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Cardiac Arrhythmias :

Treatment Principles and


Strategies
Harris Hasan,Prof,dr,SpJP(K),SpPD,FIHA
Departemen Kardiologi &KV
FK USU / RS.HAM

The Conduction system

SA node

Sumber impuls normal/


alamiah , 60 100 / menit

AV node

Bisa mengeluarkan
impuls 40-50x/menit

Berkas His
Serabut Purkinje

Ventrikel

Bisa mengeluarkan impuls


30 x/menit

1 kotak kecil
= 0.04 detik

5 kotak kecil
= 1 kotak sedang
= 0.2 detik

5 kotak sedang
= 1 kotak besar
= 1 detik

Paper speed : 25 mm/second

MEMBACA EKG
I. Sebutkan iramanya :
Sinus Rhythm

The Heartbeat

Arrhythmia
Tachyarrhythmia
(rate >100 x/min)

Bradyarrhytmia
(rate < 60 X/min)

QRS sempit (<0.12 ms)

AV blok derajat 1, 2 & 3

QRS lebar (>0.12 ms)

RBBB & LBBB

Bradyarrhytmias: general approach


Ask specifically about previous cardiac
disease, palpitations, blackouts, dizziness,
chest pain, symptoms of heart failure, and
recent drugs.
Examine carefully, noting the BP, JVP
waveform , heart sounds and murmurs, and
sign of heart failure.

Management
Haemodynamically unstable patients :
Given oxygen via facemask if the patient is
hypoxic on air.
Keep NBM until definitive therapy has been
started to reduce the risk of aspiration in case of
cardiac arrest or when the patient lies supine for
temporary wire insertion.
Secure peripheral venous access.
Bradyarrhytmias causing severe haemodynamic
compromise (cardiac arrest, asystole, SBP<90
mmHg, severe pulmonary oedema, evidence of
cerebral hypoperfusion) require immediate
treatment and temporary pacing.

Give atropine 1 mg IV bolus repeat if


necessary up to a maximum 3 mg.
Give isoprenaline 0.2 mg IV if there is a delay
in pacing and the patient remains unstable.
Set up an infusion (1 mg in 100 ml bag N
saline starting at 1 ml/min titrating to HR).
Set up external pacing system if available,
and arrange for transfer to a screening room
for trans-venous pacing.
Bradycardia in shock is a poor prognostic
sign. Look for a source of blood loss and
begin aggressive resuscitation with fluids and
inotropes.

Haemodynamically stable patients :


Admit to CCU with continous ECG monitoring.
Keep atropine drawn up and ready in case of acute
deterioration.
Does the patient require a temprorary wire
immediately?
It may be of value to have appropriate central
venous access (femoral or internal jugular vein) in
place in case of the need for emergency temporary
wire insertion.

External cardiac pacing


In emergencies, external cardiac pacing may
be used first but this is painful for the patient
and is only a temporary measure until a more
defenitive trans-venous pacing wire can be
inserted.
External cardiac pacing is useful as a standby
in patients.
Post-myocardial infarction when the risk of
prophylactic
transvenous
pacing
after
thrombolysis are high.

Haemodynamically stable patients with


anterior
myocardial
infarction
and
bifasicular block may be managed simply
by application of the external pacing
electrodes and having the pulse generator
ready if necessary.

Sinus bradycardia
The sinoatrial node (SAN) discharges <60/min. P
waves are normal but slow. It may be normal (e.g. in
sleep, healthy resting hearts).
Causes
Young athletic individual
Drug-(-blockers, morphine, amiodarone,
calcium channel blockers, lithium,
propafenone, clonidine)
Hypothyroidism
Hypothermia

Increased vagal tone


- vasovagal attack
- nausea or vomiting
- carotid sinus hypersensitivity
- acute MI (especially inferior)
Ischemia or infarction of the sinus node
Chronic degenaration of sinus or AV nodes or atria
Cholestatic jaundice
Raise intracranial pressure
Drugs-(-blockers, morphine, amiodarone, calcium
channel blockers, lithium, propafenone, clonidine).

Management
If hypotensive or pre-syncopal :
- Atropine 600 g-3 mg IV bolus repeating as
necessary.
- Isoprenaline 0.5-10 g/min IV infusion.
- Temporary pacing
- Avoid and take steps to correct prepitants
- Stop any drugs that may suppress the sinus or
AV nodes.

