Drugs used in resuscitation and certain emergency conditions

To restore spontaneous blood circulation, it is necessary to begin the administration of medications and infusion therapy as early as possible. The list of drugs currently used in primary resuscitation measures is relatively small.

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Adrenalin

Adrenomimetic, most often used in cardiopulmonary and cerebral resuscitation. Improves coronary and cerebral blood flow, increases myocardial excitability and contractility, constricts peripheral vessels.

The goal of therapy is to achieve spontaneous and stable hemodynamics with a systolic pressure of at least 100-110 mm Hg. It helps restore rhythm during asystole and electromechanical dissociation, as well as convert small-wave ventricular fibrillation to large-wave.

The initial dose of adrenaline is 1 mg (1 ml of 0.1% solution) intravenously. The intervals between adrenaline administrations are 3 to 5 minutes. For intratracheal administration, the dose of adrenaline is 3 mg (per 7 ml of isotonic sodium chloride solution).

After cardiac function is restored, there is a high risk of recurrence of ventricular fibrillation due to inadequate coronary perfusion. For this reason, adrenaline is used as inotropic support at a dose of 1-10 mcg/min.

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Vasopressin

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

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

According to the results of experimental studies, vasopressin promotes the restoration of cardiac activity and coronary perfusion.

Today, vasopressin is considered as a possible alternative to adrenaline.

It has been established that the level of endogenous vasopressin is significantly higher in individuals who were successfully resuscitated compared to those who died.

It is administered instead of the first or second administration of adrenaline, intravenously, once at a dose of 40 mg. If ineffective, it is not used again - it is recommended to switch to the administration of adrenaline.

Despite promising research results, multicenter studies have failed to show an increase in hospital survival with the use of vasopressin. Therefore, the 2005 International Consensus concluded that “there is currently no convincing evidence for or against the use of vasopressin as an alternative to or in combination with epinephrine in any rhythm during CPR.”

Cordarone

Antiarrhythmic drug of class III (repolarization inhibitor). Also has antianginal, coronary vasodilator, alpha- and beta-adrenergic blocking, and hypotensive effects. The antianginal effect of the drug is due to the coronary vasodilator, antiadrenergic effect and reduction of myocardial oxygen demand.

It has an inhibitory effect on alpha- and beta-adrenergic receptors without developing their complete blockade. It reduces sensitivity to hyperstimulation of the sympathetic nervous system, reduces the tone of the coronary vessels, increases coronary blood flow; slows the heart rate and increases the energy reserves of the myocardium (due to an increase in the content of creatine sulfate, adenosine and glycogen). It reduces total peripheral resistance and systemic arterial pressure when administered intravenously. The antiarrhythmic effect is due to the effect on electrophysiological processes in the myocardium, prolongs the action potential of cardiomyocytes, increasing the effective refractory period of the atria, ventricles, AV node, bundle of His and Purkinje fibers, and additional pathways for excitation conduction. By blocking inactivated "fast" sodium channels, it has effects characteristic of class I antiarrhythmic agents. Inhibits slow (diastolic) depolarization of the membrane of sinus node cells, causing bradycardia, inhibits AV conduction (the effect of class IV antiarrhythmics).

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

It is administered intravenously by bolus at a dose of 300 mg per 20 ml of 5% glucose. Additionally, it is recommended to carry out a maintenance infusion at a rate of 1 mg/min ^-1 for 6 hours (then 0.5 mg/min ^-1 ). An additional administration of 150 mg of the drug is possible if there is a relapse of ventricular fibrillation or ventricular tachycardia.

Sodium bicarbonate

It is a buffer solution (pH 8.1) used to correct acid-base imbalances.

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

Currently, the use of sodium bicarbonate 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 effectiveness of electrical defibrillation.

It is not recommended to use it until the heart's independent work is restored. This is due to the fact that acidosis with the introduction of sodium bicarbonate will be reduced only if the CO2 formed during its dissociation is removed through the lungs. In the case of inadequacy of pulmonary blood flow and ventilation, CO2 increases extra- and intracellular acidosis.

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

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Calcium chloride

The use of calcium preparations in cardiopulmonary resuscitation is limited due to the possible development of reperfusion lesions and disruption of energy production.

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

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

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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 (although much weaker) on H-cholinergic receptors. Atropine is thus a non-selective M-cholinergic receptor blocker. By blocking M-cholinergic receptors, it makes them insensitive to acetylcholine formed in the region of the endings of the postganglionic parasympathetic (cholinergic) nerves. It decreases the tone of the vagus nerve, increases atrioventricular conduction, reduces the likelihood of ventricular fibrillation due to hypoperfusion in severe bradycardia, and increases the heart rate in AV block (except for complete AV block). Atropine is indicated for asystole, pulseless cardiac activity with a heart rate of less than 60, and bradysystole*.

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

There is currently no convincing evidence that atropine plays a significant role in the treatment of asystole. However, the 2005 ERC and AHA guidelines recommended the drug for use because the prognosis for the treatment of asystole is extremely poor. Therefore, the use of atropine cannot make the situation worse.

The recommended dose for asystole and pulseless electrical activity with a heart rate of less than 60 beats 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 to block vagal activity in adult patients. A 1 ml ampoule of 0.1% atropine solution contains 1 mg of the drug.

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Lidocaine

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

Lidocaine increases the threshold for the development of ventricular fibrillation, stops ventricular tachycardia, promotes the conversion of ventricular fibrillation to ventricular tachycardia, and is effective in ventricular extrasystoles (frequent, polytopic, group extrasystoles and allorhythmias).

Currently, it is considered as an alternative to cordarone only when the latter is unavailable. Lidocaine should not be administered after cordarone. The combined administration of these two drugs leads to a real threat of potentiation of cardiac weakness and manifestation of proarrhythmic action.

A loading dose of lidocaine of 80-100 mg (1.5 mg/kg) is administered intravenously by jet stream. After achieving spontaneous circulation, a maintenance infusion of lidocaine at a dose of 2-4 mg/min is administered.

Magnesium sulfate

Magnesium sulfate has an antiarrhythmic effect in cases of water-electrolyte imbalance (hypomagnesemia, etc.). Magnesium is an important component of the body's enzyme systems (the process of energy formation in muscle tissue), and is necessary for neurochemical transmission (inhibition of acetylcholine release and decreased sensitivity of postsynaptic membranes).

It is used as an additional antifibrillatory agent in case of circulatory arrest due to hypomagnesemia. The drug of choice for ventricular tachycardia torsades de pointes - pirouette tachycardia (Fig. 4.1).

Hypomagnesemia is often combined with hypokalemia, which can also cause cardiac arrest.

Magnesium sulfate is administered as a bolus of 1-2 g intravenously over 1-2 minutes. If the effect is insufficient, repeated administration at the same dose is indicated after 5-10 minutes (a 10 ml 25% ampoule contains 2.5 g of the drug).

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Glucose solutions

Currently, it is not recommended to use glucose infusion during resuscitation because it enters the ischemic area of the brain, where it is included in anaerobic metabolism and is broken down into lactic acid. Local accumulation of lactate in brain tissue increases its damage. It is more preferable to use physiological saline or Ringer's solution. After resuscitation, it is necessary to strictly monitor the blood glucose level.

Further studies are needed to determine the threshold glucose level that requires insulin administration and the acceptable range of target blood glucose concentrations.