Result of the heart ceasing to beat, or alternatively beating too fast, ultimately resulting in inadequate tissue perfusion - particularly to the brain
Importance of cardiac arrest
Our brain requires oxygen and nutrients when cardiac arrest occurs it does not receive these. After around 2 - 3 minutes without oxygen brain injury begins to occur. After 8 - 10 minutes irreparable brain damage can occur and chances of recovery plummet.
Causes of cardiac arrest
Ischemic heart disease (such as CAD or atherosclerosis)
Non-shockable (Everything else, ranging from asystole to normal sinus)
Manual defibrillation
Ensure pads are applied correctly
Have an energy select button, charge button, and shock button
Analyse every 2 minutes (equivalent to 5 cycles of 30:2 CPR)
Coached method
1. Continue Compressions
2. Oxygen Away
3. All Else Clear
4. Charging
5. Hands off
6. Evaluate Rhythm
7. Defibrillate/ Disarm
Advanced airways
Switch to continuous compressions
Ventilate once every 6 seconds
Do not squeeze the bag too hard
No need to remove oxygen when defibrillating
Be careful with SGA (Superaglottic airway) positioning and perform patency checks
Cannulation
Patient likely peripherally shut down, making access harder
Use a large bore cannula if possible
Consider timing relative to defibrillation
Prioritise safety and prepare for success
Drugs
Adrenaline
Amiodarone
Fluids
Adrenaline
Helps in cardiac arrest by increasing arterial pressure and coronary perfusion. Dose: 1mg administered via IV every 4 minutes (every second cycle)
Amiodarone
An antiarrhythmic that works by slowing down cardiac cell metabolism, to help slow the heart down. In paramedic scope only.
Fluids
Can cause injury or poor morbidity when used inappropriately, so use with caution.
Waveform Capnography
Measurement of exhaled carbon dioxide (CO2), displayed as a waveform and mmHg value on the monitor. Provides valuable information on patient's ventilationstatus.
Use of waveform capnography in cardiac arrest
Indicator for effectiveness of compression (aim for output of 20 mmHg or more, minimum of 10 mmHg)
One of the most effective and reliable indicators for ROSC (sudden increase indicates rebreathing)
Normal EtCO2 is 35-40mmHg
Paediatric considerations
Not a full head tilt in paediatrics, neutral position in infants
Anterior posterior pad placement when <8 years
One hand technique for <8 years and small children, two finger for infants
Two initial rescue breaths prior to commencing CPR
2:15 ventilation to compression ratio (no pause when advanced airway in situ)
Defibrillation Joules: 4 J/kg
No cannulation and drug administration for paediatrics
Correctable causes of cardiac arrest (Hs & Ts)
Things to consider as causes for the arrest, some can be fixed
Post ROSC cares
Prepare for rearrest
Manage patient with advanced airway supine
Work out resp rate and supplement if needed
Measure appropriate vital signs early and repeatedly
Obtain 12-lead early
Treat precipitating causes of arrest (think Hs and Ts)
Aim for Sp02 94-98%, normocapnia, normoglycaemia
Provide temperature management (aim for 32-36 degrees Celsius)
During CPR
Airway Adjuncts (LMA / ETT)
O2
Waveform Capnography
IV/IO access
Plan actions before interruptions compressions (e.g charge manual defib)
Drugs
Shockable rhythms
Adrenaline (1 mg after 2nd shock, then every 2nd loop)
Amiodarone (300mg after 3 shocks, Only in paramedic scope)
Non-shockable rhythms
Adrenaline (1mg immediately, then every 2nd loop)
Why do we shock these Rhythms?
The hope is that once defibrillation has knocked out all electrical activity, one of the hearts intrinsic pacemaker sites (preferably the SA node or at least the AV node) will resume function and set a more normal rhythm
Defibrillation Considerations
Do not defib conscious pts in our setting
Sedative is generally administered if necessary to shock a conscious pt → prepare for potential asystole
Do not defib pulse-producing rhythm even if the rhythm is weak and may deteriorate → natural pacemaker rhythm is better than manual cardiac compressions
Manual Defibrillation
1. Operator(s) must determine whether ECG is pulseless VT, TdP or VF
2. If one of these rhythms, administer shock
3. If not a shockable rhythm, defib must be disarmed and compressions continued
Paediatrics
1. Rhythm analysis performed using AED
2. Operator turn to manual defib to adjust the correct joules of defib for pt weight
3. Proceed in AED setting for first shock before switching to manual
Reversible Causes (4 Hʼs and 4Tʼs)
Hypovolemia
Hypoxia
Hydrogen Ions
Hypo/Hyperkalemia
Hypoglycaemia
Hypothermia
Toxins
Tamponade
Tension Pneumothorax
Thrombosis PE
Hypovolemia
Decreased volume in vasculature Less blood in blood vessels
Decreased tissue perfusion Less blood flow to bodyʼs tissues
Hypoxia
Low lvls of O2 in tissues of body
Body tissues are not getting enough oxygenated blood flow and oxygen supply
Hydrogen Ions
Acidosis in the blood → making blood acidic
Hypo/Hyperkalemia
Hypo = 3.5 seconds ECG changes<2.7
Hyper = 5.5 seconds
Hypoglycaemia
Low blood sugar
Hypothermia
Temp 35 degrees
Toxins
Calcium channel blockers
Beta blockers
Digoxin
TCAs
Cocaine
Tamponade
Fluid buildup around heart
Prevents filling of heart → reduced cardiac output CO
Tension Pneumothorax
Can happen during broken ribs from CPR that puncture lung or over-ventilation. Over-ventilation can cause alveoli in lungs to rupture
Thrombosis PE
Partial or complete pulmonary vessel blockage Stops or reduce flow of blood back to heart Pulmonary Vessel Occlusion)
COACHED - Process of pausing for rhythm check and defib