Long term treatment :


- If all possible underlying causes removed and if
symptomatic bradycardia remains, refer for
permanent pacing.
- Consider Holter monitoring in patient with possible
episodic bradycardia. R-R intervals >2.5 seconds
may
require permanent pacing, especially if
associated with symptoms.

Sick sinus syndrome


This syndrome encompasses a number of
conduction system problems: persistent sinus
bradycardia not caused by drugs, sinus pauses, AV
conduction disturbances, and paroxyms of atrial or
junctional tachyarrythmias. It is usually diagnosed by
ambulatory cardiac monitoring.

Atrioventricular block
This can occur at the AVN (nodal) or His-Purkinje
system (infranodal). Common causes are ischaemic
heart disease, conduction system fibrosis (aging),
calcific aortic stenosis, congenital, cardiomyopathy,
hypothermia, hypothyroidism, trauma, radiotherapy,
infection, connective tissue disease, sarcoidosis,
and anti-arrhytmic drugs. AV block is further
classified :

First degree AV block


Every impulse conducts to the ventricle but
conduction time is prolonged. Every P wave is
followed by a QRS but with a prolonged PR interval
(>200 ms). If the QRS width is normal then the block
is at the AV node, if the QRS shows aberration
(RBBB or LBBB) then the block may be at the AV
node or the His-Purkinje system.

Second degree AV block


Mobitz 1. (Wenckebach). ECG shows the PR interval
prolongs until a P wave is not conducted P wave. The
PR interval following the dropped P wave must be the
shortest. The RR interval is therefore irregular. This
block is characteristic of the AVN.
Mobitz 2. ECG shows a fixed P to QRS ratio of 2:1,
3:1 or 4:1. Block is predominantly at the His bundle
and ther is often an aberrant pattern to the QRS
complex.

Third degree AV block (complete heart block)


There is no conduction to the ventricle. The ECG
shows dissociation between P and QRS complexes.
An escape pacemaker rhythm takes over. A narrow
QRS indicates AVN block and the His bundle is the
pacemaker, which is faster and more stable than
more distal sites. A wide QRS indicates infra nodal
block and a distal ventricular pacemaker site. This
carries a worse prognosis.

Causes of atrioventricular block


Associated with acute infraction or ischaemia.
Drugs (-blockers, digitalis, CA2+-blockers).
Conduction system fibrosis (Lev and Lenegre
syndromes).
Increased vagal tone.
Trauma of following cardiac surgery.
Hypothyroidism (rarely thyrotoxicosis).
Hypothermia.
Hyperkalaemia.
Hypoxia

Vavular disease (Aortic stenosis incompetence,


endocarditis).
Myocarditis (diphtheria, rheumatic fever, viral,
Chagas disease).
Associated with neuromuscular disease i.e.
myotonic dystrophy.
Collagen vascular disease (SLE, RA,
sclerodema).
Cardiomyopathies (haemochromotosis,
amyloidosis).
Granulomatous disease (sarcoid).
Congenital heart block.
Congenital heart disease (ASD, Ebsteins, PDA).

Bundle branch block


Due to disease in the His-Purkinje system causing a QRS
>120 ms. Common causes are conduction system fibrosis
(aging), ischaemic heart disease, hypertension,
cardiomyopathies, cardiac surgery, infiltrative disease
LBB : left ventricular depolarization is delayed giving large
notched R waves in leads I and V6 and M pattern in V1.
block confined to the anterior or posterior fascicle of the left
bundle gives left axis or right axis deviation respectively on
the ECG. BBB leads to asynchronous contraction of the left
and right ventricle which worsens function.

RBBB : right ventricular depolarization is delayed giving an


RSR pattern in V1 and a prominent S wave in I and V6. This
can be a normal variant but more commonly by causes listed
above and in addition: AS, PE, corpulmonale.
Bifasicular block = RBBB + left anterior hemiblock (left axis
deviation on ECG), RBBB + left posterior hemiblock (right axis
deviation on ECG) or LBBB. All of these may progress to
complete AV block. Trifasicular block = bifasicular block + 1st
degree AV block.

Management
Interventricular conduction disturbance on their
own do not require temporary pacing. However,
when associated with haemodynamic disturbance
or progression to higher levels of block (even if
intermittent) must consider insertion of a
transvenous pacing wire. The need for longer term
pacing is dependent on the persistence of
symptoms and underlying cause.

Common causes of bundle branch block


Ischaemic heart disease.
Hypertensive heart disease.
Valve disease (especially aortic stenosis).
Conduction system fibrosis (Lev and Lenegre syndromes).
Myocarditis or endocarditis.
Cardiomyopathies.
Cor pulmonale (RBBB) (acute or chronic).
Trauma or post-cardiac surgery.
Neuromuscular disorder (myotonic dystrophy).
Polymyositis.

