Physiology of ECG ,localisation of MI

11/09/20142:15 pm 1

..• HISTORY

• REVIEW OF HEART AND

ELECTRICITY AND MECHANICS

• LEADS APPLICATION

• ECG READING

• MI PATHOPHYSIOLOGY

• ECG IN MI

LUIGI GALVANI

He is a physicist and scientist.

While working in lab, he noticed contraction of leg muscles of frog when he touched the nerve with a scalpel.

Proposed mechanism-ANIMAL ELECTRICITY

This formed the basis of

ELECTRICITY & CONTRACTION OF HEART

1780- LUIGI GALVANI

SIR HANS CHRISTIAN OERSTED

PLATINUM WIRE HEATING WITH ELECTRICITY CAUSED

MOVEMENT OF COMPASS NEEDLE.

JOHANN SCHWEIGGER

• Proposed that current carrying wire

produces magnetic field.

• He invented GALVANOMETER

1872 –capillary electrometer by GABRIAL

LIPPMANN

Open the chest ,expose the heart and connect

electrodes and measure the rise /fall of potential

AUGUSTUS DESIRE

WALLER -Electrogram

• 1ST person to attempt NON

INVASIVE measuring of heart s

electricity.

• As the voltage in heart is <1 mv he

tried a new technique.

• He shone a light through meniscus

and projected on to a moving

photographic plate

AUGUSTUS DESIRE

WALLER

• ECF surrounding heart acts as a

continuous conducting medium

between heart and skin.

• Postulated that spread of electricity is

from apex to atria

WILLEM EINTHOVEN

• Enhanced electrometer

• Deflections naming as P,q ,r,s,t – followed

RENE DISCARTES, mathematician and

metaphysicist of 17th century who

represented mathematic depictions with p

,q, …..

Einthoven triangle• Based on various permutations and

combinations of placing

electrodes,einthoven finally used 3

leads – LIMB LEADS I, II, III

• LEAD III EQUALS DIFFERENCE

BETWEEN LEAD II AND I

.

WILLEM EINTHOVEN

Nobel prize -1924

For contribution to medicine

WILSON TERMINAL

Wilson’ s central terminal

• Wilson incorporated 5 k ohms

resistance to each electrode and

combined 3 electrodes to form

wilson’s central terminal

• Leads-

• VR-R arm paired with average of left

arm and left foot

• VF-left foot paired with average of

right and left arms

• VL-left arm paired with average of

left foot and right arm

Goldberger’s augmented

leads

• He increased the voltages by 50

percent by increasing resistance

• V=IR

• avR, avL, avF……

ORIENTATION OF HEART

Applications of ECG

• Cardiac Arrhythmias

• Myocardial ischemia and

infarction

• Pericarditis

• Chamber hypertrophy

• Electrolyte disturbances

• Drug effects and toxicity

ECG BASICS

• ECG /EKG is the graphic recording

of electric potentials generated by

heart.

• Signals are detected by means of

metal eletrodes attached to the

extremities and chest wall and

recorded by electrocardiograph.

• Ecg leads display the instantaneous

differences in potential between the

electrodes.

Electocardiograph is a

sophisticated galvanometer

• Heart is at the center of electric

field generated by it ,and intensity

of electric field diminishes

algebraically with the distance

from it s center.

ECG BASICS

• Depolarization of heart-the initiating

event for cardiac contraction

• Electric currents-produced by three

components

–Cardiac pace-maker cells

–Specialized conduction tissue

–Heart muscle itself

• ECG, however, records only

depolarization (stimulation) &

repolarization (recovery) potentials

generated by atrial & ventricular

myocardium

GENESIS OF CARDIAC

CONTRACTION• Depolarization stimulus- Sinoatrial (SA) node or

sinus node

– A collection of pacemaker cells

– Fire spontaneously

– Exhibit automaticity

– Fire at maximum rate, hence pace-maker

• First phase of cardiac electrical activation-

spread of depolarization wave through right &

left atria,followed by atrial contraction

• 3 bundles of atrial fibres that has purkinje type

fibres , connect SA to AV node,internodal

tracts

– Anterior BACHMAN

– Middle WENKEBACH

– Posterior THOREL

GENESIS OF CARDIAC

CONTRACTION

Next,the impulse stimulates pacemaker & specialized

conduction tissues in AV nodal & His bundle areas

Together,these two regions constitute AV junction

HIS bundle bifurcates into right & left bundles(actually

continues as right,left arises from main trunk),which

rapidly transmit depolarization wavefronts to right &

left ventricular myocardium by Purkinje fibers

Left main bundle bifurcates into left anterior

fascicle & left posterior fascicle

Depolarization wavefronts then spread through

ventricular wall, from ENDOCARDIUM TO

EPICARDIUM,triggering ventricular contraction

.

