II. Definitions
- Return of Spontaneous Circulation (ROSC)
- Palpable pulse (BLS) OR
- Return of Blood Pressure sufficient to perfuse critical organs (e.g. SBP >50 mmHg by Arterial Line)
- Orman and Weingart in Herbert (2017) EM:Rap 17(5): 12-3
- Out-of hospital Cardiac Arrest (OHCA)
- More than 70% of Out-of hospital Cardiac Arrests are due to cardiac cause
III. Pathophysiology: Primary Post-Cardiac Arrest Syndrome Components
- Systemic ischemic perfusion response
- Cytokine mediated injury with severity increasing with duration of downtime, comorbities and arrest mechanism
- Triggers intravascular volume depletion and altered vasoregulation
- Responds to IV hydration and Vasopressors
- Anoxic brain injury
- Most common early cause of post-Cardiac Arrest related mortality (first 24 hours)
- Oxygen free-radical mediated cellular injury (Protein peroxidation and apoptosis)
- Results in cerebral edema and decreased cerebral autoregulation
- Responds to targeted temperarture management and Seizure management
- Myocardial dysfunction (Post-Cardiac Arrest Shock)
- Leading cause of death for patients surviving to ICU after ROSC
- Stunned Myocardium with both Systolic Dysfunction and Diastolic Dysfunction in 70% of post-arrest patients
- Associated with vasoplegia (paradoxical low Systemic Vascular Resistance) and capillary leak
- Onset within hours of ROSC and improves after 3-4 days with intensive supportive care
- Smaller subset had myocardial wall motion abnormalities due to Myocardial Infarction
- Responds to inotropes and mechanical circulatory devices (IABP, pLVAD, ECMO)
- See Management below
- References
- Mechanism behind original Cardiac Arrest
IV. Pathophysiology: Other Post-Cardiac Arrest Syndrome Components
- Pulmonary Dysfunction (with risk of ARDS and other lung injury)
- Aspiration
- Ventilation-perfusion mismatch
- Pulmonary Edema
- Recurrent Cardiac Arrest
- Remain vigilant for signs of non-perfusing rhythm
- Loss of EtCO2 wave form may be first warning (esp. if rhythm is PEA)
V. Evaluation
-
Electrocardiogram (EKG)
- Obtain on Return of Spontaneous Circulation, and again in 15 minutes (see explanation below)
- Immediate Coronary Angiography for ST Elevation on EKG after Resuscitation of out of hospital Cardiac Arrest
- Consider emergent Coronary Angiography for presumed cardiac origin of arrest
-
Point Of Care Cardiac Ultrasound (provider performed Echocardiogram)
- Evaluate overall contractility (estimate global function)
- Evaluate Inferior Vena Cava Ultrasound for Volume Status
- Evaluate Differential Diagnosis (e.g. Cardiac Tamponade, D-Sign in Pulmonary Embolism, Pneumothorax, valvular rupture)
VI. Management: Respiratory: Lung Protective Strategy
- Consider Pulmonary Embolism as precipitating factor for Cardiac Arrest
- Avoid hyperoxia
- Titrate FIO2
- Keep Oxygen Saturation 93-97%
- Keep PaO2 near 100 mmHg
- Poor outcomes associated with PaO2 >300 mmHg or PaO2 <60 mmHg
- Kilgannon (2010) JAMA 303(21): 2165-71 [PubMed]
- Titrate FIO2
- Avoid Hyperventilation
- Keep Tidal Volumes low: 6-8 ml/kg Ideal Body Weight
- Requires higher PEEP (use PEEP Tables)
- Additional PEEP may be needed for Pulmonary Edema
- Keep ventilation rates low (titrate to etCO2 or PaCO2)
- End-Tidal CO2: 35-40
- PaCO2: 35-45 mmHg
- Risk of falsely elevated PaCO2 in hypothermic patients (discuss with lab)
- Hyperventilation decreases cerebral perfusion
- Hyperventilation increases intrathoracic pressure and decreases venous return and Cardiac Output
- Hyperventilation results in decreased CO2 and compensatory cerebral Vasoconstriction
- Keep Tidal Volumes low: 6-8 ml/kg Ideal Body Weight
- Prevent Ventilator Associated Pneumonia
- Elevate head of bed
- Oral care and Decontamination
- Subglottic suction
- Gastric Decontamination
VII. Management: Circulatory
- Prevent Hypotension
- Keep Mean arterial pressure (MAP) >65 mmHg (best neurologic outcomes if MAP kept at 80-100 mmHg)
- Keep Systolic Blood Pressure > 90 mmHg
