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Dear Doctor, This ECG presentation is an attempt to illustrate some of the fundamentals in ECG interpretation. We have advanced level courses also on ECG. In addition, we have several educational resource materials in the form of PowerPoint based CD-Rom

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Fore word l.jpg

Dear Doctor,

This ECG presentation is an attempt to illustrate some of the

fundamentals in ECG interpretation. We have advanced level

courses also on ECG. In addition, we have several educational

resource materials in the form of PowerPoint based CD-Rom

presentations. Also are available several philosophical and

religious works of all time great masters, translated into simple

English and presented as PowerPoint slide shows on CD-Rom.

A list of such materials is appended. Pl. request for your copy of

any of them at a nominal cost of Rs.100/ per CD.

Wishing You a happy learning experience !!

Fore word


The objectives l.jpg
The Objectives

  • To sensitize doctors towards learning ECG

  • To explain the clinical concepts involved

  • To illustrate them with diagrams, drawings, tables

  • To show real life ECG charts and interpret

  • Differential diagnosis on similar looking ECG changes

  • Spot light on ECG and Ischemic Heart Disease

    Not Included are

  • Electrophysiological basis of ECG changes

  • Details on arrhythmias, conduction disorders

  • Sensitivity and specificity of different patterns

  • Atypical presentations, combination of pathologies

  • Scoring systems and predictive values


Ecg resources consulted l.jpg

Alan Lindsay’s Cyber ECG learning center (on line)

Interactive Electrocardiography by Novartis – CD Rom

Frank H Netter's medical drawings

American Heart Association (AHA) sites

American Heart Lung and Blood Institute (AHLBI) sites

J.G. Webster’s Cyber ECG library

Braunwald’s text book of cardiology - 6 ed. 2004

Goldberger’s text book on ECG

Our personal collection of interesting ECGs

ECG Resources consulted


Ecg graph paper l.jpg
ECG Graph Paper

Y- Axis Amplitude in mill volts

X- Axis time in seconds


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X-Axis represents time - Scale X-Axis – 1 mm = 0.04 sec

Y-Axis represents voltage - Scale Y-Axis – 1 mm = 0.1 mV

One big square on X-Axis = 0.2 sec (big box)

Two big squares on Y-Axis = 1 milli volt (mV)

Each small square is 0.04 sec (1 mm in size)

Each big square on the ECG represents 5 small squares

= 0.04 x 5 = 0.2 seconds

5 such big squares = 0.2 x 5 = 1sec = 25 mm

One second is 25 mm or 5 big squares

One minute is 5 x 60 = 300 big squares

ECG Graph Paper


Ecg complex l.jpg
ECG Complex

P wave

PR Interval

QRS complex

ST segment

T Wave

QT Interval

RR Interval


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ECG Complex

  • P Wave is Atrial contraction – Normal 0.12 sec

  • PR interval is from the beginning of P wave to the beginning of QRS – Normal up to 0.2 sec

  • QRS is Ventricular contraction –Normal 0.08 sec

  • ST segment – Normal Isoelectic (electric silence)

  • QT Interval – From the beginning of QRS to the end of T wave – Normal – 0.40 sec

  • RR Interval – One Cardiac cycle 0.80 sec


Identify the ecg complex l.jpg
Identify the ECG Complex

3

4

5

1

8

2

6

7


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Identify the ECG Complex

The Wave or Interval Duration # of Boxes

  • P wave : Atrial contraction 0.12 sec (3)

  • PR interval – P to begin. of QRS 0.20 sec (5)

  • QRS complex - Ventricular 0.08 sec (2)

  • ST segment - Electrical silence Isoelectric

  • T wave - repolarization 0.12 sec (3)

  • QRS interval – Ventricular cont. 0.08 sec (2)

  • QT interval - From Q to T end 0.40 sec (10)

  • TP segment - Electrical silence 0.20 sec (5)


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Let us Identify the waves

4

7

1

8

6

2

3

5


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Let us Identify the waves

  • P wave – Atrial contraction = 0.12 sec (3 small boxes)

  • PR Interval – P + AV delay = 0.20 sec (5 small boxes)

  • Q wave – Septal = < 3 mm, < 0.04 sec (1 small box)

