LECTURE # 3

ASTHMATIC SYNDROME
Time – 2h.
Lecture plan:
Introduction
Topicality of the topic
Etiopathogenetic features and their significance
Clinical features. Differential diagnosis
Value of additional research methods
Complications. Prevention
Basics of therapy. Differentiation of treatment.
BRONCHIAL ASTHMA (BA)
 chronic persistent inflammatory disease of the respiratory tract (mainly the bronchi) with
their reversible obstruction, manifested by attacks of suffocation or asthmatic status.
Etiology and pathogenesis.
 AD is an etiologically and pathogenetically heterogeneous disease. The etiological
factors of AD are schematically divided into exogenous and endogenous.
 exogenous factors include:
 1) allergization of the population (urbanization);
 2) air pollution;
 3) introduction of chemistry in agriculture, industry and everyday life;
 4) widespread use of antibiotics, vaccines, serums, etc.;
 5) climatic and natural features of the region (for example, cold and wet climate,
abundance of flowering plants, dustiness, etc.).
 Endogenous factors of asthma are various infectious and inflammatory diseases of the
respiratory system (acute pneumonia, acute and chronic bronchitis), congenital or
acquired defects and disorders of the immune, endocrine, neuropsychic, neurohumoral
and other body systems.
 The main manifestation of asthma is more or less pronounced paroxysmal disorders of
bronchial patency, i.e. reversible (spontaneously or as a result of treatment) bronchial
obstruction. Restoration of bronchial patency in BA is due to the fact that the main
pathophysiological mechanisms of a suffocation attack are such reversible components of
 bronchial obstruction as inflammatory mucosal edema, excess mucus in the bronchial
tree (hypercrinia) and spasm of bronchial smooth muscles.
 Irreversible components-hyperplastic and fibrous changes in the bronchi, expiratory
collapse of small bronchi, hypotonic dyskinesia of the trachea and large bronchi with
prolapse of the membranous part on exhalation-play a much smaller role in the formation
of bronchial obstruction in BA, which appear in the case of a combination of BA with
chronic obstructive bronchitis and emphysema of the lungs.
Patients with severe asthma develop persistent, refractory to conventional therapy
bronchoobturation syndrome - asthmatic status(AS). The causes of AS are acute
infections and exacerbations of chronic infections of the upper respiratory tract,
bronchopulmonary apparatus, viral diseases, unjustified dose reduction or withdrawal of
glucocorticosteroids, overdose of sympathomimetic agents, excessive use of sleeping
pills, sedatives and antihistamines, the use of nonsteroidal anti-inflammatory drugs
(aspirin, brufen, metindol), pyrazolone drugs, analgin, enzyme mucolytics (trypsin,
chymotrypsin), antibiotics, and sulfonamides.
classification
 There are the following clinical forms:
 - allergic and close to it atopic
 - infectious
 - aspirin
 - asthma of physical effort
 - nutritious
 - steroid-dependent

Clinical picture and diagnosis

 The clinical picture of asthma is diverse: from rare mild manifestations to prolonged and
painful attacks of suffocation.
 The central place is occupied by asthmatic attacks. They usually occur at night, often
unexpectedly, sometimes after unclear harbingers in the form of a feeling of tightness in
the chest, difficulty breathing.
 At the beginning, suffocation attacks are mostly short-from a few minutes to half an hour;
later they become more prolonged, persistent, dragging on for a whole day and
sometimes turning into AS.
 Often, during an attack (usually towards the end), a small amount of mucosal, sticky
sputum is released with coughing. In its grayish lumps, it is sometimes possible to see
spirally twisted swirls of mucus (Courschmann spirals) and casts of small bronchi.
 In all clinical and pathogenetic variants, the following are distinguished:
 easy,
 average
 and a severe degree of asthma.
Mild episodic course of AD:
 *suffocation attacks are short-term and occur no more than 1-2 times a week;
 * nocturnal symptoms no more than 2 times a month;
 • in the inter-approach period, the state of health is not disturbed;
 *indicators of external respiratory function - PSV or FEV-not less than 80% of the
required values;
 *daily fluctuations in PSV or FEV do not exceed 20 %;
 *after inhalation of the bronchodilator (in case of exacerbation), the PSV and FEV
indicators return to normal values.
