Medications used in resuscitation and certain emergencies

To restore self-circulation, it is necessary to start the introduction of medications as soon as possible and infusion therapy. The list of drugs currently used for primary resuscitation is relatively small.

[1], [2]

Adrenalin

Adrenomimetic, most often used in cardiopulmonary and cerebral resuscitation. Improves coronary and cerebral blood flow, increases excitability and contractility of the myocardium, narrows peripheral vessels.

The goal of therapy is to achieve spontaneous and stable hemodynamics with a systolic pressure of at least 100-110 mm Hg. Art. It contributes to the restoration of rhythm with asystole and electromechanical dissociation, as well as the transfer of small-scale ventricular fibrillation into large-wave.

The primary dose of epinephrine is 1 mg (1 ml 0.1% solution) intravenously. Intervals between adrenaline administration are from 3 to 5 minutes. With intratracheal administration, the adrenaline dose is 3 mg (per 7 ml isotonic sodium chloride solution).

After the restoration of cardiac activity, there is a high risk of recurrence of ventricular fibrillation due to inadequate coronary perfusion. For this reason, epinephrine is used as inotropic support at a dose of 1-10 μg / min.

[3]

Vasopressin

Vasopressin (antidiuretic hormone - ADH) is the hormone of the posterior lobe of the pituitary gland. It is secreted when the osmolarity of the blood plasma increases and when the volume of extracellular fluid decreases.

Increases the reabsorption of water by the kidneys, increasing the concentration of urine and reducing its secreted volume. It also has a number of effects on blood vessels and the brain.

Based on the results of experimental studies, vasopressin helps restore cardiac activity and coronary perfusion.

To date, vasopressin is considered as a possible alternative to adrenaline.

It has been established that the level of endogenous vasopressin is significantly higher in persons successfully resuscitated, in comparison with the deceased.

Introduced instead of the first or second injection of epinephrine once intravenously in a dose of 40 mg. If inefficiency is not re-applied, it is recommended to switch to adrenaline.

Despite the promising results of the studies, in multi-center studies there was no increase in hospital survival with vasopressin. Therefore, the International Consensus of 2005 concluded that "at present there is no conclusive evidence for both, and against the use of vasopressin as an alternative or in combination with adrenaline at any heart rate during CPR."

Kordaron

Antiarrhythmic drug of the III class (inhibitor of repolarization). It also has antianginal, coronarodilating, alpha and beta-adrenergic blocking, as well as hypotensive action. The antianginal effect of the drug is due to coronary dilatory, antiadrenergic action and a decrease in myocardial oxygen demand.

Has a retarding effect on alpha and beta-adrenergic receptors without developing their complete blockade. Reduces sensitivity to hyperstimulation of the sympathetic nervous system, reduces the tone of the coronary vessels, increases coronary blood flow; reduces the heart rate and increases the energy reserves of the myocardium (by increasing the content of creatine sulfate, adenosine and glycogen). Reduces overall peripheral resistance and systemic arterial pressure when administered intravenously. The antiarrhythmic effect is caused by the effect on the electrophysiological processes in the myocardium, lengthens the action potential of the cardiomyocytes, increasing the effective refractory period of the atria, ventricles, AV-node, bundle of His and Purkinje fibers, additional ways of carrying out the stimulation. Blocking inactivated "fast" sodium channels, has the effects characteristic for antiarrhythmic drugs of the first class. It inhibits slow (diastolic) depolarization of the cell membrane of the sinus node, causing bradycardia, inhibits AV-conduction (the effect of antiarrhythmics IV class).

The effectiveness of Cordarone in resuscitation activities has been confirmed in many studies. It is considered the drug of choice in patients with ventricular fibrillation and ventricular tachycardia, refractory to the three initial categories of the defibrillator.

Introduced intravenously bolus in a dose of 300 mg per 20 ml of 5% glucose. Additionally, it is recommended to maintain a maintenance infusion at a rate of 1 mg / min ^-1 for 6 hours (then 0.5 mg / min ^-1 ). Possible additional administration of 150 mg of the drug, if there is a recurrence of ventricular fibrillation or ventricular tachycardia.

Sodium bicarbonate

It is a buffer solution (pH 8.1), used to correct the disturbances of the acid-base state.

Apply in the form of 4.2 and 8.4% solution (8.4% solution of sodium bicarbonate is called a molar, since 1 ml contains 1 mmol of Na and 1 mmol of HCO2).

At the moment, the use of sodium hydrogen carbonate during resuscitation is limited due to the fact that uncontrolled administration of the drug can cause metabolic alkalosis, lead to inactivation of adrenaline and a decrease in the efficiency of electrical defibrillation.

It is not recommended to apply it before the restoration of the independent work of the heart. This is due to the fact that acidosis with the introduction of sodium bicarbonate will be reduced only in the case of removal through the lungs formed during its dissociation of CO2. In the case of inadequate pulmonary flow and ventilation, CO2 enhances extra- and intracellular acidosis.

Indications for the introduction of the drug are hyperkalemia, metabolic acidosis, an overdose of tricyclic antidepressants and antidepressants. Sodium bicarbonate is administered at a dose of 0.5-1.0 mmol / kg if the resuscitation process is delayed more than 15-20 minutes.

