Cardiovascular Disease is the Leading Cause of Death in Almost All Industrialized Nations
Nearly 50% of All Cardiovascular Mortality is from Sudden Cardiac Death
Out-of-Hospital Cardiac Arrest Affects 325k Persons Per Year in the US
Age: average age of cardiac arrest in the US is 60 y/o
After Age 40, an American Male Has a 1 in 8 Chance of Having Sudden Cardiac Death
Etiology
Acute Coronary Syndrome (ACS) (see Coronary Artery Disease, [[Coronary Artery Disease]]): may result in cardiac arrest either via myocardial dysfunction or via ventricular arrhythmia resulting from ischemia or prior scar formation
In Cardiopulmonary Arrest, Systemic and Pulmonary Vascular Perfusion is Very Low Despite Optimal Cardiopulmonary Resuscitation (CPR): for this reason, ventilation-perfusion relationships can be maintained with low minute ventilation
Clinical Manifestations
General Comments
Post-Cardiac Arrest Syndrome
General Comments
Determination of Severity of Post-Cardiac Arrest Syndrome: SOFA score at ICU admission is associated with the 28-day mortality rate [MEDLINE]
Hypotension/Shock (see Hypotension, [[Hypotension]])
Physiologic Mechanisms
Intravascular Volume Depletion
Myocardial Dysfunction
Therapeutic Hypothermia (see Therapeutic Hypothermia, [[Therapeutic Hypothermia]]): if used, may cause hypotension in some cases (although therapeutic hypothermia usually increases SVR)
American Academy of Neurology Practice Parameter (Neurology, 2006) [MEDLINE]: burst suppression or generalized epileptiform discharges predict poor outcome, but with insufficient prognostic accuracy (recommendation level C)
Intracranial Pressure (ICP) Monitoring/Brain Oxygenation Monitoring: ICP >20 mm Hg has been associated with poor outcome in comatose patients in some studies
American Academy of Neurology Practice Parameter (Neurology, 2006) [MEDLINE]: insufficient data to determine the utility of monitoring of brain oxygenation (SjO2) and intracranial pressure monitoring
Neurologic Exam
Peripheral Blood Neuron-Specific Enolase (NSE) and S100 Beta (see Neuron-Specific Enolase, [[Neuron-Specific Enolase]])
Neuron-specific enolase is released into cerebrospinal fluid, cerebral circulation, and systemic circulation after brain injury: elevated levels 72 hrs after cardiac arrest are an indicator of hypoxic brain damage and correlate significantly with neurologic outcome
American Academy of Neurology Practice Parameter (Neurology, 2006) [MEDLINE]: serum neuro-specific enolase level >33 g/L at days 1-3 post-CPR accurately predicts poor outcome (recommendation level B)
American Academy of Neurology Practice Parameter (Neurology, 2006) [MEDLINE]: the assessment of poor prognosis can be guided by the bilateral absence of cortical SSEPs (N2O response) within 1-3 days (recommendation level B)
However, the presence of somatosensory evoked potentials does not necessarily guarantee a good neurological outcome
Physiology: post-mortem studies indicate severe ischemic brain/brainstem/spinal cord damage (a pathologic pattern which is distinct from that of status epilepticus) [MEDLINE]
Clinical
Persistent Bilaterally Synchronous Myoclonus in the Face/Limbs/Axial Musculature, Often with Eye Opening and Upward Deviation of the Eyes: importantly this must be distinguished from status epilepticus (see Seizures, [[Seizures]])
Prognosis
Myoclonic Status Epilepticus has Been associated with Poor Outcome (Even in Patients with Intact Brainstem Reflexes and Some Motor Response): however, cases with good recovery have been reported where the circulatory arrest was secondary to respiratory failure
American Academy of Neurology Practice Parameter (Neurology, 2006) [MEDLINE]: myoclonic status epilepticus within the first day after a primary circulatory arrest carries a poor prognosis (Recommendation Level B)
Active Chest Compression-Decompression Cardiopulmonary Resuscitation (CPR)
Rationale: xxx
Clinical Efficacy
Systematic Review of Active Chest Compression-Decompression CPR Device in In-Hospital/Out-of-Hospital Cardiac Arrest (Cochrane Database Syst Rev, 2013) [MEDLINE]: device had no clinical benefit
Review of the Use of Bicarbonate in Cardiac Arrest (J Clin Med Res 2016) [MEDLINE]
