Acute Coronary Syndrome (ACS) (see 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]
Therapeutic Hypothermia (see 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
Serum 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)
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)
After Out-of-Hospital Cardiac Arrest, Therapeutic Hypothermia was Associated with Increased Risk of Early-Onset Pneumonia (Am J Respir Crit Care Med, 2011) [MEDLINE]
Post-Cardiac Arrest Early-Onset Pneumonia was Associated with Increased Need for Prolonged Respiratory Support and Longer ICU Stay
Post-Cardiac Arrest Early-Onset Pneumonia Did Not Impact the Probablilty of Favorable Neurologic Outcome or the Mortality Rate
Chest Compressions During Cardiopulmonary Resuscitation (CPR)
Key Determinants of Successful Cardiopulmonary Resuscitation (CPR)
Quality Chest Compressions (100-120/min with 2-2.4” Depth and Full Chest Recoil Between Compressions
Early Defibrillation
American Heart Association Guidelines Recommend Maintaining a Chest Compression Fraction of ≥60% (Meaning on Average, There Chest Compressions Should Be Withheld<40% of the Intra-Arrest Time (J Emerg Med, 2018) [MEDLINE]
There May Be Additional Benefit with Maintaining a Chest Compression Fraction of ≥80% (Circulation, 2009) [MEDLINE] (Resuscitation, 2011) [MEDLINE]
Multiple Interventions May Interrupt Chest Compressions: some of which have unclear benefit
Administration of Resuscitation Medications
Endotracheal Intubation: supraglottic airway insertion can be quicker than endotracheal intubation, don’t interfere with chest compressions, and have a loer complication than endotracheal intubation
Intravenous/Arterial Access Attempts: intraosseous access can be quicker than intravenous access and doesn’t interfere with chest compressions
Respiratory Support During Cardiopulmonary Resuscitation (CPR)
Rationale
In Cardiopulmonary Arrest, Systemic and Pulmonary Vascular Perfusion is Very Low Despite Optimal Cardiopulmonary Resuscitation (CPR)
Therefore, Ventilation/Perfusion Relationships Can Be Maintained with Low Minute Ventilation
Hyperventilation Should Be Avoided During CPR, as Increased Intrathoracic Pressure Can Impede Effective Chest Compressions
Laryngeal Mask Airway (LMA) or Other Similar Supraglottic Airway Device (see Airway Management)
Clinical Efficacy of Airway Management Techniques in Out-of-Hospital Cardiac Arrest
Randomized Trial of Bag-Mask Ventilation vs Endotracheal Intubation During Cardiopulmonary Resuscitation in Out-of-Hospital Cardiac Arrest (JAMA 2018) [MEDLINE]: n= 2043
Bag-Mask Ventilation and Endotracheal Intubation were Equivalent in Terms of 28-Day Neurologic Outcome for Out-of-Hospital Cardiac Arrest
AIRWAYS-2 Randomized Trial of Supraglottic Airway Device vs Endotracheal Intubation in Out-of-Hospital Cardiac Arrest ( JAMA, 2018) [MEDLINE]: n = 9296
Supraglottic Airway Device and Tracheal Intubation Were Equivalent in Terms of 30-Day Outcome in Out-of-Hospital Cardiac Arrest
Trial of Laryngeal Tube Insertion vs Endotracheal Intubation in Out-of-Hospital Cardiac Arrest (JAMA, 2018) [MEDLINE]: n = 3000
Laryngeal Tube Insertion was Superior to Endotracheal Intubation in Terms of 72 hr Mortality Rate in Out-of-Hospital Cardiac Arrest
Etiology of False-Positive Capnography (Carbon Dioxide Detection with Esophageal Intubation)
Ingestion of Carbonated Liquids
Etiology of False-Negative Capnography (No Carbon Dioxide Detection with Endotracheal Intubation)
Acute Pulmonary Embolism (PE) (see Acute Pulmonary Embolism): due to decreased pulmonary blood flow and decreased delivery of carbon dioxide to the lungs
Contamination of the Detector with Gastric Contents
