Kuliah Ekg Unwar 2013

ECG InterpretationUNWAR Medical Student Lecture

A.A.Gede Budhitresna MD,Int,Ph.D,FINASIM

Objectives The Basics Interpretation Clinical Pearls Practice

Recognition

3

QUICK REVIEW OF HEART

Purpose Pumps bloodBasic Anatomy 4 chambers 2 sides 4 valves

Circulatory System Three basic components

Heart Serves as pump that establishes the pressure

gradient needed for blood to flow to tissues Blood vessels

Passageways through which blood is distributed from heart to all parts of body and back to heart

Blood Transport medium within which materials

being transported are dissolved or suspended

Circulatory System Pulmonary

circulation Closed loop of vessels

carrying blood between heart and lungs

Systemic circulation Circuit of vessels

carrying blood between heart and other body systems

Functions of the Heart Generating blood pressure Routing blood

Heart separates pulmonary and systemic circulations

Ensuring one-way blood flow Regulating blood supply

Changes in contraction rate and force match blood delivery to changing metabolic needs

Blood Flow Through and Pump Action of the Heart

Blood Flow Through Heart

Sel otot jantung 2 macam sel :

Sel autoritmik (1%) Potential pace maker Hanya terdapat pada NSA – NAV – berkas

his cabang kanan dan kiri – serabut purkinye

Sel kontraktil (99%) Sel yang berkontraksi sebagai respon thd

impuls dari sel autoritmik

Muatan listrik sel otot jantungKeadaan sel otot jantung

Muatan listrik

intraseluler ekstraseluler

Istirahat/repolarisasi

- (relatif lebih negatif)

+ (relatif lebih positif)

depolarisasi + (relatif lebih positif)

- (relatif lebih negatif)

Sel istirahat

+ + + + + + +

Sel sedang depolarisasi

--- --- --- + + + +

-- -- -- --- --- ---

--- --- --- --- ---

+ + + +

+ + + +

--- --- ---

--- --- ---

+ + + + + + +

Sel telah depolarisasi

--- --- --- --- ---

--- --- --- + + + + +

Sel mulai repolarisasi

--- --- --- + + + +

+ + + + + + +

+ + + + + + +

+ + + +

+ + + +

--- --- ---

--- --- ---

--- --- --- --- --- --- --- + + + +

Elektrokardiogram Fase depolarisasi (SISTOLE)

bagian yang terjadi akibat penyebaran impuls

Fase repolarisasi (DIASTOLE) bagian yang terjadi bila sel otot

jantung kembali istrirahat Arah defleksi , ditentukan :

Arah penyebaran impuls depolarisasi Letak elektroda

Hubungan arah impuls – defleksi elektrokardiogram

Arah impuls depolarisasi

Arah defleksi Gambar

Menuju elektroda +

Positif (ke atas)

Menuju - meninggalkan

Bifasik

Meninggalkan elektroda +

Negatif (ke bawah)

The Normal Conduction System

CONDUCTION SYSTEM

Normal Impulse Conduction

Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers

18

RELATIONSHIP

Putting the A&P with the EKG

Normal Adult ECG

CARDIAC CYCLES

SANDAPAN (LEAD) EKG Sandapan rutin 12 leads

3 bipolar standard leads ( I, II, III) 3 unipolar lead ekstremitas (aVR, aVL, aVF) 6 unipolar chest leads (V1, V2, V3, V4, V5, V6)

Bipolar standard lead & unipolar lead ekstremitas menggambarkan keadaan medan bioelektrik aktivitas jantung pada bidang frontal

Chest lead Bidang horizontal

Lead Placement

aVF

All Limb Leads

12 Lead Placement

Precordial Leads

Precordial Leads

I and AVL

II, III and AVF

V3 & v4

V1 & v2

V5 & v6 Where the positive

electrode is positioned, determines what part of the heart is seen!