Bicarbonate Can Have Deleterious Effects During Cardiac Arrest, Including Increasing Intracellular Acidosis, Decreasing Cardiac Output, Shifting the Oxygen Dissociation Curve to the Left (with Increased Affinity of Hemoglobin for Oxygen Resulting in Decreased Oxygen Release to Tissues), Causing Hypernatremia, and Causing Hyperosmolarity
Recommendations (2010 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
Routine Use of Sodium Bicarbonate is Not Recommended for Patients in Cardiac Arrest
Sodium Bicarbonate (1 mL/kg Boluses as Required) is Indicated to Maintain Hemodynamic Stability (Adequate MAP) and QRS Narrowing in Cases of Severe Cardiotoxicity or Cardiac Arrest from Hyperkalemia or Tricyclic Antidepressant Overdose (see Hyperkalemia, [[Hyperkalemia]] and Tricyclic Antidepressants, [[Tricyclic Antidepressants]])
Bystander Cardiopulmonary Resuscitation (CPR)
Rationale: xxx
Clinical Efficacy
Meta-Analysis of Predictors of Outcome After Out-of-Hospital Cardiac Arrest (n = 142,740 Patients from 79 Studies) (2010) [MEDLINE]: although 53% (95% CI, 45.0% to 59.9%) of out out-of-hospital cardiac arrests are witnessed by a bystander, only 32% (95% CI, 26.7% to 37.8%) receive bystander CPR
Implementation of Bystander Compression-Only CPR for Out-of-Hospital Cardiac Arrest in Arizona (JAMA, 2010) [MEDLINE]
Program significantly increased the rate of CPR
Lay person compression-only CPR increased survival, as compared with conventional CPR and no bystander CPR
Lay person compression-only CPR improved neurologic outcome
Early Defibrillation (see Defibrillation, [[Defibrillation]])
Rationale: xxx
Clinical Efficacy
Study of Continuous Quality Improvement Approach in Out-of-Hospital Cardiac Arrest in Arizona (2013) [MEDLINE]
Early defibrillation is associated with improved outcome
Bystander CPR is associated with improved outcome
CPR witnessed by emergency medical personnel is associated with improved outcome
Early Echocardiographic Assessment
Rationale: early echocardiography allows assessment of degree of myocardial dysfunction and allows exclusion of pericardial effusion as an etiology
Mechanical Chest Compressions with Defibrillation During Ongoing Compressions (Mechanical CPR)
Rationale: xxx
Clinical Efficacy
LINC Trial Studying Mechanical Chest Compressions with Defibrillation During Ongoing Compressions (Mechanical CPR) in Out-of-Hospital Cardiac Arrest (JAMA, 2014) [MEDLINE]: mechanical CPR with defibrillation during CPR did not improve mortality rate at 4 hrs or nurologic outcomes at 6 mo
Mechanical Ventilation
Avoidance of Hyperventilation: positive pressure ventilation during CPR (especially if aggressive) increases intrathoracic pressure, resulting in a decrease in venous return and an undesirable increase in intracerebral pressure
History: protocol was developed at the University of Arizona Sarver Heart Center and was first instituted in Tucson, Arizona, in late 2003
Rationale: protocol focuses on maximizing myocardial and cerebral perfusion via various features
Minimization of Interruption of Chest Compressions
Provision of Immediate Preshock Chest Compressions for Prolonged Ventricular Fibrillation (VF)
Decrease in the Time Interval to Intravenous Epinephrine Administration
Delay/Elimination in Endotracheal Intubation
Minimization of Positive Pressure Ventilation: positive pressure ventilation during CPR (especially if aggressive) increases intrathoracic pressure, resulting in a decrease in venous return and an undesirable increase in intracerebral pressure
For These Reasons, Passive Oxygenation May Instead Be Preferred
Clinical Efficacy
Study of Minimally Interrupted Cardiac Resuscitation (MICR) by Emergency Services Personnel in Out-of-Hospital Cardiac Arrest (JAMA, 2008) [MEDLINE]: MICR improved survival to hospital discharge
Study of Cardiocerebral Resuscitation (J Am Coll Cardiol, 2013) [MEDLINE]: cardiocerebral resuscitation increased survival of patients with primary cardiac arrest in Arizona over a 5-year period from 17.7% to 33.7%
Pre-Hospital Therapeutic Hypothermia (see Therapeutic Hypothermia, [[Therapeutic Hypothermia]])
Clinical Efficacy
Pre-Hospital Mild Hypothermia After Cardiac Arrest (JAMA, 2014) [MEDLINE]: pre-hospital cooling reduced core temperature by hospital arrival and reduced the time to reach a temperature of 34°C, but it did not improve survival or neurological outcome
Pre-Hospital Mild Hypothermia After Cardiac Arrest (J Am Heart Assoc, 2015) [MEDLINE]: pre-hospital hypothermia did not improve neurological outcome or 1‐year mortality rate
