Post-Cardiac Arrest

Immediate Priorities at ROSC

• Secure and confirm airway (intubate if comatose; waveform capnography)
• Obtain IV/IO access, continuous ECG, SpO₂, invasive arterial BP
• 12-lead ECG immediately post-ROSC
• Identify and treat reversible causes (4Hs & 4Ts)
• Transfer to ICU

Pathophysiology

• Endothelial response to prolonged hypoxia is pro-inflammatory mimicking Septic Shock; the hypotension is similarly responsive to noradrenaline
• There is post-cardiac arrest myocardial stunning for 48-72 hours during which period the heart is responsive to inotropes
• Adrenal dysfunction may exist despite elevated cortisol levels (i.e. relative adrenal insufficiency); can consider administration of corticosteroids in patients unresponsive to vasopressors
• Hypoxic brain injury
  • After restoration of circulation, the cerebral bloodflow autoregulation mechanism is impaired resulting in cerebral vasodilation and hyperaemia
  • Excess oxygen can genereate free radicals and neuronal lipid peroxidation
• Renal failure
• Ulceration of the gastric mucosa from hypoxia and other CPR related stomach injuries
• ARDS
  • Which can occur in a plethora of ways probably in tandem:
    • Failing left ventricle
    • Aspirated stomach contents
    • Pulmonary contusion from CPR Endothelial dysfunction
  • Lowering body temperature to result in lower $\dot{V}\mathrm{CO}{}_2$ means lower minute volume requirements which means lower tidal volumes (protective lung ventilation)
• Ischaemic Hepatitis

Aetiologies

• Cardiac arrest is the common pathway of any severe illness and therefore the differentials remain quite broad, nontheless here is a list of common causes:
  • Arrhythmia
    • VT/VF related to structural heart disease (remote MI, acute MI, HOCM, ARVC, myocarditis, cardiac sarcoidosis, amyloidosis)
    • VT/VF with a structurally normal heart (Torsades de pointes, WPW plus AF, Brudgada syndrome, Commotio cordis)
    • Bradycardia (e.g. heart block)
  • Primary respiratory arrest - note that agonal respirations are nonspecific and do not necessarily indicate a primary respiratory aetiology
    • Upper airway obstruction
    • Severe asthma or COPD
    • Tension pneumothorax
  • Primary neurologic arrest
    • Intracranial haemorrhage
    • Seizures (SUDEP = sudden unexpected death in epilepsy), status epilepticus
  • Toxicologic/metabolic
    • Overdose (e.g. opioids)
    • Hypoglycaemia
    • Hyperkalaemia, hypokalaemia, hypomagnesaemia
  • Any cause of profound shock

Assessment

• ECG immediately post ROSC with particular attention to:
  • Ischaemia
  • Brugada pattern
  • ARVC
  • QT interval (long QT syndrome)
  • Early repolarisation
  • Wolff-Parkinson-White pattern
  • Hypertrophic Cardiomyopathy
  • Evidence of PE
• Labs
  • Glucose
  • Basic labs (CMP, EUC, FBC, Coags, LFTs)
  • ABG/VBG
  • Troponin
    • Troponins at 12 hours post arrest (with a cut-off of 0.6 ng/ml, or 600 ng/L) had 96% sensitivity and 80% specificity for myocardial infarction which is probably not very useful
    • Mainly for monitoring for reinfarction
  • CRP
  • Blood cultures if concern for sepsis
  • B-HCG if required
  • Urine toxicology
• X-ray chest
• POCUS:
  • Lung POCUS
  • Echocardiogram
  • Abdominal USS evaluating for peritoneal blood or ascites
• CT head to pelvis
  • Purpose:
    • Find cause of cardiac arrest
    • Evaluate for complications of CPR (e.g. liver laceration)
    • CT head may provide information about neuroprognostication
    • Evaluate for evidence of aspiration/pneumonia
  • Protocol
    • Head CT: non-contrast is often adequate unless concern for a primary CNS pathology in which case consider CT angiography
    • Chest CT: Obtain CT angiography to exclude PE if this is a possibility
    • CT abdomen/pelvis with contrast is usually adequate
  • Timing
    • After initial resuscitation and stabilisation
• EEG

