CRACKCast E198 – Brain Resuscitation

In CRACKCast, Featured, Podcast by Owen ScheirerLeave a Comment

Care of the brain injured patient (traumatic, increased ICP, or post-arrest) is something we need to know about in the ED. Sit back, grab a cup of coffee, and get ready for some brain resus pearls.

This month, we have Sey Shwetz (@SeyShwetz), rockstar EM chief resident and incoming PEM fellow, as our very special guest host!

Shownotes – PDF Here


[1] What is cerebral autoregulation?

Cerebral autoregulation is the process by which the brain controls the amount of perfusing blood flow it receives. Under optimal conditions, the brain is able to accommodate changes in intracranial pressure and mean arterial pressure by altering cerebral vascular resistance. ICP is typically low, so cerebral perfusion is largely dependant in MAP. As MAP increases, cerebral blood vessels vasoconstrict to prevent vasogenic edema and increasing ICP. Conversely, if MAP decreases, the brain attempts to increase cerebral blood flow by vasodilation of cerebral vasculature. 

When MAPs are out of the range of <60 mmHg and >160 mmHg, the brain is unable adequately autoregulate, and as a result, cerebral perfusion is not optimized. In the setting of increasing ICP, the brain attempts to increase cerebral blood flow by causing vasodilation, which often increases ICP and worsens neurogenic ischemia.

[2] Describe your parameters for post-arrest care of a brain injured patient.


  1. Avoid hypotension: MAP > 65 mmHg
    1. Injured brain loses ability to autoregulate effectively
  2. Avoid hypertension: aim for SBP <140 mmHg
    1. Hypertension may disrupt BBB and lead to worsening vasogenic edema.
  3. Avoid hypoxia or hyperoxia: PaO2 80-120
    1. Hypoxia – obviously avoid.
    2. Hyperoxia – increased oxidative brain injury in animal models.
  4. Avoid hyper/hypocarbia
    1. Caveat – hyperventilation can be used if patient is herniating. Otherwise aim for PaCO2 35-45
  5. Maintain euthermia (avoid fever/spikes in temperature)
    1. Metabolic demand increases by 8-13% for every ºC.
    2. Increased free radical production, BBB damage, vasogenic edema
  6. Maintain euglycemia
    1. Target BG <10mmol/L, avoid hypoglycemia
    2. Hyperglycemia after brain injury = worse outcomes. Increased levels of lactate in brain, increased cell death.
  7. Consider therapeutic hypothermia <36º (will discuss in later questions)
  8. Aggressively treat seizures
    1. Seizures increase brain metabolism by 300-400%.
    2. Consider EEG monitoring if concerned about nonconvulsive SE.
  9. Avoid ICP triggers
    1. head in neutral position
    2. collar LOOSELY applied if C spine injured (avoid impeding head’s venous drainage)
    3. prevent Valsalva (coughing/gagging)
    4. avoid unnecessary stimulation and noisy environment
    5. sedate and paralyze (consider EEG for subclinical SE)

[3] List 7 interventions for management of a patient with elevated ICP.

  1. Elevate HOB 30º 
  2. Neutral position of head and neck to avoid jugular venous compression.
  3. Treat fever
  4. Minimize triggers of ICP increases
    1. Treat pain
    2. Adequate sedation to avoid coughing (propofol decreases cerebral metabolic activity and CBF)
  5. Initiate osmolar therapy (mannitol or HTS)
    1. Use mannitol in cases of fluid overload (is a diuretic)
    2. Use HTS in other settings (can be used as a resuscitative fluid)
  6. Consider barbiturate coma if refractory to other therapies. (further decreases CBF and lowers ICP)
  7. Hypothermia can be considered in highly refractory cases.
  8. Surgical management – craniectomy can be considered in refractory ICP or if herniation present.

[4] What are the equations for cerebral blood flow and cerebral perfusion pressure?


(Cerebral Perfusion Pressure = Mean Arterial Pressure – Intracranial Pressure) 

Normal Range: 50-70 mmHg


(Cerebral Blood Flow = Cerebral Perfusion Pressure/Cerebral Vascular Resistance)

Normal Range: 50 ml / 100 g min (typically less in white matter and higher in grey matter)

[5] Describe a protocol for induced hypothermia after cardiac arrest.

