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7/17/2019 Advanced_Life_Support.pdf
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Advanced Life Support
Doç.Dr.Oktay DEMİRKIRAN
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Chain of survival
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CARDIAC MONITORING
&
RHYTHM RECOGNITION
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Objectives
To understand:• Indications & techniques for ECG
monitoring• Basic electrocardiography
• How to read a rhythm strip –cardiac arrest rhythms
–peri-arrest arrhythmias
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How to monitor the ECG (1):
Monitoring leads
• 3-lead systemapproximates to I, II, III
• Colour coded
• Remove hair
• Apply over bone
• Lead setting (II)
• Gain
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How to monitor the ECG (2):
Defibrillator paddles
• Suitable for “quick-look”
• Movement artefact
• Risk of spurious
asystole
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Cardiac arrest rhythms
• Ventricular fibrillation• Pulseless ventricular tachycardia
• Asystole• Pulseless Electrical Activity (PEA)
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How to monitor the ECG (3):
Adhesive monitoring electrodes
• “Hands-free”
monitoring and
defibrillation
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12-lead ECG
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12-lead ECG
• 3D electrical activity from heart
• More sophisticated ECG
interpretation
• ST segment analysis
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• Depolarisationinitiated in SA node
• Slow conduction
through AV node
• Rapid conduction
through Purkinjefibres
Basic electrocardiography (1)
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Basic electrocardiography
(2)
• P wave = atrialdepolarisation
• QRS = ventricular
depolarisation (< 0.12 s)
• T wave = ventricular
repolarisation
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Ventricular fibrillation
• Bizarre irregular waveform
• No recognisable QRS complexes• Random frequency and amplitude
• Unco-ordinated electrical activity
• Coarse / fine
• Exclude artifact
– movement
– electrical interference
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Asystole
• Absent ventricular (QRS) activity
• Atrial activity (P waves) may persist• Rarely a straight line trace
• Consider fine VF
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Pulseless Electrical Activity
• Clinical features of cardiac arrest
• ECG normally associated with anoutput
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How to read a rhythm strip
1. Is there any electrical activity?
2. What is the ventricular (QRS) rate?3. Is the QRS rhythm regular or irregular?
4. Is the QRS width normal or prolonged?
5. Is atrial activity present?6. How is it related to ventricular activity?
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ECG rhythm interpretation
• Effective treatment often possiblewithout precise ECG diagnosis
• Haemodynamic consequences of anygiven rhythm will vary
• Treat the patient not the rhythm
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What is the ventricular rate?
• Normal 60-100 min-1
• Bradycardia < 60 min-1
• Tachycardia > 100 min-1
Rate = 300
Number of large squares between
consecutive QRS complexes*
* At standard paper speed of 25 mm sec-1
, 5 large squares = 1 second
I th QRS h th l
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Is the QRS rhythm regular or
irregular?• Unclear at rapid heart rates
• Compare R-R intervals
• Irregularly irregular = AF
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DEFIBRILLATION
Cardiac Arrest
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Precordial Thump if appropriate
BLS Algorithm if appropriate
Attach Defib-Monitor
Assess
Rhythm
+/- Check PulseVF/VT Non-VF/VT
Defibrillate X 3
as necessary
CPR 1 min
CPR 3 min** 1 min if immediately
after defibrillation
During CPRCorrect reversible causes
If not already:•check electrodes, paddle position and contact•attempt / verify: airway & O2,
i.v. access•give epinephrine every 3 min•give amiodarone after 3 unsuccessful shocks
Consider: buffers, magnesium, atropine
Potential reversible causes:• Hypoxia
• Hypovolaemia
• Hypo/hyperkalaemia & metabolic disorders
• Hypothermia
• Tension pneumothorax• Tamponade
• Toxic/therapeutic disorders
• Thrombo-embolic & mechanical obstruction
Universal ALSAlgorithm
Unresponsive?