  • R wave – Ventricular contraction < 15 mm

  • S wave – complimentary to R < 15 mm

  • ST segment – Isoelectric – decides our fate

  • T wave – ventricular repolarization – friend of ST

  • TP segment – ventricular relaxation – shortened in tachycardia


Important precautions l.jpg
Important Precautions

  • Correct Lead placement and good contact

  • Proper earth connection, avoid other gadgets

  • Deep inspiration record of L3, aVF

  • Compare serial ECGs if available

  • Relate the changes to Age, Sex, Clinical history

  • Consider the co-morbidities that may effect ECG

  • Make a xerox copy of the record for future use

  • Interpret systematically to avoid errors



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Normal ECG

  • Standardization – 10 mm (2 boxes) = 1 mV

  • Double and half standardization if required

  • Sinus Rhythm – Each P followed by QRS, R-R constant

  • P waves – always examine for in L2, V1, L1

  • QRS positive in L1, L2, L3, aVF and aVL. – Neg in aVR

  • QRS is < 0.08 narrow, Q in V5, V6 < 0.04, < 3 mm

  • R wave progression from V1 to V6, QT interval < 0.4

  • Axis normal – L1, L3, and aVF all will be positive

  • ST Isoelectric, T waves ↑, Normal T↓ in aVR,V1, V2



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Pediatric ECG

  • This is the ECG of a 6 year old child

  • Heart rate is 100 – Normal for the age

  • See V1 + V5 R >> 35 – Not LVH – Normal

  • T↓ in V1, V2, V3 – Normal in child

  • Base line disturbances in V5, V6 – due to movement by child



Be aware of normal ecg l.jpg

Normal Resting ECG – cannot exclude disease

Ischemia may be covert – supply / demand equation

Changes of MI take some time to develop in ECG

Mild Ventricular hypertrophy - not detectable in ECG

Some of the ECG abnormalities are non specific

Single ECG cannot give progress – Need serial ECGs

ECG changes not always correlate with Angio results

Paroxysmal events will be missed in single ECG

Be aware of normal ECG


Normal variations in ecg l.jpg
Normal Variations in ECG

  • May have slight left axis due to rotation of heart

  • May have high voltage QRS – simulating LVH

  • Mild slurring of QRS but duration < 0.09

  • J point depression, early repolarization

  • T inversions in V2, V3 and V4 – Juvenile T ↓

  • Similarly in women also T↓

  • Low voltages in obese women and men

  • Non cardiac causes of ECG changes may occur


Early repolarization l.jpg
Early Repolarization

This ECG has all normal features

The ST-T (J) Junction point is

elevated. T waves are tall, May be inverted in LIII, The ST

segment initial portion is concave. This does not signify Ischemia


Pseudo normalization l.jpg
Pseudo Normalization

T↓

Before Chest pain

T↑

During Chest pain

T↓

Chest pain Relieved


Rate determination l.jpg
Rate Determination

QRS

Next QRS


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Rate Determination

T ACHY

NORMA L

BRADY


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What is the Heart Rate ?

Answer on next slide


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What is the Heart Rate ?

  • To find out the heart rate we need to know

    • The R-R interval in terms of # of big squares

    • If the R-R intervals are constant

  • In this ECG the R-R intervals are constant

  • R-R are approximately 3 big squares apart

  • So the heart rate is 300 ÷ 3 = 100


What is the heart rate26 l.jpg
What is the Heart Rate ?

Answer on next slide


What is the heart rate27 l.jpg
What is the Heart Rate ?

  • To find out the heart rate we need to know

    • The R-R interval in terms of # of big squares

    • If the R-R intervals are constant

  • In this ECG the R-R intervals are constant

  • R-R are approximately 4.5 big squares apart

  • So the heart rate is 300 ÷ 4.5 = 67


What is the heart rate28 l.jpg
What is the Heart Rate ?

Answer on next slide


What is the heart rate29 l.jpg
What is the Heart Rate ?

  • To find out the heart rate we need to know

    • The R-R interval in terms of # of Big Squares

    • If the R-R intervals are constant

  • In this ECG the R-R intervals are not constant

  • R-R are varying from 2 boxes to 3 boxes

  • It is an irregular rhythm –Sinus arrhythmia

  • Heart rate is 300 ÷ 2 to 3 = 150 to 100 approx


Slide30 l.jpg

ECG Bipolar Limb Leads

-

+

-

-

L

R

L

R

F

+

+

F


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ECG Bipolar Limb Leads

  • Standard ECG is recorded in 12 leads

  • Six Limb leads – L1, L2, L3, aVR, aVL, aVF

  • Six Chest Leads – V1 V2 V3 V4 V5 and V6

  • L1, L2 and L3 are called bipolar leads

  • L1 between LA and RA

  • L2 between LF and RA

  • L3 between LF and LA


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ECG Unipolar Limb Leads

+

+

R

L

+

F

Lead aVR

Lead aVL

Lead aVF


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ECG Unipolar Limb Leads

  • Standard ECG is recorded in 12 leads

  • Six Limb leads – L1, L2, L3, aVR, aVL, aVF

  • Six Chest Leads – V1 V2 V3 V4 V5 and V6

  • aVR, aVL, aVF are called unipolar leads

  • aVR – from Right Arm Positive

  • aVL – from Left Arm Positive

  • aVF – from Left Foot Positive



Ecg chest leads35 l.jpg
ECG Chest Leads

Precardial (chest) Lead Position

  • V1 Fourth ICS, right sternal border

  • V2 Fourth ICS, left sternal border

  • V3 Equidistant between V2 and V4

  • V4 Fifth ICS, left Mid clavicular Line

  • V5 Fifth ICS Left anterior axillary line

  • V6 Fifth ICS Left mid axillary line


Atrial ectopics l.jpg

APC

APC

APC

APC

Atrial Ectopics


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Atrial Ectopics

  • Note the premature (ectopic) beats marked as

  • APC (Atrial Premature Contractions)

  • These occurred before the next expected QRS complex (premature)

  • Each APC has a P wave preceding the QRS of that beat – So impulse has originated in the atria

  • The QRS duration is normal < 0.08, not wide



Atrial fibrillation39 l.jpg
Atrial Fibrillation

  • Note ECG changes of Atrial Fibrillation

  • The heart rate is irregularly irregular

  • The R-R intervals are very different from beat to beat

  • There is narrow QRS tachycardia

  • There are no P waves – instead small fibrillary waves called ‘ f ’ waves are seen



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Atrial Flutter

Heart rate Rhythm P wave PR interval QRS in sec


Slide42 l.jpg

Atrial Flutter

  • Note ECG changes of Atrial Flutter

  • The heart rate is regular or variable

  • Atrial rate is 300 per minute

  • All P waves are not conducted to ventricles

  • The R-R intervals very depending on the AV conduction ratio

  • The QRS is narrow – < 0.12 sec

  • The P waves have a ‘saw toothed’ appearance called ‘F’ waves


Ventricular ectopics l.jpg

VPC

VPC

VPC

VPC

Ventricular Ectopics


Slide44 l.jpg

Ventricular Ectopics

  • Note the premature (ectopic) beats marked as VPC (Ventricular Premature Contractions)

