Dynamic Hyperinflation

Dynamic hyperinflation is a rise in end-expiratory lung volume above the resting relaxation volume, caused by expiratory flow limitation that prevents the lungs from emptying before the next breath. This article concerns the spontaneously breathing patient with obstructive lung disease. It is most important in chronic obstructive pulmonary disease and severe asthma.

Static hyperinflation (a raised resting volume) comes from loss of elastic recoil in emphysema and air trapping in small airways. Dynamic hyperinflation is superimposed on it whenever ventilatory demand rises, for example during exercise, fever, anxiety or an exacerbation. Faster breathing leaves less expiratory time, so volume climbs with every breath.

Consequences

• The inspiratory capacity falls, so tidal volume cannot rise when demand does.
• Flattened diaphragms shorten and lose force-generating ability.
• The inspiratory muscles must first overcome the elastic recoil of the trapped gas (a threshold load).
• Ventilation and neural drive become uncoupled, which produces disabling dyspnea.
• Venous return and cardiac output fall.

An inspiratory capacity to total lung capacity ratio under 0.25 predicts mortality independently of FEV1. Up to 70% of patients with moderate to severe disease hyperinflate during exercise, and this, rather than FEV1, explains much of their exertional breathlessness. Complications: exercise intolerance, respiratory muscle fatigue, hypercapnia, pneumothorax, reduced cardiac output and acute respiratory failure during exacerbations.

• Exertional breathlessness with a feeling of being unable to take a full breath
• Barrel chest, low-set flattened diaphragm with reduced chest expansion, hyper-resonant percussion, quiet heart sounds and reduced cardiac dullness
• Pursed-lip breathing, tripod posture and use of accessory muscles
• Hoover sign: inward movement of the lower rib cage during inspiration
• Prolonged expiration, wheeze and weight loss in advanced emphysema
• Red flags: hypotension, confusion, inability to speak in sentences, sudden pleuritic pain (pneumothorax), cyanosis and a rising pulse during an exacerbation

1. Post-bronchodilator spirometry: FEV1 to FVC ratio under 0.70 confirms airflow obstruction.
2. Full lung volumes by body plethysmography: residual volume over 140% predicted, residual volume to total lung capacity ratio over 40%, and total lung capacity over 120% predicted. Gas dilution methods under-measure trapped gas.
3. Inspiratory capacity at rest and during exercise: a fall of over 150 mL from rest to peak exercise indicates dynamic hyperinflation (measured on cardiopulmonary exercise testing or a shuttle walk with portable spirometry).
4. Chest radiograph: flattened diaphragms, increased retrosternal airspace and a long narrow heart. High-resolution CT shows emphysema distribution and fissure integrity.
5. Arterial blood gas during exacerbation, and diffusing capacity for carbon monoxide.
6. Alpha-1 antitrypsin level in patients under 45 years or with basal emphysema, and echocardiography to look for pulmonary hypertension or heart disease.

Differentials: heart failure, pulmonary hypertension, deconditioning, anemia, interstitial lung disease, obesity hypoventilation and anxiety.

1. Smoking cessation: varenicline 0.5 mg orally once daily for 3 days, then 0.5 mg twice daily for 4 days, then 1 mg twice daily for 12 weeks (reduce in renal impairment). Annual influenza vaccine and pneumococcal vaccination.
2. Long-acting bronchodilators (first-line, they lower hyperinflation within 1 to 2 hours and improve inspiratory capacity):
   • Tiotropium 18 micrograms capsule inhaled once daily by dry powder device, or 5 micrograms (2 actuations of 2.5 micrograms) once daily by soft mist inhaler. Adverse effects: dry mouth, urinary retention, glaucoma. Use with caution in bladder outlet obstruction.
   • Indacaterol 150 micrograms inhaled once daily (maximum 300 micrograms), or olodaterol 5 micrograms once daily.
   • Combined glycopyrronium and indacaterol 50/110 micrograms once daily when symptoms persist.
   • Add an inhaled corticosteroid (beclometasone, formoterol and glycopyrronium 2 actuations twice daily) for frequent exacerbations with blood eosinophils of at least 300 cells per microliter. The pneumonia risk rises.
3. Rescue: salbutamol 100 micrograms, 2 to 4 puffs by spacer, up to every 4 hours as needed.
4. Pulmonary rehabilitation for 6 to 8 weeks, at least twice a week, with interval and strength training and breathing retraining (pursed-lip breathing, paced breathing). Exertional oxygen when saturation falls under 88%, titrated to 90%.
5. Exacerbations: salbutamol 2.5 to 5 mg with ipratropium 500 micrograms nebulized every 4 to 6 hours, prednisolone 40 mg orally once daily for 5 days, amoxicillin-clavulanate 625 mg orally three times daily for 5 days (or doxycycline 200 mg on day 1 then 100 mg daily) if sputum is purulent, and controlled oxygen to a saturation of 88 to 92%.
6. Non-invasive ventilation for respiratory acidosis (pH under 7.35 with PaCO2 over 6.5 kPa): inspiratory pressure starting at 10 cmH2O and raised to 20 cmH2O, expiratory pressure 4 to 5 cmH2O.
7. Exacerbation prevention: azithromycin 250 mg orally once daily for a year in former smokers (check QTc, hearing and liver tests).
8. Lung volume reduction for severe emphysema with disabling dyspnea (FEV1 15 to 45% predicted, residual volume over 175% predicted):
   • Endobronchial one-way valves for heterogeneous emphysema with an intact interlobar fissure (over 90%). Pneumothorax occurs in about 20 to 30%, usually within 3 days.
   • Lung volume reduction surgery for upper lobe predominant emphysema with low exercise capacity.
   • Bullectomy for a giant bulla, and transplant assessment for suitable patients.

Follow-up at 6 to 12 weeks after treatment changes, then every 6 to 12 months with spirometry and inhaler technique review. Counsel on pacing activity and on early treatment of exacerbations.