NORMAL ECG,

INFARCTION
&
ARRHYTHMIA
S

Iqbal Lahmadi
Departement of Internal Medicine
Sintang - 2013
 5 kotak kecil
= 1 kotak sedang
= 0.2 detik Paper speed : 25 mm/second
1 kotak kecil
= 0.04 detik

5 kotak sedang
= 1 kotak besar
= 1 detik
 Heart abnormality
 Preload
 Afterload + anti remodelling
 Vascular and myocard
 Arrythmias
 Chambers
 Valves
 Contractility
 Remodelling
 Utk menurunkan Preload

• Morphine

• Furosemide

• Nitroglycerin

• Dopamine

• Dobutamine
 Heart abnormality
 Preload
 Afterload + anti remodelling
 Vascular and myocard
 Arrythmias
 Chambers
 Valves
 Contractility
 Remodelling
Afterload controls + cardiac
anti remodelling agents

 ACE-inhibitor(Captopril, Lisinopril, Enalapril)

 ARB (Valsartan)
 Beta blockers
 Heart abnormality
 Preload
 Afterload + anti remodelling
 Vascular and myocard
 Arrythmias
 Chambers
 Valves
 Contractility
 Remodelling
 Vascular and myocard
 Ischaemia (early condition of vascular injury)
 Inverted T
 Depression ST segment
 Flattening ST segment

 Injury (life threatening/ acute condition)

 Elevation ST segment
 Deep inverted T wave = Sub endocard injury = Transmural injury
 Depression ST segment  as mirror image at lead V1-V4

 Necrosis/ OMI (advance after injury without intervention)

 Pathologic Q wave
 QS pattern
Designations of different QRS patterns
ST elevasi ST depresi
Electrocardiographic DDx of T wave abnormalities in non-ACS
(perbedaan makna dari kelainan gelombang T)  gak penting…!!!
ECG DDx of ST segment elevation and depression on ACS
 Lead Groups

I aVR VI V4

II aVL V2 V5

III aVF V3 V6
Limb Leads Chest Leads

Warna yg sama, menunjukkan lokasi kelainan myocard

(selanjutnya liat slide berikut2nya)
 12 Lead ECG Interpretation (jgn pake ini, bingung ntar)

Derek J Rowlands (Clinical ECG);1991:180

Lokasi Infark Leads yang mendukung

Anteroseptal V1, V2, V3

Anterior Some of the group V1-V3 +
some of the group V4-V6
Anterolateral V4, V5, V6, I, AVL and possibly II
Extensive Anterior V1-V6 + I & AVL
High Lateral AVL
Inferior II, III, AVF

Inferolateral (Apical) II, III, AVF, V5, V6 and sometime

also I and AVL
Inferoseptal II, III, AVF, V1, V2, V3

Posterior V1, V2 (inverse of the usual

changes elsewhere)
 Cara praktis menentukan lokasi myocard yang terlibat
berdasar kelainan tiap-tiap lead pada ECG

Anteroseptal Anteroseptal Anteroseptal High

(Low septal) (Mid septal) (Apical) Lateral

V1 V2 V3 V4 V5 V6 I AVL

Anterior Anterolateral

Anterior Extensive

Schamrodt, 1994
Lead II, III + AVF: kelainan di myocard inferior
Ini yg terbaru, tp bikin bingung juga
buat pemula
Adapted with permission from Smith SW, Zvosec DL, Sharkey SW, Henry TD.
The ECG in acute MI: Philadelphia: Lippincott, Williams, and Wilkins; 2002. p. 358.
There is great variation among patients. Use this for guidelines only.
 Heart abnormality
 Preload
 Afterload + anti remodelling
 Vascular and myocard
 Arrythmias
 Chambers
 Valves
 Contractility
 Remodelling
 Arrythmias
1. Altered Automaticity
2. Reentry
3. Conduction Block
12 Lead ECG Interpretation
(ini jembatan keledai)

