a short but strong effect. Creates well-controlled muscle relaxation. Main side effects: prolonged apnea, increased blood pressure. It has no specific antidote. Similar action have medications listenone, succinylcholine, muscle relaxant.

Diplatz in. Non-polarizing muscle relaxant. Lasts about 30 minutes. The dose sufficient for one operation is 450-700 mg. No significant side effects were observed with its use.

Pipecuronium. The anesthesia dose is 0.02 mg/kg. Effective for a long time, for 1.5 hours. Unlike other drugs, it is more selective and does not affect the cardiovascular system.

Esmeron(rocuronium). The dose for intubation is 0.45-0.6 mg/kg. Valid for up to 70 minutes. Bolus doses during surgery: 0.15 mg/kg.

Pancuronium. Known as Pavulon. The dose sufficient for induction of anesthesia is 0.08-0.1 mg/kg. A maintenance dose of 0.01-0.02 mg/kg is administered every 40 minutes. It has multiple side effects on the cardiovascular system, as it is a non-selective drug. May cause arrhythmia, hypertension, tachycardia. Significantly affects intraocular pressure. Can be used for operations Caesarean section, as it does not penetrate the placenta well.

All these drugs are used exclusively by anesthesiologists and resuscitators with specialized breathing equipment!

In medicine, there are often situations when it is necessary to relax muscle fibers. For these purposes, those introduced into the body are used, neuromuscular impulses are blocked, and the striated muscles relax.

Medicines in this group are often used in surgery, to relieve seizures, before reversing a dislocated joint, and even during exacerbations of osteochondrosis.

Mechanism of action of drugs

With strong pain A spasm may occur in the muscles, which ultimately limits movement in the joints, which can lead to complete immobility. This issue is especially acute in osteochondrosis. Constant spasm interferes with the proper functioning of muscle fibers, and, accordingly, treatment is extended indefinitely.

To bring the patient's general well-being back to normal, muscle relaxants are prescribed. Drugs for osteochondrosis are quite capable of relaxing muscles and reducing inflammation.

Considering the properties of muscle relaxants, we can say that they find their use at any stage of the treatment of osteochondrosis. The following procedures are more effective when using them:

• Massage. Relaxed muscles respond best to stimulation.
• Manual therapy. It's no secret that the doctor's influence is more effective and safer, the more relaxed the muscles are.
• Physiotherapeutic procedures.
• The effect of painkillers is enhanced.

If you often experience or suffer from osteochondrosis, then you should not prescribe muscle relaxants for yourself; drugs in this group should only be prescribed by a doctor. The fact is that they have a fairly extensive list of contraindications and side effects, so only a doctor can choose a medicine for you.

Classification of muscle relaxants

The division of drugs in this group into different categories can be viewed from different points of view. If we talk about what muscle relaxants there are, there are different classifications. Analyzing the mechanism of action on the human body, we can distinguish only two types:

1. Peripheral acting drugs.
2. Central muscle relaxants.

Medicines can have effects of varying duration, depending on this they are distinguished:

• Ultra-short action.
• Short.
• Average.
• Long lasting.

Only a doctor can know exactly which drug is right for you. fits better in each specific case, so do not self-medicate.

Peripheral muscle relaxants

Able to block nerve impulses that pass to muscle fibers. They are widely used: during anesthesia, during convulsions, during paralysis during tetanus.

Muscle relaxants, peripherally acting drugs, can be divided into the following groups:

All of these medications affect cholinergic receptors in skeletal muscles, which is why they are effective for muscle spasms and pain. They act quite gently, which allows them to be used in various surgical interventions.

Centrally acting drugs

Muscle relaxants in this group can also be divided into the following types, taking into account their chemical composition:

1. Glycerol derivatives. These are Meprotan, Prenderol, Isoprotan.
2. Based on benzimidazole - "Flexin".
3. Mixed drugs, for example "Mydocalm", "Baclofen".

Central muscle relaxants are able to block reflexes that have many synapses in muscle tissue. They do this by reducing the activity of interneurons in spinal cord. These medications not only relax, but have a broader effect, which is why their use in treatment various diseases which are accompanied by increased muscle tone.

These muscle relaxants have virtually no effect on monosynaptic reflexes, so they can be used for relief without stopping natural breathing.

If you are prescribed muscle relaxants (drugs), you may come across the following names:

• "Metacarbamol".
• "Baclofen."
• "Tolperisone".
• "Tizanidine" and others.

It is better to start taking medications under the supervision of a doctor.

The principle of using muscle relaxants

If we talk about the use of these drugs in anesthesiology, we can note the following principles:

1. Muscle relaxants should only be used when the patient is unconscious.
2. The use of such drugs greatly facilitates artificial ventilation lungs.
3. Removing is not the most important thing, the main task is to carry out comprehensive measures to carry out gas exchange and maintain blood circulation.
4. If muscle relaxants are used during anesthesia, this does not exclude the use of anesthetics.

