Post-Cardiac Arrest Care

Aka: Post-Cardiac Arrest Care, Stabilization following Cardiac Arrest, Post-Resuscitation Care, Post-ROSC Care, Post-Cardiac Arrest Syndrome, Post-Cardiac Arrest Shock, Myocardial Dysfunction after Cardiac Arrest, Stabilization following CPR, Return of Spontaneous Circulation, ROSC, Cardiac Arrest with Successful Resuscitation, Resuscitated Cardiac Arrest Event, Coronary Angiography After Cardiac Arrest, Cardiac Catheterization After ROSC, Head to Pelvis Sudden Death CT, Neurologic Prognostic Factors After ROSC, Neurologic Multimodal Prognostication After Cardiac Arrest

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II. Definitions

  1. Return of Spontaneous Circulation (ROSC)
    1. Palpable pulse (BLS) OR
    2. Return of Blood Pressure sufficient to perfuse critical organs (e.g. SBP >50 mmHg by Arterial Line)
    3. Orman and Weingart in Herbert (2017) EM:Rap 17(5): 12-3
  2. Out-of hospital Cardiac Arrest (OHCA)
    1. More than 70% of Out-of hospital Cardiac Arrests are due to cardiac cause

III. Pathophysiology: Primary Post-Cardiac Arrest Syndrome Components

  1. Systemic ischemic perfusion response
    1. Cytokine mediated injury with severity increasing with duration of downtime, comorbities and arrest mechanism
    2. Triggers intravascular volume depletion and altered vasoregulation
    3. Responds to IV hydration and Vasopressors
  2. Anoxic brain injury
    1. Most common early cause of post-Cardiac Arrest related mortality (first 24 hours)
    2. Oxygen free-radical mediated cellular injury (Protein peroxidation and apoptosis)
    3. Results in cerebral edema and decreased cerebral autoregulation
    4. Responds to targeted temperarture management and Seizure management
  3. Myocardial dysfunction (Post-Cardiac Arrest Shock)
    1. Leading cause of death for patients surviving to ICU after ROSC
    2. Stunned Myocardium with both Systolic Dysfunction and Diastolic Dysfunction in 70% of post-arrest patients
      1. Associated with Vasoplegia (paradoxical low Systemic Vascular Resistance) and capillary leak
      2. Onset within hours of ROSC and improves after 3-4 days with intensive supportive care
      3. Smaller subset had myocardial wall motion abnormalities due to Myocardial Infarction
    3. Responds to inotropes and mechanical circulatory devices (IABP, pLVAD, ECMO)
      1. See Management below
    4. References
      1. Cha (2016) Resuscitation 106(S1):e79 [PubMed]
      2. Ortuno (2022) Eur J Emerg Med 29(3): 188-94 [PubMed]
  4. Mechanism behind original Cardiac Arrest
    1. See Reversible Causes of Cardiopulmonary Arrest (6H6T)
    2. Acute Coronary Syndrome
    3. Pulmonary Embolism
    4. Hypoxemia
    5. Acidosis
    6. Sepsis
    7. Intracranial Hemorrhage (e.g. Subarachnoid Hemorrhage)
    8. Cardiac Tamponade

IV. Pathophysiology: Other Post-Cardiac Arrest Syndrome Components

  1. Pulmonary Dysfunction (with risk of ARDS and other lung injury)
    1. Aspiration
    2. Ventilation-perfusion mismatch
    3. Pulmonary Edema
  2. Recurrent Cardiac Arrest
    1. Remain vigilant for signs of non-perfusing rhythm
    2. Loss of EtCO2 wave form may be first warning (esp. if rhythm is PEA)

V. Evaluation

  1. Electrocardiogram (EKG)
    1. Obtain on Return of Spontaneous Circulation, and again in 15 minutes (see explanation below)
    2. Immediate Coronary Angiography for ST Elevation on EKG after Resuscitation of out of hospital Cardiac Arrest
    3. Consider emergent Coronary Angiography for presumed cardiac origin of arrest
  2. Point Of Care Cardiac Ultrasound (provider performed Echocardiogram)
    1. Evaluate overall contractility (estimate global function)
    2. Evaluate Inferior Vena Cava Ultrasound for Volume Status
    3. Evaluate Differential Diagnosis (e.g. Cardiac Tamponade, D-Sign in Pulmonary Embolism, Pneumothorax, valvular rupture)

