CRACKCast E008 – Brain Resuscitation

In CRACKCast, Podcast by Adam Thomas2 Comments

This episode of CRACKCast cover’s Rosen’s Chapter 08, Brain Resuscitation. This complex topic is essential for critical care management in the ED.

For the PDF version of this file click HERE


Rosen’s in Perspective – Why Cerebral Resuscitation?

We frequently see post-cardiac arrest patients in the ED

  • prognostic significance of immediate post-ROSC period is limited
  • no laboratory or clinical predictors exist (yet) for the ED physician to make accurate predictions on who will survive and who will not
    • each patient should be given a chance of recovery

In any shock state (see episode 6) we know that cerebral blood flow is often compromised

  • cerebral resuscitation is just as important as cardiac resuscitation
  • post-ischemic encephalopathy is a huge contributor to poor outcomes after ROSC
  • deprivation of blood flow leads to neuronal cell death in minutes of ischemia
  • re-perfusion injury also contributor to negative sequelae

Rosen’s thinks this topic is important enough to include complex figures in the textbook:

  • Decreased cerebral blood flow (CBF) — > cellular hypoxia — > inability to produce ATP –> (impairment of the ATPase pump leads to) excess intracellular Na+ —> cytotoxic edema –> excess Ca+ and GABA release –> metabolic failure –> oxygen radical formation –> DNA damage/apoptosis/membrane degradation/cytoskeleton destruction –> membrane attack complexes –> demargination / proteases –> increased cerebrovascular resistance which leads to more decreases in cerebral blood flow[bg_faq_end]

1) Describe 6 therapeutic interventions for the post-arrest brain

Goal of therapeutic interventions are two-fold:

  •  1) restore cerebral blood flow
  • 2) prevent secondary injury

Standard Strategies:

For anyone still in cardiac arrest our first goal is ROSC

  •  good quality CPR is vital to ROSC (good depth, speed, and minimize interuptions) – inverse correlation between brain survival and CPR time

After we have achieved ROSC, a nice way to think about the post arrest brain is ““keep their vitals and ABG in the normal range and keep their brain asleep”

General Goals:

  • 1) avoid hypotension: MAP > 65 mmHg
  • 2) avoid hypertension: diastolic < 120 mmHg
  • 3) avoid hypoxia or hyperoxia
  • 4) avoid hyper/hypocarbia
  • 5) maintain euthermia (avoid fever/spikes in temperature)
  • 6) maintain euglycemia
  • 7) consider therapeutic hypothermia
  • 8) aggressively treat seizures
  • 9) supportive and IMPORTANT care
    • a) head in neutral position
    • b) collar LOOSELY applied if C spine injured (avoid impeding head’s venous drainage)
    • c) prevent Valsalva (coughing/gagging)
    • d) avoid unnecessary stimulation and noisy environment
    • e) sedate and paralyze (consider EEG for subclinical SE)

Specific Management Strategies:

Treatment of hypotension, hypoperfusion, and hypoxia

  • the injured brain loses its ability to auto-regulate
    • Keep MAP > 65 and diastolic BP < 120
  •  avoid inadvertent hyperventilation unless patient is imminently herniating
    • PaCO2 = 35-45
  • avoid hypoxia and hyperoxia
    • PaO2: 80-120 (18% higher mortality when PaO2 =300 for long periods)

Maintenance of body temperature

  • fever is damaging to the brain (increases metabolic demand 10% per degree C)
  • monitor core body temp: rectal, esophageal, bladder or vaginal
  • temp managed with antipyretics, cooling with fans +/- misting, commercial cooling devices

What about resuscitative mild hypothermia?

  • stay tuned for question 3 but no clear mechanism

Treatment of HYPERglycemia

  • profound hyperglycemia leads to increased cellular pH, increased brain lactate, and increased neuronal loss
  • cautiously use insulin for high sugars

Seizure management

  • seizures increase brain metabolism by 400% o increases oxygen delivery / demand mismatch
  • no evidence to support seizure prophylaxis, but if they occur need rapid treatment
  • treatment o benzos, phenytoin, barbiturates

Immobilization/Sedation/Head position

  • appropriate sedation and paralysis can prevent brain stimulation
  • ensure quiet environment
  • preventing coughing, unnecessary suctioning, neck compression
  • ensure neck in neutral position It all comes back to keeping the patient’s values NORMAL![bg_faq_end]

2) List 5 techniques for initiating therapeutic hypothermia

1) Cold saline infusion
2) Misting and fans
3) Ice packs in the groin and axilla
4) Cooling blankets (commercial cooling devices)
5) Internal cooling (bladder irrigation, chest tubes, ECMO)

Why care? The reported NNT for a good neurologic outcome is 7 (from Rosen’s)

The most recent edition of Rosen’s quotes the 2010 American and European guidelines for out of hospital cardiac arrest (VF)

  • target temperature was 330C for 12-24 hrs
  • ideally begun in the ED after ROSC achieved
    • insert esophageal probe
    • 2 L of cold saline
    • expose patient
  • avoid hypotension or hypoxia / do NOT delay PCI if needed
  • pharmacologic prevention of shivering:
    • paralytic, sedation, fentanyl

The new 2015 AHA guidelines suggest targeted therapy management between 32-360C for 24 hours with prognostication at 72 hours post arrest or post cooling.

