# Calculating Pplateau with HAMILTON-C1/T1/MR1 ventilators

Article

Author: Simon Franz

Date of first publication: 14.07.2017

A common question asked by users of HAMILTON-C1/T1/MR1 ventilators is how to measure/calculate Pplateau with their device.

### Background

Even if the idea of a “safe” plateau pressure is already being questioned, it is still standard of care to use it for tailoring lung-protective ventilation in acute respiratory distress (ARDS) patients Loring SH, Weiss JW. Plateau pressures in the ARDSnet protocol: cause of injury or indication of disease?. Am J Respir Crit Care Med. 2007;176(1):99-101. doi:10.1164/ajrccm.176.1.99b1​.

### Display of Pplateau as monitoring parameter

Due to the valveless pneumatics in the HAMILTON-C1/T1/MR1 ventilators, it is not possible to obtain the Pplateau by performing an inspiratory hold maneuver. Nevertheless, Pplateau is still available as a monitoring parameter and maybe displayed depending on your ventilator's software.

HAMILTON-C1/T1/MR1 SW < v2.2.0 HAMILTON-C1/T1/MR1 SW ≥ v2.2.0
End-inspiratory pressure always displayed as Pplateau. Please consider that if an end-inspiratory flow is present, the Pplateau displayed is higher than the actual Pplateau. Pplateau is only displayed if the end-inspiratory flow is close to zero. The Pplateau displayed can still be higher than the actual Pplateau.

### Calculating Pplateau if end-insp flow not near zero

A possible workaround for calculating Pplateau in situations where the end-inspiratory flow is not close to zero or the pressure measured end-inspiratory seems inaccurate:

• Calculate driving pressure (P): P = VTE/Cstat
• Calculate Pplateau: Pplateau = P + PEEP

This calculation is dependent on an accurate Cstat measurement, which means there is no significant patient effort occurring. Pinsp should be at least ~10cmH2O.

Pplateau = (VTE ml  / Cstat ml/cmH2O) + PEEP cmH2O

Example
VTE: 450 ml; Cstat: 50 ml/cmH2O; PEEP: 8 cmH2O

(450 ml / 50 ml/cmH2O) + 8 cmH2O = 17 cmH2O

Pplateau = 17 cmH2O
P = 9 cmH2O

Another benefit is that you get the P as a side product of your calculations. P is strongly associated with survival in ADRS patients and may therefore be the more interesting parameter Amato MB, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372(8):747-755. doi:10.1056/NEJMsa14106392​.

Relevant devices: HAMILTON-C1/T1/MR1 (all software versions)

#### Plateau pressures in the ARDSnet protocol: cause of injury or indication of disease?

Loring SH, Weiss JW. Plateau pressures in the ARDSnet protocol: cause of injury or indication of disease?. Am J Respir Crit Care Med. 2007;176(1):99-101. doi:10.1164/ajrccm.176.1.99b

#### Driving pressure and survival in the acute respiratory distress syndrome.

Amato MB, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372(8):747-755. doi:10.1056/NEJMsa1410639

BACKGROUND

Mechanical-ventilation strategies that use lower end-inspiratory (plateau) airway pressures, lower tidal volumes (VT), and higher positive end-expiratory pressures (PEEPs) can improve survival in patients with the acute respiratory distress syndrome (ARDS), but the relative importance of each of these components is uncertain. Because respiratory-system compliance (CRS) is strongly related to the volume of aerated remaining functional lung during disease (termed functional lung size), we hypothesized that driving pressure (ΔP=VT/CRS), in which VT is intrinsically normalized to functional lung size (instead of predicted lung size in healthy persons), would be an index more strongly associated with survival than VT or PEEP in patients who are not actively breathing.

METHODS

Using a statistical tool known as multilevel mediation analysis to analyze individual data from 3562 patients with ARDS enrolled in nine previously reported randomized trials, we examined ΔP as an independent variable associated with survival. In the mediation analysis, we estimated the isolated effects of changes in ΔP resulting from randomized ventilator settings while minimizing confounding due to the baseline severity of lung disease.

RESULTS

Among ventilation variables, ΔP was most strongly associated with survival. A 1-SD increment in ΔP (approximately 7 cm of water) was associated with increased mortality (relative risk, 1.41; 95% confidence interval [CI], 1.31 to 1.51; P<0.001), even in patients receiving "protective" plateau pressures and VT (relative risk, 1.36; 95% CI, 1.17 to 1.58; P<0.001). Individual changes in VT or PEEP after randomization were not independently associated with survival; they were associated only if they were among the changes that led to reductions in ΔP (mediation effects of ΔP, P=0.004 and P=0.001, respectively).

CONCLUSIONS

We found that ΔP was the ventilation variable that best stratified risk. Decreases in ΔP owing to changes in ventilator settings were strongly associated with increased survival. (Funded by Fundação de Amparo e Pesquisa do Estado de São Paulo and others.).