Home

helps physicians and healthcare professionals

Erectile Dysfunction

helps physicians and healthcare professionals

Doctor123.org

helps physicians and healthcare professionals

Ventricular Tachycardia, Emergency Medicine


Basics


Description


  • A wide complex tachydysrhythmia with a quasirandom signal (QRS) >120 and a rate >100
  • Rapid and regular depolarization of the ventricles independent of the atria and the normal conduction system
  • Re-entry:
    • Structural heart disease most common
    • Seen in dilated cardiomyopathy, ischemia, and infiltrative heart disease, previous MI, scarring
    • May be pharmacologically induced
    • Usually produces a regular and monomorphic rhythm
  • Triggered automaticity:
    • Minority of ventricular tachycardia (VT)
    • Caused by repetitive firing of a ventricular focus
  • Torsades de pointes:
    • Polymorphic form of VT
    • Alternating electrical polarity and amplitude
    • Prolongation in repolarization necessary
    • Usually pharmacologically induced
  • Regardless of the mechanism, all VT may degenerate to ventricular fibrillation (VF).

Etiology


  • Wide complex tachycardia:
    • 80% likelihood of being VT
    • 20% supraventricular tachycardia (SVT) with a baseline left bundle branch block (LBBB) or aberrancy
  • Wide complex tachycardia and a history of MI:
    • >98% likelihood of being VT
    • Age >35: 80% risk of VT
    • Age <35: 75% risk of SVT
  • Incidence of nonsustained VT:
    • 0 " “4% in the general population
    • Up to 60% of patients with dilated cardiomyopathy
  • Associated with increased risk for sudden cardiac death (SCD)

Diagnosis


Signs and Symptoms


History
  • Asymptomatic
  • Syncope/near syncope
  • Lightheadedness/dizziness
  • Shortness of breath
  • Palpitations
  • Chest discomfort/pain
  • Diaphoresis
  • Cannon A-waves
  • Hypotension
  • CHF
  • Beat-to-beat variability of systolic BP
  • Variability in heart tones, especially S1

Physical Exam
  • Establish presence of pulses, mental status and vital sign abnormalities.
  • Auscultation of heart will reveal tachycardia.

Essential Workup


  • EKG:
    • Most important initial test to differentiate VT from SVT with aberrancy or LBBB
  • VT definition:
    • ≥3 consecutive QRS complexes with a ventricular rate over 100 bpm and a QRS duration >120 msec
  • Torsades de pointes:
    • Polymorphic VT that rotates its axis every 10 " “20 beats
  • Criteria to determine VT:
    • Atrial ventricular (AV) dissociation (present in 60 " “75%)
    • Fusion beats (P-wave partially activates ventricle in advance of next VT cycle), capture beats (P-wave totally activates ventricle)
    • Uniform morphology (except in the case of torsades)
    • Extreme axis deviation ( " “90 ‚ ° to +180 ‚ °)
    • QRS >140 msec, with right bundle branch block (RBBB) morphology; or QRS >160 msec, with LBBB morphology, but >160 suggests VT regardless of bunch branch morphology
    • QRS concordance in the precordial leads
    • RBBB pattern V1 with R > R ' is VT 50:1.
    • LBBB pattern with Q or QS pattern in V 6 is VT 50:1.
    • Brugada criteria defines VT in wide complex tachycardia:
      • 99% sensitivity, 97% specificity
      • Only need to meet 1 criterion
      • AV dissociation
      • R-S interval absent in all precordial leads
      • QRS onset to the nadir of S >100 msec in any precordial lead
      • V1 R-wave >30 msec; R-S interval >70 msec, slurred, notched S
      • Wide QRS with LBBB in precordium
    • Indicators of SVT with aberrancy include:
      • Normal-axis QRS <140 msec
      • Absence of Q-waves
      • RBBB in V1 with rsR " ² triphasic pattern
      • AV nodal blockade: Slowing of impulse conduction velocity seen with antiarrhythmic drugs is more pronounced at faster rates, so may result in wide complex SVT (SVT with aberrancy)

Diagnosis Tests & Interpretation


Lab
  • Cardiac enzymes
  • Electrolytes, BUN, creatinine, glucose
  • Magnesium level
  • Calcium level
  • Digoxin level if toxicity suspected

Imaging
CXR: ‚  
  • Cardiomegaly or other cardiac anomalies may be apparent.