ATRIUM
SUPRAVENTRIKEL
QRS compl: S E M P I T
Tx dgn DC shock: 25 – 100 J
Kelainan EKG tersering :
A. fibril, A. flutter, SVES, SVT

VENTRIKEL
QRS compl: LEBAR
DC shock: 200 – 360 J
Kelainan EKG tersering :
VT, V. Fibril. V. flutter, PVC
 Jadi untuk mudahnya, berdasar kelainan ECG,
jantung dibagi 2:

ATAS BAWAH
(Atrium dan Supraventrikel) (Ventrikel)

Gelombang QRS sempit Gelombang QRS lebar

(durasi QRS complex ≤ 12 detik/ (durasi QRS complex > 12 detik/
3 kotak kecil)) 3 kotak kecil))

4 kelainan 4 kelainan

AF A. Flut SVES SVT PVC VT VF V . Flut

 Kelainan
Atrium dan Supraventrikel

Atrial Fibrilasi:
hilangnya gelombang P, dgn interval
RR yg BERBEDA

Atrial Flutter:
Terbentuknya gelombang yg khas
(bentuk mata gergaji) diantara R dgn R

SVES:
Dasarnya sinus (normal), tp ada
minimal 1 complex QRS yg kehilangan
P, diikuti interval RR yg memanjang

SVT:
hilangnya gelombang P, dgn
interval RR yg SAMA
 Normal Sinus Rhythm

www.uptodate.com

Implies normal sequence of conduction, originating in the sinus node and

proceeding to the ventricles via the AV node and His-Purkinje system.

EKG Characteristics: Regular narrow-complex rhythm

Rate 60-100 bpm
Each QRS complex is proceeded by a P wave
P wave is upright in lead II & downgoing in lead aVR
\
 Heart abnormality
 Preload
 Afterload + anti remodelling
 Vascular and myocard
 Arrythmias
 Chambers
 Valves
 Contractility
 Remodelling
 Chamber
Atrial Enlargement

Ventricular Hipertrophy
Biphasic P wave
Left Atrial Enlargement
Right Atrial Enlargement
Left Ventricular Hypertrophy
ECG criteria for LVH
Right Ventricular Hypertrophy
 Heart blocks
 Branch block
 AV block
 Hemiblock (LAFB and LPFB)
 Bifascicular block
 Trifascicular block
 SA Block **
 ECG criteria for right
bundle branch block

ECG criteria for left

bundle branch block
Right bundle branch block
Differential diagnosis
 Myocardial infarction
 Pulmonary embolism
 Chronic obstructive lung disease/cor pulmonale
 Pulmonary hypertension (primary or secondary)
 Hypertensive heart disease
 Degenerative disease of the conduction system
 Brugada syndrome
 Cardiomyopathy
 Chagas disease
 Congenital heart disease (eg, Ebstein anomaly)
Right bundle branch block

• The Framingham study has shown that the

presence of a new RBBB after previously

having had a normal ECG is suggestive of

organic heart disease.

•CAD is among many causes of a new RBBB.

 Left bundle branch block
The differential diagnosis of LBBB include:

• (1) CAD, (2) Cardiomyopathy,

• (3) HHD, and (4) Degenerative disease of the

conduction system.

The presence of LBBB portends a poor long-term prognosis. One study

showed that 50% of patients who have an LBBB die of a cardiac event

within 10 years.
 Left anterior fascicular block

When LAFB occurs newly in the presence of an anterior MI,

there is a slightly increased risk for progression to advanced

heart block. The most common vessel involved in this setting

is typically the left anterior descending artery.

 Left anterior fascicular block
 Note the left QRS axis deviation (60 to 90),
 The rS morphology in leads II, III, and aVF, and
 The small Q wave preceding a larger R wave in leads I and
aVL.
Left Posterior fascicular block

 Rightward deviation of the QRS axis (þ120), rS pattern in

leads I and
 aVL, and qR pattern in leads II, III, and aVF.
 Bifascicular blocks
 Bifascicular block is the combination RBBB and LAFB,

or RBBB plus LPFB.

