advanced_life_support.pdf

7/17/2019 Advanced_Life_Support.pdf

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ERC

Advanced Life Support

Doç.Dr.Oktay DEMİRKIRAN



ERC

Chain of survival



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CARDIAC MONITORING

&

RHYTHM RECOGNITION


http://slidepdf.com/reader/full/advancedlifesupportpdf 4/136ERC

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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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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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


•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


• Hypovolaemia


• Hypothermia• Tension pneumothorax

• Tamponade



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




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• 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


•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


• Hypovolaemia


• Hypothermia




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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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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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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• Hypovolaemia• Hypo/hyperkalaemia & metabolic disorders

• Hypothermia


• 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)



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


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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• Clinical features of cardiac arrest

• ECG normally associated with an

output




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• 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




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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:


– 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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– 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



ERC

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

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