- Start low dose pressor and increase if Blood Pressure begins to fall
- Replace fluids to treat Hypovolemia
- Cold fluids if initiating Therapeutic Hypothermia
- Anticipate significant diuresis with induced Hypothermia (risk of Hypovolemia, Electrolyte disturbance)
- Consider Passive Leg Raise Maneuver to assess fluid responsiveness
- Follow serum Lactic Acid levels
- Monitor for decreased cardiac contractility with bedside Echocardiogram and consult cardiology early
- Fluid bolus trials of 500 ml each to reach CVP 8 cm H2O
- Consider Red Blood Cell Transfusion for significant Anemia
- Consider Passive Leg Raise Maneuver to assess fluid responsiveness
- Inotropes are indicated for poor cardiac contractility (consider for goal ScvO2>65%)
- Epinephrine (e.g. 10 mcg/kg/min)
- Consider for combined Vasoconstriction and inotropy
- Anticipate Blood Pressure drop with other inotropes
- Dobutamine 2.5-10 mcg/kg/min
- Milrinone
- Epinephrine (e.g. 10 mcg/kg/min)
- Vasopressors are indicated for Hypotension with adequate contractility to reach MAP 80 mmHg
- Start with Norepinephrine
- Consider Vasopressin
- Vasopressin appears to maintain its Vasopressor efficacy even at low arterial pH
- Some argue that Epinephrine and Norepinephrine are ineffective at low arterial pH <7.2
- However, studies show Epinephrine and Norepinephrine are effective at low pH
- Vidal (2014) J Thorac Cardiovasc Surg 147(5):1698-705 [PubMed]
- Consider pituitary-Adrenal Insufficiency as contributing to refractory shock
- Consider Hydrocortisone
- Consider intra-aortic balloon pump, ECMO - see below
- References
- Fluid bolus trials of 500 ml each to reach CVP 8 cm H2O
- Consider Arterial Line
- Allows for closer titration of Vasopressors and inotropes
- Allows for serial Arterial Blood Gas monitoring (PaO2 and PaCO2)
- Doppler Ultrasound of Arterial Pulse may be used until Arterial Line available
- Consider Venoarterial ECMO (or intra-aortic balloon pump, percutaneous Left Ventricular Assist Device)
- May be indicated as bridging supportive therapy to post-arrest definitive management (e.g. PTCA)
- Improved neurologic outcomes
- Younger patients (<65 to 75 years old)
- Witnessed Cardiac Arrest and CPR started immediately
- Reversible cause (e.g. Acute Coronary Syndrome)
- Consider causes of Hypotension
- See Rapid Ultrasound in Shock
- Pneumothorax (including Tension Pneumothorax)
- Pericardial Effusion
- Post-arrest Cardiogenic Shock
- Massive Myocardial Infarction (as initial cause of Cardiac Arrest)
-
Hypertension
- Transient Hypertension and Tachycardia may occur with Epinephrine
- Arterial Line is preferred for systolic and diastolic Blood Pressure Monitoring
- Low Systemic Vascular Resistance (vasoplegia) may result in a wide Pulse Pressure
- Results in low diastolic Blood Pressure with a high systolic Blood Pressure
- Maintain diastolic Blood Pressure >40 mmHg to ensure adequate coronary perfusion
- Poor left ventricular function may trigger peripheral Vasoconstriction
- Perform bedside Echocardiogram to evaluate left ventricular function
- Afterload reduction may be needed to prevent further left ventricular strain
- Hypertensive Emergency Intravenous Antihypertensives (e.g. Clevidipine, Nicardipine)
- Target systolic Blood Pressure 160 to 180 mmHg OR reduce Blood Pressure 15 to 20%
- References
- Mallemat and Swaminathan (2024) Post-ROSC Hypertension, EM:Rap, 4/29/2024
-
Arrhythmia
- Maintain normal Serum Potassium, Serum Calcium, Serum Magnesium, Serum Phosphorus
- Allow Temperature to rise to 36 C if undergoing Targeted Temperature Management
- Antiarrhythmics as needed
VIII. Management: Circulatory - Arrest Cause Evaluation and Intervention
- Head to Pelvis Sudden Death CT (SDCT)
- Consider in non-Traumatic post-ROSC Cardiac Arrest without underlying arrest cause (e.g. Cardiomyopathy, CAD)
- CT Protocol (assumes patient stability for CT, no contraindication to contrast)
- Noncontrast Head CT
- EKG-gated Thoracic CT Coronary Angiography