When drugs from this group became firmly established in medicine, we could safely talk about the beginning new era in anesthesiology. Their use made it possible to simultaneously solve several problems:

After the introduction of such drugs into practice, anesthesiology had the opportunity to become an independent industry.

Area of ​​application of muscle relaxants

Considering that substances from this group of drugs have a broad effect on the body, they are widely used in medical practice. The following areas can be listed:

1. During treatment neurological diseases which are accompanied by increased tone.
2. If you use muscle relaxants (drugs), the lower back pain will also subside.
3. Before surgical intervention into the abdominal cavity.
4. During difficult diagnostic procedures for some diseases.
5. During electroconvulsive therapy.
6. When performing anesthesiology without stopping natural breathing.
7. To prevent complications after injuries.
8. Muscle relaxants (drugs) for osteochondrosis are often prescribed to patients.
9. To facilitate the recovery process after
10. Availability intervertebral hernia is also an indication for taking muscle relaxants.

Despite such an extensive list of uses for these drugs, you should not prescribe them yourself, without consulting a doctor.

Side effects after taking

If you have been prescribed muscle relaxants (drugs), lower back pain should definitely leave you alone; only when taking these medications can you experience side effects. Some are possible, but there are also more serious ones, among them it is worth noting the following:

• Decreased concentration, which is most dangerous for people driving a car.
• Decreased blood pressure.
• Increased nervous excitability.
• Bed-wetting.
• Allergic manifestations.
• Problems with the gastrointestinal tract.
• Convulsive states.

Especially often, all these manifestations can be diagnosed with the wrong dosage of drugs. This is especially true for anti-depolarizing drugs. It is urgent to stop taking them and consult a doctor. Neostigmine solution is usually prescribed intravenously.

Depolarizing muscle relaxants are more harmless in this regard. When they are canceled, the patient's condition normalizes, and the use of medications to eliminate symptoms is not required.

You should be careful when taking muscle relaxants (drugs) whose names are unfamiliar to you. In this case, it is better to consult a doctor.

Contraindications for use

You should start taking any medications only after consulting a doctor, and these medications even more so. They have a whole list of contraindications, among them are:

1. They should not be taken by people who have kidney problems.
2. Contraindicated for pregnant women and nursing mothers.
3. Psychological disorders.
4. Alcoholism.
5. Epilepsy.
6. Parkinson's disease.
7. Liver failure.
8. Children's age up to 1 year.
9. Peptic ulcer disease.
10. Myasthenia.
11. Allergic reactions to the drug and its components.

As you can see, muscle relaxants (drugs) have many contraindications, so you should not cause further harm to your health and start taking them at your own peril and risk.

Requirements for muscle relaxants

Modern drugs must not only be effective in relieving muscle spasms, but also meet certain requirements:

One such drug that practically meets all the requirements is Mydocalm. This is probably why it has been used in medical practice for more than 40 years, not only in our country, but also in many others.

Among central muscle relaxants, it differs significantly from others in better side. This drug acts on several levels at once: removes increased impulses, suppresses the formation of pain receptors, slows down hyperactive reflexes.

As a result of taking the drug, not only does it decrease muscle tension, but its vasodilating effect is also observed. This is perhaps the only medicine that relieves spasm of muscle fibers, but does not cause muscle weakness, and also does not interact with alcohol.

Osteochondrosis and muscle relaxants

This disease is quite common in modern world. Our lifestyle gradually leads to back pain, to which we try not to react. But there comes a time when the pain can no longer be ignored.

We turn to a doctor for help, but precious time is often lost. The question arises: “Is it possible to use muscle relaxants for diseases of the musculoskeletal system?”

Since one of the symptoms of osteochondrosis is muscle spasm, that is, it makes sense to talk about using drugs to relax spasming muscles. During therapy, the following drugs from the group of muscle relaxants are most often used.

In therapy, it is usually not customary to take several drugs at the same time. This is provided so that side effects, if any, can be immediately identified and a different medicine can be prescribed.

Almost all drugs are produced not only in the form of tablets, but there are also injections. Most often when severe spasm and expressed pain syndrome For emergency assistance, the second form is prescribed, that is, in the form of injections. Active substance penetrates the blood faster and begins its therapeutic effect.

Tablets are usually not taken on an empty stomach, so as not to harm the mucous membrane. You need to drink water. Both injections and tablets are prescribed to be taken twice a day, unless there are special recommendations.

The use of muscle relaxants will only bring the desired effect if they are used in complex therapy, must be combined with physiotherapeutic procedures, therapeutic exercises, and massage.

Despite their high effectiveness, you should not take these drugs without first consulting your doctor. You cannot independently determine which medicine is suitable for your case and will bring greater effect.

Do not forget that there are a lot of contraindications and side effects that should not be discounted. Only competent treatment will allow you to forget about pain and spasming muscles forever.