Mild persistent course of asthma:
 *suffocation attacks more often than 2 times a week, but not daily;
 *exacerbations (seizures) may interfere with physical activity and sleep.
  * nocturnal symptoms more often than 2 times a month;
 *PSV or FEV indicators of at least 80% of the required ones;
 *daily fluctuations of the PSV of 20-30 %.
Moderate course of asthma:
 symptoms daily.
 *the need for daily use of short-acting beta-2agonists;
 *nocturnal symptoms more than once a week;
 *exacerbations interfere with physical activity and sleep.
 *PSV or FEV is 60-80 % of the required values;
 *daily fluctuations in the PSV of more than 30 %.
Severe course of asthma:
 *symptoms are persistent with frequent exacerbations.
 *physical activity is limited.
 *frequent nocturnal symptoms.
 *PSV or FEV indicators of less than 60 % of the required ones;
 *daily fluctuations in the PSV of more than 30 %.
At the heart of allergic asthma
 there is an immunological mechanism with excessive production of IgE, with a massive
release of mast cell mediators at every contact of the patient with the” guilty " allergen.
 It occurs more often in people with a burdened family or personal allergic history, usually
begins in childhood, and such patients have other allergic manifestations (allergic rhinitis,
conjunctivitis, atonic dermatitis).
For non-allergic bronchial asthma
 sensitization to a particular allergen cannot be detected. The onset of the disease occurs at
a more mature age, and the trigger factor, as well as the” culprit " of exacerbation, is most
often a previous respiratory viral infection.
 A few days after the onset of the viral disease, shortness of breath, cough, and suffocation
attacks appear, which can last from several days to several months.
Reliable diagnosis of AD
 It is possible only by excluding secondary bronchospastic syndrome (BS). Secondary BS
is most often found in anaphylactic shock, serum sickness,SLE, pneumoconiosis,
bronchitis, pneumonia, tuberculosis, malignant and benign tumors, hysteria, mechanical
irritation of the vagus nerve, overdose with vagostimulants, such as beta-blockers,
intratracheal anesthesia, primary pulmonary arterial hypertension, PE, congestive left
ventricular failure
Treatment.
 The general treatment program for patients with asthma should include:
 1) an educational program;
 2) assessment and monitoring of the severity of the disease;
 3) exclusion of factors that provoke an exacerbation of the disease, or control over them;
 4) development of an individual drug treatment regimen;
 5) development of a treatment plan for exacerbation of the disease, emergency therapy in
case of an attack of suffocation and (or) AS;
6) medical supervision.
Individual drug treatment regimen
 It is primarily determined by the severity of asthma. Prescribing medications is carried
out in the form of four stages with an increasing bronchodilating and anti-inflammatory
effect.
 The stage of treatment corresponds to the degree of BA severity: I - mild BA, II and / or
III-moderate BA, IV-severe BA.
Stage 1. Mild episodic course of the disease
  there is no need to prescribe basic anti-inflammatory therapy and treatment consists of
elimination measures (avoid exposure to triggers) and seizure relief with short-actingbeta-
2agonists.
 Prophylactic use of beta-2agonists or sodium cromoglycate is possible before exercise or
exposure to other provoking factors.
The patient's training at this stage should consist of:
 *basic information about asthma;
 *rules for using the inhaler (spacer); explanations of the role of drugs;
 *developing a self-monitoring plan;
 *development of an action plan in case of exacerbation;
 *discuss measures to control environmental factors (allergens and other triggers).
Stage 2. Light persistent flow
 Basic treatment begins with cromoglycate or nedokromil (especially at a young age)
sodium. If the effect is insufficient, you should switch to inhaled glucocorticosteroids in
low doses or combine them with cromolins.
 Prolonged-acting theophylline (serum concentration 5-15 mcg / ml) or antileukotriene
drugs (zafirlukast, zileuton).
The training program includes all questions of the 1st stage, as well as:
 *self-control training;
 *periodically review and update the treatment plan;
 *referral to an asthma school.
Stage 3. Moderate flow
 therapy includes inhaled glucocorticosteroids in medium doses or a combination of low
doses with long-acting beta-2agonists. Long-acting beta-2 agonists can be replacedwith prolonged-
acting theophylline.
