Lab: Asthma Case Introduction

This laboratory session applies lung function test interpretation and arterial blood gas analysis to a clinical case of acute asthma, integrating the physiology of obstructive lung disease with practical diagnostics.

Asthma is characterised by reversible airflow obstruction, airway inflammation, and airway hyperresponsiveness. During an acute exacerbation, bronchoconstriction, mucous plugging, and mucosal oedema combine to narrow the airways and increase resistance to airflow. On spirometry this produces the classic obstructive pattern: FEV1 is reduced more than FVC, lowering the FEV1/FVC ratio below 0.70. Administration of a short-acting beta-2 agonist such as salbutamol causes bronchodilation; an improvement in FEV1 of more than 12% and more than 200 mL confirms reversible airflow obstruction consistent with asthma.

Peak expiratory flow rate (PEFR) is reduced during an acute asthma attack and is expressed as a percentage of the patient's predicted or best personal value. A PEFR of 50–75% of best indicates a moderate exacerbation; below 33% indicates life-threatening asthma.

Arterial blood gas analysis during an acute asthma attack reveals a characteristic progression. In mild to moderate asthma, the patient hyperventilates to compensate for hypoxaemia and in response to the effort of breathing, lowering PaCO2 and raising pH — a respiratory alkalosis. As the attack worsens and the patient tires, ventilatory effort falls, PaCO2 returns to normal. A normal PaCO2 in the context of a severe asthma attack is therefore a warning sign of impending respiratory failure, not reassurance. As fatigue progresses further, PaCO2 rises above normal (hypercapnia), indicating Type II respiratory failure and the need for immediate escalation of care.

ABG interpretation follows a systematic approach: first assess pH (acidosis or alkalosis), then PaCO2 (respiratory component), then HCO3⁻ (metabolic component), then assess whether compensation is appropriate. In respiratory alkalosis from hyperventilation, pH is elevated, PaCO2 is low, and HCO3⁻ may be slightly reduced as metabolic compensation. Mixed disturbances are common in severe illness.

Tachypnoea (rapid breathing rate) is both a symptom and a clinical sign of increased respiratory drive. In acute asthma, tachypnoea initially maintains alveolar ventilation despite airways obstruction. As the patient fatigues, breathing rate may paradoxically normalise or slow even as gas exchange deteriorates — a dangerous sign.