Ramb - Janeiro

7 / 100

It is impossible to know the way if we do not know where to start: tidal volume , driving pressure , and positive end- expiratory pressure
Rev Assoc Med B ras 2017; 63(1):1-3 1
EDITORIAL
It is impossible to know the way if we do not know where to start:
tidal volume, driving pressure, and positive end-expiratory pressure
É impossível saber o caminho se não soubermos por onde começar: volume corrente,
driving pressure e pressão expiratória final positiva
Marcelo Cunio Machado Fonseca1, Werther Brunow de Carvalho2*
1Health Technologies Assessment Center, Universidade Federal de São Paulo, São Paulo, SP, Brazil
2Full Professor of Pediatric Intensive Care/Neonatology of the Department of Pediatrics, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil
*Correspondence:
Like many other technologies, mechanical ventilation has
emerged out of necessity. Today, it is the basis of cardiopul-
monary resuscitation, intensive medicine and anesthesia.
Implementation of mechanical ventilation allows the treat-
ment of several diseases that were previously lethal, and
increases the survival of thousands of patients every day.
The lungs in acute respiratory distress syndrome
(ARDS) are characteristically heterogeneous with an aer-
eted area, called the baby lung, primarily located in non-de-
pendent regions of the lung1 and areas where there is great
inflammation, and the alveoli are filled with residual in-
flammatory material. It has been described that lungs
with ARDS are not hardened but small, and that the com-
pliance of this specific small aerated area is practically
normal.2,3 The complacency of the respiratory system, in
turn, is related to the functional size of the lung, that is,
the remaining aerated volume.1
When this syndrome was described, the mechanical
ventilation strategy used high flow volumes (10-15 mL/kg)
and relatively low positive end-expiratory pressure (PEEP)
(5-15 cmH2O) with FiO2 ≤ 0.70. 4
Initially, we learned that this ventilatory strategy usu-
ally leads to ventilatory-induced lung injury (VILI) because
it causes mechanical stress of the lung with overdistension
and stretching of the pulmonary parenchyma (volutrauma).5
We know that VILI also occurs when there is low final ex-
piratory volume. In this case, some bronchioles and alveo-
li will collapse during exhalation and reopen at the next
inspiration, a process that damages the pulmonary paren-
chyma (atelectrauma) if this takes place repeatedly.5 Later,
it was identified that the forms of mechanical ventilation
that cause atelectrauma or volutrauma can lead to the re-
lease of inflammatory mediators in the lung, characterizing
biotrauma.5 Together, it is theorized that there may be
translocation of inflammatory mediators, bacteria or en-
dotoxins into the systemic circulation due to the increased
permeability caused by the underlying disease or biotrauma.
This could eventually lead to multiple organ failure.6-8
In this context, and because we have not yet been able
to demonstrate that a specific mode of mechanical venti-
lation improves patient survival,9 one of the major advanc-
es in the last decades has been the recognition of its com-
plications, as described above, and the development of
ventilatory techniques that minimize these complications.10
Ventilatory strategies that reduce the adverse effects
of mechanical ventilation and at the same time are asso-
ciated with better survival are referred to, in all, as pro-
tective ventilatory strategies. In general, these strategies
involve the use of low tidal volume, low pressure at the
end of inspiration ( plateau pressure), and high PEEP.
Two systematic reviews by The Cochrane Collabora-
tion,11,12 including six studies on ARDS,13-18 concluded
that protective ventilatory strategies, specifically low tid-
al volume and low inspiratory plateau pressure, reduce
hospital mortality and morbidity.
However, distinguishing which element has the great-
est value for improving the clinical effects resulting from
the protective ventilatory strategy is challenging, since
each of them – low tidal volume, low inspiratory pressure
(plateau pressure), and high positive end-expiratory pres-
sure –, is closely connected to the others.
Therefore, considering that, in ARDS, respiratory
system complacency is related to the functional size of
the lung, Amato et al. 19 theorized that the ratio between
tidal volume and respiratory system complacency, that is,
driving pressure, would be an independent risk factor for
survival in patients with ARDS.
To prove their theory, Amato et al.19 conducted a me-
ta-analysis of individual patients with data from 3,562
patients enrolled in nine randomized clinical trials com-
paring mechanical ventilation strategies in ARDS. The
authors’ regression model showed that only four variables