Wk 8 – Arrhythmia

Wk 8 – Arrhythmia



CARDIAC ANATOMY AND PHYSIOLOGY

Revise cardiac anatomy, electrophysiology:(a) describe the mechanisms responsible for the generation and

distribution of action potentials in cardiac muscle



An ACTION POTENTIAL (electrolyte changes that occur across the cell membrane during depolarisation and

repolarisation) spreads across adjacent tissue, propagating the original signal. Depolarisation is electrical activation of

myocardial cells:

1. Atrial and ventricular cells: Rapid influx of sodium into cell

2. His-Purkinje system: There is a slow time-dependent decrease in potassium permeability and increase in

sodium permeability

3. Sinus node and AV node: Slow inward flow of calcium



Repolarisation is the process by which cells return to their resting state. It is rapid at first, reaches a plateau, and then a

longer rapid surge occurs until the resting state is reached.









Sinus Node AP:

 Repolarisation to about –60mV

 Slow depolarisation until about –40mV then faster depolarisation until about 0mV

 Followed by repolarisation



The slow drift from –60mV to –40mV characterises cells which can fire automatically (pacemaker/damaged cells). This

depolarisation is due to an increased inward calcium channel (T-type Ca channels), together with a constant inward

Na current and decreased outward K current. When the threshold is reached, L-type Ca channels are opened to allow

more calcium influx and thus depolarisation. Repolarisation occurs by potassium efflux following the opening of voltage-

gated K channels.



Phases of the Action Potential (Myocardial cells):

 Stable RMP of –80 to –90mV

 In resting cell, Na concentrations are much higher in the extracellular fluid, whilst potassium concentrations are much

higher inside the cell. Calcium concentrations vary during diastole and systole, but are always at least 100 lower

inside the cell that in the extracellular fluid



Phase 0 = Fast depolarisation. An electrical

impulse arrives and (critical threshold of about –

60mV reached) causes a rapid influx of Na ions

through fast Na channels which depolarise the

cell to about +20mV



Phase I = Slow repolarisation. Opening of some

K channels allows efflux of K and produces a

partial repolarisation.



Phase 2 = Plateau. Whilst a little K is leaving the

cell (K conductance falls to a low level when the

membrane is depolarised) slow Ca L-channels

allow the influx of Ca.



Phase 3 = Repolarisation: Opening of K

channels causing potassium efflux



Phase 4 = Ion concentrations are normalised

during diastole by the sodium pump –

Na/K/ATPase which uses ATP to pump sodium

and potassium ions against their concentration

gradients (3 Na out and 2 K in) to bring the RMP

back to –80mV to -90mV.

(b) Predict the effect of altered electrolyte or permeability changes on the cardiac muscle action potential



BASICALLY:

If you make intracellular fluid (ICF) more +ve  quicker depolarisation, and faster refractory period.

If you make ICF more –ve  slower depolarisation, and longer refractory period.



Ectopic Pacemakers

A contractile cell may begin to drift towards threshold before than the SA-node impulse can reach it, eg. oxidative stress

 low ATP  failure of Na+/K+ pump  inability to maintain RMP  drift to threshold & depolarisation



Hyperkalaemia:

 Membrane potential will become less negative (as the difference in the quantity of cations between the inside and

outside of the cell is less pronounced)  inactivation of the fast Na channels in the myocardial cells and a reduction

in the speed of repolarisation as the diffusion gradient has fallen

 Reduced heart rate, reduced force of contraction, cardiac arrest



Hypokalaemia:

 Membrane potential is more negative and more Na channels are “reset” so an AP is easier to achieve, occurs rapidly

and depolarises quickly. The interval between APs also decreases

 Tachycardias, over-excitable ventricle  ventricular tachycardia or fibrillation



↑ Hyper ↓Hypo

ECF Calcium Increased influx into cell  quicker Decreased influx into cell  harder to reach

depolarisation  contractions powerful and threshold, shorter plateau period, slowed rate

prolonged. Very high = extended contraction, and low force of contraction. Very low =

fatal. weak contractions, can cease altogether.

ECF Potassium Decreased K+ gradient  K+ efflux can‟t Increased K+ gradient  K+ efflux too

occur  repolarisation inhibited  cells stay effective and cells become hyperpolarised &

depolarised in extreme cases  contractions unable to reach threshold as easily. Heart

become weak and irregular and will rate slows at nodes. Blood pressure falls and

eventually stops in diastole. heart eventually stops in systole.



Hypomagnesia:

 Magnesium activates the Na/K pump  magnesium deficiency = impaired pump function = insufficient potassium can

be pumped into the cell = gradients can‟t be maintained

 It also affects the Na/Ca pump and the Ca ATPase that pumps Ca into the SR from the cytosol= calcium overload

(hypercontractility)



Sodium:

 Disturbance doesn‟t significantly affect the heart – this is because in the face of a dramatic fall in Na, there is still a

large enough diffusion difference to allow adequate Na influx into the cell and rapid depolarisation



Caffeine: Increases rate of depolarisation at SA node.

Nicotine: Indirectly stimulate the sympathetic effects on the heart.

Temperature: Cold temperatures slow the rate of depolarisation by slowing down channel function  slows down heart

rate and reduces strength of cardiac contractions. Elevated body temperature accelerates heart rate & contractile force 

heart seems to race and pound when you have a fever.



Autonomic Innervation

Paranymp effects @ SA / AV node: Acetylcholine is released by neurons  opens ACh-gated K+ channels  K+

outflow  slows rate of spontaneous depolarisation, and prolongs refractory period  slows heart rate.

2+

Symp effects @ SA / AV node: Noradrenaline is released by neurons  binds to B1 receptors  opens Ca

channels  influx of calcium shortens time to threshold, and shortens refractory period  speeds up heart rate.





