What are the key components of post cardiac arrest management?

Post-Cardiac Arrest Management

Implement a comprehensive, structured, multidisciplinary system of care immediately after return of spontaneous circulation (ROSC) that includes hemodynamic optimization, targeted temperature management, early coronary intervention when indicated, optimized ventilation and oxygenation, and neuroprognostication—this bundled approach improves survival and neurological outcomes. 1, 2

Immediate Priorities After ROSC

Hemodynamic Stabilization

Target mean arterial pressure (MAP) ≥65 mmHg within the first 6 hours using goal-directed therapy. 2

• Administer 1-2 L IV bolus of normal saline or lactated Ringer's solution for hypotension (SBP <90 mmHg); if inducing hypothermia, consider using 4°C fluid 1
• If hypotension persists despite fluid resuscitation, initiate vasopressor support: 1, 2
  • Norepinephrine (preferred): 0.1-0.5 mcg/kg/min (7-35 mcg/min in 70-kg adult) 1, 3
  • Epinephrine: 0.1-0.5 mcg/kg/min (7-35 mcg/min in 70-kg adult) 1
  • Dopamine: 5-10 mcg/kg/min 1
• Target central venous pressure (CVP) >12 mmHg and central venous oxygen saturation (ScvO2) >70% within 6 hours 2
• Most deaths occur within the first 24 hours, with cardiovascular failure accounting for most deaths in the first 3 days 1, 2
• Post-cardiac arrest myocardial dysfunction peaks in the first 24 hours but typically recovers by 2-3 days 2, 4

Oxygenation Management

Titrate inspired oxygen to achieve arterial oxygen saturation of 94%—avoid both hypoxemia and hyperoxemia as both worsen outcomes. 1, 2, 5

• Initially use 100% oxygen during resuscitation, then titrate down once SpO2 monitoring is available 1
• Hyperoxemia (PaO2 >300 mmHg) is associated with worse neurological outcomes 4, 6
• Hypoxemia (PaO2 <60 mmHg) exacerbates secondary brain injury 4, 6
• Use facemask if saturation <94% for patients requiring supplemental oxygen only 2
• Continuously monitor with pulse oximetry 1

Ventilation Management

Avoid hyperventilation—target normocapnia with PETCO2 of 35-40 mmHg or PaCO2 of 40-45 mmHg. 1, 2

• Establish advanced airway (endotracheal intubation or supraglottic device) for mechanical ventilation 1, 2
• Confirm correct placement using waveform capnography 1, 2
• Start ventilation at 10-12 breaths/min and titrate to target 1
• Hyperventilation decreases cerebral blood flow and cardiac output—this is a common and harmful error 1, 4
• Elevate head of bed 30° if tolerated to reduce cerebral edema, aspiration, and ventilator-associated pneumonia 1
• Avoid circumferential ties around the neck that may obstruct venous return from the brain 1

Targeted Temperature Management (TTM)

Initiate targeted temperature management immediately for all comatose survivors (unable to follow verbal commands) to optimize neurological recovery. 1, 2

• Control body temperature to 32-34°C (therapeutic hypothermia) for 24 hours 1, 2
• Therapeutic hypothermia is the only intervention demonstrated to improve neurological recovery 1
• Prevent hyperthermia/pyrexia which exacerbates brain injury 2
• Manage shivering aggressively during TTM: 1
  • Use sedation deep enough to prevent awareness if neuromuscular blockade is employed
  • Be aware that neuromuscular blockade can mask clinical manifestations of seizures 1
• Drug metabolism and clearance are altered considerably during TTM, which can delay accurate neuroprognostication 1

Identify and Treat Underlying Cause

Acute Coronary Syndrome

Obtain 12-lead ECG as soon as possible and activate coronary reperfusion protocols for ST-elevation or high suspicion of acute myocardial infarction. 1, 2

• Perform early coronary angiography for patients with suspected cardiac cause and ST-segment elevation 1, 2
• Transport patients to facilities with percutaneous coronary intervention (PCI) capabilities 2
• Do not defer coronary intervention in the presence of coma or in conjunction with therapeutic hypothermia 1
• Coronary ischemia is the most common cause of cardiac arrest 1

Reversible Causes (H's and T's)

Systematically evaluate and treat all potentially reversible causes: 1

• Hypovolemia, Hypoxia, Hydrogen ion (acidosis) 1
• Hypo-/hyperkalemia, Hypothermia 1
• Tension pneumothorax, Tamponade (cardiac) 1
• Toxins, Thrombosis (pulmonary), Thrombosis (coronary) 1
• STEMI (ST-elevation myocardial infarction) 1

Prevent Secondary Complications

Neurological Monitoring and Protection

Avoid all factors that exacerbate brain injury: 2

• Prevent hypotension, hypercarbia, hypoxemia, and hyperoxemia 2
• Prevent pyrexia, hypoglycemia, and hyperglycemia 2
• Monitor for and treat seizures aggressively 2
• Post-cardiac arrest brain injury causes approximately two-thirds of deaths after out-of-hospital cardiac arrest 2

Metabolic Management

Maintain normoglycemia—both hypoglycemia and hyperglycemia worsen brain injury. 1, 2

• Implement glycemic control as part of structured interventions 1
• Provide appropriate nutrition support 2

Infection Prevention

Up to 70% of patients experience early infection after cardiac arrest, with the respiratory tract being the most common source. 6

• Maintain vigilance for early-onset pneumonia 6
• Implement aggressive diagnosis and early antimicrobial administration when infection is suspected 6
• Patients are at risk for ARDS due to aspiration, pulmonary contusions from chest compressions, systemic inflammation, and reperfusion injury 6

Systems of Care Approach

Transport patients to comprehensive post-cardiac arrest treatment centers with capabilities for acute coronary interventions, neurological care, goal-directed critical care, and therapeutic hypothermia. 1, 2

• Hospitals with higher cardiac arrest case volumes have better survival outcomes 1
• Implement multidisciplinary early goal-directed therapy protocols as a bundle of care rather than single interventions 1, 2
• For out-of-hospital cardiac arrest, transport to appropriate hospital with comprehensive post-cardiac arrest treatment system 1
• For in-hospital cardiac arrest, transport to appropriate critical-care unit capable of providing comprehensive care 1

Neuroprognostication

Delay prognostication and avoid early withdrawal of life-sustaining therapy—comatose patients on arrival may have good one-year neurological outcome. 1, 5

• Perform objective assessment of prognosis for recovery using structured protocols 1
• Drug accumulation during therapeutic hypothermia can confound neurological examination 1
• Excessively deep or prolonged sedation delays neuroprognostication 1
• Place patients in critical-care units where expert neurological evaluation and appropriate testing can be performed in a timely manner 1

Common Pitfalls to Avoid

• Do not hyperventilate—this is extremely common and harmful 1, 4
• Do not use excessive inspired oxygen once SpO2 monitoring is available 1, 2
• Do not use circumferential neck ties for airway securement 1
• Do not defer coronary intervention due to coma or therapeutic hypothermia 1
• Do not prognosticate too early, especially in patients treated with therapeutic hypothermia 1, 5
• Do not allow sedation to be excessively deep or prolonged—this increases complications including delirium, infections, prolonged ventilation, and ICU length of stay 1