THE SYNDROME OF BRONCHIAL

OBSTRUCTION.
BRONCHIAL ASTHMA. COPD. ASTHMATIC
STATUS.
 BRONCHIAL OBSTRUCTION SYNDROME

- This is a clinical complex of symptoms, characterized by narrowing of the bronchi

due to:
1) bronchospasm,
2) swelling of the mucous membrane of the bronchi,
3) dyskrinia and resulting obstructive ventilation failure,
manifested by expiratory dyspnea.
Dyskrinia- is an increased production of pathological bronchial secretions of
increased viscosity, which violates the mucociliary clearance and causes obstruction
of the bronchi.
 CLASSIFICATION
Depending on the mechanism of narrowing
(obstruction) of the bronchi, there are:
• Organic and
• Functional bronchial obstruction
 FUNCTIONAL BRONCHIAL
OBSTRUCTION
Causes of functional bronchial obstruction:
• Bronchial asthma
Mechanism: Bronchial hyperreactivity, characterized by
narrowing of the bronchi due to spasm of smooth muscles
(bronchospasm).
Functional bronchial obstruction syndrome is characterized by
damage to the small bronchi and bronchioles.
Only these bronchi can narrow due to spasm, because they lack
cartilage.
FUNCTIONAL BRONCHIAL OBSTRUCTION
SYNDROME.

The main complaints.

• Choking
• cough.
 DETAILING COMPLAINS:
Choking of an expiratory character, occurs when exposed to specific and non-
specific factors.
Specific factor s causing an asthma attack are allergens: house dust and book
dust, plant pollen, animal hair, eggs, chocolate, citrus fruits, etc.
Non-specific factors may include inhalation of hot and cold air, pungent odors,
and physical exertion.
Functional bronchial obstruction syndrome is also characterized by the
appearance of asthma attacks at night closer to morning, which is explained by
an increased tone of the parasympathetic nervous system at this time.
The attack is stopped in the orthopedic position with the fixation of the shoulder
girdle, which helps to facilitate the work of the auxiliary respiratory muscles.
Also, an attack of suffocation is stopped by taking bronchodilators.
 THE COUGH. DETALING.
The cough is paroxysmal, occurs when exposed to allergens, cold
air, pungent odors or a respiratory infection, during exercise, often
occurs at night. The cough is caused by bronchospasm, so
bronchodilator therapy has a significant facilitating effect. After an
attack of dry cough, choking may develop.
At the end of the asthma attack, a cough with sputum appears.
Sputum is mucous, viscous, vitreous, difficult to separate. Its
appearance is associated with hypersecretion in the distal parts of
the bronchial tree of mucus, which can lead to blockage of the
lumen of the bronchi with mucous plugs. After sputum discharge,
the patient's condition improves.
GENERAL INSPECTION DATA.
With functional bronchial obstruction syndrome, all changes during an
objective examination are present only during bronchospasm, there are no
changes outside the attack.
The state and consciousness are determined by the degree of violation of
bronchial patency and the severity of respiratory failure.
The patient's position - forced - orthopedic with a fixed shoulder girdle.
At the time of the attack - diffuse cyanosis and swelling of the jugular veins.
CHEST EXAMINATION DATA.
The barrel-shaped form of the chest, the participation of auxiliary
muscles and wings of the nose in the act of breathing. Difficulty
breathing, with extended exhalation.
Data palpation of the chest.
Rigid chest. Voice trembling is weakened.
 PERCUSSION AND
AUSCULTTION
Data percussion of the lungs.
Boxed sound. An increase in the height of the apices of the lungs.
The omission of the lower boundaries of the lungs. Decreased
mobility of the lower edge of the lungs.
Auscultation data of the lungs.
During an attack: hard breathing, weakened vesicular or vesicular
with prolonged exhalation. Many wheezing heard from a
distance/ Single rhonci.
 BRONCHIAL ASTHMA

