Emphysema = destruction of lung tissue (elastin in particular).
This causes changes in both static and dynamic characteristics of the lung/chest wall:

total lung volume and FRC (reduced elastic recoil).
dead space (destruction of alveolar units).
respiratory muscle efficiency ( chest wall expansion leads to shortening of diaphragm inspiratory intercostals and accessory muscles.

Airway compression, expiratory flow limitation and intrinsic PEEP (PEEPi) results from the reduction in elastic recoil (less negative pleural pressures holding the airways open).
Attempts to increase the expiratory flow by the use of accessory muscles results in further airway narrowing, hyperinflation, and PEEPi.
work of breathing (in inspiration to overcome PEEPi and in expiration due to higher resistance).
PEEPi (positive alveolar pressure at end expiration) means a greater negative pressure, and therefore effort, has to be generated to initiate inspiration.

Excess mucus production, inflammation,and bronchoconstriction results in further airway narrowing with resistance and expiratory flow limitation.

Expiratory flow limitation with associated dynamic hyperinflation and intrinsic PEEP.
Increased dead space.
Reduction in respiratory muscle efficiency.
Increased work of breathing.

Lung function tests

- FEV1, FVC, FEV1/FVC, diffusing capacity

Clinical effects

Stable State
The dead space means minute volume (MV) needs to be but the expiratory flow limitation and muscle efficiency means this is not possible.
A compromise solution results with a manageable MV and an
in PCO2 with a metabolically compensated respiratory acidosis.


Infective with need for ABX if 2 of -
SOB, sputum production, purulence of sputum.

An even greater load is placed on the respiratory muscles (the bronchoconstriction, inflammation and mucous production caused by an exacerbation causes work of breathing due to resistance and PEEPi as above.
Progressive muscular exhaustion leads to worsening respiratory acidosis which further impairs the contractility of the diaphragm and results in a ‘vicious cycle’ of respiratory decline.

Dynamic hyperinflation and intrinsic PEEP

Dynamic hyperinflation is the progressive increase in lung volumes consequent to incomplete emptying. Hyperinflation is made worse by:

Larger tidal volumes
Decreased expiratory time
Higher lung compliance
Increased expiratory airflow resistance

Positive alveolar pressure at end expiration (PEEPi) has 2 mechanisms for its generation - dynamic airway compression and/or incomplete expiration. In asthmatics airway narrowing means there is not enough time to complete expiration. In COPD patients the reduced elastic recoil causes distal airway collapse with trapping of gas. Bronchoconstriction also causes a more rapid pressure drop from the alveoli to the atmosphere making distal airway collapse more likely.

Dynamic hyperinflation is prevented by using low tidal volumes and prolonged expiratory time.
Intrinsic-PEEP from dynamic airway collapse may be treated by the application of external PEEP (PEEPe). Provided PEEPe is less than PEEPi there will be no
in total PEEP (PEEPt). The PEEPe will prevent airway compression (and further hyperinflation of the chest) and minimise the inspiratory threshold load.
Dynamic hyperinflation should be suspected if:
There is a clinical observation of active expiration or wheezes that continue to the onset of inspiration.
The patient appears to be working very hard to trigger each breath or the patient's inspiratory efforts do not trigger airflow from the ventilator every time.
There is unexplained tachycardia, hypotension or pulseless electrical activity, especially on initiation of mechanical ventilatory support.
Plateau pressure increasing.
Expiratory flow graph not returning to baseline.
If there is CVS compromise then disconnect the ventilator and press on the chest before reconnecting.
For more info see ventilation in

Mechanical Ventilation

Rest the respiratory muscles while pharmacotherapy can take effect.
Prevent dynamic hyperinflation and it’s consequences:

Vt 6 mls/kg
Short I:E ratio ( ie 1:3 meaning high peak inspiratory flow)
Low respiratory rate (10-14)
External PEEP at 80% of auto-PEEP
Sedation as required

Provide controlled hypoventilation to minimise pH changes
Maintain pH >7.15 – 7.20
PaCO2 less important than avoidance of alkalaemia.
NaHCO3 infusion at very low pH or if there is cardiovascular instability.

Non-invasive ventilation is the mode of choice when the patient can tolerate it.


Mechanical ventilation of the Patient with Severe Chronic Obstructive Airways Disease
Gladwin, M T Pierson, D J
Intensive Care Medicine (1998); 24: 898 -910

Thanks to David Christmas for his review which I have used.