3. Failing Lung Flashcards
Principles of Ventilation in the Critically Ill
Conventional ventilation
traditional methods of ventilating patients with ALI
maximized oxygenation by using normal tidal volumes (10–12 ml kg1), which in
non-compliant lungs were associated with very high peak and plateau airways
pressures. The ventilatory mode was usually volume-controlled with synchronized
intermittent mandatory ventilation (SIMV). A major concern was barotrauma. It has
more recently become apparent that barotrauma is much less of a problem than
volutrauma (caused by over distension of the lung), atelectrauma (owing to cyclical
shearing forces generated by alveoli closing and reopening), and biotrauma
(so-called because of surfactant reduction and cytokine release in response to this
repetitive injury)
‘Lung-protective’ ventilation:
it has now become standard practice to try to minimize
ventilator-associated lung injury (VALI) by using ‘lung-protective’ ventilation in
which plateau airways pressures are limited to 30 cmH2O by means of much reduced
tidal volumes, typically of 6 ml kg1.
There are two consequences of this technique:
the minute ventilation may be insufficient for adequate removal of CO2, and low tidal
volumes will predispose to closure of alveoli and gas trapping. The first problem is
dealt with by allowing the PaCO2 to rise: this is ‘permissive hypercapnia’. The second
is addressed by adding PEEP to maximize the recruitment of alveoli.
Permissive hypercapnia:
this is a key part of current ventilatory strategies, and there are experimental data to suggest that it is safe (up to a PaCO2 of ~9.0 kPa and pH of ~7.2)
and that it might confer some protection in the context of lung
injury and associated systemic organ damage.
Hypercapnic acidosis (as opposed to metabolic acidosis)
appears to attenuate VALI,
particularly that associated with volutrauma rather than atelectrauma.
It also has some myocardial protective effects, and although a PaCO2 of >10 kPa does depress myocardial contractility,
cardiac output can still increase as a result of a decrease in systemic vascular
resistance.
In other tissues, hypercapnic acidosis attenuates reperfusion brain
injury and delays hepatocyte cell death.
Positive end-expiratory pressure (PEEP):
PEEP increases airways
pressures and may contribute to a fall in cardiac output, most clinicians consider it
essential for alveolar recruitment and prevention of atelectrauma. It does not appear
that outcomes are influenced by the use of ‘high’ (~13 cmH2O) rather than ‘low’
PEEP (~8 cmH2O). Typically PEEP is set at 5–10 cmH2O, but ideally this should be
done with reference to the static pressure–volume curve
The upper
inflection point represents probable encroachment on total lung capacity, and so
the distending pressure should be kept below this point to avoid overexpansion
lower inflection point is where small airways and alveoli open (and is effectively the
closing volume), and the inflation pressure should be just above this point to avoid
de-recruitment of alveoli. Pressure-controlled ventilation on the steep linear part of
the curve midway between the two points reduces the peak airway pressure for a
given mean airway pressure and minimizes intrinsic PEEP. In practice, however,
although modern ventilators will produce pressure–volume curves, the inflection
points are often difficult to identify.
HFJV
High frequency ventilation: ventilation at very high rates with low tidal volumes is
theoretically ‘lung-protective’. High frequency jet ventilation (HFJV) uses rates of
between 60 and 300 min1, while high frequency oscillation (HFO) uses still higher
rates of 300–1800 min1. HFJV is used for the management of ARDS in some units
and can be useful in differential lung ventilation (via a double-lumen tube) and in
patients with bronchopleural fistulae. HFO, in which there is considerable experience
in children, is probably used more widely
The
OSCILLATE trial, however, terminated early because of higher mortality in the
group receiving high frequency oscillatory ventilation (47% v 35%).
Prone ventilation
: the practice waxes and wanes in popularity, but meta-analyses of
the numerous trials that have been performed
suggest that in patients with severe ARDS, it confers a survival benefit of around 10%, and that in most, although not all patients, the PaO2 will improve.
Any positive response is usually observed within the first hour.
Prone ventilation reduces shunt and improves oxygenation by mechanisms
which are thought to include better distribution of ventilation to previously
dependent areas of lung, perfusion of less oedematous areas of lung, a rise in endexpiratory
volume and an increase in diaphragmatic excursion.
These improvements, however, are not explained by the traditional gravitational theories of improved perfusion of dependent areas and are thought to relate more to the geometry of the pulmonary airways and vasculature. This is discussed in more detail under ‘The
Prone Position in Anaesthesia’.
Inverse ratio ventilation
: changing the I:E ratio from 1:2 to 2:1 or even 3:1 will
increase the inspiratory time sufficiently to allow ventilation of lung units with
prolonged time constants. In effect, this may just be a way of increasing PEEP.
Airway Pressure Release Ventilation (APRV):
This is a technique that provides continuous positive airway pressure (CPAP)
with a brief release of minimal duration.
In effect it is inverse ratio, pressure controlled, intermittent mandatory ventilation
throughout which the patient is able to breathe spontaneously.
It is a means of providing ‘open lung’ ventilation.
Two levels of PEEP, high and low, are set, with the
time spent in high PEEP set, for example, at around 4.5–6.0 seconds
and in low PEEP at a brief 0.5–0.8 seconds.
The airway pressure release time is usually set at around 1 time constant
(the time that it takes to empty 63% of the lung volume).
As complete emptying requires 4 time constants, this short release time results in a
degree of auto PEEP which further reduces alveolar collapse.
The technique recruits alveoli and improves oxygenation while allowing spontaneous ventilation, but this may be at the
expense of increased transpulmonary pressure,
elevated work of breathing and the risk of dynamic hyperinflation.
Although APRV improves oxygenation,
there is no evidence to show that it improves mortality in ARDS because
there have been no defined standard settings,
not least because the time constants referred to previously
will vary substantially according to the degree of acute lung injury.
Nitric oxide (NO):
inhaled NO is delivered to better-recruited alveoli where it dilates
the associated pulmonary vessels and reduces shunt fraction. It improves oxygenation,
but no study has established that this is mirrored by better outcomes
Miscellaneous
: these include nebulized prostacyclin PGI2
(less effective than NO in improving oxygenation),
artificial recombinant protein C-based surfactant (evidence
is awaited of its benefit in adult patients), partial liquid ventilation with perfluorocarbons
which preferentially fill and recruit dependent atelectatic areas of lung
(there is no evidence as yet of improved outcomes), and interventional lung assist
membrane ventilator devices (such as the Novalung).
Extracorporeal membrane oxygenation (ECMO):
the indications for ECMO have wideNed from its use in
neonates with respiratory distress syndrome to adults who
require respiratory support and to those who need cardiorespiratory support after,
for example, acute myocardial infarction.
Evidence suggests that ECMO for respiratory support is safe, but its efficacy has not been established.
It was hoped that the CESAR trial would do so (Lancet 2009, 374: 1351–630),
but because ECMO was carried out in a single centre after referral from hospitals which in contrast had very heterogeneous management strategies,
the interpretation of the results was equivocal.
There are, however, data from the Extracorporeal Life Support Organization registry
which indicate that the recent survival rate for patients with ARDS and treated with
ECMO is 60–70%.
The technique is relatively straightforward. Venovenous ECMO is
appropriate for patients who do not need cardiac assistance, and involves passing
desaturated blood from the vena cava through a membrane oxygenator across which
gas exchange can take place.
Venoarterial ECMO is used if myocardial support is
also necessary.