SUMMARY: abnormalities in plasma potassium, calcium, and magnesium affect the ECG though changes in the

plasma sodium level DO NOT. The T wave and QT interval (measured from the onset of the QRS complex to the end of

the T wave) are most commonly affected.

a. Low potassium = T wave flattening and appearance of a hump (U wave) at the end of the T wave

b. High potassium = causes tall, wide, peaked T waves with disappearance of ST segment – the QRS

complex may be widened

i. Magnesium effects are similar

c. Low plasma calcium = prolongation of QT interval and high calcium shortens the QT interval

(c) Describe the function of the cardiac conducting system and AV ring



The conduction system:

 SA node  Atrial conduction channels  AV node  Bundle of His  Purkinje fibres



SA node:

 Located in the superior aspect of RA close to the SVC

 Composed of specialised pacemaker tissues which spontaneously depolarise

 Rate is governed by intrinsic cellular properties, SNS catecholamines ( K conductance so firing reached earlier),

PSNS vagal ACh (K conductance, so firing threshold reached later and  HR)



AV node:

 From SA node, the wave of excitation travels along specialised conduction channels

to the AVN (and from the RA  LA via Bachman‟s bundle)

 It then gets SLOWED down due to the AV node‟s characteristic decremental

conduction feature

o  Frequency of depolarisation  SLOWER conduction through the AV node

o Protects ventricles from  HR (e.g. atrial tachyarrhythmias like AF)



After going through the AVN, it then travels along the Bundle of His

 Right bundle branch

 Left bundle branch  left anterior fascicle and left posterior fascicle



Finally, it reaches the purkinje fibres and the ventricle (Remembering – that the conduction is very fast to the apex (so it

can beat first), moving out to the walls of the ventricles.



 Depolarisation of the ventricles occurs from the ENDOCARDIUM  PERICARDIUM (+ towards +  + QR segment)

 Repolarisation begins with the tissue last to depolarise (protects against reactivation of the myocardium by adjacent

depolarisations). Repolarisation from PERICARDIUM  ENDOCARDIUM (-away from +  + T wave)



Tachycardia = >100bpm

Bradycardia = 100bpm

o Flutter = 250-350bpm

o Fibrillation = 350+



3. RHYTHM – look at the QRS complexes

 Is it sinus rhythm? Is there a P wave for every QRS?

 Regularly regular, regularly irregular, irregularly regular, irregularly irregular



4. ELECTRICAL POSITION OF THE HEART

 Is the cardiac vector between –30 and +90? (Positive in I, avR is a quick way to check)

 Right axis or left axis deviation?



5. P WAVES

 Present? (Present = origin in SA node/atria; Absent = AV node/ventricular origin)

 Normal (Normal = origin in SA node; Abnormal = origin in atria)

6. PR SEGMENT

 Duration (3-5 small squares: 0.12-0.20s)

o Increased = blocked conduction between origin and ventricles

o Increased = can be physiological (e.g. athlete)



7. QRS COMPLEX

 Pathological Q if over ¼ height of R wave and >1sqaure wide

 Width:

o Normal (QRS = atrial flutter, atrial fibrillation, heart block



9. QT interval – start of QRS to end of T

 Normal?

 Abnormal – prolonged? Short? (Drugs, metabolic, ANS, Brugada syndrome) – long = predisposed to malignant

arrhythmias (like Torsades de pointes)



10. ST SEGMENT

 Should be isoelectric (level with T-P segment)

 Elevated = recent MI (in leads facing MI), pericarditis (globally elevated), hyperkalaemia, LV aneurysm

 Depressed = AMI, angina (ischaemia), digoxin, LVH and strain



11. T WAVES

 Normal?

 Tall/peaked = immediately after posterior AMI, hyperkalaemia

 Inverted = infarct, ischaemia, hypokalaemia, hypterophy

 Flattened = ischaemia, pericarditis

ARRHYTHMIA

1. List the causes and underlying pathophysiological mechanisms and classification of arrhythmia



Clinically, dysrhythmias are classified according to:

 The site of origin of the abnormality (atrial, junctional, ventricular)

 Whether the rate is increased/decreased (tachycardia/bradycardia)



There are four basic mechanisms underlying pathological or drug induced disturbances or cardiac rhythm:

1. Delayed after-depolarisation

2. Re-entry

3. Ectopic pacemaker activity

4. Heart block



Delayed “after-depolarisation”

 Main cause in ventricular muscle is abnormally raised Ca concentration – the amount of Ca entering the cell

2+

+ 2+

during the plateau phase increase and this activates Na -Ca exchange, transferring 1 Ca out for exchange of 3 Na

into the cell (use CCBs)  this results in net influx of one positive charge causing membrane depolarisation and

leads to repetitive discharge that does not depend on arrival of an impulse from elsewhere in the heart.



Re-entry

 In normal cardiac rhythm, the conducted impulse dies out after it has activated the ventricles because it is surrouned

by refractory tissue (absolute and relative)

 Re-entry occurs when the impulse succeeds in re-exciting regions of the myocardium after the refractory

period has ended  causes continuous circulation of APs (circus phenomenon)

 This occurs as a result of anatomical abnormalities or myocardial damage leading to a transient or uni-

directional block causing depolarisation and a disturbed pattern of conductance

 Anatomical abnormality  WPW Syndrome (re-entrant activity at AV node, so if beat goes through at

different speeds – arrhythmia)

 Myocardial damage  may result in extreme slow of AP propagation due to partial or complete

inactivation of fast Na channels, thus favouring re-entry because if the beat finally comes out of the tissue at

nd

the end of the refractory period, a 2 impulse occurs independent of the SA node



Ectopic pacemaker activity

 Although the SA node (and if that fails, the AV node) is the normal pacemaker, other areas of the heart can resume

the job (safety mechanism BUT it can also trigger tachyarrhythmias)

 Ectopic pacemaker activity is encourage by sympathetic activity (catecholamine action) and by partial

depolarisation, which may occur during ischaemia

o Catecholamines (on 1-adrenoceptors) increase rate of depolarisation in phase 4 and can cause normally

quiescent parts of the heart to take on a spontaneous rhythm (can be from adrenal gland, or as a sympathetic

response to pain (e.g. during MI) causing several tachyarrhythmias)

o Partial depolarisation as a result of ischaemic damage is probably result of decreased activity of the

+

electrogenic Na pump (so –90mV RMP not maintained and the cell starts off closer to the threshold)



Heart block

 Results from fibrosis or ischaemic damage of the conducting system (most commonly, the AV node)

 In complete heart block, the atria and ventricles beat completely independently of one another – the ventricles beat at

a slow rate, depending on what pacemaker picks up distal to the block.



Arrhythmias are abnormal heartbeats, either fast (tachyarrhythmias) or slow (bradyarrhythmias). Minor arrhythmias are

universal. The most common sustained arrhythmia – atrial fibrillation – occurs in 1% of those over 50 years and in 10% of

all over 80 years. Sudden cardiac death is often due to arrhythmia and causes 5-40% of cardiac deaths in coronary artery

disease or heart failure.





TACHYARRHYTHMIAS



Clinical features

 May be asymptomatic or cause intermittent minor palpitations or be the cause of blackouts, severe cardiovascular

compromise or cardiac arrest.

 Palpitation describes an abnormal awareness of the heartbeat (but it doesn‟t always mean the heart rhythm is

abnormal).