  • These occurred before the next expected QRS complex (premature)

  • Each VPC has no definite P wave preceding the QRS of that beat – So impulse has originated in the ventricles

  • The QRS complexes are wide with abnormal duration of > 0.12 and their shapes are bizarre



Ventricular tachycardia46 l.jpg
Ventricular Tachycardia

  • A wide QRS tachycardia is VT until proved

  • otherwise. Features suggesting VT include

  • Evidence of AV dissociation

  • Independent P waves (shown by arrows here)

  • Beat to beat variability of the QRS morphology

  • Very wide complexes (> 0.14 ms)

  • The QRS is similar to that in ventricular ectopics

  • Concordance (chest leads all positive or negative)


The six limb leads l.jpg
The Six Limb Leads

FRONTAL PLANE

RIGHT

LEFT

INFERIOR


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The 12 Camera Photography

  • There SIX cameras photographing frontal plane

  • Lead 1 and aVL are horizontal left sided cameras

  • Lead 2, aVF, Lead 3 are vertical inferior cameras

  • aVR is horizontal Rt. sided camera (cavitary lead)

  • Lateral Leads – L1, aVL, V5 and V6

  • Inferior Leads – L2, aVF, and L3 leads

  • Septal Leads – V1 and V2

  • Anterior Leads – V3 and V4

  • Anterio-lateral leads – V3, V4, V5, V6, L1 and aVL


The six chest leads l.jpg
The Six Chest Leads

TRANSVERSE PLANE


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The 12 Camera Photography

  • There SIX cameras photographing in transverse or anterio-posterior plane

    • V1 and V2 record events of septum

    • V3 and V4 record events of the anterior wall

    • V5 and V6 record events of left lateral wall

  • To record right side events V2R to V6R are needed – In dextrocardia, in RV infarction



Cardiac impulse52 l.jpg
Cardiac Impulse

  • Cardiac impulse originates in the SA node

  • Traverses the atria simultaneously – no special conduction wires in atria – so the delay

  • Reaches AV node – the check post – so delay

  • Enters bundle of His and branches – through specialized conducting wires called Purkinje network - activates both ventricles – quick QRS

  • First the septum from L to R, then right ventricle and then the left ventricle and finally the apex

  • Then the ventricles recover for next impulse


Qrs axis l.jpg
QRS Axis

NW

NE

SE

SW


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QRS Axis

  • The QRS electrical (vector) axis can have 4 directions

  • Normal Axis - when it is downward and to the left – southeast quadrant – from -30 to +90 degrees

  • Right Axis – when it is downward and to the right – southwest quadrant – from +90 to 180 degrees

  • Left Axis – when it is upward and to the left – Northeast quadrant –from -30 to -90 degrees

  • Indeterminate Axis – when it is upward & to the right – Northwest quadrant – from -90 to +180


Axis determination l.jpg
Axis Determination

ALL UPRIGHT

MEET

LEAVE

NORMAL RIGHT LEFT



Slide57 l.jpg

LEAD 1

aVR

aVL

LEAD 2

LEAD 3

aVF

What is the Axis ?


Ecg with normal axis l.jpg
ECG With Normal Axis

  • Note the QRS voltages are positive and upright in the leads - L1, L2, L3 and aVF

  • L2, L3 and aVF tell that it is downward

  • L1, aVL tell that it is to the left

  • Downward and leftward is Normal Axis

  • Normal QRS axis


Slide59 l.jpg

What is the Axis ?

LEAD 1

LEAD 2

LEAD 3


Ecg with right axis l.jpg
ECG With Right Axis

  • Note the QRS voltages are positive and upright in leads L2, L3

  • Negative in Lead 1

  • L2, L3 tell that it is downward

  • L1 tells that it is not to the left but to right

  • Downward and rightward is Right Axis

  • See the Right –Meet criterion QRS in L1 and L3 meet

  • Right Axis Deviation - RAD


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What is the Axis ?