Tachyarrhytmias: general approach

Tachyarrhythmias may present with symptoms and


haemodynamic compromise. The approach to patients
depends upon:
1. The effects of the rhythm on the patient.
2. The diagnosis from the ECG and rhythm.
3. Any underlying cardiac abnormality or
identifiable precipitant.

The effect of the rhythm on the patient


1. Patients with sign of severe haemodynamic
compromise:
- Impending cardiac arrest.
- Severe pulmonary oedema.
- Shock-systolic BP <90 mmHg.
- Depressed conciousness.
Treat immediately with unsynchronized external
defibrillation for tachy arrhythmia and temporary
pacing for bradyarrhythmia.

2. Patients with mild-moderate compromise:


- Mild pulmonary oedema.
- Low cardiac output with cool peripheries
and oliguria.
- Angina at rest.
Try to record an ECG and long rhythm strip
before giving any pharmacological agents and/or
defibrillation. This will be invaluable for long-term
management. If they deteriorate, treat as above.

Diagnosing the arrhythmia


The main distinctions to make are :
Tachy- (>120/min) vs brady- (<60/min)
arrhythmia.
Narrow (<120 ms or 3 small sq.) vs. broad QRS
complex.
Regular vs irregular rhythm.

Precipitating factors
Underlying cardiac disease
Ischaemic heart disease
Acute or recent MI
Angina
Mitral valve disease
LV aneurysm
Congenital heart disease
LV aneurysm
Congenital heart disease
Abnormalities of resting ECG
Pre excitation (short PR interval)
Long QT (congenital or acquired).

Narrow complex tachycardias originate in the atria or AV


node (i.e. supraventricular tachycardias SVT).
Irregular, narrow complex tachycardia is most commonly
AF or atrial flutter with varying AV block.
Broad complex tachyarrhythmias may originate from either
the ventricles (VT) or from the atria or AV node (SVT) with
aberrant conduction to the ventricles (RBBB or LBBB
configuration).
If the patients has previous documented arryhthmias,
compare the morphology of the current arrhythmia to old
ECGs. The diagnosis of VT vs. SVT and therapy may be
evident from the last admission.

QRS sempit : Supraventricular origin


QRS sempit

Irama
Tidak teratur

Irama Teratur

Sinus Tachycardia

Atrial Flutter

Supraventricular
Tachycardia

Atrial Fibrillation

SVT :
-due to re-entry mechanism
-narrow QRS complex
-regular
-retrograde atrial depolarization
-P wave ?

Atrial Fibrillation :
-from multiple area of re-entry within atria
-or from multiple ectopic foci
-irregular, narrow QRS complex
-very rapid atrial electrical activity
(400-700 x/min).
-no uniform atrial depolarization

Atrial Flutter :
-The result of a re-entry circuit within
the atria
-Irregular / regular QRS rate
-Narrow QRS complex
-Rapid P waves (300x/min), sawtooth

VENTRIKEL EXTRA SYSTOLE

SR

VES

Sinus rhythm
with
Multifocal VES

VES

VES

SR

SR

SR

SR

SR

SR

Sinus rhythm with VES couplet

Sinus Rhythm with VES, R on T

QRS Lebar : Ventricular origin

QRS lebar

Irama
tidak teratur

Irama Teratur

Ventricular
Tachycardia

Ventricular
Fibrillation

Ventricular Tachycardia

Torsade de Pointes

Ventricular Fibrillation

VT

VF

Management of Tachyarrhytmia
TACHYCARDIA

Stabil

Tidak
stabil

Tidak stabil
Cardioversi :
VT
Non VT

: mulai dgn 100 joule


: mulai dgn 50 joule

Defibrilasi :
VT / VF

: mulai dgn 360 joule

Stabil
QRS sempit
Irama Teratur
Supraventricular
Tachycardia
(SVT)

Adenosin
6 mg 12 mg -12mg

Irama
Tidak teratur
Atrial Fibrilation
(AF)

Diltiazem
15 25 mg
10 mg / 8jam

Stabil
QRS lebar

Irama
tidak teratur

Irama Teratur

Ventricular
Tachycardia

Amiodarone 150 mg

AF dgn MPW ?
VF ?

Consult expert

. ECG
diagnosis of
tachycardia

Types of
supraventricular
tachycardia.

Drug treatment of tachyarrhythmias