Key facts for understanding arrhythmias

 The heartbeat is controlled by the fastest pacemaker focus

 During a tachyarrhythmia, the normal SA node depolarisations are “suppressed” by the faster

depolarisations of the abnormal focus

 The surface ECG is a “superimposed” graph of both atrial and ventricular activity (atrial and ventricular activities are

not necessarily linked during arrhythmia), so atrial and ventricular activity need to be considered separately.

 Arrhythmias are categorised according to where the initial depolarisation originates:



1. Supraventricular arrhythmias – originate in the atria or around the AV node (junctional)

2. Ventricular arrhythmias – originate in the ventricles



 In the normal heart, the only communication between the atria and ventricles is the AV node, so the ventricular rate

during arrhythmias arising in the atria is governed not just be the arrhythmia itself but by conduction

through the AV node

 The normal AV node acts as a “turnstile” because it conducts depolarisations slowly and is refractory for a relatively

long period after each depolarisation

 Abnormal additional conducting pathways between the atria and ventricles (“accessory pathways”) are common, and

in some people, may allow depolarisations to spread from atria to ventricles, or from ventricles to atria without

necessarily passing through the AV node – this allows ”re-entry” circuits to be set up, and in some circumstances,

bypasses the normal “safety valve” of the AV node.



Supraventricular tachyarrhythmias (SVT)

- AV reciprocating tachycardias



 Paroxysmal SVT; AV or AV node re-entrant tachycardias



Pathogenesis – a re-entrant circuit is set up by the presence of an accessory pathway, an additional conducting

pathway:

 Between the atria and ventricles – causing an AV re-entrant tachycardia (AVRT). This additional pathway may be

seen in the ECG during normal sinus rhythm

 Between the atrium and the AV node to form a complete circuit within the AV node. This is the most common

additional pathway and underlies the AV nodal re-entrant tachycardias (AVNRT).



ECG diagnosis

 Regular, narrow QRS complex tachycardia (usually a rate of 150-200bpm)

 Regular P waves may be visible interspersed between the QRS complexes



Clinical features

 Usually presents as recurrent attacks of rapid palpitation, lasting from a few minutes  hours/days



Treatment

Slowing conduction through the AV node may stop the tachycardia:

 Vagotonic manoeuvres that increase vagal tone (e.g. Valsalva, swallowing cold drinks or carotid sinus massage)

 Drug treatment – slows or blocks conduction in the AV node

 IV adenosine – transiently (200 shocks and provide arrhythmia surveillance for up to 5 years

(implantation formerly involved limited thoracotomy, but now over 95% are transvenous electrodes)



Radiofrequency ablation:

 If an arrhythmia is caused by a small discrete pathway or generator, the pathway can be destroyed

 Gentle heating of tissue to 60 using an electrode catheter creates RF lesions 90% are expected for accessory pathway tachycardias, para-AV nodal re-entry tachycardia, atrial

tachycardia & right ventricular outflow tract tachycardia

 AV node ablation (used for ventricular rate control in AF) is possible in >99% of patients

 Success rates of 85% for the cure of atrial flutter (which involves a line of RF lesions preventing conduction through

an important narrow isthmus of atrial myocardium near the orifice of the coronary sinus)



Surgery:

 Can be performed to resect alternative pathways, as in WPW syndrome – the anatomical basis of WPW is well

understood and can be accurately localised (however, with the advent of RF ablation, this is largely obsolete)

 Surgery also has a place in the treatment of post-infarction VT by removal of the ischaemic tissue after acute intra-

operative localisation and mapping



Most cardiac arrhythmias cause no symptoms, have no haemodynamic importance and have no prognostic significance,

but may cause anxiety in a patient who becomes aware of them. Some patients with benign arrhythmias remain disabled

despite reassurance. Behaviour modification therapy often helps when reassurance has failed. In rare cases, a

precipitating factor may be identified and modified (e.g. excessive intake of caffeine or alcohol).

ANXIETY

1. Describe the symptoms and neurochemical basis of anxiety



GIT Respiratory CVS Genitourinary Nervous Psychological

 Dry mouth  Chest tightness  Palpitations  Increased  Fatigue &  Apprehension

 Dysphagia  Dyspnoea  Awareness frequency sleep and fear

 Epigastric  Hyperventilation of missed  Erectile disturbance  Irritability and

discomfort beats dysfunction  Blurred restlessness

 Aerophagy  Feeling of  Loss of vision  Reduced

(air gulping) pain over libido  Dizziness concentration and

 Diarrhoea heart  Headache easily distracted

 Sensitivity to

noise

 Depersonalisation

 Derealization



DDx of this wide range of non-specific symptoms:

Psychiatric disorders Physical disorders

 Depression  Hyperthyroidism

 Dementia  Hypoglycaemia

 Alcohol dependence  Phaeochromocytoma

 Drug dependence

 BDZ withdrawal









2. Describe the acute management of an anxious patient, and the clinical manifestation and management

principles of the varieties of anxiety.



Panic attacks may occur in ANY anxiety disorder, usually in situations tied to the core features of the disorder (eg a

person with a specific phobia of snakes may get a panic attack when they see one)

(What makes panic „disorder‟ different, as opposed to a simple panic „attack‟ is that in PD, the panic attacks are

spontaneous or „out of the blue‟, at least initially).



Anxiety is a complex interrelationship between genetics, CNS mechanisms, cognitive & social factors. There are

many forms of anxiety:



Main DSM-IV categories:

1. Panic disorders

2. Phobic disorders (specific, agora, social)

3. Generalised anxiety disorders

4. Obsessive-compulsive disorders

5. Post-traumatic stress disorders



Aetiology of neuroses in general:

 MULTIFACTORIAL

 Genetics (moderate penetrance) -  predisposition to developing anxiety symptoms

 CNS mechanisms: Change in 5-HT and NA (may mediate the anxiety symptoms)

 Cognitive factors & behavioural conditioning: Important psychological processes that accounts from HOW different

people react to the same stimulus

 Social factors: Adaptive and coping strategies of the individual

Anxiety disorder type Clinical features Management

Panic disorder  Fear of dying, madness, loss of  CBT

 F>M control  Relaxation and breathing

 Episodic  Automatic arousal (physiological  Medication: SHORT term

 Transient symptoms feedback with cognition) anxiolytics, antidepressants

 Unpredictable timing

 Inexplicable trigger

Phobic disorders  Specific phobia  Behavioural – exposure and

 F>M  Agoraphobia (open spaces desensitisation

where they can‟t escape)  Medication: SHORT term

 Social phobia (social humiliation anxiolytics, SSRs, MAOis

and meeting unfamiliar people)