LEAD 1

aVR

aVL

LEAD 2

aVF

LEAD 3


Ecg with left axis l.jpg
ECG With Left Axis

  • Note the QRS voltages are positive and upright in leads L1and aVL

  • Negative in L2, L3 and aVF

  • L1, aVL tell that it is leftward

  • L2, L3, and aVF tell that it is not down ward - instead it is upward

  • Upward and Leftward is Left Axis

  • See the Left - Leave criterion QRS in L1 and L3 leave each other

  • Left Axis Deviation - LAD




Right atrial enlargement65 l.jpg
Right Atrial Enlargement

P wave voltage is 4 boxes or 4 mm


Right atrial enlargement66 l.jpg
Right Atrial Enlargement

  • Always examine Lead 2 for RAE

  • Tall Peaked P Waves, Arrow head P waves

  • Amplitude is 4 mm ( 0.4 mV) - abnormal

  • Pulmonary Hypertension, Mitral Stenosis

  • Tricuspid Stenosis, Regurgitation

  • Pulmonary Valvular Stenosis

  • Pulmonary Embolism

  • Atrial Septal Defect with L to R shunt


Atrial enlargements l.jpg
Atrial Enlargements

RIGHT ATRIAL ENLARGEMENT LEFT ATRIAL ENLARGEMENT



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Left Atrial Enlargement

P wave duration is 4 boxes-0.04 x 4 = 0.16


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Left Atrial Enlargement

  • Always examine V 1 and Lead 1 for LAE

  • Biphasic P Waves, Prolonged P waves

  • P wave 0.16 sec, ↑ Downward component

  • Systemic Hypertension, MS and or MR

  • Aortic Stenosis and Regurgitation

  • Left ventricular hypertrophy with dysfunction

  • Atrial Septal Defect with R to L shunt


Ventricular hypertrophy l.jpg

Ventricular Muscle Hypertrophy

QRS voltages in V1 and V6, L 1 and aVL

We may have to record to ½ standardization

T wave changes opposite to QRS direction

Associated Axis shifts

Associated Atrial hypertrophy

Ventricular Hypertrophy



Right ventricular hypertrophy73 l.jpg
Right Ventricular Hypertrophy

  • Tall R in V1 with R >> S, or R/S ratio > 1

  • Deep S waves in V4, V5 and V6

  • The DD is RVH, Posterior MI, Anti-clock wise rotation of Heart

  • Associated Right Axis Deviation, RAE

  • Deep T inversions in V1, V2 and V3

  • Absence of Inferior MI



Slide75 l.jpg

Criteria and Causes of LVH

Criteria of RVH

  • Tall R in V1 with R >> S, or R/S ratio > 1

  • Deep S waves in V4, V5 and V6

  • The DD is RVH, Posterior MI, Rotation

  • Associated Right Axis Deviation, RAE

  • Deep T inversion in V1, V2 and V3

    Cause of RVH

  • Long standing Mitral Stenosis

  • Pulmonary Hypertension of any cause

  • VSD or ASD with initial L to R shunt

  • Congenital heart with RV over load

  • Tricuspid regurgitation, Pulmonary stenosis



Ecg of ms with rvh rae l.jpg
ECG OF MS with RVH, RAE

  • Classical changes seen are

  • Right ventricular hypertrophy

  • Right axis deviation

  • Right Bundle Branch Block

  • P – Pulmonale - Right Atrial enlargement

  • P – Mitrale – Left Atrial enlargement

  • If Atrial Fibrillation develops – ‘P’ disappears



Left ventricular hypertrophy79 l.jpg
Left Ventricular Hypertrophy

  • High QRS voltages in limb leads

  • R in Lead I + S in Lead III > 25 mm

  • S in V1 + R in V5 > 35 mm

  • R in aVL > 11 mm or S V3 + R aVL > 24 ♂, > 20 ♀

  • Deep symmetric T inversion in V4, V5 & V6

  • QRS duration > 0.09 sec

  • Associated Left Axis Deviation, LAE

  • Cornell Voltage criteria, Estes point scoring



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Causes and Criteria of LVH

Causes of LVH

  • Pressure overload - Systemic Hypertension, Aortic Stenosis

  • Volume overload - AR or MR - dilated cardiomyopathy

  • VSD - cause both right & left ventricular volume overload

  • Hypertrophic cardiomyopathy – No pressure or volume overload

    Criteria of LVH

  • High QRS voltages in limb leads

  • R in Lead I + S in Lead III > 25 mm or S in V1 + R in V5 > 35 mm

  • R in aVL > 11 mm or S V3 + R aVL > 24 ♂, > 20 ♀

  • Deep symmetric T inversion in V4, V5 & V6

  • QRS duration > 0.09 sec, Associated Left Axis Deviation, LAE


Lvh types l.jpg
LVH Types

Pressure Over Load

Volume Over Load


Lvh types83 l.jpg
LVH Types

Pressure Over load

  • Like in hypertension, IHD

  • LV strain pattern – ST depression with T ↓

    in V5, V6, L1 and aVL leads

    Volume Over load

  • Like in Mitral or Aortic regurgitation

  • Shows prominent positive T waves in

    V5, V6, L1 and aVL



Causes of conduction block l.jpg
Causes of Conduction Block

  • Clinically normal individual

  • CAD, Acute MI, Remote MI, Pulmonay embolism

  • Aortic stenosis, SABE + abscesses in conduction

  • Cardiac trauma, Hyperkalemia, Rapid heart rates

  • Lenegre's disease (idiopathic fibrosis of conduction)

  • Lev's disease (calcification of the cardiac skeleton)

  • Cardiomyopathy - Dilated and Hypertrophic

  • Infiltrative Tumor – Chaga’s disease

  • Myxedema, Amyloidosis, Ventricular hypertrophy



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Complete RBBB

  • Complete RBBB has a QRS duration > 0.12 sec

  • R' wave in lead V1 (usually see rSR' complex)

  • S waves in leads I, aVL, V6, R wave in lead aVR

  • QRS axis in RBBB is -30 to +90 (Normal)

  • Incomplete RBBB has a QRS duration of 0.10 to 0.12 sec with the same QRS features as above

  • The "normal" ST-T waves in RBBB should be oriented opposite to the direction of the QRS




Complete lbbb90 l.jpg
Complete LBBB

  • Complete LBBB has a QRS duration > 0.12 sec

  • Prominent S waves in lead V1, R in L I, aVL, V6

  • Usually broad, Bizarre R waves are seen, M pattern

  • Poor R progression from V1 to V3 is common.

  • The "normal" ST-T waves in LBBB should be oriented opposite to the direction of the QRS

  • Incomplete LBBB looks like LBBB but QRS duration is 0.10 to 0.12 sec, with less ST-T change.

  • This is often a progression of LVH changes.




Rate dependent lbbb93 l.jpg
Rate Dependent LBBB

  • Complete LBBB is sometimes rate dependent

  • See the LBBB pattern when the HR is 75 per minute

  • But, LBBB pattern disappeared when the HR is < 50

  • Some times the LBBB appears and disappears with out any change in heart rate. This is called stuttering LBBB. It signifies underlying Ischemia.

