Mnemonic

Smoking and Respiratory Physiology

A memory aid for the physiological effects of cigarette smoking.

Expansion

Impaired clearance, carboxyhaemoglobin, protease imbalance and accelerated decline in FEV1

Expansion

Immediate

  • Carboxyhaemoglobin of 5 to 10 per cent, reducing oxygen carriage and shifting the curve left
  • Nicotine-induced tachycardia, hypertension and vasoconstriction
  • Bronchoconstriction and increased airway resistance

Short term

  • Cilia are slowed and destroyed, so mucociliary clearance fails
  • Goblet cell hyperplasia with mucus hypersecretion

Long term

  • Protease-antiprotease imbalance: smoke recruits neutrophils and macrophages releasing elastase, and oxidises alpha-1 antitrypsin so that it cannot inhibit it. The result is emphysema
  • Accelerated FEV1 decline, from about 30 ml per year to 60 to 90 ml per year in susceptible smokers
  • Small airway fibrosis, and loss of the alveolar capillary bed

Reversibility is an important point for counselling. Carbon monoxide clears within a day and cilia recover over months. The rate of FEV1 decline returns towards normal after stopping, so lung function already lost is not regained but further loss is slowed, and stopping is beneficial at any age.