Bronchial asthma (BA) is a heterogeneous disease,

characterized by chronic inflammation of the airways, the
presence of respiratory symptoms such as wheezing,
shortness of breath, chest tightness, and cough, which vary in
time and intensity, and manifest along with variable airway
obstruction.
 ETIOLOGY AND
PATHOGENESIS
Internal factors:
Genetic predisposition to atopy
Genetic predisposition to bronchial hyperreactivity
Sex (in childhood, BA more often develops in boys; in
teenage and adult - in women)
 Obesity
 ETIOLOGY AND
PATHOGENESIS
The environment factors:
 Allergens: house dust mites, house allergens, animals, cockroach allergens,
fungal allergens, pollen plants, fungal allergens
 Infectious agents (mainly viral)
 Occupational factors
 Air pollutants: ozone, sulfur dioxide and nitrogen, products combustion of
diesel fuel, tobacco smoke (active and second hand smoke)
 Diet: increased intake of high-grade foods processing, increased intake of
omega-6 polyunsaturated fatty acid and reduced antioxidants (in the form of
fruits and vegetables) and omega-3 polyunsaturated fatty acid (as part of fatty
varieties of fish)
 EPIDEMIOLOGY
At least 300 million patients worldwide suffer from BA.
  The prevalence of BA: affecting 1-18% of population in
different countries.
 PHENOTYPE OF BRONCHIAL
ASTHMA
Allergic BA: the most easily recognized phenotype in which BA usually
begins in childhood is associated with the presence of other allergic diseases
(atopic dermatitis, allergic rhinitis, food allergies) in the patient or relatives.
Eosinophilic airway inflammation is characteristic of this phenotype. Patients
with allergic asthma usually respond well to inhaled glucocorticosteroid
therapy.
Non-allergic BA: occurs in adults, is not associated with allergies. The
profile of airway inflammation in patients with this phenotype can be
eosinophilic, neutrophilic, mixed or small-granulocytic. Depending on the
nature of the inflammation, patients with non-allergic asthma may not
respond to GCS therapy.
 PHENOTYPE OF BRONCHIAL
ASTHMA
BA with a late debut: in some patients, especially women, asthma
develops for the first time in adulthood. These patients are often non
allergic and, as a rule, are refractory to steroid therapy or higher doses
of IGCS are required.
BA with fixed airway obstruction: in some patients with a long
history of BA, apparently due to remodeling of bronchial wall
develops a fixed airway obstruction.
BA in obese patients: Obese and BA patients often have
pronounced respiratory symptoms not associated with eosinophilic
inflammation.
 MAKING THE INITIAL
DIAGNOSIS
Making the diagnosis of asthma is based on identifying both a characteristic pattern of
respiratory symptoms such as wheezing, shortness of breath (dyspnea), chest tightness or
cough, and variable expiratory airflow limitation.
The pattern of symptoms is important, as respiratory symptoms may be due to acute or
chronic conditions other than asthma.
If possible, the evidence supporting a diagnosis of asthma should be documented when the
patient first presents, as the features that are characteristic of asthma may improve
spontaneously or with treatment; as a result, it is often more difficult to confirm a diagnosis
of asthma once the patient has been started on controller treatment.
 PATTERNS OF RESPIRATORY SYMPTOMS THAT ARE
CHARACTERISTIC OF ASTHMA

