Updates on

Post Cardiac Arrest Care

Nor’azim Mohd Yunos

Intensive Care Unit, Universiti Malaya Medical Centre
Chains of survival
October 2020

April 2021
June 2021

Nov 2022

Jan 2024
Post-Cardiac Arrest Care
• Managing the brain injury
• To cool or not to cool
• Organ systems management
• Neuroprognostication
•Managing the brain injury
• To cool or not to cool
• Organ systems management
• Neuroprognostication
Normal 70-year-old man 48-year-old man 40 h post-arrest
Sandroni et al. Intensive Care Med 2021
Post-Cardiac Arrest Brain Injury (PCABI)
Primary Injury
• No-flow phase from onset of cardiac arrest until partial reperfusion is
established by cardiopulmonary resuscitation (CPR)
• The brain (only 2% of body weight) receives 15–20% of total cardiac
output → cessation of cerebral blood flow (CBF) severely affects oxygen
and glucose delivery, and thus brain tissue viability
Secondary Injury
• Begins with suboptimal low flow during CPR (at most 25% of CBF)
• With return of spontaneous circulation (ROSC), CBF is restored but
reperfusion of ischaemic tissue triggers secondary brain injury

Sandroni et al. Intensive Care Med 2021

 Secondary Brain Injury – reperfusion mechanisms

Calcium and intracellular changes in reperfusion injury

Immune inflammatory response in reperfusion injury

Sandroni et al. Intensive Care Med 2021
PCABI: Cerebral Autoregulation

• Narrower or right-shifted in 30-50% of patients

after cardiac arrest.
• If cerebral autoregulation is impaired:
↑ MAP → hyperemia → ↑ intracranial hypertension

Ameloot et al. Resuscitation 2021

Sekhon MS. Crit Care Med 2019
PCABI: Intracranial Hypertension

• Accumulating evidence of intracranial

hypertension in PCABI
Mechanisms:
• Cytotoxic oedema: cell swelling caused by
intracellular accumulation of fluid
• Vasogenic oedema: extracellular accumulation of
fluid from disruption of the blood-brain barrier
(BBB) and extravasation of serum proteins
Seizures
• Rates of clinical seizures in comatose patients after cardiac arrest
reported between 9-36%
• Often clinically silent and diagnosed only with EEG
• Sedation and neuromuscular blockade may mask clinical seizures

• Limited guidance on how often and how long should EEG be done
after cardiac arrest
• EEG also has a role in neuroprognostication
• To optimize cerebral O2 delivery, maintain haemoglobin > 7 g/dL and
arterial oxyhaemoglobin saturation between 92% and 98%
• In ICUs where advanced cerebral monitoring is not in routine use, target
an MAP > 80 mm Hg unless there are clinical concerns
65-75 mmHg vs 80-100 mmHg
• To optimize cerebral O2 delivery, maintain haemoglobin > 7 g/dL and
arterial oxyhaemoglobin saturation between 92% and 98%
• In ICUs where advanced cerebral monitoring is not in routine use, target
an MAP > 80 mm Hg unless there are clinical concerns
• In survivors with cerebral edema and elevated ICP (as measured by CT
brain, optic nerve ultrasound, or deterioration of clinical condition),
consider invasive ICP monitoring
• Monitor for seizures and status epilepticus with EEG as early as possible
after cardiac arrest and during the rewarming phase if hypothermia target
is used
• Monitor patients who fail to recover consciousness with cEEG to screen
for seizures or status epilepticus.
• Valproic acid and levetiracetam are reasonable first-line agents for seizure
treatment after CA
• Managing the brain injury
•To cool or not to cool
• Organ systems management
• Neuroprognostication
 939 pts,
80% shockable rhythm

531 pts,
non- shockable rhythm

1,900 pts,
all rhythms

Belur et al. Cardiol Ther 2023

A target temperature on the higher end of this range (36.0 to 37.5°C; maintenance of
normothermia) may be appropriate for patients with mild brain injury, higher bleeding
risk, trauma, recent surgery, septic shock, or patients with severe underlying comorbid
medical conditions since the risks of bleeding, arrhythmias, and electrolyte disturbances
are lower at this temperature compared with TH.

Patients who may benefit from a temperature target on the lower end of this range (33 to
36°C) include patients with stroke, severe brain injury (e.g., loss of motor response or
brainstem reflexes, malignant EEG patterns, or early CT scan changes suggesting the
development of cerebral edema), subarachnoid hemorrhage, or hepatic encephalopathy.
In these patients, a greater degree of hypothermia may help reduce cerebral edema and
seizure activity.
• Managing the brain injury
• To cool or not to cool
•Organ systems management
• Neuroprognostication
25
• Managing the brain injury
• To cool or not to cool
• Organ systems management
•Neuroprognostication

26
 Outcomes of Post-Cardiac Arrest Brain Injury
• 48-72 hours after ROSC:
mortality predominantly from cardiovascular
instability or multiorgan failure

• > 72 h after ROSC:

PCABI accounts for approximately two thirds of
mortality

• Massive cerebral oedema is common in these

patients

Risk factors for brain death:

• non-shockable initial rhythm,
• lower serum levels of sodium
Multimodal Neuroprognostication. AHA 2020.
Quantitative pupillometry
30
 Post-Cardiac Arrest Care
• Managing the brain injury
• To cool or not to cool
• Organ systems management
• Neuroprognostication
 Thank You
norazim@ummc.edu.my