KURSK STATE MEDICAL UNIVERSITY

DEPARTMENT OF PROPAEDEUTICS OF INTERNAL DESEASES

Bronchial asthma

BRONCHIAL ASTHMA Definition

BA is a chronic inflammatory disease of the small airways, characterized by episodic, reversible bronchial obstruction due to hyperresponsiveness of tracheobronchial tree to a multiplicity of intrinsic and extrinsic stimuli manifested clinically by paroxysms of polyphonic wheeze, dyspnea and cough which may be relieved spontaneously or as a result of therapy

Definition of BA (American Thoracic Society)

The disease is characterized by increased responsiveness of the bronchi to various stimuli, manifested by widespread narrowing of the airways that changes in severity either spontaneously or as a result of treatment.

Asthma is a common condition that caused considerable morbidity

In adult -5% (1:1 male/female) Children -10% (2:1 male/female preponderance) 56,8 cases per 100.000 population in Russia (2001y.) BA occurs at all ages, but predominantly in early life: 1/2 cases before age 10, 1/3 cases before age 40

Asthma is a common condition that caused considerable morbidity and results in approximately 2000 deaths per year in the UK. In the United States, a national survey by the Public Health Service estimated that 4-5% of the population had asthma. Mortality from asthma in the USA over the last 30 years appears to be stable at less than 0.4 deaths per 100000 population.

In New Zealand 4.0 deaths per 100000.

It is much less common in most Asian countries.

Etiology
BA is a heterogeneous disease. Two broad types of asthma:

Allergic (extrinsic, atopic, early onset)

Idiosyncratic (intrinsic, nonatopic, late onset)

Allergic asthma

Often associated with a personal and/or family history of allergic diseases (rhinitis, urticaria, eczema) with positive wheal-and-flare skin reactions to intradermal injection of extracts of airborne antigens, with increased level of IgE in serum, and/or with a positive response to provocation tests involving the inhalation of specific antigen.

Idiosyncratic asthma

Patients without personal or family history of allergy, with negative skin test, with normal level of serum IgE

Pathogenesis

1. Airway reactivity (Nonspecific hyperirritability of the tracheo-bronchial tree).

2. Genetic mechanism (screening families has identified multiple chromosomal regions that relate to atopy, elevated IgE and airway hyperresponsiveness).

Stimuli that interact with airway responsiveness and incite acute episodes of BA.

Allergens Pharmacological stimuli Environmental and air pollution Occupational factors Infections Exercise Emotional stress

Allergens: 1. immediate response in minutes.

2. late reaction after 6-10 h (30-50% patients).

Allergic asthma is dependent on an Ig E response controlled by T and B lymphocytes and activated by the interaction of antigen with mast cell bound Ig E molecules Frequently seasonal; nonseasonal forms: allergy to feathers, animal danders, dust mites, environment antigens Most often in children and young adults

Pharmacological stimuli

Aspirin Tartrazine Beta-adrenergic antagonists Sulfiting agents [potassium and sodium bisulfate widely used in the food (salads, fresh fruit, potatoes, shellfish, wine) and pharmaceutical industry] Aspirin-sensitive respiratory syndrome primarily affects adults, associated with vasomotor rhinitis (hyperplastic rhinosinusitis with nasal polyps)

Environment & air pollution

Climatic conditions Heavy industrial urban areas

Atmospheric pollutants:

Ozone Nitrogen dioxide Sulfur dioxide (in high concentration)

Occupational factors

Metal salts (platinum, chrome, nickel) Wood and vegetable dusts (oak, western red cedar, grain, flour) Pharmaceutical agents (antibiotics, piperazine, cimetidine) Industrial chemicals and plastics Biological enzymes (laundry detergents, pancreatic enzymes) Animal and insect dusts, serums and secretions

Infections
Respiratory infections the most common stimuli

The respiratory viruses (not bacteria or allergy!) the most etiologic factors. Syncytial virus and parainfluenza [in young children] Rhinovirus and influenza [in older children and adults]

Exercise
Initiation of bronchospasm by exercise is operative to some extent in every asthmatic patient, and in some it may be the only trigger mechanism that will produce symptoms

Activities such as ice hockey, cross country skiing, or ice skating are more provocative than is swimming in an indoor heated pool

Emotional stress
Psychological factors can interact with BA to worsen the disease (vagal efferent activity, endorphins)

Pathophysiology
Reduction in air way diameter by contraction of smooth muscle, vascular congestion, edema of the bronchial wall, thick tenacious secretion

Increased air way resistance, decreased forced expiratory volume and flow rates, hyperinflation, increased work of breathing, alterations in respiratory muscle function, changes in elastic recoil, altered arterial blood gases

Pathogenesis of bronchial asthma

eosinophile
allergens
Affection of the epithelium mucosal edema

mast cells degranulation

Endogenic factors

Inflammatory and allergic mediators

Hypercrinia and dyscrinia bronchospasm Excitation of the nerve endings

b r o n c h o o b s t r u c t i o n

B R O N C H I A L

A S T H M A

Morphological examination
1. Overdistention of the lungs.