  • Appearance of new LBBB in a patient with chest pain is enough evidence of MI. It presents primary T changes


Blood supply of heart l.jpg
Blood Supply of Heart

RCA

LCX

LAD

RCA

LCA


Blood supply of heart95 l.jpg
Blood Supply of Heart

  • Heart has four surfaces

  • Anterior surface – LAD, Left Circumflex (LCx)

  • Left lateral surface – LCx, partly LAD

  • Inferior surface – RCA, LAD terminal portion

  • Posterior surface – RCA, LCx branches

  • Rt. and Lt. coronary arteries arise from aorta

  • They are 2.5 mm at origin, 0.5 mm at the end

  • Coronary arteries fill during diastole

  • Flow - epicardium to endocardium – poverty/plenty


Ischemia injury infarction l.jpg

Ischemia produces ST segment depression with or without T inversion

Injury causes ST segment elevation with or without loss of R wave voltage

Infarction causes deep Q waves with loss of R wave voltage.

Myocardial Ischemia

Myocardial Injury

Myocardial Infarction

Ischemia, Injury & Infarction


Ischemia and infarction l.jpg
Ischemia and Infarction without T inversion

TRANSMURAL Injury ST Elevation


Ischemic heart disease ihd l.jpg
Ischemic Heart Disease (IHD) without T inversion


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Types of Angina without T inversion

CHRONIC STABLE ANGINA


Types of angina100 l.jpg
Types of Angina without T inversion

  • Chronic Stable Angina – Dynamic occlusion + Micro vascular dysfunction – Progressive

  • Micro vascular Angina – No flow limiting stenosis – Angio normal – less severe IHD

  • Unstable Angina – Dynamic occlusion + Micro vascular dysfunction + Active Thromb

  • Prinzemetal Angina – Occlusive spasm, No Micro vascular dys, No thrombus – ST ↑


Micro vascular angina l.jpg
Micro Vascular Angina without T inversion


Micro vascular angina102 l.jpg
Micro Vascular Angina without T inversion

  • Normal Coronary blood flow by angiogram

  • No significant CAD in epicardial blood vessels

  • Cardiac micro circulation is at fault

  • Poor collateral connections – younger age

  • More common in women – Syndrome X

  • ECG or TMT show ST - T changes repeatedly

  • Patient will be symptomatic for IHD


St segment depression l.jpg

Upward sloping depression of ST segment is not indicative of IHD

It is called J point depression or sagging ST seg

Downward slopping or Horizontal depression of ST segment leading to T↓is significant of IHD

ST Segment Depression


Lateral wall ischemia l.jpg

Note the classical ischemic ST depressions IHD

ST ↓ are seen in V4,V5,V6 – lateral wall

His ST segments retuned to base line after sublingual nitroglycerine

His pain is precipitated by effort

Notice the tachycardia – heart rate = 140

Lateral Wall Ischemia



T wave inversion106 l.jpg
T Wave Inversion IHD

  • Deep symmetric inverted T waves

  • In more than 2 precardial leads

  • 85% of the patients with such T wave↓had > 75% stenosis of the coronary artery

  • T wave ↓are significantly associated with MI or death during follow up


Acute coronary syndromes l.jpg
Acute Coronary Syndromes IHD

Minor Plaque Disruption

Occlusive

Thrombus

Non-Occlusive Thrombus

Non-Vulnerable Atherosclerotic Plaque

Vulnerable Atherosclerotic Plaque

Myocardial Infarction or Sudden Cardiac Death

Asymptomatic

Unstable Angina or Non-Q-MI

Major Plaque Disruption

Occlusive

Thrombus


Slide108 l.jpg

ACUTE CORONARY SYNDROMES IHD

No ST Elevation

ST Elevation

NSTEMI

Unstable Angina

NQMI QWMI

Myocardial Infarction



Slide110 l.jpg

Pathogenesis of ACS IHD

Platelet rupture

Platelet Adhesion

Platelet Activation

  • Sequence of events

  • Plaque Rupture

  • Platelet Adhesion

  • Platelet Activation

  • Platelet Aggregation

  • Thrombotic Occlusion

Platelet Aggregation

Thrombotic Occlusion

Anti-platelet drugs


Acs pathophysiology plaque rupture thrombosis and microembolization l.jpg

Marker IHD

CholesterolLDL, LP (a), HCy

C-Reactive ProteinsICAM

Interleukin 6, TNFa,

sCD-40 ligand, SAA

MDA Modified LDL,

MMP-9, sICAM,

D-dimer, Neopterin Complement,

Fibrinogen, Troponin, CRP, CD40L

ACS PathophysiologyPlaque Rupture, Thrombosis, and Microembolization

Quiescent plaque

Process

Plaque formation

InflammationMultiple factors

? Infection

Plaque Rupture

? Macrophages

Metalloproteinases

ThrombosisPlatelet ActivationThrombin

Lipid core

Vulnerable plaque

TF  Clotting Cascade

Inflammation

Collagen  platelet activation

Foam Cells

Macrophages

Metalloproteinases

Platelet-thrombin micro-emboli

Plaquerupture


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Thrombus Formation and ACS IHD

Plaque Disruption/Fissure/Erosion

Thrombus Formation

Old

Terminology:

UA

NQMI

STE-MI

New

Terminology:

Non-ST-Segment Elevation Acute Coronary Syndrome (ACS)

ST-Segment Elevation Acute Coronary Syndrome (ACS)