Electrode Placement

Lead V1 is placed over the 4th intercostal space, to the right of the sternum

Lead V2 is placed over the 4th intercostal space, to the left of the sternum

Lead V4 is placed over the 5th intercostal space in the mid-clavicular line

Lead V3 is placed midway between V2 and V4 Lead V5 is placed on the same horizontal level

as V4 but at the anterior axilliary line Lead V6 is placed on the same horizontal level

as V4 and V5 but on the mid axilliary line

EKG Distributions

Anteroseptal: V1, V2, V3, V4 Anterior: V1–V4 Anterolateral: V4–V6, I, aVL Lateral: I and aVL Inferior: II, III, and aVF Inferolateral: II, III, aVF, and

V5 and V6

2004 Anna Story

The ECG Tracing: Waves P- wave

Marks the beginning of the cardiac cycle and measures the electrical impulse that causes atrial depolarization and mechanical contraction

QRS- Complex Measures the impulse that causes ventricular

depolarization Q-wave- may or may not be evident on the ECG R-wave- first upward deflection following P wave S-wave- the first downward deflection following the

R-wave T- wave

Marks ventricular repolarization that ends the cardiac cycle

Intervals and Segments P-R interval-

Time interval for impulse to go from the SA to the AV node

normal 0.12-0.20 secs QRS Interval

Time interval for impulse to go from AV node to stimulate Purkinjie fibers

Less than 0.12 secs QT Interval

Time interval from beginning of depolarization to the end of repolarization

Should not exceed ½ the length of the R-R ST segment

end of the S to the beginning of the T

Waveforms

Interpretation Develop a systematic approach to

reading EKGs and use it every time The system we will practice is:

Rate Rhythm (including intervals and

blocks) Axis Hypertrophy Ischemia

RATE2 More Methods to Count Rate

1. When the rhythm is regular, the heart rate is 300 divided by the number of large squares between the QRS complexes.

For example, if there are 4 large squares between regular QRS complexes, the heart rate is 75 (300/4=75).

2. The second method can be used with an irregular rhythm to estimate the rate. Count the number of R waves in a 6 second strip and multiply by 10.

For example, if there are 7 R waves in a 6 second strip, the heart rate is 70 (7x10=70).

Heart Rate: 300, 150, 100, 75, 60, 50, 43, 37 bpm

Rate

HR of 60-100 per minute is normal HR > 100 = tachycardia HR < 60 = bradycardia

Differential Diagnosis of Tachycardia

Tachycardia

Narrow Complex Wide Complex

Regular STSVTAtrial flutter

ST w/ aberrancySVT w/ aberrancy

VT

Irregular A-fibA-flutter w/ variable conductionMAT

A-fib w/ aberrancy

A-fib w/ WPWVT

What is the heart rate?

(300 / 6) = 50 bpm

www.uptodate.com

Asystole V-Tach to V-Fib

can lead to….

Asystole

Rhythm

Sinus Originating

from SA node P wave before

every QRS P wave in same

direction as QRS

What is this rhythm?Normal Sinus Rythm

Normal Intervals PR

0.20 sec (less than one large box)

QRS 0.08 – 0.10 sec (1-2

small boxes) QT

450 ms in men, 460 ms in women

Based on sex / heart rate

Half the R-R interval with normal HR

Prolonged QT Normal

Men 450ms Women 460ms

Corrected QT (QTc) QTm/√(R-R)

Causes Drugs (Na channel blockers) Hypocalcemia, hypomagnesemia, hypokalemia Hypothermia AMI Congenital Increased ICP

Blocks AV blocks

First degree block PR interval fixed and > 0.2 sec

Second degree block, Mobitz type 1 PR gradually lengthened, then drop QRS

Second degree block, Mobitz type 2 PR fixed, but drop QRS randomly

Type 3 block PR and QRS dissociated

What is this rhythm?

First degree AV block PR is fixed and longer than 0.2 sec

What is this rhythm?

Type 1 second degree block (Wenckebach)

What is this rhythm?

Type 2 second degree AV block Dropped QRS

What is this rhythm?

3rd degree heart block (complete)

Bundle Branch Block - BBB

The QRS Axis

Represents the overall direction of the heart’s activity

Axis of –30 to +90 degrees is normal

The Quadrant Approach

QRS up in I and up in aVF = Normal

What is the axis?

Normal- QRS up in I and aVF

Hypertrophy Add the larger S wave of V1 or V2

in mm, to the larger R wave of V5 or V6.

Sum is > 35mm = LVH

Ischemia

Usually indicated by ST changes Elevation = Acute infarction Depression = Ischemia

Can manifest as T wave changes Remote ischemia shown by q

waves

Acute Coronary Syndrome

PEMBULUH DARAH PEMBULUH DARAH KORONERKORONER

RCA

LM

LAD LCx

Normal : Isoelektris

Kepentingan : Elevasi Pada injuri/infark akutDepresi Pada iskemia

Segmen STDiukur dari akhir QRS s/d awal gel

T

NSTEMI dan STEMI

ECG Changes : Ischemia T-wave inversion ( flipped T) ST segment depression T wave flattening Biphasic T-waves

Baseline

ECG Changes: Injury ST segment elevation of greater than 1mm in

at least 2 contiguous leads Heightened or peaked T waves Directly related to portions of myocardium

rendered electrically inactive

Baseline

ECG Changes: Infarct Significant Q-wave where none previously existed

Why? Impulse traveling away from the positive lead Necrotic tissue is electrically dead

No Q-wave in Subendocardial infarcts Why?