2. Gelatinous plugs of exudate in the bronchial branches down to the terminal bronchioles.

Morphologic examination
1.
2.

3.

4.

5. 6.

Infiltration with eosinophils Thickening of the basement membrane Hypertrophy of the airway smooth muscle Desquamation of the epithelium Mucosal edema Mucus plugs containing shed epithelial cells and cellular components of the inflammatory reaction

Symptoms
1.

2.
3.

4.

Severe expiratory dyspnea. Attacks of dyspnea arise suddenly, gradually increase in strength and lost from a few minutes to several hours and even days (status asthmaticus). Sense of the compression in the chest. At the beginning - nonproductive cough. At the peak poorly expectorated thick and tenacious sputum. Inability to speak.

Objective examination
1.

2. 3. 4.

Forced (tripod) posture: sitting with the upper part of the body slightly inclined forward, leaning against the edge of the chair back or laps. Cyanosis. Cold perspiration The mouth is open, the nostrils participate in breathing.

Examination of the respiratory system. Form of the chest

pigeon chest in asthmatic children

Barrel shaped chest

1.

2.
3.

4.
5.

Chest is held in phase of maximal inspiration. Added muscles are involved. Intercostal spaces and supraclavicular fosses depressed in inspiration. Anteroposterior diameter of the chest increased. Paradoxical abdominal and diaphragmatic movement on inspiration indicates diaphragmatic fatigue

Examination of the respiratory system.

Normal expiration.

Expiration is prolonged (edema of the mucus, bronchospasm, accumulation of the sputum). Distant wheezes.

Examination of the respiratory system.

Palpation: Increased rigidity of the chest.

Decreased vocal fremitus.

Examination of the respiratory system.

Percussion: 1. bandbox sound. 2. low borders of the lungs displaced downward. 3. mobility is decreased.

Examination of the respiratory system. Auscultation.

Hash breathing with prolonged expiration. Wheezes (distant).

Examination of the cardiovascular system.

Jugular veins are overfilled.

Examination of the cardiovascular system.

Tachycardia. Pulsus paradoxus (decreased amplitude on inspiration). Systolic pressure decreases by more than 10 mm Hg during inspiration

Examination of the cardiovascular system.

Palpation: Cardiac beat. Percussion: Borders of the absolute dullness of the heart cant be determined because of the acute hyperinflation of the lungs. Auscultation: Decreased heart sounds. Presystolic gallop accentuated during inspiration.

The end of an episode of BA is frequently marked by a cough that produces thick, stringy mucus, which often takes the form of casts of the distal airways (Curshmanns spirals).
Patients with uncomplicated BA have no symptoms during periods clear of attacks.

The diagnosis of BA is established by demonstrating reversible airway obstruction.

Laboratory investigation.

Blood test: eosinophilia. Immunologic test: IgE. T Suppressors

Laboratory investigation.
Sputum: Increased eosinophils.

Crystals of Charkot Leyden. Curshmann's spirals.

Instrumental investigation
Spirometry: FVC. FEV1. (reversibility: 15% or more increase in FEV1 after 2 puffs of B adrenergic agonists; provocation tests with histamine, methacholine, isocapnic hyperventilation of cold air) Peak flow metry: PEF (daily variation).

Making a diagnosis of asthma

>15% improvement in FEV1 or PEF following administration of a bronchodilator > 15% spontaneous change in PEF during 1week of home monitoring.

X-ray of the chest

Diaphragm is low and flattened. Bronchovascular shadow do not extend to the periphery of the lungs. Cardiac silchouette is lengthened and narrowed. Overinflation.

ECG (COR - pulmonale).

increased P wave in III and AVF leads (P-pulmonale) increased R wave in V1-2 Increased S wave in V5-6 Right limb block of His bundle.

