What the hell is EIP ?

Low tidal volume ventilation in ARDS (acute respiratory distress syndrome) have been shown to improve mortality. However, low tidal volume ventilation invariably leads to hypercapnia.

Many strategies have been employed to optimize the ventilation in ARDS using increases in respiratory rate , use of active humidifiers  and the tracheal gas insufflation or aspiration of dead space.

Hernan Aguirre-Bermeo,  Indalecio Morán et el  published in Annals of Intensive care in August, 2016 issue about improving respiratory system mechanics in  ARDS patients when mild hypercapnia by prolonging EIP. 

 

BACKGROUND

We all use end inspiratory pause on ventilators to achieve a zero flow status, which gives us the plateau pressure.

 

If we add this pause at the end of  each inspiration, it will be called EIP.

In different ventilators, its named differently. This is also called t-pause in Servo or Drager but called T plateau in Puritan Bennett .

Most of the time, it is set to 0. But it can be increased up to 1.5 Sec or up to 30% of breath cycle.

See pictures below

Several authors (Aboab J, Niklason LUttman L, Jonson BMercat A, Diehl JLDevaquet J, Jonson B)  have shown that EIP prolongation can enhance CO2 elimination and decrease partial pressure of carbon dioxide in arterial blood (PaCO2) and also reduce physiological dead space (Vdphys).

None of these authors investigated  the potential physiological benefits  in terms of Vt reduction in ARDS.

 

WHAT THEY DID

In patient’s with ARDS (total 13 patients), after following standard low tidal volume ventilation protocol, EIP was prolonged.

EIP was prolonged until one of the following parameters was reached:

(1) EIP of 0.7 s;

(2) intrinsic positive end-expiratory pressure (PEEPi) ≥1 cmH2O; or

(3) inspiratory–expiratory ratio (I/E) of 1:1.

Then, Vt(Tidal volume) was diminished in steps of 30 mL every 30 min until PaCO2 reached baseline levels.

 

WHAT THEY FOUND

  1. EIP prolongation decreased Vdphys and PaCO2 significantly with respect to basal conditions (267 ± 71 to 244 ± 65 mL and 54 ± 9 to 50 ± 8 mmHg, respectively; p < 0.001 for both comparisons).

2. Prolonging EIP allowed to reduce Vt by 11 % (from 6.3 ± 0.8 to 5.6 ± 0.8 mL/kg of PBW; p < 0.001), maintaining PaCO2 levels equal to baseline.

3. A slight but not statistically significant decrease in mean arterial pressure was observed.

LIMITATIONS

  1. Small sample
  2. Most patients had pneumonia
  3. No measurement of other parameters such as inflammatory mediators, lung volumes or Shunt.
  4. Only moderate reduction in tidal volume.
  5. Can cause patient ventilator asynchrony.

BOTTOMLINE

Interesting new area to explore in a larger study.