Severe Airflow Obstruction: due to poor carbon dioxide exchange across the obstructed airway (Emerg Med J, 2003) [MEDLINE]
Significant Hypotension/Cardiac Arrest (Especially with Poor Quality CPR) (see Hypotension): due to decreased pulmonary blood flow and decreased delivery of carbon dioxide to the lungs
Can Be Used to Confirm Endotracheal Tube Placement
However, There is No Evidence that These Devices are Accurate for Continued Monitoring of Endotracheal Tube Placement
In Addition, Since a Minimum Threshold Carbon Dioxide Must Be Reached to Activate the Detector and Exhaled Carbon Dioxide is Low in the Setting of Cardiac Arrest, Carbon Dioxide Might Not Be Detectable During CPR (Particularly with Low Quality CPR)
General Recommendations
Bag-Valve-Mask Ventilation and Supraglottic Airways are Probably Preferred Over Endotracheal Intubation in the Prehospital Out-of-Hospital Cardiac Arrest Setting
Recommendations (American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, 2015) (Circulation, 2015) [MEDLINE]
Use the Maximal Feasible Inspired Oxygen Concentration During CPR (Class IIb, LOE C-EO)
Method of Oxygenation/Ventilation
Inadequate Evidence to Demonstrate a Difference in Survival or Favorable Neurologic Outcome with the Use of Bag-Mask Ventilation, as Compared to Endotracheal Intubation During CPR
Either a Bag-Mask Device or an Advanced Airway May Be Used for Oxygenation/Ventilation During CPR in Both the In-Hospital and Out-of-Hospital Settings (Class IIb, LOE C-LD)
For Healthcare Providers Trained in Their Use, Either a Supraglottic Airway Device or an Endotracheal Tube May Be Used as the Initial Advanced Airway During CPR (Class IIb, LOE C-LD)
Confirmation of Endotracheal Tube Placement
Continuous Waveform Capnography is Recommended in Addition to Clinical Assessment as the Most Reliable Method of Confirming and Monitoring Correct Endotracheal Tube Placement (Class I, LOE C-LD)
If Continuous Waveform Capnometry is Not Available, a Nonwaveform CO2 Detector, Esophageal Detector Device, or Ultrasound Used by an Experienced Operator is a Reasonable Alternative (Class IIa, LOE C-LD)
Ventilation After Advanced Airway Placement
After Placement of Advanced Airway, it is Reasonable to Deliver 1 Breath Every 6 sec (10 Breaths/min) While Continuous Chest Compressions are Being Performed (Class IIb, LOE C-LD)
Monitoring Physiologic Parameters During Cardiopulmonary Resuscitation (CPR)
Recommendations (American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, 2015) (Circulation, 2015) [MEDLINE]
Although No Clinical Study Has Examined Whether Titrating Resuscitative Efforts to Physiologic Parameters During CPR Improves Outcome, it is Reasonable to Utilize Physiologic Parameters (Quantitative Waveform Capnography, Arterial Relaxation Diastolic Pressure, Arterial Pressure Monitoring, and Central Venous Oxygen Saturation) When Feasible to Optimize Quality of CPR, Guide Vasopressor Therapy and Detect ROSC (Class IIb, LOE C-EO)
In Intubated Patients with Cardiac Arrest, Failure to Achieve an ETCO2 >10 mm Hg by Waveform Capnography After 20 minutes of CPR May Be Considered as One Component of a Multimodal Approach to Decide When to End Resuscitative Efforts, But it Should Not Be Used in Isolation (Class IIb, LOE C-LD)
Studies from Which this Recommendation is Derived Only Included Intubated Patients
Use of Ultrasound During Cardiopulmonary Resuscitation (CPR)
Rationale
Early Echocardiography Allows Assessment of Degree of Myocardial Dysfunction and Allows for the Exclusion of Pericardial Effusion as an Etiology
Recommendations (American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, 2015) (Circulation, 2015) [MEDLINE]
Ultrasound (Cardiac or Noncardiac) May Be Considered During the Management of Cardiac Arrest, Although its Usefulness Has Not Been Well Established (Class IIb, LOE C-EO)