 Alternatively, anticholinergic drugs (ipratropium bromide) or a combination thereof with
a beta-2 agonist may be used, especially if beta-2agonists are poorly tolerated.
Stage 4. Heavy flow
 * regular use of inhaled glucocorticoids in high doses;
 * long-term oral corticosteroid use (usually no more than 60 mg of prednisone per day);
 * taking long-acting bronchodilators (long-acting beta-2agonists or prolonged-acting
theophylline).
 With severe adverse reactions to these bronchodilators, they can be replaced or combined
with cholinolytics (ipratropium bromide).
Emergency care for AS.
 A mild attack of suffocation is stopped by taking inside tablets of eufillin, theophedrine or
antastman, no-shpa, papaverine or halidor, 30-60 drops of solutan.
 Distracting activities are effective (talking to the patient, taking a hot foot bath, putting
mustard plasters or cans on your back).
 Sometimes one inhalation of epinephrine derivatives - isoprenaline (novodrin, euspiran),
orciprenaline (astmopent, alupent), hexaprenaline (ipradol), ventolin (salbutamol),
berothec (fenoterol) - is enough to stop an attack.
Moderate suffocation attack
 stop 0.1 % p-om of epinephrine in a dose of 0.5-1 ml subcutaneously or in the form of an
aerosol. To preserve the bronchospasmolytic effect simultaneously with epinephrine, it is
advisable to introduce 5 % ephedrine solution in a dose of 0.5-1 ml subcutaneously or
intramuscularly;
 If there are contraindications to the administration of epinephrine, some of its derivatives
can be used - orciprenaline (alupent), hexaprenaline (ipradol), ventolin (salbutamol),
berotec (fenoterol). Alupent is used in the form of injections (0.5 mg), aerosol (2 % and
5% solutions, up to 1 mg). Modern bronchospasmolytics (berotek, ventolin) are used as
an aerosol. Ipradol is administered intravenously at a dose of 5-10 mcg (1-2 ampoules).
  In the absence of an effect from epinephrine and its derivatives, eufillin (aminophylline,
diphylline) is used in the form of a 2.4% solution, 10 ml IV slowly. For side effects of
eufillin, the following solutions are used simultaneously: 2 % - papaverine, 2 ml, 2 % -
noshpa, 2 ml, 1 % - dibazole, 4-6 ml.
 At night attacks of suffocation and bradycardia-subcutaneous administration of 1 ml of
0.2 % solution of platifillin or 0.5-1 ml of 0.1 % solution of atropine, a good effect is
given by inhaling nitrous oxide mixed with oxygen.
 In case of allergic manifestations, intravenous or intravenous administration of
diphenhydramine, suprastin or pipolfen is indicated.
Severe attack of suffocation
 if the patient does not respond to the above-mentioned therapy and threatens to go into a
hypercapnic coma, it is necessary to call a specialized NSR team.
 At the prehospital stage, the patient should be given intravenous epinephrine, eufillin in
the usual dosage, alupent-0.5 mg in 1 ml of sodium chloride solution slowly for 5
minutes or 5-20 mg in 250 mg of 5 % glucose solution at a rate of 10-15 drops per
minute, ipradol-1-2 ampoules iv within 5 min.
 Along with this, intravenous glucocorticoid hormones are administered - prednisone, 30-
60 mg, or hydrocortisone, 100-250 mg, per 250-500 ml of 5 % glucose solution.
Asthmatic status (AS)
 It is the most serious complication of asthma. It is an ODN due to airway obstruction that
is resistant to sympathomimetic and eufillin therapy.
 Emergency care for AS consists of three mandatory components: oxygen therapy,
infusion and drug therapy (eufillin and its analogues, glucocorticosteroid hormones).
 Oxygen therapy is performed in the form of continuous insufflation of an oxygen-air
mixture with a relatively low oxygen content (30-40%); infusion therapy is performed
with heparinized 5 % glucose solution, Ringer's solution, polyglucin, and rheopolyglucin.
The total volume of infusion therapy is 3-3. 5 liters on the 1st day, and in the following
days-at the rate of 1.6 liters/m2 of body surface.
 Drug treatment of AS is carried out with the most narrowed range of drugs, including the
complete rejection of adrenostimulants.