VI. Management: Respiratory: Lung Protective Strategy

  1. Consider Pulmonary Embolism as precipitating factor for Cardiac Arrest
  2. Avoid hyperoxia
    1. Titrate FIO2
      1. Keep Oxygen Saturation 93-97%
      2. Keep PaO2 near 100 mmHg
    2. Poor outcomes associated with PaO2 >300 mmHg or PaO2 <60 mmHg
    3. Kilgannon (2010) JAMA 303(21): 2165-71 [PubMed]
  3. Avoid Hyperventilation
    1. Keep Tidal Volumes low: 6-8 ml/kg Ideal Body Weight
      1. Requires higher PEEP (use PEEP Tables)
      2. Additional PEEP may be needed for Pulmonary Edema
    2. Keep ventilation rates low (titrate to etCO2 or PaCO2)
      1. End-Tidal CO2: 35-40
      2. PaCO2: 35-45 mmHg
        1. Risk of falsely elevated PaCO2 in hypothermic patients (discuss with lab)
    3. Hyperventilation decreases cerebral perfusion
      1. Hyperventilation increases intrathoracic pressure and decreases venous return and Cardiac Output
      2. Hyperventilation results in decreased CO2 and compensatory cerebral Vasoconstriction
  4. Prevent Ventilator Associated Pneumonia
    1. Elevate head of bed
    2. Oral care and Decontamination
    3. Subglottic suction
    4. Gastric Decontamination

VII. Management: Circulatory

  1. Prevent Hypotension
    1. Keep Mean arterial pressure (MAP) >65 mmHg
      1. Best neurologic outcomes with MAP 80-100 mmHg in some studies
      2. However, BOX Trial found no significant outcome difference between MAP of 63 and 77 mmHg
        1. Kjaergaard (2022) N Engl J Med 387(16):1456-66 +PMID: 36027564 [PubMed]
    2. Keep Systolic Blood Pressure > 90 mmHg
    3. Start low dose pressor and increase if Blood Pressure begins to fall
    4. Replace fluids to treat Hypovolemia
      1. Cold fluids if initiating Therapeutic Hypothermia
      2. Anticipate significant diuresis with induced Hypothermia (risk of Hypovolemia, Electrolyte disturbance)
      3. Consider Passive Leg Raise Maneuver to assess fluid responsiveness
    5. Follow serum Lactic Acid levels
    6. Monitor for decreased cardiac contractility with bedside Echocardiogram and consult cardiology early
      1. Fluid bolus trials of 500 ml each to reach CVP 8 cm H2O
        1. Consider Red Blood Cell Transfusion for significant Anemia
        2. Consider Passive Leg Raise Maneuver to assess fluid responsiveness
      2. Inotropes are indicated for poor cardiac contractility (consider for goal ScvO2>65%)
        1. Epinephrine (e.g. 10 mcg/kg/min)
          1. Consider for combined Vasoconstriction and inotropy
        2. Anticipate Blood Pressure drop with other inotropes
          1. Dobutamine 2.5-10 mcg/kg/min
          2. Milrinone
      3. Vasopressors are indicated for Hypotension with adequate contractility to reach MAP 80 mmHg
        1. Start with Norepinephrine
        2. Consider Vasopressin
          1. Vasopressin appears to maintain its Vasopressor efficacy even at low arterial pH
          2. Some argue that Epinephrine and Norepinephrine are ineffective at low arterial pH <7.2
            1. However, studies show Epinephrine and Norepinephrine are effective at low pH
            2. Vidal (2014) J Thorac Cardiovasc Surg 147(5):1698-705 [PubMed]
      4. Consider pituitary-Adrenal Insufficiency as contributing to refractory shock
        1. Consider Hydrocortisone
      5. Consider intra-aortic balloon pump, ECMO - see below
      6. References
        1. Gaieski (2009) Resuscitation 80(4): 418-24 [PubMed]
    7. Consider Arterial Line
      1. Allows for closer titration of Vasopressors and inotropes
      2. Allows for serial Arterial Blood Gas monitoring (PaO2 and PaCO2)
      3. Doppler Ultrasound of Arterial Pulse may be used until Arterial Line available
    8. Consider Venoarterial ECMO (or intra-aortic balloon pump, percutaneous Left Ventricular Assist Device)
      1. May be indicated as bridging supportive therapy to post-arrest definitive management (e.g. PTCA)
      2. Indications (no current official established guidelines as of 2024)
        1. Good prognosis and neurologic functional outcome expected with adequate Resuscitation
          1. Younger patients (<65 to 75 years old)
          2. Witnessed Cardiac Arrest and CPR started immediately
        2. Single Organ Failure (esp. reversible causes)
          1. High risk Acute Coronary Syndrome (e.g. planned emergent PTCA)
          2. Massive Pulmonary Embolism (e.g. with PE Thrombolysis)
          3. Refractory Cardiogenic Shock (e.g. bridge to LVAD or Heart Transplant, or reversible cause)
          4. Acute Respiratory Distress Syndrome (ARDS) with cardiac dysfunction
          5. Refractory Ventricular Fibrillation arrest
      3. References
        1. Mattu and Swaminathan (2024) EM:Rap 10/7/2024, accessed 10/31/2024
    9. Consider causes of Hypotension
      1. See Rapid Ultrasound in Shock
      2. Pneumothorax (including Tension Pneumothorax)
      3. Pericardial Effusion
      4. Post-arrest Cardiogenic Shock
      5. Massive Myocardial Infarction (as initial cause of Cardiac Arrest)
  2. Hypertension
    1. Transient Hypertension and Tachycardia may occur with Epinephrine
    2. Arterial Line is preferred for systolic and diastolic Blood Pressure Monitoring
    3. Low Systemic Vascular Resistance (Vasoplegia) may result in a wide Pulse Pressure
      1. Results in low diastolic Blood Pressure with a high systolic Blood Pressure
      2. Maintain diastolic Blood Pressure >40 mmHg to ensure adequate coronary perfusion
    4. Poor left ventricular function may trigger peripheral Vasoconstriction
      1. Perform bedside Echocardiogram to evaluate left ventricular function
      2. Afterload reduction may be needed to prevent further left ventricular strain
        1. Hypertensive Emergency Intravenous Antihypertensives (e.g. Clevidipine, Nicardipine)
        2. Target systolic Blood Pressure 160 to 180 mmHg OR reduce Blood Pressure 15 to 20%
    5. References
      1. Mallemat and Swaminathan (2024) Post-ROSC Hypertension, EM:Rap, 4/29/2024
  3. Arrhythmia
    1. Maintain normal Serum Potassium, Serum Calcium, Serum Magnesium, Serum Phosphorus
    2. Allow Temperature to rise to 36 C if undergoing Targeted Temperature Management
    3. Antiarrhythmics as needed

