RESUSCITATION COUNCIL (UK)

ADVANCED LIFE SUPPORT PROVIDER COURSE

RC (UK)

Cardiovascular Disease
In Europe cardiovascular disease accounts for 40% of all deaths < 75 yrs One third of all people developing an MI die before reaching hospital Presenting rhythm in most of these cases is VF/VT In-hospital cardiac arrest more likely non-VF/VT
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Chain of Survival

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Cardiac Arrest
Precordial Thump if appropriate

Universal ALS Algorithm

BLS Algorithm if appropriate Attach Defib-Monitor

Assess Rhythm

VF/VT
Defibrillate X 3 as necessary CPR 1 min

+/- Check Pulse

Non-VF/VT

During CPR
Correct reversible causes If not already: check electrodes, paddle position and contact attempt / verify airway & O2 i.v. access give epinephrine every 3 min Consider: amiodarone, atropine / pacing buffers

CPR 3 min*
* 1 min if immediately after defibrillation

Potential reversible causes:

Hypoxia Hypovolaemia Hypo/hyperkalaemia & metabolic disorders Hypothermia Tension pneumothorax Tamponade Toxic/therapeutic disorders Thrombo-embolic & mechanical obstruction

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ALS Course Objectives

Standardised CPR for adults Multidisciplinary: Doctors, senior nurses & other healthcare personnel throughout Europe Resuscitation team members Resuscitation team leaders
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ALS Course Format

Manual common to RC (UK) and ERC Lectures Skill stations Cardiac arrest simulation (CAS) training
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ALS Course Assessment

MCQ Practical skills Cardiac arrest simulation (CASTest) Provider certificate valid for 3 years Revalidation

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CAUSES AND PREVENTION OF CARDIORESPIRATORY ARREST

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Objectives
To understand: The causes of cardiorespiratory arrest in adults How to identify patients at risk The role of a Medical Emergency Team The initial management of patients at risk of a cardiorespiratory arrest

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Causes of cardiorespiratory arrest 1. Airway obstruction

CNS depression Blood, vomit, foreign body Trauma Infection, inflammation Laryngospasm Bronchospasm
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Causes of cardiorespiratory arrest 2. Breathing inadequacy

Decreased respiratory drive
CNS depression

Decreased respiratory effort

neurological lesion muscle weakness restrictive chest defect

Pulmonary disorders
pneumothorax, lung pathology
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Causes of cardiorespiratory arrest 3. Cardiac abnormalities

Primary Secondary Ischaemia Asphyxia Myocardial infarction Hypoxaemia Hypertensive heart disease Blood loss Valve disease Septic shock Drugs Electrolyte abnormalities

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Recognition of patients at risk

History, examination, investigations Clinical indicators of deterioration before inhospital cardiac arrest in 80% tachypnoea tachycardia hypotension reduced conscious level

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Medical Emergency Team (MET) Calling Criteria

Airway -threatened Breathing Respiratory arrest RR < 5 or RR >36 Circulation cardiac arrest PR < 40 or PR >140 Systolic BP < 90

Neurology sudden fall in GCS > 2 Any other worries

RR = respiratory rate
PR = pulse rate
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Airway obstruction
Symptoms and signs Difficulty breathing, distressed, choking Shortness of breath Stridor, wheeze, gurgling See-saw respiratory pattern Actions Suction, positioning BLS manoeuvres Advanced airway intervention

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Breathing inadequacy
Symptoms and signs Short of breath, anxious, irritable Decrease in conscious level Tachypnoea Cyanosis

Action Oxygen Ventilatory support Treat underlying cause where possible

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Acute Coronary Syndromes

Clinical syndromes form spectrum of the same disease process:
Unstable angina Non-Q wave myocardial infarction Q wave myocardial infarction
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Stable angina
Pain from myocardial ischaemia tightness/ache across chest radiating to throat/arms/back/epigastrium provoked by exercise settles when exercise ceases NOT an acute coronary syndrome

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Unstable angina
Angina of effort with increasing frequency and provoked by less exertion Angina occurring recurrently and unpredictably - not specific to exercise Unprovoked and prolonged episode of chest pain - no ECG or laboratory evidence of MI

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Non-Q wave myocardial infarction

Symptoms suggesting MI Non-specific ECG abnormalities ST segment depression T wave inversion Elevated cardiac enzymes Unstable coronary artery disease unstable angina non-Q wave MI
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Non-Q wave myocardial infarction

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Q wave myocardial infarction

Prolonged chest pain Acute ST segment elevation Q waves Elevated cardiac enzymes creatine kinase troponins
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Anterolateral myocardial infarction

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Immediate treatment in all acute coronary syndromes

MONA Morphine (or diamorphine) Oxygen Nitroglycerine (GTN spray or tablet) Aspirin 300 mg orally (crushed/chewed)

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Patients with ST segment elevation MI or MI with LBBB

Early coronary reperfusion therapy: Thrombolytic therapy
streptokinase alteplase

Percutaneous transluminal coronary angioplasty (PTCA) Coronary artery bypass surgery (CABG)

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Indications for thrombolytic therapy for MI

Presentation < 12 h of typical chest pain, and: ST segment elevation: > 0.2 mV in 2 adjacent chest leads, or > 0.1 mV in 2 or more limb leads New onset left bundle branch block Dominant R waves and ST depression in V1-V3 Presentation 12-24 h after onset of pain with continuing pain +/- evolving MI on ECG
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Absolute contraindications to thrombolytic therapy

Previous haemorrhagic stroke Other stroke or CVA within 6 months Active internal bleeding Aortic dissection

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 MONA Heparin continuous infusion unfractionated, or subcutaneous low molecular weight Intravenous nitrate If high risk: glycoprotein IIb/IIIa inhibitor Consider beta-blockers
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Unstable angina and non-Q wave MI

Any Questions?

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Summary
Airway, breathing or cardiac problems can cause cardiorespiratory arrest Patients often have warning symptoms and signs Early recognition may allow arrest prevention In acute coronary syndromes consider MONA and start reperfusion therapy early, if indicated

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BASIC LIFE SUPPORT

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Objectives
To understand: The risks to the rescuer during resuscitation How to perform BLS The differences between layperson and in-hospital BLS
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Risks to the rescuer

Eliminate or minimise risk Manual Handling Beware of environmental danger: traffic electricity gas water
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Risks to the rescuer: poisoning

Hydrogen cyanide or hydrogen sulphide gas mask and non-return Corrosive chemicals absorbed through skin and respiratory tract protective clothing
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Risks to the rescuer: infection

15 documented cases of CPR related infection - mainly Neisseria meningitidis Tuberculosis Not hepatitis B or C, or CMV 3 cases of HIV transmission from high-risk cutaneous exposure
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Risks to the rescuer: precautions against infection

Gloves and eye protection Sharps box Face-mask with one-way valves Manikins clean regularly
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Assessment
Ensure safety of rescuer and victim

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Shake and Shout

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Is the victim responsive? YES

Check for injuries Reassess Get help
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Is the victim responsive? NO

