Chronic Bronchitis

Grade the obstruction - Spirometry before and after a bronchodilator: FEV1/FVC below 0.7 confirms COPD, and the FEV1 sets the GOLD severity class. Pair it with resting pulse oximetry or an arterial blood gas so you know their baseline oxygenation and CO2 before you choose a ventilation strategy.

Is this an exacerbation? - Fever is uncommon in stable chronic bronchitis, and when present suggests influenza or pneumonia. Chest x-ray, CBC with differential, sputum culture, and a serum procalcitonin separate bacterial infection from a harmless color change in the sputum - leukocyte peroxidase alone will turn sputum green. That is the data behind proceed versus delay.

Secretions - Mucus hypersecretion with poor ciliary clearance plugs small airways, and it will plug a tube. Humidify, suction before extubation, and think about case length before committing to a small-bore airway.

Reactive airway - The hyperactive airway wheezes and bronchospasms intermittently. Short-acting beta-2 agonist, short-acting anticholinergic, or both before induction; get depth before instrumenting; treat new intraoperative wheeze as bronchospasm until proven otherwise.

Air trapping - Airway collapse on exhalation is the defining intraoperative problem. Give a long expiratory time, keep the rate down, and disconnect to check for breath stacking whenever the blood pressure sags after a ventilator change.

Right heart - COPD is the most common cause of cor pulmonale, and its severity tracks the magnitude of hypoxemia, hypercapnia, and airflow obstruction. Pulmonary hypertension here is usually modest, mean PA pressure 40 mmHg or less, but hypoxic vasoconstriction makes it worse - oxygen is the first pulmonary vasodilator you have.

Screen for the overlap - The chronic bronchitis phenotype runs with a higher BMI and a higher rate of obstructive sleep apnea than the emphysema phenotype. Ask about witnessed apneas and CPAP use; overlap syndrome carries worse nocturnal desaturation and worse outcomes than either condition alone.

Smoking cessation is the intervention that works - It improves mucociliary function and reduces goblet cell hyperplasia. Every preoperative visit is a chance to make the ask.

Regional where it fits - Anything that keeps you off an airway this reactive and this wet is worth considering.

Chronic bronchitis is the mucus phenotype of chronic obstructive pulmonary disease (COPD): a productive cough on most days for at least 3 months in each of 2 consecutive years. Cigarette smoke and other inhaled irritants drive goblet cell hyperplasia and submucosal gland hypertrophy - the Reid index, normally about 0.4, rises - while the epithelium releases interleukin-8 and other pro-inflammatory mediators.

Mucociliary clearance falls as mucus output climbs, so small airways clog with secretions and debris. What that buys us is expiratory airflow limitation with air trapping: the airway collapses on exhalation, the lung hyperinflates, and CO2 is not fully cleared. Chronic hypoxic vasoconstriction then remodels small pulmonary arteries and raises pulmonary vascular resistance, which is why COPD is the most common cause of cor pulmonale.