Systematic Review of Pre-hospital Versus In-Hospital Therapeutic Hypothermia After Out-of-Hospital Cardiac Arrest (Cochrane Database Syst Rev, 2016) [MEDLINE]: no convincing evidence to delineate beneficial or harmful effects of pre-hospital induction of cooling, as compared to in-hospital induction of cooling (based on low quality evidence)
Recommendations (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
Pre-Hospital Hypothermia with Rapid Infusion of Cold Intravenous Fluids is Not Recommended: no evidence that this intervention has clinical benefit
Treatment-First 24 Hours of Hospital Care
Acute Coronary Syndrome (ACS) Management
Rationale
Early Coronary Angiogram is Often Required: since 40% of cardiac arrests caused by unstable coronary plaques may be missed if decision making is based on EKG criteria alone
In the cardiac arrest population with ST elevation, significant coronary lesions amenable to treatment are found in 96% of cases [MEDLINE]
In the cardiac arrest population without ST elevation, significant coronary lesions amenable to treatment are found in 58% of patients [MEDLINE]
Although Many Clinicians Advocate Waiting to Assess for Neurologic Recovery Prior to Coronary Angiogram, the Probablity for Neurologic Recovery Cannot Usually Be Determined Reliably at the Time that Emergency Cardiovascular Interventions are to Be Performed
Combination Hypothermia and Coronary Intervention: may be more efficacious than each therapy alone
Clinical Efficacy
PROCAT Registry Data (Circ Cardiovasc Interv, 2010) [MEDLINE]: PCI is an independent predictor of survival regardless of the initial EKG findings
Recommendations (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
Coronary Angiogram Should Be Performed Emergently For Out-of-Hospital Cardiac Arrest with Suspected Cardiac Etiology and ST Elevation
Coronary Angiogram is Reasonable for Comatose Adult Patients with Out-of-Hospital Cardiac Arrest with Suspected Cardiac Etiology and Without ST Elevation
Coronary Angiogram is Reasonable in Post–Cardiac Arrest Patients for Whom Coronary Angiogram is Indicated Regardless of Whether the Patient is Comatose or Awake
Early Echocardiographic Assessment
Rationale: early echocardiography allows assessment of degree of myocardial dysfunction and allows exclusion of pericardial effusion as an etiology
Recommendations (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
It is Reasonable to Prevent/Treat Fever in the Post-Cardiac Arrest Period (After the Period of Therapeutic Hypothermia): although data on treating fever in the post-cardiac arrest period is poor, fever is associated with worsened neurologic injury in other clinical situations
Glucose Management
Recommendations (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
No Clear Glucose Goals Can Be Recommended
Hemodynamic Management
Rationale: optimal hemodynamic targets are unknown in the post-cardiac arrest period
Swan-Ganz Catheter Monitoring (see Swan-Ganz Catheter, [[Swan-Ganz Catheter]])
Clinical Efficacy
Systematic Review/Meta-Analysis of Clinical Efficacy of IABP in STEMI (Eur Heart J, 2009) [MEDLINE]
Pooled randomized data do not support the use of IABP in patients with high-risk STEMI
There is insufficient evidence endorsing the current guideline recommendation for the use of IABP therapy in the setting of STEMI complicated by cardiogenic shock
Single Center Trial Using a Post-Resuscitation Algorithm, Including Early Initiation of Therapeutic Hypothermia (Resuscitation, 2009 [MEDLINE]: post-resuscitative algorithm resulted in a non-statistically significant 28% improvement in mortality in 20 patients compared with historical controls
Recommendations (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
Target MAP: unclear, but published guidelines suggest anywhere from 65-80+ mm Hg (accounting for patient’s normal blood pressure and the degree of myocardial dysfunction)
Respiratory Management
Clinical Efficacy
Following Out-of-Hospital Arrest, Arterial Hyperoxia is Associated with Increased Mortality Rate [MEDLINE]
Recommendations (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
Maintain Normoxia: avoid hyperoxia and hypoxia
Maintain Normal pCO2 (Eucapnia)
When Patient Temperature is Below Normal (During Hypothermia), Laboratory Values Reported for pCO2 Might Be Higher than the Actual Values in the Patient