Generalised anxiety disorder  Apprehensive expectations  Reassurance

 F>M  Hypervigilence  CBT

 Aetiology - ? Genetics, childhood  Disturbed sleep  Medication: Short term anxiolytics,

separations, current stressors  Muscle tension antidepressants, -blockers

 Autonomic arousal and

physiological feedback

Obsessive Compulsive Disorder  Distressing, time consuming & life  SSRIs and clomipramine (TCA)

 M=F interfering obsessions and  Response prevention

 Peak incidence: 15-30 y.o. compulsions  Thought stopping (CBT)

 Genetic? 5-HT underactivity?  Obsession: in the mind

 Compulsion: Resulting behaviour

(acting on obsession to alleviate

anxiety)

Post-Traumatic Stress Disorder  Flashbacks  Debriefing and deconstructing

 Traumatic events  Avoidance event

 Onset after weeks/months  Anxiety  CBT

 Autonomic arousal (HR, RR,  Antidepressants

sweats)  EMDR (eye movement

 Emotional numbness (reduced desensitisation & reprogramming)

emotions)









ACUTE panic attack: Discrete period of intense fear or discomfort in which 4 (or more) of the following

symptoms develop abruptly and reach a peak within 10 minutes:

Palpitations, pounding heart or  HR

Trembling or shaking (carpopedal spasms) Sometimes known as ‘hyperventilation

Dyspnoea or smothered feeling syndrome’ since the cause is due to

Choking sensation OVERBREATHING

Chest pain or discomfort - So get a decrease in PaCO2

Nausea or abdominal distress - & Increase in pH (resp alkalosis)

Dizziness, unsteady, light-headed or faint

Derealisation (Feelings of unreality) or depersonalisation (being detached from oneself)

Fear of losing control or going crazy

Fear of dying

Paraesthesia (tingling, pricking or burning sensations)

Chills or hot flushes



Managing the ACUTE attack:

- For ISOLATED panic attacks – treatments should generally be non-Rx

 Re-breathing from a large paper bag (to  PaCO2)  respiratory alkalosis causes cerebral vasoconstriction,

leading to hypoxia and impaired CNS function with various depersonalising symptoms

 Counselling and reassurance

 Relaxation techniques and slow breathing

 CBT – including identification and challenging of negative thoughts

 Residual anxiety can be treated with benzodiazapenes

3. Describe the pharmacology of anxiolytic agents

ANXIOLYTICS:



Benzodiazepines: (Diazepam, oxazepam, Temazepam)

 Work by potentiating the effect of GABAA (inhibitory NT) throughout the CNS (increases the time Cl channels are

open for)  inhibitory effect

 Also has allosteric effect to increase the affinity of the receptor for GABA itself

NB: GAGA receptors are ligand gated Cl channels, leading to hyperpolarisation of the post-synaptic neuron ( less

excitable)



Buspirone (“Buspar”)

 Partial agonist for 5-HT1A receptors (non BZ MOA)



“Z” Drugs – Zopiclone (Imovane) and Zolpidem (Stilnox)

 Newer drugs – promoted as having less tolerance and dependence (but they don‟t)

Both work via potentiation of GABA (like BDZ but have different chemical structures)

CLINICAL REASONING

1. Demonstrate clinical reasoning by interpretation of „palpitations‟



Palpitation: Forcible or irregular pulsation of the heart, perceptible to the patient, usually with an increase in

frequency or force, with or without irregularity in rhythm.



 Generally, they are non-specific and often reflect a functional rather than organic problem

 They may be the only manifestation of important cardiac arrhythmias, or they may be benign and related to structural

heart disease, requiring no treatment

 Patients with various anxiety states may describe palpitations resulting from normal heart action and may be

convinced they are due to underlying heart disease (cause great apprehension, increase ANS and often create a

vicious cycle that results in emotional disability and cardiac neurosis).



BOTTOM LINE – PALPITATIONS DESERVE CAREFUL ASSESSMENT.



Evaluation of the patient with palpitations includes:

 Defining symptom severity

 Determining the underlying patho-physiologic mechanism

 Defining the presence/absence of structural heart disease

 Establishing whether the symptoms correlate with cardiac rhythm disturbances



Initial evaluation includes:

 History

 Physical examination

 Basic laboratory evaluation

 ECG (12 lead)



Further testing is directed by information derived from this initial assessment

 If symptoms are mild and there is no evidence of associated cardiac/non-cardiac disorders, further workup is

generally not necessary

 Patients who have findings suggestive of underlying heart disease or who have severe symptoms usually require

additional evaluation including:

o Echocardiography to define the extent of structural heart disease

o Ambulatory ECG monitoring or trans-telephonic ECG transmission to correlate cardiac rhythm and symptoms

o Treadmill testing to evaluate for exercise-induced arrhythmias and underlying CAD



Based on these results (non-invasive studies), selected patients may require invasive assessment with cardiac

catheterisation or electrophysiological study.



Description of palpitations Likely cause

Occasional “flip flops”, skipped beats Premature beats

Sudden onset, rapid, regular Supraventricular tachycardia

Sudden onset, rapid, irregular Paroxysmal atrial fibrillation

Gradual onset, regular with exercise Sinus tachycardia

Associated with drugs Tobacco, coffee, tea, catecholamines, xanthines, thyroid

hormone

Associated with atypical chest pain and hyperventilation Anxiety state, mitral valve prolapse syndrome

syndromes

CVS CLINICAL SKILLS

1. Review history taking and cardiovascular examination skills

2. Demonstrate interpretation of cardiac symptoms and signs.



Cardiac symptoms:

Chest pain/heaviness – must Angina: Often “discomfort” not pain, central, can radiate to jaw/arm, worse of

ascertain location, duration, exertion and relived by rest/GTN, unaffected by respiration

quality, precipitating, aggravating & MI: Often at rest, more severe and lasts longer (>30mins) than angina pain.

relieving factors and other Associated symptoms: dyspnoea, sweating, anxiety, nausea, faintness

symptoms Pleuritic: Worse on inspiration, not brought on by exertion and often relived by

sitting up and leaning forward

Chest wall pain: Localised, sharp, associated with respiration or shoulder

movement

Dissecting aneurysm: Very severe “tearing” pain, more severe at time of onset.

Radiates to the back

Massive PE: Sudden onset of retrosternal pain. Associated with collapse, cyanosis,

and dyspnoea. Often pleuritic in nature but can be identical to angina

Oesophageal spasm: Retrosternal chest pain/discomfort. May come on after

eating/drinking and may be associated with dysphagia. May be relieved by nitrates

and can be hard to distinguish from angina.