QMI


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Management of ACS IHD

A = Aspirin, B = Beta-blocker, C = Clopidogrel, G = GPIIb/IIIa Inhibitor


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1. Markers of Plaque formation IHD (Stable

Plaque) LDLc, LP(a),Homocysteine

2. Markers of Inflammation

(Vulnerable Plaque)

HS CRP – High Sensitivity C Reactive

Protein

sICAM – Soluble Intercellular Adhesion

Molecule

IL 6 – Interleukin 6

TNFα- Tumor Necrosis Factor Alpha

SAA – Serum Amyloid Alpha

sCD 40 – serum CD 40 Ligand

New Markers of CHD

3. Markers of Plaque Rupture

MDA Modified LDL – Oxidized LDL

MMP-9 – Matrix Metallo Proteinase

sICAM – Soluble Intercellular

Adhesion Molecule

4. Markers of Thrombosis

D-dimer, Complement

Neopterin, Fibrinogen

Troponins, CRP, CD 40 L


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Lipid Profile Report IHD

We have 2 types of fats in our body – the cholesterol and the triglyceride


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Diabetes Mellitus – FBG > 110, PPBG > 140 IHD

Hypertension – SBP > 140, DBP > 90

Dyslipidemia – LDL > 100, TG > 150, HDL < 50

Overweight – BMI > 25, Waist girth > 34 ♀ 38 ♂

Micro-albuminuria > 20 mg / L or GFR < 60 ml / min.

Male Sex up to age 55 yrs – Equal after 55

Smoking, Alcohol, sedentary life, couch potatoes

Family H/o premature CAD – 1º blood relative < 50

Presence of LVH by Echo or ECG

Emerging new risk factors – HCy, LP(a)

CHD Risk Factors


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Extension / Ischemia IHD

Pericarditis

Acute MI

RV Infarct

Expansion / Aneurysm

Mechanical

Heart Failure

Mural Thrombus

Complications of Acute MI

Arrhythmia


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HT + DM ACEi, ARB IHD

HT + IHD ACEi, Perindopril + BB (Meto, Carva)

HT + MRD ACEi + / or Methyl dopa (MD)

HT + CHF ARB, ACEi, Diuretics, No CCB

HT + Pregnancy MD or CCB (Amlo) No ACEi

HT + Asthma, COPD No beta blockers, Alpha blockers OK

HT + Tachycardia No CCBs, Give BB

HT + Dyslipidemia No Diuretics- give ACEi, ARB, CCB

HT in elderly, ISH Indapamide, Diuretics, CCB

Which BP Drug to Choose ?



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Unstable Angina IHD

  • Presence of one or more of the three features,

  • Crescendo Angina- more severe, prolonged, or frequent. Decrease in exercise capacity

  • New onset (1 month) & brought on by minimal exertion. Not relieved by Nitrates

  • Angina at rest as well as with minimal exertion. There are 3 classes – 1 to 3

  • This may progress to NSTEMI or STEMI



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Prinzemetal Angina IHD

  • Transient ST-segment elevation during chest pain due to coronary vasospasm – variant angina

  • ECG with ST ↑. Becomes normal soon, No Q wave

  • Intermittent chest pain

    • often repetitive, usually at rest, early morning

  • Other vasospasms - syncope, Raynaud’s, migraine

  • βblockers contraindicated. CCB, α blockers Rx.



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NSTEMI IHD

Non ST ↑ MI or NSTEMI, Non Q MI

  • Or also called sub-endocardial Infarction

  • Non transmural, restricted to the sub-endocardial region - there will be no ST ↑ or Q waves

  • ST depressions in anterio-lateral & inferior leads

  • Prolonged chest pain, autonomic symptoms like nausea, vomiting, diaphoresis

  • Persistent ST-segment ↓even after resolution of pain



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STEMI and QWMI IHD

STEMI and QWMI

  • ST ↑ signifies severe transmural myocardial injury – This is early stage before death of the muscle tissue – the infarction

  • Q waves signify muscle death – They appear late in the sequence of MI and remain for a long time

  • Presence of either is an indication for thrombolysis


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A – Normal ST segment and T waves IHD

B – ST mild ↑ and prominent T waves

C – Marked ST ↑ + merging upright T

D – ST elevation reduced, T↓,Q starts

E – Deep Q waves, ST segment returning to baseline, T wave is inverted

F – ST became normal, T Upright, Only Q+

Evolution of Acute MI




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Holter & TMT in CAD IHD

  • Holter is an ambulatory ECG, BP monitor

  • Look at the Stress Test – Deep ST ↓

  • The Holter recordings show the changing patterns in ST segments and Heart rate during different activities

  • Worst ST changes during vigorous physical activity like playing tennis


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Normal Q waves IHD

Notice the small

Normal Q in Lead I


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Normal Q Waves IHD

  • The normal Q wave in lead I is due to septal depolarization

  • It is small in amplitude – less than 25% of the succeeding R wave, or less than 3 mm

  • Its duration is < 0.04 sec or one small box

  • It is seen in L1 and some times in V5, V6


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Pathological Q wave IHD

Notice the deep & wide

Infarction Q in Lead I


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Pathological Q wave IHD

  • The pathological Q wave of infarction in the respective leads is due to dead muscle

  • It is deep in amplitude – more than 25% of the succeeding R wave, or more than 4 mm

  • Its duration is > 0.04 sec or > 1 small box

  • It is seen in Leads facing the infarcted muscle mass



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Q Wave of Cardiomyopathy IHD

  • In idiopathic hypertrophic cardiomyopathy the septal Q wave in lead 1 is deep and prolonged because of excessive septal thickness. Similar to MI Q wave,

    but

  • There will be marked LVH evidence and

  • The R wave amplitude is very tall unlike in infarction – where R waves are reduced



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Serial ECG Changes of MI IHD

  • Normal ECG does not exclude MI or IHD

  • First few hours of MI – Hyper acute T with ST segment elevation starting

  • Drop in R wave voltage and ST elevation

  • Significant Q, R wave none, ST ↑, T↓

  • No R, Marked Q, ST baseline, T↓

  • Small R starts, Q remains, ST normal, T↓

  • In some Q waves disappear, R improves, ECG becomes nearly normal.