[4], [5], [6], [7], [8],

Calcium chloride

The use of calcium in cardiopulmonary resuscitation is limited in connection with the possible development of reperfusion injuries and disruption of energy production.

The introduction of calcium preparations during resuscitation is indicated in the presence of hypocalcemia, hyperkalemia and overdose of calcium antagonists.

Introduced in a dose of 5-10 ml of 10% solution (2-4 mg / kg or) for 5-10 minutes (10 ml of 10% solution contains 1000 mg of the drug).

[9], [10], [11], [12], [13]

Atropine sulfate

Atropine sulfate belongs to the group of anticholinergic drugs. The ability of atropine to bind to cholinergic receptors is explained by the presence in its structure of a fragment that makes it related to the molecule of the endogenous ligand, acetylcholine.

The main pharmacological feature of atropine is its ability to block M-cholinergic receptors; it also acts (albeit considerably weaker) on H-cholinergic receptors. Atropine therefore refers to non-selective blockers of M-cholinergic receptors. Blocking m-holinoretseptory, he makes them insensitive to acetylcholine, formed in the region of the postganglionic parasympathetic (cholinergic) nerves. Reduces the tone of the vagus nerve, increases the atrioventricular conduction conductivity, reduces the chance of developing ventricular fibrillation due to hypoperfusion with severe bradycardia, increases the heart rate with AV blockade (except for the full AV block). The use of atropine is indicated with asystole, cardiac activity without pulse, with a heart rate of less than 60, and also with bradisystolia *.

* According to the recommendations of ERC and AHA 2010, atropine is not recommended for the therapy of electromechanical dissociation / asystole and is excluded from the intensive care algorithm for maintaining cardiovascular activity in cardiac arrest.

At present, there is no conclusive evidence that atropine plays a significant role in the treatment of asystole. Nevertheless, in the recommendations of ERC and AHA 2005 the drug was recommended for use, as the prognosis for the treatment of asystole is extremely unfavorable. In this regard, the use of atropine can not further worsen the situation.

The recommended dose for asystole and electrical activity without a pulse with a heart rate of less than 60 per minute is 3 mg. The drug is administered once. Recommendations for the frequency of administration of the drug have now changed: it is proposed to limit its administration to a single dose of 3 mg intravenously. This dose is sufficient for a block of vagal activity in adult patients. In the ampoule, 1 ml of a 0.1% solution of atropine contains 1 mg of the drug.

[14], [15], [16], [17], [18], [19]

Lidocaine

Antiarrhythmic activity of the drug is due to the inhibition of phase 4 (diastolic depolarization) in Purkinje fibers, a decrease in automatism and suppression of ectopic foci of excitation. The speed of rapid depolarization (phase 0) does not affect or slightly reduces it. Increases the permeability of membranes for potassium ions, accelerates the process of repolarization, and shortens the action potential. Does not change the excitability of the sinus-atrial node, has little effect on the conductance and contractility of the myocardium. When administered intravenously, it acts quickly and briefly (10-20 min).

Lidocaine increases the threshold of ventricular fibrillation, stops ventricular tachycardia, promotes the transfer of ventricular fibrillation into the ventricular tachycardia, is effective in ventricular extrasystoles (frequent, polytopic, group extrasystoles and allorhythmias).

Currently considered as an alternative to Kordaron only when the latter is unavailable. Do not administer lidocaine after the administration of cordarone. The combined administration of these two drugs leads to a real threat of potentiation of cardiac weakness and the manifestation of proarrhythmic action.

A loading dose of lidocaine 80-100 mg (1.5 mg / kg) is injected intravenously. After achieving self-circulation, a maintenance infusion of lidocaine in a dose of 2-4 mg / min is carried out.

Magnesium sulfate

Magnesium sulphate has an antiarrhythmic effect in disturbances of water-electrolyte balance (hypomagnesemia, etc.). Magnesium is an important component of the body's enzyme systems (the process of energy generation in muscle tissue), is necessary for the implementation of neurochemical transmission (inhibition of acetylcholine release and decrease in the sensitivity of postsynaptic membranes).

It is used as an additional antifibrillatory agent in stopping blood circulation against hypomagnesemia. The choice agent for ventricular tachycardia torsades de pointes is pirouette tachycardia (Figure 4.1).

Hypomagnesemia is often combined with hypokalemia, which can also serve as a cause of cardiac arrest.

Magnesium sulphate is administered bolus 1-2 g intravenously for 1-2 minutes. If the effect is insufficient, repeated administration in the same dose after 5-10 minutes is shown (in an ampoule of 10 ml of 25% contains 2.5 g of the drug).

[20], [21], [22], [23], [24], [25], [26], [27], [28]

Solutions of glucose

Currently, it is not recommended to use glucose infusion during resuscitation because it enters the ischemic area of the brain, where, when included in anaerobic metabolism, it is split into lactic acid. Local accumulation in the brain tissue of lactate increases its damage. More preferably, saline or Ringer's solution is used. After resuscitation, you must strictly monitor the level of glucose in the blood.

To determine the borderline glucose level, which requires the introduction of insulin, as well as allowable fluctuations in the target glucose concentration in the blood, further studies are needed.