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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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Which patients?• Cardiac arrest or other important
arrhythmias• Chest pain• Heart failure• Collapse / syncope• Shock / hypotension• Palpitations
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How to monitor the ECG (1):Monitoring leads
• 3-lead system approximates 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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• Depolarisation initiated in SA node
• Slow conduction through AV node
• Rapid conduction through Purkinje fibres
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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Pulseless ventricular tachycardia
• Monomorphic VT–Broad complex rhythm–Rapid rate–Constant QRS morphology
• Polymorphic VT–Torsade de pointes
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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 an
output
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How to read a rhythm strip1. 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 possible without precise ECG diagnosis
• Haemodynamic consequences of any given 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 = 300Number of large squares between consecutive QRS complexes*
* At standard paper speed of 25 mm sec-1, 5 large squares = 1 second
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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
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Cardiac ArrestPrecordial Thump if appropriate
BLS Algorithm if appropriate
Attach Defib-Monitor
AssessRhythm
+/- Check PulseVF/VT Non-VF/VT
Defibrillate X 3as necessary
CPR 1 minCPR 3 min*
* 1 min if immediatelyafter 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
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Unresponsive?
Open airwayLook for signs of life
Call resuscitation team
CPR 30:2Until Defib-Monitor Attach
AssessRhythm
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 of VF/VT at 5 seconds after shock delivery”
• Critical mass of myocardium depolarised• Natural pacemaker tissue resumes control
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DefibrillationSuccess depends on delivery of current to the myocardium
Current 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 shocks have higher success rate for terminating VF/VT than escalating monophasic shocks
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Goals for in-hospital defibrillation
• “Healthcare providers with a duty to perform 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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Automated external defibrillators• Analyse cardiac
rhythm• Prepare for shock
delivery• Specificity for
recognition of shockable rhythm close to 100%
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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
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Automated External Defibrillation• Attach adhesive
electrodes• Follow audible and visual
instructions• Automated ECG analysis
- stand clear • Charges automatically if
shockable rhythm • +/- manual override
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Assess VictimAccording to BLS guidelines
BLSIf AED not immediately available
Switch defibrillator ONAttach electrodes
Follow spoken/visual directions
ANALYSEShock
IndicatedNo shockIndicated
After every 3 shocks
CPR 1 minute
If nocirculation
CPR 1 minute
AED Algorithm
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AED Use:• Airports• Bus terminals• Shopping malls• Hotels• Schools• Hospital wards• Aircrafts
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Manual Defibrillation
Relies upon:• Operator recognition of
ECG rhythm• Operator charging machine
and delivering shock• Can be used for
synchronised cardioversion
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Defibrillator Safety
• Never hold both paddles in one hand• Charge only with paddles on casualty’s
chest• Avoid direct or indirect contact • Wipe any water from the patient’s chest• Remove high-flow oxygen from zone of
defibrillation
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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, start again at 200J*
*or biphasic equivalent
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Defibrillation
A series of 3 shocks should be delivered rapidly, do not interrupt the sequence for CPR or a pulse check unless:
• Possible restoration of cardiac output• Uncertain ECG rhythm
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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
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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
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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• 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 UNIVERSAL TREATMENT ALGORITHM
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Objectives
To understand:• Treatment of patients in:
–ventricular fibrillation and pulseless ventricular tachycardia
–asystole or pulseless electrical activity (non-VF/VT rhythms)
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Unresponsive?
Open airwayLook for signs of life
Call resuscitation team
CPR 30:2Until Defib-Monitor Attach
AssessRhythm
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 ALSAlgorithm
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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 for
a 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 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 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 that
VF/VT persists.
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– If organised electrical activity compatible with a cardiac output is seen, check for a pulse• 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 and
switch to the non-shockable algorithm.
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Cardiac ArrestPrecordial Thump if appropriate
BLS Algorithm if appropriate
Attach Defib-Monitor
AssessRhythm
+/- 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
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In-hospital Basic Life Support Patient Collapsed
Shout for HELP and assess responsiveness
Not responsive Responsive
Call cardiac arrest team / Get defibrillatorStart BLS if defibrillator not immediately
available
Call for medical assistance
Definite Pulse and Breathing Present?
Apply pads / monitorDefibrillate if appropriate
Ventilate with oxygenChest compressions
ALS on arrival of Cardiac Arrest Team
Airway manoeuvresOxygen, monitor, i.v.
