Asthmatic status

Asthmatic status is a severe prolonged attack of bronchial asthma, characterized by severe or acutely progressive respiratory failure caused by obstruction of the airways, with the formation of the patient's resistance to therapy (V.Schelkunov, 1996).

[1],

What causes asthmatic status?

1. Bacterial and viral inflammatory diseases in the bronchopulmonary system (acute or chronic in the acute phase);
2. Hyposensitization therapy conducted in the phase of exacerbation of bronchial asthma.
3. Excess use of sedatives and hypnotic drugs (they can cause a significant violation of the drainage function of the bronchi).
4. Cancellation of glucocorticoids after prolonged use (withdrawal syndrome);
5. Drugs that cause an allergic reaction from the bronchi with their subsequent obstruction - salicylates, pyramidone, analgin, antibiotics, vaccines, serums.
6. Excessive intake of sympathomimetics (while adrenaline is converted to metanephrine, and izadrin into 3-methoxyisoprenaline, which block beta receptors and contribute to bronchial obstruction; in addition, sympathomimetics relax the walls of the bronchial vessels and increase the swelling of the bronchi - “lung locking effect”).

How does asthmatic status develop?

Slowly developing asthmatic status. The main pathogenetic factors are:

• deep blockade of beta-adrenergic receptors, the predominance of alpha-adrenergic receptors, causing bronchospasm;
• pronounced deficiency of glucocorticoids, which exacerbates the blockade of beta 2 -adrenoreceptors;
• inflammatory obstruction of the bronchi infectious or allergic origin;
• suppression of the cough reflex, the natural drainage mechanisms of the bronchi and the respiratory center;
• the prevalence of cholinergic bronchoconstricting effects.
• expiratory collapse of small and medium bronchi.

Anaphylactic asthmatic status (immediately developing): an immediate-type hyperergic anaphylactic reaction with the release of mediators of allergy and inflammation, which leads to a total bronchospasm, asphyxiation at the moment of contact with the allergen.

Anaphylactoid asthmatic status:

• reflex bronchospasm in response to irritation of the respiratory tract receptors by mechanical, chemical, physical stimuli (cold air, strong odors, etc.) due to bronchial hyperreactivity;
• the direct histamine-activating effect of various non-specific irritants (outside the immunological process), under the influence of which histamine is released from mast cells and basophils. According to the speed of development, this variant of asthmatic status can be considered immediately evolving, but unlike the anaphylactic asthmatic status, it is not associated with immunological mechanisms.

In addition to the above pathogenetic features of various types of asthmatic status, there are mechanisms common to all forms. Due to bronchial obstruction, residual lung volume increases, reserve inhalation and exhalation decrease, acute pulmonary emphysema develops, the mobilization mechanism of venous return of blood to the heart is disturbed, and the stroke volume of the right ventricle decreases. Increased intrathoracic and intraalveolar pressure contributes to the development of pulmonary hypertension. A decrease in venous blood return contributes to water retention in the body due to an increase in the level of antidiuretic hormone and aldosterone. In addition, high intrathoracic pressure interferes with the return of lymph through the thoracic lymphatic duct into the venous bed, which contributes to the development of hypoproteinemia and decrease oncotic pressure of the blood, increasing the amount of interstitial fluid. The increased permeability of the vascular wall against the background of hypoxia contributes to the release into the interstitial space of protein molecules and sodium ions, which leads to an increase in osmotic pressure in the interstitial sector, resulting in intracellular dehydration. Impaired respiratory function and the cardiovascular system leads to disruption of the acid-base balance and blood gas composition. In the early stages of asthmatic status, hypoxemia develops on the background of hyperventilation and respiratory alkalosis. With advanced airway obstruction, hypercapnia develops with decompensated metabolic acidosis.

In the pathogenesis of asthmatic status, depletion of the functional activity of the adrenal glands and an increase in the biological inactivation of cortisol are also important.

[2], [3]

Symptoms of asthmatic status

The first stage of the asthmatic status is characterized by relative compensation, when there are still no pronounced violations of ventilation of the lungs. There is a prolonged dyspnea. An asthmatic attack is characterized by difficulty in exhaling while maintaining inspiration. The ratio of inspiration and expiration is 1: 2, 1: 2.5. Dyspnea, moderate diffuse cyanosis, bronchospasm, congestion in the lungs, hyperventilation, disorders of the acid-base state and blood gas composition are characteristic. Cough is unproductive. The phlegm is difficult to separate.