Shout for help Open their airway Check for breathing

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Opening the airway

Head tilt Chin lift If cervical spine injury suspected: jaw thrust

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Assess Breathing
Look for chest movement Listen for breath sounds Feel for expired air Assess for 10 seconds before deciding breathing is absent
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Is the victim breathing? YES

If safe, use recovery position Telephone for help Reassess at intervals
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Recovery Position 1st Stage

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Recovery Position 2nd Stage

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Recovery Position 3rd Stage

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Recovery Position 4th Stage

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Is the victim breathing? NO

Telephone for help Give two slow effective rescue breaths Make up to 5 attempts

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Rescue breathing (Expired air ventilation)

Occlude victims nose Maintain chin lift Take a deep breath Ensure a good mouth-to-mouth seal
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Rescue breathing (Expired air ventilation)

Blow steadily (2 sec) into victims mouth Watch for chest rise Maintain chin lift, remove mouth Watch chest fall
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Watch for chest fall

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Finger sweep

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Assess Circulation
Look, listen and feel for normal breathing, coughing, or movement by the victim Check the carotid pulse (if trained) Take no more than 10 seconds

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Is a circulation present? YES

Continue with rescue breathing Reassess for signs of a circulation about every minute
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Is a circulation present? NO
Start chest compressions Continue with rescue breathing

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Identify costal margin

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Identify xiphisternum

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Identify hand position on sternum

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Chest compressions:
Depress sternum 4-5 cm Rate: 100 per minute

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Chest compressions

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One Person CPR

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Chest compression: breath ratio

15 compressions : 2 breaths for 1-person CPR 2-person CPR

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When to go for help?

Go for help immediately: More than one rescuer Single rescuer: adult with cardiac problem, once established that patient not breathing CPR for 1 minute first: Trauma Drowning Drug or alcohol intoxication Infant or child

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Continue resuscitation until:

Qualified help arrives and takes over The victim shows signs of life You become exhausted

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Mouth-to-nose ventilation
If mouth-to-mouth technically difficult If mouth seriously injured Rescue from water Resuscitation carried out by a child Aesthetic reasons
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Compression-only CPR
Reluctance to perform mouth-tomouth ventilation Chest compression alone better than no CPR If possible combine with head tilt Appropriate for telephone-CPR
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Cervical spine injury?

If possible, maintain alignment of head, neck and chest Minimum head tilt only Jaw thrust preferable Assistance often required

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Choking: Back Blows

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Abdominal Thrusts

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In-hospital Basic Life Support

Not responsive

Patient Collapsed

Shout for HELP and assess responsiveness Responsive

Definite Pulse and Breathing Present? No Call cardiac arrest team / Get defibrillator Start BLS if defibrillator not immediately available Apply pads / monitor Defibrillate if appropriate Ventilate with oxygen Chest compressions ALS on arrival of Cardiac Arrest Team Yes Call for medical assistance

Airway manoeuvres Oxygen, monitor, i.v.

Find notes Prepare handover RC (UK)

Any Questions?

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Summary
ABC of basic life support rescue breathing chest compressions modifications

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AIRWAY MANAGEMENT AND VENTILATION

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Airway management and ventilation

Basic airway management and ventilation The laryngeal mask airway and Combitube Advanced techniques of airway management Basic mechanical ventilation
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Basic airway management and ventilation Objectives

Causes of airway obstruction Recognition of airway obstruction Basic techniques for airway management Simple airway adjuncts Simple devices to ventilate the patients lungs
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 Upper Airway

Common causes of airway obstruction

tongue soft tissue oedema, foreign material blood, vomit

Larynx

laryngospasm, foreign material

Lower Airway

secretions, oedema, blood bronchospasm aspiration of gastric contents

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Recognition of airway obstruction

LOOK LISTEN
for chest/abdominal movement at mouth and nose for breath sounds, snoring, gurgling at mouth and nose for expired air
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FEEL

Opening the airway

Head tilt Chin lift Jaw thrust

CAUTION! cervical spine injury

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Head Tilt and Chin Lift

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Jaw Thrust

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Suction

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Simple airway adjuncts

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Sizing an oropharyngeal airway

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Oropharyngeal airway insertion

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Nasopharyngeal airway insertion

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Mouth to mask ventilation

Advantages: Avoids direct person to person contact Decreases potential for cross infection Allows oxygen enrichment Limitations: Maintenance of airtight seal Gastric inflation
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Bag-valve-mask, 2-person ventilation

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Advantages Limitations Avoids direct person When used with a to person contact facemask: Allows oxygen Risk of inadequate supplementation up ventilation to 85% Risk of gastric Can be used with inflation facemask, LMA, Need two persons Combitube, tracheal for optimal use tube
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Ventilation using self inflating bag

The Laryngeal Mask Airway and Combitube Objectives

To understand: The role of the LMA and Combitube during CPR

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Limitations Rapidly and easily No absolute inserted guarantee against Variety of sizes aspiration More efficient Not suitable if very ventilation than high inflation facemask pressures needed Avoids the need Unable to aspirate for laryngoscopy airway
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The Laryngeal Mask Airway Advantages

LMA Insertion

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The Combitube
Advantages Rapidly and easily inserted Avoids need for laryngoscopy Protects against aspiration Can be used if inflation pressures high Limitations Available in 2 sizes only Potential for ventilation via wrong lumen Damage to cuffs on insertion Trauma on insertion Single use RC (UK)

Ventilation with the Combitube

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Advanced techniques of airway management Objectives

To understand: The advantages and limitations of tracheal intubation during CPR The technique of tracheal intubation Methods for confirming correct placement of a tracheal tube The role of needle cricothyroidotomy
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Tracheal Intubation
Advantages Limitations Allows ventilation Training and with up to 100% O2 experience essential Isolates airway, Failed insertion, preventing aspiration oesophageal placement Allows aspiration of the airway Potential to worsen cervical cord or head Alternative route for injury drug administration
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Tracheal Intubation
Attempting intubation: Pre-oxygenate the patient Allow 30 seconds only for attempt Insert tube through larynx under direct vision If in doubt or difficulty, re-oxygenate before further attempts Patients are harmed by failure of oxygenation, not failure of intubation!
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Insertion of tracheal tube

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Confirming correct placement of a tracheal tube Direct visualisation at laryngoscopy

Auscultation:

Bilaterally, mid-axillary line Over the epigastrium

Symmetrical movement of the chest during ventilation Oesophageal detector device Capnometry
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Cricoid Pressure
Anteroposterior pressure on cricoid cartilage by an assistant to occlude the oesophagus against cervical vertebra
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Cricoid Pressure
Advantages Limitations Reduces risk of May make regurgitation and intubation more aspiration difficult Useful during May impair intubation, ventilation via ventilation with facemask , LMA facemask or LMA Avoid if active vomiting
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Needle Cricothyroidotomy

Indication Failure to provide an airway by any other means Complications Malposition of cannula

Emphysema Haemorrhage Oesophageal perforation

Hypoventilation
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Basic Mechanical Ventilation Objective

To understand: The role of simple automatic ventilators in the peri-arrest period

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Basic Mechanical Ventilation

Automatic ventilators: Free rescuer when patient is intubated Allow two hands to hold facemask if unintubated Provides specific tidal volume and rate High FiO2 Can be used with facemask, LMA, Combitube, tracheal tube
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Any Questions?