Management

Targets

Domain	Target / Recommendation	Guideline Source
O₂ (initial)	100% FiO₂ until SpO₂ measurable	AHA 2025, RCUK 2025
O₂ (maintenance)	SpO₂ 94–98% / PaO₂ 60–105 mmHg	AHA 2025, RCUK 2025
Ventilation	PaCO₂ 35–45 mmHg	AHA 2025, RCUK 2025
MAP	≥65 mmHg	AHA 2025, RCUK 2025
Temperature (comatose)	≤37.5°C (fever prevention); hypothermia 32–34°C uncertain benefit	ANZCOR 2024, RCUK 2025
Fever avoidance duration	≥72 hours post-ROSC	ANZCOR 2024, RCUK 2025
Glucose	4–10 mmol/L (avoid hypo and hyperglycaemia)	AHA 2025, RCUK 2025
ECG post-ROSC	Immediate 12-lead	AHA 2025
Coronary angiography	Immediate if STEMI; delayed if no ST↑ (OHCA)	RCUK 2025, BMJ BP
Neuroprognostication timing	≥72 hrs post-ROSC or post-rewarming	AHA 2025, ERC/ESICM 2021
Seizures (treatment)	Levetiracetam or valproate; no prophylaxis	RCUK 2025
Antibiotics	Not routine; low threshold if pneumonia suspected	AHA 2025, RCUK 2025

• Normoxia:
  • Aim for a $P_{\text{a}}\mathrm{O}{}_2$ of around 100 mmHg
• Aim for normocapnoea
• In the first 24 hours aim for a termpature of 32-36 degrees (targeted temperature management) except in:
  • Those with obvious good neurology
  • Those with uncontrollable bleeding (colder temperatures cause less platelet aggregation)
• Aim for a MAP ≥ 65 mmHg and a SBP > 100 mmHg
• Aim for a BSL between 8-10
  • NG feeding can commence during TTM
• Sedation
  • Avoid benzodiazepines as their clearance is decreased with hypothermia
  • Propofol and ramifentanil may be the most suitable combination

Ventilator Management

• Comatose patients post-ROSC should be intubated with waveform capnography confirmation
• Use 100% $F_{\text{i}}\mathrm{O}{}_2$ initially and once reliable $S_{\text{p}}\mathrm{O}{}_2$/ABG available titrate for normoxia ($S_{\text{p}}\mathrm{O}{}_2$ 94-98%, $P_{\text{a}}\mathrm{O}{}_2$ 75-100 mmHg)
• Aim for normocapnoea $P_{\text{a}}\mathrm{CO}{}_2$ 35-45 mmHg with lung protective tidal volumes and avoid hypocapnoea (causes cerebral vasoconstriction)
  • Strategy
    • Immediately after intubation, adjust the minute ventilation to achieve an end-tidal $\mathrm{CO}{}_2$ of 30-25 mmHg
      • Since $P_{\text{a}}\mathrm{CO}{}_2$ > end-tidal $\mathrm{CO}{}_2$, this will generally put $P_{\text{a}}\mathrm{CO}{}_2$ in the safe range
      • Then obtain an ABG/VBG to verify that $P_{\text{a}}\mathrm{CO}{}_2$ is within the target range
  • Exceptions
    • Patients with chronic hypercapnoea may benefit from being maintained at their chronic baseline $P_{\text{a}}\mathrm{CO}{}_2$
    • Patients with severe metabolic acidosis may benefit from a degree of respiratory comepensation if necessary to maintain a safe pH
• Nursing position 30° head up
• If significant aspiration can consider early antibiotics
• Do not routinely give bicarbonate for all cardiac arrest as it may cause increased intracellular acidosis as the bicarbonate is converted to $\mathrm{CO}{}_2$ with the release of $\mathrm{H}{}^{+}$ ions
  • Give bicarbonate in cardiac arrest associated with hyperkalaemia or tricyclic overdose

Haemodynamic Management

• Target MAP ≥ 65 mmHg
  • MAP goals can later be adjusted and individualised for example:
    • A higher MAP goal in a patient with oliguria and chronic hypertension
    • A lower MAP goal in a patient with cardiogenic shock
  • Additionally ARC guidelines recommends a MAP required to achieve a urine output > 1 mL/kg/hr and normal or decreasing plasma lactate
• Initiate vasopressors and fluid resuscitation as needed
  • Noradrenaline and fluid with/without dobutamine is usually most effective
  • ARC ALS 2 guidelines suggest insertion of an IABP where the above is inadequate
• Obtain continues ECG monitoring, invasive arterial BP and central venous access in comatose patients
• Avoid steroids routinely for post-arrest shock

Coronary Investigation

• ACS accounts for ~65% of out of hospital cardiac arrests with a shockable rhythm
• Indications for emergent angiogram
  • OMI on ECG
  • Cardiogenic shock attributable to coronary artery disease
  • Recurrent ventricular arrhythmias
  • Evidence of significant ongoing myocardial ischaemia
• Indications for delayed angiogram prior to discharge
  • Those with suspected cardiac aetiology especially in the presence of
    • An initial shockable rhythm
    • Unexplained left ventricular systolic dysfunction
    • Evidence of severe myocardial ischaemia
• Medical therapies may be indicated for patients with probably/definite type 1 MI