- CT Pulmonary Angiography
- CT Abdomen and Pelvis
- Efficacy
- Diagnostic yield: 72 to 92%
- Decreased time to diagnosis by 11 hours
- Does not modify survival to discharge
- References
- Consider CT Pulmonary Embolism or CTA Chest for Aortic Dissection
- Indicated for suspected vascular cause of Cardiac Arrest
- Consider obtaining CTA on transfer from Emergency Department to ICU
- Early Coronary Angiography (PCI) for Acute Coronary Syndrome
- Background
- Coronary events are responsible for 40% of Cardiac Arrests
- In medical centers distant from PCI, Thrombolytics could be considered
- Immediate angiography in presumed cardiac origin arrest has better outcomes than if done day 1-2
- Obtain immediate post-arrest Electrocardiogram (and repeat in 10-15 minutes)
- Initial EKG (first 10-15 minutes) may demonstrate ST changes due to Defibrillation, Epinephrine
- Early cardiac catheterization (PCI) indications (within 2 hours)
- History of Chest Pain prior to Cardiac Arrest
- Post-arrest EKG signs of ST Elevation Myocardial Infarction (STEMI)
- Ventricular Fibrillation (or Pulseless Ventricular Tachycardia) as initial heart rhythm from EMS
- Any shockable rhythm may predict benefit with early PCI
- STEMI and Ventricular Fibrillation is associated with acute coronary Occlusion in 70-80%
- NSTEMI and Ventricular Fibrillation is associated with acute coronary Occlusion in 25-35%
- Delayed cardiac catheterization (PCI) Indications (up to 5 days after Cardiac Arrest)
- Of NSTEMI patients, up to 32% had Cardiac Arrest due to coronary lesion (esp. if Ventricular Fibrillation)
- NSTEMI and shockable rhythm had similar outcomes with delayed PCI (up to 5 days later) as with early (2 hours)
- Relative contraindications to early PCI (unfavorable Resuscitation features, patients less likely to benefit)
- Unwitnessed arrest
- No bystander CPR
- Duration of Cardiac Arrest to ROSC >30 minutes
- Ongoing CPR
- Arterial pH <7.2
- Serum Lactic Acid >7
- Age over 85 years old
- End-stage renal disease
- Noncardiac cause of Cardiac Arrest (e.g. Traumatic Arrest)
- Rab (2015) J Am Coll Cardiol 66(1): 62-73 +PMID:26139060 [PubMed]
- References
- Orman and Mattu in Herbert (2015) EM:Rap 15(11): 8-9
- Swaminathan and Mattu in Herbert (2019) EM:Rap 19(10): 9-11
- Dumas (2010) Circ Cardiovasc Interv 3(3):200-7 [PubMed]
- Hollenbeck (2014) Resuscitation 85(1): 88-95 [PubMed]
- Rab (2015) J Am Coll Cardiol 66(1): 62-73 +PMID:26139060 [PubMed]
- Background
IX. Management: Neurologic
-
Pupillary response is a strong predictor of outcome
- Absent pupillary response is associated with a worse outcome
- Induced Therapeutic Hypothermia (Targeted Temperature Management)
- Goal is Return of Neurologic Function (RONF)
- Class I indications
- Comatose patient with STEMI
- Out of hospital Cardiac Arrest with Ventricular Fibrillation or Pulseless Ventricular Tachycardia
- Class 2b Indications
- All comatose patients with ROSC following Cardiac Arrest, regardless of initial rhythm
- Seizures (20% of cases)
- Imaging
- Consider Intracranial Hemorrhage, cerebral edema, Brainstem Herniation
- Head CT indications
- Any case of unwitnessed Cardiac Arrest
- Intracranial Hemorrhage is found in 11% of out of hospital Cardiac Arrest
- Focal neurologic changes
- Atypical Arrhythmia
- Evaluation for catastrophic anoxic brain injury
- Diffuse cerebral edema
- Severe loss of grey-white differentiation (grey-white ratio or GWR)
- Any case of unwitnessed Cardiac Arrest
- Neurologic outcome prognosis
- Initial Neurologic Exam (coma, pupils, motor activity) after ROSC does not accurately predict outcome
- Avoid estimating neurologic prognosis for 72 hours after ROSC or completed Targeted Temperature Management
- Prognosis may be later evaluated with MRI, EEG, somatosensory-evoked potentials, Neuron specific enolase levels
- Early CT Head with specific findings is one exception, that may accurately predict poor neurologic outcome