If a Qualified Sonographer is Present and Use of Ultrasound Does Not Interfere with the Standard Cardiac Arrest Treatment Protocol, then Ultrasound May Be Considered as an Adjunct to Standard Patient Evaluation (Class IIb, LOE C-EO)
Active Chest Compression-Decompression Cardiopulmonary Resuscitation (ACD-CPR)
Rationale
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Clinical Efficacy
Pilot Study of Mechanical Active Compression-Decompression Cardiopulmonary Resuscitation (ACD-CPR) vs Manual CPR in Out-of-Hospital Cardiac Arrest (Resuscitation, 2009) [MEDLINE]
As Compared to Manual CPR, Mechanical Active Compression-Decompression Cardiopulmonary Resuscitation (ACD-CPR) Generated Higher Initial, Minimum and Average End-Tidal pCO2 Values
Systematic Review of Active Chest Compression-Decompression CPR (ACD-CPR) Device in In-Hospital/Out-of-Hospital Cardiac Arrest (Cochrane Database Syst Rev, 2013) [MEDLINE]
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 and Tricyclic Antidepressants)
Bystander Cardiopulmonary Resuscitation (CPR)
Rationale
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Clinical Efficacy
Meta-Analysis of Predictors of Outcome After Out-of-Hospital Cardiac Arrest (n = 142,740 Patients from 79 Studies) (Circ Cardiovasc Qual Outcomes, 2010) [MEDLINE]
Although 53% (95% CI, 45.0% to 59.9%) of Out-of-Hospital Cardiac Arrests are Witnessed by a Bystander, Only 32% (95% CI, 26.7% to 37.8%) Receive Bystander CPR
Survival to Hospital Dicharge was Predicted by the Following Variables
Witnessed Arrest by Bystander or Emergency Medical Personnel
Receipt of Bystander CPR
Initial Rhythm of Ventricular Tachycardia/Fibrillation
Achieved Return of Spontaneous Circulation (ROSC)
The Aggregate Survival Rate for Out-of-Hospital Cardiac Arrest (7.6%) Has Not Significantly Changed in Almost Three Decades
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
Study of Continuous Quality Improvement Approach in Out-of-Hospital Cardiac Arrest in Arizona (J Am Coll Cardiol, 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
American Heart Association Scientific Statement on Lay Responder Experience in Out-of-Hospital Cardiac Arrest (Circulation, 2022) [MEDLINE]: n = 232,703 out-of-hospital cardiac arrest patients (meta-analysis of 19 studies) CPR from a Witness Increased Survival (Odds Ratio 1.95)Patients who received CPR were more likely to have initial shockable rhythm (80.9% vs 61.4%; P <.01) and to survive hospital discharge (18.3% vs 8.4%; P <.001)Most common barrier for bystanders to intervene is lack of confidence in their skills
Animal Studies Suggest that Performing CPR for 90-180 sec Prior to Defibrillation Improves Coronary Perfusion, Improve the Metabolic State of the Heart, and Increase the Chance that Defibrillation Will Be Successful
Clinical Efficacy
Prospective Registry Study of CPR + Defibrillation (for VF/VT) in Out-of-Hospital Cardiac Arrest (Resuscitation, 2010) [MEDLINE]
Between 46-195 sec of Emergency Medical Services CPR Prior to Defibrillation was Associated with Improved Survival, as Compared to ≤45 sec of CPR
Asian Randomized Study of Compression First vs Analyze First Strategies in Out-of-Hospital Cardiac Arrest (Resuscitation, 2012) [MEDLINE]
In This Study with Low Rates of Shockable Rhythms, No Difference in Return of Spontaneous Circulation Between Compression First vs Analyze First Strategies
Study of Continuous Quality Improvement Approach in Out-of-Hospital Cardiac Arrest in Arizona (J Am Coll Cardiol, 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
Cochrane Systematic of CPR + Defibrillation vs Early Defibrillation for Out-of-Hospital Cardiac Arrest (Cochrane Database Syst Rev, 2014) [MEDLINE]
