Exam

Post-Cardiac Arrest Care

Post-Cardiac Arrest Care, Stabilization following Cardiac Arrest, Post-Resuscitation Care, Post-Cardiac Arrest Syndrome, Stabilization following CPR, Return of Spontaneous Circulation, ROSC, Cardiac Arrest with Successful Resuscitation, Resuscitated Cardiac Arrest Event

Definitions

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
Out-of hospital Cardiac Arrest (OHCA)
1. More than 70% of Out-of hospital Cardiac Arrests are due to cardiac cause

Pathophysiology
Primary Post-Cardiac Arrest Syndrome Components

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
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
Myocardial dysfunction
1. Stunned Myocardium with both Systolic Dysfunction and Diastolic Dysfunction in 70% of post-arrest patients
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
4. Responds to inotropes and mechanical circulatory devices (IABP, pLVAD, ECMO)
5. Cha (2016) Resuscitation 106(S1):e79 [PubMed]
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

Pathophysiology
Other Post-Cardiac Arrest Syndrome Components

Pulmonary Dysfunction (with risk of ARDS and other lung injury)
1. Aspiration
2. Ventilation-perfusion mismatch
3. Pulmonary edema
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)

Evaluation

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

Management
Respiratory: Lung Protective Strategy

Consider Pulmonary Embolism as precipitating factor for Cardiac Arrest
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]
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
Prevent Ventilator Associated Pneumonia
1. Elevate head of bed
2. Oral care and Decontamination
3. Subglottic suction
4. Gastric Decontamination

Management
Circulatory

Prevent Hypotension
1. Keep Mean arterial pressure (MAP) >65 mmHg (best neurologic outcomes if MAP kept at 80-100 mmHg)
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
        However, studies show Epinephrine and Norepinephrine are effective at low pH
        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. Improved neurologic outcomes
    1. Younger patients (<65 to 75 years old)
    2. Witnessed Cardiac Arrest and CPR started immediately
    3. Reversible cause (e.g. Acute Coronary Syndrome)
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)
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 (and repeat in 10-15 minutes)
  1. Initial EKG (first 10-15 minutes) may demonstrate ST changes due to Defibrillation, Epinephrine
3. Early Angioplasty (PCI) indications
  1. History of Chest Pain prior to Cardiac Arrest
  2. Post-arrest EKG signs of ST Elevation Myocardial Infarction (STEMI)
    1. However even 32% without ST Elevation had Cardiac Arrest due to coronary lesion
    2. Millan (2016) Resuscitation 108:54-60 [PubMed]
  3. Ventricular Fibrillation as initial heart rhythm from EMS
    1. Any shockable rhythm may predict benefit with early PCI
4. Relative contraindications to early PCI (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]
5. References
  1. Orman and Mattu in Herbert (2015) EM:Rap 15(11): 8-9
  2. Dumas (2010) Circ Cardiovasc Interv 3(3):200-7 [PubMed]
  3. Hollenbeck (2014) Resuscitation 85(1): 88-95 [PubMed]
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

Management
Neurologic

Pupillary response is a strong predictor of outcome
1. Absent pupillary response is associated with a worse outcome
Induced Therapeutic Hypothermia (Targeted Temperature Management)
1. Goal is Return of Neurologic Function (RONF)
2. Class I indications
  1. Comatose patient with STEMI
  2. Out of hospital Cardiac Arrest with Ventricular Fibrillation or Pulseless Ventricular Tachycardia
3. Class 2b Indications
  1. All comatose patients with ROSC following Cardiac Arrest, regardless of initial rhythm
Seizures (20% of cases)
1. Consider continuous EEG monitoring
2. Treat with Ativan
3. Prophylaxis not initially needed unless Seizure occurs
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)
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

Management
Miscellaneous

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
Avoid Hyperglycemia (and Hypoglycemia)
1. Target Blood Glucose near 150 mg/dl with Insulin as needed
Elevate head of bed
1. Prevents aspiration in intubated patients
2. Decreases Intracranial Pressure
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
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)
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]
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
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
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)

Prognosis

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

References

Herbert and Crager in Herbert (2019) EM:Rap 19(2): 1-2
Mattu and Herbert (2012) EM: Rap 12(4): 5-6
Winters et al in Majoewsky (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]