 Intravenously, 15 ml of a 2.4 % eufillin solution on an isotonic solution of glucose or
sodium chloride is administered for 4-6 minutes together with 5000 units of heparin. The
daily dose of eufillin is 1.5-2 g. Prednisone is administered intravenously: from 30 to 90
mg.
 During decompensation, along with the above measures, therapeutic bronchoscopy is
performed with segmental lavage of the bronchi, the patient is transferred to a ventilator.
CARDIAC ASTHMA (CA)
 Paroxysmal forms of severe breathing difficulties caused by the exudation of serous fluid
into the lung tissue with the formation (increase) of edema — interstitial (in cardiac
asthma) and alveolar, with foaming of protein-rich transudate (in pulmonary edema).
Etiology and pathogenesis.
 The causes of SA and AL are primary ALN (myocardial infarction, other acute and
subacute forms of IHD, hypertensive crisis and other paroxysmal forms of hypertension,
acute nephritis, ALN in patients with myocardiopathy, etc.) or acute manifestations of
CLN (mitral or aortic malformation, chronic heart aneurysm, other chronic forms of IHD,
etc.).
 The main pathogenetic factor — an increase in hydrostatic pressure in the pulmonary
capillaries-is usually accompanied by additional factors that provoke seizures: physical or
emotional stress, hypervolemia, increased blood flow to the small circle system during
the transition to a horizontal position and violation of central regulation during sleep, and
other factors.
  Accompanying the attack, arousal, rising blood pressure, tachycardia, tachypnea,
increased work of the respiratory and auxiliary muscles increase the load on the heart and
reduce its efficiency.
 The suction effect of forced inspiration leads to an additional increase in blood filling of
the lungs.
 Hypoxia and acidosis are accompanied by further deterioration of the heart, violation of
central regulation, increased permeability of the alveolar membrane and reduce the
effectiveness of drug therapy.
Symptoms and course.
 Harbinger and erased forms: increased (appearance) of dyspnea, orthopnea. Choking,
coughing, or only stinging behind the sternum with little physical exertion or when
moving to a horizontal position.
 Usually-weak breathing and scanty wheezing below the shoulder blades. suffocation with
coughing, wheezing.
Cardiac Asthma (CA):
 Orthopnea, forced rapid breathing. Excitement, fear of death. Cyanosis, tachycardia,
often-increased blood pressure. Auscultation — on the background of weakened
breathing, dry, often scanty small—bubbly wheezes. In severe cases-cold sweat, "gray"
cyanosis, swelling of the cervical veins, prostration.
 Swelling of the bronchial mucosa may be accompanied by a violation of bronchial
patency ("mixed asthma").
 Differential diagnosis with AD is very important, because in AD, narcotic analgesics are
contraindicated (dangerous) and indicated (beta-adrenergic drugs).
 It is necessary to evaluate the medical history (heart or lung disease, effectiveness (of
beta-adrenergic drugs) and pay attention to difficult, prolonged exhalation (in BA).
Pulmonary edema (OL)
 it occurs more or less suddenly, or as a result of an increase in the severity of AS. The
appearance of profuse small - and medium-bubbly wheezing in SA, extending to the
anteroposterior parts of the lungs, indicates developing ("grade II") OL.
 The appearance of foamy, usually pink sputum (an admixture of red blood cells) is a
reliable sign of AL. Wheezing is clearly audible at a distance ("Grade III").
 Other objective and subjective signs as in severe SA. Stage IV of AL is characterized by
severe orthopnea and cold sweats.
 Distinguish between lightning-fast (death within a few minutes),
 acute (duration of attack from 0.5 to 2-3 hours)
 prolonged (up to a day or more) course. Foamy sputum in AL should be distinguished
from foamy, often blood-stained, saliva released during an epileptic attack and hysteria.
 "bubbling" breathing in extremely severe (agonizing) patients is not a specific sign of
AL.
Treatment
 emergency is already at the stage of harbingers (possible death). The sequence of
therapeutic measures is largely determined by their availability and the time required for
their implementation.
1. Relief of emotional stress
 A significant role of the emotional factor in this pathology determines the increased
requirements for the doctor's behavior.
 In SA and its precursors, attempts to calm the patient down by assessing his condition as
relatively harmless lead to the opposite result.
 The patient should make sure that the doctor takes his complaints and condition
seriously, acts decisively and confidently.
