Management of Cardiac Arrest

Dr. Michael J. Baffsky

Intensive Care Registrar
Concord ICU
Concord Hospital
23rd February 2004
 Definition of Cardiac Arrest

• Abrupt cessation of cardiac pump function

which may be reversible by a prompt
intervention but will lead to death in its
absence

• Sudden Cardiac Death is the most common

cause of sudden natural death
 Definition of Cardiac Arrest

• Out Of Hospital

• In Hospital
 Incidence

• 1 in 100,000 per year in young adults

• 1 in 1000 per year in aged 45-75

 Causes Of Cardiac Arrest
 Coronary heart disease (most
common)
 Myocardial hypertrophy
 Cardiac inflammatory diseases
 Cardiac valvular disease
 Electrophysiologic
Abnormalities (e.g. WPW)
 Electrolyte disturbances
 Abnormal metabolic states
 Sympathetic nervous system
disorders
 Proarrhythmic toxic exposures
 Electrocution
 Tension pneumothorax
 Trauma
 Drowning
 Pulmonary embolism
 Causes Of Cardiac Arrest
 Coronary heart disease (most
common)
 Myocardial hypertrophy
 Cardiac inflammatory diseases
 Cardiac valvular disease
 Electrophysiologic
Abnormalities (e.g. WPW)
 Electrolyte disturbances
 Abnormal metabolic states
 Sympathetic nervous system
disorders
 Proarrhythmic toxic exposures
 Electrocution
 Tension pneumothorax
 Trauma
 Drowning
 Pulmonary embolism
 Causes Of Cardiac Arrest
 Coronary heart disease (most
common)
 Myocardial hypertrophy
 Cardiac inflammatory diseases
 Cardiac valvular disease
 Electrophysiologic
Abnormalities (e.g. WPW)
 Electrolyte disturbances
 Abnormal metabolic states
 Sympathetic nervous system
disorders
 Proarrhythmic toxic exposures
 Electrocution
 Tension pneumothorax
 Trauma
 Drowning
 Pulmonary embolism
 Are Arrests Predictable?

• Genetic
– general
– specific
• Congenital long QT interval syndromes
• Right ventricular dysplasia
• Brugada Syndrome (RBBB with non-ischemic ST-
segment elevations
 Survival Of A Cardiac Arrest

• <5% of people survive an “out of hospital”

arrest

• Statistics vary on “in hospital” arrests

 The 'chain of survival' concept

• To improve survival in an arrest:-

 Recognition of the cardiac arrest
 Early activation of emergency services
 Early basic life support
 Early defibrillation
 Early advanced life support
 How Does An Arrest Present?

• Patient found, usually unconscious

– most often by a nurse
• An arrest is called
– (Do YOU know the emergency number?)
• BLS should commence immediately
• The nature of the arrest identified quickly
• Appropriate action should be taken
 How Does An Arrest Present?
• Ventricular Fibrillation/Flutter (60%-80%)
• Ventricular Tachycardia
– Conscious and Unconscious (Pulseless)
• Supraventricular Tachycardia
• Pulseless Electrical Activity (EMD) (~10%)
• Cardiac Standstill (Asystole) (20%-40%)
– More difficult to treat with worse prognosis
 Ventricular Fibrillation (VF)

• Survivability decreases by 10% per minute

until normal rhythm restored
• Coarse or fine
• Fine may looks like asystole
– Could be equipment gain
– If any doubt, shock
Ventricular Fibrillation
 Ventricular Tachycardia (VT)

• Conscious
– Treat pharmacologically

• Unconscious
– Treat as for VF
AF with WPW
 Causes of Pulseless Activity
• PE • Tension PTx
• Hypovolaemia • Cardiac Tamponade
• Acidosis • Hypoxaemia

Treat the cause

 Asystole

• Impaired automaticity of SA node

• Problems with conduction pathways
– usually due to ischaemia/hypoxea
• Sympathetic reflex failure
• Acidotic and Ischaemic Environment
– may affect the efficacy of adrenalin
 Will My Efforts Be Successful?