Low Quality of Evidence Prevents Conclusion Regarding Superiority of CPR (1.5-3 min) + Defibrillation vs Immediate Defibrillation for Out-of-Hospital Cardiac Arrest: further studies are required
Recommendations (2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) (Circulation, 2010)
Performing CPR While a Defibrillator is Readied is Strongly Recommended in All Patients with Cardiac Arrest (Class I Recommendation, Level of Evidence B)
This was Not Reviewed in the 2015 AHA Guidelines
Benefit of Delaying Defibrillation to Perform CPR Before Defibrillation is Unclear (Class IIb Recommendation, Level of Evidence B)
This was Not Reviewed in the 2015 AHA Guidelines, But the Following are General Considerations
For Unwitnessed Cardiac Arrest in the Out-of-Hospital Setting (with EMS Response Times Usually >5 min), CPR x 2 min Prior to Defibrillation May Be Reasonable
Otherwise, For VF/Pulseless VT, the 2015 Adult Cardiac Arrest Algorithm Specifies Starting CPR with Immediate Assessment for a Shockable Rhythm (Followed by Defibrillation)
Mechanical Chest Compressions with Defibrillation During Ongoing Compressions (Mechanical CPR)
Rationale
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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 Neurologic Outcome at 6 mo
Avoid 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
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 interventions
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
Retrospective Analysis of Passive Oxygen vs Bag-Valve-Mask Ventilation in Witnessed Ventricular Fibrillation Out-of-Hospital Cardiac Arrest (Ann Emerg Med, 2009) [MEDLINE]
MICR with Initial Passive Ventilation Increased Neurologically Intact Survival to Hospital Discharge, as Compared to Initial Bag-Valve-Mask Ventilation
Study of Cardiocerebral Resuscitation (J Am Coll Cardiol, 2013) [MEDLINE]
Cardiocerebral Resuscitation Increased Survival of Patients with Primary Cardiac Arrest Over a 5 yr Period in Arizona from 17.7% to 33.7%
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 Cooling, as Compared to In-Hospital 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 are Recommended
Hemodynamic Management
Rationale
Optimal hemodynamic targets are unknown in the post-cardiac arrest period
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
Randomized Controlled Trial of Blood Pressure Target in Patients with Shock After Acute Myocardial Infarction and Cardiac Arrest (J Am Coll Cardiol, 2020) [MEDLINE]
Study Used Pooled Analysis of Post-Cardiac Arrest Patients with Shock After Acute Myocardial Infarction Randomized in the Neuroprotect (Neuroprotective Goal Directed Hemodynamic Optimization in Post-cardiac Arrest Patients; NCT02541591) and COMACARE (Carbon Dioxide, Oxygen and Mean Arterial Pressure After Cardiac Arrest and Resuscitation; NCT02698917) Trials
In Post-Cardiac Arrest Patients with Shock After Acute Myocardial Infarction and Cardiac Arrest, Targeting a Mean Arterial Pressure (MAP) Between 80/85 and 100 mm Hg with Additional Use of Inotropes and Vasopressors was Associated with Smaller Myocardial Injury
Recommendations (2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) [MEDLINE]
Target Mean Arterial Pressure (MAP) is Unclear, But Published Guidelines Suggest Anywhere from 65-80+ mm Hg (Accounting for the 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): may be used
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): 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
