Control of a bronchial asthma attack

Emergency therapy

The mechanism of action of drugs used to stop an attack of bronchial asthma is described in the article " Treatment of bronchial asthma ".

Non-selective adrenergic agonists

Non-selective adrenergic agents have a stimulating effect on beta1- beta2- and alpha-adrenergic receptors.

Adrenaline is the drug of choice for stopping an attack of bronchial asthma due to the rapid stopping effect of the drug.

In adult patients during an asthma attack, subcutaneous administration of adrenaline at a dose of 0.25 mg (i.e. 0.25 ml of a 0.1% solution) is characterized by the following features: onset of action - after 15 minutes; maximum action - after 45 minutes; duration of action - about 2.5 hours; maximum expiratory air flow rate (MEAF) increases by 20%; no changes in heart rate are noted; systemic diastolic blood pressure decreases slightly.

An injection of 0.5 mg of adrenaline produces the same effect, but with the following features: the duration of action increases to 3 hours or more; the MAP increases by 40%; the heart rate increases slightly.

S. A. Sun (1986) recommends administering adrenaline subcutaneously in the following doses to relieve an attack of bronchial asthma, depending on the patient’s body weight:

• less than 60 kg - 0.3 ml of 0.1% solution (0.3 mg);
• 60-80 kg - 0.4 ml of 0.1% solution (0.4 mg);
• more than 80 kg - 0.5 ml of 0.1% solution (0.5 mg).

If there is no effect, the administration of adrenaline in the same dose is repeated after 20 minutes; adrenaline can be administered again no more than 3 times.

Subcutaneous administration of adrenaline is the drug of choice for initial therapy of patients during an asthma attack.

The administration of adrenaline is not recommended for elderly patients suffering from coronary heart disease, hypertension, parkinsonism, toxic goiter due to the possible increase in blood pressure, tachycardia, increased tremor, agitation, and sometimes worsening of myocardial ischemia.

Ephedrine - can also be used to relieve an attack of bronchial asthma, but its effect is less pronounced, it begins after 30-40 minutes, but lasts a little longer, up to 3-4 hours. To relieve bronchial asthma, 0.5-1.0 ml of a 5% solution is administered subcutaneously or intramuscularly.

Ephedrine should not be used in patients for whom adrenaline is contraindicated.

Selective or partially selective beta2-adrenergic agonists

Drugs of this subgroup selectively stimulate beta2-adrenergic receptors and cause relaxation of the bronchi, do not stimulate or almost do not stimulate beta1-adrenergic receptors of the myocardium (when used in acceptable optimal doses).

Alupent (asthmopent, orciprenaline) - is used as a metered aerosol (1-2 deep breaths). The effect begins in 1-2 minutes, the attack is completely stopped in 15-20 minutes, the duration of action is about 3 hours. If the attack resumes, the same dose is inhaled. Alupent can be used 3-4 times a day. To stop an attack of bronchial asthma, you can also use subcutaneous or intramuscular administration of 1 ml of a 0.05% solution of Alupent, intravenous drip administration is also possible (1 ml of a 0.05% solution in 300 ml of a 5% glucose solution at a rate of 30 drops / min).

Alupent is a partially selective beta2-adrenergic agonist, therefore, with frequent inhalations of the drug, palpitations and extrasystole are possible.

Salbutamol (Ventolin) - used to stop an asthma attack, a metered aerosol is used - 1-2 inhalations. In severe cases, if there is no effect after 5 minutes, another 1-2 inhalations can be taken. The permissible daily dose is 6-10 single inhalation doses.

The bronchodilatory effect of the drug begins in 1-5 minutes. The maximum effect occurs in 30 minutes, the duration of action is 2-3 hours.

Terbutaline (Bricanil) is a selective beta2-adrenergic agonist, used to relieve an attack of bronchial asthma in the form of a metered aerosol (1-2 inhalations). The bronchodilator effect is noted after 1-5 minutes, maximum after 45 minutes (according to some data after 60 minutes), the duration of action is at least 5 hours.

There is no significant change in heart rate and systolic blood pressure after inhalation of terbutaline. To stop an attack of bronchial asthma, it can also be used intramuscularly - 0.5 ml of a 0.05% solution up to 4 times a day.

