GINA (Global Initiatives for Asthma)

DefinitionNHLBI defines asthma as a chronic inflammatory disease manifested by recurrent episodes of wheezing, breathlessness, chest tightness and coughing. It also identifies 3 key features essential to the diagnosis and understanding the pathophysiology and treatment :• Variable airflow obstruction that is often reversible (spontaneously or with treatment)• Airway inflammation• Increased bronchial (or airway) responsiveness to a variety of stimuli

Airflow obstruction

This part of the definition refers to asthma's classification as an "obstructive" lung disease and is caused by a number of changes in the airways, all of which result in a narrowing of the airway lumen, a slowing of air flow, and an increased resistance to air flow.

Airflow obstruction is best demonstrated by characteristic changes in pulmonary function: 1. Spirometry in asthma demonstrates

a. FEV1/FVC (see Figure 3)b. FEV1 (see Figure 3)c. PEFR (see Figure  4)d. expiratory time

2. Peak expiratory flow rates ("peak flow" or PEFR) can be measured from spirometric maneuvers or with peak flow meters. As with spirometry, the normal value is related to age, height, and gender. (Typical 70 kg 24 y/o man, expected PEF 500 l/min and for a 55kg 24 y/o woman, 400 l/min.)

3. Additional characteristics of obstruction :a. Hyperinflation of the lungs due to air

trappingb. RV (residual volume)

c. FRC (functional residual capacity) d. TLC (total lung capacity)

e. Compliance change: left shift due to changes in elastic recoil

f. Unequal distribution of regional ventilation and perfusion resulting in

hypoxemia.

4. A single measurement of FEV1 or PEFR can be used to assess severity. Serial measurements can be used to monitor the response to therapy, either acutely during an exacerbation or chronically as an outpatient.

Reversible airflow obstructionThis refers to the fact that the airflow obstruction demonstrated above is either partially or completely reversible in someone with asthma, in contrast to someone with chronic obstructive pulmonary disease (COPD). This may occur spontaneously over hours to days and may be accelerated by the administration of a bronchodilating agent (effects begin in minutes). The most effective class of agents for asthma is the -2 adrenergic agonists. Other potential bronchodilators include the theophyllines and the anticholinergic drugs (ipratropium bromide). These last two options are associated with either more side effects or less bronchodilation.

PathogenesisAs you can see from reviewing the pathology of asthma, changes in smooth muscle, blood vessels, goblet cells and mucus glands as well as airway secretions all lead to a reduction in airway diameter in asthma. In between all of this is a whole complex world of inflammatory cells, mediators and cytokines which interact to initiate, sustain and modulate both the inflammatory response and airway hyperresponsiveness, leading to the clinical features of asthma. Our knowledge of these has expanded tremendously due to the explosion of research in this area, increasing both our understanding of the disease process and identifying potential therapeutic targets. In addition, neural mechanisms may contribute to, or modify the inflammatory events.

Patofisiologi Asma1. Mekanisme Imunologis Inflamasi Saluran Respiratori

Patofisiologi Asma2. Inflamasi Akut dan Kronik

Patofisiologi Asma3. Remodeling Saluran Respiratorik

Gambaran saluran nafas normal dan pada penderita asma

Gambar : A. Mukosa Normal, B. Mukosa Penderita Asma

A B

Differential Diagnosis

A. COPDB. Heart failureC. Pulmonary embolismD. Upper airway obstructionE. Foreign body aspirationF. Acute bronchiolitis (in kids)

Clinical Manifestations

A. Triggers vs. risk factors1. Triggers—those that sometimes cause

exacerbations of the disease or provoke airway narrowing :

a. Allergen exposure b. Exercise

c. Hyperventilation cold, dry air (osmotic stimuli)

d. Infections, especially virale. Sulfur dioxide (produced by metabisulfite

found in some food, beer and wines or air pollution

f. Air pollution—ozone, sulfur dioxide, nitrogen dioxide

g. Miscellaneous factors—weather, stress, irritant odors or fumes, gastroesophageal reflux