Find notesPrepare handover
YesNo
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Cardiac ArrestPrecordial Thump if appropriate
BLS Algorithm if appropriate
Attach Defib-Monitor
AssessRhythm
+/- Check Pulse
VF/VT Non-VF/VT
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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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Pulseless Ventricular Tachycardia
• Monomorphic VT–Broad complex rhythm–Rapid rate–Constant QRS morphology
• Polymorphic VT–Torsade de pointes
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AssessRhythm
VF/VT
Defibrillate X 3as necessary
CPR 1 min
Ventricular Fibrillation/Pulseless Ventricular Tachycardia
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Assess the rhytm
Shockable(VF / pulseless VT)
Shockable150-200 J Biphasic or
360 J monophasic
Immediately resume:CPR 30:2
2 min(without reassesing the rhytm or feeling a pulse)
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Check the monitor
VF / pulseless VT persist
2nd shock150-200 J Biphasic or
360 J monophasic
Immediately resume:CPR 30:2
2 min
VF / pulseless VT persist
Adrenaline 1 mg (IV)
3rd shock150-200 J Biphasic or
360 J monophasic
Immediately resume:CPR 30:2
2 min
Check the monitor
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 30:2
2 min
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• Drug-shock-CPR-rhytm check
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During CPRCorrect 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
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Chest compressions, airway and ventilation
• Secure airway:–Tracheal tube–Laryngeal mask airway (LMA)–Combitube
• Once airway secured, if possible, do not interrupt chest compressions for ventilation
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Intravenous access and drugs VF/VT
• Central veins versus peripheral• Epinephrine / adrenaline 1 mg i.v. or
2-3 mg tracheal tube• Consider amiodarone 300 mg if
VF/VT persists after 3rd shock • Alternatively - lidocaine 100 mg• Consider magnesium 8 mmol (2g)
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Epinephrine/AdrenalineActions: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)
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Amiodarone
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
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Sodium BicarbonateActions:
• Alkalinising agent (increases pH)But may:– increase carbon dioxide load– inhibit release of oxygen to tissues– impair myocardial contractility– cause hypernatraemia
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Non-VF/VT
CPR 3 min** 1 min if immediately
after defibrillation
AssessRhythm
+/- Check Pulse
AsystolePulseless Electrical Activity (PEA)
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Assess the rhytm
CPR30:2
Check the leads are attachedwithout stopping CPR
Adrenaline 1 mg (İV)Every 3-5 min
Atropine 3 mg (İV)
CPR 2 min30:2
(Until airway secured)
VF/VT recurs
Shockable rhytm algoritm
Adrenaline 1 mg (İV)Every 3-5 min
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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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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 tracheal tube)
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Atropine
Actions:
• Blocks effects of vagus nerve• Increases sinus node automaticity• Increases atrioventricular conduction
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‘Spurious’ asystole
• Only occurs after shock delivered and subsequent monitoring with paddles and gel pads
• More likely with increasing number of shocks and high chest impedance
• Displays apparent ‘asystole’• Confirm rhythm with monitoring leads
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Pulseless Electrical Activity
• Clinical features of cardiac arrest• ECG normally associated with an
output
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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)
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Non-VF/VT immediately after defibrillation
• Withhold epinephrine /adrenaline and atropine - check rhythm and pulse after 1 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 DELIVERY DURING CPR
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Objectives
• Understand the reasons for venous access
• Review the equipment used • Outline the routes used for
venous access• Understand the associated
complications
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Access to the circulation allows:
• Drug administration
• Fluid administration
• Taking blood samples
• Insertion of a pacing wire
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Peripheral venous access
• Upper limb–Dorsum of the hand–Forearm, antecubital fossa
• Neck–External jugular vein
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Complications of peripheral venous access
Early• Failure to cannulate vein• Haematoma formation• Extravasation of drugs, fluid• Damage to surrounding
structures• Air embolus• Shearing/fracture of cannula
or needle
Late• Thrombophlebitis• Cellulitis
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Central venous access
• Internal jugular vein
• Subclavian vein
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Complications of central venous cannulation
• Arterial puncture• Haematoma• Haemothorax• Pneumothorax• Air embolism• Damage to surrounding structures• Arrhythmias
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Tracheal administration of drugs
• Inability to cannulate a vein• Need for tracheal tube in situ• Adjustment of dose and volume• Dispersal into bronchial tree
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Tracheal administration of drugs
Drugs that canbe given via the trachea:
• Epinephrine• Lidocaine• Atropine• Naloxone
Drugs that cannot be given via the trachea
• Amiodarone• Sodium bicarbonate• Calcium
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Summary• 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
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Objectives
• To understand the indications, doses and actions of drugs used in resuscitation
• To understand the indications, doses and actions of some of the common drugs used to treat peri-arrest arrhythmias
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EpinephrineIndications:
• All cardiac arrest rhythms• Bradycardia• Special circumstances:
–anaphylaxis
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EpinephrineDose:• 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
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EpinephrineActions: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)
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Atropine
Indications:
• Asystole• Symptomatic bradycardias• PEA (rate < 60 beats min-1)
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AtropineDose:• 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
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AtropineActions:• Blocks effects of vagus nerve
• Increases sinus node automaticity
• Increases atrioventricular conduction
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Amiodarone
Indications:
• Refractory VF / Pulseless VT• Haemodynamically stable VT• Other resistant tachyarrhythmias
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AmiodaroneDose:
• 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
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Amiodarone
Actions:
• Lengthens duration of action potential• Prolongs Q-T interval• Mild negative inotrope - may cause
hypotension
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MagnesiumIndications:
• Shock refractory VF (with possible hypomagnesaemia)
• Ventricular tachyarrhythmias (with possible hypomagnesaemia)
• Torsades de pointes
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MagnesiumDose:
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
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Magnesium
Actions:
• Depresses neurological and myocardial function
• Acts as a physiological calcium blocker
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LidocaineIndications:
• Refractory VF / Pulseless VT– when amiodarone is unavailable
• Haemodynamically stable VT– as an alternative to amiodarone
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LidocaineDose:• 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
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Sodium Bicarbonate
Indications:
• Severe metabolic acidosis (pH < 7.1)• Hyperkalaemia• Special circumstance
–Tricyclic antidepressant poisoning
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Sodium Bicarbonate
Dose:
• 50 mmol (50 ml of 8.4% solution) i.v.