Inoline is a selective beta2-adrenergic agonist, used to relieve an attack of bronchial asthma in the form of metered aerosols (1-2 inhalations), as well as subcutaneously - 1 ml (0.1 mg).

Ipradol is a selective beta2-adrenergic agonist, used to relieve an attack of bronchial asthma in the form of a metered aerosol (1-2 inhalations) or intravenously by drip 2 ml of a 1% solution.

Berotek (fenoterol) is a partially selective beta2-adrenergic agonist, used to relieve an attack of bronchial asthma in the form of a metered aerosol (1-2 inhalations). The onset of bronchodilating action is observed after 1-5 minutes, the maximum effect is after 45 minutes, the duration of action is 5-6 hours (even up to 7-8 hours).

Yu.B. Belousov (1993) considers Berotek as the drug of choice due to its sufficient duration of action.

Combined beta2-adrenergic agonists

Berodual is a combination of the beta2-adrenergic agonist fenoterol (berotek) and the anticholinergic iprapropium bromide, which is an atropine derivative. It is produced as a metered-dose aerosol and is used to relieve an asthma attack (1-2 inhalations). If necessary, the drug can be inhaled up to 3-4 times a day. The drug has a pronounced bronchodilating effect.

Ditek is a combined dosed aerosol consisting of fenoterol (berotek) and a mast cell stabilizer - intal. With the help of Ditek, it is possible to stop attacks of bronchial asthma of mild and moderate severity (1-2 inhalations of aerosol), if there is no effect, the inhalation can be repeated after 5 minutes in the same dose.

Use of beta1, beta2-adrenergic stimulants

Isodrin (isoproterenol, novodrin) - stimulates beta1- and beta2-adrenoreceptors and thus dilates the bronchi and increases the heart rate. To relieve an attack of bronchial asthma, it is used in the form of metered aerosols of 125 and 75 mcg in one dose (1-2 inhalations), the maximum daily dose is 1-4 inhalations 4 times a day. In some cases, it is possible to increase the number of doses to 6-8 times a day.

It should be remembered that in case of overdose of the drug, severe arrhythmias may develop. It is inappropriate to use the drug in ischemic heart disease, as well as in severe chronic circulatory failure.

Treatment with euphyllin

If after 15-30 minutes after the use of adrenaline or other beta2-adrenergic receptor stimulants the attack of bronchial asthma is not relieved, intravenous administration of euphyllin should be started.

As M.E. Gershwin points out, euphyllin plays a central role in the therapy of reversible bronchospasm.

Euphyllin is available in ampoules of 10 ml of 2.4% solution, i.e. 1 ml of solution contains 24 mg of euphyllin.

Euphyllin is administered intravenously initially at a dose of 3 mg/kg, and then a maintenance dose is infused intravenously at a rate of 0.6 mg/kg/h.

According to S.A. San (1986), euphyllin should be administered intravenously by drip:

• at a dose of 0.6 ml/kg per hour to patients who previously received theophylline;
• at a dose of 3-5 mg/kg over 20 minutes for individuals who have not received theophylline, and then switch to a maintenance dose (0.6 mg/kg in 1 hour).

Euphyllin is administered intravenously by drip until the condition improves, but under control of the concentration of theophylline in the blood. The therapeutic concentration of theophylline in the blood should be within 10-20 mcg/ml.

Unfortunately, in practice it is not always possible to determine the theophylline content in the blood. Therefore, it should be remembered that the maximum daily dose of aminophylline is 1.5-2 g (i.e. 62-83 ml of 2.4% aminophylline solution).

To stop an attack of bronchial asthma, it is not always necessary to administer this daily dose of euphyllin; such a need arises when asthmatic status develops.

If it is not possible to determine the concentration of theophylline in the blood and there are no automated systems - pumps that regulate the administration of the drug at a given rate, you can do the following.

Example.

An attack of bronchial asthma in a patient weighing 70 kg who did not receive theophylline.

First, we administer euphyllin intravenously at a dose of 3 mg/kg, i.e. 3x70= 210 mg (approximately 10 ml of a 2.4% solution of euphyllin), in 10-20 ml of isotonic sodium chloride solution very slowly over 5-7 minutes or intravenously by drip over 20 minutes.