• The probability of achieving successful

resuscitation from cardiac arrest is related
to the interval from onset to institution of
resuscitative efforts, the setting in which the
event occurs, the mechanism (VF, VT,
PEA, asystole) and the clinical status of the
patient prior to the cardiac arrest
 Point To Note

• VF or asystole without CPR within the first

4 to 6 min has a poor outcome, and there
are few survivors among patients who had
no life support activities for the first 8 min
after onset
 General Management

• Defibrillate (if indicated)

• AIRWAY
• BREATHING
• CIRCULATION
• ALS Measures
 In A WITNESSED Arrest

• A praecordial “thump” delivered to the

junction of the middle and lower third of
the sternum may occasionally revert VT or
VF
• It may convert VT to VF
• Works by delivering a 4J shock
 BLS vs ALS
• BLS = EAR + ECC = CPR
– (A,B,C)

• ALS = BLS +
Advanced Airway Management
IV meds
Defibrillation
Fluids
 Defibrillation
• When?
– VF/pulseless VT
– Torsades
– ? Asystole / fine VF (often post adrenalin)
• How much?
– 200/200/360 (mono)
– 120-150 (biphasic) can max to 200
– Biphasic may have less post-resus myocardial dysfunction (less
energy/thermal effects)
• When to sync?
 Defibrillation

• Paddle position
– Where should they be?
 Expired Air Resuscitation (EAR)

• “Mouth to Mouth”
• Bag mask….Aim 6-7 ml/kg TV
– Usually 100% O2 (EAR a misnomer here)
– LOS tone less… more TV increases risk of
gastric inflation
– Difficult to be accurate
• If you cant intubate, don’t waste time trying
 External Cardiac Compression
(ECC)

• Current ratio is 15:2 with one OR two

operators

• Compression rate 100/min

– Improves Coronary Perfusion Pressure
– Improves success of defibrillation
 EAR + ECC = CPR
• Rate of respiration = 12-15/min
– otherwise may cause positive pressure in the chest
and impair the venous return generated
• Must allow chest to recoil fully during ECC
– to gain full benefit of negative pressure
• ECC deliver about 1/3 normal SV
• Start without delay
– Don’t wait for the defibrillator
 IV Access

• Central line best

– direct access to heart
• Often peripheral access only one available
– Best is antecubital fossa or EJV
• Avoid veins below the diaphragm and distal
to the antecubital fossa
• Lots of flushes
 Most Commonly Used Drugs
• Adrenaline • CaCl2
• Atropine – Hypocalcaemia
• Amiodarone – Hyperkalaemia
– Ca++ channel blocker
• Adenosine
OD
• Lignocaine • MgSO4
• Sotalol – Torsades
• NaHCO3 – Refractory VF
 Adrenalin
• Mainstay of drug therapy
• Naturally occurring inotropic agent
• Both  and  effects
• Positive inotrope
• Increases SVR (and afterload)
• Short acting
• Can be given via ETT if no IV access
 Adrenalin

• Increasing doses (cumulatively) may

produce poor neurological outcomes post
VF arrest
– May be as low as 6mg
– If given 3-5 minutely, may be a time factor
 Atropine
• Anticholingeric
• Increases heart rate
• Useful in bradycardia
• May be of use in asystole (after adrenalin)
• Give enough
– at LEAST 300 mcg (usually 500mcg to 1mg)
– Otherwise may get paradoxical effects
• Can be given via ETT if not IV access
 Amiodarone

• Anti Arrhythmic
• Useful in refractory VF or Pulseless VT
• Give 300mg as bolus
– Then an infusion
 Adenosine

• Useful in SVT
• May be helpful in obtaining the diagnosis
• Ultra short acting
• Must be followed by large bolus flush
 Lignocaine

• Local anaesthetic
• Membrane stabilizing properties
• Dose 1mg/kg
– for refractory VF/VT
 Vasopressin
• Potent endogenous vasoconstrictor
• Unsure of its value
• Levels found to be higher in patients in whom CPR effective
(rather than died)
• Improves Coronary Perfusion Pressure
– (Diastolic aortic pressure - diastolic RAP)
• Improves Cerebral O2 delivery
• May have better neurological recovery
• May be of use in catecholamine resistance
• Its use is still under investigation
 Goals In A Cardiac Arrest

• Restore spontaneous pulse

• Restore BP
• Aim for no neurological deficit
• Know when to STOP