The Skeleton Protocol (Box 7.1)

  1. Evaluate adult survivors of cardiac arrest by following institutional criteria for appropriateness for induced hypothermia.
  2. Begin cooling by rapidly infusing 2L of cold (4 degrees Celsius) intravenous saline immediately after arrival or ROSC.
  3. Expose patient, avoid external warming – no blankets and no heated ventilator circuit.
  4. Place temperature-sensing urinary catheter and esophageal temperature probe.
  5. Initiate definitive endovascular temperature control device at maximal rate ot target temperature of 33 degrees Celsius.
  6. Prevent shivering with sedation and non-depolarizing paralytic – bolus in ED, bolus or drip in ICU.
  7. Avoid hypotension and hypoxia.
  8. Most ED diagnostic evaluation, if needed, should follow initiation of cooling (in patients with acute myocardial infarction who are going to primary coronary intervention, cooling should not delay door-to-balloon time. Coling is initiated in the ED if there is time before catheterization laboratory is ready; otherwise, cooling is initiated in the laboratory).
  9. Admit to ICU.
  10. Continuous EEG monitoring for occult status epilepticus recommended. Treat seizures if present.
  11. Manage ABG in a consistent manner (may choose pH stat or alpha stat).
  12. At 24 hours after initiation of cooling, initiate rewarming to a target temperature of 36.5 degrees Celsius at a rate of 0.15 degrees Celsius per hour.
  13. Discontinue paralytics at the onset of warming. Control shivering with sedation, narcotics, and surface counter-warming.
  14. Lighten sedation as tolerated as rewarming progresses.
  15. Discontinue endovascular temperature control device after 48 hours (may use the device to maintain normothermia after rewarming is complete until it is removed).
  16. Remove or minimize sedation to allow neurologic evaluation before 72 hours to allow the best possible clinical prognostication at that time point; neurology consultation recommended.

[6] In the patient with a traumatic brain injury, what is the optimal drug for and duration of seizure prophylaxis?

Seizure activity has been noted to increase brain metabolism by 300-400%, which can significantly worsen neurological damage in our patients with an injured brain. Yikes.

In the setting of traumatic brain injury, it is recommended that seizure prophylaxis instituted. The benefit of seizure prophylaxis has been demonstrated with phenytoin, reducing seizures during the first seven days after TBI. While this can be accomplished with phenytoin, the side effect profile is not ideal. As such, Rosen’s recommends 7 days of levetiracetam 500 mg PO BID.




[1] What are Lundberg A waves?

On ICP monitoring devices, Lundberg A waves represent periods of refractory ICP elevation. These appear as increases in ICP from baseline, plateauing ICP for several minutes, and then spontaneous return of ICP to near-baseline levels. These are generally the result of increasing ICP that leads to increased cerebral vasodilation that further increased ICP and diminished CPP. The return to baseline is the result of the Cushing Response.

[2] What is the relationship between PaCO2 and CBF?

As well all know, carbon dioxide is a vasodilator. We also know that lowering the PaCO2 in the patient suspected to be herniating is a life-saving measure, but just how important is it? Well, here you go: for every 1 mmHg reduction in PaCO2, you see a rapid reduction in CBF by 2% Remember, however, that this comes at a price. There is profound reduction in CBF with hyperventilation, so this strategy should only be used when the patient is herniating or when there is critically high ICP that is not responding to hyperosmolar therapies.

[3] What is the Monro-Kellie hypothesis?

The Monro-Kellie hypothesis  states that the skull is a rigid container with three non-compressible elements: brain, blood, and cerebrospinal fluid.

Increases in one substance will cause displacement of others from the box or increases in ICP. The first vault content to be displaced is CSF. CSF is shunted from the intracranial compartment to the spinal subarachnoid space. Next to be displaced is blood. Displacement of blood is achieved by compression  of the dural sinuses and cerebral veins. Last to go is the brain. Herniation will eventually occur, and death or permanent neurologic injury will result if intervention is not undertaken.

[4] What is the probability that a survivor of cardiac arrest has a full neurologic recovery? How do these values change in patients with severe coma?

Outcome prognostication in patients who survive cardiac arrest is difficult. However, Rosen’s cites the following probabilities for neurologic recovery after cardiac arrest:

  • Normal patients: 14-55% chance of full neurologic recovery
  • Patients with severe coma (defined as having motor plus brainstem four score <4 in the absence of sedatives and paralytics): 5-10%

Again, these numbers may not be the most accurate. However, it is important to remember that for most patients, the likelihood that they will make a full recovery is not insignificant, so you should endeavour to intervene appropriately and in accordance with a patient’s wishes to best treat them.


Copyedit and upload by @O_Scheirer




Owen Scheirer

Owen is a resident in the FRCPC Emergency Medicine program at the University of Saskatchewan. When he's not running around the emergency department, he's hanging out with his wife, new baby girl, and dog. Spare time = climbing and cycling!

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Dillan Radomske

Dillan Radomske is an Emergency Medicine resident at the University of Saskatchewan. He is passionate about technology-enhanced medical education, podcast creation and production, and Indigenous advocacy. He is one of the new CRACKCast hosts, and aspires to continue to contribute to the field of FOAMed in the future.

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