After this, we switch to intravenous infusion of a maintenance dose of 0.6 mg/kg/h, i.e. 0.6 mg χ 70 = 42 mg/h, or approximately 2 ml of 2.4% solution per hour (4 ml of 2.4% solution in 240 ml of isotonic sodium chloride solution at a rate of 40 drops per minute).

Treatment with glucocorticoids

If there is no effect from euphyllin within 1-2 hours from the start of the above-mentioned maintenance dose, treatment with glucocorticoids is started. 100 mg of water-soluble hydrocortisone (hemisuccinate or phosphate) or 30-60 mg of prednisolone are administered intravenously by jet stream, sometimes after 2-3 hours they have to be administered again.

If there is no effect after prednisolone administration, euphyllin can be administered again, and beta2-adrenergic stimulants can be used in inhalations. The effectiveness of these agents often increases after the use of glucocorticoids.

Oxygen inhalation

Oxygen inhalations help relieve asthma attacks. Humidified oxygen is inhaled through nasal catheters at a rate of 2-6 l/min.

Chest massage

Vibration massage of the chest and acupressure can be used in complex therapy of an asthma attack to achieve a faster effect from other measures.

General treatment plan

S.A. Sun (1986) recommends the following measures:

1. Oxygen inhalation through a nasal catheter at 2-6 l/min (oxygen can also be given through a mask).
2. Prescribing one of the beta-adrenergic drugs:
   • adrenaline subcutaneously;
   • terbutaline sulfate subcutaneously;
   • inhalation of orciprenaline.
3. If there is no improvement within 15-30 minutes, the administration of beta-adrenergic substances is repeated.
4. If after another 15-30 minutes there is no improvement, intravenous drip infusion of euphyllin is started.
5. The absence of improvement within 1-2 hours after the start of administration of euphyllin requires additional administration of atropine or atrovent by inhalation (for patients with moderate cough) or intravenous corticosteroids (100 mg hydrocortisone or an equivalent amount of another drug).
6. Continue inhalation of beta-adrenergic agents and intravenous administration of euphyllin.

Treatment of status asthmaticus

Asthmatic status (AS) is a syndrome of acute respiratory failure that develops as a result of severe bronchial obstruction that is resistant to standard therapy.

There is no generally accepted definition of asthmatic status. Most often, asthmatic status develops with bronchial asthma, obstructive bronchitis. Taking into account the etiology and treatment measures carried out before the development of asthmatic status, other definitions of asthmatic status can be given.

According to S. A. Sun (1986), asthmatic status is an acute attack of asthma in which treatment with beta-adrenergic agents, fluid infusions and euphyllin is ineffective. The development of asthmatic status also requires the use of other treatment methods due to the emergence of an immediate and serious threat to life.

According to Hitlari Don (1984), asthmatic status is defined as a marked, potentially life-threatening deterioration in the condition of a patient with bronchial asthma that does not respond to conventional therapy. This therapy should include three subcutaneous injections of adrenaline at 15-minute intervals.

Depending on the pathogenetic features of asthmatic status, three variants are distinguished:

1. Slowly developing asthmatic status caused by increasing inflammatory obstruction of the bronchi, edema, thickening of sputum, deep blockade of beta2-adrenergic receptors and severe glucocorticoid deficiency, which aggravates the blockade of beta2-adrenergic receptors.
2. An immediately developing asthmatic status (anaphylactic), caused by the development of a hyperergic anaphylactic reaction of the immediate type with the release of mediators of allergy and inflammation, which leads to total bronchospasm and asphyxia at the moment of contact with the allergen.
3. Anaphylactoid asthmatic status caused by reflex cholinergic bronchospasm in response to irritation of respiratory tract receptors by various irritants; release of histamine from mast cells under the influence of non-specific irritants (without the participation of immunological mechanisms); primary bronchial hyperreactivity.

All patients with status asthmaticus should be immediately hospitalized in the intensive care unit.

Treatment of slowly developing status asthmaticus

Stage I - the stage of formed resistance to sympathomimetics, or the stage of relative compensation

Treatment with glucocorticoids

The use of glucocorticoids is mandatory in the treatment of status asthmaticus once this life-threatening condition is diagnosed.