Physiology

• Resting membrane potential of cardiac cell is -90mV

• Depolarization 2 ms

• Plateau phase & repolarization 200 msor more

• Changes in EC potassium concentration affects RMP of cardiac cell

• EC sodium concentration affects magnitude of action potential of cardiac cell

Cardiac action potential

Cell depolarisation

Ecg wave forms and

cardiac action potential

• Factors that decrease slope of

phase 0

– Impairing influx of Na + e.g.,

hyperkalemia, flecainide

– Increase QRS duration

• Conditions that prolong phase 2

–Amiodarone, hypocalcemia etc

– Increase QT interval

• Shortening of ventricular

repolarization (phase 2)

–Digitalis ,hypercalcemia etc

–Shortens QT segment

Ecg basics

• Paper speed 25 mm/sec

• 5 large squares =1 sec

• 1 small square =0.04 sec

• Voltage – 1 large square = 0.5 mv

• Small square = 0.1 mv

Wave forms

• HR(beats/min)-from interbeat (R-R) interval

• HR=300/no.of large squares

• Or 1500 /no. small squares between RR

• PR interval –time between atrial & ventricular

depolarization,includes physiologic delay at AV

junction- 120 to 200 ms

• QRS interval-duration of ventricular depolarization-

100 to 110 ms or less

• QT interval

– Includes both ventricular depolarization &

repolarization times

– Varies inversely with heart rate

– A rate corrected QT interval, QTc ( QT/√RR)

– Normally is ≤0.44 s

QT interval

• Bazett formula for measuring QTc– QTc = QT/(Square root of RR

interval)

• Hodges method– QTc = QT + 1.75(HR-60)

• Normal 330 to 440 ms

• As a general rule,with HR 60-100/min,QT should not exceed half the R-R interval

QTc interval

• QT prolongation– Sleep– Drugs– Hypocalcemia– Hypothermia– SAH– Torsades de pointes– Jervel-Lange-Nielson/Romano-ward

syndromes

• QT shortening– Digitalis– Hypercalcemia– Hyperthermia– Vagal stimulation

ECG Leads

Leads are electrodes which measure the

difference in electrical potential between

either:

1. Two different points on the body

(bipolar leads)

2. One point on the body and a virtual

reference point with zero electrical

potential, located in the center of the

heart (unipolar leads)

Standard Limb Leads

Standard Limb Leads

AUGMENTED LIMB LEADSLEEEDS

ALL LIMB LEADS

Augmented voltage leads• aVR-augmented unipolar right arm

lead

– Its oriented to face heart from right shoulder

– Oriented to the cavity of heart

• aVL-augmented unipolar left arm lead

– Face heart from left shoulder

– Oriented to anterolateral/superior surface of LV

• aVF-augmented unipolar left leg lead

– Face heart from below

– Oriented to inferior surface of heart

Leads II,III,aVF –oriented to

inferior surface of heart

Leads I,aVL-oriented to

high/superior left lateral wall

Lead aVR,(V1)-oriented to cavity

of heart

• Anteroseptal leads V1 to V4

• Apical or lateral leads V5 & V6

V1 to V6-oriented to

anterior wall of heart

Dominance of left ventricle

Right ventricle thickness -0.3-0.5 cm

Left ventricle wall thickness -1.3-1.5 cm

Electro cardiologically and electrophysiologically Left ventricle is dominant..

Free wall of right ventricle is anatomical anterior wall of heart .electrocardiological anterior wall of heart is inter ventricular septum

Electrical axisCardinal rules

– If a vector is directed at right angles or

perpendicular to a particular lead axis,then net

impression on that lead is nil/small

equiphasic/null deflexion

– If a vector courses parallel to a particular lead,it

records a maximum deflection on that lead

– If a vector is obliquely oriented to a particular

lead,the voltage obtained will have a lesser

magnitude

Electrical axis

Electrical axis

• Paired leads that are perpendicular to each other

–Lead I is perpendicular to aVF

–Lead II is perpendicular to aVL

–Lead III is perpendicular to aVR

Principles of axis Measurement

• Examine the 6 frontal leads

• Determine the most equiphasicdeflection of qrs

• Inspect the perpendicular lead and see the qrs wave in that lead .

• Positive wave /negative will decide the axis.

P WAVE

• Wave form in lead II

–P wave best studied in lead II

–Because,frontal plane P wave axis is directed to positive pole of this lead

–Pyramidal shape with rounded apex

–Duration 0.08 to 0.10 s, no greater than 0.11 s

–Normal amplitude is <2mm,max 2.5mm

P wave

• Wave form in V1

–Here initial & terminal parts of P wave easily identified

–Normally biphasic ,initial positive & terminal negative

• Reason being RA is anterior & LA is posterior

–Duration of P wave 0.05 s

P wave• Frontal plane P wave axis

– Directed to region of +45* to +65*

– Best studied in lead II , because waves most aligned with & directed towards positive pole of this lead

– P wave axis >70* - Right axis deviation

• Here,its most aligned with aVF

• So,best evaluated in aVF

– P wave axis <45* - Left axis deviation

• Here,its most aligned with lead I

• So,best evaluated in lead I

P wave

• Widened,notched(camel-hump) P wave/LA abnormality

– Duration > 0.11 s

– Duration of notch > 0.04 s

– Terminal component deviated more leftward

– Seen in lead II,if axis is +50*

– If axis is deviated leftward,seen in aVL,lead I

– Also seen in V5,v6

P wave in v 1

• MORRIS INDEX-depth of terminal p wave in v1 * duration in seconds

• =/> 0.o8 mm.sec is abnormal.

Right atrial abnormality

• Lead II p wave amplitude >0.25 mv

QRS complex

• QRS complex is subdivided into specific deflections or waves

– Initial QRS deflection in a given lead if negative-Q wave

– First positive deflection-R wave

– A negative deflection after an R wave -S wave

– Subsequent positive or negative waves are labeled R′ & S′, respectively

– Lowercase letters (qrs)-small amplitude waves

Q wave

• Q wave-initial QRS vector directed away from positive electrode

• More likely seen in inferior leads when QRS axis is vertical,& in leads I & aVLwhen QRS axis is horizontal

• Q wave-present in 1 or more of inferior leads (leads II, III, aVF) in >50%of normal adults & in leads I & aVL in < 50%

• Duration-Important in diagnosis of MI

Q wave

• Lead III,duration occasionally as long as 0.04 s,rarely 0.05 s

• This lead accounts for most of erroneous diagnoses of MI

• Amplitude– < 0.4 mV in all limb leads except lead

III,where it may reach 0.5 mV

• Depth – <25% of R wave,exception lead III

• Normal in V5,V6…..abnormal in V1-V3

R wave

• Maximum R wave amplitude in the lead in which axis is most parallel & has same polarity as maximum vector

• Upper Limit for R wave– Lead I 1.5 mV

– Lead aVL 1.0 mV

– Leads II, III,aVF, 1.9 mV

• Amplitude increases from V1 to V4,V5,V6. Larger amplitudes-young subjects

R wave in V1,V6

Poor progression of R wave

• Old anterior MI

• Lead misplacement (frequently in obese women)

• LBBB/LAFB

• LVH

• WPW syndrome

• Dextrocardia

• Tension pneumothorax with mediastinal shift

• Congenital heart disease

S wave

• Most prominent in lead aVR,amplitude up to 1.6 mV in young subjects

• Relatively large S wave in leads III & aVL (occasionally) depending on QRS axis,magnitude usually does not exceed 0.9 mV

• In leads I, II & aVF, S wave amplitudes are <0.5 mV

• In general,S waves are large in V1,V2,progressively smaller from V3 to V6

• Chamber hypertrophy

– Progression altered

T wave

• Ventricular repolarisation– Return of stimulated muscle to resting

state

• Always positive in lead II,left sided leads(V4 to V6),negative in aVR

• As a rule

– T wave follows the direction of main QRS deflection

– If positive in any chest lead,it must remain positive in all chest leads to the left of that lead

LVH

ROMHILT ESTES CRITERIA

• Criterion• 1. Amplitude {any of the following}: 3• Largest R or S wave in any limb

lead ≥ 20mm• S in V1 or V2 ≥ 30mm• R in V5 or V6 ≥ 30mm• 2. LV strain: Without digoxin: 3 • With digoxin: 1• 3. Left atrial enlargement: 3• 4. Left axis deviation: 2• 5. QRS duration ≥ 90 ms: 1• 6. Intrinsicoid deflection in V5 or V6 ≥ 50

ms :1• (4-PROBABLE• 5 –DEFINITIVE)

Deep T inversions(>3mm)

• Normal variant-early repolarisation/Juvenile T

• Recurrent MI

• Takotsubo cardiomyopathy

• CVA

• LV/RV overload

• Bundle branch blocks,WPW

• Memory T waves

Frontal plane T wave axis

• T wave deflection is nearest to equiphasic in lead III

• Lead perpendicular to III is aVR,hence it will show maximum deflection(negative)

• So,mean T wave axis would be at negative pole of aVR at +30*

• If T wave is not absolutely equiphasic,slight adjustment in resultant value can be made

ST segment

• Early phase of ventricular repolarisation

• <1 mm deviations are normal

S-T segment axis

• Normal ST segment is isoelectric,so it has no manifest axis

• Mean manifest frontal plane S-T segment axis is directed towards site of injury

• Inferior wall MI

– S-T axis directed inferior & to right in region of 120*

– hence ST elevation in II,III & aVF & vice versa in I,aVL

• Anterolateral MI

– S-T axis directed superior & to left-30* to -60*

– hence ST elevation in I,aVL & vice versa in III,aVF

U wave

• Normally absent or small wave after ‘T’ wave

• Last phase of ventricular repolarisation

• Prominent in

– Hypokalemia

– Patients on sotalol,phenothiazines

– CVA

U wave

• Prominent U waves can predispose to ventricular arrhythmias

• Same direction as ‘T’ with 10% of its amplitude

• Prominent in V2-V4

• Larger at slower heart rates

• MI,LVH can be associated with negative U & positive T waves

ECG reporting

• Standardisation• Rate- per min• Rhythm- sinus & arrhythmia• P wave morphology• PR interval• QRS complex

– Width– Axis – Configuration(comment on Q,R,S waves)

• ST segment• T wave morphology• U wave morphology• QTc interval• Comments eg: P pulmonale,RAD,1st degree

AV block, AF etc• Conclusions – normal/abnormal ECG

Normal variants

• Persistent Juvenile Pattern

• Early Repolarisation Syndrome(ERPS): the athletes heart-

• prominent j waves

• Concave upwards ,minimally elevated ST segments

• Tall ,symmetrical T waves

• Inverted T waves ,occasionally.

• prominent ,narrow q waves in left oriented leads.

• Tall R in left precordial leads

• Non specific T wave variants.

Prominent mid precordial U waves.

Sinus brady cardia

Non specific T wave variants-

Inversion of T waves may occur in

1 response to anxiety/fear

2 as an orthostatic response

3 as a post prandial response

4 result of hyper ventilation

All features are normalised after administration of Potassium salts

Coronary circulation

LCX • 97% from LCA• 2% from Separate

Ostium• 1% RCA

Obtuse margin of heart and entire posterior wall. LA, posterior IV septum if PD arises from LCX

OM • 97% LCA Obtuse margin of heart adjacent to LV

Posterolateral branch

• 80% LCA• 20% RCA

Posterior and diaphragm LV wall

PD • 82% RCA• 18% LCA

Posterior IV septum and Diaphragm LV

RCA RA and part of LA, RV, Posteriosuperior IV septum. SN, AV node

Acute Marginal Inferior and diaphragmaticsurface of RV

Conus Branch Outflow track of RV

SN branch RA, LA,SN

RV Branch RV

Atrial Branch Right Atrium

ECG

Ischemia Injury infarction

.

Using ECG one can localize the site of Ischemia / Injury/ Infarction.

Chief diagnostic tool to identify

.

Why Localize ?

Culprit Artery

To decide further

management.

Localization - Left Coronary Artery (LCA)

Left Main (proximal LCA) occlusion

• Extensive Anterior injury

Left Circumflex (LCX) occlusion

• Lateral injury

Left Anterior Descending (LAD) occlusion

• Anteroseptal injury

LocalizationRight Coronary Artery (RCA)

Proximal RCA

occlusion

• Right Ventricle injured

• Posterior wall of left ventricle injured

• Inferior wall of left ventricle injured

Posterior descending

artery (PDA)

occlusion

• Inferior wall of left ventricle injured

Prevalence of Culprit Artery

RCA 45%

LCX 12%

LAD 36%

INCIDENCEof STEMI

Inferior 58%

Anterior 39%

Other 3%

Post Ischemic T wave changes

ST elevation MI Non-ST Elevation Infarction

ST depression, peaked T-waves, then T-wave inversion

ST elevation &

appearance of Q-

waves

ST segments and T-

waves return to

normal, but Q-

waves persist

Ischemia

Infarction

Fibrosis

ST

depression

& T-wave

inversion

ST

depression

& T-wave

inversion

ST returns to

baseline, but

T-wave

inversion

persists

Infarcti

on

Fibrosis

Ischemia

Localization

I

Lateral

II Inferior

III Inferior

aVR

aVL Lateral

V1 Septal

aVF Inferior

V2 Septal

V3 Anterior

V4 Anterior

V5 Lateral

V6 Lateral

The changes of ischemia/injury/infarction are seen in the leads

Over lying the area involved

Localization

Inferior: II, III, AVFSeptal: V1, V2Anterior: V3, V4Lateral: I, AVL, V5, V6

Anterior Wall

V3, V4

• Left anterior chest

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Septum

V1, V2

◦ Along sternal borders

◦ Look through right ventricle & see septal wall

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

.

Anteroseptal MI

ST elevations V1, V2, V3, V4

Levels of occlusion of LAD

S1D1

Terminology

• Proximal LAD – origin to S1

• Mid LAD – S1- S2

• Distal LAD – Beyond S2

PROXIMAL LAD BEFORE S1

• ST ↑ in lead aVR and v1-v4

• Complete RBBB

• ST ↑ in V1 > 2.5 mm

• ST ↓ in V5

• ST ↓ in lead II, lead III > 1mm

• ST ↓ in lead aVF > 2 mm

PROXIMAL TO D1

PROXIMAL TO D1

• Lateral wall

• Q in aVL

• ST ↓ in lead II, lead III, lead aVF > 1mm

DISTAL LAD

DISTAL TO D1

• ST ↓ in aVL

• Absence of ST ↓ in lead II, lead III ,aVF

Lateral Wall

I and aVL

◦ View from Left Arm

◦ lateral wall of left ventricle

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Lateral Wall

V5 and V6

◦ Left lateral chest

◦ lateral wall of left ventricle

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Lateral Wall

–I, aVL, V5, V6

–ST elevation suspect lateral wall injury

Lateral

Wall

Lateral MI

Localization - Extensive Anterior MI

. .

Evidence in septal, anterior, and lateral leads

Often from proximal LCA

lesion

Complications common

• Left ventricular failure

• CHF / Pulmonary Edema

• Cardiogenic Shock

.

Practice 1

Anterior MI with lateral involvement

ST elevations V2, V3, V4

ST elevations II, AVL, V5

Inferior Wall

II, III, aVF

◦ View from Left Leg

◦ inferior wall of left ventricle

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Inferior MI

Inferior MI

ST elevation 2,3 AVF

?

Inferior lateral MI

ST elevations 2, 3, AVF

ST elevations V5

LOCALISATION OF IWMI

Posterior Leads

• Posterior leads – Posterior Infarct with ST

Depressions and/ tall R wave

– RCA and/or LCX Artery

ST elevation in V7,V8,V9.

• Understand Reciprocal changes

– The posterior aspect of the heart is viewed as a mirror image and therefore depressions versus elevations indicate Mi

Localization - Myocardial Infarct

Localization ST

elevation

Reciprocal

ST depression

Coronary

Artery

Anterior MI V1-V6 None LAD

Septal Mi

V1-V4,

Disappearan

ce of

septum Q in

leads V5,V6

none LAD

Lateral MII, aVL, V5,

V6

II,III, aVF

(inferior leads)LCX

Inferior MI II, III, aVF I, aVL (lateral

lead)

RCA (80%) or

LCX (20%)

Posterior MI V7, V8, V9

high R in V1-V3

with ST

depression V1-

V3 > 2mm

(mirror view)

RCA or LCX

Right Ventricle

MI V1, V4R I, aVL RCA

Atrial MIPTa in

I,V5,V6 PTa in I,II, or III RCA

Sgarbossa criteriaMI in presence of LBBB

• ST elevation >/= 1 mm and concordant with predominantly negative QRS complex ( score 5)

• ST depression in >/= 1 mm in leads v1,v2,v3(score 3 )

• ST Elevation >/=5 mm and discordant with predominantly negative QRS complex (score 2)

• QR complexes in leads I ,V5 ,orv6 or lead II ,III

• Chronic infarction-

• Chronic infarction

• CABRERA SIGN sign- notching of ascending part of a wide s wave in mid precordial leads.

• 0R

• CHAPMAN SIGN-Notching of ascending limb of wide R wave in lead I,Avl,v5 ,or v6

MI in presence of RBBB

• Diagnosis in q wave infarction is same as that of normal conduction

Atrial infarction

• PR elevations in v5 or v6 or inferior leads,changes in p wave morphology

• Atrial arrhythmias

WELLEN S SYNDROME

– Inverted or biphasic T-waves in V2 and V3

– T wave changes may also be present in V1, V4-V6

–Changes appear when pain free

– Little to no ST change

–No loss of precordial R waves

–No pathologic Q waves

• Concern:

–Highly specific for LAD lesions

–At risk for extensive AMI or sudden death

PROGNOSIS IN MI

• The immediate prognosis in patients with AMI is inversely related to the amount of myocardial reserves.(ischaemic area at risk),

ESTIMATING SIZE OF ISCHEMIC MYOCARDIUM AT

RISK

• Sclarovsky-Birnbaum

• Aldrich score:

• % of myocardium at risk=3[0.6(# ST elevation II,III,aVF)+2]

• % of myocardium at risk=3[1.5(#leads with of ST elevation)-0.4]

PROGNOSIS FROM ECG

• Predictors of size of MI

– Presence of Q waves with ST elevation

– Number of leads with ST Elevation

– Sum of ST Elevation in 12 leads

– ST elevation in V4 with Inferior MI

– Abnormal R in V1 (R/S>1) with inferior MI

– Conduction disturbances

• Predictors of in hospital mortality

– Anterior location of MI

– ST elevation in anterior and inferior leads

– Evidence of earlier remote MI

– Marked ventricular ectopic activity

• KILLIP CLASSIFICATION FOR PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION

•

•

• KILLIP CLASS HOSPITAL MORTALITY (%)

• I No congestive heart failure 6

•

• II Mild congestive heart failure, rales, S3, congestion on chest radiograph

• 17

• III Pulmonary edema 38

•

• IV Cardiogenic shock 81

•

•

•

Role of 12 lead ecg in risk stratification in ACS

Normal ecg or T wave inversions in < 5 leads is low risk

ST depression or ST depression and elevation if present indicates highest incidence of death ,highest chance of re infarction,recurrentchest pain.

Infart size proportional to mortality.

Infarct size correlation –a) degree and extent of st elevation

b)Coronary artery involved mortality more if left involved

c)Distortion of terminal qrs complex is indicative of very poor outcome

• Acute anterior wall MI due to proximal LAD occlusion has the worst short and long term prognosis

• In inferior wall MI proximal RCA occlusion carries worst prognosis.

• Reference:Schweitzer P, Keller.

• BETH ISRAEL MEDICAL CENTER,NY,2001

.

References

1 Harrisons internal medicine -18th

edition

2 Marriot ‘s practical electrocardiography 12th edition

3 leo schamroths introduction to electrocardiography 7th edition

4 Braunwald s 9 th edition

5 Hurst The heart ,13th edition .

Treat the patient ,not ecg

. .

• ‘From inability to let well alone

• From too much zeal for the new and contempt for what is old

• From putting knowledge before wisdom, science before art, and

• Cleverness before common sense;

• From treating patients as cases;

• And from making the cure of the disease more grievous than the

• Endurance of the same, Good Lord, deliver us.’ –

SIR ROBERT HUTCHISON