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Summary of Post-Cardiac Arrest Syndrome 2008 Guidelines

Four Processes of Post-Cardiac Arrest Syndrome

  1. Post-Cardiac arrest brain injury
  2. Post-cardiac arrest myocardial injury
  3. Systemic ischemia/reperfusion response
  4. Treatment of precipitating pathology

Post-Cardiac arrest brain injury
Failure of cerebral microcirculation
No-reflow (transient intravascular thrombi when untreated cardiac arrest exceeds 15 minutes – thrombolytics may help)
Hyperoxia during the early stages of reperfusion harms postischemic neurons by causing oxidative stress (goal O2 sat is 94-96%)
MAP during first two hours after ROSC positively correlated with neurological outcome
Pyrexia > 37.8 associated with increased risk of brain death
Hyperglycemia is associated with poor neurological outcomes
Seizures associated with worse neurological prognosis
No benefit to “protective hypercapnia”

Post-cardiac arrest myocardial injury
Decreased LVEF is usual due to hibernation and reverses over time
CI nadirs at 8 hours and improves by 24 hours and normal by 72 hours

Systemic ischemia/reperfusion response
CPR only partial reverses ischemia and leaves an oxygen debt
“Endotoxin tolerance” leads to increased risk of infection
Coagulation/anticoagulation/fibrinolysis/antifibrinolysis systems are activated
Relative adrenal insufficiency is common after ROSC

Treatment of precipitating pathology
50% of out-of-hospital arrest is ACS whereas only 11% of in-patient arrest is ACS
Identify cause:
ACS
Pulmonary embolism
Respiratory arrest from COPD/asthma or PNA
Asphyxiation
Sepsis
Hypovolemia
Hypo/hyperkalemia and metabolic disorders
Cardiac tamponade
Tension PTX
Cerebrovascular catastrophes
Drug overdose, toxins and intoxication
Trauma

Treatment

Goals
CVP 8-12 mmHg
MAP 65-90 mmHg (higher MAP for longer time to ROSC, lower MAPs for those undergoing evolving MI)
Scvo2 > 70%
Hct > 30%
Lactate <= 2 mmol/L or decreasing
UOP >= 0.5 (or 1.0 mL/kg/hr in therapeutic hypothermia)
CPP is primarily dependent on maintaining MAP
Oxygenation Saturation 94-96%
Normocarbia

Pathology that can elevate CVP independent of volume status
Cardiac tamponade
Right-sided MI
PE
Tension PTX

Circulatory Support
Dysrhythmias
No evidence to support prophylactic antiarrhythmics
Reperfusion is the best way to correct dysrhythmias due to focal ischemia

Hypotension
IVF (3.5-6.5L crystalloid within 24 hours in one study)

Low Cardiac Index
Inotropes and vasopressors
Early echocardiography
Inotropes may exacerbate ACS
Intra-aortic balloon pump to augement myocardial perfusion
ECMO

Management of ACS
Chest pain and ST elevation are poor predictors of acute coronary occlusion
Early PCI in patients with ST-elevation MI or when ACS is suspected
Therapeutic Hypothermia (PCI may be done while cooling is being initiated)

Complications of Hypothermia Protocol
Bradycardia
Hypothermia increases SVR which may decrease CO
Hypothermia induced diuresis leads to loss of electrolytes which may cause dysrhythmias
Pyrexia is common after rewarming even in the absence of infection

Seizure Control and Prevention
Clonazepam is the DOC for myoclonus
EEG monitoring of paralyzed patients

Adrenal Dysfunction
Consider for refractory hypotension
Routine use is not recommended

Renal Failure
In one study 7% of patient required HD regardless of whether hypothermia was used

Infection
High risk for aspiration and PNA within 48 hours of intubation

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