VIII. Management: Circulatory - Arrest Cause Evaluation and Intervention

  1. Head to Pelvis Sudden Death CT (SDCT)
    1. Consider in non-Traumatic post-ROSC Cardiac Arrest without underlying arrest cause (e.g. Cardiomyopathy, CAD)
    2. CT Protocol (assumes patient stability for CT, no contraindication to contrast)
      1. Noncontrast Head CT
      2. EKG-gated Thoracic CT Coronary Angiography
      3. CT Pulmonary Angiography
      4. CT Abdomen and Pelvis
    3. Efficacy
      1. Diagnostic yield: 72 to 92%
      2. Decreased time to diagnosis by 11 hours
      3. Does not modify survival to discharge
    4. References
      1. Adel (2022) Front Cardiovasc Med 9:799446 +PMID: 35187123 [PubMed]
      2. Branch (2023) Resuscitation 188:109785 +PMID: 37019352 [PubMed]
      3. Branch (2021) Acad Emerg Med 28(4):394-403 +PMID: 33606342 [PubMed]
  2. Consider CT Pulmonary Embolism or CTA Chest for Aortic Dissection
    1. Indicated for suspected vascular cause of Cardiac Arrest
    2. Consider obtaining CTA on transfer from Emergency Department to ICU
    3. Manage as massive Pulmonary Embolism if identified
      1. See Thrombolysis in Massive Pulmonary Embolism
  3. Early Coronary Angiography (PCI) for Acute Coronary Syndrome
    1. Background
      1. Coronary events are responsible for 40% of Cardiac Arrests
      2. In medical centers distant from PCI, Thrombolytics could be considered
      3. Immediate angiography in presumed cardiac origin arrest has better outcomes than if done day 1-2
    2. Obtain immediate post-arrest Electrocardiogram (at 8 to 15 minutes after ROSC)
      1. Initial EKG within first 8 minutes may demonstrate ST changes due to Defibrillation, Epinephrine
    3. Early cardiac catheterization (PCI) indications (within 2 hours)
      1. Post-arrest EKG signs of ST Elevation Myocardial Infarction (STEMI)
        1. STEMI on EKG is the only absolute indication for emergent PCI
        2. PCI is a level I recommendation unless poor prognosis (e.g. Dementia, Intracranial Hemorrhage)
        3. Predicts Cardiac Arrest causative lesion in 80% of cases
      2. History of Chest Pain prior to Cardiac Arrest (consult cardiology)
      3. Persistent hemodynamic or electrical instability
      4. Ventricular Fibrillation (or Pulseless Ventricular Tachycardia) as initial heart rhythm from EMS
        1. Any shockable rhythm may predict benefit with early PCI (consult cardiology)
        2. STEMI and Ventricular Fibrillation is associated with acute coronary Occlusion in 70-80%
        3. NSTEMI and Ventricular Fibrillation is associated with acute coronary Occlusion in 25-35%
    4. Delayed cardiac catheterization (PCI) Indications (up to 5 days after Cardiac Arrest)
      1. Of NSTEMI patients, up to 32% had Cardiac Arrest due to coronary lesion (esp. if Ventricular Fibrillation)
        1. Millan (2016) Resuscitation 108:54-60 [PubMed]
      2. NSTEMI and shockable rhythm had similar outcomes with delayed PCI (up to 5 days later) as with early (2 hours)
        1. Lemkes (2019) N Engl J Med 380(15): 1397-407 +PMID:30883057 [PubMed]
    5. Relative contraindications to early PCI (unfavorable Resuscitation features, patients less likely to benefit)
      1. Unwitnessed arrest
      2. No bystander CPR
      3. Duration of Cardiac Arrest to ROSC >30 minutes
      4. Ongoing CPR
      5. Arterial pH <7.2
      6. Serum Lactic Acid >7
      7. Age over 85 years old
      8. End-stage renal disease
      9. Noncardiac cause of Cardiac Arrest (e.g. Traumatic Arrest)
      10. Rab (2015) J Am Coll Cardiol 66(1): 62-73 +PMID:26139060 [PubMed]
    6. References
      1. Orman and Mattu in Herbert (2015) EM:Rap 15(11): 8-9
      2. Swaminathan and Mattu in Herbert (2019) EM:Rap 19(10): 9-11
      3. Dumas (2010) Circ Cardiovasc Interv 3(3):200-7 [PubMed]
      4. Hollenbeck (2014) Resuscitation 85(1): 88-95 [PubMed]
      5. Rab (2015) J Am Coll Cardiol 66(1): 62-73 +PMID:26139060 [PubMed]
      6. Tamis-Holland (2024) Circulation 149(5):e274-95 +PMID: 38112086 [PubMed]