The following features are typical of asthma and, if present, increase the probability that
the patient has asthma:
More than one symptom (wheeze, shortness of breath, cough, chest tightness), especially
in adults
• Symptoms often worse at night or in the early morning
• Symptoms vary over time and in intensity
• Symptoms are triggered by viral infections (colds), exercise, allergen exposure,
changes in weather, laughter, or irritants such as car exhaust fumes, smoke or strong
smells.
 HISTORY AND FAMILY
HISTORY
Commencement of respiratory symptoms in childhood, a
history of allergic rhinitis or eczema, or a family history of
asthma or allergy, increases the probability that the
respiratory symptoms are due to asthma.
Patients with allergic rhinitis or atopic dermatitis should be
asked specifically about respiratory symptoms.
 PHYSICAL EXAMINATION
Physical examination
Physical examination in people with asthma is often normal.
The most frequent abnormality is expiratory wheezing (rhonchi) on
auscultation, but this may be absent or only heard on forced
expiration.
Wheezing may also be absent during severe asthma exacerbations,
due to severely reduced airflow (so called ‘silent chest'), but at such
times, other physical signs of respiratory failure are usually present.
Examination of the nose may reveal signs of allergic rhinitis or nasal
polyposis.
 LUNG FUNCTION TESTING TO
DOCUMENT VARIABLE
EXPIRATORY AIRFLOW
LIMITATION
Asthma is characterized by variable expiratory airflow limitation, i.e.
expiratory lung function varies over time and in magnitude to a
greater extent than in healthy populations.
In asthma, lung function may vary between completely normal and
severely obstructed in the same patient. Poorly controlled asthma is
associated with greater variability in lung function than well-
controlled asthma
 LUNG FUNCTION TESTING
Lung function testing should be carried out by well-trained operators with well-
maintained and regularly calibrated equipment.
Forced expiratory volume in 1 second (FEV1 from spirometry is more reliable
than peak expiratory flow (PEF).
If PEF is used, the same meter should be used each time, as measurements may
differ from meter to meter by up to 20%.
PEAK FLOW METER
 LUNG FUNCTION TESTING
A reduced FEV-1 may be found with many other lung diseases (or poor
spirometric technique), but a reduced ratio of FEV1 to FVC indicates airflow
limitation.
From population studies, the FEV1/FVC ratio is usually greater than 0.75 to
0.80 in adults, and usually greater than 0.90 in children.
Any values less than these suggest airflow limitation.
Many spirometers now include mutt-ethnic age-specific predicted values.
 ‘VARIABILITY’ AND
‘REVERSIBILITY’
In clinical practice, once an obstructive defect has been confirmed, variation in airflow
limitation is generally assessed from variation in FEV1 or PEF.
‘Variability’refers to improvement and/or deterioration in symptoms and lung function.
Excessive variability may be identified over the course of one day (diurnal variability),
from day to day, from visit to visit, or seasonally, or from a reversibility test.
‘Reversibility’ generally refers to rapid improvements in FEV1 (or PEF), measured
within minutes after inhalation of a rapid-acting bronchodilator such as 200-400 mcg
salbutamol, or more sustained improvement over days or weeks after the introduction of
effective controller treatment such as ICS.
 LUNG FUNCTION AS AN
ESSENTIAL COMPONENT
In a patient with typical respiratory symptoms, obtaining evidence of
excessive variability in expiratory lung function is an essential component
of the diagnosis of asthma. Some specific examples are:
• An increase in lung function after administration of a bronchodilator,
or after a trial of controller treatment.
• A decrease in lung function after exercise or during a bronchial
provocation test.
• Variation in lung function beyond the normal range when it is repeated
over time, either on separate visits,or on home monitoring over at least 1-2
weeks.
 HOW MUCH VARIATION IN EXPIRATORY
AIRFLOW IS CONSISTENT WITH ASTHMA?
There is overlap in bronchodilator reversibility and other measures
of variation between health and disease. In a patient with respiratory
symptoms, the greater the variations in their lung function, or the
more times excess variation is seen, the more likely the diagnosis is
to be asthma.
Generally, in adults with respiratory symptoms typical of asthma, an
increase or decrease in FEV1 of >12% and >200 mL from
baseline, or (if spirometry is not available) a change in PEF of at
least 20%, is accepted as being consistent with asthma.
 PEAK EXPIRATORY FLOW
(PEF).
Diurnal PEF variability is calculated from twice daily readings as the daily
amplitude percent mean, i.e. ([Day's highest - day's lowest]/mean of day's
highest and lowest) x 100, then the average of each day’s value is calculated
over 1-2 weeks.
The upper 95% confidence limit of diurnal variability (amplitude percent
mean) from twice daily readings is 9% in healthy adults, and 12.3% in
healthy children, so in general, diurnal variability >10% for adults and >13%
for children is regarded as excessive.
 WHEN CAN VARIABLE AIRFLOW
LIMITATION BE DOCUMENTED?
When can variable airflow limitation be documented?
If possible, evidence of variable airflow limitation should be documented
before treatment is started. This is because variability usually decreases with
treatment as lung function improves.
In addition, any increase in lung function after initiating controller treatment
can help to confirm the diagnosis of asthma. Bronchodilator reversibility may
not be present between symptoms, during viral infections or if the patient has
used a beta2-agonist within the previous few hours; and in some patients
airflow limitation may become persistent or irreversible over time.
 Diagnostic criteria for asthma in adults, adolescents, and children 6-11 years