This does not apply to other types of brain injury. Cooling for adults/children with TBI and acute ischemic stroke have shown NO benefits from therapeutic hypothermia[bg_faq_end] [bg_faq_start]

3) List 4 mechanisms of therapeutic hypothermia in improving neurologic outcome

No clear mechanism known; however, Rosen’s suggests 4:

1) decreases metabolic demand
2) decreases free radical formation
3) decreases production of inflammatory cytokines
4) prevents programmed neuronal cell death

Bottom line:

  • initially comatose e in ER does not always mean bad long term outcome! Give everyone the best chance of recovery
  • Prevent:
    • hypotension, hypoperfusion, hypoxia
    • hyperthermia, hyperglycemia
    • seizures/coughing/vasalva
    • body/head/neck positions that increase ICP[bg_faq_end]



1) What components make up cerebral blood flow and CPP?


Taken from

  • any change in BP between 50-150 mmHg doesn’t increase the cerebral blood flow because your brain is able to AUTOREGULATE the size of the cerebral blood vessels.
  • after 150 mmHg the brain is maximally vasoconstricted and the cerebral blood flow spikes upwards again
  • ideally we should keep the injured brain in 50-150mmHg sweet spot – ideally more than 100mmHg and less than 150mmHg

Some equations:

  • Cerebral Perfusion Pressure (CPP) = MAP – ICP or CVP (whichever is highest)
  • Cerebral Blood Flow (CBF) = CPP/CVR (Cerebral Vascular Resistance)

Brain Trauma Foundation support a CPP of 50-70mmHg in patients with severe traumatic brain injury (this is usually calculated for patients once in the neuro-ICU)

Note: this is a gross oversimplification of a complicated fellowship topic. The key take home point is that we need to do whatever we can to protect the injured brain because it does a finite ability to auto-regulate![bg_faq_end] [bg_faq_start]

2) Wisecracks Essential Evidence: Target Temperature Management at 330C versus 360C after Cardiac Arrest (Nielsen et al. 2013)1

Worldwide, Nielsen et al.’s TTM study has been a practice changing multi-center randomized controlled trial comparing targeted 330C vs 360C temperature management for post-cardiac arrest patients.

See original paper below:

Quick overview:

  • Very well executed/designed multi-center randomized controlled trial based out of Europe and Australia
  • n = 939 (see original paper for full inclusion/exclusion criteria) BUT patients with an unwitnessed arrest with initial rhythm of asystole were excluded. Thus, this study looked mainly at post-VF arrest patients and thus the generalizability to other initial rhythms can be debated.
  • modified intention-to-treat analysis
  • No difference in primary outcome of mortality at 180 days
    • 50% for 330C
    • 48% for 360C
    • hazard ratio for T33°C, 1.06; 95%CI 0.89-1.28; P=0.51
  • No difference in secondary outcome of neurological performance (cerebral performance score and modified rankin scale)
  • Differences in:
    • duration of mechanical ventilation shorter in 360C
    • serious events marginally higher in 330C group
    • higher rates of hypokalemia in the 330C group

Bottom line: No difference in primary or secondary outcomes between 360C and 330C groups.

  • It is important to note that both arms of the trial had active monitoring and regulation of temperature (temperature was not left to fluctuate naturally)
  • **Thus, the target (330C vs 360C) might not be as important as actively maintaining euthermia/mild hypothermia and preventing fever and spikes in temperature (previously shown to result in poor outcomes)[bg_faq_end]

This post was copyedited and uploaded by Robert Carey (@_RobCarey)

Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013;369(23):2197-2206. [PubMed]

Adam Thomas

CRACKCast Co-founder and newly minted FRCPC emergency physician from the University of British Columbia. Currently spending his days between a fellowship in critical care and making sure his toddler survives past age 5.
Chris Lipp is one of the founding Fathers for CrackCast. He currently divides his time as an EM Physician in Calgary (SHC/FMC) and in Sports Medicine (Innovative Sport Medicine Calgary). His interests are in paediatrics, endurance sports, exercise as medicine, and wilderness medical education. When he isn’t outdoors with his family, he's brewing a coffee or dreaming up an adventure…..