Respiratory System

Diagnosis and reasoning

This young man has presented with wheezing and dyspnea of acute onset; given the history of bronchial asthma, this is most likely an acute exacerbation.

The examination provides further supportive evidence, by demonstrating diffuse inspiratory and expiratory wheezes, and most importantly, prolongation of expiratory phase.

Note also the history suggestive of a preceding respiratory tract infection - this might very well have been the trigger for this episode.

It should be kept in mind that certain other respiratory conditions (such as pneumonia) and cardiac conditions (such as acute left ventricular failure) may also present with similar symptoms - these should not be written off merely due to the history of asthma.

However, note that there are no other associated clinical features which would hint towards an alternative diagnosis.

The next step in his evaluation should be to clinically quantify the severity of the exacerbation; here, the inability to complete a sentence in one bre

ath, respiratory rate of > 25 cycles/min and pulse > 110 bpm is suggestive of an acute severe exacerbation.

His investigations should be directed at confirming the clinical diagnosis, assessing the degree of respiratory compromise and airflow limitation, and excluding complications.

Note that pneumonia is both the most common complication of asthma, as well as a potential mimicker of the condition. Thus a full blood count and chest x-ray are justifiable in these patients - but turn out to be normal here.

An arterial blood gas assay (ABG) will allow estimation of the degree of respiratory compromise. The findings in this patient are suggestive of hypoxia and respiratory alkalosis (probably due to hyperventilation), i.e. type 1 respiratory failure.

Lung function tests are important in objectively assessing the airflow limitation, and establishing a baseline. This patient's peak expiratory flow rate is between 33% to 50% of the predicted value for his age, gender and height, providing another indicator that this is acute severe asthma.

Inhaled short-acting beta-2 agonists (such as salbutamol) are indicated here, as this may result in quick relief of the bronchospasm; addition of ipratropium bromide should also be considered. Corticosteroids should also be commenced in parallel.

If he fails to respond to these drugs, IV or inhaled magnesium sulfate should be administered.

Note that although methylxanthines (such as theophylline) were once the primary treatment for acute asthma, they are considerably less effective than the sympathomimetics, with potentially significant side effects. Most current data indicate little benefit in acute situations, and thus they are not generally recommended.

Antibiotics are also probably not indicated here, given the absence of clinical, biochemical or radiological features suggestive of an infection.


An asthma exacerbation is defined as an acute or subacute episode of progressively worsening dyspnea, cough, wheezing, chest tightness, or some combination of these symptoms, along with decreases in expiratory airflow and objective measures of lung function (spirometry and peak flow).

In the USA alone, these account for 15 million outpatient visits, 2 million emergency room visits, and 500,000 hospitalizations each year.

Important precipitants of acute asthma exacerbations include viruses, allergens (such dust mites, pollen, and animal dander), occupational exposures (grains, flours, cleaning agents, certain metals, irritants), hormones (i.e. menstrual asthma), drugs (NSAIDs, beta-blockers), exercise, stress, and air pollutants.

Note that overall, rhinoviruses are the most common precipitant in both children and adults.

The key symptoms of an acute exacerbation include dyspnea, cough, and wheezing; important physical signs include tachypnea, tachycardia, wheeze, hyperinflation, accessory muscle use, pulsus paradoxus, diaphoresis, cyanosis, and obtundation.

Asthma exacerbations can be classified as "brittle", moderate, severe, or life threatening; this is key to the management. The classification is based upon the clinical findings, lung functions and oxygen saturation.

- Brittle exacerbation: these are classified as either type 1 or type 2.

Type 1: >40% variability of PEFR over 50% of time within a period >150 days

Type 2: sudden attack in a patient with apparently well controlled asthma

- Moderate exacerbation: worsening symptoms; PEFR between 50% to 75% of best or predicted; no features of acute severe asthma.

- Acute severe exacerbation: inability to complete sentences in one breath, respiratory rate ≥ 25 cycles/min, heart rate ≥110/min, PEFR between 33% of 50% best or predicted.

- Life threatening exacerbation: silent chest; cyanosis; poor respiratory effort; arrhythmia; exhaustion; altered mentation; PEFR < 33% best or predicted; SpO2 <92%; PO2 < 60 mmHg; normal PCO2 (35 - 45 mmHg).

- Near fatal: elevated PCO2 (which may or may not require mechanical ventilation with raised inflation pressures).

Note that arterial blood gases (ABG) should be measured in asthmatic patients requiring admission to hospital - especially if the SpO2 is < 92% or other features of life threatening asthma are present.

A chest x-ray should be performed if there is a suspected pneumomediastinum or pneumothorax, suspected consolidation, life threatening asthma, failure to respond to treatment satisfactorily and requirement for ventilation.

The key principle in managing an acute asthma exacerbation are to stabilize the patient as rapidly as possible, to ensure adequate oxygenation, and to reverse bronchial narrowing with a minimum of side effects.

Urgent oxygen supplementation via face mask, venturi mask, or nasal cannula is indicated for a patient with acute severe asthma, in order to prevent hypoxemia.

Nebulized beta-2 agonists such as salbutamol or terbutaline have a rapid onset of action and provide more bronchodilation than methylxanthines and anticholinergics. They should be administered with oxygen as the driving gas.

Nebulized anticholinergics (ipratropium bromide) are the next line of therapy, particularly in patients resistant to beta-2 agonists.

If no improvement occurs with nebulized therapy, IV beta agonists and/or magnesium sulfate should be used.

Note that IV methylxanthines are not used in the treatment of acute asthma anymore as they produce significant side effects and trials show no benefit.

Corticosteroids are used in all cases of acute asthma. IV hydrocortisone is used initially, followed by oral prednisolone.

If the patient’s condition deteriorates despite the above measures, ventilation should be considered.

In patients with hypercapnic respiratory failure who can cooperate and are able to protect their airways, non invasive ventilation can be administered.

Indications for invasive ventilation include progressive CO2 retention, obtundation, and impending cardiopulmonary collapse.

Important (but rare) complications include Pneumothorax (potentially associated with pneumomediastinum), subcutaneous emphysema, pneumopericardium and tracheoesophageal fistulas (in the mechanically ventilated patient).

Other potential complications include theophylline toxicity, lactic acidosis, electrolyte disturbances (hypokalemia, hypophosphatemia, hypomagnesemia), myopathy and ultimately anoxic brain injury.

Severe asthma carries a significant mortality ranging between 1% to 10%. However early diagnosis, aggressive medical treatment, and improvements in mechanical ventilation can greatly improve the prognosis.


Take home messages

1. The key symptoms of an acute asthmatic exacerbation include dyspnea, cough, and wheezing.

2. ABGs are indicated in all asthmatic patients requiring admission to hospital - particularly if features of life-threatening asthma are present.

3. IV methylxanthines are not used in the treatment of acute asthma anymore.


  1. Thorax. 2008 May;63 Suppl 4:iv1-121. doi: 10.1136/thx.2008.097741. British Guideline on the Management of Asthma; revised in January 2012
  2. American Journal of Respiratory and Critical Care Medicine, Vol. 168, No. 7 (2003), pp. 740-759, doi: 10.1164/rccm.200208-902SO, Acute Severe Asthma, E. R. McFadden,Jr.
  3. Clin Exp Allergy. 2009 Feb;39(2):193-202. doi: 10.1111/j.1365-2222.2008.03157.x, Acute exacerbations of asthma: epidemiology, biology and the exacerbation-prone phenotype, Dougherty RH, Fahy JV.