Myoclonic Status Epilepticus Management
Clonazepam (Klonopin, Rivotril, Clonotril) (see Clonazepam, [[Clonazepam]]): may be used
Valproic Acid (see Valproic Acid, [[Valproic Acid]]): may be useful
Propofol (Diprivan) (see Propofol, [[Propofol]]): limited data suggests utility
Recommendations (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
EEG Should Be Performed in Comatose Patients After Cardiac Arrest to Detect Seizure Activity
If Present, Seizures Should Be Treated By Standard Therapies
Impact of Continuous EEG During Therapeutic Hypothermia Following Cardiac Arrest (Neurology, 2013) [MEDLINE]: grades 1 and 3 EEG severity grading scale during therapeutic hypothermia and normothermia correlated with outcome -> however, treatment of seizures did not improve outcome
Combination Hypothermia and Coronary Intervention: may be more efficacious than each therapy alone
Indications
Coma Post-Cardiac Arrest: inability to follow commands or demonstrate purposeful movements
Patients Receiving Thrombolytics: therapeutic hypothermia is associated with an increased risk of hemorrhage in this population
Patients Undergoing Coronary Catheterization: therapeutic hypothermia is associated with an increased risk of hemorrhage in this population [MEDLINE]
Contraindications: pregnancy and hemodynamic instability are not considered specific contraindications to therapeutic hypothermia
Active Non-Compressible Hemorrhage: although temperature management to 36 degrees C or below in this population may still be attempted
Systematic Review and Meta-Analysis of the Impact of Therapeutic Hypothermia on the Risk of Hemorrhage (Medicine, 2015) [MEDLINE]
Therapeutic Hypothermia was Not Associated with an Increased Risk of Hemorrhage, Despite Increased Risk of Thrombocytopenia and Increased Transfusion Requirements
However, Prolonged Duration of Cooling May Be Associated with an Increased Risk of Hemorrhage
Advanced Directive Stating No Desire for Aggressive Care
Technique: most are easily managed in the intensive care unit
Arctic Sun Device
Surface Cooling with Cooling Blankets/Ice Packs
Endovascular Cooling Catheters: more accurate and reliable at maintaining target temperature than other methods
Gaymar Medi-Therm II
Transnasal Evaporation: novel method which may be used during cardiac arrest
Physiologic Effects of Therapeutic Hypothermia
Cardiovascular
Decreased Heart Rate
Decreased Infarct Size with Cardiac Arrest or Acute Myocardial Infarction
Increased Myocardial Salvage: with use of therapeutic hypothermia before revascularization in STEMI
Increased Systemic Vascular Resistance (SVR)
Neurologic
Decreased Cerebral Oxygen Demand
Decreased Formation of Reactive Oxygen Species in Brain
Coagulopathy (see Coagulopathy, [[Coagulopathy]]): usually mild (occurs due to impairment of both clotting factor and platelet function below 35 degrees C)
“Cold Diuresis”: may result in hypovolemia, hypokalemia, hypomagnesemia, and hypophosphatemia
Decreased Metabolism/Excretion of Medications
Electrolyte Abnormalities
Hyperkalemia (see Hyperkalemia, [[Hyperkalemia]]): during rewarming from hypothermia (potassium shifts extracellularly)
Hypokalemia (see Hypokalemia, [[Hypokalemia]]): during induction of hypothermia (potassium shifts intracellularly)
Hyperglycemia (see Hyperglycemia, [[Hyperglycemia]]): due to insulin resistance
Increased Risk of Infection: hypothermia impairs leukocyte function
No Effect on Vasopressor Requirement
Therapeutic Hypothermia May Impair the Prognostic Utility of Somatosensory Evoked Potentials and Serum Neuron-Specific Enolase (NSE) (see Somatosensory Evoked Potentials, [[Somatosensory Evoked Potentials]] and Serum Neuron-Specific Enolase, [[Serum Neuron-Specific Enolase]]) [MEDLINE] [MEDLINE]: for this reason, caution must be exercised with regard to determining prognosis in the setting of therapeutic hypothermia
Clinical Efficacy
Hypothermia After Cardiac Arrest Study Group (HACA) Trial (NEJM, 2002) [MEDLINE]: therapeutic hypothermia (32-34 degrees C) improved neurologic outcome after cardiac arrest due to ventricular fibrillation
Trial of Therapeutic Hypothermia in Comatose Survivors of Out-of-Hospital Cardiac Arrest (NEJM, 2002) [MEDLINE]: therapeutic hypothermia (33 degrees C) improved neurologic outcome after cardiac arrest