In this case, glucocorticoids have the following effect:

• restore the sensitivity of beta2-adrenergic receptors;
• enhance the bronchodilating effect of endogenous catecholamines;
• eliminate allergic edema, reduce inflammatory obstruction of the bronchi;
• reduce the hyperreactivity of mast cells and basophils and, thus, inhibit the release of histamine and other mediators of allergy and inflammation;
• eliminate the threat of acute adrenal insufficiency due to hypoxia.

Glucocorticoids are administered intravenously by injection or jet every 3-4 hours.

N. V. Putova recommends using prednisolone at 60 mg every 4 hours until the asthmatic status is eliminated (the daily dose can reach 10 mcg/kg of the patient’s body weight).

According to the recommendations of T. A. Sorokina (1987), the initial dose of prednisolone is 60 mg; if the condition does not improve within the next 2-3 hours, the single dose is increased to 90 mg or hydrocortisone hemisuccinate or phosphate is added to prednisolone intravenously at 125 mg every 6-8 hours.

If the patient's condition improves with the start of treatment, prednisolone is continued at 30 mg every 3 hours, then the intervals are lengthened.

In recent years, along with parenteral administration of prednisolone, it has been prescribed orally at 30-40 mg per day.

After withdrawal from the status, the daily dose of prednisolone is reduced by 20-25% daily.

In 1987, a method for treating status asthmaticus by Yu. V. Anshelevich was published. The initial dose of intravenous prednisolone is 250-300 mg, after which the drug is continued by jet injection every 2 hours at 250 mg or continuously by drip until a dose of 900-1000 mg is reached over 6 hours. If status asthmaticus persists, prednisolone should be continued at 250 mg every 3-4 hours in a total dose of 2000-3500 mg for 1-2 days until a relief effect is achieved. After relief of status asthmaticus, the dose of prednisolone is reduced every day by 25-50% in relation to the initial dose.

Treatment with euphyllin

Euphyllin is the most important drug for bringing a patient out of asthmatic status. Against the background of glucocorticoid administration, the bronchodilating effect of euphyllin increases. Euphyllin, in addition to the bronchodilating effect, reduces pressure in the pulmonary circulation, reduces the partial pressure of carbon dioxide in the blood and reduces platelet aggregation.

Euphyllin is administered intravenously at an initial dose of 5-6 mg/kg (i.e. approximately 15 ml of a 2.4% solution for a person weighing 70 kg), the administration is performed very slowly over 10-15 minutes, after which the drug is administered intravenously by drip at a rate of 0.9 mg/kg per hour (i.e. approximately 2.5 ml of a 2.4% solution per hour) until the condition improves, and then the same dose for 6-8 hours (maintenance dose).

Intravenous drip infusion of euphyllin at the above-mentioned rate is most conveniently performed using an automatic dosing device. If one is not available, one can simply "inject" approximately 2.5 ml of a 2.4% solution of euphyllin into the system every hour or establish intravenous drip infusion of euphyllin 10 ml of 2.4% euphyllin in 480-500 ml of isotonic sodium chloride solution at a rate of 40 drops per minute, in which case the rate of euphyllin infusion will approach 0.9 mcg/kg per hour.

When providing assistance to a patient in a state of asthmatic status, it is permissible to administer 1.5-2 g of euphyllin per day (62-83 ml of 2.4% solution).

Instead of euphyllin, similar drugs can be administered - diaphylline and aminophylline.

Infusion therapy

It is carried out for the purpose of hydration, improvement of microcirculation. This therapy replenishes the deficit of BCC and extracellular fluid, eliminates hemoconcentration, promotes the discharge and liquefaction of sputum.

Infusion therapy is performed by intravenous drip infusion of 5% glucose, Ringer's solution, isotonic sodium chloride solution. In case of severe hypovolemia, low arterial pressure, it is advisable to administer rheopolyglycin. The total volume of infusion therapy is about 3-3.5 liters on the first day, in the following days - about 1.6 l/m2 ^of body surface, i.e. about 2.5-2.8 liters per day. The solutions are heparinized (2,500 U of heparin per 500 ml of liquid).