ECHO: ‚  
  • Structural disease may be identified.

Diagnostic Procedures/Surgery
Esophageal pacing catheters: ‚  
  • May be able to detect atrial activity to establish AV dissociation and therefore diagnose VT
  • Catheters can then be used to overdrive pace if refractory to cardioversion/antiarrhythmics.

Differential Diagnosis


  • SVT with aberrancy or baseline LBBB
  • Proarrhythmia secondary to antidysrhythmia medications; suspect if:
    • VT morphology is different than previous episodes of VT
    • Medications have recently been started or changed
    • QT interval is >440 msec.
    • Torsades de pointes
    • If VT continues to recur after cardioversion

Treatment


Pre-Hospital


  • Cautions:
    • Transport stable patients suspected of being in VT without attempting to convert them.
    • Synchronized cardioversion for unstable patients with a pulse
    • Defibrillation for pulseless VT
  • Controversies:
    • Lidocaine:
      • No benefit in the prevention of VT in patients with isolated premature ventricular contractions, regardless of the frequency

Initial Stabilization/Therapy


Pulseless VT: Defibrillate immediately and follow the VF treatment plan. ‚  

Ed Treatment/Procedures


  • Unstable patient:
    • Definition:
      • Chest pain
      • Hypotension
      • Evidence of worsening heart failure
    • Initiate immediate synchronized cardioversion with 100 J, quickly progressing to 200 J, 300 J, and 360 J if no response.
      • If the VT is polymorphic, begin cardioversion at 200 J.
    • Sedate the patient before cardioversion if at all possible.
    • If unable to terminate the VT, administer lidocaine and repeat the cardioversion.
    • Antitachycardia overdrive pacing if torsades
    • After successful return of sinus rhythm, begin amiodarone.
  • Stable patient, monomorphic VT:
    • Normal cardiac function at baseline:
      • Procainamideorsotalol; may also consider amiodarone or lidocaine
      • Avoid sotalol if evidence of prolonged QT or known long QT syndrome.
    • Impaired cardiac function at baseline:
      • Amiodarone bolus, then infusion or lidocaine, then synchronized cardioversion
  • Stable patient, polymorphic VT:
    • Normal QT interval at baseline:
      • Correct electrolyte abnormalities.
      • Treat ischemia if present.
      • Then begin 1 of the following: b2-blockers, lidocaine, amiodarone, procainamide, or sotalol.
    • Prolonged QT Torsades de pointes:
      • Correct electrolytes.
      • Magnesium sulfateor overdrive pacing or 1 of the following: Isoproterenol, phenytoin, lidocaine
      • Isoproterenol is used to overdrive the tachycardia if the patient has no history of coronary artery disease or long QT syndrome.
      • Temporizing measure until external pacing available
    • Impaired cardiac function at baseline
    • Amiodarone bolus or lidocaine bolus then synchronized cardioversion

  • Primary cardiac arrest and VT are rare in children.
  • Usually secondary to hypoxia and acidosis
  • VT is tolerated for longer periods in children than adults and is less likely to degenerate to VF.
  • Infants in VT most commonly present with CHF.
  • VT in children results from:
    • Cardiomyopathy
    • Congenital structural heart disease
    • Congenital prolonged QT syndromes
    • Coronary artery disease secondary to vasculitis
    • Toxins, poisons, drugs
    • Severe electrolyte imbalances, especially of potassium

