Targeted temperature management
›Target and duration
›Active temperature control targeting a constant temperature of 32 to 36 C
›Class I recommendation for comatose adults after ROSC from cardiac arrest
›Maintained for at least 24 hours
›Fever avoidance for at least 72 hours after reaching target temperature
›Sustained fever after ROSC is independently associated with worse neurologic outcome
›Initiation
›Surface cooling devices or intravascular cooling catheters preferred
›Prehospital or ED cold IV fluid boluses for induction are not recommended
›Large volume cold crystalloid infusion increased rearrest and pulmonary edema without improving outcome in trial evidence
›Rewarming
›Controlled rewarming rate of 0.25 to 0.5 C per hour
›Rapid rewarming risks rebound hyperkalemia, vasodilatory hypotension, and cerebral edema
›Electrolyte and hemodynamic monitoring intensified during the rewarming phase
›Shivering control ladder
›Counter-warming of the hands and face
›Acetaminophen 1000 mg PO, NG, or IV every 6 hours, maximum 4000 mg per day
›Adjunct antipyretic only, not a substitute for device-based temperature control
›Buspirone 30 mg PO or via nasogastric tube every 8 hours
›Magnesium sulfate infusion to a target serum magnesium of 1.2 to 1.7 mmol/l
›Mild therapeutic hypermagnesemia for shivering suppression, kept below the neuromuscular toxicity threshold near 2 to 2.5 mmol/l
›Escalation to sedative infusion titrated to shivering control
›Neuromuscular blockade as a last resort
›Rocuronium 0.6 mg per kg IV bolus or vecuronium 0.1 mg per kg IV bolus, repeated as needed, or a continuous infusion titrated to train-of-four
›Requires continuous EEG monitoring because paralysis masks ongoing seizure or status epilepticus
›Train-of-four monitoring during infusion
›Minimize duration to reduce ICU-acquired weakness risk
Oxygenation and ventilation targets
›Oxygenation
›SpO2 94 to 98 percent
›Avoid PaO2 above 300 mmHg
›Hyperoxia promotes oxidative injury in reperfused, previously ischemic brain tissue
›Avoid hypoxemia
›Exception populations for the oxygen target
›Chronic hypercapnic respiratory failure, target individualized to baseline
›Carbon monoxide poisoning as the arrest cause, high FiO2 continued until carboxyhemoglobin clears
›Ventilation
›PaCO2 35 to 45 mmHg
›Hypocapnia causes cerebral vasoconstriction and worsens ischemic injury
›Hypercapnia causes cerebral vasodilation and can raise intracranial pressure
›Lung protective ventilation
›Tidal volume 6 to 8 mL per kg predicted body weight
›Plateau pressure limited below 30 cm H2O
›Exception populations for the ventilation target
›Chronic hypercapnia at baseline, target individualized to the patient's usual PaCO2
›Pre-existing pulmonary hypertension, avoid hypoxemia and acidemia more strictly given risk of right ventricular decompensation
Hemodynamic targets and vasopressor strategy
›Blood pressure and perfusion targets
›MAP at least 65 mmHg
›Impaired cerebral autoregulation after arrest makes cerebral perfusion pressure-passive
›Exception populations for the MAP target
›Chronic hypertension, higher MAP target of 80 to 100 mmHg considered given a right-shifted autoregulation curve
›Where available, cerebral oximetry or autoregulation monitoring used to individualize the target
›Avoid hypotension
›SBP under 90 mmHg associated with worse neurologic outcome
›Fluid strategy
›Cautious isotonic crystalloid boluses guided by dynamic assessment
›Avoid large volume rapid boluses
›Post-cardiac-arrest myocardial stunning limits tolerance for rapid volume loading
›Risk of precipitating pulmonary edema
›Vasopressor and inotrope selection
›Norepinephrine
›Initiate 0.05 mcg per kg per minute
›Titrate every 2 to 5 minutes to MAP target
›Typical maximum 1 mcg per kg per minute before escalation of strategy
›First line for the vasoplegic component of the systemic ischemia reperfusion response
›Dobutamine
›Initiate 2.5 mcg per kg per minute
›Titrate to perfusion and cardiac output every 10 to 15 minutes
›Typical range up to 10 mcg per kg per minute
›Added for low cardiac output from myocardial stunning, not a substitute for norepinephrine in vasoplegia
›Epinephrine infusion
›Initiate 0.05 mcg per kg per minute
›Titrate to hemodynamic response
›Reserved for combined vasoplegia and severe myocardial dysfunction
›Troubleshooting when the MAP target is not reached
›Reassess volume status and cardiac function with point of care echocardiography
›Consider stress dose hydrocortisone for suspected relative adrenal insufficiency from the systemic ischemia reperfusion response
›Hydrocortisone 50 mg IV every 6 hours
›Escalate to mechanical circulatory support evaluation if refractory
›Recognize transient myocardial stunning
›Typically improves over 24 to 48 hours with supportive care
›Avoid excess inotrope exposure that increases myocardial oxygen demand in stunned, recently ischemic tissue
Sedation, analgesia, and neuromuscular blockade
›Sedation strategy
›Propofol infusion
›Initiate 5 mcg per kg per minute
›Titrate every 5 to 10 minutes to sedation target
›Typical range up to 50 mcg per kg per minute
›Hypertriglyceridemia and propofol infusion syndrome risk with prolonged high dose use
›Midazolam infusion as an alternative
›Initiate 0.02 mg per kg per hour
›Titrate every 15 to 30 minutes
