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PROCAINAMIDE
DISOPIRAMIDE
LIDOCAINE
PHENITOINE
MEXILETINE
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
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)
ASSOCIATED WITH
RECCURENT ISCHEMIA
SEVERE LEFT VENTRICLE DYSFUNCTION
HYPOTENSION
HYPOKALEMIA
LARGE INFARCTION
Fusion
beat
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
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
VT
Irregular
Atrial fibrillation
II
Pace-maker rhythms