I.

Sodium channel blockers

II. Beta- blockers

III. Potassium channel blockers

IV. Calcium channel blockers

I. Sodium channel blockers:

I.a.increase the duration of the action potential (slow phase 0):

QUINIDINE (also class III effects)

PROCAINAMIDE

DISOPIRAMIDE

I.b.decrease the duration of the action potential :

LIDOCAINE

PHENITOINE

MEXILETINE

I.c.dont influence the duration of the action potential:

PROPAFENONE

FLECAINIDE
II. Beta- blockers (metoprolol, bisoprolol)
III. Potassium channel blockers (prolong the
refractory period):
AMIODARONE
SOTALOL
IBUTILIDE
DOFETILIDE
VERNAKALANT
IV. Calcium channel blockers
DILTIAZEM

VERAPAMIL

V. Unclassified
DIGOXIN
ADENOSINE
Digoxin
Cardiac glycoside
Inhibits the sodium-potassium ATPase pump
Positive inotropeimproves the strength of
cardiac contraction
Allows more calcium to be available for
contraction
Used for CHF and atrial dysrhythmias
Monitor potassium levels, drug levels, and
for toxicity
adenosine (Adenocard)
Slows conduction through the AV node
Used to convert paroxysmal supraventricular
tachycardia to sinus rhythm
Very short half-life
Only administered as fast IV push
May cause asystole for a few seconds
Other side effects minimal
 Early afterdepolarization
(EAD)-amiodarone

Delayed afterdepolarization
(DAD) -digoxin
 VPB appear in both normal or pathological hearts
Monomorphic VT is usually associated with a
pathological heart, but it can appear on a
structurally normal heart.
Polimorphic VT in cardiac ischemia or in
conditions that delay the ventricular
repolarization
Dyselectrolytemia, hypoxia are other causes
 LOWN CLASSIFICATION
CLASS 0 ABSENT VPB
CLASS I MOMOMORPHIC VPB, < 30/ HOUR
CLASS II MONOMORPHIC VPB, > 30/ HOUR
CLASS III A POLIMORPHIC VPB
CLASS III B SISTEMATIC VPB (BI/ TRIGEMINISM)
CLASS IV A CUPLES
CLASS IV B NONSUSTAINED VT
CLASS V - R/ T PHENOMENA VPB
Ventricular premature beat (VPB)

Compensatory
pause
VPB: Ventricular Bigeminism
VPB: Ventricular Trigeminism
Ventricular monomorphic premature beats
(VPB)

VENTRICULAR VENTRICULAR
couplet BIGEMINISM
VENTRICULAR
TRIPLET
Types of VT
Monomorphic
Polimorphic
Bidirectional
Fascicular
 Succesiune rapid, regulat de bti ventricular ectopice cu frecven= 150-
300/, n contextul unei afectri cardiace severe
TV pot fi
susinute >30
nesusinute<30
Mecanism
ectopie
Reintrare
ECG
complexe QRS largi >0.12 sec., deformate aspect BRD/BRS
activitate atrial (P) vizibil uneori sau absenta, fr relaie cu QRS
(disociaie A-V)
rar dar patognomonic pot apare
capturi ventricular - intermitent complexe QRS suple rezultat al
impulsului sinus la ventricul
bti de fuziune - complex cu morfologie intermediar ntre cel de baz
i al TV
 Usually without hemodinamic impact
EES
BETA BLOCKERS
AMIODARONE
 HEMODINAMIC INSTABILITY
ELECTRIC CONVERSION- SYNCRONOUS EES
TREATMENT
Amiodarone
Lidocaine
Beta blockers
CORECTION OF DYSELECTROLYTEMIA
POLIMORPHIC VT WITH HEMODINAMIC
INSTABILITY
ELECTRIC CONVERSION, SYNCRONOUS EES
TREATMENT
NORMAL QTc
AMIODARONE, LIDOCAINE, BETABLOCKER
LONG QTc
ELECTROLITE CORRECTION, ISOPROTERENOL,
(MAGNEZIUM SULPHATE)
 AV
Dissociation
ATRIA AND VENTRICLES
ACT INDEPENDENTLY

SA
Node

Ventricular
Focus
 Ventricular
Tachycardia (VT)
V1

Rates range from 100-250 beats/min

Non-sustained or sustained
P waves often dissociated (as seen here)
Sustained VT: Degeneration to VF
 Ladder Diagram of AV Dissociation
During Ventricular Tachycardia
Slower atrial rate

Faster ventricular rate

Impulses invade the AV node retrogradely and anterogradely,

creating physiologic interference and block. Under the right
conditions, some anterograde impulses may slip through.