IX. Management: Neurologic

  1. Pupillary response is a strong predictor of outcome
    1. Absent pupillary response is associated with a worse outcome
  2. Induced Therapeutic Hypothermia (Targeted Temperature Management)
    1. Goal is Return of Neurologic Function (RONF)
    2. Current AHA guideline is to target 32 to 37.5 C and preventing fever
      1. As of 2024, no outcome difference between 36 to 37.5 C (96.8 to 99.5 F) and lower Temperatures
    3. Class I indications
      1. Comatose patient with STEMI
      2. Out of hospital Cardiac Arrest with Ventricular Fibrillation or Pulseless Ventricular Tachycardia
    4. Class 2b Indications
      1. All comatose patients with ROSC following Cardiac Arrest, regardless of initial rhythm
  3. Seizures (20% of cases)
    1. Consider continuous EEG monitoring
    2. Treat with Ativan
    3. Prophylaxis not initially needed unless Seizure occurs
  4. Imaging
    1. Consider Intracranial Hemorrhage, cerebral edema, Brainstem Herniation
    2. Head CT indications
      1. Any case of unwitnessed Cardiac Arrest
        1. Intracranial Hemorrhage is found in 11% of out of hospital Cardiac Arrest
      2. Focal neurologic changes
      3. Atypical Arrhythmia
      4. Evaluation for catastrophic anoxic brain injury
        1. Diffuse cerebral edema
        2. Severe loss of grey-white differentiation (grey-white ratio or GWR)
  5. Neurologic outcome prognosis
    1. Initial Neurologic Exam (coma, pupils, motor activity) after ROSC does not accurately predict outcome
    2. Avoid estimating neurologic prognosis for 72 hours after ROSC or completed Targeted Temperature Management
    3. Prognosis may be later evaluated with MRI, EEG, somatosensory-evoked potentials, Neuron specific enolase levels
    4. Early CT Head with specific findings is one exception, that may accurately predict poor neurologic outcome
      1. CT Head may demonstrate Intracranial Hemorrhage or catastrophic anoxic brain injury (see above)
    5. In one study, initial GCS 3 and lack of Brainstem reflexes, yet favorable neurologic outcome in 20% of patients
      1. Merrill (2016) Am J Emerg Med 34(6): 975-9 [PubMed]
    6. Witnessed arrest with initial shockable rhythm, who survive to discharge, have 57% favorable neurologic outcome
    7. Multimodal Prognostic Factors (Avoid prognostication until >72 hours after normothermia)
      1. Imaging and Lab
        1. CT Head (first 24 Hours)
        2. MRI Brain (>24 hours)
        3. Neuron-Specific Enolase or Serum NSE (24 to 72 hours)
      2. Electrophysiology
        1. Somatosensory Evoked Potentials (SSEP) with N20 Amplitudes (>24 hours)
        2. Burst Suppression (>72 hours)
        3. Persistent Status Epilepticus (>72 hours)
        4. Status Myoclonus on EEG (24 to 72 hours)
      3. Exam (>72 hours)
        1. Pupillary Light Reflex
        2. Quantitative Pupillometry
        3. Corneal Reflex
      4. References
        1. (2022) ACLS Guidelines, AHA, reviewed online 8/5/2022

