2VT - DefinitionA general term that applies to any rhythm faster than 100 bpm arising distal to the bundle of HIS.Sustained VT with haemodynaic instability (syncope, hypotention) is life threatening.Based on ECG, can be either:Monomorphic VTPolymorphic VTCan also be classified as ‘sustained’ (>30 secs) or ‘non-sustained’
3VTpolymorphicmonomorphicVTNon-sustainedsustainedKumar and ClarkLife threatening ventricular tachyarrhythmiasSustained ventricular tachycardiaventricular fibrillationTorsades de pointesNormal heart ventricular tachycardiaNon-sustained ventricular tachycardia
4Monomorphic VTOccurs when the ventricular activation sequence is the same, resulting in a uniform ECG pattern.
5Most typically seen with patients with a structural heart abnormality. Monomorphic VT – Structural abnormalitiesMost typically seen with patients with a structural heart abnormality.Usually there is a region of slow conductionCauses include scarring and fibrillar disarray due to: infract, cardiomyopathy, hypertrophy, surgical scar and muscle degeneration.Re-entrant tachycardias occur when there is scar tissue or an abnormal area that causes the electrical wavefront to move through it slowly. By the time it reaches the normal (fast) conducting area has already repolarized, causing it to depolarize again and start a loop.
6Monomorphic VT – non structural abnormalities A minority of pt with monomorphic VT have structurally normal hearts (idiopathic VT).Usually a benign condition with good prognosis.The VT arises from either a focus in the right ventricular outflow tract or in the left ventricular septum.In symptomatic pt, radiofrequency catheter ablation of the area causing the VT results in a cure in >90% pt.
7Polymorphic VT The ECG trace shows a varying pattern. Causes very broadly include:Drug inducedInherited and Cardiac ion channel defectsIschaemia and myocarditis (most common causes when no drug and ion channel defects)
8Polymorphic VT - Torsades de pointes Torsades de pointes is a polymorphic VT following a long resting long QT interval (>0.44 seconds). The ECG waves are rapid, and irregular (i.e. polymorphic) and continuously change from an upright to inverted position.
9Torsades de pointes Causes include (congenital vs acquired) Congenital – Long QT syndrome: Jervell-Lange-Nielsen or Romano-Ward syndrome.Acquired:Electrolyte abnormalities – hypokalaemia, hypomagnesaemia, hypocalcaemiaDrugs – quinidine, erythromyocine, haloperidol, disopyramide, etc.Misc – bradycardia, mitral valve prolapse, AMIPathophysiology is complex – related to ionic flow, which leads to broad QT, which then leads to early after depolarisations.
10Torsades de pointes Clinical presentation: Causes palpitations, syncope and dizziness, but usually spontaneously resolves.It can lead to VF and sudden deathAcute management –Any electrolyte imbalances correctedCauasative drugs stoppedHeart rate maintained with atrial or ventricular pacing.Magnesium sulfate 8mmol over 10-15mins. This stops early after depolarisations through causing an influx of Ca.
11Torsades de pointes - Long term management Acquired –Avoidance of all drugs known to prolong QT intervalCongenital –Beta blockadeLeft cardiac sympathetic denervationPacemaker therapy
12Polymorphic VT - others There is a list of other syndromes caused by different channels being affected, Kumar and Clark only highlights:Brugada Syndrome – inherited condition that leads to patients having idiopathic ventricular fibrillations with no evidence of causative structural cardiac disease.Only successful treatment in symptomatic patients is ICD.
13Brugada syndromeCharacteristic ECG: right bundle branch block (rsR pattern in V1 with T wave inversion) with ST elevations in V1 –V3
14Brugada syndromePatient may present with: sudden death during sleep, resuscitated cardiac arrest and syncope or they may be asymptomatic and their ECG may lead to diagnosis.High risk of sudden death.Only successful treatment is ICD
15Sustained Ventricular Tachycardia PresentationSustained ventricular tachycardia (>30secs) often with: presyncope, syncope, hypotention and cardiac arrest. Nb: some pt may tolerate it very well.Ex.bpmOften signs of atriaoventricular dissociation – cannon ‘a’ waves in neck
16Ix: ECGBroad (>0.12) abnormal QRS complexes. May have some capture beats (intermittent narrow QRS complex from normal ventricular contraction via AV node)
17NB: 80% of all broad complex tachycardias are due to VT NB: 80% of all broad complex tachycardias are due to VT. Other causes include SVT with either a right or left bundle branch block.Mx:If patient haemodynamically compromised (i.e. Is hypotensive, has pulmonary oedema) emergency DC conversion may be needed.If blood pressure and CO are maintained, IV therapy with class 1 drugs used: lidocaine.
18VT vs SVT with BBB VT more likely if A very broad QRS>0.14s AV dissociationA bifid, upright QRS with a taller first peak in V1A deep S wave in V6Same polarity QRS direction in all chest leads v1 – v6.
20Non-sustained VT (NSVT) > than 5 consecutive beats, but lasts less than 30 secs.Found in up to 6% of pt with normal heart and does not require treatment.Found in up to 60-80% of pt with heart disease. In patients with particularly poor left ventricular function (ejection fraction <30%) ICD may help.
21VTpolymorphicmonomorphicVTNon-sustainedsustainedKumar and ClarkLife threatening ventricular tachyarrhythmiasSustained ventricular tachycardiaventricular fibrillationTorsades de pointesNormal heart ventricular tachycardiaNon-sustained ventricular tachycardia