This phenomenon is not equivalent to third degree AV block

 Ladder Diagram of AV Dissociation
During Third Degree AV Block

Faster atrial rate

Slower ventricular (escape) rhythm

Note that impulses block anterogradely and retrogradely

within the AV conduction system
Monomorphic
VT
 Polymorphic
VT

V1
MI Scar-Related Sustained
Monomorphic VT Circuit
 RBBB +
ASHB

FASCICULAR VT
RBBB + PIHB
Torsade de Pointes

Treatment:
Stop amiodarone
Magnezium sulphate
 Ventricular Flutter

250 b/min,
Ventricular Fibrillation
(VF)

Totally chaotic rapid ventricular rhythm

Often precipitated by VT
Fatal unless promptly terminated (DC shock)
Sustained VT : Degenerates to VF
Atrial fibrillation with fast
conduction on the accesory
pathway degenerates toVF
Ventricular arrhythmias in the
acute myocardial infarction
 PRIMARY VF ( <48 h) post MI

ASSOCIATED WITH INCREASED INHOSPITAL

MORTALITY
DOES NOT AFFECT THE LONG TERM PROGNOSIS
SECONDARY VF ( >48h) post MI

ASSOCIATED WITH
RECCURENT ISCHEMIA
SEVERE LEFT VENTRICLE DYSFUNCTION
HYPOTENSION
HYPOKALEMIA
LARGE INFARCTION

ASYNCRONOUS EES ELECTRIC CONVERSION

INCREASED EARLY/ LONG TERM MORTALITY
STUDY THE POSSIBILITY OF DEFIBRILLATOR
IMPLANTATION FOR THE PREVENTION OF SUDDEN
CARDIAC DEATH
 Accelerated Idioventricular
Rhythm
( Ventricular Escape Rate, but
100 bpm)

Fusion
beat

Ectopic Sinus Normal

ventricular activation acceleration ventricular activation
 ACCELERATED IDIOVENTRICULAR
RHYTHM
 INCREASED AUTOMATISM
20% OF STEMI
FREQUENTLY AFTER SUCCESSFUL
REPERFUSION
DOES NOT AFFECT THE PROGNOSIS
DOES NOT NEED TREATMENT
 CORECTING THE CAUSES
RECURRENT ISCHEMIA
DYSELECTROLYTEMIA
BRADYCARDIA
SIMPATHETIC STIMULATION

TREATMENT
AMIODARONE
LIDOCAINE
 RECURRENT VF - >4/h, >20/24h
TREATMENT
BETA BLOCKERS
AMIODARON
MECHANIC VENTILATION
CONTRAPULSATION BALOON
PREMATURE BEAT ABLATION
 Ventricular arrhythmias after a myocardial
infarction

Acute phase arrhythmias (first hour)

Subacute phase arrhythmias (3h 72h)

Chronic phase arrhythmias (>72h)

Reperfusion arrhythmias
 REMEMBER: VT does not invariably cause
hemodynamic collapse; patients may be
conscious and stable
History of heart disease, especially prior
myocardial infarction, suggests VT
Occurrence in a young patient with no known
heart disease suggests SVT
12-lead EKG (if patient stable) should be
obtained
 Regular
SVT with bundle branch block

Pre-existent

Frequency dependent (abberant conduction)

Antidromic AVRT

Atrial flutter/atrial tachycardia with abberant conduction or with an accesory pathway

VT

Irregular
Atrial fibrillation

Atrial flutter / Multifocal atrial tachycardia with variable conduction

Bundle branch block

Frequency dependent (abberant conduction)

Antegrade conduction through an accesory pathway

More R than p- VT!

II
Pace-maker rhythms