Auscultation is determined by hard breathing with the presence of mixed whistling and humming rales. Breathing is carried out in all parts of the lungs.

Normal ventilation / perfusion ratio is disrupted. Peak expiratory flow rate is reduced to 50-80% of normal. Emphysema increases. Due to this, heart sounds are muffled. There is tachycardia, arterial hypertension. Signs of general dehydration appear.

In general, hyperventilation, hypocapnia, and moderate hypoxemia are characteristic of this stage. Alveolar ventilation is less than 4 l / min. The frequency of respiratory movements more than 26 per minute. Sa O2> 90% with Fi O2 = 0.3.

Sympathomimetic and bronchodilator drugs do not relieve an attack of suffocation.

The second stage of asthmatic status is characterized by an increase in obstructive-ventilation disorders and the development of respiratory decompensation.

Observed pronounced bronchospasm with sharply obstructed exhalation. The work of the respiratory muscles is ineffective (even due to hyperventilation) and is not able to prevent the development of hypoxia and hypercapnia. Peak expiratory flow rate is less than 50% of the proper value.

Motor excitement becomes drowsy. Perhaps the development of muscle twitches and cramps.

Breathing is noisy, frequent (more than 30 per minute). Respiratory noises can be heard at a distance of several meters.

Auscultatory, the number of wheezing decreases, in some zones of the lungs there is no breathing (“silent lung” areas). A total pulmonary obstruction may develop (“silent lungs”). Phlegm is not separated.

Tachycardia over 110-120 per minute. Alveolar ventilation <3.5 l / min. SaO,> 90% at PYu2 = 0.6. Marked dehydration of the body.

With the progression of disorders, hyperventilation is replaced by hypoventilation.

The third stage of asthmatic status can be called the stage of hypoxic / hypercapnic coma.

Pupils are sharply dilated, sluggish reaction to light. Breathing is arrhythmic, superficial. Respiratory rate more than 40-60 per minute (can go to bradypnea). There is an extreme degree of hypoxia with a pronounced hypercapnia. Sa O2 <90% with Fi O2 = 1.0. Total bronchospasm and bronchial obstruction with viscous mucus develop. Auscultative noises over the lungs are not heard ("mute" lung). Decompensation of cardiac activity is observed, leading to asystole and ventricular fibrillation.

[4]

Stage I asthmatic status

Stage of relative compensation, formed sympathomimetic resistance.

The main clinical symptoms

1. The frequent occurrence during the day of prolonged, not stoped choking attacks, in the interictal period, breathing is not fully restored.
2. Hot, agonizing, dry cough with sputum difficult to separate.
3. Forced position (orthopnea), rapid breathing (up to 40 in 1 min) with the participation of auxiliary respiratory muscles.
4. At a distance, breathing noises, dry wheezing.
5. Pronounced cyanosis and pallor of the skin and visible mucous membranes.
6. With percussion of the lungs - a boxed sound (emphysema of the lungs), auscultation - “mosaic” breathing: in the lower parts of the lungs breathing is not heard, in the upper parts - hard with a moderate amount of dry rales.
7. On the part of the cardiovascular system - tachycardia up to 120 per minute, arrhythmias, pain in the heart, arterial pressure is normal or elevated, as a manifestation of right ventricular insufficiency - swelling of the neck veins and enlarged liver.
8. Signs of dysfunction of the central nervous system - irritability, agitation, sometimes nonsense, hallucinations.

Laboratory data

1. Complete blood count: polycythemia.
2. Biochemical analysis of blood: increased levels of a1- and y-globulins, fibrin, seromucoid, sialic acids.
3. Study of blood gas composition: moderate arterial hypoxemia (PaO2 60-70 mm Hg) and normocapnia (PaCO2 35-45 mm Hg).

Instrumental studies. ECG: signs of overload of the right atrium, right ventricle, deviation of the electrical axis of the heart to the right.

[5], [6], [7],

Stage II asthmatic status

The stage of decompensation, "silent light", progressive ventilation disorders.