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p
Open airway
Look for signs of life
Call resuscitation team
CPR 30:2
Until Defib-Monitor Attach
Assess
Rhythm
Shockable(VF/pulslessVT)
Non shockable(PEA/ Asystole)
1 Shock150-3600J biphasic or
360 J monophasic
Immediately resume:
CPR 30:2 for
2 min
Immediately resume:
CPR 30:2 for
2 min
During CPRCorrect reversible causes
•check electrodes, paddle position and contact•attempt / verify: airway & O2,
i.v. accessGive interrupted compressions when airwaysecure•give epinephrine every 3-5 min
Consider: amiodarone, magnesium, atropine
Potential reversible causes:• Hypoxia
• Hypovolaemia
• Hypo/hyperkalaemia & metabolic disorders
• Hypothermia• Tension pneumothorax
• Tamponade
• Toxic/therapeutic disorders
• Thrombo-embolic & mechanical obstruction
Universal ALSAlgorithm
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Mechanism of defibrillation
• Definition
“The termination of fibrillation or absence ofVF/VT at 5 seconds after shock delivery”
• Critical mass of myocardium depolarised
• Natural pacemaker tissue resumes control
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Defibrillation
Success depends on delivery
of current to the myocardiumCurrent flow depends upon:
• Electrode position
• Transthoracic impedance
• Energy delivered
• Body size
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Transthoracic Impedance
Dependent upon:• Electrode size
• Electrode/skin interface• Contact pressure
• Phase of respiration• Sequential shocks
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Defibrillators• Design
– Power source
– Capacitor – Electrodes
• Types – Manual
– Automated – Monophasic or Biphasic waveform
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Defibrillator waveforms
Damped Monophasic Truncated Biphasic
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Biphasic Defibrillators
• Require less energy for defibrillation
– smaller capacitors and batteries
– lighter and more transportable
• Repeated < 200 J biphasic shockshave higher success rate for
terminating VF/VT than escalatingmonophasic shocks
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Goals for in-hospital defibrillation
• “Healthcare providers with a duty toperform CPR should be trained,
equipped, and authorised to
perform defibrillation”
• “The goal should be a collapse-to-
shock interval of less than 3
minutes in all areas of the hospital”
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A t t d t l d fib ill t
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Automated external defibrillators
• Analyse cardiacrhythm
• Prepare for shockdelivery
• Specificity forrecognition ofshockable rhythm
close to 100%
Automated external
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Automated external
defibrillators Advantages:
• Less training required
– no need for ECG interpretation
• Suitable for “first-responder” defibrillation
• Public access defibrillation (PAD)
programs
Automated External Defibrillation
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Automated External Defibrillation
• Attach adhesiveelectrodes
• Follow audible and visualinstructions
• Automated ECG analysis
- stand clear• Charges automatically if
shockable rhythm
• +/- manual override
Assess Victim
According to BLS guidelines
AED
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According to BLS guidelines
BLSIf AED not immediately available
Switch defibrillator ON
Attach electrodesFollow spoken/visual directions
ANALYSEShock
Indicated
No shock
Indicated
After every
3 shocksCPR 1 minute
If no
circulationCPR 1 minute
AED
Algorithm
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AED U
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AED Use:
• Airports
• Bus terminals• Shopping malls
• Hotels• Schools
• Hospital wards• Aircrafts
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Manual Defibrillation
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Manual Defibrillation
Relies upon:
• Operator recognition ofECG rhythm
• Operator charging machine
and delivering shock
• Can be used for
synchronised cardioversion
Defibrillator Safety
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Defibrillator Safety
• Never hold both paddles in one hand
• Charge only with paddles on casualty’schest
• Avoid direct or indirect contact
• Wipe any water from the patient’s chest
• Remove high-flow oxygen from zone of
defibrillation
Shock Energy
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Shock Energy
• Initial shock energy 200 J*, repeat
once if unsuccessful
• Subsequent shocks at 360 J*
• Shocks delivered in groups of three• If defibrillation restores the patient’s
circulation and VF/VT recurs, startagain at 200J*
*or biphasic equivalent
Defibrillation
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Defibrillation
A series of 3 shocks should bedelivered rapidly, do not interrupt thesequence for CPR or a pulse check
unless:
• Possible restoration of cardiac output• Uncertain ECG rhythm
Manual Defibrillation (1)
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Manual Defibrillation (1)• Diagnose VF/VT from
ECG and signs of cardiac
arrest• Select correct energy level
• Charge paddles on patient
• Shout “stand clear”
• Visual check of area
• Check monitor • Deliver shock
Manual Defibrillation (2)
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Manual Defibrillation (2)
• Reassess rhythm
• Keep paddles on chest between shocks
• Increase energy level
– use assistant, or
– replace paddle/s in defibrillator and select
energy level yourself
• No BLS between shocks unless prolonged
delays
Synchronised cardioversion
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Synchronised cardioversion
• Convert atrial or ventricular tachyarrhythmias
• Shock synchronised to occur with the R wave• Short delay after pressing discharge buttons -
keep defibrillator electrodes in place• Conscious patients: sedation or anaesthesia
• Check mode if further shock/s required
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Pulseless VT is treated with an
unsynchronised shock using
the VF protocol
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Stres points• Wet chest
• Hairy chest
• Plasters
• “Pacemaker”
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Summary
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Summary
• Defibrillation is the only effective means
of restoring cardiac output for the patient
in VF or pulseless VT
• Defibrillation must be performed
promptly, efficiently and safely
• New technology has improved machine
performance and simplified use
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ALS UNIVERSALTREATMENT ALGORITHM
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ObjectivesTo understand:
• Treatment of patients in:
–ventricular fibrillation andpulseless ventricular tachycardia
–asystole or pulseless electricalactivity (non-VF/VT rhythms)
Unresponsive?