 In addition, because the left bundle branch is composed of an anterior and
a posterior fascicle, LBBB can be thought of as a bifascicular block (rare).
 Bifascicular blocks are of particular importance in the setting of an acute
MI, because their presence may suggest impending complete heart block.
 When LPFB does exist, coronary artery disease, hypertensive disease, or
aortic valvular disease are common etiologies .
Bifascicular blocks
LAFB + RBBB
Bifascicular blocks
LPFB + RBBB
 Trifascicular blocks

 Complete trifascicular block can present as a bifascicular block plus a third-

degree AV block.

 Patients who have multi-fascicular block have advanced conduction system

disease that ultimately may progress to complete heart block and sudden cardiac

death.

 Based on the Framingham study & several other, it has been estimated that

approximately 1% of patients/ year with bifascicular block may progress to

complete heart block

 AV block
Rhythms Produced by Conduction Block

 1st degree AV block

 Type 1 2nd degree AV block
 Type 2 2nd degree AV block
 3rd degree AV block
Trifascicular blocks
WARMING UP CARDIOLOGY AND HYPERTENSION

Classification of Arrhythmias

Narrow complex arrhythmias

Arise above the bifurcation of the bundle of His. The QRS duration is
less than 0.1s (2.5 small squares)
Sinus arrhythmia, Sinus tachycardia, Sinus bradycardia, Junctional / AV
nodal tachycardia, Atrial tachycardia, atrial flutter, AF, Atrial ectopics.

Broad complex arrhythmias

Usually arise either from the ventricles or less commonly are conducted
abnormally from a site above the ventricles so that delay occurs (this is
called aberrant conduction). The QRS duration is greater than 0.1s (2.5
small squares).
Ventricular ectopics, VT, SVT with aberrant conduction, VF. 
WARMING UP CARDIOLOGY AND HYPERTENSION

Antiarrhythmic drug classes:

( Vaughan Williams Classifications )

Class I - Sodium Channel Blocker

Class II - Beta blocker
Class III - Potassium Channel Blocker
Class IV - CCB
Miscellaneous -
- Adenosine
- Electroliyte supplement (magnesium and potassium salts)
- Digitalis compounds (cardiac glycosides)
- Atropine (muscarinic receptor antagonist)
WARMING UP CARDIOLOGY AND HYPERTENSION

Sodium-Channel Blockers (Class I Antiarrhythmics)

Class IA:  atrial fibrillation, flutter; supraventricular & ventricular tachyarrhythmias

cinchonism (blurred vision, tinnitus,
   quinidine* anticholinergic (moderate) headache, psychosis); cramping and
nausea; enhances digitalis toxicity
anticholinergic (weak);
   procainamide lupus-like syndrome in 25-30% of patients
relatively short half-life
   disopryamide anticholinergic (strong) negative inotropic effect
Class IB:  ventricular tachyarrhythmias (VT)
   lidocaine* IV only; VT and PVCs good efficacy in ischemic myocardium
   tocainide orally active lidocaine analog can cause pulmonary fibrosis
   mexiletine orally active lidocaine analog good efficacy in ischemic myocardium
   phenytoin digitalis-induced arrhythmias  
Class IC:  life-threatening supraventricular tachyarrhythmias (SVT) and ventricular
tachyarrhythmias (VT)
   flecainide* SVT can induce life-threatening VT
b-blocking and Ca++-channel blocking
   propafenone SVT & VT;
activity can worsen heart failure
   moricizine VT; IB activity   
WARMING UP CARDIOLOGY AND HYPERTENSION

Beta Blockers (Class II Antiarrhythmics)