2. Risk factors—those that are associated with the cause of the diseasea. Genetics—although often positive family

history of asthma and/or allergy, twinstudies do not show strong geneticcomponent. May be more complicated i.e., some genetic factors predispose toallergy and additional ones predisposeallergic individuals to then develop asthma

b. Atopy and allergens

c. Respiratory infections?d. Passive smokinge. Occupational exposure

Symptoms

1. Chest tightness, cough, wheezing, dyspnea2. Patient may experience any, all or none

(between attacks) of these3. May or may not be able to identify cause or

trigger4. Onset may be slow or rapid 5. Frequency of recurrence variable: from years

to nearly continuous

Signs

1. None (between attacks)2. Tachypnea3. Wheezing4. Prolonged expiratory phase5. Cough6. Accessory muscle use

7. Severe attacka. Respiratory rate > 30b. Pulse rate > 120c. Pulsus paradoxus > 15 mmHg (normal <10)d. PEFR < 100 l/mine. Mental status changes

(confusion, agitation, lethargy)f. ABG abnormalities (see below)

Laboratory evaluation

1. Routine biochemistry and hematology values normal with exception of mild eosinophilia in 30-50% patients

2. Chest x- ray findings: (can be normal also) hyperinflation, peribronchial cuffing, atelectasis from mucus plugging. In most cases, the x-ray is most helpful for ruling out other pulmonary diseases or complications such as pneumonia, pneumothorax, or heart failure.

3. ABG’s typically mildly low PaO2 and PCO2. Why?

a. Abnormal distribution of both pulmonary blood flow and ventilation seen due to unequal airflow obstruction and mucus plugging results in abnormal V/Q relationships and arterial hypoxemia.

b. Reduced PCO2 less well understood, but chemoreceptors and carotid bodies seem to play a role in the hyperventilation seen.

c. Severe airflow obstruction and possibly impending respiratory failure suggested by more significant decreases in PaO2, normal or increasing levels of PCO2 (i.e. respiratory acidosis), and the presence of a lactic acidosis

4. Respiratory function: reduced FEV1, FEV1/FVC or PEFR

a. Objective assessment important since signs and symptoms of an asthma exacerbation (whether assessed by patient or doctor) are not very good guides to severity until the attack is severe.

Gangguan kesadaran Cyanosis Distress respiratory berat Periode akut setelah satu periode pendek (2-5 hari) Peningkatan kebutuhan bronchodilator dengan minimal penyembuhan

Gejala Klinis Status Asmatikus yang mengancam jiwa

Pulsus pradoksus > 15-18 mmHg Kontraksi m. sternokleidomastoideus, retraksi interkostal Wheezing pada inspirasi Takipnea >30 kali/menit Takikardi > 120 kali/menit PEFR <100-120 L permenit atau <25-40% PVC < 1-1,5 / < 25-40% PEV1 < 1 L / < 25-40% Pa O2 < 60mmHg Pa CO2 >40-45 mmHg Abnormalitas EKG, hipotensi Adanya pneumothorak, pneumomediastinum, pneumonia.

Asma menurut consensus internasional Clin Exper Allergi 1992 dan GINA adalah kelainan radang yang kronis pada saluran nafas dimana banyak sel memainkan peranan, termasuk sel mast, eosinofil dan limfosit. Pada individu yang rentan, radang ini menyebabkan episode mengi/wheezing berulang, sesak nafas, rasa dada tertekan dan batuk, khususnya pada malam hari dan dini hari. Gejala biasanya berhubungan dengan penyempitan jalan nafas yang luas namun bervariasi. Penyempitan ini bersifat reversibel dan derajat penyempitannya bisa berubah-ubah, baik secara spontan maupun karena pemberian obat-obatan.

DEFINISI

Status asmatikus adalah suatu serangan asma yang berat, berlangsung dalam beberapa jam sampai beberapa hari, yang tidak memberikan respon perbaikan pada pengobatan yang biasa digunakan seperti brankhodilator. Merupakan suatu penyumbatan aliran udara pernafasan yang berat sehingga dapat menyebabkan kematian.

DEFINISI

1. Infeksi (sering infeksi virus)2. Iklim (perubahan mendadak suhu, kelembaban dan tekanan

udara)3. Inhalan /eksposure allergen (debu, kapuk, tungau, bulu

binatang, serbuk sari, asap)4. Makanan (susu sapi, udang, ikan laut)5. Obat-obatan (Aspirin)6. Kegiatan fisik (olah raga berat, kecapaian, tertawa terbahak-

bahak)

Etiologi