Cholecystitis: Causes chest pain. Usually presents with right upper quadrant

abdominal tenderness



Dyspnoea Cardiac: Typically chronic and associated with exertion. Associated with an acute

rise in LV end diastolic pressure, raised pulmonary venous pressure, interstitial fluid

leakage and reduced lung compliance.

Can be hard to distinguish from respiratory causes (good history).

Presence of orthopnoea and PND is more suggestive of cardiac failure

Dyspnoea associated with anxiety is recognised by the presence of deep

respiration punctuated with sighs



Ankle swelling Symmetrical, worse in evenings, improves overnight. May be due to biventricualar

failure or right heart failure secondary to chronic lung disease (cor pulmonale)

Oedema that affects the face is more likely due to nephrotic syndrome.



Palpitations Unexpected awareness of the heart beat. Cardiac arrhythmias are usually sudden

onset and offset, whereas sinus tachycardia is more gradual. Completely irregular

rhythm is suggestive of AF.

Check for associated features of pain, dyspnoea, faintness or syncope



Syncope Must establish whether the patient actually lost consciousness and under what

circumstances.

If syncope is associated with arrhythmia, it is often a sudden loss of consciousness

regardless of posture. Chest pain may occur in patient has IHD or aortic stnosis.

Exertional syncope may occur with LV outflow obstruction (e.g. hypertrophic

cardiomyopathy or aortic stenosis)

Dizziness is more likely to be neurological in origin

Cardiac signs:

Physical Sign Interpretation

HANDS: Clubbing Cardiac causes of clubbing include cyanotic congenital

heart disease and infective endocarditis

Peripheral Cyanosis Cardiac cause is reduced cardiac output due to left

ventricular failure

Cachexia Sign of systemic disease

Splinter haemorrhages Can be traumatic or a sign of infective endocarditis

Osler‟s nodes Red, raised, tender nodules on pulps of fingers, rare

sign of infective endocarditis

Janeway Lesions Non-tender erythematous maculopapular lesions

containing bacteria, very rare sign of infective

endocarditis

Tendon Xanthomata Yellow or orange deposits of lipid over the tendons

which occur in type II hyperlipidaemia

FACE: Jaundice Can occur in severe congestive cardiac failure or

hepatic congestion

Xanthelasma May indicate type II or III hyperlipidaemia

Mitral facies Associated with pulmonary hypertension and low

cardiac output (eg. Mitral valve stenosis)

High arched palate Sign of Marfan‟s syndrome, associated with congenital

heart disease

Central Cyanosis Due to presence of deoxygenated haemoglobin in

superficial blood vessels. Cardiac cause is cor

pulmonale.

Petechiae May indicate infective endocarditis

Dentition Possible source of infective endocarditis

NECK: JVP When JVP is above 3cm the right heart filling pressure

is raised, sign of right ventricular failure or volume

overload

PRAECORDIUM: Apex beat If laterally displaced can indicate left ventricular

hypertrophy or mediastinal shift

Thrills Palpable murmur

Heaves Indicates right ventricular or left atrial enlargement

Heart sounds

Added sounds Indicate presence of murmur

BACK: Percussion note Dullness indicates pulmonary oedema possibly due to

left heart failure

Inspiratory crackles Pulmonary oedema due to left heart failure

Sacral oedema Indicates right heart failure

OTHER: Peripheral oedema Indication of right heart failure

Hepatomegaly Indication of right heart failure



Bradycardia:

 Regular

o Physiological (athlete, increased vagal tone)

o Drugs (-blockers, digoxin, amiodarone)

o Hypothyroidism

o Hypothermia

o Jaundice (only when severe)

o Raised intracranial pressure (effect on sympathetic outflow)

rd nd

o 3 degree AV block or 2 degree AV block

o MI

o Paroxysmal bradycardia (vasovagal syncope, acute hypoxia, acute hypertension)

 Regularly irregular

o Sinus arrhythmia (normal slowing of the pulse with expiration)

nd

o 2 degree AV block

 Irregularly irregular

o AF

o AV nodal disease

o Drugs

o Frequent extrasystoles

Tachycardia

 Regular

o Hyperdynamic circulation (exercise, emotion, fever, pregnancy, thyrotoxicosis, anaemia, beri beri)

o Congestive heart failure

o Constrictive pericarditis

o Drugs (salbutamol (other sympathetomimetics, atropine)

o Normal variant

o Diabetes

o Hypovolemic shock

o Supraventricular/ventricular tachycardia

o Atrial flutter with regular 2:1 AV block

 Irregular

o AF (due to myocardial ischaemia, mitral valve disease or any cause of LH enlargement, thyrotoxicosis, HTN

heart disease, sick sinus syndrome, PE, myocarditis, fever, acute hypoxia, alcohol)

o Multifocal atrial tachycardia

o Atrial flutter with variable block



Chest pain – things to consider:

1. Could the chest discomfort be due to an acute, potentially life-threatening condition that warrants immediate

hospitalisation and aggressive evaluation?

Acute ischaemic disease, pulmonary embolism, aortic dissection, spontaneous pneumothorax

2. If not, could the discomfort be due to a chronic condition likely to lead to serious complications?

Stable angina, aortic stenosis, pulmonary hypertension

3. If not, could the discomfort be due to an acute condition that warrants specific treatment?

Pericarditis, pneumonia/pleuritis, herpes zoster

4. If not, could the discomfort be due to another treatable chronic condition?Oesophageal reflux/spasm, cervical

disc disease, arthritis of the shoulder or spine, peptic ulcer disease, gallbladder, anxiety state



3. Interpret an ECG showing a common arrhythmia



Questions to ask of arrhythmias:

1. Is it fast or slow (tachyarrhythmia or bradyarrhythmia)

2. Is the origin of the rhythm disturbance ventricular or supraventricular (look at width of QRS)

3. Is the patient haemodynamically compromised

4. Does the arrhythmia need management

5. What is the underlying substrate that predisposed to the arrhythmia (re-entry, ectopic beats, delayed after

depolarisation, blocks)

6. What triggered the arrhythmia

7. Will it recur



LOOKING AT THE ECG:



ECG Leads:

 Limb leads: (frontal plane view of heart)

o Lead I: current movement RHS  LHS

o Lead II: right arm  left leg

o Lead III: left arm  left leg

 Augmented leads: (electrical activity between one limb +

a single electrode)

o aVR: right

o aVL: left

o aVf: foot

 Precordial leads: (horizontal plane view)

th

o V1: 4 ICS, R sternal border

th

o V2: 4 ICS, L sternal border

o V3: between leads 2 & 4

th

o V4: 4 ICS, mid-clavicular

o V5: Btw 4 & 6 (same horizontal level as V4)

o V6: Mid-axillary (same horizontal level as V4)

The ECG complex:



The P wave: (Atrial depolarisation)

 Precedes QRS complex

 2-3 mm high

 Usually rounded + upright

 Peaked or notched P waves  atria hypertrophy/enlargement

 Inverted P wave  retrograde or reverse conduction from AV junction toward atria

 Varying P waves  ectopic sites

 Absent P waves  non-SA node conduction e.g. AF



PR interval:

 Time for atrial impulse  atria  AV node  bundle of HIS  left + right bundle branches

 Measured from beginning of P wave to beginning of QRS complex

 0.12 – 0.2 second

 0.20 second  conduction delay through atria or AV junction



QRS complex: (Ventricular depolarisation)

 Ventricles contract immediately after QRS complex

 Follows PR interval

 0.06 – 0.10 second (intraventricular conduction time)

 Q wave – 1 negative deflection after P wave

st



 R wave – 1 positive deflection after P wave or Q wave

st



 S wave – 1 negative deflection after the R wave

st



 Deep, wide Q waves  may represent MI

 Notched R wave  may signify bundle branch block

 Broad QRS complex  ventricular conduction delay

 Absent QRS  AV block or ventricular standstill



ST segment: (end of ventricular depolarisation + beginning of ventricular repolarisation)

 J point = beginning of ST segment

 Extends from S wave to beginning of T wave

 Usually isoelectric

 ST depression  myocardial ischemia or digoxin toxicity

 ST elevation  MI



T wave: (ventricular repolarisation)

 Follows S wave

 Round and smooth; 0.5mm in limb leads; up to 1mm in chest leads

 Bumpy T wave – hidden P wave (Peak of T wave  relative refractory period of ventricle repolarisation  cells are

prone to extra stimuli)

 Tall, peaked T wave: myocardial injury or hyperkalaemia

 Inverted T wave in certain leads  mycocardial ischaemia

 Heavily notched or pointed T waves  Pericarditis



QT interval: (time for ventricular depolarisation + repolarisation)

  HR  es QT interval and vice versa

 Beginning of QRS complex to end of T wave

 0.36 – 0.44 second (should not be > 50% of R-R interval)

 Prolonged QT interval  relative refractory period is longer  increases risk of life-threatening arrhythmias „torsades

de points‟.

 Short QT interval  hypercalcaemia or digoxin toxicity

ECG Analysis:

1. Correct patient details

2. Note any clinical notes on ECG

3. Rate

a. Tachycardia >100bpm

b. Bradycardia than ventricular rate

o P waves  abnormal with „saw tooth‟ appearance

o T wave unidentifiable, QT interval unmeasurable, QRS

complex usually normal.

o Conduction ratio e.g. 2:1 (most common), 4:1 etc.

o Causes: conditions that enlarge atria +  atrial pressure – severe mitral

valve disease, hyperthyroidism, pericardial disease + primary

myocardial disease.

 Atrial fibrillation (>400bpm)

o Rhythm grossly irregular; atrial rates (>400) + ventricular rates (100-

150)

o P waves absent  replaced by f (fibrillatory) waves, R-R intervals

have wide variations, normal QRS complex

o Causes: post-cardiac surgery, long-standing hypotension, PE,

electrolyte imbalances, mitral insufficiency, CAD, hyperthyroidism, acute MI, hypoxia + ASD.









WPW

3. Junctional arrhythmias

 Wolff-Parkinson-White syndrome

o PR interval 0.10sec; delta

waves @ beginning of complex (slurred appearance)







 Premature Junctional contraction

o Irregular rhythm, rate varies with rhythm; compensatory pause

after PJC

o P wave inverted or absent – occurs before, during or after QRS PJC

complex; PR interval 0.44sec.







Ventricular tachycardia VT

o Atrial rhythm + rate undetermined; ventricular rhythm

o Regular or slightly irregular + rate (100-250bpm)

o P wave absent, PR unmeasurable

o QRS wide with ed amplitude

o T wave opposite deflection to QRS, possible TDP



Torsade de pointes (TDP) TDP

o Irregular ventricular rhythm; rate (150-250bpm)

o P wave absent, PR unmeasurable, QRS

wide + rotates around the baseline +

deflection  +  for several beats

Ventricular fibrillation

o Rhythm, rate, P wave, PR interval, QRS complex, T waves  all

undetermined; QT interval not applicable

o Variations in size of fibrillatory waves



 Pulseless electrical activity

o Electrical activity on ECG but heart muscle can‟t

contract

 Asystole (ventricular standstill + cardiac arrest)

o Lack of electrical activity on ECG  flat line









5. Atrioventricular blocks

 1 degree AV block

st



o Normal sinus rhythm with prolonged PR interval (>0.2sec); P wave, QRS complex + QT interval normal

o Causes: myocardial ischaemia, myocarditis, degenerative heart changes, drugs

 2 degree AV block type I (Mobitz I)

nd



o Atrial rhythm regular, ventricular rhythm abnormal; Atrial rates > ventricular rates

o PR interval progressive gets longer with each beat until P waves fails to conduct to ventricles

o P wave, QRS complex + T wave normal

o Causes: CAD, inferior-wall MI, rheumatic fever, drugs, ed vagal stimulation

 2 degree AV block type II (Mobitz II)

nd



o Atrial rhythm regular, ventricular rhythm (regular if constant block 2:1 or 3:1; irregular if intermittent block)

o PR interval constant, QRS complex usually wide, T wave normal

o Causes: anterior-wall MI, severe CAD, degenerative changes in conduction system (Bundle His or bundle

branches)

 3 degree AV block/Complete heart block

rd



o Regular atrial + ventricular rhythms; atrial rate > ventricular rates

o P wave, QRS complex + T wave normal; PR interval  variations with no regularity

o Causes: congenital, CAD, anterior or inferior-wall MI, drug, surgical injury.



 AV dissociation (atria + ventricles beat independently by its own pacemaker)

o Regular rhythm; Atrial + ventricular rates are nearly equal with ventricular rates slightly faster

o PR interval no relation to QRS; QRS may be normal or abnormal





st

1 degree









Mobitz I









Mobitz II









CHB

ETHICS

1. Explain the ethical bases of consent to medical treatment, the ethical and legal requirements for valid consent,

and the legal implications of failure to obtain consent.



