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Asthma. SS Visser, Lung Unit, UP. Contents. Definition Disease Pattern Prevalence Mortality Etiology Pathogenesis Triggers of acute attacks. Contents. Pathophysiology Manifestations of Resp failure Diagnosis: clinical,physiologic,immunologic and radiologic Differential diagnosis

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SS Visser, Lung Unit, UP


  • Definition

  • Disease Pattern

  • Prevalence

  • Mortality

  • Etiology

  • Pathogenesis

  • Triggers of acute attacks


  • Pathophysiology

  • Manifestations of Resp failure

  • Diagnosis: clinical,physiologic,immunologic and radiologic

  • Differential diagnosis

  • Management


  • Chronic inflammatory disease of airways (AW)

  •  responsiveness of tracheobronchial tree

  • Physiologic manifestation: AW narrowing relieved spontaneously or with BD  Cster

  • Clinical manifestations: a triad of paroxysms of cough, dyspnea and wheezing.

Disease pattern
Disease Pattern

  • Episodic --- acute exacerbations interspersed with symptom-free periods

  • Chronic --- daily AW obstruction which may be mild, moderate or severe  superimposed acute exacerbations

  • Life-threatening--- slow-onset or fast-onset (fatal within 2 hours)


  • All ages, predominantly early life

  • Adults: 2-5% population

  • Children: 15% population

  • 50% dx <10y,85% dx <40y, 15% dx > 40y

  • 2:1 male/female preponderance in childhood


  • Fatal asthma 1-7% asthmatics

  • ing death rate ?abuse of inhaled BDs

  • Risks for death:previous life-threatening asthma, severe disease, recent hospitalization or emergency room Rx, non-compliant and confusion re Rx, under- treatment with Corticosteroids, discontinued Rx, severe AW hyperreactivity.


  • Allergic/atopic/early onset asthma---rhinitis, urticaria,eczema,(+)skin tests,IgE,(+) response to provocation tests with aeroallergens.

  • Idiosyncratic/non-atopic/late onset asthma--- no allergic diseases,(-)skin tests,normal IgE, symptoms when upper resp infection, sx lasting days or months.

  • Mixed group---usually onset later in life

Pathogenesis 1
Pathogenesis - 1

  • Non-specific AW hyperreactivity:

    Sx more severe & persistent

    Nocturnal  early awakening with dyspnea

    diurnal fluctuation in lung function

    Unstable lung function

     BD response,  therapeutic needs

  • Cause of hyperreactivity = inflammation

Pathogenesis 2
Pathogenesis - 2

  • Dual AW response to AG challenge

    1.Early bronchospastic response- type1reaction

    within min after IH of AG:

    Mechanism: IH of aeroallergensensitizatiom formation of IgE & expression on mast cells re-exposure to AG mast cell degranulation & mediator release bronchospasm

Pathogenesis 3
Pathogenesis - 3

2.Late-bronchospastic reaction: in 30-50%, 6-10 hours after AG exposure. Minority only a late response

Mechanism: recruitment of E, N, L and macro-phagesrelease lipid mediators(PG E2, F2 ,D2; LT C,D,E , PAF), O2radicals, toxic granule proteins, cytokines (TH1:IL-2, IFN; TH2: IL-4, IL-5) bronchoconstriction, vascular congestion, mucosal edema, mucus production, mucociliary transport.

Pathogenesis 4
Pathogenesis - 4

  • Chronic asthmatic response:

    Destruction of AW epithelium by toxic granule contentsepithelial shedding into bronchial lumen exposure of sensory nerve endings and imbalance in cholinergic and peptidergic neuronal control AW remodelling with subendothelial fibrosis, goblet cell hyperplasia, smooth muscle hyper- trophy, vascular changes fixed AW obstruction.

Triggers of acute asthmatic episodes

Allergens - pollen

Pharmacol stimuli such as aspirin, NSAIDS, - adrenergic blockers, preservatives,col agent

Environment pollution- ozone, SO2, NO2

Occupational- metal salts, biol enzymes

Infection- resp viruses

Exercise –IH cold dry airthermally-induced hyperemia and micro-vascular engorgement

Emotional stress

Triggers of acute asthmatic episodes


  • Reduction in AW diameterAW resistance  FeV and flow rates hyperinflation work of breathing altered respiratory muscle Fx and elastic recoil abnormal ventilation

  • Vascular congestion and edema of bronchial walls abnormal perfusion

  • V/P mismatch altered blood gases hypoxemia and hypocapnia with respiratory alkalosis, but with impending ventilatory failure  normocapnia and later hypercapnia and respiratory acidosis

Manifestations of respiratory failure
Manifestations of respiratory failure

  • Hypoxemia: cyanosis- very late sign, not


  • Hypercapnia: sweating, tachycardia,widened pulse pressure

  • Acidosis: tachypnea

  • Blood gases the only accurate assessment of ventilatory status

Diagnosis clinical

  • Episodic asthma: Paroxysms of wheeze, dyspnoea and cough, asymptomatic between attacks.