  Clinical Uses  
Class/Drug HTN Angina Arrhy MI CHF Comments

Non-selective b1/b2            

ISA; long acting; also used for

   carteolol X        
glaucoma
   carvedilol X       X -blocking activity

   labetalol X X       ISA; -blocking activity

   nadolol X X X X   long acting

   penbutolol X X       ISA

   pindolol X X       ISA; MSA

   propranolol X X X X   MSA; prototypical beta-blocker

   sotalol     X     several other significant mechanisms

   timolol X X X X   primarily used for glaucoma

b1-selective            

   acebutolol X X X     ISA

   atenolol X X X X    

   betaxolol X X X     MSA

   bisoprolol X X X      
ultra short acting; intra or postoperative
   esmolol X   X    
HTN
   metoprolol X X X X X MSA
WARMING UP CARDIOLOGY AND HYPERTENSION

Potassium Channel Blockers (Class III Antiarrhythmics)

Drug Therapeutic Uses Comments

very long half-life (25-60 days);
Class I, II, III & IV actions and
severe supraventricular and ventricular therefore decreases phase 4 slope
amiodarone
arrhythmias and conduction velocity; potentially
serious side effects (e.g., pulmonary
fibrosis; hypothyroidism)
IV only; initial sympathomimetic
life-threatening ventricular tachycardia effect (norepinephrine release)
bretylium
and fibrillation followed by inhibition, which can
lead to hypotension
ventricular arrhythmias; atrial flutter
sotalol also has Class II activity
and fibrillation
slow inward Na+ activator, which
supraventricular arrhythmias; atrial delays repolarization; inhibits Na+-
ibutilide channel inactivation, which
flutter and fibrillation conversion
increases ERP; IV only
supraventricular arrhythmias; atrial
dofetilide very selective K+-channel blocker
flutter and fibrillation conversion
WARMING UP CARDIOLOGY AND HYPERTENSION

CCB (Class IV Antiarrhythmics)

Dihydropyridines include the following specific drugs: 

amlodipine
felodipine
isradipine
nicardipine
nifedipine
nimodipine
nitrendipine

Non-dihydropyridines,
Verapamil (phenylalkylamine class),
Diltiazem (benzothiazepine class)
WARMING UP CARDIOLOGY AND HYPERTENSION

Choices for Treatment of Arrhythmias

Condition Drug Comments
Sinus tachycardia Class II, IV Other underlying causes may
need treatment
Atrial Class IA, IC, II, III, Ventricular rate control is
fibrillation/flutter IV important goal; anticoagulation
digitalis; adenosine required
Paroxysmal Class IA, IC, II, III,  
supraventricular IV
tachycardia adenosine
AV block atropine Acute reversal
Ventricular Class I, II, III  
tachycardia
Premature Class II, IV;  PVCs are often benign and not
ventricular Mg  salts
++
treated
complexes
Digitalis toxicity Class IB  
Mg  salts; KCl
++
WARMING UP CARDIOLOGY AND HYPERTENSION

Efek POSITIF NEGATIF

Inotropik Calcium
( muscular contractions) Calcium sensitisers
oLevosimendan
Cardiac glycosides
oDigoxin
Catecholamines
oDopamine
oDobutamine
oDopexamine
oEpinephrine (adrenaline)
oIsoprenaline (isoproterenol)
oNorepinephrine
(noradrenaline)
Eicosanoids
oProstaglandins
Phosphodiesterase inhibitors
oEnoximone
oMilrinone
oTheophylline

Inotropik Beta blockers

Diltiazem
Verapamil
WARMING UP CARDIOLOGY AND HYPERTENSION

Efek POSITIF NEGATIF

Kronotropik Atropine
(heart rate) Quinidine
Dopamine
Dobutamine
Epinephrine
Isuprel

Kronotropik Beta-blockers
Acetylcholine
Digoxin
Diltiazem
Verapamil
Ivabradine
Metoprolol
WARMING UP CARDIOLOGY AND HYPERTENSION

Management Of Hypertension In Women and

Pregnancy

Classification

1. Preeclampsia-eclampsia
2. Chronic hypertension
3. Preeclampsia superimposed upon chronic hypertension
4. Gestational hypertension (only during pregnancy)
5. Transient hypertension (only after pregnancy)
WARMING UP CARDIOLOGY AND HYPERTENSION