The main clinical symptoms

1. Extremely serious condition of patients.
2. Severe shortness of breath, shallow breathing, the patient gasping for breath.
3. The situation is forced, orthopnea.
4. The neck veins are swollen.
5. The skin is pale gray, moist.
6. Arousal is periodically noted, again alternating with indifference.
7. During auscultation of the lungs - no respiratory sounds are heard over the whole lung or in a large area of both lungs (“mute lung”, obstruction of the bronchioles and bronchi), only a small amount of wheezing can be heard in a small area.
8. Cardiovascular system - pulse is frequent (up to 140 per minute), weak filling, arrhythmias, arterial hypotension, deaf heart sounds, canter rhythm is possible.

Laboratory data

1. General and biochemical blood tests: the data are the same as in stage I.
2. The study of blood gas composition - severe arterial hypoxemia (PaO250-60 mm Hg) and hypercapnia (PaCO2 50-70 or more mm Hg).
3. The study of acid-base balance - respiratory acidosis.

[8]

Instrumental data

ECG: signs of overload of the right atrium and right ventricle, diffuse decrease in the amplitude of the T wave, various arrhythmias.

[9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21]

III stage of asthmatic status

Hypercapnic coma.

The main clinical symptoms

1. Unconscious patient, before loss of consciousness, convulsions are possible.
2. Diffuse diffuse "red" cyanosis, cold sweat.
3. Breathing is shallow, rare, arrhythmic (perhaps Cheyne-Stokes breathing).
4. With auscultation of the lungs: the absence of respiratory noise or a sharp weakening.
5. Cardiovascular system: the pulse is thread-like, arrhythmic, blood pressure is sharply reduced or not detected, collapse, heart sounds are deaf, often canter rhythm, ventricular fibrillation is possible.

Laboratory data

1. General and biochemical blood tests: the data are the same as in stage I. Significant increase in hematocrit.
2. The study of blood gas composition - severe arterial hypoxemia (PaO2 40-55 mm Hg) and pronounced hypercapnia (PaCO2 80-90 mm Hg).
3. The study of acid-base balance - metabolic acidosis.

[22], [23]

Classification of asthmatic status

1. Pathogenetic options.
   1. Slowly developing asthmatic status.
   2. Anaphylactic asthmatic status.
   3. Anaphylactoid asthmatic status.
2. Stage.
   1. The first is relative compensation.
   2. The second is decompensation or "dumb lung."
   3. The third is hypoxic hypercapnic coma.

[24], [25], [26], [27], [28],

Diagnosis of asthmatic status

[29], [30], [31]

Survey program

1. General blood and urine tests.
2. Biochemical analysis of blood: total protein, protein fractions, seromucoid, fibrin, sialic acids, urea, creatinine, coagulogram, potassium, sodium, chlorides.
3. EKG.
4. Acid-base balance.
5. Gas composition of blood.

[32], [33], [34], [35]

Examples of the wording of the diagnosis

1. Infectious-dependent bronchial asthma, severe course, acute phase. Asthmatic status, slowly developing. Stage II Chronic suppurative bronchitis.
2. Bronchial asthma, atonic form (pollen and home dust allergy), severe course, acute phase. Asthmatic status slowly developing, I stage.

[36], [37], [38], [39], [40]

Emergency care for asthmatic status

Emergency care for asthmatic status necessarily includes oxygen therapy, restoration of airway patency, elimination of hypovolemia, relief of inflammation and edema of the mucous bronchioles, stimulation of beta-adrenergic receptors.

[41], [42], [43], [44],

Hydroxytherapy

All patients with a prolonged asthmatic attack and status are indicated with oxygen therapy with humidified oxygen of 3-5 l / min, which maintains its concentration in the inhaled mixture within 30-40%. Higher concentrations are not appropriate, since hyperoxygenation can lead to inhibition of the respiratory center.

[45], [46]

Infusion therapy

Rehydration therapy is required. Its goal is to compensate for a deficit in the volume of circulating blood and extracellular fluid, which makes it possible to normalize hemodynamics and reduce bronchial obstruction by improving the rehabilitation of the tracheobronchial tree (liquefaction of sputum, etc.).

For conducting infusion therapy and controlling central hemodynamics, catheterization of one of the central veins is desirable.

It should be remembered that patients with asthmatic status have an increased risk of damage to the pleura and the development of pneumothorax, therefore, it is safer to catheterize the femoral or external jugular vein at the prehospital stage.

