Broad complex tachycardia

Ventricular Tachycardia (VT)

• Regular, 100-300 (although an irregular rhythm does not exclude it as a diagnosis)
• P waves continue, disassociated from QRS
• An arrhythmia that originates from tissue below the penetrating AV bundle
• A wide-complex tachycardia should be treated as VT until proven otherwise (and ∼80% of the time the diagnosis will prove to be VT, especially in patients aged >35 years)
• 90% of patients with monomorphic VT have a structurally abnormal heart, 10% have idiopathic VT (and in 80% of these, VT is from right ventricle outflow tract)
• Outflow tract VTs are associated with characteristically tall QRS complexes in the inferior leads. Important to exclude an arrhythmogenic cardiomyopathy in these instances
• Outflow tract arrhythmias are frequently amenable to successful catheter ablation
• Risk of recurrence after treated STEMI is low, but high in NSTEMI
• VT is likely to be RBBB morphology  (VT usually comes from left ventricular outflow tract)
• If VT comes from right ventricle, it has LBBB pattern and inferior leads have positive deflection and there can be Q waves in V6. Can treat with a betablocker
• VT storm – defined as 3 appropriate therapies for VT over 24 hours
• Causes of VT
  • • Ischaemia
    • Cardiomyopathy
    • Electrolyte imbalance
    • Myocarditis
    • Prolonged QT and Brugada
    • Drugs (cocaine, erythromycin, haloperidol, digoxin)
• Get an ECG once VT resolves – may see signs of cause eg ischaemia, long QT, delta waves (ie. ‘VT’ was actually antidromic AVRT)

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Distinguishing VT from other rhythms

• It is not possible to definitively distinguish between rhythms of ventricular or supraventricular origin solely based on ventricular rate, the presence or absence of structural heart disease, or whether a rhythm is haemodynamically tolerated.
• A definitive diagnosis of VT requires the demonstration of ventriculoatrial dissociation – the number of spontaneous ventricular activations exceeds the number of atrial activations, capture and fusion beats. However, this is often not possible in real world
• VT can run at 140-150, so called ‘slow VT’. It can look a bit atypical to classical monomorphic VT, so don’t be fooled
• If diagnosis of VT is missed, and the blood pressure is low, giving vasopressors can be very dangerous
• Response to adenosine or Valsalva does not rule out VT
• Vereckei protocol:
  • • LOOK ONLY AT AVR if not sure whether it’s VT or a tachycardia with bundle branch block
    • Usually: usually QRS negative, p wave negative, t wave positive
    • Is there a positive R wave in AVR, initial R wave >1 small square in AVR (>40m/s), or notch on downward stroke of QRS in AVR?
    • If yes to any, you can confidently say it’s VT. If none – SVT. Up to 98% sensitive.
• Also, probable VT if
  • • AV disassociation (50% prevalence, highly specific)
    • +ive wave in AVR
    • History of IHD
    • Capture (normal QRS) and fusion beats (normal QRS and wide QRS fused). Highly specific but only 7% prevalence
    • All precordial chest leads concord, but especially if all negative (highly specific). Positive QRS in all chest leads also suggests VT
    • R to S interval > 100ms in one precordial lead
    • Very broad (QRS > 140 msec)
    • LBBB pattern with RAD
    • Q waves in precordial leads
    • Right rabbit ear taller than left in typical BBB, left rabbit ear taller in VT
    • Overall QRS duration >140 ms in a RBBB configuration or >160 ms in a LBBB configuration favours VT.
    • A QRS axis in the precordial leads between −90 and −180°, or ‘northwest’.
    • Left-axis deviation in RBBB morphology tachycardias and right axis deviation in LBBB tachycardias

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Differential of VT

• SVT with BBB – if this likely, treat as narrow complex tachycardia. More likely if:
  • • RBBB – double R waves in V1, first one smaller (If 2^nd R smaller than first, more likely VT). S wave present in V6
    • LBBB – usually rS in V1 and R pattern in V6
    • Rapid early deflection in the QRS complex. In VT, there is a less steep initial portion of the QRS complex. This has been quantified as an RS interval in any precordial lead of >100 ms
• AF with BBB – irregular, treat as AF
• Electrolyte abnormalities
• Pre-excited AF (antidromic AVRT)
• Pacemaker-mediated tachycardia (can’t always see the pacing spike with modern pacemakers)
• SVT conducted with a delay in myocardial propagation (often because of medication, including class 1A, 1C and class III anti-arrhythmic drugs) or systemic disturbances resulting in abnormal myocardial electrical propagation
• If regular, possible causes include VT, SVT with BBB, Class 1 anti-arrhythmic drugs, PPM
• If irregular, possible causes include AF with BBB, Polymorphic VT (though adverse features very likely), pre-excited AF (rare, unstable patient, sometimes WPW on baseline ECG but not always)