DIAGNOSTIC FEATURE CRITERIA FOR MAKING THE DIAGNOSIS OF ASTHMA

1 1 1. History of variable respiratory symptoms
Wheeze, shortness of breath, chest tightness and • Generally more than one type of respiratory symptom
cough (in adults, isolated cough is seldom due to asthma)
Descriptors may vary between cultures and by age,
eg. children may be described as having heavy • Symptoms occur variably over time and vary in intensity
breathing • Symptoms are often worse at night or on waking
• Symptoms are often triggered by exercise, laughter, allergens, cold air
• Symptoms often appear or worsen with viral infections
2. Confirmed variable expiratory airflow limitation
Documented excessive variability in lung function* The greater the variations, or the more occasions excess variation is seen, the
(one or more of the tests below) more confident the diagnosis
AND documented expiratory airflow limitation* .O'
At a time when FEV, is reduced, confirm that FEVi/FVC is reduced (it is usually
>0.75-0.80 in adults, >0.90 in children8)
G
Positive bronchodilator (BD) reversibility test* Adults: increase in FEV, of >12% and >200 mL from baseline, 10-15 minutes
(more likely to be positive if BD medication is after 200-400 mcg albuterol or equivalent (greater confidence if increase is >15%
withheld before test: SABA 24 hours, LABA 215 and >400 mL).
hours) Children: increase in FEV, of >12% predicted
Excessive variability in twice-daily PEF over 2 Adults: average daily diurnal PEF variability >10%**
weeks* Children: average daily diurnal PEF variability >13%**
Significant increase in lung function after 4 Adults: increase in FEV, by >12% and >200 mL (or PEF* by >20%) from baseline
 SYNDROME OF
ORGANIC BRONCHIAL
OBSTRUCTION
 REASONS FOR THE DEVELOPMENT OF
ORGANIC BRONCHIAL OBSTRUCTION:
1. COPD
2. Acute bronchitis
3. Often manifestations of bronchial obstruction are found in bronchiectatic disease, bronchial
tuberculosis, bronchogenic cancer.
Mechanism:
The development of organic bronchial obstruction is due to morphofunctional restructuring of the
wall of the entire bronchi with prolonged exposure to tobacco smoke, dust, pollutants, and
repeated respiratory infections. Persistent inflammation develops (the main cells are neutrophils,
eosinophils, macrophages, mast cells), which leads to a thickening of the bronchial wall due to:
• swelling of the mucous membrane,
• hyperplasia of the bronchial glands,
• smooth muscle hypertrophy,
• fibrotic changes.
PATHOGENESIS OF ORGANIC
BRONCHIAL OBSTRUCTION
In the early stages of the development of the pathological process,
inflammatory swelling of the mucous membrane of the bronchi occurs and the
number of goblet cells increases, which is accompanied by an increase in the
production of mucus.
The functional activity of the microvilli of the ciliated epithelium decreases.
As a result of these changes, mucociliary insufficiency occurs: a viscous
mucous secretion sticks to the walls of the bronchi, narrowing their lumen.
Further exposure to damaging factors contributes to an increase in the
production of inflammatory mediators that cause proliferation of smooth
myocytes and fibroblasts; a thickening of the bronchial wall occurs, which
exacerbates the obstruction.
SYNDROME OF ORGANIC
BRONCHIAL OBSTRUCTION
The syndrome of organic bronchial obstruction is characterized by
a defeat in the first place of large and medium bronchi, and only
later the inflammatory process can go on to small bronchi.
 SYNDROME OF ORGANIC BRONCHIAL OBSTRUCTION.
THE MAIN COMPLAINTS.