Hypothermia was associated with a lower cardiac index, higher systemic vascular resistance, and hyperglycemia
TTM Trial: Therapeutic Hypothermia (33°C versus 36°C) After Cardiac Arrest (NEJM, 2013) [MEDLINE]: hypothermia to 33°C did not confer a benefit as compared with hypothermia to 36°C
Pre-Hospital Mild Hypothermia After Cardiac Arrest (JAMA, 2014) [MEDLINE]: pre-hospital cooling reduced core temperature by hospital arrival and reduced the time to reach a temperature of 34°C, but it did not improve survival or neurological outcome
Pre-Hospital Mild Hypothermia After Cardiac Arrest (J Am Heart Assoc, 2015) [MEDLINE]: pre-hospital hypothermia did not improve neurological outcome or 1‐year mortality rate
Systematic Review of Pre-hospital Versus In-Hospital Therapeutic Hypothermia After Out-of-Hospital Cardiac Arrest (Cochrane Database Syst Rev, 2016) [MEDLINE]: no convincing evidence to delineate beneficial or harmful effects of pre-hospital induction of cooling, as compared to in-hospital induction of cooling (based on low quality data)
Systematic Review of Therapeutic Hypothermia After Cardiac Arrest (Cochrane Database Syst Rev, 2016) [MEDLINE]: therapeutic hypothermia improves neurologic outcome after cardiac arrest (based on moderate quality evidence)
Insufficient evidence to show the effects of therapeutic hypothermia with in-hospital cardiac arrest, asystole, non-cardiac causes of arrest
Recommendations (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
Therapeutic Hypothermia is Recommended (Between 32-36 Degrees) for At Least 24 hrs for Comatose Adult Patients with Return of Spontaneous Circulation After Cardiac Arrest (Including In-Hospital Cardiac Arrest)
The temperature sensitivity of the brain after cardiac arrest may persist as long as the brain dysfunction (coma) is present: consequently, the upper limit time duration for temperature management is unknown
Similar recommendation was provided from the 2015 Recommendations from the International Liaison Committee on Resuscitation (ILCOR)
Pre-Hospital Hypothermia with Rapid Infusion of Cold Intravenous Fluids is Not Recommended: no evidence that this intervention has clinical benefit
Treatment-Further Care
Consideration of Need for Automatic Implantable Cardioverter-Defibrillator (AICD) Placement (see Automatic Implantable Cardioverter-Defibrillator, [[Automatic Implantable Cardioverter-Defibrillator]])
Indications
xxx
Consideration of Need for Rehabilitation
xxx
Prognosis
Survival from Out-of-Hospital Cardiac Arrest (2010 Meta-Analysis) [MEDLINE]
Survival Rates from Out-of-Hospital Cardiac Arrest Have Been Stable for the Past 30 Years
Survival Rate to Hospital Admission: 23.8% (95% CI, 21.1 to 26.6)
Survival Rate to Hospital Discharge: 7.6% (95% CI, 6.7 to 8.4)
Positive Predictors of Survival to Hospital Discharge in Out-of-Hospital Cardiac Arrest
Cardiac Arrest Witnessed by a Bystander: survival to hospital discharge increased from 6.4% to 13.5%
Witnessed by Emergency Medical Services Personnel: survival to hospital discharge increased from 4.9% to 18.2%
Patient Received Bystander CPR: survival to hospital discharge increased from 3.9% to 16.1%
Patient was Found in Ventricular Fibrillation/Ventricular Tachycardia: survival to hospital discharge increased from 14.8% to 23.0%
Arrests due to asystole/pulseless electrical activity (PEA) (non-shockable rhythms) generally have poorer outcomes than arrest from ventricular tachycardia/ventricular fibrillation (shockable rhythms)
Patient Achieved Return of Spontaneous Circulation: survival to hospital discharge increased from 15.5% to 33.6%
Neurologic Prognosis Related to the Duration of Cardiopulmonary Resuscitation (CPR)
Study of Survival After CPR for Out-of-Hospital Cardiac Arrest (Eur Neurol, 1997) [MEDLINE]: no patient who required >15 min of CP survived >6 wks
Initial Survival: 44% of patients
Survival at 24 hrs: 30% of patients
Survival at 1 mo: 13% of patients
Survival at 6 mo: 6% of patients
Neurologic Prognosis Related to Clinical Findings [MEDLINE]
Clinical Parameters Associated with Poor Prognosis
Duration of Anoxia: >8-10 min
Duration of CPR: >30 min
Pupillary Light Response: absent on day 3
Motor Response to Pain: absent on day 3
Brainstem Reflexes: absent
Blood Glucose on Admission: >300 mg/dL
Glasgow Coma Scale: <5 on day 3
Glasgow-Pittsburgh Coma Score (GPCS): <22 on day 3
Patients with Virtually No Chance of Regaining Independence
