Wide complex tachycardia overview: Difference between revisions
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:*There are positive or negative [[QRS]] complexes in all the precordial leads | :*There are positive or negative [[QRS]] complexes in all the precordial leads | ||
:*The morphology of the [[QRS]] complexes resembles that of a previous [[premature ventricular contraction]] ([[PVC]]). | :*The morphology of the [[QRS]] complexes resembles that of a previous [[premature ventricular contraction]] ([[PVC]]). | ||
:*Patients with ventricular tachycardia can often be hemodynamically stable, and stable vital signs do not rule out ventricular tachycardia. This is often a major mistake on the part of clinicians and can lead to inappropriate treatment of [[VT]] as [[SVT]] with poor outcomes. <ref name="pmid4057488">{{cite journal |author=Morady F, Baerman JM, DiCarlo LA, DeBuitleir M, Krol RB, Wahr DW |title=A prevalent misconception regarding wide-complex tachycardias |journal=[[JAMA : the Journal of the American Medical Association]] |volume=254 |issue=19 |pages=2790–2 |year=1985 |month=November |pmid=4057488 |doi= |url=http://jama.jamanetwork.com/article.aspx?volume=254&page=2790 |issn= |accessdate=2013-08-04}}</ref> | |||
===Supraventricular Tachycardia with Aberrant Conduction=== | ===Supraventricular Tachycardia with Aberrant Conduction=== | ||
Revision as of 20:05, 4 August 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Wide complex tachycardia is a cardiac rhythm of more than 100 beats per minute with a QRS duration of 120 milliseconds or more. It is critical to differentiate whether the wide complex tachycardia is of ventricular origin and is ventricular tachycardia (VT), or if it is of supraventricular origin with aberrant conduction (SVT with aberrancy). Rapid differentiation between these two causes of wide complex tachycardia is absolutely critical because the treatment options are quite different for VT versus SVT with aberrancy.
Causes
A wide complex tachycardia is either of ventricular origin (ventricular tachycardia or VT), or is of supraventricular origin with aberrant conduction (SVT with aberrancy) such as occurs with conduction down a bypass tract. Approximately 80% of wide complex tachycardias are due to ventricular tachycardia.[1]
Differential Diagnosis of Wide Complex Tachycardia: Distinguishing VT from SVT
Differentiating between VT and SVT as the cause of wide complex tachycardia is absolutely critical because the treatment options are quite different for VT versus SVT with aberrancy.
Ventricular Tachycardia
The diagnosis of VT is more likely if:
- There is a history of myocardial infarction or structural heart disease
- The electrical axis is -90 to -180 degrees (a “northwest” or “superior” axis)
- The QRS is > 140 msec
- There is AV dissociation
- There are positive or negative QRS complexes in all the precordial leads
- The morphology of the QRS complexes resembles that of a previous premature ventricular contraction (PVC).
- Patients with ventricular tachycardia can often be hemodynamically stable, and stable vital signs do not rule out ventricular tachycardia. This is often a major mistake on the part of clinicians and can lead to inappropriate treatment of VT as SVT with poor outcomes. [2]
Supraventricular Tachycardia with Aberrant Conduction
The diagnosis of atrial fibrillation with aberrant conduction down a bypass tract should be considered if
- The heart rate is over 200 beats per minute
- If the rhythm is grossly irregularly irregular
For more detailed information regarding how to differentiate VT from SVT please view the differential diagnosis page or click here.
Epidemiology and Demographics
The underlying cause of wide complex tachycardia tends to be ventricular tachycardia (VT) in older patients and supraventricular tachycardia (SVT) with aberrancy in younger patients.
Risk Factors
Wide complex tachycardia will be due to VT in 80% of cases if there is a history of myocardial infarction (MI). Only 7% of patients with SVT with aberrancy will have had a prior myocardial infarction (MI). Wide complex tachycardia will be due to VT in 98% of cases if there's a history of structural heart disease.
Electrocardiogram
Laboratory Studies
Electroyte abnormalities such as hypokalemia (which can be associated with ventricular tachycardia), hypomagnesemia (which can lead to Torsade de Pointes) and hyperkalemia (which can cause a sinusoidal rhythm) should be ruled out.
Medical Therapy
The management of wide complex tachycardia should begin by assessing the patient's ABCs (airway, breathing, and circulation). If the patient is unstable and either hypotension, altered mental status, chest pain, heart failure or seizures are present, then immediate synchronized cardioversion should be performed. If the patient is stable, the optimal management depends upon the differentiation of ventricular tachycardia versus supraventricular tachycardia with aberrant conduction as a cause of the wide complex tachycardia. Treatment targeted at the underlying cause can then be initiated.
| Wide complex tachycardia QRS ≥ 120ms | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Do the following simultaneously: - Assess and support ABC's as needed - Give oxygen - Monitor ECG, BP, oxymetry - Identify and treat reversible causes (hypokalemia, hypomagnesemia | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Is the patient stable? Unstable signs include: - Chest pain - Congestive heart failure - Hypotension - Loss of consciousness - Seizures | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Yes | No | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Is the rhythm regular? | Immediate synchronized cardioversion -Establish IV access - Give IV sedation if the patient is conscious - Consider expert consultation | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Regular rhythm | Irregular rhythm | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Ventricular tachycardia or uncertain rhythm? | Confirmed SVT with aberrancy? | Afib with aberrancy? | Pre-excited Afib (Afib + WPW)? | Recurrent polymorphic VT? | Torsade de pointes? | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| - Give amiodarone 150 mg IV over 10 min - Repeat amiodarone as needed for a maximal dose of 2.2g/24h - Prepare for elective synchronized cardioversion | - If certain VT is not present, give adenosine 6 mg rapid IV push - If no conversion give 12 mg IV push - May repeat 12 mg dose once | - Consider expert consultation - Control rate e.g diltiazem or beta blockers Use beta blockers with caution in pulmonary diseases or CHF | - Consider expert consultation - Avoid AV nodal blocking agents e.g adenosine, digoxin, diltiazem and verapamil - Consider amiodarone 150 mg IV over 10 min | Consider expert consultation | Load with Magnesium 1-2 g over 5-60 min, then infusion | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Algorithm based on ACLS guidelines for the management of tachycardia.
References
- ↑ Lam P, Saba S (2002). "Approach to the evaluation and management of wide complex tachycardias". Indian Pacing and Electrophysiology Journal. 2 (4): 120–6. PMC 1557420. PMID 16951728. Retrieved 2013-08-04.
- ↑ Morady F, Baerman JM, DiCarlo LA, DeBuitleir M, Krol RB, Wahr DW (1985). "A prevalent misconception regarding wide-complex tachycardias". JAMA : the Journal of the American Medical Association. 254 (19): 2790–2. PMID 4057488. Retrieved 2013-08-04. Unknown parameter
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