• Cough
• shortness of breath
Cough detail: cough with sputum, more worrying in the morning. Sometimes
patients cough so rarely during the day that they do not notice their cough.
Sputum is moderate, it is excreted heavily, more in the morning after an
attack of prolonged cough. During remission, sputum is usually of a mucous
nature, very viscous, and in the period of exacerbation of the disease,
mucopurulent.
 DETAILS OF DYSPNEA:
expiratory dyspnea of ​varying severity. In the late stages of the disease,
when the pathological process is complicated by emphysema,
pneumosclerosis, and pulmonary heart disease, dyspnea becomes
mixed.
The clinical feature of dyspnea is its relatively constant nature during
the day at rest and intensification after physical exertion, as well as in
bad weather conditions.
The more pronounced obstructive ventilation failure, the lower the
threshold for physical exertion, causing increased shortness of breath.
 DATA FROM PHYSICAL RESEARCH
METHODS.
General inspection data.
The state and consciousness are determined by the degree of violation of
bronchial obstruction, the severity of respiratory failure, the presence of
intoxication. Changes identified during an objective examination are
amplified during an exacerbation of the inflammatory process.
Forced position - orthopnea with a fixed shoulder girdle.
The physique is wrong due to the emphysematous chest.
A person during an exacerbation of a disease accompanied by fever is the
face of a febrile patient.
GENERAL INSPECTION DATA.
Erythrocyanosis - purplish-cyanotic cheeks, an expanded capillary
network on the face. This is a sign of respiratory failure and
compensatory erythrocytosis.
Skin with diffuse cyanosis, during the period of decompensation of
right ventricular failure (decompensated pulmonary heart) - appears
acrocyanosis, swelling on the legs and swollen jugular veins.
When viewed by region, you can identify nails in the form of "watch
glasses" and fingers in the form of "drum sticks"
CHEST EXAMINATION DATA.
With a static examination before the development of emphysema, no changes
are observed.
The emphysematous form of the chest appears with increased airiness of the
lung tissue.
The mechanism of development of emphysema with organic bronchial
obstruction is associated with the presence of increased resistance to the path of
air exit from the alveoli through the narrowed bronchi, resulting in an increase
in the residual air volume in the alveoli, which leads to an overstretching of
their wall and a decrease in the elasticity of the lung tissue.
 A DYNAMIC EXAMINATION OF THE CHEST
REVEALS SIGNS OF SHORTNESS OF BREATH.

