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Brain Trust

Oxygenation and Ventilation in Brain Injury: Getting the Porridge Just Right

Wright, Brian MD

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Emergency Medicine News: May 2017 - Volume 39 - Issue 5 - p 10
doi: 10.1097/01.EEM.0000516456.54650.d0
    brain injury
    brain injury:
    brain injury
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    Neuroresuscitation of the emergency department patient with severe brain injury is based on the time-honored premise of “do no harm.” One way to minimize secondary injury is to modify oxygenation and ventilation targets. The jury is still out on the best targets for PO2 and PaCO2, but newer (albeit retrospective) data consistently show that targeting “normal” PO2 and PaCO2 while avoiding extremes of high and low is associated with better outcomes.

    We have known for some time that hypoxia and hyperoxia are associated with mortality in traumatic brain injury (TBI) (Acta Neurochir Suppl [Wien] 1993;59:121; J Pediatr Surg 1993;28[3]:310; J Neurotrauma 2009;26[12]:2217) and anoxic brain injury. (JAMA 2010;303[21]:2165; Crit Care 2015;19:348.) We have the mantra of avoiding hypoxia in brain-injured patients, but we should also avoid hyperoxia and truly target normoxia. This requires attention to detail. A small prospective ICU trial by Girardis, et al., looking at critically ill patients showed improved outcomes in the oxygen conservative group (targeting SpO2 at 94-98%) versus the oxygen liberal group (targeting SpO2 >98%). (JAMA 2016;316[15]:1583.) Current evidence suggests targeting an oxygen saturation of 95% in brain injury patients. (Circulation 2015;132[18 Suppl 2]:S465; Neurosurgery 2016 [Epub ahead of print].)

    Think PEEP in Oxygenation

    The pathophysiology of hypoxemia in acute brain-injured patients is surprisingly uniform — shunt or low cardiac output. We typically address this by increasing FiO2 or PEEP, but leaving patients on high FiO2 for extended time is suboptimal, exposing them to oxygen toxicity without resolving the underlying shunt. Resorption atelectasis occurs when oxygen replaces nitrogen and gets absorbed into the bloodstream at a faster rate, resulting in reduced alveolar volume and subsequent collapse. A better strategy is to increase PEEP to increase mean airway pressure and recruit alveoli. There is, however, a fear that increased PEEP will lead to increased venous pressure, impaired cerebral blood flow, and increased intracranial pressure (ICP), especially in brain-injured patients. Is this truth or myth?

    Huynh, et al., examined this issue in 28 trauma patients with severe TBI and a need for increased PEEP to treat hypoxemia through ICP monitors. (J Trauma 2002;53[3]:488.) They found no increase in ICP or decrease in cerebral perfusion pressure (CPP) as they increased PEEP from zero to 10 and 11 to 15 cm H2O. Caricato, et al., also looked at the use of PEEP in 21 patients with severe brain injury or subarachnoid hemorrhage (SAH), and found increased jugular venous pressure, a drop in MAP and CPP with increased PEEP, and ICP mostly stayed the same in patients with normal lung compliance. (J Trauma 2005;58[3]:571.) Conversely, patients with low lung compliance had no increase in ICP and no decrease in MAP and CPP with increased PEEP. These findings are important because they show that PEEP titration is safe in brain-injured patients, and those with “stiff lung” and low lung compliance are most likely to benefit from PEEP titration. These findings also highlight an often-forgotten side effect of PEEP — decreased cardiac output and decreased MAP. The decrease in MAP and CPP caused by PEEP titration will necessitate “non-neurological” interventions, namely fluids, vasopressors, or inotropic support, which carry other complications.

    A New Look at Ventilation

    Ventilation and PaCO2 goals are also important in brain injuries. PaCO2 and cerebral pH are directly related to cerebral blood flow, and current evidence suggests that hyperventilation and hypocapnia lead to worse outcomes in brain injury. Helmerhost, et al., in cardiac arrest patients with anoxic brain injury found a “U-shaped” phenomenon, with worse outcomes in hypercapnia and hypocapnia compared with normocapnia (35-45 mm Hg) patients. (Crit Care 2015;19:348.) Muizelaar, et al., found that long-term prophylactic hyperventilation led to worse outcomes in TBI patients. (J Neurosurg 1991;75[5]:731.) Hyperventilation can be used as a temporizing measure in a patient who is herniating while preparing the patient for definitive treatment such as craniectomy. Prolonged hyperventilation, however, is not recommended by the Brain Trauma Foundation unless advanced measures of brain oxygenation can be monitored to ensure that hyperventilation is not causing cerebral ischemia. (Neurosurgery 2016 [Epub ahead of print].)

    Preliminary feasibility data by Westermaier, et al., showed improved cerebral blood flow (CBF) and oxygen delivery in SAH, while Eastwood, et al., found decreased release of brain injury-specific biomarkers, both in post-cardiac arrest patients with controlled hypoventilation and PaCO2 augmentation. (Neurocrit Care 2016;25[2]:205; Resuscitation 2016;104:83.) These therapies are not quite ready for prime time, but could change the way we think about mechanical ventilation in brain-injured patients. Concern for increased intracranial pressure has usually been a contraindication for the “permissive hypercapnia” strategy that is used in most other areas of critical care medicine.

    In the meantime, it is important to remember to use safe ventilation strategies when targeting normocapnia. A tidal volume of 6-8 cc/kg of ideal body weight (based on sex and height) targeting a low Pplat (<30 cm H2O) will help prevent ventilator-induced lung injury. It is critical, however, to provide an adequate respiratory rate to avoid extremes of PaCO2. End-tidal CO2 won't eliminate the need for arterial blood gases, but can provide another tool to help reach and stay within PaCO2 targets. This is important because sedation requirements, spontaneous ventilation, and therefore, total minute ventilation and carbon dioxide exhalation can vary tremendously in these patients. If end-tidal CO2 is not available, you will have to keep track of exhaled minute ventilation and correlate it with your patient's PaCO2. A change in exhaled minute ventilation will likely mean a change in your patient's PaCO2. You may need to adjust sedation, respiratory rate, or tidal volume to get your patient back to his PaCO2.

    Thanks to Evie Marcolini, MD, for lending me her column this month.

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