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Summary
Recognise and relieve airway obstruction using basic techniques Oxygen The role of the LMA, Combitube and tracheal intubation in managing the airway during CPR Ventilation techniques during CPR
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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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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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Basic electrocardiography (1)

Depolarisation initiated in SA node Slow conduction through AV node Rapid conduction through Purkinje fibres
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Basic electrocardiography (2)

P wave = atrial depolarisation QRS = ventricular depolarisation (< 0.12 s) T wave = ventricular repolarisation

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Cardiac arrest rhythms

Ventricular fibrillation Pulseless ventricular tachycardia Asystole Pulseless Electrical Activity (PEA)

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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 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 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 Bradycardia Tachycardia Rate = 60-100 min-1 < 60 min-1 > 100 min-1

300 Number 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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Is the QRS width normal or prolonged?

Normal QRS: < 0.12 s (< 3 small squares) originates from above bifurcation of bundle of His

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Is the QRS width normal or prolonged?

Prolonged QRS (> 0.12 s) arises from: ventricular myocardium, or supraventricular with aberrant conduction

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A broad complex tachycardia should be assumed to be ventricular in origin unless there is a very good reason to suspect otherwise.

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Is atrial activity present?

P waves (leads II and V1) Rate, regularity, morphology Flutter waves Atrial activity may be revealed by slowing QRS rate with adenosine

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How is atrial activity related to ventricular activity?

Consistent, fixed PR interval Variable, but recognisable pattern No relationship - atrioventricular dissociation

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Heart Block: First Degree

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Heart Block: Second Degree

Mbitz Type I (Wenckebach) Block

Mbitz Type II Block

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Heart Block: Third Degree

Site of pacemaker:
AV node 40 - 50 min-1 Ventricular myocardium 30 - 40 min-1
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Any Questions?

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Summary
Monitoring which patients techniques Recognition cardiac arrest rhythms other rhythms
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DEFIBRILLATION

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Objectives
To understand: What is meant by defibrillation The indications for defibrillation How to deliver a shock safely using: a manual defibrillator an automated external defibrillator (AED)
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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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Defibrillation
Success 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-toshock 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 Victim According to BLS guidelines

BLS
If AED not immediately available Switch defibrillator ON Attach electrodes Follow spoken/visual directions

AED Algorithm

ANALYSE
Shock Indicated
After every 3 shocks CPR 1 minute

No shock Indicated
If no circulation CPR 1 minute

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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 casualtys chest Avoid direct or indirect contact Wipe any water from the patients 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 patients 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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Any Questions?

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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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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 Late Failure to cannulate vein Thrombophlebitis Haematoma formation Extravasation of drugs, fluid Cellulitis Damage to surrounding structures Air embolus Shearing/fracture of cannula or needle

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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 can be given via the trachea: Epinephrine Lidocaine Atropine Naloxone Drugs that cannot be given via the trachea Amiodarone Sodium bicarbonate Calcium

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Any Questions?

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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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Epinephrine
Indications: All cardiac arrest rhythms Bradycardia Special circumstances: anaphylaxis
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Epinephrine
Dose: 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 210 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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Epinephrine
Actions: agonist vasoconstriction resistance arterial

systemic vascular

cerebral and coronary blood flow agonist

heart rate force of contraction

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Atropine
Indications: Asystole Symptomatic bradycardias PEA (rate < 60 beats min-1)
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Atropine
Dose: 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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Atropine
Actions: 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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Amiodarone
Dose:

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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Magnesium
Indications:

Shock refractory VF
(with possible hypomagnesaemia) Ventricular tachyarrhythmias (with possible hypomagnesaemia) Torsades de pointes

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Magnesium
Dose: Shock Refractory VF 24 ml 50% (48 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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Lidocaine
Indications:
Refractory VF / Pulseless VT when amiodarone is unavailable Haemodynamically stable VT as an alternative to amiodarone
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Lidocaine
Dose: 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 Bicarbonate
Actions: 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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Calcium
Indications: Pulseless electrical activity caused by: severe hyperkalaemia severe hypocalcaemia overdose of calcium channel blocking drugs Dose 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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Adenosine
Dose:
6 mg intravenously, by rapid injection If necessary, three further doses each of 12 mg can be given every 12 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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Naloxone
Dose: 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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Naloxone
Actions: Opioid receptor antagonist Reverses all opioid effects, particularly respiratory and cerebral May cause severe agitation in opioid dependence

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Any Questions?

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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
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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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Cardiac Arrest
Precordial Thump if appropriate

Universal ALS Algorithm

BLS Algorithm if appropriate Attach Defib-Monitor

Assess Rhythm

VF/VT
Defibrillate X 3 as necessary CPR 1 min

+/- Check Pulse

Non-VF/VT

During CPR
Correct reversible causes If not already: check electrodes, paddle position and contact attempt / verify airway & O2 i.v. access give epinephrine every 3 min Consider: amiodarone, atropine / pacing buffers

CPR 3 min*
* 1 min if immediately after defibrillation

Potential reversible causes:

Hypoxia Hypovolaemia Hypo/hyperkalaemia & metabolic disorders Hypothermia Tension pneumothorax Tamponade Toxic/therapeutic disorders Thrombo-embolic & mechanical obstruction

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Precordial thump
Indication: witnessed or monitored cardiac arrest

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Cardiac Arrest
Precordial Thump if appropriate BLS Algorithm if appropriate

Attach Defib-Monitor

Assess Rhythm +/- Check Pulse

VF/VT

Non-VF/VT
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Assess Rhythm +/- Check Pulse

VF/VT
Defibrillate X 3 as necessary

CPR 1 min

Ventricular Fibrillation/ Pulseless Ventricular Tachycardia

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VF/VT
Shock 200 J* Shock 200 J* Shock 360 J*

Deliver 3 shocks, if required, in < 1 minute Do not interrupt shock sequence for BLS After shock/s, palpate carotid pulse only if waveform compatible with a cardiac output

*or biphasic equivalent

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During CPR
Correct reversible causes If not already: check electrodes, paddle position and contact attempt / verify: airway & O2 i.v. access give epinephrine every 3 min Consider: amiodarone, atropine / pacing, buffers
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Chest compressions, airway and ventilation

Secure airway: tracheal tube LMA Combitube Once airway secured, do not interrupt chest compressions for ventilation
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Intravenous access and drugs VF/VT

Central veins versus peripheral Epinephrine 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
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VF/VT (continued)
Shock 360 J* Shock 360 J* Shock 360 J* Epinephrine every 3 minutes Consider bicarbonate 50 mmol if pH < 7.1 Consider paddle positions
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*or biphasic equivalent

Assess Rhythm +/- Check Pulse

Non-VF/VT
Asystole Pulseless Electrical Activity

CPR 3 min*
* 1 min if immediately after defibrillation
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Non-VF/VT immediately after defibrillation

Withhold epinephrine/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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Potential reversible causes:

Hypoxia Hypovolaemia Hypo/hyperkalaemia & metabolic disorders Hypothermia Tension pneumothorax Tamponade Toxic/therapeutic disorders Thrombo-embolic & mechanical obstruction
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Asystole
Confirm: check leads - view via leads I and II check gain Epinephrine 1 mg every 3 minutes Atropine 3 mg i.v. or 6 mg via tracheal tube
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Spurious asystole
When monitoring with paddle-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

Exclude/treat reversible causes Epinephrine 1 mg every 3 minutes Atropine 3 mg if PEA with rate < 60 min-1

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Any Questions?