Deep breathing with a predominance of obstructive

ventilation disorders, superficial and frequent with the
development of emphysema - mixed ventilation disorders.
The exhalation is extended.
The participation of auxiliary muscles and wings of the nose
in the act of breathing
 PALPATION AND PERCUSSION
DATA
On palpation and percussion before the addition of emphysema,
no changes are detected.
When emphysema is attached during palpation of the chest, its
stiffness and weakening of voice trembling are revealed, with
percussion - a box sound, an increase in the height of the apices
of the lungs, lowering of the lower borders of the lungs, a
decrease in the mobility of the lower edge of the lungs.
 AUSCULTATION OF THE LUNGS
is the main physical method to detect bronchial obstruction.
Before the development of emphysema, harsh vesicular breathing is heard - a
sign of an uneven narrowing of the lumen of the bronchi and
dry, mostly low rales = rhonchi
When small-caliber bronchi are involved in the process - during an exacerbation of
the disease - you can hear a few wheezing.
When liquid contents, for example, purulent sputum appear in the lumen of the
bronchi, during the period of exacerbation, sonorous, moist, fine and medium
crakles are heard.
With the development of emphysema, the main respiratory noise becomes
weakened vesicular breathing or breathing with an extended expiration.
Chronic Obstructive Pulmonary Disease
(COPD)
COPD. DEFENITION.
• Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable
and treatable disease that is characterized by persistent respiratory
symptoms and airflow limitation that is due to airway and/or alveolar
abnormalities usually caused by significant exposure to noxious particles or
gases.
 OVERALL KEY POINTS
• The most common respiratory symptoms include dyspnea, cough and/or sputum production.
These symptoms may be under-reported by patients.
• The main risk factor for COPD is tobacco smoking but other environmental exposures such
as biomass fuel exposure and air pollution may contribute. Besides exposures, host factors
predispose individuals to develop COPD. These include genetic abnormalities, abnormal lung
development and accelerated aging.
• COPD may be punctuated by periods of acute worsening of respiratory symptoms, called
exacerbations.
• In most patients, COPD is associated with significant concomitant chronic diseases, which
increase its morbidity and mortality.
 EPIDEMIOLOGY
Chronic Obstructive Pulmonary Disease (COPD) is currently the fourth leading cause of
death in the world but is projected to be the 3rd leading cause of death by 2020. More than
3 million people died of COPD in 2012 accounting for 6% of all deaths globally.
COPD represents an important public health challenge that is both preventable and
treatable.
COPD is a major cause of chronic morbidity and mortality throughout the world; many
people suffer from this disease for years, and die prematurely from it or its complications.
Globally, the COPD burden is projected to increase incoming decades because of
continued exposure to COPD risk factors and aging of the population.
 WHAT IS CHRONIC
OBSTRUCTIVE PULMONARY
DISEASE (COPD)?
Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and
treatable disease that is characterized by persistent respiratory symptoms and
airflow limitation that is due to airway and/or alveolar abnormalities usually
caused by significant exposure to noxious particles or gases.
The chronic airflow limitation that is characteristic of COPD is caused by a
mixture of small airways disease (e.g., obstructive bronchiolitis) and parenchymal
destruction (emphysema), the relative contributions of which vary from person to
person
 WHAT CAUSES COPD?
Worldwide, the most commonly encountered risk factor for COPD is tobacco smoking.
Nonsmokers may also develop COPD. COPD is the result of a complex interplay of
long-term cumulative exposure to noxious gases and particles, combined with a variety
of host factors including genetics, airway hyper-responsiveness and poor lung growth
during childhood.
The risk of developing COPD is related to the following factors:
Tobacco smoke - cigarette smokers have a higher prevalence of respiratory symptoms
and lung function abnormalities, a greater annual rate of decline in FEVi, and a greater
COPD mortality rate than non-smokers. Other types of tobacco (e.g., pipe, cigar, water
pipe) and marijuana are also risk factors for COPD, as well as environmental tobacco
smoke
 THE RISK OF DEVELOPING
COPD
Indoor air pollution - resulting from the burning of wood and other biomass
fuels used for cooking and heating in poorly vented dwellings, is a risk
factor that particularly affects women in developing countries.
Occupational exposures - including organic and inorganic dusts, chemical
agents and fumes, are under-appreciated risk factors for COPD.
Outdoor air pollution - also contributes to the lungs' total burden of inhaled
particles, although it appears to have a relatively small effect in causing
COPD.
 THE RISK OF DEVELOPING
COPD
Genetic factors - such as severe hereditary deficiency of alpha-1
antitrypsin (AATD); the gene encoding matrix metalloproteinase 12
(MMP-12) and glutathione S-transferase have also been related to a
decline in lung function or risk of COPD.
Age and sex - aging and female sex increase COPD risk.
Lung growth and development - any factor that affects lung growth
during gestation and childhood (low birth weight, respiratory
infections, etc.) has the potential to increase an individual's risk of
developing COPD. 
 THE RISK OF DEVELOPING
COPD
Socioeconomic status. lower socioeconomic status associated with airflow
obstruction and an increased risk of developing COPD. It is not clear,
however, whether this pattern reflects exposures to indoor and outdoor air.
Asthma and airway hyper-reactivity - asthma may be a risk factor for the
development of airflow limitation and COPD.
Chronic bronchitis - may increase the frequency of total and severe
exacerbations.
Infections - a history of severe childhood respiratory infection has been
associated with reduced lung function and increased respiratory symptoms in
adulthood.
 DIAGNOSIS
• COPD should be considered in any patient who has dyspnea, chronic cough or sputum
production, a history of recurrent lower respiratory tract infections and/or a history of
exposure to risk factors for the disease.
• Spirometry is required to make the diagnosis; the presence of a post-bronchodilator
FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation. and thus of
COPD in patients with appropriate symptoms and significant exposures to noxious stimuli.
Spirometry is the most reproducible and objective measurement of airflow limitation. It is a
noninvasive and readily available test.
Despite peak expiratory flow measurement alone cannot be reliably used as the only
diagnostic test because of its weak specificity.
 THE GOALS OF COPD
The goals of COPD assessment are to determine the level of airflow
limitation, the impact of disease on the patient's health status, and the
risk of future events (such as exacerbations, hospital admissions, or
death), in order to guide therapy.
 CONCOMITANT CHRONIC
DISEASES FOR COPD
• Concomitant chronic diseases occur frequently in COPD patients
including: cardiovascular disease, skeletal muscle dysfunction,
metabolic syndrome, osteoporosis, depression, anxiety, and lung
cancer.
These comorbidities should be actively sought and treated
appropriately when present as they can influence'mortality and
hospitalizations independently.
 KEY INDICATORS FOR CONSIDERING A DIAGNOSIS OF COPD
Consider COPD, and perform spirometry, if any of these indicators are present in an individual over age 40.
These indicators are not diagnostic themselves, but the presence of multiple key indicators increases the probability of a
diagnosis of COPD. Spirometry is required to establish a diagnosis of COPD.