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Sodium BicarbonateActions:• Alkalinizing agent (increases pH)
But may:– increase carbon dioxide load– inhibit release of oxygen to tissues– impair myocardial contractility– cause hypernatraemia– interact with adrenaline
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Calcium
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
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CalciumIndications:• Pulseless electrical activity caused by:
– severe hyperkalaemia– severe hypocalcaemia– overdose of calcium channel blocking
drugsDose• 10 ml 10% calcium chloride (6.8 mmol)
Do not give immediately before or after sodium bicarbonate
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Adenosine
Indications:
• Broad complex tachycardia, uncertain aetiology
• Paroxysmal supraventricular tachycardia
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AdenosineDose:
• 6 mg intravenously, by rapid injection
If necessary, three further doses each of 12 mg can be given every 1–2 mins
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Adenosine
Actions:• Slows conduction across the AV node
Must only be used in a monitored environment
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NaloxoneDose:
• 0.2 - 2.0 mg i.v.• May need to be repeated up to a
maximum of 10 mg• May need an infusion
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Naloxone
Indications:
• Opioid overdose• Respiratory depression secondary to
opioid administration
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NaloxoneActions:
• Opioid receptor antagonist• Reverses all opioid effects, particularly
respiratory and cerebral• May cause severe agitation in opioid dependence
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Summary
• Indications, dose and actions of drugs used during cardiac arrest
• Indications, dose and actions of drugs used in the management of peri-arrest arrhythmias
Advanced Life SupportChain of survivalCARDIAC MONITORING �& �RHYTHM RECOGNITIONObjectivesWhich patients?How to monitor the ECG (1):�Monitoring leadsHow to monitor the ECG (2):�Defibrillator paddlesCardiac arrest rhythmsHow to monitor the ECG (3):�Adhesive monitoring electrodes12-lead ECG12-lead ECGBasic electrocardiography (1)Basic electrocardiography (2)Ventricular fibrillationPulseless ventricular tachycardiaAsystolePulseless Electrical ActivityHow to read a rhythm stripECG rhythm interpretationWhat is the ventricular rate?Is the QRS rhythm regular or irregular?DEFIBRILLATIONMechanism of defibrillationDefibrillationTransthoracic ImpedanceDefibrillatorsDefibrillator waveformsBiphasic DefibrillatorsGoals for in-hospital defibrillationAutomated external defibrillatorsAutomated external defibrillatorsAutomated External DefibrillationAED Use:Manual DefibrillationDefibrillator SafetyShock EnergyDefibrillationManual Defibrillation (1)Manual Defibrillation (2)Synchronised cardioversionStres pointsSummaryALS UNIVERSAL �TREATMENT ALGORITHM�ObjectivesPrecordial thumpPrecordial thumpVentricular FibrillationPulseless Ventricular TachycardiaChest compressions, airway and ventilationIntravenous access and drugs �VF/VTEpinephrine/AdrenalineAmiodaroneMagnesiumSodium BicarbonateAsystoleAsystoleAtropine‘Spurious’ asystolePulseless Electrical ActivityPulseless Electrical ActivityNon-VF/VT immediately after defibrillationDRUG DELIVERY DURING CPRObjectivesPeripheral venous accessComplications of peripheral �venous accessCentral venous accessComplications of central venous cannulationTracheal administration �of drugsTracheal administration of drugsSummary�DRUGSObjectivesEpinephrineEpinephrineEpinephrineAtropineAtropineAtropineAmiodaroneAmiodaroneAmiodaroneMagnesiumMagnesiumMagnesiumLidocaineLidocaineSodium BicarbonateSodium BicarbonateSodium BicarbonateCalciumCalciumAdenosineAdenosineAdenosineNaloxoneNaloxoneNaloxoneSummary