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Summary
In patients in VF/pulseless VT attempt defibrillation without delay In patients in refractory VF or with a non-VF/VT rhythm identify and treat any reversible cause

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CARDIAC PACING

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Objectives
To understand: The peri-arrest indications for cardiac pacing How to perform percussion pacing How to apply safely transcutaneous electrical pacing The problems with temporary transvenous pacing
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The Cardiac Impulse

Normal heart beat arises in the sino- atrial (SA) node Regular spontaneous depolarisation- automaticity Natural pacemaker

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The Cardiac Conducting System

Sinoatrial node Intrinsic rate 60-70 per min Atrioventricular node

Atrioventricular junctional region Intrinsic rate 40-50 per min - Narrow QRS complex Distal His-Purkinje fibres Intrinsic rate 0 - 30 per min - Broad QRS complex
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Complete Heart Block (CHB)

Interruption between AV node and ventricles CHB at level of AV node Narrow QRS if pacemaker above division of bundle of His Intrinsic rate may be 50 beats min-1 CHB low in ventricle QRS broad and slow
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Artificial Pacemakers
Indicated when natural pacemaker too slow or unreliable Rarely successful in straight-line asystole Mechanical pacing Electrical pacing

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Artificial Pacemakers
Classification
Non-invasive Percussion pacing Transcutaneous pacing Invasive Temporary transvenous pacing Permanent implanted pacing Implantable cardioverter defibrillators (ICDs)
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Non-invasive Techniques Percussion Pacing

First described 35 years ago May produce good cardiac output Gentle blows lateral to lower left sternal edge

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Non-invasive Techniques Transcutaneous Pacing

Very quick to establish Easy to perform Avoids risks of central venous cannulation Applicable to nurses and paramedics as well as doctors
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Transcutaneous Pacing: Technique (1)

Remove excess chest hair Attach adhesive pads (and ECG electrodes if required) Pacing only = antero-posterior Multi-function = antero-lateral
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Transcutaneous Pacing: Technique (2)

Select demand mode Select rate (60 - 90 per min) Set pacing current to lowest value Turn on pacemaker Increase current until electrical capture (50 - 100 mA)

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Transcutaneous Pacing

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Transcutaneous Pacing Technique (3)

Palpable pulse = mechanical capture Analgesia and sedation may be required CPR is safe with electrodes attached Temporising measure Seek expert help
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Artificial Pacemakers
Classification
Non-invasive Percussion pacing Transcutaneous pacing Invasive Temporary transvenous pacing Permanent implanted pacing Implantable cardioverter - defibrillators (ICDs)
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Temporary Transvenous Pacing

Reasons for Failure
Problem 1. High threshold - loss of capture 2. Loss of electrical continuity - loss of pacing spike 3. Electrode displacement Solution Increase output
- displaced electrode?

Check power is on Check connections

Use non-invasive pacing

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Permanent Implanted Pacing Systems

Problems are rare Fracture of electrode is possible May fail to sense smaller QRS after infarct Place defibrillator paddles 12 - 15 cm from implanted pacing unit

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Implantable Cardioverter Defibrillator Systems (ICDs)

Overdrive pacing or DC shock Inappropriate response is possible Temporarily disabled by holding magnet over unit No risk of DC shock to rescuer
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Any Questions?

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Summary
Non-invasive pacing is easily performed Therapy of choice for immediate management of drug resistant bradyarrhythmias Non-invasive pacing is a temporising manoeuvre Seek expert help

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PERI-ARREST ARRHYTHMIAS

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Peri-arrest arrhythmias
To understand: The importance of arrhythmias that occur in the peri-arrest period The principles of management of these arrhythmias

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Peri-arrest arrhythmias
Principles of treatment
How is the patient? What is the arrhythmia?

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Adverse signs (1)

Low cardiac output Chest pain, pallor,cool peripheries, hypotension, reduced level of consciousness Excessive tachycardia Narrow complex >200 beats min-1 Broad complex >150 beats min-1
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Adverse signs (2)

Excessive bradycardia <40 beats min-1 or <60 beats min-1 if poor cardiac reserve Heart failure Pulmonary oedema, raised JVP, hepatic enlargement

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Treatment options
Bradycardias Cardiac pacing Tachycardias Cardioversion All Arrhythmias Antiarrhythmic and other drugs
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Cardiac pacing
Reliable method of treating bradycardias Requires expert help to insert transvenous pacing system Used in presence of adverse signs or when drugs have failed
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Cardioversion
Effective at converting tachyarrhythmias

to sinus rhythm
Used when adverse signs Drugs are relatively ineffective May cause VF ! Must use a synchronised shock Need for sedation / anaesthesia
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Antiarrhythmic and other drugs

May convert a tachyarrhythmia to sinus rhythm Less reliable than cardioversion Use when no adverse signs Used to treat bradycardias initially Less effective if cardiac output reduced

All drugs that are used to treat arrhythmias can cause arrhythmias !
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Bradycardia
Are there any adverse signs? Systolic blood pressure < 90 mmHg Heart rate < 40 beats min-1 Ventricular arrhythmias requiring suppression Heart failure If YES give atropine 500 g i.v. and assess response

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Bradycardia
If there is a satisfactory response to atropine, and There are NO adverse signs Determine the risk of asystole: Recent episode of asystole? Mobitz type II heart block? Complete heart block with wide QRS? Ventricular pause > 3 seconds?
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Bradycardia
1. 2. 3. 4. There is a risk of asystole If there is NO response to atropine Further doses of atropine, 3 mg maximum External pacing Epinephrine infusion, 2-10 g min-1 Arrange transvenous pacing SEEK EXPERT HELP !
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Bradycardia
If there is a response to atropine, and: There is NO risk of asystole
Observe the patient

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BRADYCARDIA
(Rate <40 beat min-1 or inappropriately slow for haemodynamic state)
Adverse signs? Systolic BP <90 mm Hg Rate < 40 beat min-1 Ventricular arrhythmias requiring suppression Heart failure

YES Atropine 500 g i.v. Satisfactory response?

NO

YES

NO YES Interim measures: Atropine 500 g i.v. repeat to maximum of 3 mg External pacing Epinephrine 2-10 g min-1 Seek expert help Arrange transvenous pacing

Risk of asystole? Recent asystole Mobitz II AV block Complete heart block with broad QRS Ventricular pause >3 s

NO Observe

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Broad complex tachycardia

Does the patient have a pulse? NO! follow the VF protocol
YES are there any adverse signs?
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Broad complex tachycardia

Adverse signs
Systolic blood pressure < 90 mmHg Chest pain Heart failure Rate > 150 beats min-1 NO
Antiarrhythmics

YES
Seek expert help

Seek expert help

Cardioversion

Cardioversion
Antiarrhythmics
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Correct hypokalaemia, give magnesium

Broad complex tachycardia

(Treat as sustained ventricular tachycardia)
If not already done, give oxygen and establish i.v. access

Pulse?

