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
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 V˙COX2 means lower minute volume requirements which means lower tidal volumes (protective lung ventilation)
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
Management
Targets
Normoxia:
Aim for a PaOX2 of around 100 mmHg
Aim for normocapnoea
In the first 24 hours aim for a termpature of 32-36 degrees (targeted temperature management)
Aim for a MAP > 65 mmHg and a SBP > 90 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
Other Considerations
Consider angiogram especially in patients with ECG evidence of myocardial ischaemia