 2. Sit the patient down (with his legs down).
  3. Nitroglycerin 1-1.5 mg (2-3 tablets or 5-10 drops) under the tongue every 5-10
minutes under the control of blood pressure until a noticeable improvement or decrease in
blood pressure occurs. Possible intravenous administration of nitroglycerin at a rate of 5-
20 mg per 1 min. In some cases, nitroglycerin monotherapy is sufficient, and a noticeable
improvement occurs after 5-15 minutes.
 If nitroglycerin is not effective enough or it is impossible to use it, treatment is
carried out according to the following scheme.
 4. A 1% morphine solution of 1 to 2 ml is administered subcutaneously or intravenously
(slowly, in an isotonic solution of glucose or sodium chloride). If there are
contraindications to the use of morphine (respiratory depression, bronchospasm, brain
edema) or relative contraindications in elderly patients, 2 ml of 0.25% droperidol solution
is administered intravenously or intravenously under the control of blood pressure.
5. Furosemide — from 2 to 8 ml of 1% solution iv (do not use with low blood pressure,
hypovolemia); with low diuresis — monitoring of effectiveness using a urinary catheter.
 6. Use oxygen inhalation (nasal catheters or a mask, but not a pillow). In severe cases,
OL — breathing under high pressure (mechanical ventilation, anesthesia machine).
 7. Digoxin solutions of 0.025% in a dose of 1-2 ml or strophanthin-0.05% in a dose
of 0.5-1 ml are administered intravenously simultaneously or dropwise in an isotonic
solution of sodium chloride or glucose. According to indications, they are re-
administered in half a dose after 1 and 2 hours. Limited indications for acute forms of
coronary heart disease.
 8. If the alveolar membrane is affected (pneumonia, allergic component) and
hypotension, prednisone or hydrocortisone is used.
 9. With mixed asthma with a bronchospastic component, prednisone or
hydrocortisone is administered; slow intravenous administration of 10 ml of 2.4 %
zufillin solution is possible (keep in mind the possible threat of tachycardia, extrasystole).
 10. According to indications-suction of foam and liquid from the tracheobronchial tree
(electric pump), inhalation of foam gel (10% solution of antifomsilane), antibiotics.
 Treatment is carried out under constant monitoring of systolic blood pressure,
which should not decrease by more than 1/3/3 of the initial or below 100-110 mm Hg.
 Special care should be taken with concomitant use of drugs, as well as in elderly patients
with a history of high hypertension. With a sharp decrease in systolic blood pressure,
emergency measures are necessary (lower the head, raise the legs, start mezaton
administration using a pre-prepared backup system for drip infusion).
 At low blood pressure, long-term (up to 1-2 or more) administration of high doses (up to
1.5 g/day) of prednisone and, in some cases, high-pressure mechanical ventilation is of
the greatest importance in the treatment of AL.
 Venous tourniquets on the extremity (alternately for 15 minutes) or venous
bloodletting (200-300 ml) can be recommended as a forced replacement for "internal
bloodletting" of blood-filling redistribution performed with nitroglycerin, furosemide, or
(and) ganglioblockers.
 Inhalation of ethyl alcohol vapors is ineffective and is accompanied by undesirable
irritation of the respiratory tract mucosa.
 The volume of infusion therapy and administration of sodium salts should be limited to
the necessary minimum.
Main literature:
1. Manual of Pulmonology " ed. Putova Publ., 1986.
2. Differential diagnosis of internal diseases. A.V. Vinogradov, 1980.
3. "Clinical Cardiology" ed. by A. V. Sumarokov, 1986.
4. Internal diseases: Textbook: in 2 volumes / Ed. by A. I. Martynov, N. A. Mukhin, V. S.
Moiseev, A. S. Glyavich. - 3rd ed., ispr. - Moscow: GEOTAR-Media, 2005
5. "Guide to cardiology" ed. by E. I. Chazov, 1-1U t., 1982.
6. "The complete cardiologist's handbook", Moscow: Eksmo Publishing House, 2005, 800 p.
7. "Handbook of clinical pharmacology of cardiovascular drugs". 2nd ed., reprint. Moscow:
BINOM Publishing House-St. Petersburg: Nevsky Dialect 2002. - 926 p.