NO

Use VF protocol

YES Adverse signs? Systolic BP <90 mm Hg Chest pain Heart failure Rate >150 beat min-1

NO

YES

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NO

Adverse signs? Systolic BP <90 mm Hg Chest pain Heart failure Rate >150 beat min-1

If potassium known to be low see panel

Amiodarone 150 mg i.v. over 10 mins or Lidocaine i.v. 50 mg over 2 mins repeated every 5 mins to maximum dose of 200mg; Seek expert help Synchronised DC shock 100 J: 200 J: 360 J or equivalent biphasic energy

Give potassium chloride up to 60 mmol, max rate 30mmol h-1 Give magnesium sulphate i.v. 5ml 50% in 30min

If necessary, further amiodarone 150 mg i.v. over 10 mins, then 300 mg over I hour

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Adverse signs? Systolic BP <90 mm Hg Chest pain Heart failure Rate >150 beat min-1

YES Seek expert help Synchronised DC shock 100 J:200J: 360 J or equivalent biphasic energy If potassium known to be low, see panel Amiodarone 150 mg i.v. over 10 mins Further cardioversion as necessary For refractory cases consider additional pharmacological agents: amiodarone, lidocaine, procainamide or sotalol or overdrive pacing Caution drug-induced myocardial depression

Give potassium chloride up to 60 mmol, max rate 30mmol h-1 Give magnesium sulphate i.v. 5ml 50% in 30min

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BROAD COMPLEX TACHYCARDIA

(Treat as sustained ventricular tachycardia)
If not already done, give oxygen and establish i.v. access Pulse? YES Adverse signs? Systolic BP <90 mm Hg Chest pain Heart failure Rate >150 beat min-1 NO Use VF protocol

NO

YES

Seek expert help If potassium known to be low see panel Synchronised DC shock 100 J:200J: 360 J or equivalent biphasic energy

Amiodarone 150 mg i.v. over 10 mins or Lidocaine i.v. 50 mg over 2 mins repeated every 5 mins to maximum dose of 200mg;

Give potassium chloride up to 60 mmol, max rate 30mmol h-1 Give magnesium sulphate i.v. 5ml 50% in 30min

If potassium known to be low, see panel

Amiodarone 150 mg i.v. over 10 mins Seek expert help Further cardioversion as necessary

Synchronised DC shock 100 J: 200 J: 360 J or equivalent biphasic energy

For refractory cases consider additional pharmacological agents: amiodarone, lidocaine, procainamide or sotalol or overdrive pacing Caution drug-induced myocardial depression

If necessary, further amiodarone 150 mg i.v. over 10 mins, then 300 mg over I hour

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Atrial fibrillation
Treatment based on risk to patient from the arrhythmia

High risk
Rate > 150 beats min-1 Chest pain Critical perfusion

Low risk
Rate < 100 beats min-1 Mild or no symptoms Good perfusion

Intermediate risk
Rate 100-150 beats min-1 Breathlessness

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Atrial fibrillation
High risk
Rate > 150 bpm Chest pain Critical perfusion

SEEK EXPERT HELP !

1. Heparinisation 2. Synchronised shock 100J, 200J, 360J (or biphasic equivalent) 3. Amiodarone 300mg over 1 hour (may repeat once)
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Atrial Fibrillation: high risk

High risk? Rate > 150 beats min-1 Chest pain Critical perfusion YES

Seek expert help

Immediate heparin and synchronised DC shock 100J, 200J:360J or equivalent biphasic energy Amiodarone 300mg over 1 hour, may be repeated once if necessary

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Atrial fibrillation
Intermediate risk Rate 100-150 beats min-1 Breathlessness SEEK EXPERT HELP !
1. Poor perfusion or structural heart disease? 2. Onset within 24 hours?

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Atrial fibrillation
Intermediate risk
NO structural heart disease/poor perfusion
Onset > 24 hours ago: Control rate with drugs Onset < 24 hours ago: Heparinisation

OR
Anticoagulation Later synchronised DC shock

Antiarrhythmics
Synchronised DC shock if indicated

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Atrial fibrillation
Intermediate risk
structural heart disease / poor perfusion
Onset > 24 hours ago: Control rate with amiodarone (with anticoagulation) Later synchronised DC shock if indicated Onset < 24 hours ago: Heparinisation

Synchronised DC shock if indicated

Amiodarone

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Atrial fibrillation
Low risk Rate < 100 beats min-1 Mild or no symptoms Good perfusion
Onset > 24 hours ago: Consider anticoagulation Onset < 24 hours ago: Heparinisation

Later DC shock if indicated

Antiarrhythmics
DC shock if indicated
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Atrial Fibrillation
High risk? Rate > 150 beats min-1 Chest pain Critical perfusion Intermediate risk? Rate 100-150 beats min-1 Breathlessness Low risk? Rate < 100 beats min-1 Mild or no symptoms Good perfusion

YES

YES

YES

Seek expert help Seek expert help Immediate heparin and synchronised DC shock 100J, 200J:360J or equivalent biphasic energy

NO

Onset known to be within 24 hours?

YES

Anticoagulate with: Heparin Warfarin For later synchronised DC shock if indicated

Amiodarone 300mg over 1 hour, may be repeated once if necessary

Heparin Amiodarone: 300mg over 1 hr repeated once if necessary OR Flecainide 100-150 mg i.v. over 30 mins and/or DC shock if indicated

NO

Poor perfusion and/or known structural heart disease?

YES

NO Rate control with: Beta blockers, or Verapamil, or Diltiazem, or Digoxin, or Anticoagulate with: Heparin Warfarin, then Later DC shock if indicated

Onset known to be within 24 hours?

Onset known to be within 24 hours?

YES

YES Attempt cardioversion Heparin Flecainide 100-150 mg i.v., or Amiodarone 300 mg i.v. over 1 h Synchronised DC shock if indicated

NO

Initial rate control: Amiodarone 300mg over 1hour, may be repeated once if necessary AND Anticoagulation: Heparin Warfarin Later synchronised DC shock if indicated

Heparin Synchronised DC shock 100J, 200J, 360J or biphasic equivalent

Amiodarone 300mg over 1hour, may be repeated once if necessary

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Narrow complex tachycardia

(Presumed supraventricular tachycardia)

1. Rate > 250 beats min-1, pulseless 1. synchronised DC shock

2. Rapid AF 1. follow AF algorithm 3. Narrow complex, with pulse

follow SVT algorithm

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Narrow complex tachycardia

(Presumed supraventricular tachycardia)

1. Vagal manoeuvres
Valsalva Carotid sinus massage

2. Adenosine i.v.
6mg, rapid bolus 12mg, every 1-2 minutes, (max 3 doses)

If no effect: SEEK EXPERT HELP!