›Typical range up to 0.2 mg per kg per hour
›Prefer the shortest-acting agent that achieves comfort, since accumulated long-acting sedation delays the reliable exam needed for prognostication
›Analgesia
›Fentanyl infusion
›Initiate 0.5 mcg per kg per hour
›Titrate every 15 to 30 minutes
›Typical range up to 2 mcg per kg per hour
›Respiratory depression and hypotension risk
›Neuromuscular blockade
›Rocuronium or vecuronium bolus dosing for refractory shivering or ventilator dyssynchrony
›Requires continuous EEG whenever used
›Paralysis eliminates the only clinical sign of an ongoing seizure
›Minimize cumulative dose and duration
›ICU-acquired weakness risk increases with prolonged exposure
Seizure and myoclonus management
›EEG monitoring
›Continuous EEG initiated as soon as possible after ROSC
›Maintained for at least 24 to 48 hours or until an unequivocal interpretation is reached
›Indications for urgent EEG
›Clinical seizure activity or myoclonus
›Any patient receiving neuromuscular blockade
›Unexplained failure to awaken
›First line antiseizure therapy
›Levetiracetam IV
›Loading 60 mg per kg IV, maximum 4500 mg, infused over 10 to 15 minutes
›Minimal hemodynamic effect makes it preferred in this hemodynamically fragile population
›Valproate IV as an alternative
›Loading 20 to 40 mg per kg IV, maximum 3000 mg, infused over 10 to 15 minutes
›Avoid in known hepatic failure
›Refractory seizure escalation
›Escalate per the standard refractory status epilepticus pathway with continuous infusion sedation if seizures persist after first line loading
›Troubleshooting when seizures do not respond
›Confirm therapeutic antiseizure drug levels rather than assuming failure
›Reassess for a concurrent reversible cause, including electrolyte derangement from cooling or rewarming
›Prognostic caution
›Status myoclonus or seizure within the first 24 to 48 hours is an unfavorable marker but is not by itself sufficient to declare a poor prognosis or withdraw care
›Lance-Adams syndrome, a delayed post-hypoxic action myoclonus with potential for meaningful recovery, is distinct from early status myoclonus
Glucose and metabolic control
›Glucose target
›7.8 to 10 mmol/l
›Tighter control below 6 mmol/l avoided due to hypoglycemia risk in an already injured brain
›Insulin infusion
›Initiate 0.05 to 0.1 units per kg per hour
›Titrate per weight-based sliding scale protocol to the target range
›Hourly glucose checks during active titration
›Electrolyte repletion during TTM
›Potassium
›Permissive mild hypokalemia during the cooling phase, replete only if potassium under 3 mmol/l
›Full correction during cooling risks rebound hyperkalemia on rewarming
›Potassium chloride 10 mmol IV over 1 hour peripherally, up to 20 mmol IV over 1 hour via central access with continuous cardiac monitoring
›Magnesium
›Magnesium sulfate replacement to a target serum magnesium of 1.2 to 1.7 mmol/l, also supporting shivering control
Iatrogenic harms of routine interventions in this syndrome
›Intubation
›Laryngoscopy can provoke vagally mediated bradycardia or rearrest in the immediate post-ROSC period
›Induction agent choice affects hemodynamics in an already vasoplegic or stunned circulation
›Etomidate has less hypotension but may worsen relative adrenal insufficiency
›Ketamine preserves blood pressure but caution with catecholamine-depleted shock states
›Confirm placement with continuous waveform capnography, not auscultation alone
›Sedation
›Oversedation with long-acting agents delays the reliable exam needed for prognostication and can be mistaken for irreversible injury
›Undersedation risks awareness, shivering, and ventilator dyssynchrony during active cooling
›Fluid loading
›Rapid large volume crystalloid, especially cold fluid used for cooling induction, increases rearrest and pulmonary edema risk without outcome benefit
›Myocardial stunning limits the ability to tolerate rapid preload increases
›Oxygen
›Fixed high FiO2 continued after ROSC drives hyperoxia and worsens oxidative brain injury
›Titrate down as soon as pulse oximetry is reliable
›Vasopressors
›Excess catecholamine exposure increases myocardial oxygen demand in stunned, recently ischemic myocardium and raises arrhythmia risk
›Guide dosing with the lowest effective agent and dose rather than reflexive escalation
›Mechanical circulatory support
›Intra-aortic balloon pump is not routinely beneficial and is not indicated as a default adjunct for post-arrest cardiogenic shock
›ECMO or ECPR is selective, reserved for refractory shockable arrest with short low flow time and rapid access to a capable center, not a routine post-ROSC intervention
›Anticoagulation
›Needed for cath lab and PCI, but hypothermia-associated platelet dysfunction and coagulopathy from the systemic ischemia reperfusion response raise bleeding risk
›Balance thrombotic risk against bleeding risk when selecting anticoagulant intensity
›Fibrinolysis
›Not indicated for cardiac arrest broadly
›Selective use when massive pulmonary embolism is the confirmed or strongly suspected precipitant
›Trial evidence does not support routine unselected use in undifferentiated arrest
›Analgesia
›Opioids can mask the neurologic exam and contribute to hypotension in a vasoplegic circulation
›Use the lowest effective dose and prefer short-acting agents