Dyspnea that is: Progressive over time.

Characteristically worse with exercise.
Persistent.

May be intermittent and may be unproductive. Recurrent wheeze.

Chronic Cough:
Chronic Sputum Production: Any pattern of chronic sputum production may indicate COPD.

Recurrent Lower Respiratory Tract Infections

------------------------
Host factors (such as genetic factors, congenital/developifl^ntal abnormalities etc.). Tobacco smoke (including popular
local preparations).
History of Risk Factors: Smoke from home cooking and heating fuels. CQ Occupational dusts, vapors, fumes, gases
and other chemicals.
------------------------------------------------------------ -------------------------------------------------------
Family History of COPD For example low birthweight, childhood^espiratory infections etc.
and/or Childhood Factors:
Status asthmaticus
 DEFENITION
Status asthmaticus ( 'AS) - is one of the most severe complications of
asthma, visible role in which play a pronounced and progressive
respiratory failure caused by obstruction of the airway of the patient
with full resistance to common therapy.
AS - an episode of acute respiratory failure due to severe
exacerbation of bronchial asthma
 DIAGNOSTIC CRITERIA FOR
ASTHMATIC STATUS
1. Resistance to sympathomimetics and other bronchodilators.
2. A severe attack of suffocation, which can be complicated by the
syndromes of total pulmonary obstruction, the development of acute
respiratory failure, acute pulmonary heart, transform into a hypoxemic coma.
3. A sharp violation of the drainage function of the bronchial tree. An
unproductive and ineffective cough exhausts the patient. Mucociliary
insufficiency is pronounced.
4. Hypercapnia and respiratory acidosis.
5. Secondary polycythemia.
 THE MAIN SYNDROMES OF
ASTHMATIC STATUS
1. Respiratory syndrome - intense shortness of breath (from 30 to 60
breaths per minute), participation in the breathing of the auxiliary
respiratory muscles, pronounced diffuse cyanosis, difficulty and sharply
elongated exhalation, weakening of respiratory sounds, breathing is
practically not heard over individual parts of the lungs, cough and sputum
are absent.
The patient takes a forced position (orthopnea) - sitting on the bed, resting
his hands on the edge of the bed (as if hanging on his hands), chest in a
state of maximum breath. The extreme severity of acute respiratory failure
contrasts with poor physical and radiological findings.
 THE MAIN SYNDROMES OF
ASTHMATIC STATUS
2. Cardiovascular syndrome - sinus tachycardia (more than 120 per minute),
increased systolic blood pressure to 200-220 mm RT. Art. followed by arterial
hypotension and collapse. There are signs of right ventricular failure (cervical
vein swelling, enlarged and sore liver, pasty lower limbs, high P wave and
symptom QIII-S1 on the ECG).
 In severe cases, there is a violation of the heart rhythm (supraventricular and
ventricular extrasystoles, atrial fibrillation, blockade of the legs of the bundle
of His, etc.).
The cardiotoxic effect of sympathomimetics enhances the manifestations of the
cardiovascular syndrome.
 THE MAIN SYNDROMES OF
ASTHMATIC STATUS
3. Psychomotor syndrome — agitation, anxiety, anxiety,
“respiratory panic”, trembling in the extremities, short delirious
episodes are replaced by inhibition, up to the development of
hypercapnic-hypoxemic coma.
 STAGES OF ASTHMATIC STATUS
Stage 1 asthmatic status - stage of relative compensation. It is clinically
characterized by a prolonged, non-stopable attack of bronchial asthma with a
formed resistance to sympathomimetics and other bronchodilators.
Patients are conscious, adequate. Objectively: diffuse pale cyanosis, tachypnea.
The mismatch between the intensity of respiratory sounds, determined remotely,
and their weak severity during auscultation of the lungs.
Percussion - mobility of the lower pulmonary margin is limited, above the lungs a
sound with a boxy tint.
The auscultatory picture of the lungs is very diverse - in places weakened
breathing is heard, in places - hard. It is important that breathing is carried out in
all pulmonary fields. The exhalation is sharply intensified, dry scattered
whistling, buzzing rales, but their number is small. Relative cardiac dullness due