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NARROW COMPLEX TACHYCARDIA

(Presumed supraventricular tachycardia)
Pulseless (heart rate usually > 250 beats min-1) Narrow complex tachycardia Atrial fibrillation

Synchronised DC shock 100J, 200 J, 360 J or equivalent biphasic

Follow AF algorithm

If not already done, give oxygen and establish i.v. access Vagal manoeuvres (caution if possible digitalis toxicity, acute ischaemia, or presence of carotid bruit for carotid sinus massage) Adenosine 6 mg by rapid bolus injection; if unsuccessful, follow, if necessary, with up to 3 doses each of 12mg every 1-2 mins* Caution adenosine with known Wolf-Parkinson-White syndrome

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Narrow complex tachycardia

(Presumed supraventricular tachycardia Adverse signs Systolic BP < 90 mmHg Chest pain Heart failure Rate > 200 beats min-1 NO Antiarrhythmics (caution drug interactions)

YES Synchronised DC shock Amiodarone if necessary

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NARROW COMPLEX TACHYCARDIA

(Presumed supraventricular tachycardia)
Seek expert help Adverse signs? Systolic BP< 90 mm Hg Chest pain Heart failure Rate >200 beats min-1

NO

YES

Choose from: Esmolol: 40 mg over 1 min + infusion 4 mg min-1 (i.v. injection can be repeated with increments of infusion to 12 mg min-1 OR Verapamil 5-10 mg i.v. OR Amiodarone: 300 mg over 1 hour, may be repeated once if necessary OR Digoxin: maximum dose 500 g over 30 mins x2

Synchronised DC shock 100 J:200J: 360 J or equivalent biphasic energy

If necessary, amiodarone 150 mg over 10 mins then 300 mg over 1 hour, and repeat shock

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NARROW COMPLEX TACHYCARDIA

(Presumed supraventricular tachycardia)
Pulseless (heart rate usually > 250 beats min-1) Narrow complex tachycardia If not already done, give oxygen and establish i.v. access Synchronised DC shock 100J, 200 J, 360 J or equivalent biphasic Vagal manoeuvres (caution if possible digitalis toxicity, acute ischaemia, or presence of carotid bruit for carotid sinus massage) Adenosine 6 mg by rapid bolus injection; if unsuccessful, follow, if necessary, with up to 3 doses each of 12mg every 1-2 mins* Caution adenosine with known Wolf-Parkinson-White syndrome Follow AF algorithm Atrial fibrillation

Seek expert help

NO

Adverse signs? Systolic BP< 90 mm Hg Chest pain Heart failure Rate >200 beats min-1

YES

Choose from: Esmolol: 40 mg over 1 min + infusion 4 mg min-1 (i.v. injection can be repeated with increments of infusion to 12 mg min-1 OR Verapamil 5-10 mg i.v. OR Amiodarone: 300 mg over 1 hour, may be repeated once if necessary OR Digoxin: maximum dose 500 g over 30 mins x2

Synchronised DC shock 100 J:200J: 360 J or equivalent biphasic energy

If necessary, amiodarone 150 mg over 10 mins then 300 mg over 1 hour, and repeat shock

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Any Questions?

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Summary
Peri-arrest arrhythmias may need treatment to prevent cardiac arrest or to restore haemodynamic stability Treatment depends upon both the patients condition and the arrhythmia SEEK EXPERT HELP early

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CARDIAC ARREST IN SPECIAL CIRCUMSTANCES 1

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Objectives
To understand how resuscitation techniques should be modified in the special circumstances of:

Hypothermia Immersion and submersion Poisoning

Pregnancy Electrocution Anaphylaxis Acute severe asthma Trauma

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Special Circumstances
Common cause of cardiopulmonary arrest in younger age group Cardiac arrest often preventable Suitable patients may require a prolonged period of resuscitation
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Hypothermia
Definition: Core temp < 35 C (low reading thermometer) Mild Moderate Severe 32 - 35 C 30 - 32 C < 30 C
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Hypothermia
Special problems of: Immersion Elderly Very young Injury/illness Drugs/alcohol

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Clinical Features of Hypothermia

Pulse: BP: Pupils: CNS: slow, irregular, small volume or unrecordable dilated depressed conscious level, coma

Primary versus secondary hypothermia?

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Caution
The clinical features of hypothermia can mimic death Cerebral protective effect Not Dead until Warm and Dead, except: obvious lethal injuries body so frozen - resuscitation impossible in-hospital - clinical judgement

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Airway and breathing

Warm (40-46 C), humidified, high concentration oxygen Tracheal intubation as indicated on ALS algorithm with care Ventilation to make chest rise visibly

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Circulation
Beware extreme bradycardia Consider use of Doppler probe Oesophageal temperature Chest wall stiffness Central or large proximal veins
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Arrhythmias associated with hypothermia

Sinus bradycardia Atrial fibrillation Ventricular fibrillation Asystole

Temp

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Circulation
Defibrillation may not be successful until core temp > 30C Other arrhythmias spontaneously improve with warming alone Reduced efficacy of drugs < 30 C Bradycardia may be physiological in severe hypothermia

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Rewarming
Remove from cold environment Movement may precipitate arrhythmias Prevent further heat loss Rapid transfer to hospital Remove cold/wet clothing

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Active Rewarming
External
Forced air warming blankets

Internal (core)
Cardiopulmonary bypass Ventilation with warm humidified 02 Warm i.v. fluids (40 C) Gastric, peritoneal, pleural, bladder lavage Continuous veno-venous haemofiltration
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Monitoring and investigations

Continuous haemodynamic monitoring Repeated arterial blood gas analysis do not use temperature correction Electrolytes hyperkalaemia during rewarming Thyroid function (elderly)

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Immersion and Submersion

Immersion - head above water hypothermia cardiovascular instability Submersion - head below water asphyxiation hypoxia - secondary cardiac arrest Drowning - death within 24 hours of submersion event
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Decision to resuscitate
Full recovery possible even after prolonged immersion High risk of hypothermia if water temperature < 25C Submersion related to epilepsy or alcohol?

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Rescue from water

Minimise risks to rescuers Consider spinal injury Keep patient horizontal Do not attempt resuscitation in water unless trained

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Airway and breathing

Caution: possible spinal injury Give 100% oxygen Do not attempt to drain lungs Vomiting is common Early intubation if unconscious High risk of ARDS
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Circulation
Beware extreme bradycardia Hypovolaemia from squeeze effect Intravenous fluids Nasogastric tube Salt/fresh water unimportant

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Investigations
Arterial blood gas analysis Electrolytes Glucose ECG CXR
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Further management
If not had cardiac arrest consider discharge after 6 hours observation in hospital ONLY if: No clinical symptoms or abnormal clinical signs Normal Pa02 breathing room air Normal CXR No other worrying symptoms There is a small risk of late pulmonary oedema
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Poisoning and drug intoxication

A leading cause of death < 40 years Most commonly self-poisoning with therapeutic or recreational drugs Industrial accidents or warfare: chemical contamination radiation
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Resuscitation: Airway
Decreased conscious level common: airway obstruction respiratory arrest Avoid mouth-to-mouth ventilation if:
cyanide hydrogen sulphide corrosives organophosphates
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Breathing
High concentration of 02 (except paraquat) Intubate unconscious patients Arterial blood gas analysis Rapid sequence induction with cricoid pressure (expert help required)
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Circulation
Drug-induced hypotension is common Fluid therapy +/- inotropes Correct acid-base status Cardioversion for life-threatening arrhythmias

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Specific therapeutic measures

Limiting absorption of ingested poisons < 1 hour - gastric lavage & charcoal Enhance elimination haemodialysis haemoperfusion Specific antidotes

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Poisons Information
National Poisons Information Service TOXBASE Edinburgh NPIS

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Specific antidotes
Paracetamol Organophosphates Cyanides - N-acetylcysteine - Atropine - Sodium nitrite - Sodium thiosulphate - Dicobalt edetate - Fab antibodies - Naloxone
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Digoxin Opioids

Further Management
Prolonged coma - rhabdomyolysis Electrolytes (K+) and glucose Arterial blood gases Temperature

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Any Questions?