Early-Onset Pneumonia (see Aspiration Pneumonia) -After Out-of-Hospital Cardiac Arrest, Therapeutic Hypothermia was Associated with Increased Risk of Early-Onset Pneumonia (Am J Respir Crit Care Med, 2011)* [MEDLINE] – Post-Cardiac Arrest Early-Onset Pneumonia was Associated with Increased Need for Prolonged Respiratory Support and Longer ICU Stay – Post-Cardiac Arrest Early-Onset Pneumonia Did Not Impact the Probablilty of Favorable Neurologic Outcome or the Mortality Rate
Electrolyte Abnormalities
Hyperkalemia (see Hyperkalemia): during rewarming from hypothermia (potassium shifts extracellularly)
Hypokalemia (see Hypokalemia): during induction of hypothermia (potassium shifts intracellularly)
Hyperglycemia (see 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 and 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 of Therapeutic Hypothermia (33°C versus 36°C) After Out-of-Hospital 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 Demonstrate the Effects of Therapeutic Hypothermia with In-Hospital Cardiac Arrest, Asystole, Non-Cardiac Causes of Arrest
Observational Study of the Effect of Therapeutic Hypothermia on Survival After In-Hospital Cardiac Arrest (JAMA, 2016) [MEDLINE]
After In-Hospital Cardiac Arrest, Therapeutic Hypothermia Decreased Survival to Hospital Discharge and Decreased Likelihood of Favorable Neurologic Outcome
Temperature Data was Only Available for 23.9% of Hypothermia Group and 16.3% of Non-Hypothermia Group
Median Lowest Temperature in Hypothermia Group: 33.1 C (Interquartile Range: 32.3-35.7 C)
Approximately 20.9% of Patients were Below the Recommended Nadir of 32 C in the Hypothermia Group
Median Lowest Temperature in Non-Hypothermia Group: 36.3 (Interquartile Range: 35.6-36.8 C)
Randomized Trial is Warranted to Confirm These Findings
French Open Label, Randomized HYPERION Trial of Targeted Temperature Management Following In-Hospital Cardiac Arrest with a Non-Shockable Rhythm (NEJM, 2019) [MEDLINE]: n = 584 (25 ICU’s)
Among Patients with Coma Who Had Been Resuscitated from Cardiac Arrest with a Non-Shockable Rhythm, Moderate Therapeutic Hypothermia at 33°C for 24 hrs Led to a Higher Percentage of Patients Who Survived with a Favorable Neurologic Outcome at Day 90 than was Observed with Targeted Normothermia
TTM-2 Randomized Open-Label Trial (with Blinded Outcomes) of Therapeutic Hypothermia Following Adult Out-of-Hospital Cardiac Arrest (NEJM, 2021) [MEDLINE]: n = 1,850
6-Month Mortality Rate was Not Statistically Significantly Different Between the Therapeutic Hypothermia Group (33°C) and the Normothermia Group (with Early Treatment of Fever for Body Temperature ≥37.8°C) (Relative Risk with Hypothermia 1.04; 95% CI: 0.94 to 1.14; P = 0.37)
In the Hypothermia Group, 55% Had Moderately Severe Disability or Worse (Modified Rankin Scale Score ≥4), as Compared to 55% in the Normothermia Group (Relative Risk with Hypothermia 1.00; 95% CI: 0.92 to 1.09)
Arrhythmia Resulting in Hemodynamic Compromise was More Common in the Hypothermia Group, as Compared to the Normothermia Group (24% vs 17%, P<0.001) -Incidence of Other Adverse Events Did Not Differ Significantly Between the Groups
Canadian Single-Center CAPITAL CHILL Randomized Trial of Therapeutic Hypothermia (31°C vs 34°C) in Comatose Survivors of Out-of-Hospital Cardiac Arrest (JAMA, 2021) [MEDLINE]: n = 367
In Comatose Survivors of Out-of-Hospital cardiac Arrest, a Target Temperature of 31°C Did Not Significantly Decrease the Mortality Rate or Poor Neurologic Outcome at 180 Days, as Compared with a Target Temperature of 34°C
Study May Have Been Underpowered to Detect a Clinically Important Difference
Post-Hoc Analysis of HYPERION Trial of Targeted Temperature Management Following In-Hospital Cardiac Arrest with a Non-Shockable Rhythm (Chest, 2022) [MEDLINE]