Open airway
U i l ALS
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Look for signs of life
Call resuscitation team
CPR 30:2
Until Defib-Monitor Attach
Assess
Rhythm
Shockable(VF/pulslessVT)
Non shockable(PEA/ Asystole)
1 Shock150-200J biphasic or
360 J monophasic
Immediately resume:
CPR 30:2 for
2 min
Immediately resume:
CPR 30:2 for
2 min
During CPRCorrect reversible causes
•check electrodes, paddle position and contact•attempt / verify: airway & O2,
i.v. accessGive interrupted compressions when airwaysecure•give epinephrine every 3-5 min
Consider: amiodarone, magnesium, atropine
Potential reversible causes:• Hypoxia
• Hypovolaemia
• Hypo/hyperkalaemia & metabolic disorders
• Hypothermia
• Tension pneumothorax• Tamponade
• Toxic/therapeutic disorders
• Thrombo-embolic & mechanical obstruction
Universal ALS
Algorithm
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• Attempt defibrillation. Give one shock of 150-200 J biphasic (360 J monophasic).
• Immediately resume chest compressions (30:2) without reassessing the rhythm or feeling fora pulse
• Continue CPR for 2 min, then pause briefly to check the monitor:
– If VF/VT persists
• Give a further (2nd) shock of 150-360 J biphasic (360 J monophasic).
• Resume CPR immediately and continue for 2 min.
• Pause briefly to check the monitor.
• If VF/VT persists give adrenaline 1 mg IV followed immediately by a (3rd) shock of150-360 J biphasic (360 J monophasic).
• Resume CPR immediately and continue for 2 min.
• Pause briefly to check the monitor.
• If VF/VT persists give amiodarone 300 mg IV followed immediately by a (4th)shock of 150-360 J biphasic (360 J monophasic).
• Resume CPR immediately and continue for 2 min.• Give adrenaline 1 mg IV immediately before alternate shocks (i.e. approximately
every 3-5 min).
• Give further shocks after each 2 min period of CPR and after confirming thatVF/VT persists.
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– If organised electrical activity compatible
with a cardiac output is seen, check for apulse
• If a pulse is present, start post-
resuscitation care• If no pulse is present, continue CPR and
switch to the non-shockable algorithm
– If asystole is seen, continue CPR andswitch to the non-shockable algorithm.
Cardiac Arrest
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Precordial Thump if appropriate
BLS Algorithm if appropriate
Attach Defib-Monitor
Assess
Rhythm
+/- Check Pulse
VF/VT Non-VF/VT
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Precordial thump• Mechanical
shock
• Indication:
–witnessed or
monitored
cardiac arrest
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Precordial thump• Lower half of the sternum
• From a height of about 20 cm
• In first 10 seconds
In-hospitalBasic Life Support Patient Collapsed
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ppShout for HELP and assess responsiveness
Not responsive Responsive
Call cardiac arrest team / Get defibrillator
Start BLS if defibrillator not immediately
available
Call for medical assistance
Definite Pulse and Breathing Present?