Consent Vs Agreement

Consent implies more than just an agreement, in a sense it is and agreement, but the pt plays more of an active roll, they

are AUTHORISING a doctor to do something which if done without consent would be an infringement on their freedom or

their bodily integrity and illegal.



However, the paradigm case of consent is that relating to the performance of a medical procedure or investigation, which

usually involves some risk to the person.



Elements of consent (competent, informed and not under duress)

Not surprisingly, all of the following requirements relate to the person's autonomy:

1. The authorisation must be free and voluntary.

o Consider the difference between coercing and influencing patient decisions, ultimately the patient must

feel like they are free to decide.

2. The patient must be competent.

o The patient must comprehend, believe, and understand the information provided (e.g. NESP may

need interpreter)

3. The patient must be adequately informed.

o Authorising a treatment without adequate knowledge of its broad nature means a pt might authorise

something they do not want to happen.



Legally valid consent

As well as the ethical requirements there are legal ones:

1. The patient's consent must cover the actual procedure to be performed, and not a different one.

o Breach if pt consents to an appendectomy and is sterilised (REALLY BAD!)

o Exceptions-> written into most consent forms is a clause about consent to any necessary lifesaving

/morbidity preventing actions

2. The procedure must be legal in itself. (eg can not get consent to euthanasia)

3. The consent given a doctor to perform a procedure refers to only that doctor, except in public hospital situations

where consent is given to a management team.









Consent and trespass

Invalid consent = unauthorised invasion = Trespass

Failure to satisfy requirements of consent can result in legal Case Studies

proceedings against doctors. 1. Doctor sedates patients in order to

indulge in sexual acts with them

In case 1 and 2, something has occurred without the patient's 2. Saving of a pt's life by blood transfusion,

authorisation - an invasion of the person's body to which he did not despite advance directive refusing

properly consent – legally, this amounts to a trespass on that consent to any such transfusion.

patient's person. 3. Pt consents to operation on left arm,

but doctor operates on right.

Trespass is a tort (a civil wrong) involving a wrongful direct 4. Pt consents to operation on left arm,

interference with another person or with his land or property. having a general idea of the kind of

2 types operation, which will be performed.

o An assault is an intentional or reckless act causing someone The operation is performed on her left

to be put in fear of harm. arm, but complications follow, about

o A battery is an intentional or reckless application of physical which she was not fully appraised.

force to someone without his consent.



Criminal or Tort Law?

o Criminal Criminal law punishes common assaults. Medical assaults / batteries resulting from, say, fraud,

deception, or physical force may also be punished as crimes eg Case 1

o Tort Usually, medical assault / battery dealt with under the civil law tort of trespass, because most cases are

unintentional, and pt wants compensation.



Tort LawTrespass

o Trespass is actionable per se, ie pt does not have to prove damage occurred, to win the legal suit, just that no

consent was obtained. Eg

Trespass VS negligence

o Trespass only actions where no consent to the procedure done has been given which can be pursued in trespass.

 Trespassconsider case 2, JW pt refused life-saving treatment: pt saved, can sue because procedure

was done without their consent. (intentional)

 Trespass consider case 3, pt did not consent to procedure on other arm (reckless) Trespass

o Negligence

 Negligence Consider case 4, The doctor has not failed to obtain the patient's consent, nor acted

without her consent, nor overridden her refusal, but in failing to disclose certain relevant risks, the

"quality" of the consent is reduced/less informed. This pt could sue for negligence, based on the claim

that she was inadequately informed in terms of what was significant to her, and that certain conditions

pertaining to disclosure must be satisfied in order to satisfy the legal standard of care relevant to

disclosure.

PPH – CLINICAL EPIDEMIOLOGY (BAYESIAN THEORY)

1. Be able to apply Bayesian theory for multi-level diagnostic tests and use this to aid selection of screening

measures for ischaemic heart disease



DISEASE

Present Absent

Positive True False a+b

TEST Positive a b Positive all tested positive

Negative False True c+d

Negative c d Negative all tested negative

a+c b+d

All have disease All are disease-

free



Sensitivity = a/(a+c) – proportion of people with the disease who have a positive test result

 This means that a very sensitive test doesn‟t miss the disease if it is present (so SnOUT – you can rule it out)

 Low number of false negatives



Specificity = d/(b+d) – people without the disease, who have a negative test result.

 A very specific test will rarely be positive in the absence of disease (low number of false positives) (so SPIN – if

positive, can rule disease in)



Clinically:

 If you are worried that your patient may have a serious disease, then it is best to use a very sensitive test. You will get

more false positives, but at least you won‟t miss the disease if it is present

 If you want to rule the disease “in”, use a specific test. If the person doesn‟t have the disease, the result should be

negative.



“So, we have the test result – what are the chances the results are correct?”



Positive predictive value (PPV): The probability of having the disease in a patient with a positive test result

 Proportion of people who tested positive who actually have the disease: a/(a+b)



Negative predictive value (NPV): The probability of NOT having the disease if you get a negative test result

 Proportion of people who tested negative who are actually free of disease: d/(c+d)



Determinants of Predictive values and Baye‟s Theorem:

The predictive value is determined by 2 factors:

1. The accuracy of the test (sensitivity and specificity)

2. The prevalence of the disease in the population being tested – Pre-test probability.



Baye‟s theorem relates sensitivity, specificity and prevalence to predictive value and it is important to understand the

implications of the theorem:



 The more sensitive as test, the better will be its negative predictive value (SNOUT) – the more confident you will

be that a negative test rules out a disease

 The more specific the test is, the better will be its positive predictive value (SPIN) – the more confident you will be

that a positive test result rules in the disease.

 Because predictive value is influenced by prevalence, positive results, even for a very specific test will be largely false

positives if the prevalence of the disease in the population is very low (conversely, negative results in a population

where the disease prevalence is very high are likely to be false).





TO FIND OUT THE PROBABILITY THAT A PATIENT HAS A PARTICULAR DISORDER:

1. Find out the prevalence (pre-test probability) of the disorder in the patient‟s population

2. Find out the sensitivity and specificity of the test

3. Make a 22 table and fill it in using the prevalence and sensitivity/specificity of the test

4. Calculate the predictive values

PPH - CLINICAL TRIALS

1. Discuss the use and dangers of surrogate outcome measures in clinical trials.



Surrogate outcomes/endpoints:

A laboratory or physical sign that is used in therapeutic trials as a substitute for a clinically meaningful

endpoint that is a direct measure of how a patient feels, functions, or survives and that is expected to predict

the effect of the therapy.

