INVITED REVIEW
J Neurocrit Care 2009;2 Suppl 2:S86-S87
ISSN 2005-0348
Ventilator Management in Brain-Damaged Patients with ARDS
Younsuck Koh, MD, PhD, FCCM
Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
Introduction
Acute lung injury/Acute respiratory distress syndrome (ALI/
ARDS) is a permeability pulmonary edema characterized by
refractory hypoxemia leading to multiple system organ failure.1 The mortality rate of ARDS still remains more than 40%
and survivors suffer significant decrements in their quality of
life.2 In a retrospective analysis, 27% of subarachnoid hemorrhage (SAH) developed ALI, and the development of ALI
was an independent bad prognostic factor.3 In an international
observational study, high tidal volume was associated with
the development of ALI after severe brain injury.4
Lung Protective Mechanical Ventilation
in Brain-Damaged Patients
Alveoli remain permanently open at functional residual capacity (FRC) in healthy peoples. Only if volume is reduced
forcibly to near residual volume, peripheral airways prompt
to close in normal lungs. However, alveoli close at volumes
above FRC in acute respiratory distress syndrome (ARDS)/
acute lung injury (ALI). The collapsed alveoli increase ventilation/perfusion heterogeneity resulting in intrapulmonary
shunt and severely impaired oxygenation. Numerous evidences show that inappropriate mechanical ventilator settings
can produce further lung damage to the ARDS lungs, which
has been defined as ventilator induced lung injury (VILI).
Inappropriate mechanical ventilator settings can cause proinflammory cytokines production,5 and can facilitate translocation of bacteria from the bronchial tree into the systemic circulation.
The two important aspects of VILI seem to be end-inspiratory overdistension and a low end-expiratory lung volume
Address for correspondence: Younsuck Koh, MD, PhD, FCCM
Department of Pulmonary and Critical Care Medicine, Asan Medical
Center, University of Ulsan College of Medicine, 388-1 Pungnap 2-dong,
Songpa-gu, Seoul 138-736 Korea
Tel: +82-2-3010-4710, Fax: +82-2-3010-4709
E-mail: [email protected]
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Copyright ⓒ 2009 The Korean Neurocritical Care Society
allowing repeated collapse and re-expansion with each respiratory cycle (tidal recruitment). Tidal recruitment is thought
to result in high shear force on alveolar walls and small airways during inflation, especially at the interfaces between collapsed and aerated alveoli. Therefore, low tidal volume (6
mL per Kg of predicted body weight) and limitation of plateau pressure under optimal PEEP (less than 30 cm H2O) is
a key of lung protective ventilator strategy.6
Low tidal volume without adequate PEEP may not be valid
to improve ARDS patients’ outcome. After 5 days of mechanical ventilation on zero PEEP in brain-damaged patients static
elastance and mimimal resistance were significantly increased compared with 8 cm H2O of PEEP applied patients.7
However, it is not clear how to select optimal PEEP level
to prevent the bad tidal recruitment. Moreover, a safe upper
limit for plateau pressure has not been determined in ARDS
patients.8 One way to circumvent VILI may be alveolar recruitment maneuvers (ARM) in early stage of ALI. However,
the application of early ARM with low tidal volume has not
been proved its efficacy on the mortality reduction.9,10
PEEP Setting & Other Adjunctive
Measures in a Patient with Increased
Intracranial Pressure
Application of PEEP up to 25 cm H2O did not impair intracranial pressure (ICP), brain tissue oxygenation, or regional cerebral blood flow in an animal model with SAH.11 However, stepwise elevation of PEEP resulted in a significant decrease of mean arterial pressure and cerebral blood flow in
patients with severe SAH.11 However, PEEP increasing up to
12 mm Hg did not significantly influence ICP.12 The effect
of PEEP on ICP may be different depending on the lung elastance change induced by applied PEEP. When PEEP induced
alveolar hyperinflation leaded significant increase in ICP.13
Whereas when PEEP induced alveolar recruitment, ICP did
not change.13 In another study, PEEP did not affect cerebral
hemodynamics in patients with low respiratory system com-
Ventilator Management in Brain-Damaged Patients with ARDS ■ Y Koh
pliance.14 Raising the head-of-bed by 30 degrees in euvolemic patients with traumatic brain injury and subarachnoid
haemorrhage ameliorated the PEEP effect on ICP and CPP.15
Inspiration to expiration ratio did not cause significant changes
in ICP or cerebral perfusion within 1 : 1 to 1 : 2.16
international observational study. Crit Care Med 2007;35:1815-20.
5. Ranieri VM, Suter PM, Tortorella C, et al. Effect of mechanical ven-
6.
Conclusion
In spite of the remarkable advance in the understanding of
ARDS pathogenesis, the only effective therapeutic measure
to decrease the mortality up to now is low tidal volume mechanical ventilation6 up to now. Most ARDS patients die of
multi-organ failure rather than irreversible respiratory failure,
indicating that ALI is closely associated with other organs by
neurological, biochemical, metabolic, and inflammatory reactions. Although the careful use of induced hypocapnia to
temporally decrease increased ICP remains a therapeutic tool
in current practices, hyperventilation to induce hypocapnia
may not be recommendable in brain-damaged patients with
ARDS. Hyperventilation can induce ALI, or aggravate already
developed ALI. And judicious application of PEEP increment
is feasible in ventilating neurosurgical patients with acute intracranial pathology and concomitant acute respiratory distress
syndrome (ARDS). However, it is not well addressed the optimal balance between brain and lung protection in patients
with more refractory raised ICP.
7.
8.
9.
10.
11.
12.
13.
14.
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