to emphysema is not determined.
STAGE 1 ASTHMATIC STATUS
Heart sounds are weakened, tachycardia (resistant to cardiac
glycosides). Blood pressure tends to increase, which is partially
due to an overdose of sympathomimetics. An alarming symptom is
the lack of sputum production. In the blood, moderate arterial
hypoxemia and normo- or hypocapnia. FEV is reduced to 30% of
due.
 STAGE II ASTHMATIC STATUS
II stage of asthmatic status - the stage of decompensation or the stage of
"silent lung". Characterized by total pulmonary obstruction syndrome and
increasing obstructive respiratory failure.
 The patient's condition is extremely serious: diffuse cyanosis, tachypnea,
oligopnea. There is a mismatch between noisy wheezing, the number of
respiratory movements and an almost complete absence of wheezing in the
lungs, a sharp weakening of breathing and zones of complete lack of
breathing over individual sections of the lungs - the “silent lung” zone.
The chest is emphysematically swollen.
 STAGE II ASTHMATIC STATUS
Pulse of weak filling, tachycardia up to 140 beats per minute, often
arrhythmia. Blood pressure decreases.
Acute right ventricular failure appears.
Pronounced signs of dehydration are added - negative water balance,
erythrocytosis, increased hematocrit to 50-60%.
 A significant mental disorder is noted - psychomotor agitation is replaced by
inhibition, hallucinations, a sense of fear of death, and “respiratory panic” are
possible.
Hypoxemia and hypercapnia increase. FEV, less than 20%.
 III STAGE OF ASTHMATIC
STATUS
III stage of asthmatic status - hypoxic hypercapnic coma. The condition is
extremely serious.
Cerebral and neurological disorders prevail. Rare, shallow breathing.
Diffuse cyanosis.
  Auscultation retains the picture of a "silent lung."
Pulse - filiform, hypotension, collapse. Marked hypoxemia and hypercapnia
are noted. There is a shift in the acid base syndrome towards metabolic
acidosis, and with increasing severity of the status, metabolic alkalosis
develops.
Emergency treatment for asthmatic
status
 EMERGENCY TREATMENT FOR
ASTHMATIC STATUS
1. Asthmatic status is an indication for immediate
hospitalization of the patient.
2. Sympathomimetics through the nebulizer.
3. The purpose of corticosteroids - eliminate the
functional blockade of β-adrenergic receptors, the
stopping effect of sympathomimetics is restored.
 DOSAGE OF
CORTICOSTEROIDS
In stage I asthmatic status, prednisolone is administered at a dose of 60–90 mg iv every 3
hours until the status is stopped.
At stage II of asthmatic status, prednisolone is administered at a dose of 90-120 mg iv every
1.5-2 hours.
If the patient’s condition does not improve in the next 2-3 hours, a single dose of prednisolone
increases to 240 mg. At the same time, hydrocortisone 125–250 mg every 4–6 hours is
connected. The total dose of corticosteroids for stage II asthmatic status is large - prednisolone
from 360 to 2000 mg, hydrocortisone from 500 to 1500 mg.
In stage III asthmatic status, prednisone is administered at a dose of 120-240 mg every hour
and hydrocortisone 250 mg every 2-3 hours. After stopping the asthmatic status, the daily
amount of corticosteroids administered is reduced by 25-50% with respect to the initial dose.
 TREATMENT FOR ASTHMATIC
STATUS
4. Methylxanthines - the initial dose of Euphyllin is 5-6 mg / kg of body weight with a slow
intravenous drip (within 20 minutes), then the administration of Euphyllin continues at a dose of
0.6-0.9 mg / kg per hour until improvement condition of the patient. The daily dose of Euphyllin is
up to 2 g (an average of 40-60 ml of 2.4% solution).
5. Rehydration therapy - the volume of injected fluid in the first two days should be at least 3-4 liters
or more, and in the following days - 1.6 l / m2 of the body surface.
6. Alkaline solutions - small doses of sodium bicarbonate (200-300 ml of a 4% iv solution) under the
control of acid-base balance.
7. Expectorants and mucolytics.
8. Oxygen therapy - an oxygen-air mixture with a relatively low oxygen content (35-40%) is
recommended.
9. Droperidol, antibiotics, heparin (up to 20,000 units per day).
10. In the absence of the effect of the therapy, transfer to mechanical ventilation.