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Blood Supply - MI - Leads IHD

ANTERIOR LATERAL INFERIOR POSTERIOR

LAD LAD or LCx RCA RCA + LCx

V1, V2, V3, V4 V5, V6, L1, aVL L2, L3, aVF V1, V2 Mirror


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What are the Investigations ? IHD

  • Resting 12 Lead ECG, Chest X-Ray

  • Tread Mill Test (TMT) – Provocative stress tests

  • Troponins (bed side), LDH, CPK isoenzymes

  • Echocardiography and Doppler

  • Calcium scoring and CT angiography

  • Exercise Echo, Dobutamine challenge echocardiography

  • Perfusion – Stress Thalium, Sistemibi, Dipyridamole

  • 3D Coronary Cartography (CCG), PET scan

  • Coronary Angiography (Gold Standard)



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Acute Anterior Wall MI IHD

  • Due to occlusion of the proximal LAD

  • Significant Q waves, ST elevation and T inversions in Leads V2, V3 and V4

  • Q waves and T inversion in L1

  • If only V1 and V2 show the changes it is called septal MI

  • Associated with abnormal conduction

  • Septal perforation with acquired VSD is a rare complication



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Hyper Acute MI IHD

  • Note the hyper acute elevation of ST

  • The R wave is continuing with ST and the complexes are looking rectangular

  • Some times tall and peaked T waves in the precardial leads may be the only evidence of impending infarct

  • Sudden appearance LBBB indicates MI

  • MI in Dextro-cardia – right sided leads are to be recorded


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Note the ST IHD↑in V1, V2, V3

T↓ in V1 to V5

R wave voltages of all lateral leads well preserved

No ST ↑in the Lateral leads

What is striking ?



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Acute Anterio-lateral MI IHD

  • Due to occlusion of the marginal branch or the main trunk of Left Circumflex artery

  • Or due to occlusion of the diagonal branch of Left anterior descending artery

  • Significant Q waves, ST elevation and T inversions in Lead 1, aVL, V5 and V6

  • This is the most common form of MI



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Acute Anterio-lateral MI IHD

  • Note the marked ST elevations in chest leads V2 to V5 and also ST↑ in L1 & aVL

  • T inversions have not appeared as yet

  • R wave voltages have dropped markedly in V3, V4, V5 and V6

  • Small R in L1 and aVL.



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Acute Anterio-lateral MI IHD

  • Note the marked ST elevations in chest leads V2 to V5, also ST↑ in L1 & aVL

  • T inversions have not appeared as yet

  • R wave voltages have merged with ST ↑ markedly in V3, V4, V5 and V6

  • In addition complimentary St ↓in L2, L3



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Thrombolysed Anterio-lateral MI IHD

  • Note the ST elevations in chest leads V2 to V5 are returned toward baseline

  • Deep T ↓have appeared in all leads

  • R wave voltages have improved in V2 to V5

  • No residual Q waves seen

  • This patient was thrombolysed within 2 hours and MI has become stable – Golden period

  • Thrombolytics – UK, SK, TPA, r-TPA



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Stable Anterio-lateral MI IHD

  • The coved ST↑ in chest leads V2 to V5 almost returned to baseline

  • T↓are becoming less marked in all leads

  • R wave voltages improved well in V4 to V5

  • No residual Q waves seen

  • This ECG is 4 weeks after the Acute MI



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Acute Inferior wall MI IHD

  • Due to occlusion of the right coronary artery

  • Significant Q waves, ST elevation and T inversions in Lead II, Lead III, aVF,

  • This is the associated with arrhythmias



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Acute Inferior wall MI IHD

  • Note the ST elevations in Inferior leads- namely L2, L3 and aVF

  • T inversions yet to appear

  • aVL lead shows complimentary ST↓and T inversion


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What is striking ? IHD

Acute Inf Post


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Acute Inferior wall MI IHD

  • Note the ST elevations in Inferior leads- namely L2, L3 and aVF

  • Hyper acute T waves merging with ST

  • V1, V2, aVL lead shows rsR’ pattern with ST↓and T inversion – Inferior MI

  • Associated RBBB also is present – QRS is wide > 0.12 sec


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Where are the ST IHD↑ ?

Inf Lysed


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Inferior Wall MI - Thrombolysed IHD

  • A case of inferior wall MI

  • Thrombolysed with in 2 hours

  • ST segments returned to base line

  • Deep T inversions signify residual ischemia

  • This patient became stable



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Old Inferior wall MI IHD

  • This is months after the acute event

  • Patient suffered inferior MI

  • Residual QS waves in L3 and aVF

  • T inversions in L3 and aVF

  • ST segments are isoelectric

  • L3 t inversion became normal

  • Chest leads R wave voltages are good



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Acute True Posterior MI IHD

  • Due to occlusion of the distal Left circumflex artery or posterior descending or distal right coronary artery

  • Mirror image changes or reciprocal changes in the anterior precardial leads

  • Lead V1 shows unusually tall R wave (it is the mirror image of deep Q)

  • V1 R/S > 1, Differential Diagnosis - RVH



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Acute True Posterior MI IHD

  • V2, V3 show tall R waves, Even V1 shows R

  • V2, V3, V1 leads R/s ratio is >> 1

  • These R waves are the mirrored MI – Qs

  • These leads show deep ST depression

  • This ST↓is in fact the mirrored ST↑of MI

  • The same leads show sharp T waves

  • These are the mirrored T inversions of MI



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Inferio-Posterior MI IHD

  • V1, V2 show tall R waves

  • V1, V2 leads R/s ratio is >> 1

  • These R waves are the mirrored MI – Qs

  • This ST↓ is in fact the mirrored ST ↑ of MI

  • The T ↓are the mirrored T inversions of MI

  • L2, L3 and aVF show gross ST ↑ - Inferior MI

  • V4R, V5R show ST elevations – RV – MI too.



