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Ventricular tachyarrhythmias (classification (MALIGNANT (Life…
Ventricular tachyarrhythmias
pathophysiology
Increased automaticity (acute ischaemia, catecholaminergic polimorphic ventricular tachycardia, exercise-induced arrhythmias)
Reentry mechanism (fibrosis, HCM and other)
Early afterdepolarizations and late afterdepolarizations
(LQTS, SQTS, dyselectrolitemia, drug toxicity)
etiology
• Ischeamia (ACS, stable CAD, exertion)
• Heart failure (dilated cardiomyopathy, symptoms)
• ANS balance (↑ SNS, ↓ PNS)
• Hypertrophy / fibrosis (cardiomyopathy, amyloidosis, sarcoidosis, others)
classification
BENIGN
• minimal risk of death
• Premature ventricular contractions
• without hemodynamic dysfunction
• without cardiac structural changes
• treatment:
beta-blockers may improve quality-of-life in symptomatic individuals
Class Ic and class III
ICD in clearly defined subgroups
Non-sustained ventricular tachycardia
ventricular tachycardia that is ≥5 consecutive beats but lasts <30 s
POTENTIALLY MALIGNANT
• Potentially life- threatening
• recurrent non-sustained ventricular tachycardia
• inreased risk of sudden cardiac death
• multiple premature ventricular contractions
• hemodynamic dysfunction
•
cardiac structural changes
• decreased LVEF
• needs specialist investigations and treatment
MALIGNANT
(Life-threatening)
• the highest risk of sudden cardiac death
•
sustained ventricular tachycardia
•
ventricular fibrillation
• serious hemodynamic dysfunction
• cardiac structural changes
• EF < 40%
ventricular fibrillation
usually provoked by a ventricular ectopic beat.
The only effective treatment is electrical defibrillation.
pulse rate typically between 120 and 220 b.p.m
No QRS complexes can be identified
Implantable cardioverter-defibrillators (ICDs) are first-line therapy in the management
The Brugada syndrome
idiopathic ventricular fibrillation who have no evidence of causative structural cardiac disease.
It is more common in young male adults and in South-east Asia.
20% of cases associated with loss of sodium channel function due to a mutation in the SCN5A gene.
other mutations in the SCN1B gene, glycerol-3-phosphate dehydrogenase-1-like gene (GPD1LL-type) and genes related to calcium channel subunits CACNA1C and CACNB2 have also been implicated
present with sudden death during sleep, resuscitated cardiac arrest and syncope, or the patient may be asymptomatic
high risk of sudden death
treatment is an ICD. Beta-blockade is not helpful and may be harmful in this syndrome.
sustained ventricular tachycardia sVT
lasting > 30 seconds (degenerating into VF)
common hemodynamic dysfunction correlating with sVT:
hypotension, pulmonary oedema, shock
The ECG shows a rapid ventricular rhythm with broad (often ≥0.14 s), abnormal QRS complexes.
Can progress to VFib if untreated
doesn’t qualify for treatment
Patients with:
asymptomatic, benign arrhythmias without structural heart disease
treatment
Treatment of underlying heart disease – causative therapy
Pharmacotherapy
Implantable cardioverter-defibrillator
Catheter ablation
Heart transplantation
When can we use anti-arrhythmic drugs I class?
Patients without structural heart disease:
• without heart failure
• without ischaemia
• without hypertrophy
When should we use ß-blockers?
Patients with symptomatic ventricular arrythmias:
• all of them – if drug is well tolerated
• after MI, CAD
• with hypertension
• with long QT
• with catecholaminergic polymorphic ventricular tachycardia
When should we use amiodarone?
Patients with ventricular arrhythmias and:
• with heart failure
• after MI
• with Brugada syndrome
• always after failure of previous treatment (including
catheter ablation), and arrhythmia is symptomatic (VT, or nsVT, or multiple VPCs)
When can we use sotalol?
Patients with ventricular arrhythmias and:
• after MI, CAD
• LVEF>40%, without hypertrophy (ECHO)
Patients with hypertrophy can use only amiodarone!
When can we use calcium antagonists?
Patients with:
„fascicular” idiopathic, monomorphic ventricular tachycardia
Who has got a higer risk of proarrhythmia (VT, VF)?
Patients with:
• deterioration of LV function
• persistent ischaemia
• dyselectrolitemia