How to optimise CPR
No benefit to CPR > 60mm depth. However, although pauses are associated with worse outcomes it might not be that it’s because it increases likelihood of terminating CPR.
ETCO2 is increasingly important and improvements in ETCO2 have been seen with increasing depth of CPR but not rate.
- Rate 100-120
- Depth 5-6 cm
- Minimise interruptions
- Use physiologically directed CPR (ETCO2 or blood pressure?) where possible
Drugs During CPR
- Evidence based on animal experiments
- Beta affects are detrimental
- Reduces cerebral microcirculation!
- Associated with improved short term but worsened long term outcomes
Vasopressin no better than adrenaline
Amiodarone improved ROSC but no survival benefit
However, OOHCA is different to IHCA and Greek trial suggested favourable neurological outcome with adren/vaso/steroids
Bad quality CPR won’t be saved by drugs
No benefit from high-dose (i.e. > 1mg) adrenaline
Cerebral Oximetry during and after CA
Cerebral oximeters use a variety of different arrangements of lights and detectors and assume a fixed ratio of arterial and venous blood, normally 25-30:70-75. Balance O2 delivery and uptake in real time. Normal range 60-75% and used more extensively in neurosurgical and cardiothoracic surgical settings.
Trends are probably more useful than individual values; however, really high initial values might be worth pursuing longer? Data limited. There is evidence that people with higher cerebral oxygenation values do better but overlap is significant between group and lacks specificity.
Identifying the cause of CA during CPR
Most CA are due to cardiac causes and account for 20-30% of all deaths. Most of this is IHD.
Hypoxia should be treated empirically. Hypovolaemia may be more difficult to diagnose if concealed, e.g. AAA, GI, spleen. Otherwise, follow the guidelines and get what you can from the history +/- ancillary tests such as echo.