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Old Inferio-Posterior MI IHD

  • V2 shows residual R waves of Posterior MI

  • V2 lead R/s ratio is > 1

  • The R waves are the mirrored old Qs of MI

  • This ST↓ is no longer seen – stabilized MI

  • L3 & aVF show deep QS of old Inferior MI

  • The T ↓in L3, aVF signify old inferior MI



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Dextrocardia and MI IHD

  • Note the ECG carefully – It is an eye opener

  • 55 years ♀ is sent for ECG by another doctor

  • She has dextrocardia of which she is unaware

  • She has typical clinical features of acute MI

  • Routine chest leads placed on left chest showed no evidence of MI at all

  • ECG with chest leads on the right chest – V2R to V6R - typical acute anterio-septal MI



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Right Ventricular MI IHD

  • Note the ECG carefully – It is an eye opener

  • 65 yrs ♂ has typical clinical features of acute MI

  • Routine chest leads placed on left chest showed no MI - but limb leads showed acute Inferior MI

  • ECG with chest leads on the right chest – V2R to V6R show typical changes of acute MI of the Right Ventricle. RV MI is associated with Inferior wall MI

  • His serum troponins were very high

  • Angio showed 95% block of the RCA



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Electrical Alternans IHD

  • Note the typical ECG changes

  • Every alternate QRS complex has a small and a large amplitude but of sinus origin

  • The heart rate is 110 per minute

  • There are P waves preceding all QRS waves

  • This is a feature of pericardial effusion with cardiac tamponade


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Normal IHD

VPC

Normal

VPC

Ventricular Bigeminy


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Ventricular Bigeminy IHD

  • Note this typical ECG of bigeminy

  • Each normal sinus originated ventricular complex with narrow QRS is followed by a

  • Premature beat with wide and bizarre looking QRS of ventricular origin

  • Similarly Trigeminy, Quadrigeminy

  • These ectopics signify heart failure

  • In this ECG there are features of Inferior MI


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Myxedema IHD

Heart rate Rhythm P wave PR interval QRS in sec

50


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Myxedema IHD

  • Note the ECG changes

  • Bradycardia – HR of 55 per minute

  • Low voltages of all complexes

    • Less than 5 mm Limb leads

    • Less than 8 mm chest leads

  • DD of low voltage complexes

  • Pericardial effusion, Constrictive pericarditis

  • Severe Emphysema

  • Pneumothorax or left sided pleural effusion



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S.A.H – ECG changes IHD

  • Striking ECG changes of Non Cardiac origin

  • Incredible deep and symmetric T Inversions

  • In young person with massive Sub Arachnoid Haemorrhage

  • He has no cardiac disease

  • Presumably due to autonomic dysfunction

  • Intense Head ache, Has very high B.P

  • Lumbar Puncture clinches the issue



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Hyperkalemia IHD

  • This is a 58 yr old man's with CRF

  • Serum K was 7.6 m mol/L. (Normal upto 4.2)

  • Hyperkalaemia ECG changes are

  • Small or absent P waves

  • Atrial fibrillation (not in this ECG)

  • Wide QRS

  • Shortened or absent ST segment

  • Wide, tall and tented T waves



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Hypokalemia IHD

  • This 22 year lady had prolonged vomiting

  • Her serum K was 1.8 mmol/L.

  • Normal 3.2 to 4.2

  • Hypokalaemia ECG changes are

  • Small or absent T waves or inverted T

  • Prominent U waves (see pointer)

  • T wave is the tent house of K

  • More K – tall T, less K flat or inverted T


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In non co-operative child IHD

Excessive movements of limbs

Movement disorders of CNS

Not properly earthed machine

Additional wet ground earth helps

Wandering base line


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Limb movements cause baseline fluctuations IHD

Tense muscles cause tremor of baseline

Hairy chest interferes with proper contact of chest leads – better to shave the area if needed.

Reassurance, starting recording a few minutes after the leads are placed – reduce muscle tension

Muscle Tremor


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Any electrical gadgets in the same line may interfere IHD

Like Mixie, Motor, Musical tube lights etc

Proper earthing is essential

Dedicated direct line for ECG power point

Use battery mode, Artifacts are quite misleading

AC Interference


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We have also an advanced course on ECG IHD

We have several other educative CMEs prepared

Please refer to the list at the beginning of this book

We have several religious and philosophical texts sung, translated and made as PowerPoint slides

Please request what ever you want

CME talk can also be given if you intimate ahead

The charge of Rs.100/- per CD is nominal and to cover the incidental costs only

Our Other Resources


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This only a beginning and certainly not the end IHD

We look forward for more learning experiences

Please write to us what you felt about this ECG

Contact address and phone are in the beginning

Thank YOU and

With Warm Regards,

Dr.Sarma.

THIS IS NOT THE END


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