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Treatment of a broad complex tachycardia

• If no pulse – Non-synchronised shock and ALS algorithm
• If unstable (chest pain, heart failure, low GCS, extreme tachycardia, hypotensive)
  • • Sedate
      • • Fentanyl 0.5-1mcg/kg and propofol 0.25-0.5mg/kg
        • Or ketamine 0.5-1 mg/kg
    • Synchronised shocks – up to three (125J, 200J, 360J)
    • If not effective – amiodarone 300mg over 10-20 minutes
      • • Can repeat amiodarone (150mg IV over 10 mins, after 15 mins)
        • Then 24 hour infusion – ideally with central line (and always if concentration >2mg/ml). Otherwise use a big cannula and flush well first
        • If patient has known long QT and goes into VT – try to avoid amiodarone
        • Amiodarone can cause acute hypotension – so be careful
        • Consider overdrive pacing if amiodarone not effective
• If stable
  • • Can try amiodarone 300mg IV over 10-60 mins
    • Another option is Metoprolol 5mg IV – can repeat in 30 mins), though never in acute failure / hypotension
    • Consider magnesium (2g over 15 mins) and replace K+ if required (Aim for K+> 4 and Mg>1)
    • If all ineffective – consider synchronised shock if VT susuatined, even if no unstable features
    • Lidocaine and sotalol are other options. Lidocaine can be used if no response to betablockers and contraindications to amiodarone
    • Never give calcium channel blockers
    • Ensure all ECGs are saved / scanned
    • Consider PCI or transvenous catheter overdrive pacing
• Later – once the dust settles
  • • 12 lead ECG in SR – look for Q waves, QT, Brugada pattern, epsilon wave (AVRC)
    • Check all electrolytes
    • Echo – for LV function, scar, structural disease
    • Consider coronary angio
    • CMR often used
    • Take a family history
    • Risk stratification for sudden cardiac death
    • Consider ICD
      • • In general, if VT occurs outside of systemic disturbance or a reversible cause, consider secondary prevention ICD
        • Not all VT needs an ICD – especially if structurally normal heart (consider medications or ablation) or in context of ischaemia (reassess after treatment)
        • Low EF (<35%) – likely to need ICD
    • Optimise HF treatment if present
    • Ablation in some cases, but comes with risks, so drugs generally preferred
    • In refractory cases, consider emerging approaches, such as cardiac stereotactic body radiation therapy
• If ICD in situ – if patient has ICD and is receiving lots of shocks while in VT but BP is stable, you can turn it off with a magnet

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Polymorphic VT

• Can resemble VF
• Sinusoidal pattern if Torsades – often in patients with long QT (may be due to drugs) and hypokalaemia. Often short-lived and self-terminating.
• Bigeminy in a patient with a known long QT syndrome may herald imminent torsades
• HR > 220 is more likely to degenerate into VF
• Give magnesium 2g IV over 5 or 10 minutes. Can repeat
• Might use synchronised shock first if patient compromised or episode prolonged
• Correct hypokalaemia
• Avoid drugs that prolong QT such as amioderone
• Consider overdrive pacing once arrhythmia corrected

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Pre-excited AF

• Rate 200 – 300+
• Irregular if AF but regular if flutter
• Wide QRS (stable axis, unlike VT) but some can be narrow
• Due to an abnormal connection between the atria and ventricles (outside the AV node)
• Standard AF is rate limited by the AV node, therefore no risk of VF. However if AF and a fast accessory pathway – rates can reach 300, and can cause VF
• Usually unstable on presentation
• Check old ECGs – you might see ‘manifest pre-excitation’, ie WPW (short PR and delta wave), but you may see no changes (a concealed pathway)
• Can resemble:
  • • Polymorphic VT
    • AF with LBBB (but in pre-excited AF there’s variability in QRS width, and the rate is faster. It’s too rapid to be conducted by the AV node, therefore too fast for LBBB)
    • Or even VF
• Avoid: CCB, betablockers, digoxin and adenosine (blocks AV node, and risks VF)
• Can give procainamide or ibutilide, but usually DC cardioversion preferred
• Will need catheter ablation – usually on that admission