For rehydration, 5% glucose solution, reopolyglukine, hemodez in combination with protein preparations are used. The volume of liquid introduced on the first day should be 3-4 liters (including food and drink). Subsequently, the liquid is injected at the rate of 1.6 l / m2 of the body surface. Recommended heparinization solutions at the rate of 2.5-5 thousand. Units per 500 ml.

Use with an asthmatic status of 0.9% sodium chloride solution is not recommended, as it can increase the swelling of the bronchial mucosa.

The introduction of sodium bicarbonate solutions is indicated in asthmatic status II-III stage or laboratory confirmed decompensated metabolic acidosis (in asthmatic status I degree, subcompensated metabolic acidosis is usually observed in combination with compensated respiratory alkalosis).

The adequacy of the conducted infusion therapy is assessed by changes in central venous pressure and diuresis (the rate of urination with adequate infusion therapy should be about 80 ml / h without the use of diuretic drugs).

[47], [48], [49], [50], [51]

Adrenoreceptor stimulants

When treating attacks of bronchial asthma, adrenoreceptor stimulants are used. These drugs cause relaxation of the bronchi with their subsequent expansion, have a mucokinetic effect, reduce the viscosity of sputum, reduce swelling of the mucous membrane and increase the contractility of the diaphragm. With the development of asthmatic status using short-acting drugs, which allows to correct the dose, depending on the effect obtained. It has been shown to begin treatment with selective beta2-agonists, since non-selective adrenoreceptor stimulants cause tachycardia, an increase in cardiac output and an increase in myocardial oxygen demand. Therapy begins with the inhalation of a salbutamol solution through a nebulizer. Repeated inhalations are shown every 20 minutes for the 1st hour.

The advantage of the introduction of drugs by nebulizer therapy is the possibility of inhalation of higher doses of drugs compared to aerosol dosage or powder inhalers (turbuhaler, dischaler, cyclohaler, etc.).

It is advisable to combine beta2-adrenomimetics with anticholinergics. A good effect gives a combination of salbutamol and ipratropium bromide (atrovent).

Salbutamol (ventolin) is a selective beta2-adrenoreceptor agonist. Used as a first line drug. Its action occurs in 4-5 minutes with a maximum of 40-60 minutes. Duration of action is about 4-5 hours. For inhalation using a nebulizer, 1-2 nebulas (2.5-5 mg salbutamol sulfate in 2.5 ml of 0.9% NaCl) are neatly placed in a nebulizer and the mixture is inhaled. The drug can also be used in the form of a metered-dose aerosol inhaler (2.5 mg - 1 breath).
Berotec is also a selective beta2-adrenoreceptor agonist. Its effect develops in 3-4 minutes with a maximum of action by the 45th minute. Duration of action is about 5-6 hours. It can be used with a nebulizer (inhalation of 0.5-1.5 ml of fenoterol solution in physiological solution for 5-10 minutes with repeated inhalations of the same dose every 20 minutes) or in the form of a metered-dose aerosol inhaler (100 μg - 1-2 breaths ).

Atrovent (ipratropium bromide) is an anticholinergic agent. Usually used with the ineffectiveness of beta2-agonists or in combination with them to enhance the bronchodilator effect. The drug can be administered through a nebulizer at 0.25-0.5 mg or by using a metered-dose aerosol inhaler and spacer at a dosage of 40 μg.

The lack of response to adrenomimetics indicates the development of a perverted reaction of beta-adrenergic receptors to sympathomimetics, which makes it impractical to use them (in asthmatic status, the use of adrenergic stimulants can lead to the development of rebound syndrome - deterioration caused by the accumulation of metabolic products of adrenostimulants in the blood).

[52], [53], [54], [55], [56], [57], [58], [59], [60],

Bronchodilators

Of the preparations of the bronchodilator effect, first of all, the use of aminophylline (theophylline, aminophylline) is indicated. 240 mg of the drug is administered slowly intravenously over a period of 20 minutes in the form of a 2.4% solution. Then reduce the dose to 0.5-0.6 mg / kg mass at 1 hour to improve the clinical status of the patent. The daily dose should not exceed 1.5 g. Eufillin inhibits phosphodiesterase, which leads to the accumulation of adenylcyclic adenosine monophosphate, the restoration of adrenoceptor sensitivity and the removal of bronchospasm. The drug reduces the pressure in the pulmonary artery system, increases myocardial contractility and has a slight diuretic effect.

