Cardiac arrest & anoxic brain injury

Today we discussed the case of a young man with Duchenne’s Muscular Dystrophy complicated by chronic respiratory failure and dilate cardiomyopathy who was found down at home in asystolic arrest.  Though ROSC was achieved en route to the hospital, patient suffered significant sequelae of anoxic brain injury.


Clinical Pearls

  • Most common causes of out-of-hospital cardiac arrests are
    • Acute MI
    • Cardiomyopathy
    • Primary arrhythmia
  • Most immediate threat to survival post cardiac arrest is cardiovascular collapse.
  • Most common cause of death in out-of-hospital cardiac arrests is neurologic injury.
  • Post cardiac arrest hemodynamic targets
    • SpO2 > 40%
    • PaCO2 > 40
    • MAP >65 (preferably 80-100 mmHg)
  • Read below for more info on the ongoing battle between therapeutic hypothermia (TH) and targeted temperature management (TTM) to reduce brain injury.

Post cardiac arrest management

Goals

  • Determining and treating cause of arrest
  • Minimizing brain injury
  • Managing cardiovascular dysfunction
  • Managing problems that arise from global ischemia and reperfusion injury

Most immediate threat to survival post ROSC is cardiovascular collapse.

  • Correct hypotension to maintain end-organ perfusion
  • Optimize oxygenation and ventilation
  • Correct electrolyte abnormalities

Determining cause and extent of injury:

  • Focused history
  • Exam:
    • Remember ABCs
    • Baseline neurologic exam
      • Make sure patient is off sedation or neuromuscular blocking agents
      • Brainstem reflexes:
        • Pupillary
        • Corneal
        • Oculocephalic
        • Gag
        • Cough
      • GCS ⇒ with special attention to motor score as it correlates with neurologic recovery
    • Work up
      • Causes
        • Most common are acute MI, cardiomyopathy, and primary arrhythmia ⇒ check ECG!
        • Labs
          • ABG
          • Basic electrolytes and liver function studies
          • CBC
          • Troponin q8-12 hours for 24 hours
          • Trend lactate
          • Toxicology studies
        • Management
          • Ventilator:
            • Target SpO2 >94% and PaCO2 > 40
              • Avoid hyperventilation because it leads to cerebral vasoconstriction and worsening cerebral perfusion
              • Avoid hyperoxia ⇒ a systematic review of 14 observational studies found that those with PaO2>300 mmHg had a higher in-patient mortality following cardiac arrest
          • Hemodynamics
            • Keep MAP >65 mmHg and preferably 80-100 mmHg to optimize cerebral perfusion
            • Prevent arrhythmia with meds only if patient has recurrent or ongoing unstable arrhythmia. No data on routine prophylactic use of these agents in other patients.
            • Coronary revascularization if indicated
          • Decrease brain injury
            • Targeted temperature management (TTM) and therapeutic hypothermia (TH)
              • Rationale
                • Neurologic injury is the most common cause of death in patients with out-of-hospital cardiac arrest
              • Indications
                • Anyone not following commands or showing purposeful movements following resuscitation from cardiac arrest
              • Contraindication
                • Active non-compressible bleeding
                • TH is associated with higher risk of bleeding in patients undergoing coronary cath or those who received thrombolytics
              • Timing
                • To be achieved as soon as possible and maintained for at least 48 hours
                  • Rate of good functional outcome is higher with 48 hours rather than 24
                • Avoid fever at all costs in the first 48 hours
              • Goal temperature
                • This is an area of much debate amongst neurologists and intensivists.  There are two main goal temperatures:
                  • 33ºC (TH)
                    • The studies in support of cooling to a temperature of 33 come from two landmark NEJM papers published back in 2002 (HACA and OHCA) which found that mild to moderate hypothermia improved neurologic outcomes post cardiac arrest.  The caveats were that all these patients had VF/VT arrest (not PEA/asystole), no baseline brainstem function was reported before randomization, and the sample sizes were small. Based on these findings, TH is recommended for anyone with the following:
                      • Deep coma (loss of motor response or brainstem reflexes)
                      • Malignant EEG patterns
                      • Early CT changes suggesting development of cerebral edema
                    • Adverse effects:
                      • Increased rates of infection
                      • Coagulopathy and bleeding
                      • Cold diuresis
                      • Bradycardia and QT prolongation induced cardiac arrhythmias
                  • 36ºC (TTM)
                    • The TTM trial published in 2012 is the largest study on the topic that randomized 939 patients with out-of-hospital cardiac arrests to 33 or 36 degrees temp regulation and found no difference in all cause mortality or neurologic recovery between the two groups.  They included all patients regardless of type of arrest (VF/VT/asystole/PEA).  In subgroup analyses, they found no difference in outcomes based on type of initial rhythm, shock on presentation, age, gender, or time from cardiac arrest to ROSC.
                • So what to do?
                  • General consensus seems to be that avoiding fever at all cost in the first 48 hours is the most important intervention.  Beyond that, keeping patients at 36 might be better as further cooling is associated with risks and no clear indication of benefit based on our best available evidence.
            • General critical care
              • Elevate HOB to 30 degrees
              • Stress ulcer ppx
              • DVT ppx
              • Early PT/OT
              • Seizures and myoclonic jerks
                • Common and a marker of more severe brain injury
                • Continuous EEG recommended if available
                • No benefit in prophylactic treatment

Anoxic brain injury

Nomenclature

  • Brain death: irreversible cessation of cerebral and brainstem function
  • Persistent vegetative state: subgroup that suffers from severe anoxic brain injury and progresses to a state of wakefulness without awareness
  • Minimally conscious state: can have some purposeful movements or interactions with the environment.

Clinical parameters associated with an unfavorable prognosis

Clinical parameters Unfavorable prognosis
Duration of anoxia >8-10 minutes
Duration of CPR >30 minutes
Pupillary light reaction Absent on day 3
Motor response to pain Absent on day 3
Brainstem reflexes Absent
Blood glucose on admission >300 mg/dL
Glascow coma score on day 3 <5
Table above adapted from UpToDate

Work up:

  • Somatosensory evoked potentials (SSEPs): absent response at 24-72 hours appears to be most useful in identifying those with poor prognosis
  • EEG: can be affected by sedative drugs, metabolic derangements, and sepsis so careful with interpreting its findings!
  • Lab test for neuron-specific enolase (NSE)
    • Markedly elevated levels are associated with poor outcomes but no clear cut-off established
  • Imaging:
    • CT/MRI: look for edema and inversion of gray-white densities associated with poor outcome.

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