Not full thickness dead tissue But will see a ST depression Often a precursor to full thickness MI

Criteria Depth of Q wave should be 25% the height of the R

wave Width of Q wave is 0.04 secs Diminished height of the R wave

Evolving MI and Hallmarks of AMI

1 year

Q wave

ST Elevation

T wave inversion

INFERIOR INFARCTION

Color Coding ECG- Inferior

Blue indicates leads II, III, AVF

Inferior Infarct with ST elevations

Right Coronary Artery (RCA)

1st degree Heart Block

2nd degree Type 1, 2 3rd degree Block N/V common, Brady

Inferior MI

Inferior myocardial infarction

Small inferior distal RCA occlusion

ECG changes in leads II, III, and aVF

ANTERIOR INFARCTION

ECG demonstrates large anterior infarction

Color Coding ECG’s Anterior

Yellow indicates V1, V2, V3, V4

Anterior infarct with ST elevation

Left Anterior Descending Artery (LAD)

V1 and V2 may also indicate septal involvement which extends from front to the back of the heart along the septum

Left bundle branch block Right bundle branch block 2nd Degree Type2 Complete Heart Block

Anterior MI

Mid LAD occlusion after the first septal perforator (arrow)

ECG : large anterior MI

2004 Anna Story 83

Color Coding ECG- Lateral Red indicates leads

I, AVL, V5, V6 Lateral Infarct

with ST elevations

Left Circumflex Artery

Rarely by itself Usually in combo

Lateral MI

Color Coding ECG- Posterior

Green indicates leads V1, V2

Posterior Infarct with ST Depressions and/ tall R wave RCA and/or LCX Artery

Understand Reciprocal changes The posterior aspect of the

heart is viewed as a mirror image and therefore depressions versus elevations indicate MI

Rarely by itself usually in combo

Posterior MI

Putting it ALL together

2004 Anna Story 89

Practice 1

Anterior MI with lateral involvement

ST elevations V2, V3, V4

ST elevations II, AVL, V5

Click for answer

Practice 2

Anteroseptal MI

ST elevations V1, V2, V3, V4

Click for answer

Practice 3

Click for answer

Inferior MI

ST elevation 2,3 AVF

Practice 4

Click for answer

Inferior lateral MI

ST elevations 2, 3, AVF

ST elevations V5

Practice 5

•Acute inferior MI

•Lateral ischemia

Click for answer

Cardiac Enzymes Indicating Infarct Normals

CPK- 10-155u/liter begin rise 3-6 hours and peaks 12-24 with return

to norm 3-5 days CPK-MB < than 5% IU/liter LDH 85-200 IU/liter

Begin rise 12 hours, peaks 36-72 and normal around 10 days

LDH 1- 18.1% - 29% of total LDH 2- 27.4% to 37.5% of total

Cardiac Enzymes Indicating Infarct

Troponins- Now the Gold Standard! Rises after 3-6

hours Negative Troponin

within 6 hours of onset of S&S rules out the MI

Peaks at about 20 hours

May be raised for 14 days

Cardiac Enzymes Indicating Infarct Troponin T

84% sensitivity for MI 8 hours after onset of symptoms

22% for unstable angina Advantages

Highly sensitive for detecting myocardial ischemia Levels may help to stratify risks

Disadvantages Less specific than Troponin I Increased in angina Increased in chronic renal failure

