Wide - Complex Tachycardia (WCT)



Wide - Complex Tachycardia (WCT)
Wide-Complex Tachycardia
Rate ≥ 100bpm
QRS width >120ms
(more common)
(less common)
1. Bundle-branch aberrancy
2. Metabolic or drug-induced
3. Antidromic AVRT
1. Pacemaker
2. VT
1. Afib with pre-excitation
1. Vfib/flutter
2. Long QT
3. Brugada syndrome
4. Other (catecholamineinduced VT, short QT)
Note: A therapy like verapamil can cure a patient with SVT but kill a patient with VT.
Also treatment for conditions in a given box can vary, for example VT versus AIVR.
Questions to answer immediately
1. Hemodynamically stable? Angina?
(If not, immediate electrical cardioversion/defibrillation.)
2. Any history of structural heart disease?
(If so, the etiology is almost certainly is ventricular.)
3. What did an old ECG show?
(Identify baseline bundle-branch blocks and pre-excitation.)
Common Misconceptions
1. VT is always hemodynamically significant
(Incorrect, in general VT is as well tolerated as SVT.)
2. Thinking too much
(Up to 70-80% of all WCT are VT.)
On morning rounds you are reviewing telemetry:
What is the rhythm?
How do you describe the wide-complex beat?
Cycle-length dependent aberrancy
Cycle-length dependent aberrancy can produce isolated wide-complex beats which are supraventricular (like prior).
Via concealed conduction, this phenomenon can produce runs of wide-complex, supraventricular beats (as below).
At your VA clinic that afternoon, a 59-M w/ ESRD who missed 2 days of HD
presents for an acute care visit with weakness. He is borderline tachycardic so
you obtain an ECG:
Any laboratory predictions? Do you admit this patient to the CCU or the MICU?
Metabolic/drug effects on QRS width
Tricyclic antidepressant toxicity
Other drugs which block Na-channel can cause this too (class IA and IC antiarrhythmics, diphenhydramine, cocaine)
That night on call a STEMI comes in and receives PCI. After the
cath team and fellow have left the RN calls you for the following
strip on the telemetry monitor:
What is the rhythm?
What treatment is needed?
Later that call night your code pager goes off. Upon entering the patient’s room
the monitor strip shows
What is this rhythm? What treatment is indicated?
After appropriate treatment you obtain a 12-lead ECG tracing:
What is the unifying diagnosis?
Your final call comes just before you are about to
pass off the call pager. The ER has a young man
who has palpitations and is dizzy. Thankfully he
brought an old ECG of his, of which some
representative beats are shown. His current 12lead ECG shows:
What is the treatment of choice?
Algorithm for monomorphic WCT
Absence of precordial RS complex
Presence of precordial RS complex
Duration of precordial RS interval
Measure from START of R-wave to NADIR of S-wave
AV Dissociation
QRS morphology in V1 and V6
In RBBB pattern first “rabbit ear” is taller in VT while second “rabbit ear” is taller in SVT.
In LBBB pattern the time from R-wave start to S-wave nadir is short in SVT and long in VT.
Other clues to VT
• QRS duration: >140ms with RBBB morphology or >160ms with LBBB
morphology suggests VT
• QRS axis: “extreme” axis (right upper quadrant) suggests VT
• Precordial concordance: negative concordance suggests VT, positive
concordance suggests VT or AVNRT
Energy levels for shocking
• Polymorphic: unsynchronized 200 J
• Monomorphic (unstable): synchronized 100 J
• Monomorphic (stable): synchronized 50 J
Case 1. 61-M w/ known CAD s/p multiple PCI presenting with chest pain
Case 2. 63-M w/o manifest CAD presents with several hours of palpitations
Answer Guide
Case 1 (BJ 4/22/2007). RS complex present in V1 with duration about 120ms, AV dissociation present most clearly
before/after 2 sinus beats, all of which point to VT
EPS: spontaneously converted to SR, patient left hospital AMA before work-up could be initiated
Case 2 (DT 8/6/2008). RS complex present in V5-6 with narrow duration, no AV dissociation, V1 morphology suggests
aberrant RBBB although V6 has R<S, all of which suggest SVT
EPS: adenosine revealed atrial flutter, underwent DCCV as rate was hard to control

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