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High-frequency oscillatory ventilation with tracheal gas insufflation: the rescuestrategy for brain-lung interaction


The occurrence of moderate to severe acute respiratory distress syndrome due totraumatic brain injury is not uncommon and is associated with an extremely highincidence of morbidity and mortality. Owing to the complex interaction betweenthe lung and brain, protective ventilation for the lung with lower tidal volumeand higher positive end-expiratory pressure with or without mild hypercapniamight be harmful for the brain, and maintaining normocapnia or mild hypocapniaby increasing tidal volume or respiratory rate (or both) with lower positiveend-expiratory pressure levels for protecting the brain might lead toventilator-induced lung injury. Balancing the end-point between lungs and brainbecomes a challenging issue, and non-conventional modes of mechanicalventilation might play a role in the more difficult clinical cases. In thiscommentary, the authors discuss the rationale, based on the physiologicprinciple of targeting both vital organs, of applying high-frequency oscillationand tracheal gas insufflation in acute respiratory distress syndrome patientswith traumatic brain injury.


In this issue of Critical Care, Vrettou and colleagues [1] introduce the alternative rescue strategies of high-frequency oscillation(HFO) and tracheal gas insufflation (TGI) in acute respiratory distress syndrome(ARDS) patients with traumatic brain injury (TBI). A quarter of patients with TBIdevelop subsequent pulmonary dysfunction and are associated with high mortality. Themain mechanisms of aggravating lung injury are stimulation of systemic inflammatoryresponse and decreasing of lung tolerance to stress [2]. The evidence from animal models is that massive brain injury canincrease the risk of ventilator-induced lung injury (VILI) [35].

The ventilator management in ARDS comprises low tidal volume (VT) of 6mL/kg ideal body weight, limited plateau pressure of the respiratory system at 30 cmH2O, and maintenance of the partial pressure of arterial oxygen(PaO2) at between 55 and 80 mm Hg. This strategy may cause permissivehypercapnia to negatively affect intracranial pressure (ICP) by cerebralvasodilation in patients with severe TBI. Additionally, the increased ICP incombination with low PaO2 might promote cerebral tissue hypoxia.Therefore, a low VT strategy may result in a progressive deterioration ofneurological outcome.

The main end-points of mechanical ventilator management in severe TBI are maintainingthe partial pressure of carbon dioxide (PaCO2) at between 31 and 35 mm Hgand maintaining PaO2 at more than 60 mm Hg or 100 mm Hg [6, 7]. Trying to ventilate TBI patients with VT to keep that rangeof PaCO2 can aggravate VILI in patients either at risk of ARDS or withARDS [8] (Figure 1). It was recently shown that higherVT ventilation can be associated with higher morbidity and mortalityin patients with non-previously injured lungs [9]. Consequently, most of the clinical trials about protective ventilationin ARDS exclude patients with TBI.

Figure 1
figure 1

The effect of mechanical ventilation setting and acid-base disturbance onthe brain and lung in acute respiratory distress syndrome (ARDS) andtraumatic brain injury. CPP, cerebral perfusion pressure; HFO-TGI,combination of high-frequency oscillation with tracheal gas insufflation;ICP, intracranial pressure; PCO2, partial pressure of carbondioxide; PEEP, positive end-expiratory pressure; PO2, partialpressure of arterial oxygen; VILI, ventilator-induced lung injury;VT, tidal volume.

HFO is an alternative approach in ventilating patients with severe ARDS. Severalstudies have reported a clear benefit in terms of improvement of oxygenation,prevention of further lung injury from low VT ventilation, and ability torecruit the lungs compared with conventional ventilation. However, two recent largerandomized control trials have shown clear evidence that applying HFO in moderate tosevere ARDS is not superior to low VT ventilation [10] and might even be harmful in terms of in-hospital mortality [11]. Nevertheless, the first trial did not specify whether the TBI subgroupwas included or excluded, and the second one clearly excluded the TBI subgroup. Sowe still have a question: are there any places for HFO? Vrettou and colleagues [1] make an effort to answer this question in this issue of CriticalCare. The authors demonstrate the beneficial effect of the combination ofHFO with TGI (HFO-TGI) on oxygenation, hemodynamics, cerebral perfusion pressure(CPP), and ICP in severe ARDS patients with TBI. The authors aimed to achieveoptimal oxygenation and lower-to-normal PaCO2, avoiding possible adverseeffects such as the increase of ICP and decrease of CPP.


From previous study, HFO has been shown to improve oxygenation but also has beenreported to increase CO2 retention. Another limitation is that theincrease of intrathoracic pressure in HFO might lead to a decrease of cardiac outputand consequently a worsening of CPP. Mentzelopoulos and colleagues [12] have shown that, in patients with early severe ARDS, HFO-TGI (comparedwith HFO) can improve oxygenation and conventional mechanical ventilation withouthaving adverse effects on PaCO2 and hemodynamics. TGI can enhanceCO2 elimination by (a) improving the CO2 washout from theproximal part of the anatomic dead space, (b) increasing lung volume and recruitingnon-aerated lung regions by generating additional expiratory flow resistance, and(c) increasing the lung compliance, thus promoting a less injurious ventilation andbetter CO2 removal [13]. In another study, the authors demonstrated that additional recruitmentmaneuver can improve oxygenation and lung compliance without disturbing hemodynamicsin ARDS without TBI [14]. HFO-TGI, compared with conventional ventilation, improves lungcompliance and PaO2/fraction of inspired oxygen ratio while decreasingthe plateau pressure of the respiratory system and the incidences of higher ICP andlower CPP. Furthermore, the improvements in ICP and CPP were demonstrated 4 hoursafter applying HGO-TGI. The main mechanisms of improvement of cerebral hemodynamicsduring HFO-TGI are (a) the lowering of mean tracheal pressure to below the actualmean airway pressure displayed by ventilator and (b) lung recruitment withoutover-distension by the previously mentioned mechanisms.

However, the application of TGI can lead to bronchial mucosal damage from the jetstream and retention of secretion. These complications are not reported in thisstudy. However, the authors applied HFO-TGI for less than 12 hours. The recruitmentmaneuver during pre-HFO-TGI might lead to transient hypotension and is notlife-threatening. An alternative could be the use of extracorporeal CO2removal, but this technique might pose a risk in patients with TBI [15].


HFO-TGI may be considered an alternative rescue ventilation strategy in patients withTBI and severe ARDS. This method might provide non-injurious ventilation for thelung and optimal gas-exchange to protect the brain. When these techniques are used,an intensive monitoring of the respiratory function as well as brain physiology ismandatory.



acute respiratory distress syndrome


carbon dioxide


cerebralperfusion pressure


high-frequency oscillation


combination ofhigh-frequency oscillation with tracheal gas insufflation




partial pressure of carbon dioxide


partial pressure ofarterial oxygen


traumatic brain injury


tracheal gas insufflation


ventilator-induced lung injury


tidal volume.


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Correspondence to Paolo Pelosi.

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Pelosi, P., Sutherasan, Y. High-frequency oscillatory ventilation with tracheal gas insufflation: the rescuestrategy for brain-lung interaction. Crit Care 17, R179 (2013).

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  • Traumatic Brain Injury
  • Acute Respiratory Distress Syndrome
  • Cerebral Perfusion Pressure
  • Severe Traumatic Brain Injury
  • Acute Respiratory Distress Syndrome Patient