As Compared with Targeted Normothermia for 48 hrs, Therapeutic Hypothermia at 33°C for 24 hrs was Associated with a Higher Percentage of Patients Who were Alive with Good Neurologic Outcomes at Day 90 (16.4% vs 5.8%; P = 0.03)
Day 90 Mortality was Not Significantly Different Between the Groups (68.5% vs 76.7%; P = 0.24)
By Mixed Multivariate Analysis Adjusted by Cardiac Arrest Hospital Prognosis Score and Circulatory Shock Status, Therapeutic Hypothermia was Associated Significantly with Good Day 90 Neurologic Outcomes (Odds Ratio 2.40; 95% CI: 1.17-13.03; P = 0.03)
Post-Hoc Analysis of TTM-2 Trial for Adult Out-of-Hospital Cardiac Arrest (Crit Care, 2022) [MEDLINE]
Therapeutic Hypothermia to 33°C Following Out-of-Hospital Cardiac Arrest, as Compared to Normothermia, was Not Associated with a Higher Mortality Rate in Patients Stratified According to Vasopressor Support on Admission
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)
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
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
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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]
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Respiratory Support
Effect of Bag-Mask Ventilation vs Endotracheal Intubation During Cardiopulmonary Resuscitation on Neurological Outcome After Out-of-Hospital Cardiorespiratory Arrest: A Randomized Clinical Trial. JAMA 2018; 319:779 [MEDLINE]
Effect of a Strategy of a Supraglottic Airway Device vs Tracheal Intubation During Out-of-Hospital Cardiac Arrest on Functional Outcome: The AIRWAYS-2 Randomized Clinical Trial. JAMA 2018; 320:779 [MEDLINE]
Effect of a Strategy of Initial Laryngeal Tube Insertion vs Endotracheal Intubation on 72-Hour Survival in Adults With Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial. JAMA 2018; 320:769 [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 fraction determines survival in patients with out-of-hospital ventricular fibrillation. Circulation 2009;120:1241–7 [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]
Survival increases with CPR by Emergency Medical Services before defibrillation of out-of-hospital ventricular fibrillation or ventricular tachycardia: observations from the Resuscitation Outcomes Consortium. Resuscitation. 2010 Feb;81(2):155-62. doi: 10.1016/j.resuscitation.2009.10.026. Epub 2009 Dec 6 [MEDLINE]
The impact of increased chest compression fraction on return of spontaneous circulation for out-of-hospital cardiac arrest patients not in ventricular fibrillation. Resuscitation 2011;82:1501–7 [MEDLINE]
A randomized trial of compression first or analyze first strategies in patients with out-of-hospital cardiac arrest: results from an Asian community. Resuscitation. 2012 Jul;83(7):806-12. doi: 10.1016/j.resuscitation.2012.01.009. Epub 2012 Jan 21 [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]
Cardiopulmonary resuscitation (CPR) plus delayed defibrillation versus immediate defibrillation for out-of-hospital cardiac arrest. Cochrane Database Syst Rev. 2014 Sep 12;(9):CD009803. doi: 10.1002/14651858.CD009803.pub2 [MEDLINE]
Team-focused Cardiopulmonary Resuscitation: Prehospital Principles Adapted for Emergency Department Cardiac Arrest Resuscitation. J Emerg Med. 2018 Jan;54(1):54-63. doi: 10.1016/j.jemermed.2017.08.065 [MEDLINE]
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Early Echocardiogram
Echocardiography in cardiac arrest. Curr Opin Crit Care. 2010;16:211–215 [MEDLINE]
Hemodynamic Management
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Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest. J Am Coll Cardiol. 2020 Aug 18;76(7):812-824. doi: 10.1016/j.jacc.2020.06.043 [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
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