Wide complex tachycardias

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Wide complex tachycardia Microchapters

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Overview

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Differentiating VT from SVT with aberrant conduction

Epidemiology and Demographics

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Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

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Laboratory Findings

Electrocardiogram

EKG Examples

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: WCT; fast and wide; wide and fast; wide-complex tachycardia; wide complex rhythm; SVT with aberrancy; SVT with aberrant conduction; supraventricular tachycardia with aberrancy; VT versus SVT

Diagnosis

History

The patient should be asked about drugs that are associated with ventricular tachycardia and if there is a history of ischemic heart disease which would dramatically increase the odds that the rhythm is VT. Wide complex tachycardia will be due to VT in 80% of cases and will be due to VT in 98% of cases if there's a history of either acute MI or structural heart disease. Only 7% of patients with SVT will have had a prior myocardial infarction (MI). VT or an accelerated idioventricular rhythm can be seen following reperfusion in STEMI. Digoxin, antiarrhythmics, phenothiazines, TCAs, and pheochromocytoma may also cause VT. Recent procedures such as cardiac catheterization, DC countershock, repair of congenital lesions are all associated iwth VT. A family history of sudden cardiac death, a history of a channelopathy associated with arrhythmias, and the hereditary Long QT syndrome, and Brugada syndrome are all associated with VT.

Symptoms

Physical Examination

  • Vitals should be obtained to assess hemodynamic stability and guide therapy
  • Cannon-a waves are a manifestation of AV dissociation and suggest VT
  • Carotid sinus massage (CSM)/Valsalva: ST can gradually slow. MAT, AT, Flutter, and AF may transiently slow. An AV nodal dependent WCT may terminate. AV dissociation may become more apparent with CSM in VT. VT can terminate with CSM

Electrocardiogram

EKG examples and diagnosis here:

  • Extreme axis deviation favors VT. Especially -90 to -180 or “northwest” or “superior” axis. (23% of SVT will have SAD)
  • QRS duration >140 msec favors VT (21% of VT will have QRS <140 msec)
  • AV dissociation is demonstrated in only 21% of VT
  • Morphologic Criteria
    • 4% of SVT and 6% of VT did not fulfill criteria in any lead
    • 40% will have discordance between V1/V2 and V5/V6. One lead may suggest VT while another suggests SVT.
  • An algorithmic approach was proposed by Brugada in 1991. It has a reported sensitivity of 99% and specificity of 97%.


An overview of ventricular tachycardias, follow the wide complex tachycardia flowchart
example regularity atrial frequency ventricular frequency origin (SVT/VT) p-wave effect of adenosine
Wide complex (QRS>0.12)
Ventricular Tachycardia regular (mostly) 60-100 bpm 110-250 bpm ventricle (VT) AV-dissociation no rate reduction (sometimes accelerates)
Ventricular Fibrillation irregular 60-100 bpm 400-600 bpm ventricle (VT) AV-dissociation none
Ventricular Flutter regular 60-100 bpm 150-300 bpm ventricle (VT) AV-dissociation none
Accelerated Idioventricular Rhythm regular (mostly) 60-100 bpm 50-110 bpm ventricle (VT) AV-dissociation no rate reduction (sometimes accelerates)
Torsade de Pointes regular 150-300 bpm ventricle (VT) AV-dissociation no rate reduction (sometimes accelerates)
Bundle-branch re-entrant tachycardia* regular 60-100 bpm 150-300 bpm ventricles (VT) AV-dissociation no rate reduction
* Bundle-branch re-entrant tachycardia is extremely rare

Treatment

Defibrillation

Indications for defibrillation include the following:

Acute Pharmacotherapies

  • If stable: (More patients than you think)
  • DO NOT USE Ca2+ Channel blocker, Digoxin or Adenosine if you don't not know the etiology of the Wide Complex Tachycardia. Ca2+ Channel blockers and Digoxin can lead to accelerated conduction down a bypass tract and VF.
  • Though ACLS guidelines recommend a diagnostic trial of Adenosine, it can precipitate VF in some patients with SVT. Patients who have underlying coronary disease may become ischemic from coronary steal. Rhythm can degenerate and lead to VF that cannot be resuscitated. Furthermore, some VT (esp those with structurally normal hearts) are adenosine responsive and can terminate.
    1. Etiology Uncertain
      • Pronestyl 15mg/kg load over 30 minutes then 2-6mg/min gtt
    2. Ventricular Tachycardia with active ischemia
      • Lidocaine 1 mg/kg q5-10 min up to 3 times then 2-6mg.min gtt
      • If unsuccessful, Pronestyl as above
      • If unsuccessful, IV Amiodarone 150-300 load over 15-20min. 30-60mg/hr gtt for total of 1gram
    3. Ventricular Tachycardia in Setting of Cardiomyopathy
    4. Positively SVT with aberrancy
    5. Antidromic AVRT
      • If 100% positive AF is not underlying, can terminate with a nodal blocker
      • If unsure, Pronestyl as above

Sources

Copyleft images obtained courtesy of ECGpedia, http://en.ecgpedia.org/index.php?title=Special:NewFiles&offset=&limit=500

References


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