Intravenous drip infusions are carried out under the control of CVP and diuresis. CVP should not exceed 120 mm H2O, and the diuresis rate should be at least 80 ml/hour without the use of diuretics.

If the central venous pressure increases to 150 mm H2O, 40 mg of furosemide should be administered intravenously.

It is also necessary to control the blood electrolyte levels - sodium, potassium, calcium, chlorides, and if their levels are abnormal, make corrections. In particular, potassium salts should be added to the administered fluid, since hypokalemia often occurs in asthmatic status, especially when treated with glucocorticoids.

Combating hypoxemia

Already in stage I of asthmatic status, patients have moderate arterial hypoxemia (PaO260-70 mm Hg) and normo- or hypocapnia (PaCO2 is normal, i.e. 35-45 mm Hg or less than 35 mm Hg).

Relief of arterial hypoxemia is the most important part of the complex therapy of asthmatic status.

An oxygen-air mixture with an oxygen content of 35-40% is inhaled; humidified oxygen is inhaled through nasal catheters at a rate of 2-6 l/min.

Oxygen inhalation is a replacement therapy for acute respiratory failure. It prevents the adverse effects of hypoxemia on tissue metabolism processes.

Inhalation of a helium-oxygen mixture (75% helium + 25% oxygen) for 40-60 minutes 2-3 times a day is very effective. The helium-oxygen mixture, due to its lower density compared to air, more easily penetrates poorly ventilated areas of the lungs, which significantly reduces hypoxemia.

Measures to improve sputum discharge

The dominant pathological process in asthmatic status is bronchial obstruction with viscous sputum. To improve sputum discharge, the following is recommended:

• infusion therapy to reduce dehydration and help thin mucus;
• intravenous administration of 10% sodium iodide solution - from 10 to 30 ml per day; T. Sorokina recommends administering it up to 60 ml per day intravenously and also taking a 3% solution orally, 1 tablespoon every 2 hours 5-6 times a day; sodium iodide is one of the most effective mucolytic expectorants. Being released from the blood through the mucous membrane of the bronchi, it causes their hyperemia, increased secretion and liquefaction of sputum, normalizes the tone of the bronchial muscles;
• additional humidification of inhaled air, which helps to liquefy phlegm and cough it up; humidification of inhaled air is achieved by spraying liquid; you can also inhale air humidified with warm steam;
• intravenous or intramuscular administration of vaxam (lasolvan) - 2-3 ampoules (15 mg per ampoule) 2-3 times a day, and oral administration of the drug 3 times a day, 1 tablet (30 mg). The drug stimulates the production of surfactant, normalizes bronchopulmonary secretion, reduces the viscosity of sputum, and promotes its expectoration;
• Physiotherapy methods including percussion and vibration massage of the chest.

Correction of acidosis

In stage I of asthmatic status, acidosis is not pronounced, compensated, therefore intravenous administration of soda is not always indicated. However, if the blood pH is less than 7.2, it is advisable to administer about 150-200 ml of 4% sodium bicarbonate solution intravenously slowly.

It is necessary to measure blood pH regularly in order to maintain it at a level of 7.25.

Use of proteolytic enzyme inhibitors

In some cases, it is advisable to include proteolytic enzyme inhibitors in the complex therapy of asthmatic status. These drugs block the action of allergy and inflammation mediators in the bronchopulmonary system and reduce bronchial wall edema. Contrical or trasylol is administered intravenously by drip at a rate of 1,000 U per 1 kg of body weight per day in 4 doses in 300 ml of 5% glucose.

Heparin treatment

Heparin reduces the risk of developing thromboembolism (the threat of thromboembolism exists due to dehydration and thickening of the blood in asthmatic status), has a desensitizing and anti-inflammatory effect, reduces platelet aggregation, and improves microcirculation.

It is recommended to administer heparin (in the absence of contraindications) under the skin of the abdomen at a daily dose of 20,000 IU, dividing it into 4 injections.