Initial Exam: no pupillary light reflex
Day 1 Exam: motor response no better than flexor and spontaneous eye movements neither orienting nor roving conjugate
Day 3 Exam: motor response no better than flexor, no spontaneous eye opening
Day 7 Exam: motor response not obeying commands and spontaneous eye movements neither orienting nor roving conjugate
Day 14 Exam: oculocephalic response not normal, not obeying commands, no spontaneous eye opening, eye opening not improved at least 2 grades from initial examination
Patients with Best Chance of Regaining Independence
Initial Exam: pupillary light reflexes present and motor response flexor or extensor; spontaneous eye movements roving conjugate or orienting
Day 1 Exam: motor response withdrawal or better and eye opening improved at least 2 grades
Day 3 Exam: motor response withdrawal or better and spontaneous eye movements normal
Day 7 Exam: motor response obeying commands
Day 14 Exam: normal oculocephalic response
Clinical Findings Which Predict Poor Prognosis (American Academy of Neurology Practice Parameter; Neurology, 2006) [MEDLINE]: with 100% specificity
Within First Day After Primary Circulatory Arrest: presence of myoclonic status epilepticus (recommendation level B)
Day 3 Exam: absent or extensor motor responses (recommendation level A)
Day 3 Exam: absent pupillary or corneal reflexes (recommendation level A)
Neurologic Prognostication Guidelines (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
Timing of Assessment
The Earliest Time That Neurologic Prognostication Can Usually Be Made by Clinical Exam is 72 hrs After Cardiac Arrest or After Return to Normothermia: this time period may be even longer if sedatives/paralytics are involved
In Patients Treated/Not Treated with Therapeutic Hypothermia, the Absence of Pupillary Response to Light at 72 hrs or More After Cardiac Arrest is a Reasonable Exam Finding Which Predicts Poor Neurologic Outcome
Motor Findings/Myoclonus
Absent Motor Movements or Extensor Posturing Should Not Be Used Alone to Predict Neurologic Outcome
Mycoclonus Should Not Be Used Alone to Predict Neurologic Outcome
Status Myoclonus (In Combination with Other Diagnostic Testing) at 72-120 hrs After Cardiac Arrest is a Reasonable Finding to Predict Poor Neurologic Outcome
Seizures/Electroencephalogram Findings
In Comatose Post–Cardiac Arrest Patients Who are Treated with Therapeutic Hypothermia, Persistent Absence of EEG Reactivity to External Stimuli at 72 hrs After Cardiac Arrest and Persistent Burst Suppression After Rewarming Predict a Poor Neurologic Outcome
Intractable and Persistent (>72 hrs) Status Epilepticus in the Absence of EEG Reactivity to External Stimuli Predicts a Poor Neurologic Outcome
In Comatose Post–Cardiac Arrest Patients Who are Not treated with Therapeutic Hypothermia, Burst Suppression on EEG at 72 hrs or More After Cardiac Arrest (In Combination with Other Diagnostic Testing) Predicts a Poor Neurologic Outcome
Brain Imaging
In Patients Who are Comatose After Resuscitation from Cardiac Arrest and Not Treated with Therapeutic Hypothermia, it May be Reasonable to Use the Presence of a Marked Reduction of the Gray/White Ratio on Head CT Obtained Within 2 hrs After Cardiac Arrest to Predict Poor Outcome
It May Be Reasonable to Consider Extensive Restriction of Diffusion on Brain MRI at 2-6 days After Cardiac Arrest in Combination with Other Established Predictors to Predict a Poor Neurologic Outcome
Serum Neuron-Specific Enolase (NSE)
Given the Possibility of High False-Positives, Blood Levels of NSE and S-100B Should Not Be Used Alone to Predict a Poor Neurologic Outcome
Somatosensory Evoked Potentials
In Comatose Post–Cardiac Arrest Patients Regardless of Treatment with Therapeutic Hypothermia, Bilateral Absence of the N20 Somatosensory Evoked Potential Wave 24-72 hrs After Cardiac Arrest or After Rewarming Predicts a Poor Neurologic Outcome
Neurologic Prognosis Post-Anoxic Vegetative State in Subacute Setting
Study of Coma Recovery Scale-Revised (CRS-R) (Neurology, 2013) [MEDLINE]
CRS-R >6 at 1 mo Post-Injury: predicts subsequent recovery of responsiveness within the next 24 mo
References
General
The prognostication of cerebral hypoxia after out-of-hospital cardiac arrest in adults. Eur Neurol. 1997;37(3):135 [MEDLINE]