  • Acute severe asthma: Upright position, use accessory resp muscles, can’t complete sentences in one breath, tachypnea > 25/min, tachycardia > 110/min, PEF < 50% of pred or best, pulsus paradoxus, chest hyperresonant, prolonged expiration, breath sounds decreased, inspiratory and expiratory rhonchi, cough.

Diagnosis clinical1

  • Life-threatening features: PEF < 33% of pred or best, silent chest, cyanosis, bradycardia, hypotension, feeble respiratory effort, exhaustion, confusion, coma, PaO2 < 60, PCO2 normal or increased, acidosis (low pH or high [H+]).

  • Chronic asthma: Dyspnea on exertion, wheeze, chest tightness and cough on daily basis, usually at night and early morning; intercurrent acute severe asthma (exacerbations) and productive cough (mucoid sputum), recurrent respir-atory infection, expiratory rhonchi throughout and accentuated on forced expiration.

Diagnosis physiologic

  • Demonstration of variable airflow obstruction with reversibility by means of FEV1 and PEF measurement (spirometer and peak flow meter).

  • FEV1 < 80% of pred – PEF < 80% of pred.

  • Reversibility: A good bronchodilator response is a 12% and 200ml improvement in FEV1 20 min after inhalation of 200ug salbutamol (2 puffs).

  • Diurnal peak flow variation: Normal variation: Morning PEF 15% lower than evening PEF. With asthma this variation is > 15% (morning dipping).

Diagnosis physiologic1

  • Provocation studies:

    (a) Exercise: A 15% drop in FEV1 post exercise indicates exercise induced asthma.

    (b) Metacholine challenge: A 20% reduction in FEV1 at Metacholine concentrations < 8mg/ml indicates bronchial hyperreactivity.

    This is expressed as a PC20 value of eg 0.5mg/ml (= a 20% reduction in FEV1 at 0.5mg/ml Metacholine).

Diagnosis immunologic

  • Skin prick wheal and flare response.

  • IgE and RAST.

  • Eosinophil cationic protein (ECP).

  • Peripheral blood and sputum eosinophilia.

Diagnosis radiology

  • Chest XR may be normal between attacks.

  • With attacks hyperinflation may be found.

  • In complicated asthma segmental lobar collapse (mucous plugs) and pneumothorax can occur.

Differential diagnosis

  • Upper airway obstruction – glottic dysfunction.

  • Acute LV failure – pulmonary oedema.

  • Pulmonary embolism.

  • Endobronchial disease.

  • Chronic bronchitis.

  • Eosinophilic pneumonia.

  • Carsinoid syndrome.

  • Vasculitis.

Management 1

  • Avoidance of allergen and triggers – may be impractical  adjust Rx.

  • Occasional asthma: Rarely symptomatic  2 agonist prn.

  • Mild intermittent asthma (episodic): 2 agonist prn + low dose IH corticosteroid.

  • Mild persistent asthma: 2 agonist prn + high dose IH corticosteroid or long acting 2 agonist + low dose IH corticosteroid.

  • Moderate persistent asthma: 2 agonist prn + high dose IH corticosteroid + long acting 2 agonist or SR theophylline.

Management 2

  • Severe, persistent asthma 2 agonist prn + high dose IH corticosteroid + long acting 2 agonist + SR Theophylline + oral corticosteroids.

  • Step up: If uncontrolled at any severity level, oral steroids – Prednisone 30-40-mg/day for 7-14 days.

  • Step down: When stable for at least 3 months – reduce or stop oral steroids first.

  • Leukotriene antagonists: for patients with aspirin/NSAIDS induced asthma. May also be added on for severe persistent asthma or in pts with steroid related side effects such as growth retardation or non-responsiveness to IHS or to allow low dose IHS instead of high dose.

Management 3

  • Acute severe asthma:

    1. Immediate Rx: O2 40-60% via mask or cannula + 2 agonist (salbutamol 5mg) via nebulizer + Prednisone tab 30-60mg and/or hydrocortisone 200mg IV. With life-threatening features add 0.5mg ipratropium to nebulized 2 agonist + Aminophyllin 250mg IV over 20 min orsalbutamol 250ug over 10 min.

    2. Subsequent Rx: Nebulized 2 agonist 6 hourly + Prednisone 30-60mg daily or hydrocortisone 200mg 6 hourly IV + 40-60% O2.

Management 4

  • No improvement after 15-30 min: Nebulized 2 agonist every 15-30 min + Ipratropium.

  • Still no improvement: Aminophyllin infusion 750mg/24H (small pt), 1 500mg/24H (large pt), oralternatively salbutamol infusion.

  • Monitor Rx: Aminophyllin blood levels + PEF after 15-30 min + oxymetry (maintain SaO2 > 90) + repeat blood gases after 2 hrs if initial PaO2 < 60, PaCO2 normal or raised and patient deteriorates.

  • Deterioration: ICU, intubate, ventilate + muscle relaxant.