Apply pads / monitor
Defibrillate if appropriate
Ventilate with oxygen
Chest compressions
ALS on arrival of Cardiac Arrest Team
Airway manoeuvres
Oxygen, monitor, i.v.
Find notes
Prepare handover
YesNo
Cardiac Arrest
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Precordial Thump if appropriate
BLS Algorithm if appropriate
Attach Defib-Monitor
Assess
Rhythm
+/- Check Pulse
VF/VT Non-VF/VT
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Ventricular Fibrillation
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• Bizarre irregular waveform
• No recognisable QRS complexes• Random frequency and amplitude
• Unco-ordinated electrical activity• Coarse / fine
• Exclude artifact – movement
– electrical interference
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Pulseless Ventricular Tachycardia• Monomorphic VT
–Broad complex rhythm
–Rapid rate –Constant QRS morphology
• Polymorphic VT –Torsade de pointes
Assess
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Rhythm
VF/VT
Defibrillate X 3
as necessary
CPR 1 min
Ventricular Fibrillation/
Pulseless VentricularTachycardia
Assess the rhytm
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Shockable
(VF / pulseless VT)
Shockable
150-200 J Biphasic or
360 J monophasic
Immediately resume:
CPR 30:2
2 min(without reassesing the rhytm or feeling a pulse)
Check the monitor VF / pulseless VT persistCheck the monitor
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VF / pulseless VT persist
2nd shock150-200 J Biphasic or
360 J monophasic
Immediately resume:
CPR 30:2
2 min
Adrenaline 1 mg (IV)
3rd shock150-200 J Biphasic or
360 J monophasic
Immediately resume:
CPR 30:2
2 min
VF / pulseless VT persist
Amiodarone 300 mg (IV)
4th shock150-200 J Biphasic or
360 J monophasic
Immediately resume:
CPR 30:2
2 min
Adrenaline 1 mg (İV)
Every 3-5 min
Immediately resume:
CPR 30:22 min
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• Drug-shock-CPR-rhytm check
During CPR
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gCorrect reversible causes
If not already:• check electrodes, paddle position and contact
• attempt / verify: airway & O2
i.v. access• give epinephrine / adrenaline every 3 min
• give amiodarone after 3 unsuccessful shocks
Consider: buffers, magnesium, atropine
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Potential reversible causes:• Hypoxia
• Hypovolaemia• Hypo/hyperkalaemia & metabolic disorders
• Hypothermia
• Tension pneumothorax• Tamponade
• Toxic/therapeutic disorders• Thrombo-embolic & mechanical obstruction
Chest compressions,
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airway and ventilation• Secure airway:
–Tracheal tube
–Laryngeal mask airway (LMA)
–Combitube
• Once airway secured, if possible,do not interrupt chest compressionsfor ventilation
Intravenous access and drugs
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VF/VT• Central veins versus peripheral
• Epinephrine / adrenaline 1 mg i.v. or2-3 mg tracheal tube
• Consider amiodarone 300 mg ifVF/VT persists after 3rd shock
• Alternatively - lidocaine 100 mg• Consider magnesium 8 mmol (2g)
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Amiodarone
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Actions:
• Lengthens duration of action potential
• Prolongs Q-T interval
• Mild negative inotrope - may cause
hypotension
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Magnesium Actions:
• Hypomagnesaemia often co-exists
with hypokalaemia
• Depresses neurological and
myocardial function
• Acts as a physiological calcium
blocker
Sodium Bicarbonate
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Actions:
• Alkalinising agent (increases pH)But may:
– increase carbon dioxide load – inhibit release of oxygen to tissues
– impair myocardial contractility
– cause hypernatraemia
Assess
Rh th
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Non-VF/VT
CPR 3 min** 1 min if immediately
after defibrillation
Rhythm
+/- Check Pulse
Asystole
Pulseless Electrical Activity (PEA)
Assess the rhytm VF/VT recurs
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CPR
30:2
Check the leads are attached
without stopping CPR
Adrenaline 1 mg (İV)Every 3-5 min
Atropine 3 mg (İV)
CPR 2 min
30:2
(Until airway secured)
Shockable rhytm algoritm
Adrenaline 1 mg (İV)
Every 3-5 min
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A t l
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Asystole
• Absent ventricular (QRS) activity
• Atrial activity (P waves) may persist
• Rarely a straight line trace
• Consider fine VF
A t l
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Asystole• Confirm:
