Non-invasive ventilation (NIV) in the ICU

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How NIV works — the physiology

NIV delivers positive pressure to the airway through a leak-tight interface, doing mechanical work the fatiguing patient can no longer do. Two pressure domains matter. ^[1]

EPAP / PEEP / CPAP (extrinsic, set pressure during exhalation):

• Recruits collapsed alveoli and splints them open throughout the respiratory cycle, increasing functional residual capacity and lung compliance — less work per breath.
• Overcomes intrinsic PEEP (auto-PEEP) in obstructed patients: by raising extrinsic pressure toward intrinsic PEEP, it lowers the pressure gradient the diaphragm must generate to trigger a breath. This is the principal mechanism by which BiPAP unloads the COPD patient.
• Reduces preload (decreased venous return) and LV afterload (decreased transmural LV pressure) — the haemodynamic mechanism in cardiogenic pulmonary oedema.
• Redistributes alveolar oedema out of the alveolar space (cardiogenic oedema). ^[1]

IPAP / pressure support (the inspiratory boost):

• Augments every patient-triggered breath, increasing tidal volume and minute ventilation, washing out CO2.
• The IPAP-EPAP gradient IS the pressure support: IPAP 15 / EPAP 5 = 10 cmH2O of pressure support. To increase ventilation, raise IPAP; to increase oxygenation/recruitment, raise EPAP — but raising EPAP also raises IPAP and shortens expiration, so watch for dynamic hyperinflation in COPD. ^[1]

Clinical translation. A COPD patient tiring against their intrinsic PEEP needs EPAP to lower the trigger threshold and IPAP to boost tidal volume and blow off CO2. A pulmonary-oedema patient needs the continuous pressure (CPAP is sufficient) to preload- and afterload-reduce and recruit. An immunocompromised patient needs the mask pressure to bridge while the underlying insult is treated, avoiding the infectious morbidity of a tube. ^[1]

References17ShowHide

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