Negative Pressure Pulmonary Oedema

Reviewed and revised 12 May 2014

OVERVIEW

Negative pressure pulmonary edema (NPPE) is a form of noncardiogenic pulmonary edema (PE) that results from the generation of high negative intrathoracic pressure (NIP) needed to overcome upper airway obstruction

• may occur in otherwise healthy individuals who can generate high NIP
• typically resolves over 12-48 hours with appropriate care

MECHANISM

Cause

• any cause of upper airway obstruction
• examples include laryngospasm or obstructed endotracheal tube (e.g. patient biting down)
• high NIP from patient-ventilator dysnchrony may contribute to respiratory failure (e.g. ARDS patients) and extubation failure (high NIP against increased resistance)
• Young healthy subjects can generate very high levels of NIP with a maximum of −140 cmH2O

Hydrostatic mechanism due to increased preload and increased LV afterload

• high NIP augments venous return to the right side of the heart
  -> increased pulmonary venous pressures, while decreasing perivascular interstitial hydrostatic pressure
  -> movement of fluid from the pulmonary capillaries into the interstitium and alveolar spaces
• hypoxia
  -> decreased myocardial contractility and increased pulmonary venous pressures through hypoxic vasoconstriction
• sympathetic outflow
  -> increased venous return from venoconstriction, and increased afterload due to increased SVR (peripheral arterial vasoconstriction)
• increased LV afterload due to NIP
  -> increased transmural pressure across LV wall
• increased pulmonary capillary pressure due to decreased LV function

Mechanical stress mechanism

• respiration against an obstructed upper airway
  -> increased transmural pulmonary capillary pressures
  -> disruption of the alveolar epithelial and pulmonary microvascular membranes
  -> increased pulmonary capillary permeability and protein-rich pulmonary edema

ASSESSMENT

Clinical features

• Pink frothy sputum
• Crackles
• Wheeze
• Increased JVP/CVP
• Liver engorgement
• Increased airway P, HR, RR, CVP, PCWP
• Decreased SpO2

Investigations

• CXR – basal shadowing, ULD, perihilar infiltrates, effusions, Kerley B lines, fluid in fissure, cardiomegaly
• ECG – right heart strain, ischaemic change

MANAGEMENT

Specific therapy

• apply high FiO2 to keep SpO2 >94%
• If awake – sit upright and apply CPAP
• If intubated – IPPV + PEEP, head up positioning, aspirate fluid from endotracheal tube (may need frequent changes of HME filters)
• no evidence for diuretics, and may exacerbate hypovolemia and hypoperfusion
• consider preload reduction with GTN if adequate BP (e.g. SBP >100mmHg) —  may also have beneficial afterload lowering effects

References and Links

LITFL

• CCC – Neurogenic pulmonary oedema

Journal articles

• Lemyze M, Mallat J. Understanding negative pressure pulmonary edema. Intensive Care Med. 2014 May 6. PMID: 24797685. [Free Full Text]