– check leads (view via leads I and II)
– check ‘gain’
• Epinephrine / adrenaline 1 mg i.v.every 3 minutes
• Atropine 3 mg i.v. (or 6 mg via trachealtube)
At i
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Atropine Actions:
• Blocks effects of vagus nerve• Increases sinus node automaticity
• Increases atrioventricular conduction
‘S i ’ t l
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‘Spurious’ asystole• Only occurs after shock delivered
and subsequent monitoring withpaddles and gel pads
• More likely with increasing number ofshocks and high chest impedance
• Displays apparent ‘asystole’• Confirm rhythm with monitoring leads
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P lseless Electrical Acti it
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Pulseless Electrical Activity
• Clinical features of cardiac arrest
• ECG normally associated with an
output
Pulseless Electrical Activity
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Pulseless Electrical Activity
• Exclude / treat reversible causes• Epinephrine / adrenaline 1 mg every 3
minutes• Atropine 3 mg if PEA with rate < 60 min-1
(6mg via tracheal tube)
Non-VF/VT immediately
after defibrillation
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after defibrillation• Withhold epinephrine /adrenaline and
atropine - check rhythm and pulse after1 minute of CPR
–delay in recovery of monitor display –electrical stunning - few seconds of
true asystole after defibrillation –myocardial stunning - temporarily
impaired contractility
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DRUG DELIVERYDURING CPR
Objectives
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• Understand the reasons for
venous access• Review the equipment used
• Outline the routes used forvenous access
• Understand the associatedcomplications
Access to the circulation allows:
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Access to the circulation allows:
• Drug administration
• Fluid administration
• Taking blood samples
• Insertion of a pacing wire
Peripheral venous access
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Peripheral venous access• Upper limb
–Dorsum of the hand
–Forearm, antecubital fossa
• Neck
–External jugular vein
Complications of peripheral
venous accessEarly L t
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Early
• Failure to cannulate vein
• Haematoma formation• Extravasation of drugs, fluid
• Damage to surroundingstructures
• Air embolus
• Shearing/fracture of cannulaor needle
Late
• Thrombophlebitis
• Cellulitis
Central venous access
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Central venous access
• Internal jugular vein
• Subclavian vein
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Complications of central
venous cannulation
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venous cannulation• Arterial puncture
• Haematoma• Haemothorax
• Pneumothorax• Air embolism
• Damage to surrounding structures
• Arrhythmias
Tracheal administration
of drugs
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of drugs
• Inability to cannulate a vein• Need for tracheal tube in situ
• Adjustment of dose and volume
• Dispersal into bronchial tree
Tracheal administration of drugs
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Drugs that canbe given via thetrachea:
• Epinephrine• Lidocaine
• Atropine• Naloxone
Drugs that cannot begiven via the trachea
• Amiodarone
• Sodium bicarbonate
• Calcium
Summary
• If a peripheral cannula is in place and
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If a peripheral cannula is in place and
working, use it initially
• Central veins are the route of choice if
expertise is available, but beware of
complications
• The tracheal route can be used with
appropriate adjustment of dose
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DRUGS
Objectives
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Objectives• To understand the indications, doses and
actions of drugs used in resuscitation
• To understand the indications, doses andactions of some of the common drugsused to treat peri-arrest arrhythmias
EpinephrineI di ti
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EpinephrineIndications:
• All cardiac arrest rhythms
• Bradycardia• Special circumstances:
–anaphylaxis
Epinephrine
Dose:1 i t 10 l 1 10 000 (1 l
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• 1 mg intravenous 10 ml 1:10,000 (1 ml
1:1,000) every 2-3 mins during resuscitation• 2-3 mg via tracheal tube
• 2–10 mcg min-1 for atropine resistant
bradycardia
• 0.5ml 1:1,000 i.m., 3-5 ml 1:10,000 i.v.