[61], [62], [63], [64], [65]

Glucocorticoids

Glucocorticoids inhibit various mechanisms of bronchospasm and have a nonspecific anti-inflammatory and anti-edema effect. They potentiate the effect of bronchodilator drugs, increasing the intracellular concentration of adenylcyclic adenosine monophosphate.

Corticoids reduce bronchial hyperreactivity, have an anti-inflammatory effect, increase the activity of P2-agonists and promote reactivation of beta2-adrenergic receptors.

The initial dose is at least 30 mg of prednisolone or 100 mg of hydrocortisone and 4 mg of dexamethasone. Next, prednisone administered intravenously at the rate of 1 mg / kg / h. Other hormonal drugs are administered in the appropriate dosage (5 mg of prednisolone equivalent to 0.75 mg of dexamethasone, 15 mg of cortisone, 4 mg of triamcinolone). The intervals of administration should be no more than 6 hours, the frequency of administration depends on the clinical effect. On average, to relieve asthmatic status of stage I, 200-400 mg of prednisolone (up to 1500 mg / day) is required. With asthmatic status of stage II-III, the dose of prednisone is up to 2000-3000 mg / day.
Mechanical ventilation

The indications for the transfer to artificial ventilation of the lungs of patients with asthmatic status are the progression of asthmatic status. Despite ongoing intensive therapy (signs of acute respiratory failure II-III degree), increase in PaCO2 and hypoxemia, progression of symptoms from the central nervous system and the development of coma, increasing fatigue and exhaustion. Decrease in O2 voltage to 60 mm Hg. Art. And an increase in CO2 voltage above 45 mmHg. Art. Should be considered as an absolute indication for respiratory support.

The effect of “over-inflation” of the lungs and the development of pressure in the airways over 35 cm of water should be avoided. Art., as this is fraught with the development of pneumothorax. It is possible to use short-term fluorotane anesthesia through an open circuit or intravenous steroid anesthesia. At the same time there is a pronounced bronchodilatory effect. In addition, by turning off the consciousness, the emotional background is eliminated.

[66], [67], [68], [69], [70], [71],

Other drugs

The use of antihistamines and sedatives in asthmatic status is undesirable, as they can depress respiration and suppress the cough reflex. It is also undesirable to use diuretic drugs in order to reduce the swelling of the bronchial mucous membrane, as they can aggravate the existing disturbances of water and electrolyte balance.

It is possible to consider the use of calcium antagonists, which relaxes the smooth muscles of the bronchi and dilates the peripheral vessels, thereby providing a balanced effect on ventilation and pulmonary hemodynamics. In addition, they inhibit the release of mediators from lung mast cells and histamine from blood basophils. In some cases, a good effect is given by the introduction of glucocorticoids and mucolytic enzymes into the trachea.

[72], [73], [74], [75]

Regional and neuroaxillary blockades

When arresting asthmatic status, patient’s hypersensitivity to certain drugs is very difficult. This reduces the possibilities of the intensive care physician and predetermines the search for new approaches in the treatment of this disease.

Significantly increase the effectiveness of the treatment can regional blockade. It is known that dysfunction of the central and autonomic nervous systems plays an important role in the realization of suffocation by the type of formation of congestive pathological interoceptive processes causing spasms of sensitized bronchial muscles and increased secretion of viscous sputum with obstruction of the bronchi. In cases where traditional methods of treatment of patients with bronchial asthma are ineffective, it is recommended to conduct blockages of the autonomic nervous system.

Blockade of the cervical sympathetic nodes F.G. Corner. Cervical blockade of 1-2 sympathetic ganglia is technically simple, has a minimal negative effect on the cardiovascular system, and can be effectively used at any stage of emergency care. To achieve blockade, 20-30 ml of 0.5% novocaine solution is injected.

Intradermal anterior cervical blockade is a type of intracutaneous blockade according to Speransky. The easiest to perform manipulation. The purpose of the blockade is to influence the pathological process through the nervous system in order to reduce the pathological irritation of the nervous elements and eliminate bronchospasm.

The technique of the blockade: 40-50 ml of a 0.25% solution of novocaine (lidocaine) is injected into the skin along three sides of the triangle, the base of which is located at the level of cricoid cartilage, and the top approaches the jugular fossa. To achieve a therapeutic effect, 4-6 blockades are performed at intervals of 5-7 days.

[76], [77]