X. Management: Miscellaneous

  1. Monitor serum Electrolytes including Potassium, Calcium, Magnesium and Phosphorus
    1. Replace Electrolytes as needed
    2. Risk of Arrhythmia with Electrolyte disturbance
    3. Induced Hypothermia increases risk of Electrolyte disturbance via significant diuresis
      1. Monitor hourly Urine Output and Intravenous Fluid rates
  2. Avoid Hyperglycemia (and Hypoglycemia)
    1. Target Blood Glucose near 150 mg/dl with Insulin as needed
  3. Elevate head of bed
    1. Prevents aspiration in intubated patients
    2. Decreases Intracranial Pressure
  4. Bleeding Diathesis or occult Hemorrhage
    1. Consider Disseminated Intravascular Coagulation (DIC)
    2. Hold Anticoagulation
    3. Allow Temperature to rise to 36 C if undergoing Targeted Temperature Management
  5. Treat fever
    1. Higher Body Temperatures are associated with worse neurologic outcomes
    2. See Induced Therapeutic Hypothermia
    3. Consider Sepsis, Pneumonia, bacteremia as precipitating factor for Cardiac Arrest (see Antibiotics below)
  6. Empiric Antibiotics for bacteremia (investigational)
    1. In one study, bacteremia was present in 38% of Cardiac Arrest patients who had significantly worse survival rates
    2. Hypothesized that Cardiac Arrest in some cases may be due to overwhelming Sepsis
    3. Most common Bacteria found are Gram Negative Rods and MRSA
    4. Consider obtaining Blood Cultures and administering broad spectrum Antibiotics after ROSC
    5. Coba (2014) Resuscitation 85(2): 196-202 [PubMed]
    6. Mongardon (2011) Crit Care Med 39(6): 1359-64 [PubMed]
  7. Post-arrest intubation precautions
    1. See respiratory management as above
    2. Exercise caution if patient not intubated prior to ROSC (e.g. Extraglottic Device)
    3. Right heart involvement places at high risk of recurrent and refractory Cardiac Arrest on intubation
    4. Limit RSI to cardiac-stable agents
      1. Use paralytic (Succinylcholine or Rocuronium) for maximal first-pass success
      2. Etomidate (some recommend half dose after ROSC at 0.15 mg/kg)
      3. Ketamine (some recommend half dose after ROSC at 0.75 mg/kg)
    5. Involve anesthesiology if possible
    6. Consider not intubating post-arrest unless otherwise indicated
      1. However, Extraglottic Devices are replaced with definitive airways in most cases after ROSC
      2. Definitive airway is required when Transferring to cath lab
  8. Musculoskeletal
    1. Consider Traumatic Injury as precipitating event for Cardiac Arrest
      1. Complete Trauma survey and imaging as needed
    2. Consider Rhabdomyolysis or Compartment Syndrome if prolonged down time
      1. Perform complete Musculoskeletal Exam
      2. Serum Creatine Kinase
  9. Post-arrest sedation
    1. As with RSI, use cardiac stable agents at lower dose
      1. Etomidate (half dose)
      2. Ketamine (half dose)
      3. Avoid Propofol if possible (however if used, dose at 10% the typical dose)

XI. Prognosis

  1. Out-of hospital Cardiac Arrest (OHCA) survival to discharge: 11%

XII. References

  1. Herbert and Crager in Herbert (2019) EM:Rap 19(2): 1-2
  2. Mattu and Herbert (2012) EM: Rap 12(4): 5-6
  3. Mattu and Swaminathan in Swadron (2023) EM:Rap 23(2): 4-5
  4. Winters et al in Herbert (2013) EM:Rap 13(7): 9-10
  5. Weingart and Orman in Herbert (2015) EM:Rap 15(8): 13-4
  6. Orman and Weingart in Herbert (2015) EM:Rap 15(1): 14-6
  7. Stull, Haas, Haas and Whitmore (2017) Crit Dec Emerg Med 31(10): 13-9
  8. Stub (2011) Circulation 123(13): 1428-­35 [PubMed]

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