Elektrokardiografi

Prof. dr. Peter Kabo

1. Irama : Sinus

Bukan Sinus Atrial Fibrilasi

SVT

Irama JUNSION

60-100 x/menit (normal)

2. Laju QRS : HR?

Regularitas

3. Aksis : Normal

RAD/LAD

Superior Aksis

4. Interval PR : 0.20 Detik (Normal)

5. Morfologi

a. Gelombang P : Normal P.Pulmonal P.Mitral

b. Kompleks QRS : Q patologis

RSR pattern di V1&V2

Interval-QRS (0.08 detik)

c. Segmen ST : ST-elevasi, ST-depresi

d. Gel.T : Flat-T, Inverted-T, tall-T

PA interval : 0.01-0.45 detik

P dur : 0.06 ± 0.2 detik

Max : 0.1 detik

AH interval : 0.05-0.13 detik

PR-interval: ± 0.2 detik

Max : 0.24 detik

HV interval : 0.03-0.05 detik

PRS dur : ± 0.08 detik

Max : 0.1 detik

6.7 x 20 = 134x/menit

300 : 5.8 = 52x/menit

3.3 x 50 = 165x/menit

Gambar 3.2. Perhitungan aksis

A. Aksis Normal : Lead I: I= +4.5; lead aVF : +12.5; aksis = 72°

B. Deviasi aksis ke kanan : Lead I = -10; lead aVF : +8; aksis = +140°

C. Deviasi aksis ke kiri : Lead I = +5; lead aVF : -10; aksis = - 60°

TERIMA KASIH

CARDIAC ARRHYTHMIASCLASSIFICATION :

1. Sinus Node diseases : Sinus tachycardia / bradycardiaSA blockWandering pace makerHypersensitive carotid sinus syndrome (SSS)

2. Disturbance of atrial rhytim :Atrial fibrilationAtrial flutter

3. Disturbance of AV junction rhytim :Supraventricular tachycardia

4. Pre-excitation syndrome :Woeff – Parkinson – White syndrome (S-wave)

5. Disturbance of ventricular rhytim :Ventricular extra systoleVentricular tachycardia’

6. Heart Block :1 o HB2 o HB : - Wenckebach ( Mobits type I)

- Mobitz type II3 o HB (total AV block) : - Temporary pace-maker

- Permanent pace-makerR/ : - Simpatomimetik : Ephedrin - Anti cholinergic: Atropine

COMMON UNDERLYING DISEASES CAUSING ARRHYTHMIAS

1. Ischemic Heart Disease :

Acute myocardial infarction

Myocardial ischemia ( HHD, LVH, CAD)

Left ventricle aneurysma

2. CARDIOMYOPATHY

3. Valvular Heart disease

4. Myocarditis

5. Congenital Hearth disease

6. Conduction system abnormalities :

Sinus R AV-node disease

By pass tract

7. Chronic pulmonary disease : Hypokemia

8. Endocrine : Thyrotoxicosis

9. Electrolide imbalance

10. Drug-induce : Sympathomimetic, caffeine

11. Increase Symphatetic / vagal activity

DRUG O P BIO (%)

T ½ (hari)

Doses Loading

Doses Maintenance

Quinidine

Procamamide

Disopyramide

Lidocaine

Propafenone

Amiodarone

Sotalol

+

+

+

+

+

+

+

+

+ 40 %

100%

4-10

3-4

4-10

2

2-32

25-60

10

1 mg/kg BB

800-1600

(2 weeks)

300-600

750

400-800

4-3-2-1mg/kg BB

450-900

100-400

80-320

DRUGS INDICATIONS ADVERSE EFFECTS

Quinidine

Procamamide

Disopyramide

Lidocaine

Propafenone

Amiodarone

Sotalol

AF

VES

VES

VES,VT

VES,VT,AF,SVT

VES,VT,AF,SVT

VT,VES

Cinchronism, Long QT syndrome, Hypotension, Diarrhea/Hepatitis, Thrombocytopenia

Hypotension, Nausea, Lupus

(-) miotropic, Anti cholinergic : dry mouth

Constipation, urine retention, Glaukoma attack

Hypotension, nystagmus, Seizure

Hypotension, Hepatic disfunction, Pulmonary fibrosis, Hypo/Hyper thyroidism, Cornea microdeposit

Heart failure, Bradycardia

Serious sign or symptoms prepare for immediate cardioversion

Tachycardia

Stable

Atrial fibrillation Atrial flutter

Narrow-complex tachycardias

Stable monomorphic VT or Polymorphic VT

Unstable

Verapamil, B-blokers, Digoxin, Cardioversion, Amiodarone, Sotalol, Adenosine

Digoxin, Amiodarone

Verapamil, B-blockers, Amiodarone

Vagel Stimulation Adenosine

Juctionaltachycardia

Paroxysmal SVT

Ectopic / multifocal atrial tachycardia

Heart function preserved

EF < 40%

Amiodarone, B-blokers, Verapamil

Amiodarone

Amiodarone

Heart function preserved

EF < 40%

Heart function preserved

EF < 40%

Narrow-complex Supra Ventricular Tachycardia (SVT)

If AF > 48 hours duration : use anti arrithmic agents with extreme caution patients not receiving adequate anti coagulation because of possible embolic complication.Delayed cardioversion :Anti coagulation 3 weeks cardioversion anti coagulation 4 weeks

CONTROL RATE CONVERT RHYTIM

Normal Cardiac Verapamil

Function B-Blocker

Impaired Heart Digoxin

(EF < 40% or CHF )

Amiodarone

Propafenone

Sulfas quinidine

DC Cardioversion

ATRIAL FIBRILLATION / FLUTTER

CLASSIFICATION OF ANTIARRHYTMIC DRUGS

I. Sodium channel blockers

A. Sodium channel (++)

Blocks K+ effluks (+)

B. Sodium Channel (+)

C. Sodium Channel (+++)

Disopyramide

Quinidine

Procainamide

Lidocaine

Mekiletine

Tocainide

Flecamide, Encamide,

Propafenone

II. Anti adrenergic Beta blockers

III. K+ channel effluks blockers

also Na+ BlockersAmiodarone

Sotalol

IV. Ca++ channel blockers Verapamil, Diltiazem

V. Autonomic effects

Vagal stimulation

Adenosine receptor activation

Digoxin

Adenosine

Mechanisms of Antiarrhytmic Drug Action

Decreased Phase 4 Slope B-blocker

Increased Threshold

Na+ channel blocker

Ca++ channel blocker

Increased Max-diastolic potential

Adenosine

Acetylcholine

Increased action potential duration

K+ channel blocker

Antiarrhytmic drugs can cause arrhytmias

Some arrthythmias should not be treated

Mechanisms of Cardiac Arrhytmias1. Enhanced Automaticity : Sinus tachycardia

2. Triggered Automaticity : Multifocal atrial tachycardia. VES VT. Torsade de pointes

Delayed after depolarization

Early after depolarization

3. Reentry Atrial fibrillation (AF)

Atrial Flutter

Supraventricular tachycardia (SVT)

Ventricular tachycardia (VT)

Woeff-Parkinson-White Syndrome

4. Block 1o AV block

2o AV block

3o AV block (Total AV Block)

• Narrow QRS Complex• Retrograde P• Vent-rate : 140 – 200 x / min• Vagal Maneuver Response• Wide QRS Complex, V1(+), LAD/Superior• AV dissociation / fusion beat• Vent-rate : 150 – 250 x / min• Vagal Maneuver No Response