Narrow Complex Tachycardias

• Causes
  • • Supra Ventricular Tachycardias (SVTs), include:
      • • AVNRT
        • AVRT
        • Atrial tachycardias
    • AF or Flutter
    • Sinus tachycardia

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AVNRT (Atrioventricular nodal reentrant tachycardia, the classic SVT)

• Due to very small aberrant circuit around AV node
• ECG features
  • • HR 150-250
    • P waves absent or fused with QRS
    • Sometimes slight deformation at end of QRS – p wave hiding within it – ? pseudo R’ primes. Sometimes pseudo S waves
    • QRS Alternans – phasic variation in QRS amplitude
• Occurs most often in young patients (75% female) with sudden onset and offset palpitations.
• Syncope rare and usually fairly benign
• Twice as common as AVRT
• 90% is slow-fast ie antegrade conduction down slow, retrograde up fast, and atria are repolarised retrogradely
• Cannon waves can occur, with palpitations in the neck (atria contracting against closed valves)
• Acute treatment
  • • If in ED – transfer to resus on put on defib pads
    • Try a Modified Valsalva (at end of expiration into syringe, suddenly tilt patient back and hold legs in air) – effective in 43% (compared to 17% for simple valsalva)
    • If ineffective
      • • Insert large cannula high up (ACF) and have 20ml flush ready
        • Check defib and get ready to record rhythm
        • Warn patient about upcoming symptoms (and if they don’t feel unwell, it’s probably not working)
        • Give Adenosine
          • • Can try 6mg first, then 12mg if that fails, then 18mg (10 sec half-life).
            • Some advocate starting at 12mg.
            • Small risk of precipitating AF
            • May avoid in asthma (esp if uncontrolled) or severe COPD
        • Can try Verapamil if adenosine contraindicated – 2.5-5mg over 2 minutes, or betablocker
        • Could also try a betablocker
        • Avoid mixing a rate-limiting CCB and a betablocker (doubles the negatives inotropic effect)
    • After adenosine, check the rhythm strip:
      • • If no impact of adenosine – inadequate dose or delivery, or high septal VT
        • If slows with adenosine and then reaccelerates – either ST or autonomic focal atrial tachycardia, or junctional ectopic tachycardia
        • If sudden termination – AVNRT, AVRT, sinus nodal re-entry, triggered focal atrial tachycardias (Delayed After-Depolarisations, DADS)
        • If persistent atrial tachycardia with transient AV block – flutter, micro-re-entrant focal atrial tachycardia
    • If no termination of AVNRT – give either a betablocker or CCB, d/w cardiology, and consider synchronised shock
• Follow up
  • • Always check TSH and CRP
    • Echo for LV function (tachymyopathy)
    • EP study often indicated prior to ablation
    • Sometimes ETT, EPS, stress echos, loop recorder indicated
• Ablation
  • • Most SVT is ablate-able (90-95% cure rate) – more effective than in AF
    • ECG useful to work out the likelihood of success.
    • Not useful if close to natural PPM.
    • Takes around 2 hours
    • Day cause under LA/sedation
    • Complication rate 1-2%
    • 5% need repeat
    • Unable to drive for one week.
    • Risk of needing PPM is 1 in 150
• How to distinguish SVT from ST
  • • ST less likely at rates > 150 but still possible
    • SVT – usually no visible atrial activity. With ST the P waves may be hidden in the preceding T wave, producing a ‘camel hump’ appearance, but again not specific for ST and does occur in SVT
    • ST doesn’t start or stop as abruptly as SVT (but if patient hasn’t had regular obs, you may not know much about its onset)
    • For ST, the cause is usually clear from the history (though there can be inappropriate ST with no clear cause and drugs might still be appropriate to slow down)
    • ST has more rate variability
    • Some SVTs have more than one p wave for each QRS

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AVRT (Atrioventricular reentrant tachycardia)

• Bigger circuit than AVNRT
• 70% have WPW, 30% have no pre-excitation on baseline ECG and no risk of VT.
• It’s the characteristic arrhythmia of WPW – hunt down old ECGs
• Rate 200-300
• Orthodromic conduction
  • • Narrow QRS
    • QRS Alternans (phasic variation in QRS amplitude)
    • P waves fused or invisible
    • Often TWI and ST depression (more often than in AVNRT)
    • Regular
    • Can look like AVNRT but it’s managed similarly anyway
    • DC cardiovert if unstable
    • Can try adenosine or a CCB
• Antidromic conduction
  • • Rarer (10%)
    • Wide QRS
    • Confused with VT (but can be managed similarly anyway)
    • Can tx with amiodarone or procainamide
    • Cardiovert if these ineffective, as could degenerate
    • High risk of VF if shortest pre-existed RR interval during AF is <250ms

• AVRT vs AVNRT
  • • AVNRT – no P waves or P wave inside QRS
    • AVRT – p wave just after QRS

• Wolf-Parkinson-White
  • • Extra conduction pathway connecting atria to ventricles
    • Rarely associated with Ebstein’s anomaly
    • ECG
      • • Short PR
        • Delta wave – slurring slow rise of initial portion of the QRS
        • Prolonged QRS
        • Pseudo-q waves (negative delta waves)
        • Prominent R wave in v1-v3
        • Can be intermittent on ECGs (which is less risky)
        • Type A has tall R in V1, Type B has deep S in V1
    • Pre-excitation can be asymptomatic, but WPW syndrome is technically defined as pre-excitation plus arrythmia
    • Arrythmias
      • • SVT (common)
        • AF (rarer) incl pre-excited AF
        • VF (v rare)
    • Treatment
      • • All should see cardiac EP
        • Treatments determined by symptoms, risk, patient preference and occupation. Often no specific treatment
        • Arrhythmias may respond to sotalol, amiodarone and flecainide (especially)
        • Often avoid digoxin, verapamil, beta-blockers – they block AV node. They are therefore of no use, and may be dangerous.
        • Refer some for ablation
    • Risks
      • 0.1% risk of death per annum (ablation mitigates this risk, but comes with its own risks)
      • Check for red flags
        • • Syncope
          • Frequent palpitations
          • History of AF/flutter
          • Family hx of SCD

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Other atrial tachycardias

• Focal atrial tachycardia
  • • Axis and P waves can be abnormal – look for inverted P waves in inferior leads
    • Can be subtle and misdiagnosed as SR. Old ECGs helpful (p waves may appear different)
    • Often occurs after AF catheter ablation
    • Often fixed rate which is usually quite fast but not always (and if not, can cause SOB if HR fixed and doesn’t rise with physical activity)
    • Treatment
      • Rate control with betablocker or CCB, which can terminate rhythm or slow down rate
      • Consider anti-coagulation esp if planning ablation but this is controversial
      • Ablation later
    • If treated with adenosine, P waves continue at previous rate during the ventricular pause. It can terminate

• Multifocal atrial tachycardia
  • • Irregular, 100-150
    • Intermittent P waves, of different morphology in the same lead
    • Stable baseline between Ps, no flutter waves
    • Mostly occurs in HF or COPD. Tends to resolve following treatment of the underlying disorder but is associated with poor prognosis. Often precursor to AF

• Inappropriate sinus tachycardia
  • • Not usually diagnosed in hospital, as there is almost certainly something underlying a ST in that setting
    • If HR consistent, more likely an abnormal atrial tachycardia than a simple sinus tachycardia