Cardiac Enzymes Indicating Infarct Troponin I

90% sensitivity for MI 8 hours after onset of S&S and 95% specificity

Level greater than 1.2 suggest MI Negative rules out MI Obtain two negative troponin values 4 hours

apart Normally exceedingly low Even a small elevation indicates

myocardial damage

DISKUSI KASUS

Normal Sinus Rhythm

Mattu, 2003

First Degree Heart Block

PR interval >200ms

Junctional Rhythm

Rate 40-60, no p waves, narrow complex QRS

Hyperkalemia

Tall, narrow and symmetric T waves

Premature Atrial Contractions

Trigeminy pattern

Atrial Flutter with Variable Block

Sawtooth waves Typically at HR of 150

Torsades de Pointes

Notice twisting pattern

Treatment: Magnesium 2 grams IV

Digitalis

Dubin, 4th ed. 1989

Lateral MI

Reciprocal changes

Inferolateral MI

ST elevation II, III, aVF

ST depression in aVL, V1-V3 are reciprocal changes

Anterolateral / Inferior Ischemia

LVH, AV junctional rhythm, bradycardia

Left Bundle Branch Block

Monophasic R wave in I and V6, QRS > 0.12 secLoss of R wave in precordial leadsQRS T wave discordance I, V1, V6Consider cardiac ischemia if a new finding

Right Bundle Branch Block

V1: RSR prime pattern with inverted T waveV6: Wide deep slurred S wave

First Degree Heart Block, Mobitz Type I (Wenckebach)

PR progressively lengthens until QRS drops

Supraventricular Tachycardia

Narrow complex, regular; retrograde P waves, rate <220

Retrograde P waves

Right Ventricular Myocardial Infarction

Found in 1/3 of patients with inferior MI

Increased morbidity and mortality

ST elevation in V4-V6 of Right-sided EKG

Ventricular Tachycardia

Second Degree Heart Block, Mobitz Type II

PR interval fixed, QRS dropped intermittently

Acute Pulmonary Embolism

SIQIIITIII in 10-15%

T-wave inversions, especially occurring in inferior and anteroseptal simultaneously

RAD

Hypokalemia

U wavesCan also see PVCs, ST depression, small T waves

LVH with ‘strain’

Sinus arrhythmia

Perempuan 26 th, MCU penerimaan karyawan

Lateral myocardial infarction

Perempuan 46 th, DM, Nyeri dada 10 jam yg lalu, mendadak, Trop T (+)

Acute inferoposterior myocardial infarction

Laki-laki 36 th, perokok, nyeri dada 1 jam yg lalu, mendadak, Trop T (-)

Atrial fibrillation dan STEMI inferior

Laki-laki 76 th, perokok, stroke ischemik berulang, nyeri dada memberat

Atrial flutter

Laki-laki 76 th, perokok, keluhan (-), akan operasi reseksi kolon ok tumor

premature ventricular contraction

Laki-laki 32 th, gemuk, tidak nyaman di dada hilang timbul, terutama kalau cape.

Wide complex tachycardia

Laki-laki 66 th, perokok, DM, nyeri dada 8 jam yg lalu, tiba2 kolaps

Supraventricular tachycardia

Perempuan 36 th, HT, berdebar-debar sejak 2 jam yll, hilang-timbul

Ventricular flutter

Laki-laki 36 th, dyslipidemia, nyeri dada 6 jam yg lalu, mendadak, Trop T (+), tiba-tiba kolaps di IGD

KASUS 1

EKG

Interpretasi EKG ?

Jawaban: D

Kasus 2 Pria 50 thn, CAD post PTCA, Hipertensi Berdebar & lemas 3 jam SMRS, hemodinamik

stabil

Diagnosis EKG

A. Supraventricular Tachycardia (AVNRT)

B. Atrial TachycardiaC. Atrial FlutterD. Atrial Fibrillasi

Jawaban: A

KASUS 3

Pria 67 tahun, anggota DPR Berdebar dan sesak nafas sejak 2 jam Hipertensi dan PPOK Tidak ada bukti klinis CAD

Apa diagnosis EKG ?

A. Atrial fibrillationB. Atrial TachycardiaC. Sinus arrhythmiaD. Atrial flutter

Jawaban: D

Kasus 4 Wanita 45 tahun Lemas, lekas capek dan sesak nafas

bila aktivitas

Diagnosis EKG

A. Sick Sinus Syndrome

B. AV blok derajat 2 Mobitz II

C. Sinus arrest

D. AV blok derajat 3

Jawaban: D

Kasus 5 : Laki-laki, 50 thn. Chest pain dengan Troponin T (+)

A. UAPB. STEMI Anteroseptal (fase evolusi)C. NSTEMI AnteroseptalD. NSTEMI Anterior Ekstensif

Jawaban : B

JAWABAN :

KASUS 6

EKG

Interpretasi EKG ?

Jawaban : C

KASUS 7

EKG

Interpretasi EKG ?

Jawaban : D

KASUS 8

EKG

Interpretasi EKG ?

Jawaban : B

151

THANK YOU- ANY QUESTION?