Surrogate endpoints are useful when they can be measured:

o Earlier

o More conveniently

o Or more frequently than the endpoints of interest (referred to as the “true” endpoints)



There are several main uses for surrogate endpoints (SEPs):

Replace a distal endpoint with a more proximal one (e.g. protein in urine as a marker for future renal failure)

Can be measured more easily or frequently (e.g. HR, BP, RR, Temperature, instead of “sepsis”)

Can be measured with higher precision, or less subject to competing risks (e.g. change in the reproducible GCS as a

marker for neurological state)

Less affected by other treatment modalities

Reduced sample size requirements and faster decision making.



Some of the best-known examples of SEPs include:

CD4+ count for progression of aids

When looking at treatments for arrhythmias, investigators monitor the reduction of ventricular ectopic beats (VEBs) as

SEP for reduction in mortality post-MI



Possible dangers associated with SEPs:

Surrogate endpoints/markers should correlate to the TRUE endpoint – e.g. you should not be looking at rate of hair

regrowth as a marker for the efficacy of a new anti-depressant drug

The effect of the drugs could be thought to lead to clinical benefits but may ignore other effects

o COX-2 inhibitors such as Vioxx have great effects on inhibiting COX and PG synthesis (markers) but they

failed to pick up on the increased CVS adverse effects

o Recombinant tPA is great at re-establishing blood flow (marker) following and thromboemoblic stroke, but

also increases the risk of haemorrhagic strokes

Must be cautious about association and inferences drawn from surrogate endpoints  always look at the markers

with a cynical eye

o Classic example is when promoting COX-2 inhibitors, drug reps would say “Oh, look how well it combats

morning stiffness associated with RA” (morning stiffness being the marker), but does it ACTUALLY

improve patient‟s day-to-day pain scores and quality of life overall?



2. Be able to apply results of clinical trials to patients by considering the weighing up of risks and benefits.

When reviewing a paper, one of the most important issues is whether it should lead to changes in the management of

one‟s own patients. It is vital to weigh up the risks and benefits of any treatment (including withholding treatment) before

proceeding. It could mean the difference between subjecting patients to useless therapy while denying them access to

more effective ones. Alternatively, it could be exposing them to unnecessary risks and side effects. Costs are also an

important consideration and our duty to public and population health binds us to judiciously use more expensive

treatments (“more expensive” doesn‟t always mean “more effective”)



Make sure that the hallmarks of a good clinical trial are there:

 Large studies

 Randomised trials

 Independent investigators

 Conclusions are justified by the evidence (this can be hard if one only reads conclusions).

 It is relevant to the disease/condition of the patients

 Meta analysis of randomised trials are good.

Think about the impact that a treatment is going to have on your patient. Think about the co-morbidities of the

treatment, the cost and the change in lifestyle that will ensue.

PPH – DELAY IN PRESENTATION

1. What are the reasons for patient delay in seeking early intervention?



 Lack of knowledge regarding symptoms

 Appraising symptoms as “not serious”

 Worry about troubling others

 Embarrassment about seeking help

 Denial and vulnerability

 “Too busy”



2. What are the characteristics of patients who delay seeking medical assistance?



 Low income

 Less than 12 years of education

 People who have not had any health training/CPR

 Diabetes mellitus

 A history of hypertension

 Location (rural)

 Indigenous patients (in both rural and urban areas)

 NESB patients



3. What are the consequences of delay in seeking medical care for chest pain? (BCS)



Chest pain can be the sign of serious disease or a warning of serious complications to come, so should be followed up

promptly and thoroughly.



E.g. Timeline of heart problems due to CAD

 Myocardial necrosis begins about 30mins after coronary occlusion

 Classic acute MI with extensive damage occurs when the perfusion of the myocardium is reduced severely below its

requirements for an extended period of time (usually about 2-4 hours)

o This causes profound, prolonged ischaemia and results in permanent loss of function of large regions  can

lead to arrhythmias, mechanical failure

 If however, reperfusion follows briefer periods of flow deprivation (<20 minutes), loss of cell viability can be prevented



THIS PROVIDES THE RATIONALE FOR THE VERY EARLY CLINICAL DETECTION OF ACUTE MI – TO PERMIT

EARLY THERAPY (E.G. THROMBOLYSIS), ESTABLISH REPURFUSION OF THE AREA AT RISK, SALVAGE AS

MUCH ISCHAEMIC (BUT NOT YET DEAD) MYOCARDIUM AS POSSIBLE AND CONSEQUENTLY REDUCE INFARCT

SIZE.



SUMMARY:

The interval between the onset of symptoms and administering therapies for acute myocardial infarction

(AMI) is associated with better outcomes including reduced mortality and morbidity. So, in light of the fact

that chest pain could by the sign of such a potentially serious disease process (or many other serious

disease processes that are best seen to immediately), delay in seeking medical care increases the risk of

mortality, complications and delays possible interventions that could be life saving (or at least, reduce

morbidity).

PPH ISSUES RELATING TO CARDIAC ARREST

1. What community education interventions are available to doctors and their patients?





2. Using automated defibrillators as an example, outline the factors that government/health regulatory bodies

need to take into consideration when considering the introduction of a new technology?



E.g: Experiment on automated external defibrillators:

It was a community-based, multicenter clinical trial in which they randomly assigned community units (e.g., shopping malls

and apartment complexes) to a structured and monitored emergency-response system involving lay volunteers trained in

cardiopulmonary resuscitation (CPR) alone or in CPR and the use of AEDs. The primary outcome was survival to hospital

discharge.



There were more survivors to hospital discharge in the units assigned to have volunteers trained in CPR plus the use of

AEDs (30 survivors among 128 arrests) than there were in the units assigned to have volunteers trained only in CPR.

Functional status at hospital discharge did not differ between the two groups.



Conclusions Training and equipping volunteers to attempt early defibrillation within a structured response system can

increase the number of survivors to hospital discharge after out-of-hospital cardiac arrest in public locations. Trained

laypersons can use AEDs safely and effectively.



The results of the trial pertain only to the implementation of layperson-based defibrillation systems in public settings with

an organized emergency-response system in place. Furthermore, the results only apply to locations with a defined

window of emergency-medical-services response times (i.e., 3 to 15 minutes). Locations where responses may be

delayed (e.g., aircraft, boats, and trains) were excluded because randomization to the CPR-only group would almost

completely remove any possibility of defibrillation. Locations with very rapid emergency-medical-services response times

were not included because public AED implementation could not be expected to have a large effect in such places.