COPD aka "chronic bronchitis"

• A disease of parenchymal lung destruction which destroys the attachments that maintain bronchiole patency
• This results in airways collapsing during exhalation, thus the cardinal problem in COPD is exhalation
• Difficulty exhaling gas results in alveolar distention and thus lung hyperinflation (see schematic below)

Acute treatment basics:

• Inhaled beta agonists (albuterol) intermittent or continuous administration: bronchiole smooth muscle relaxation results in bronchodilation
• Inhaled ipratropium (often co-administered with albuterol): anticholinergic which also contributes to bronchodilation
• Oral or intravenous steroids (no difference in efficacy)
• Antibiotics only for the sickest patients (requiring admission or even just for ICU patients)

Oxygen

• Although the exact mechanism is controversial, excess oxygen administration can result in worsening hypercarbia and respiratory acidosis, increasing the probability of intubation (see graph of minute ventilation and CO2 concentration when a COPD patient is placed on O2)
• For this reason, target O2 sat of 92%. Higher O2 sats are not beneficial.

Non-invasive positive pressure ventilation

• NIPPV has major benefits in terms of reducing intubation rates and decreasing overall mortality rates in acute COPD exacerbations
• Even in a patient requiring intubation, NIPPV may help in terms of preoxygenation in the severely hypoxic COPD patient

Ventilator pearls

• Expect high plateau pressures and breath stacking as patients often cannot exhale a breath fully before the ventilator administers another breath
• Counter this with: low tidal volumes (6-7 ml/kg), low RR (~10-12), setting the vent to allow more time for exhalation (I:E ratio), and judicious use of sedation agents to counter dyssynchrony with the vent
• This ventilation strategy is known as "permissive hypercarbia" as you expect PaCO2 to rise

Major pearl alert!

• Do NOT target a "normal" PCO2 with ventilator settings. COPD patients live with a mild chronic respiratory acidosis, and thus have a high HCO3 plasma concentration to compensate
• Normalizing PCO2 will this result in a harmful metabolic alkalosis and also cause the kidneys to excrete bicarb in the urine
• Then when patients are placed on minimal vent settings to wean, their CO2 will again rise, only now there isn't a buffer of HCO3, resulting in a more severe respiratory acidosis