2015 Resus council guidelines
It should be remembered that the algorithm divides patients into those with:
- 'shockable' rhythms: ventricular fibrillation/pulseless ventricular tachycardia (VF/pulseless VT)
- 'non-shockable' rhythms: asystole/pulseless-electrical activity (asystole/PEA)
Major points include:
- chest compressions
- the ratio of chest compressions to ventilation is 30:2
- chest compressions are now continued while a defibrillator is charged
- defibrillation
- a single shock for VF/pulseless VT followed by 2 minutes of CPR
- if the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then the 2015 guidelines recommend 'up to three quick successive (stacked) shocks', rather than 1 shock followed by CPR
- drug delivery
- IV access should be attempted and is first-line
- if IV access cannot be achieved then drugs should be given via the intraosseous route (IO)
- delivery of drugs via a tracheal tube is no longer recommended
- adrenaline
- adrenaline 1 mg IV as soon as possible for non-shockable rhythms
- during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock
- repeat adrenaline 1mg every 3-5 minutes whilst ALS continues (or every second rhythm check)
- amiodarone
- amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.
- a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered
- lidocaine used as an alternative if amiodarone is not available or a local decision has been made to use lidocaine instead
- thrombolytic drugs
- should be considered if a pulmonary embolus is suspected
- if given, CPR should be continued for an extended period of 60-90 minutes
Other points
- atropine is no longer recommended for routine use in asystole or pulseless electrical activity (PEA)
- following successful resuscitation oxygen should be titrated to achieve saturations of 94-98%. This is to address the potential harm caused by hyperoxaemia
Reversible causes of cardiac arrest:
