Review of Heart Electricity and Mechanics Leads Application

..• HISTORY
• REVIEW OF HEART AND
ELECTRICITYAND 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

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’ 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……

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

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 ms
or more
• Changes in EC potassium concentration
affects RMP of cardiac cell
• EC sodium concentration affects
magnitude of action potential of
cardiac cell

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

• 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)

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 axis
Cardinal 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,i
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
• 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 equiphasic
deflection 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

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 & aVL
when 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%

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

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

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

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
Postero
lateral
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, Posterio
superior IV
septum. SN, AV
node
Acute Marginal Inferior and
diaphragmatic
surface 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/
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

Localization
Right 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 t
Over lying the area involved

Localization
Inferior: II, III,
AVF
Septal: V1, V2
Anterior: V3, V4
Lateral: 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
S1
D1

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
• Lateral wall
• Q in aVL
• ST ↓ in lead II, lead III, lead aVF >
1mm

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

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
ST elevation 2,3
AVF

?
Inferior lateral MI
ST elevations 2, 3, AVF
ST elevations V5

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

Sgarbossa criteria
MI 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

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,recurrent
chest 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

Review of Heart Electricity and Mechanics Leads Application

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