Intravenous administration of sympathomimetics

As stated above, asthmatic status is characterized by resistance to sympathomimetics. However, there is no unambiguous attitude to these drugs. N. V. Putov (1984) points out that in drug treatment of asthmatic condition, the use of adrenomimetics is sharply limited or excluded. G. B. Fedoseyev and G. P. Khlopotova (1988) believe that sympathomimetics can be used as bronchodilators if there is no overdose.

S. A. Sun (1986) believes that beta-adrenergic agents (for example, isadrine) should be administered intravenously only in the most severe asthma attacks that do not respond to conventional treatment methods, including intravenous administration of euphyllin, atropine, and corticosteroids.

X. Don (1984) points out that progressive asthmatic status, which is not amenable to treatment with intravenous administration of aminophylline (euphylline), inhalation of sympathomimetics, intravenous infusions of glucocorticoids, can be treated quite successfully with intravenous administration of Shadrin.

It should be noted that during the above therapy, patients become more sensitive to sympathomimetics and, if the rules for their use are followed, a pronounced bronchodilatory effect can be achieved.

Treatment with isadrine should be started with intravenous administration at a dose of 0.1 mcg/kg per minute. If no improvement is observed, the dose should be gradually increased by 0.1 mcg/kg/min every 15 minutes. It is advisable not to exceed a heart rate of 130 beats per minute. The lack of effect from intravenous administration of isadrine is observed in approximately 15% of patients.

Treatment with isadrine should be carried out only in young patients without concomitant cardiac pathology.

The main complications are cardiac arrhythmias and toxic-necrotic changes in the myocardium.

During treatment with isadrine, heart rate and blood pressure should be constantly monitored, and the level of myocardial enzymes in the blood, especially specific MB-CK isoenzymes, should be determined daily.

Selective beta2-adrenergic agonists can be used to treat status asthmaticus. Given their ability to selectively stimulate beta2-adrenergic receptors and have almost no effect on beta1-adrenergic receptors of the myocardium and, thus, not to excessively stimulate the myocardium, the use of these drugs is preferable to isadrine.

G. B. Fedoseyev recommends intravenous or intramuscular administration of 0.5 ml of a 0.5% solution of alupent (orciprenaline), a drug with partial beta2-selectivity.

It is possible to use highly selective beta2-adrenergic agonists - terbutaline (bricanil) - 0.5 ml of 0.05% solution intramuscularly 2-3 times a day; ipradol - 2 ml of 1% solution in 300-350 ml of 5% glucose solution intravenously by drip, etc.

Thus, beta2-adrenergic receptor stimulants can be used in the treatment of progressive asthmatic status, but only in combination with complex therapy that restores the sensitivity of beta2-adrenergic receptors.

Long-term epidural block

In complex therapy of AS, a high block of the epidural space between DIII-DIV can also be used. According to A. S. Borisko (1989), for a long-term block, a 0.8 mm diameter vinyl chloride catheter is inserted through a needle into the epidural space in the DIII-DIV region. Using the catheter, 4-8 ml of a 2.5% trimecaine solution is fractionally injected every 2-3 hours. The peridural block can last from several hours to 6 days.

Long-term peridural blockade normalizes the tone of the smooth muscles of the bronchi, improves pulmonary blood flow, and allows the patient to be brought out of the asthmatic state more quickly.

In bronchial asthma, especially in the development of asthmatic status, dysfunction of the central and autonomic nervous system develops in the form of formation of congestive pathological interoceptive reflexes, causing spasm of sensitized bronchial muscles and increased secretion of viscous sputum with bronchial obstruction. Long-term epidural blockade blocks pathological interoceptive reflexes and thereby causes bronchodilation.

Fluorothane anesthesia

C. H. Scoggin points out that fgorothane has a bronchodilator effect. Therefore, patients with asthmatic status can be given general anesthesia. As a result, bronchospasm often ceases and does not occur again after the anesthesia wears off. However, in some patients, severe asthmatic conditions develop again after recovery from anesthesia.

Uses of Droperidol

Droperidol is an alpha-adrenoreceptor and neuroleptic. The drug reduces bronchospasm, removes the toxic effects of sympathomimetics, agitation, reduces arterial hypertension. Given these effects of droperidol, in some cases it is advisable to include it in the complex therapy of asthmatic status under the control of arterial pressure (1 ml of 0.25% solution intramuscularly or intravenously 2-3 times a day).