Degrees of asthma severity

Mild intermitted Symptom <1 per week Mild persistance 1 per week or more, but not every day. >2 per month. Moderate persistance Every day. Severe persistance Constant

Night <2 per month. symptoms

Acute periods

Short (few hours few days ).

Decreased physical activity and deranged sleep.

Decreased Decreased physical activity physical activity and deranged sleep.

PEF 60- 80% PEF <60% of of normal. normal. Variation>30% Variation>30%

Between acute PEF > 80% of periods normal normal. functional tests Variation 20-30% PEF > 80% of normal. Variation<20%

Treatment

1st step. Inhalation of the short-acting B2 adrenergic agents. 2nd step. Inhalation of corticosteroids(every day). 3rd step. Inhalation of corticosteroids(every day) and inhalation of the long-acting B2 adrenergic agents. 4th step. Inhalation of corticosteroids(every day) and inhalation of the long-acting B2 adrenergic agents + long-acting theophylline.

Status asthmaticus.

Prolonged acute attack of BA, characterized by progressive or severe respiratory insufficiency, due to airways obstruction and resistance to the therapy.

Status asthmaticus.

I stage (relative compensation). Severe cough.

Orthopnea. Tachypnea. Inability to speak in sentences. Added muscles are involved. Distant wheezes. Cyanosis. Bandbox sound. Ausc.: no sound over the low lobes, hash breathing over the upper parts. Tachycardia(120/min.). Nerve excitation, hallucinations. BT: polycythemia. Arterial hypoxemia: PaO2 60-70 mm Hg (N-95 -100 mm Hg). Normocapnia PaCO2 35-45 mm Hg.

Status asthmaticus.

dyspnea. Inability to speak. Superficial respiration. Orthopnea. Tachypnea. Pale-grayish skin. Bandbox sound. Ausc.: no sound over the hole lobes, small amount of rales over the small part of the lungs. Tachycardia (140/min). Pulsus paradoxus. Hypotension. Mental status changes (confusion). BT: polycythemia. Arterial hypoxemia: PaO2 50-60 mm. Hg. Hypercapnia PaCO2 50-70mmHg. Respiratory acidosis. PEF<50% of expected

II stage (decompensation, silent lung). Severe

Status asthmaticus.

III stage (hypercapnia coma).

Patient is unconscious. Diffuse cyanosis. Superficial respiration. Chain- Stock's breathing. Ausc.: no sound over the hole lobes (silent chest). Tachycardia(140/min.). Pulsus filliformis. Arrhythmia. Hypotension. Gallop rhythm. BT: polycythemia. Arterial hypoxemia: PaO2 40-55 mm. Hg. Hypercapnia PaCO2 80-90mmHg. Metabolic acidosis.

PEF unrecordable.

Pulmonary Hypertension
Increased pulmonary artery pressure: Systolic >30 mm Hg, Diastolic > 15 mm Hg (WHO) [normal syst. 23-26 mm Hg, diast. 7-9 mm Hg]

Primary (an uncommon disease characterized by increased pulmonary artery pressure and pulmonary vascular resistance without an obvious cause) Secondary

Etiology

1.
2. 3. 4.

Acute hypertension: Pulmonary thromboembolism Acute left cardiac failure Status asthmaticus Respiratory distress syndrome

Etiology
Chronic pulmonary hypertension: Increased pulmonary circulation (defect of the interventricular and interatrial septum) Increased pressure in the left atrium (mitral valve diseases, chronic left cardiac failure) Increased pulmonary vascular resistance (COPD, hypoventilatory syndrome, recurrent pulmonary thromboembolism, systemic vasculitis, diffuse diseases of connective tissue).

1.
2. 3.

Symptoms

Dyspnea (gradual onset progressing to minimal activity dyspnea) Weakness Pain in the heart region (right ventricular ischemia) Syncope Peripheral edema Hemoptysis

Objective examination
Cyanosis Clubbing symptom (in purulent bronchial disorders, congenital heart diseases) Increased JVP. Sign of Plesh. Reduced carotid pulse Palpation: cardiac beat Percussion: hypertrophy of the right heart. Heart auscultation: accentuation of the S2 over the pulmonary trunk, right-sided S3 and S4. Systolic murmur over the tricuspid valve, pulmonary valve (Graham Steels murmur).

Investigation

X-ray: enlarged central pulmonary arteries and clear lung fields. ECG: right axis deviation and right ventricular and atrial hypertrophy. Echocardiography: right ventricular enlargement, a reduction in left ventricular cavity size. Doppler studies: signs of severe pulmonary hypertension