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Summary
Prompt and correct treatment may prevent cardiac arrest Modify advanced life support techniques for special circumstances of arrest

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CARDIAC ARREST IN SPECIAL CIRCUMSTANCES 2

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Objectives
To understand how resuscitation techniques should be modified in the special circumstances of: Hypothermia Immersion and submersion Poisoning

Pregnancy Electrocution Anaphylaxis Acute severe asthma Trauma

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Pregnancy: causes of maternal cardiac arrest

Haemorrhage Pulmonary embolism Amniotic fluid embolism Placental abruption Eclampsia Drug toxicity
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Resuscitation in pregnancy
Two people to resuscitate Early involvement of obstetrician and neonatologist

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Airway
risk of regurgitation Cricoid pressure Tracheal intubation (difficult): obesity of neck breast enlargement glottic oedema

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Breathing
Difficult because of: Diaphragmatic splinting High inflation pressures may be required

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Circulation
Supine position causes caval compression Displace uterus using: sandbags or (Cardiff) wedge manual displacement left lateral tilt Volume replacement Early surgical intervention if bleeding

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Emergency caesarian section in 3rd trimester if resuscitation unsuccessful after 5 minutes

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Electrocution

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Electrocution
Electricity (AC): domestic industrial Lightning strike (DC)

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Factors influencing severity

Current type and pathway through body alternating (AC) - VF more common direct (DC) - asystole more common Voltage Magnitude of delivered energy Resistance to current flow Area and duration of contact
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Electrical injury

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Lightning
Depolarisation of myocardium asystole or VF Respiratory muscle paralysis may cause respiratory arrest Widespread neurological damage

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Rescue with Safety

Switch off / isolate supply High tension may arc / jump spread through ground

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Resuscitation
Early BLS and ALS Early intubation if burns to face/neck Muscular paralysis may persist for 30 minutes after high voltage shocks

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Indications for admission

Cardiac arrest Loss of consciousness ECG abnormalities Soft tissue damage and burns

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Anaphylaxis
Anaphylaxis - hypersensitivity reaction mediated by IgE Anaphylactoid - similar reaction but not dependent on hypersensitivity Manifestations and management similar
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Common clinical features

Angio-oedema - laryngeal oedema Rash (urticaria / erythema) Hypotension vasodilatation & vascular permeability Bronchoconstriction Rhinitis, conjunctivitis Abdominal pain, vomiting & diarrhoea

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Resuscitation
Remove likely allergen High flow oxygen Epinephrine shock, stridor, etc - 0.5 ml 1:1000 i.m. profound shock - titration of 1:10,000 i.v. Fluids Antihistamine - H1, consider H2 Hydrocortisone and inhaled 2 agonist
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Consider when compatible history of severe allergic-type reaction with respiratory difficulty and/or hypotension especially if skin changes present Oxygen Stridor, wheeze, respiratory distress or clinical signs of shock

Epinephrine (adrenaline) 1:1000 solution 0.5 ml (500 micrograms) i.m.

Repeat in 5 minutes if no clinical improvement Antihistamine (chlorpheniramine) 10-20 mg slow i.v. IN ADDITION For all severe or recurrent reactions and patients with asthma give hydrocortisone 100-500 mg i.m./or slowly i.v. If clinical manifestations of shock do not respond to drug treatment give 1-2 litres i.v. fluid. Rapid infusion may be necessary
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Caution: early recurrence

Severe reactions with slow onset Reactions in severe asthmatics Continuing to absorb allergen Previous history of biphasic reactions

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Acute severe asthma

Largely reversible Deaths considered avoidable patients seek medical help late slow response by medical personnel premature discharge home
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Asthma and cardiac arrest

Hypoxia bronchospasm mucus plugging Arrhythmias hypoxia drug toxicity Tension pneumothorax
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Near fatal asthma: features

Silent chest Cyanosis Bradycardia Hypotension Exhaustion Coma Hypoxia, acidaemia, +/-hypercarbia
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Immediate treatment (1)

High concentration oxygen Inhaled 2-agonists Early steroids Subcutaneous epinephrine 300 g Inhaled anti-cholinergics, aminophylline i.v. Fluids
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Immediate treatment (2)

Mechanical ventilation only when maximal medical therapy has failed May not be possible to achieve normal blood gases

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Resuscitation of the asthmatic patient in cardiac arrest

Ventilation of lungs difficult
Bag-valve-mask gastric inflation Early intubation

Risk of tension pneumothorax Effective chest compression difficult Allow prolonged respiratory time Consider open chest cardiac massage
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Trauma related cardiac arrest

Causes: Severe brain injury Hypovolaemia, hypoxia Injuries to vital organs Tension pneumothorax Cardiac tamponade Underlying medical problems
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Resuscitation for trauma

Identify and treat life-threatening injuries before cardiac arrest Protect cervical spine Hypoxia and/or hypovolaemia PEA Oxygen, stop bleeding, fluids Resuscitative thoracotomy for cardiac arrest associated with penetrating injury
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Open chest cardiac massage: Indications

Recent cardiothoracic surgery PEA after penetrating trauma Hyperinflated lungs or fixed rib cage During abdominal or thoracic surgery

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Any Questions?

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Summary
Prompt and correct treatment may prevent cardiac arrest Modify advanced life support techniques for special circumstances of arrest

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POST RESUSCITATION CARE

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Objectives
To understand: The need for continued resuscitation after return of spontaneous circulation The need for monitoring and investigations How to facilitate safe transfer How to optimise organ function Prognostication after cardiac arrest

RC (UK)

The return of spontaneous circulation is the first step in the continuum of resuscitation

RC (UK)

Post Resuscitation Care

The goal: Normal cerebral function Stable cardiac rhythm Adequate organ perfusion

RC (UK)

Continued resuscitation: airway and breathing

Aim: to ensure a clear airway, adequate oxygenation and ventilation

Consider continued intubation, sedation and controlled ventilation in patients with obtunded cerebral function Avoid excessive hyperventilation
RC (UK)

Airway and breathing

Assess chest movement Listen for breath sounds Endobronchial intubation Simple/tension pneumothorax Collapse/consolidation Pulmonary oedema

RC (UK)

Continued resuscitation: circulation

Aim: the maintenance of normal sinus rhythm and a cardiac output adequate for perfusion of vital organs

RC (UK)

Circulation
Pulse and blood pressure Peripheral perfusion Right ventricular failure distended neck veins Left ventricular failure pulmonary oedema Measurement of CVP +/- PAP