Stage II - stage of decompensation (stage of "silent lung", stage of progressive ventilation disorders)

In stage II, the patient’s condition is extremely severe, there is a pronounced degree of respiratory failure, although consciousness is still preserved.

Treatment with glucocorticoids

Compared with stage I asthmatic status, a single dose of prednisolone is increased by 1.5-3 times and is administered every 1-1.5 hours or continuously intravenously by drip. 90 mg of prednisolone is administered intravenously every 1.5 hours, and if there is no effect in the next 2 hours, the single dose is increased to 150 mg and hydrocortisone hemisuccinate is administered at the same time at 125-150 mg every 4-6 hours. If the patient's condition improves with the start of treatment, 60 mg and then 30 mg of prednisolone are administered every 3 hours.

The absence of an effect within 1.5-3 hours and the persistence of the “silent lung” picture indicate the need for bronchoscopy and segmental lavage of the bronchi.

Against the background of glucocorticosteroid therapy, oxygen inhalation therapy, infusion therapy, intravenous administration of euphyllin, and measures to improve the drainage function of the bronchi are continued.

Endotrocheal intubation and artificial ventilation of the lungs with bronchial tree sanation

If treatment with high doses of glucocorticoids and the rest of the above therapy do not eliminate the picture of "silent lung" within 1.5 hours, it is necessary to perform endotracheal intubation and transfer the patient to artificial lung ventilation (ALV).

S. A. Sun and M. E. Gershwin formulate indications for artificial ventilation as follows:

• deterioration of the patient's mental status with the development of anxiety, irritability, confusion, and, finally, coma;
• progressive clinical deterioration despite vigorous drug therapy;
• pronounced tension of the accessory muscles and retraction of the intercostal spaces, pronounced fatigue and the danger of complete exhaustion of the patient;
• cardiopulmonary failure;
• progressive increase in the level of CO2 in arterial blood, determined by determining blood gases;
• reduction or absence of respiratory sounds during inhalation, as the respiratory volume decreases, which is accompanied by a reduction or disappearance of expiratory wheezing.

Predion (viadril) is used for induction anesthesia at a rate of 10-12 mg/kg as a 5% solution. Before intubation, 100 mg of the muscle relaxant listenone is administered intravenously. Basic anesthesia is performed using nitrous oxide and fluorothane. Nitrous oxide is used in a mixture with oxygen in a ratio of 1:2.

Simultaneously with artificial ventilation, emergency therapeutic bronchoscopy with segmental bronchial lavage is performed. The bronchial tree is washed with a 1.4% sodium bicarbonate solution heated to 30-35 °C, followed by suction of the bronchial contents.

In intensive therapy of asthmatic status, A. P. Zilber recommends performing artificial ventilation in the positive end-expiratory pressure (PEEP) mode. However, in right ventricular failure, the PEEP mode can further disrupt hemodynamics. This is especially dangerous when artificial ventilation is started against the background of epidural anesthesia with uncorrected hypovolemia, which leads to collapse that is difficult to correct.

Against the background of artificial ventilation of the lungs, the therapy described in the section on the treatment of stage I asthmatic status is continued, as well as correction of acidosis (200 ml of 4% sodium bicarbonate solution intravenously) under the control of blood pH.

Mechanical ventilation is stopped after the relief of stage II AS (“silent lung”), but bronchodilator therapy, treatment with glucocorticoids in decreasing doses, and expectorants are continued.

Stage II - hypoxemic hypercapnic coma

In stage III, the following scope of treatment measures is carried out.

Artificial ventilation of the lungs

The patient is immediately transferred to artificial ventilation. During this period, the blood oxygen tension, carbon dioxide, and blood pH are determined every 4 hours.

Bronchoscopic sanitation

Bronchoscopic sanitation is also a mandatory treatment measure; segmental lavage of the bronchial tree is performed.

Glucocorticoid therapy

Prednisolone doses in stage III are increased to 120 mg intravenously every hour.

Correction of acidosis

Correction of acidosis is performed by intravenous infusions of 200-400 ml of 4% sodium bicarbonate solution under the control of blood pH and buffer base deficiency.