CLASSIFICATION OF HYPERTENSION IN PREGNANCY

BP≥140 mmHg systolic or 90 mmHg diastolic prior to

CHRONIC
pregnancy or before 20 weeks gestation
HYPERTENSION
Persists >12 weeks postpartum

BP ≥ 140 mm Hg systolic or 90 mm Hg diastolic with

PREECLAMPSIA
proteinuria (>300 mg/24 hr) after 20 weeks gestation
Can progress to eclampsia (seizures)
More common in nulliparous women, multiple gestation,
women with hypertension for ≥4 years, family history of
preeclampsia, hypertension in previous pregnancy, renal disease
New onset after 20 weeks in a woman with hypertension
CHRONIC
In a woman with hypertension and proteinuria prior to 20
HYPERTENSION
weeks gestation:
WITH
Sudden 2- to 3-fold increase in proteinuria
SUPERIMPOSED
Sudden increase in BP
PREECLAMPSIA
Thrombocytopenia
Elevated AST or ALT
 WARMING UP CARDIOLOGY AND HYPERTENSION

CLASSIFICATION OF HYPERTENSION IN PREGNANCY

Chronic
BP hypertension

GESTATIONAL Hypertension without proteinuria occurring after 20

HYPERTENSION weeks’ gestation
Temporary diagnosis (only during pregnancy)
May represent pre-proteinuric phase of preeclampsia or
recurrence of chronic hypertension abated in
midpregnancy
May evolve to preeclampsia
If severe, may result in higher rates of premature
delivery and growth retardation than mild preeclampsia
TRANSIENT Retrospective diagnosis (only after pregnancy)
HYPERTENSION BP normal by 12 weeks postpartum
May recur in subsequent pregnancies
Predictive of future essential hypertension
WARMING UP CARDIOLOGY AND HYPERTENSION

CLASSIFICATION OF HYPERTENSION IN PREGNANCY

0 bulan 20 minggu lahir 12 minggu

POST PARTUM
HAMIL

1 3 2

5 6

1/2. HT kronis 5. HT gestasional

3. PE/ E 6. Transient HT
4. 1 / 2 superimpose no. 3
WARMING UP CARDIOLOGY AND HYPERTENSION

ACUTE TREATMENT OF HTN IN PREGNANCY

AGENT DOSAGE
Hydralazine 5 mg iv bolus, then 10 mg every 20 to 30 minutes to a
(preferred) maximum of 25 mg, repeat in several hours as
necessary
Labetalol 20 mg iv bolus, then 40 mg 10 minutes later, 80 mg
(second line) every 10 minutes for 2 additional doses to a maximum
of 220 mg
Nifedipine 10 mg po, repeat every 20 minutes to a maximum of 30
(controversial) mg
Cautious use with magnesium sulfate, can see
precipitous blood pressure drop
Short acting nifedipine is not approved by FDA for
managing hypertension
Sodium nitroprusside 0.5 ug/kg/min to a maximum of 5 ug/kg/min
Fetal cyanide poisoning may occur if used for more
(rarely when others than 4 hour
fail)
WARMING UP CARDIOLOGY AND HYPERTENSION

ORAL TREATMENT OF HYPERTENSION IN PREGNANCY

AGENT COMMENTS
Methyldopa Preferred based on long term studies of child
development and uteroplacental blood flow
Beta Blockers Reports of intrauterine growth retardation,
particularly for atenolol exposure at conception or
in the first trimester; generally safe
Labetalol Increasingly preferred for efficacy and few side
effects
Clonidine Limited data

CCB Limited data

Most experience with nifedipine and isradipine
No increase in major teratogenicity with exposure
Diuretics Not first line agents, probably safe

ACE Contraindicated, reports of fetal toxicity and death

ARB Contraindicated, reports of fetal toxicity and death

CARDIAC ARREST
KASUS TAKIKARDI
CATATAN
Acute Coronary Syndrome

Depression ST segment