Medication


First Line
  • Procainamide: 3 " “6 mg/kg over 5 min, may repeat every 5 " “10 min to max. total dose of 15 mg/kg. Do not exceed 100 mg/dose or 500 mg in 30 min (peds: 15 mg/kg IV/IO over 30 " “60 min).
  • Amiodarone: 150 mg IV bolus over 10 min, may repeat; arrest dose is 300 mg IV/IO max. cumulative dose 2.2 g IV/24 h; followed by 1 mg/min for 6 hr, then 0.5 mg/min for 18 hr. (peds: 5 mg/kg IV or IO over 20 " “60 min, max. 15 mg/kg/d)
  • MgSO4: 2 g in D5W over 5 " “10 min followed by infusion of 0.5 " “1 g/h IV, titrate to control torsades (peds: 25 " “50 mg/kg IV/IO over 10 min, max. dose 2 g)

Second Line
  • Lidocaine: 1 " “1.5 mg/kg bolus IV push 1st dose, 0.5 " “0.75 mg/kg 2nd dose, and q5 " “10min for a max. of 3 mg/kg; tracheal administration 2 " “4 mg/kg; maintenance infusion 1 " “4 mg/min if converted. Not recommended for ACS induced VT(peds: 1 mg/kg bolus with infusion 20 " “50 Ž Όg/kg/min)
  • Adenosine: 6 mg IV push followed by 12 mg IV push if needed in 1 " “2 min (peds: 1 mg/kg, max. 6 mg). Note: Does not convert VT, do not use if unstable or irregular WCT.
  • Isoproterenol: 2 " “10 Ž Όg/min, titrate to heart rate (peds: 0.1 Ž Όg/kg/min). Note: Do not give with epinephrine, may precipitate VT/VF (no longer part of ACLS protocol), do not give if prolonged QT.
  • Sotalol: 100 mg IV over 5 min. (peds: Use not recommended for initial management). Note: Do not give if prolonged QT.

Follow-Up


Disposition


Admission Criteria
  • Admit sustained VT to a critical care setting.
  • Admit nonsustained VT and a history of MI or dilated cardiomyopathy for electrophysiologic studies.

Discharge Criteria
  • Rare patients with nonsustained VT and a previous evaluation that revealed no structural heart disease can be discharged:
    • At low risk for SCD
  • Patients with automatic internal cardiac defibrillators that are well functioning can also be discharged.

Issues for Referral
All patients discharged with VT should be followed by a cardiologist within 48 hr. ‚  

Followup Recommendations


Patients should follow-up with a cardiologist. ‚  

Pearls and Pitfalls


  • Search for contributing factors such as toxins, metabolic abnormalities, trauma, hypothermia, thrombosis.
  • Unstable VT requires early cardioversion.
  • Administer postresuscitation maintenance medications to prevent recurrence.
  • Watch for bradycardia and GI toxicity after amiodarone administration.
  • Discontinue any proarrhythmic drugs
  • Consider b2-blockade for ischemia-induced VT and polymorphic VT.

Additional Reading


  • Connolly ‚  SJ, Dorian ‚  P, Roberts ‚  RS, et al. Comparison of beta-blocker, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: The OPTIC Study: A randomized trial. JAMA.  2006;295:165 " “171.
  • Pellegrini ‚  CN, Scheinman ‚  MM. Clinical management of ventricular tachycardia. Curr Probl Cardiol.  2010;35(9):453 " “504.
  • Zipes ‚  DP, Camm ‚  AJ, Borggrefe ‚  M, et al. ACC/AHA ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death " ”executive summary. J Am Coll Cardiol.  2006;48:1064 " “1108.

Acknowledgments


Thank you to the prior authors of this chapter, Jennifer Audi and Shannon Straszewski ‚  

See Also (Topic, Algorithm, Electronic Media Element)


2010 AHA Guidelines for CPR and ECC ‚  

Codes


ICD9


427.1 Paroxysmal ventricular tachycardia ‚  

ICD10


I47.2 Ventricular tachycardia ‚  

SNOMED


  • 25569003 Ventricular tachycardia (disorder)
  • 31722008 Torsades de pointes (disorder)
Copyright © 2016 - 2017
Doctor123.org | Disclaimer