Extracorporeal membrane oxygenation of blood

In acute respiratory failure, artificial ventilation does not always give a positive result even with a high oxygen concentration (up to 100%). Therefore, extracorporeal membrane oxygenation of blood is sometimes used. It allows to gain time and prolong the life of the patient, giving the opportunity for acute respiratory failure to decline under the influence of therapy.

In addition to the above-mentioned measures, treatment with zufillin, rehydration, measures to improve sputum discharge and others described in the section "Treatment in stage I asthmatic status" are also continued.

Treatment of anaphylactic variant of asthmatic status

1. 0.3-0.5 ml of 0.1% adrenaline solution in 10-20 ml of isotonic sodium chloride solution is administered intravenously. If there is no effect after 15 minutes, intravenous drip infusion of 0.5 ml of 0.1% adrenaline solution in 250 ml of isotonic sodium chloride solution is established. If difficulties arise with intravenous infusion of adrenaline into the cubital vein, adrenaline is administered into the sublingual region. Due to the abundant vascularization of this area, adrenaline quickly enters the systemic bloodstream (0.3-0.5 ml of 0.1% adrenaline solution is administered) and simultaneously into the trachea using the cricoid-thyroid membrane protocol.

Shadrin can be administered intravenously by drip at 0.1-0.5 mcg/kg per minute.

Adrenaline or isadrine stimulate beta2-adrenergic receptors of the bronchi, reduce bronchial edema, relieve bronchospasm, increase cardiac output by stimulating beta1-adrenergic receptors.

2. Intensive glucocorticoid therapy is administered. Immediately, 200-400 mg of hydrocortisone hemisuccinate or phosphate or 120 mg of prednisolone are administered intravenously by jet stream, followed by a transition to intravenous drip infusion of the same dose in 250 ml of 5% glucose solution at a rate of 40 drops per minute. If there is no effect, 90-120 mg of prednisolone can be administered intravenously by jet stream again.
3. 0.5-1 ml of 0.1% atropine sulfate solution per 10 ml of isotonic sodium chloride solution is administered intravenously. The drug is a peripheral M-anticholinergic, relaxes the bronchi, eliminates anaphylactic bronchospasm, and reduces sputum hypersecretion.
4. 10 ml of a 2.4% solution of euphyllin in 10-20 ml of isotonic sodium chloride solution is administered intravenously slowly (over 3-5 minutes).
5. Antihistamines (suprastin, tavegil, diphenhydramine) are administered intravenously at 2-3 ml per 10 ml of isotonic sodium chloride solution.

Antihistamines block H1-histamine receptors, promote relaxation of the bronchial muscles, and reduce swelling of the bronchial mucosa.

6. If the above measures are ineffective, fluorothane anesthesia is administered, and if there is no effect from it, artificial ventilation is administered. Inhalation of 1.5-2% fluorothane solution as the anesthesia deepens eliminates bronchospasm and alleviates the patient's condition.
7. Direct lung massage is performed manually (inhalation is performed using the anesthetic device bag, exhalation is performed by squeezing the chest with hands). Direct lung massage is performed in case of total bronchospasm with "lung arrest" in the position of maximum inhalation and impossibility of exhalation.
8. Elimination of metabolic acidosis is carried out under the control of pH, deficiency of buffer bases by intravenous infusion of 200-300 ml of 4% sodium bicarbonate solution.
9. Improvement of blood rheological properties is achieved by intravenous or subcutaneous administration of heparin in a daily dose of 20,000-30,000 U (divided into 4 injections). Heparin reduces platelet aggregation and bronchial mucosal edema.
10. To combat cerebral edema, 80-160 mg of Lasix and 20-40 ml of hypertonic 40% glucose solution are administered intravenously.
11. The use of alpha-adrenergic blockers (droperidol) intravenously at a dose of 1-2 ml of 0.25% solution in 10 ml of isotonic sodium chloride solution under the control of blood pressure reduces the activity of alpha-adrenergic receptors and helps relieve bronchospasm.

Treatment of anaphylactoid variant of status asthmaticus

The basic principles of bringing a patient out of anaphylactoid status are similar to those in providing emergency care for the anaphylactic variant of asthmatic status.

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