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A number of adjunct therapies are
available, none have proven effective. Prone positioning and inhaled
nitric oxide are the most commonly used. It is
uncertain what the lowest safe PaO2 is. Profound hypoxia will lead to
death. In this situation it is necessary to oxygenate the patient at all
costs – if this means increasing the FiO2, tidal volume or peak pressure,
then so be it. Often neuromuscular blocking agents are required to improve
patient-ventilator interaction, and increase chest wall compliance. It is
my practice to assume mucus plugging and derecruitment until otherwise
proven. The therapy involves aggressive suctioning with or without
bronchoscopy, followed by recruitment
maneuvers. There are many different
methods of performing this: e.g. switch off the control breaths, and
gradually increase the CPAP level to 10cmH2O above the peak airway
pressure, and hold it there for 30 to 40 seconds. Multiple methods of lung
recruitment have been described (1-3).
The efficacy and safety of recruitment maneuvers has not been established.
Another method of improving oxygenation is to alter the
alveolar gas content. This is achieved by washing carbon dioxide out of
the anatomical dead space by insufflating oxygen at the level of the
carina during expiration. When the next breath is delivered this dead
space gas is the first to arrive into the alveoli. This process, tracheal
gas insufflation (TGI) can be performed by placing a catheter at the level
of the catheter and delivering a flow of gas. The catheter can be inside
or outside the endotracheal tube (outside is better as it does not
increase airways resistance). The problem with this technique is in the
application: the easiest method is continuous gas flow at 2 to 5 liters
per minute. Unfortunately, this will significantly increase end
inspiratory volumes, even in pressure control ventilation. Care must be
taken that the patient does not develop large amounts of
auto-PEEP.
In addition, there are a number of unproven adjunct therapies available,
which may, at least in the short term, improve oxygenation:
1. Turn the patient prone – this improves ventilation-perfusion matching,
although the exact mechanism is unknown (4).
2. Administer inhaled nitric oxide – this is a local vasodilator, which
dilates up the capillaries around the well-ventilated alveoli, potentially
improving ventilation-perfusion matching(5;6). Due to the high cost of
administering this agent, nebulized prostacyclin has been used as an
alternative.
3. Add almitrine – which enhances hypoxic pulmonary vasoconstriction, and
may reduce right to left shunt (7). This agent is not available in the
USA; phenylephrine can be used instead.
4. High frequency oscillation – full tidal volume ventilation, with no
cyclic opening and closing of lung units. Experience with this mode has
been very good in pediatric and neonatal practice; there is little
published data in adults. 5. Tracheal gas insufflation
- 2 or more litres of oxgen are delivered into the major bronchi in
expiration to wash out dead space gas.
6. Partial liquid ventilation (PLV) with perfuocarbons, which carry
oxygen. This very attractive proposition of “liquid PEEP” has been
underutilized, due to lack of availability. The FRC is filled with the
liquid, and the patient ventilated above it. PLV has the added advantage
of lavaging the airways and removing cellular debris (7;8). Although of
academic interest, this strategy is not currently available.
6. Extracorporeal membrane oxygenation: the patient is put on an
extracorporeal circuit and oxygenated by a type of heart-lung bypass
machine: there is little evidence of efficacy in adults (9).
Although none of these techniques have been shown to improve outcome, when
a patient is severely hypoxemic many physicians feel that their backs are
to the wall, and there is little alternative but to go down the road of
adjunct therapy.
References
(1) Foti G, Cereda M, Sparacino ME, De Marchi L, Villa F, Pesenti A.
Effects of periodic lung recruitment maneuvers on gas exchange and
respiratory mechanics in mechanically ventilated acute respiratory
distress syndrome (ARDS) patients. Intensive Care Med 2000; 26(5):501-507.
(2) Mancebo J. PEEP, ARDS, and alveolar recruitment. Intensive Care Med
1992; 18(7):383-385.
(3) Medoff BD, Harris RS, Kesselman H, Venegas J, Amato MB, Hess D. Use of
recruitment maneuvers and high-positive end-expiratory pressure in a
patient with acute respiratory distress syndrome. Crit Care Med 2000;
28(4):1210-1216.
(4) Fridrich P, Krafft P, Hochleuthner H, Mauritz W. The effects of
long-term prone positioning in patients with trauma- induced adult
respiratory distress syndrome. Anesth Analg 1996; 83(6):1206-1211.
(5) Cuthbertson BH, Dellinger P, Dyar OJ, Evans TE, Higenbottam T, Latimer
R et al. UK guidelines for the use of inhaled nitric oxide therapy in
adult ICUs. American-European Consensus Conference on ALI/ARDS. Intensive
Care Med 1997; 23(12):1212-1218.
(6) Troncy E, Collet JP, Shapiro S, Guimond JG, Blair L, Ducruet T et al.
Inhaled nitric oxide in acute respiratory distress syndrome: a pilot
randomized controlled study. Am J Respir Crit Care Med 1998; 157(5 Pt
1):1483-1488.
(7) Gallart L, Lu Q, Puybasset L, Umamaheswara Rao GS, Coriat P, Rouby JJ.
Intravenous almitrine combined with inhaled nitric oxide for acute
respiratory distress syndrome. The NO Almitrine Study Group. Am J Respir
Crit Care Med 1998; 158(6):1770-1777.
(8) Hirschl RB, Conrad S, Kaiser R, Zwischenberger JB, Bartlett RH, Booth
F et al. Partial liquid ventilation in adult patients with ARDS: a
multicenter phase I-II trial. Adult PLV Study Group. Ann Surg 1998;
228(5):692-700.
(9) Ullrich R, Lorber C, Roder G, Urak G, Faryniak B, Sladen RN et al.
Controlled airway pressure therapy, nitric oxide inhalation, prone
position, and extracorporeal membrane oxygenation (ECMO) as components of
an integrated approach to ARDS. Anesthesiology 1999; 91(6):1577-1586.
Copyright Patrick Neligan
2001-2002 |
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