Cardio - Post Cardiac Arrest

Question 1

Mortality follow cardiac arrest

Answer 1

All cause out of hospital - 8.6%OOH with early CPR and defib > in hospital with deterioration (usually non-shockable)Depends on cause, age, and setting

Question 2

What makes up the post caridac arrest syndome

Answer 2

Triad of:
Myocardial Dysfunction
Reperfusion injury
Hypoxic brain injury

Question 3

Describe the myocardial dysfunction

Answer 3

Known as myocaridal stunning
Early echo - poor global function, generally improves
May be so severe that there is low cardiac output —> responds to inotropes
Early echo should be avoided unless suspicious of valve rupture or LV aneurysm

Question 4

Describe the Reperfusion Syndrome

Answer 4

Ischaemic tissue re-perfused
Cytokines and hypoxic metabolites released
Leads to VASOPLEGIA
Impaired oxygen utilisation
Hypotension —> may respond to vasopressors and filling

Question 5

Describe the hypoxic brain injury

Answer 5

Hypoxaemia —> primary injuiry by brain cell apoptosis
Secondary injury —> impaired cerebral autoregulation and cerebral oedema
Neuroprotection as per head injury
Attention to oxygenation and ventilation
Maintain CPP, Na, glucose and seizure control

Question 6

Management priorities post cardiac arrest

Answer 6

Airway - specially when GCS is lowAdequate oxygenation and maintain normal CO2.Maintain CPP —> raise MAP, fluid, vasopressor, inotropesSedationFind the cause —> pPCIAvoid hyperthermiaMaintain normoglycaemiaControl of seizures

Question 7

Poor prognostic indicators in OOHCA

Answer 7

Unwitnessed arrest - no bystander
PEA as initial rhythm
BLS longer than 10 minutes
ALS longer than 20-25 minutes

Question 8

Neuro prognostication

Answer 8

Absences of pupil/corneal reflexesMotor score < 2 Myoclonus status, NOT post hypoxic myoclonus (Lance Adams Syndrome)Neurone specific enolase levelsAbsence of N2O spike on SSEPBurst supression/epileptiform discharges —> hypoxic encephalopathy

Question 9

What investigations can be used in neuropronostication?

Answer 9

Electroencephalogram (EEG):
EEG features are associated with a poor outcome: generalized suppression, burst
suppression and an isoelectric EEG. An EEG may demonstrate subclinical
seizure activity. [1]
Bispectral index (BIS):
A modified EEG is obtained by attaching a specially designed electrode to the head and
gives a BIS value between 0 and 100, indicating the level of cerebral activity. A BIS
value of 0 predicts a poor neurological outcome. BIS scores > 0 have limited
prognostic value. Using suppression ratios alongside an actual BIS value may
improve predictive capability. [1]
Somatosensory-evoked potentials (SSEP):
A useful tool with a low false positive rate.
Evoked potentials are signals generated in the central nervous system after sensory
stimulation. The main response normally seen is the ‘N20’ signal in the primary
somatosensory cortex. This is a negative ‘N’ signal deflection 20 μs after electrical
stimulation of the median nerve. Bilateral loss of this response indicates cortical cell
death, provided that nerve function is intact at the brachial plexus. [1]
Radiological:
CT scanning of the head is of limited value and is often useful to exclude an initial
intracerebral event such as an intracerebral haemorrhage. Loss of grey–white
matter differentiation has not been shown as a useful prognostic indicator of the
long-term neurological outcome at an early stage. [1]
Biochemical markers:
Certain biochemical entities are thought to indicate cerebral damage. These include
neuronal specific enolase (NSE) and S-100b calcium binding protein. However,
biomarkers are still largely a research tool. Raised levels, after cardiac arrest, are
associated with the increased likelihood of a poor neurological outcome