Systematic review of early prediction of poor outcome in anoxic-ischaemic coma. Lancet. 1998;352(9143):1808 [MEDLINE]
Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation. JAMA. 1999;281:1182-1188
Time course of serum neuron-specific enolase: A predictor of neurological outcome in patients resuscitated from cardiac arrest. Stroke 1999; 30:1598-1603 [MEDLINE]
The prognostic value of evoked responses from primary somatosensory and auditory cortex in comatose patients. Clin Neurophysiol 2003; 114:1615-1627 [MEDLINE]
Serum neuron-specific enolase predicts outcome in post-anoxic coma: A prospective cohort study. Intensive Care Med 2003; 29:189-195 [MEDLINE]
Is this patient dead, vegetative, or severely neurologically impaired? Assessing outcome for comatose survivors of cardiac arrest. JAMA. 2004;291(7):870 [MEDLINE]
International Liaison Committee on Resuscitation. 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care with Treatment Recommendations. Circulation. 2005;112:III–1-III–136
Predicting survival from out-of-hospital cardiac arrest: a graphic model. Ann Emerg Med. 1993;22:1652-1658
Estimating effectiveness of cardiac arrest interventions: a logistic regression survival model. Circulation. 1997;96:3308-3313
Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006;67(2):203 [MEDLINE]
Scientific knowledge gaps and clinical research priorities for cardiopulmonary resuscitation and emergency cardiovascular care identified during the 2005 International Consensus Conference on ECC and CPR Science with Treatment Recommendations. Resuscitation 2007; 75(3):400-411
Predictors of survival from out-of-hospital cardiac arrest. A systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes 2010;3:63-81 [MEDLINE]
Post cardiac arrest syndrome: a review of therapeutic strategies. Circulation. 2011 Apr 5;123(13):1428-35 [MEDLINE]
Cerebral Performance Category and long-term prognosis following out-of-hospital cardiac arrest. Crit Care Med. 2013 May;41(5):1252-7. doi: 10.1097/CCM.0b013e31827ca975 [MEDLINE]
Predictors of recovery of responsiveness in prolonged anoxic vegetative state. Neurology. 2013 Jan;80(5):464-70. Epub 2013 Jan 9 [MEDLINE]
SOFA score to assess the severity of the post-cardiac arrest syndrome. Resuscitation. 2016 Mar 7;102:110-115. doi: 10.1016/j.resuscitation.2016.03.001 [MEDLINE]
Treatment
General
Passive oxygen insufflation is superior to bag-valve-mask ventilation for witnessed ventricular fibrillation out-of-hospital cardiac arrest. Ann Emerg Med. 2009;54:656–660 [MEDLINE]
Improved patient survival using a modified resuscitation protocol for out-of-hospital cardiac arrest. Circulation. 2009;119:2597–2605 [MEDLINE]
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 8: Adult advanced cardiovascular life support. Circulation 2010; 122(18 Suppl 3):S729-S767
Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S829-861 [MEDLINE]
Prognostication after cardiac arrest and hypothermia: a prospective study. Ann Neurol 2010;67(3):301 [MEDLINE]
Long-term cognitive outcomes following out-of-hospital cardiac arrest: a population-based study. Neurology. 2011;77(15):1438 [MEDLINE]
Timing of neuroprognostication in postcardiac arrest therapeutic hypothermia. Crit Care Med. 2012 Mar;40(3):719-24 [MEDLINE]
Alternative approach to improving survival of patients with out-of-hospital primary cardiac arrest. J Am Coll Cardiol 2013;61:113-118 [MEDLINE]
Part 8: Post-Cardiac Arrest Care: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015 Nov 3;132(18 Suppl 2):S465-82. doi: 10.1161/CIR.0000000000000262 [MEDLINE]
Cardiocerebral Resuscitation: An Approach to Improving Survival of Patients With Primary Cardiac Arrest. J Intensive Care Med. 2016 Jan;31(1):24-33. doi: 10.1177/0885066614544450. Epub 2014 Jul 30 [MEDLINE]
Acute Coronary Syndrome (ACS) Management
Coronary angiography predicts improved outcome following cardiac arrest: propensity-adjusted analysis. J Intensive Care Med. 2009;24(3):17 [MEDLINE]
Immediate percutaneous coronary intervention is associated with better survival after out-of-hospital cardiac arrest: insights from the PROCAT (Parisian Region Out of hospital Cardiac ArresT) registry. Circ Cardiovasc Interv. 2010;3:200–207 [MEDLINE]
Defibrillation/Chest Compression
Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: a randomized trial. JAMA. 2003;289:1389-1395
Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest. JAMA. 2008 Mar 12;299(10):1158-65. doi: 10.1001/jama.299.10.1158 [MEDLINE]
Chest compression-only CPR by lay rescuers and survival from out-of-hospital cardiac arrest. JAMA. 2010 Oct 6;304(13):1447-54. doi: 10.1001/jama.2010.1392 [MEDLINE]
Active chest compression-decompression for cardiopulmonary resuscitation. Cochrane Database Syst Rev 2013 Sep 20;9:CD002751 [MEDLINE]
Mechanical chest compressions and simultaneous defibrillation vs conventional cardiopulmonary resuscitations in out-of-hospital cardiac arrest. The LINC randomized trial. JAMA. 2014 Jan 1;311(1):53-61. doi: 10.1001/jama.2013.282538 [MEDLINE]
Early Echocardiogram
Echocardiography in cardiac arrest. Curr Opin Crit Care. 2010;16:211–215 [MEDLINE]
Hemodynamic Management
Early goal-directed hemodynamic optimization combined with therapeutic hypothermia in comatose survivors of out-of-hospital cardiac arrest. Resuscitation. 2009;80:418-424 [MEDLINE]
A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? Eur Heart J. 2009;30:459-468 [MEDLINE]
Respiratory Management
Emergency Medicine Shock Research Network Investigators. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010; 303:2165–2171 [MEDLINE]
Seizure Management
Continuous EEG in therapeutic hypothermia after cardiac arrest: prognostic and clinical value. Neurology. 2013 Jan;80(4):339-44. Epub 2013 Jan 2 [MEDLINE]
Sodium Bicarbonate
Use of Sodium Bicarbonate in Cardiac Arrest: Current Guidelines and Literature Review. J Clin Med Res. 2016 Apr;8(4):277-83. doi: 10.14740/jocmr2456w. Epub 2016 Feb 27 [MEDLINE]
Therapeutic Hypothermia
Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557–63 [MEDLINE]
Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346: 549–56 [MEDLINE]
Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. Hypothermia after Cardiac Arrest Study Group. N Engl J Med. 2002;346(8):549 [MEDLINE]
Therapeutic hypothermia after cardiac arrest. N Engl J Med 2002;346:612 [MEDLINE]
From evidence to clinical practice: Effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest. Crit Care Med 2006;34:1865 [MEDLINE]
Induced hypothermia and fever control for prevention and treatment of neurological injuries. Lancet 2008;371:1955 [MEDLINE]
Early goal-directed hemodynamic optimization combined with therapeutic hypothermia in comatose survivors of out-of-hospital cardiac arrest. Resuscitation. 2009;80:418-424 [MEDLINE]
Outcome, timing and adverse events in therapeutic hypothermia after out-of-hospital cardiac arrest. Acta Anaesthesiol Scand. 2009;53(7):926 [MEDLINE]
Targeted temperature management for comatose survivors of cardiac arrest. N Engl J Med. 2010 Sep 23;363(13):1256-64. doi: 10.1056/NEJMct1002402 [MEDLINE]
Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013 Dec 5;369(23):2197-206. doi: 10.1056/NEJMoa1310519. Epub 2013 Nov 17 [MEDLINE]
Effect of prehospital induction of mild hypothermia on survival and neurological status among adults with cardiac arrest: a randomized clinical trial. JAMA. 2014 Jan 1;311(1):45-52. doi: 10.1001/jama.2013.282173 [MEDLINE]
Effect of prehospital induction of mild hypothermia on 3-month neurological status and 1-year survival among adults with cardiac arrest: long-term follow-up of a randomized, clinical trial. J Am Heart Assoc. 2015 Mar 11;4(3):e001693. doi: 10.1161/JAHA.114.001693 [MEDLINE]
Cardiac arrest and therapeutic hypothermia. Trends Cardiovasc Med. 2015 Oct 22. pii: S1050-1738(15)00240-6. doi: 10.1016/j.tcm.2015.10.002 [MEDLINE]
Therapeutic hypothermia for acute brain injuries. Scand J Trauma Resusc Emerg Med. 2015 Jun 5;23:42. doi: 10.1186/s13049-015-0121-3 [MEDLINE]
Therapeutic Hypothermia and the Risk of Hemorrhage: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Medicine (Baltimore). 2015 Nov;94(47):e2152. doi: 10.1097/MD.0000000000002152 [MEDLINE]
Pre-hospital versus in-hospital initiation of cooling for survival and neuroprotection after out-of-hospital cardiac arrest. Cochrane Database Syst Rev. 2016 Mar 15;3:CD010570 [MEDLINE]
Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database Syst Rev. 2016 Feb 15;2:CD004128. doi: 10.1002/14651858.CD004128.pub4 [MEDLINE]
Association between therapeutic hypothermia and long-term quality of life in survivors of cardiac arrest: A systematic review. Resuscitation. 2016 Jun;103:54-9. doi: 10.1016/j.resuscitation.2016.03.024. Epub 2016 Apr 7 [MEDLINE]