- CT Head may demonstrate Intracranial Hemorrhage or catastrophic anoxic brain injury (see above)
- In one study, initial GCS 3 and lack of Brainstem reflexes, yet favorable neurologic outcome in 20% of patients
- Witnessed arrest with initial shockable rhythm, who survive to discharge, have 57% favorable neurologic outcome
- Multimodal Prognostic Factors (Avoid prognostication until >72 hours after normothermia)
- Imaging and Lab
- Electrophysiology
- Somatosensory Evoked Potentials (SSEP) with N20 Amplitudes (>24 hours)
- Burst Suppression (>72 hours)
- Persistent Status Epilepticus (>72 hours)
- Status Myoclonus on EEG (24 to 72 hours)
- Exam (>72 hours)
- Pupillary Light Reflex
- Quantitative Pupillometry
- Corneal Reflex
- References
- (2022) ACLS Guidelines, AHA, reviewed online 8/5/2022
X. Management: Miscellaneous
- Monitor serum Electrolytes including Potassium, Calcium, Magnesium and Phosphorus
- Replace Electrolytes as needed
- Risk of Arrhythmia with Electrolyte disturbance
- Induced Hypothermia increases risk of Electrolyte disturbance via significant diuresis
- Monitor hourly Urine Output and Intravenous Fluid rates
- Avoid Hyperglycemia (and Hypoglycemia)
- Target Blood Glucose near 150 mg/dl with Insulin as needed
- Elevate head of bed
- Prevents aspiration in intubated patients
- Decreases Intracranial Pressure
-
Bleeding Diathesis or occult Hemorrhage
- Consider Disseminated Intravascular Coagulation (DIC)
- Hold Anticoagulation
- Allow Temperature to rise to 36 C if undergoing Targeted Temperature Management
- Treat fever
- Higher Body Temperatures are associated with worse neurologic outcomes
- See Induced Therapeutic Hypothermia
- Consider Sepsis, Pneumonia, bacteremia as precipitating factor for Cardiac Arrest (see Antibiotics below)
- Empiric Antibiotics for bacteremia (investigational)
- In one study, bacteremia was present in 38% of Cardiac Arrest patients who had significantly worse survival rates
- Hypothesized that Cardiac Arrest in some cases may be due to overwhelming Sepsis
- Most common Bacteria found are Gram Negative Rods and MRSA
- Consider obtaining Blood Cultures and administering broad spectrum Antibiotics after ROSC
- Coba (2014) Resuscitation 85(2): 196-202 [PubMed]
- Mongardon (2011) Crit Care Med 39(6): 1359-64 [PubMed]
- Post-arrest intubation precautions
- See respiratory management as above
- Exercise caution if patient not intubated prior to ROSC (e.g. Extraglottic Device)
- Right heart involvement places at high risk of recurrent and refractory Cardiac Arrest on intubation
- Limit RSI to cardiac-stable agents
- Use paralytic (Succinylcholine or Rocuronium) for maximal first-pass success
- Etomidate (some recommend half dose after ROSC at 0.15 mg/kg)
- Ketamine (some recommend half dose after ROSC at 0.75 mg/kg)
- Involve anesthesiology if possible
- Consider not intubating post-arrest unless otherwise indicated
- However, Extraglottic Devices are replaced with definitive airways in most cases after ROSC
- Definitive airway is required when Transferring to cath lab
- Musculoskeletal
- Consider Traumatic Injury as precipitating event for Cardiac Arrest
- Complete Trauma survey and imaging as needed
- Consider Rhabdomyolysis or Compartment Syndrome if prolonged down time
- Perform complete Musculoskeletal Exam
- Serum Creatine Kinase
- Consider Traumatic Injury as precipitating event for Cardiac Arrest
- Post-arrest sedation
XI. Prognosis
- Out-of hospital Cardiac Arrest (OHCA) survival to discharge: 11%
XII. References
- Herbert and Crager in Herbert (2019) EM:Rap 19(2): 1-2
- Mattu and Herbert (2012) EM: Rap 12(4): 5-6
- Mattu and Swaminathan in Swadron (2023) EM:Rap 23(2): 4-5
- Winters et al in Herbert (2013) EM:Rap 13(7): 9-10
- Weingart and Orman in Herbert (2015) EM:Rap 15(8): 13-4
- Orman and Weingart in Herbert (2015) EM:Rap 15(1): 14-6
- Stull, Haas, Haas and Whitmore (2017) Crit Dec Emerg Med 31(10): 13-9
- Stub (2011) Circulation 123(13): 1428-35 [PubMed]