RC (UK)

Continued resuscitation: neurological assessment

Glasgow Coma Scale Pupils Limb tone and movement Posture

RC (UK)

Further Assessment History

Health prior to the cardiac arrest Time delay before resuscitation Duration of resuscitation Cause of the cardiac arrest

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Further assessment Monitoring

ECG Pulse oximetry Blood pressure End tidal carbon dioxide Urine output Temperature
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Further assessment Investigations

Full blood count Biochemistry 12-lead ECG Chest X-ray Arterial blood gases

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RC (UK)

Post Resuscitation Care Chest X-ray

Fractured ribs, pneumothorax, aspiration, sub-diaphragmatic gas Tracheal tube CVP line Chest drain Nasogastric tube Pacing wire
RC (UK)

Arterial blood gases

Metabolic acidosis low pH (acidaemia), base deficit treatment increase cardiac output (fluids +/- inotropes) Respiratory acidosis low pH, high PaCO2 treatment increase ventilation
RC (UK)

Transfer of the patient

Aim: to facilitate a safe transfer of the patient between the site of resuscitation and an appropriate place of definitive care (critical care area)

RC (UK)

Transfer of the patient

Discuss with admitting team Cannulae, drains, tubes secured Chest drains Monitoring Patients notes Reassessment before leaving

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Optimising organ function Heart

Poor myocardial function despite optimal filling: seek expert help inotropes or mechanical support Reperfusion injury: arrhythmias myocardial stunning
RC (UK)

Optimising organ function Brain

Hyperaemia followed by hypoperfusion No cerebral autoregulation Maintain normal arterial pressure Control seizures Maintain normoglycaemia Do not rewarm patients with mild hypothermia (>33C)
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Prognostication
No neurological signs that can predict outcome in the first hours after ROSC Serum S-100 protein Somatosensory evoked potentials Poor outcome predicted at 3 days by: absent pupillary light reflexes absent motor response to pain
RC (UK)

Any Questions?

RC (UK)

Summary
The return of a spontaneous circulation does not mark the end of resuscitation Post-resuscitation care influences outcome Appropriate monitoring, safe transfer and continued organ support Prognostication difficult

RC (UK)

ETHICS AND LEGAL ASPECTS OF RESUSCITATION

RC (UK)

Objectives
To understand: The ethical and legal implications of the duty of care in regard to resuscitation The implications of Do Not Attempt Resuscitation orders and Advanced Directives The involvement of relatives in witnessing resuscitation attempts The considerations involved in the decision to stop a resuscitation attempt
RC (UK)

Failure to start resuscitation

Failure to recognise cardiac arrest has occurred Rescuer inadequacy Real or perceived risk to rescuer from attempting resuscitation

RC (UK)

CPR should be commenced routinely unless:

The patients condition indicates that successful resuscitation is unlikely to result in length or quality of life acceptable to the patient It is not in accord with the recorded, sustained wishes of a mentally competent patient
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The overall responsibility for the decision to perform resuscitation rests with the senior clinician in charge of the patients care.
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The appropriateness of resuscitation may be raised by:

The patient Relatives or close friends General Practitioner Medical staff Nursing staff

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Do Not Attempt Resuscitation (DNAR) Policy

Regularly reviewed and recorded in: Medical notes Nursing notes
Where possible must include prior consent of patient, explanation and justification.
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DNAR Orders apply to resuscitation only

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Deciding when to stop

Place
People Time

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Prolonged resuscitation
Indicated in special circumstances: Hypothermia Near drowning Drug overdose Children

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Advance Directives
Refusing CPR can be legally binding if certain safeguards are met and doctor is satisfied that request is genuine May be difficult in emergencies If in any doubt - Resuscitate
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Advanced Directives
Safeguards: Adult Patient mentally competent when decision made Circumstances foreseen Not under duress Patient aware of the implications

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Should relatives witness resuscitation?

May help in bereavement process Exclusion may be distressing Must be accompanied by appropriate person Team aware Patient takes priority Staff stress and training recognised

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Any Questions?

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Summary
It is important to commence resuscitation promptly and effectively To know when such measures are contraindicated To know when resuscitation attempts should cease

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A colleague states that she doesnt want to be resuscitated if she ever has a cardiac arrest. The next week she sustains a cardiac arrest in front of you. Do you start resuscitation? You find out that she was diagnosed last week with cancer and is taking anti-depressants. Do you continue resuscitation? Her partner arrives and asks you to reverse your decision What do you do?
RC (UK)

An 82 year old woman falls and sustains a fractured neck of femur. She lives in sheltered housing, is prone to forgetfulness, and has been unwell for the last 2 days. A resuscitation decision needs to be made. Who should be involved with this decision? What makes a DNAR order valid?
RC (UK)

It is 3 am and 54 year old Albert Jones is recovering from a routine hernia operation when he collapses, is unsuccessfully resuscitated, and dies. How do you contact the relatives who live an hour away? How do you receive them as they arrive on the ward? Who should discuss the collapse with them and how?
RC (UK)

In the A&E department, a 42 year old man is brought in by his wife suffering from a suspected MI. They are in the cubicle together when he collapses in VF
What do you do with his wife? She wants to stay what support do you offer her? Should relatives be present during resuscitation?
RC (UK)

A 48 year old man collapses in a public place as you are driving past. Would you stop to assist? Would you start resuscitation if needed? What is the legal and professional view in this situation? The Ambulance Service arrive and, on monitoring, he is found to be asystolic and remains in this rhythm. When do you decide to stop? RC (UK)

Your elderly next door neighbour has not been seen out today. You find him on the floor, collapsed, not breathing, but with a weak pulse. There are a number of empty drug and brandy bottles around him. Pinned to his chest is a note saying DO NOT RESUSCITATE What do you do?
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SUPPORTING THE RELATIVE IN RESUSCITATION PRACTICE

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Objectives
To understand: How to support relatives witnessing attempted resuscitation How to care for the recently bereaved Religious and ethnic requirements Legal and practical arrangements
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Supporting relatives
In groups of 4 - 6, brainstorm the considerations before inviting a relative/close friend to witness the resuscitation

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Supporting relatives
Clear explanation of what they will see Clear explanation of the events leading to the arrest Provide an opt-out clause Direct not to interfere Use simple language Ensure they are supported by a member of the team

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Dealing with the recently bereaved

In groups of 4 - 6, brainstorm the principles of supporting a relative/close friend when breaking bad news or supporting the recently bereaved
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Dealing with the recently bereaved

Early contact with one person, usually a nurse Provision of a suitable room Recognising the grief response Encouraging and arranging viewing of the body Establishing religious requirements
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Dealing with the recently bereaved

Possible responses to grief: Acute emotional distress Anger Denial Guilt Catatony
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Religious, legal and practical arrangements

Notification of coroner Notification of General Practitioner Information: what to do in the event of death Involvement of religious ministers Information relating to social service support Long term counselling
RC (UK)

Any Questions?

RC (UK)

Summary
Many relatives want the opportunity to be present during the attempted resuscitation. This may help their grieving process Communication with bereaved relatives should be honest, simple and supportive
RC (UK)