in anaphylaxis, depending on severity
Epinephrine
Actions:
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α agonist arterial vasoconstriction
↑ systemic vascular resistance ↑ cerebral and coronary blood flow
β agonist ↑ heart rate
↑ force of contraction↑ myocardial O2 demand
(may increase ischaemia)
Atropine
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Indications:
• Asystole• Symptomatic bradycardias
• PEA (rate < 60 beats min-1)
Atropine
Dose:
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• Asystole / PEA (rate < 60 beats min-1)
– 3 mg i.v., once only – 6 mg via tracheal tube
• Bradycardia
– 0.5 mg i.v., repeated as necessary,maximum 3 mg
Atropine
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Actions:
• Blocks effects of vagus nerve
• Increases sinus node automaticity
• Increases atrioventricular conduction
Amiodarone
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Indications:
• Refractory VF / Pulseless VT
• Haemodynamically stable VT• Other resistant tachyarrhythmias
Amiodarone
Dose:
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• Refractory VF / Pulseless VT – 300 mg in 20 ml 5% dextrose, bolus i.v.
• Stable tachyarrhythmias
– 150 mg in 20 ml 5% dextrose over 10 mins
– Repeat 150 mg if necessary
– 300 mg in 100 ml 5% dextrose over 1 hour
Amiodarone
Actions:
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Actions:
• Lengthens duration of action potential
• Prolongs Q-T interval• Mild negative inotrope - may cause
hypotension
Magnesium
Indications:
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• Shock refractory VF(with possible hypomagnesaemia)
• Ventricular tachyarrhythmias(with possible hypomagnesaemia)
• Torsades de pointes
Magnesium
Dose:
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Shock Refractory VF• 2–4 ml 50% (4–8 mmol) i.v. over 1-2 mins
• Can be repeated after 10-15 minutes
Other circumstances
• 5 ml of 50% (10 mmol) i.v. over 30 mins
Magnesium
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Actions:
• Depresses neurological and
myocardial function• Acts as a physiological calcium
blocker
Lidocaine
I di ti
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Indications:
• Refractory VF / Pulseless VT
– when amiodarone is unavailable• Haemodynamically stable VT
– as an alternative to amiodarone
Lidocaine
Dose:
R f t VF / P l l VT
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• Refractory VF / Pulseless VT
– 100 mg i.v. – further boluses of 50 mg, max 200 mg
• Haemodynamically stable VT – 50 mg i.v.
– further boluses of 50 mg, max 200 mg
• Reduce dose in elderly or hepatic failure
Sodium Bicarbonate
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Indications:
• Severe metabolic acidosis (pH < 7.1)
• Hyperkalaemia
• Special circumstance –Tricyclic antidepressant poisoning
Sodium Bicarbonate
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Dose:
• 50 mmol (50 ml of 8.4% solution) i.v.
Sodium Bicarbonate
Actions:
( )
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• Alkalinizing agent (increases pH)
But may: – increase carbon dioxide load
– inhibit release of oxygen to tissues – impair myocardial contractility
– cause hypernatraemia – interact with adrenaline
Calcium
A ti
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Actions:
• Essential for normal cardiac contraction
• Excess may lead to arrhythmias
• The trigger for cell death in the
ischaemic myocardium
•Excess may impair cerebral recovery
Calcium
Indications:• Pulseless electrical activity caused by:
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Pulseless electrical activity caused by:
– severe hyperkalaemia – severe hypocalcaemia
– overdose of calcium channel blockingdrugs
Dose
• 10 ml 10% calcium chloride (6.8 mmol)Do not give immediately before or after
sodium bicarbonate
Adenosine
Indications:
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Indications:
• Broad complex tachycardia, uncertain
aetiology
• Paroxysmal supraventricular tachycardia
Adenosine
Dose:
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Dose:
• 6 mg intravenously, by rapid injection
If necessary, three further doses each
of 12 mg can be given every 1–2mins
Adenosine
A ti
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Actions:
• Slows conduction across the AV node
Must only be used in a monitored
environment
Naloxone
Dose:
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Dose:
• 0.2 - 2.0 mg i.v.
• May need to be repeated up to a
maximum of 10 mg
• May need an infusion
Naloxone
I di ti
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Indications:
• Opioid overdose
• Respiratory depression secondary to
opioid administration
Naloxone
Actions:
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• Opioid receptor antagonist
• Reverses all opioid effects, particularly
respiratory and cerebral• May cause severe agitation in opioid
dependence
Summary
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• Indications, dose and actions of drugsused during cardiac arrest
• Indications, dose and actions of drugsused in the management of peri-
arrest arrhythmias