Temperature Control

• Actively prevent fever by targeting temperature ≤37.5°C for comatose patients post-ROSC
• Avoid fever ≥ 37.7°C for at least 72 hours post-ROSC in comatose patients
• Duration of termpature control should be at least 24 hours from achieving target and fever prevention should continue for 36-72 hours

Antiarrhythmic Therapy

• For most patients observation without antiarrhythmic therapy is recommended however consider in:
  • Recurrent arrhythmias
  • VT/VF arrest pending catheterisation
  • Persistent hypertension (e.g. propranolol)
• Electrolyte repletion
  • Aggressive magnesium repletion may be useful for shivering prevention and for some arrhythmias
  • Potassium repletion
• Refer all patients who had cardiac arrest in a shockable rhythm outside the context of STEMI or non-cardiac arrhythmogenic causes for ICD insertion prior to discharge

Seizure Management

• Use EEG to diagnose seizures
• First line anti-epileptic medications are levetiracetam and sodium valproate but routine seizure prophylaxis is not recommended

Targeted Temperature Management

• Patients who are able to follow commands only require supportive care, for those unable to follow commands the following applies
• Temperature control is recommended for:
  • OOHCA with initially shockable rhythm who remain unresponsive after ROSC
• Temperature control is suggested for:
  • OOHCA with initial non-shockable rhythm who remain unresponsive after ROSC
  • IHCA with any intiial rhythm who remain unresponsive after ROSC
• Temperature control
  • Target a temperature of 37.5°C in most patients especially if those who shiver when targeting lower temperatures (e.g. 36°C)
• Methods
  • Simple ice packs and/or wet towels
  • Cooling blankets or pads
  • Transnasal evaporative cooling
  • Intravascular heat exchanger placed in the femoral or subclavian veins
  • Infusion of cold saline or Hartmann’s solution
• Paracetamol 1000 mg q6hrly as an antipyretic, analgesic and anti-shivering agent
• If temperature control is used it should continue for at least 24 hours
• Rewarming should occur at 0.25-0.5°C/hour

Neuromanagement

• Sedation:
  • Typically propofol is the agent of choice initially; other alternatives include dexmedetomidine
• Ketamine infusion (0.1-0.3 mg/hr) is often helpful for both analgesia and shivering
• Avoid benzodiazepines or opioids as they may delay awakening and confound neuroprognostication
• EEG monitoring

Gastrointestinal Management

• Nutrition should be managed as usual
• Patients are at high risk of stress ulcerations so prophylaxis is recommended

Neuroprognostication

• Should not occur earlier than 72 hours post-ROSC or ≥72 hours from rewarming in cooled patients
• Examination
  • Pupillary and corneal reflexes
    • Between 0-24 hours:
      • A lack of pupillary response is nonspecific.
      • The presence of pupillary responses may be an encouraging sign (especially if they occur rapidly after cardiac arrest).
      • If both pupillary and corneal reflexes are present soon after ROSC, this suggests a favorable outcome.
    • After 72 hours:
      • The absence of any pupillary response is ~20% sensitive and ~99% specific for poor neurological outcome¹
      • The absence of any corneal reflex is ~30% sensitive and ~97-100% specific for poor neurologic outcome.
    • After 96 hours:
      • The lack of any pupillary response bilaterally approaches 100% specificity for poor neurological outcome.
      • The absence of corneal reflexes may approach 100% specificity for a poor neurologic outcome.
• Somatosensory evoked potentials
  • In short, the idea is that Per nerve stimulation should evoke a response in the cortical central neurons
• EEG at 24 hours after arrest
  • Hold any sedative infusions
  • Administer paralytics if necessary

Sources

• Deranged Physiology
  • Post-cardiac arrest syndrome (“Post-Resuscitation Syndrome”)
  • Approach to cardiac arrest and peri-arrest scenarios
  • Supportive management of the recently resuscitated patient
  • Mild therapeutic hypothermia for survivors of cardiac arrest
• IBCC
  • Post-cardiac arrest management (including neuroprognostication) - EMCrit Project
• Resuscitation Council (UK):
  • lms.resus.org.uk/modules/m30-v2-post-resuscitation/10346/resources/chapter_13.pdf
• American Heart Association
  • cpr.heart.org/-/media/CPR-Files/CPR-Guidelines-Files/2025-Algorithms/PCAC-Algorithm-ACLS-PCAC-250527.pdf?sc_lang=en
• Australia Resuscitation Guidelines: Advanced Life Support Level 2. Third Australian Edition. Gale M. et. al. March 2016

Footnotes

1. i.e. If the pupillary reflex is absent, then there’s a 99% change the patient will have a poor neurological outcome. If the pupillary reflex is present, then it does not say much (only 20% of patients with poor outcomes show absent pupils at 72 hours) ↩