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A. Overview navigator

  1. Ventricular Tachycardia (VT)
  2. Torsade de Pontes (TDP)
  3. Accelerated Idioventricular Rhythm (AIVR)
  4. Ventricular Fibrillation (VF)
  5. Agonal Rhythm
  6. Sudden Cardiac Death

B. Ventricular Tachycardia (VTach) navigator

  1. Classifications
    1. Reentrant versus Ectopic
    2. Monomorphic versus Polymorphic (such as Torsades de Pointes)
  2. Reentrant
    1. Atrioventircular (AV) Nodal Reentry
    2. Wolff-Parkinson-White Syndrome (WPW, pre-excitation)
  3. Ectopic
    1. R or qR in V1 (taller left peak)
    2. V6: no q, small r, deep wide S
    3. QS in V6; LA deviation or in "no man's land" (that is, I - ; aVF -)
    4. Fusion beats common
  4. VTach in Healthy Hearts [1]
    1. Usually presents in young persons
    2. VTach originates in RV outflow tract or in LV near the septum
    3. Present with specific abnormal ECG depending on origin of VTach
    4. For RV outflow tract, ECG shows LBBB and inferior or right axis deviation
    5. For LV septum, ECG shows RBBB and left axis deviation
    6. Catheter directed radiofrequency (RF) ablation is preferred treatment [2]
  5. Types of Monomorphic VTach [3]
    1. Focal origin - nonstructural versus structural heart disease
    2. Bundle-branch reentry - consuction system, valve, nonischemic, muscular, ischemic
    3. Scar-related reentry - post-MI, ARVD, cardiomyopathy, sarcoidosis
    4. Uncommon scar-related reentry - scleroderma, giant-cell myocarditis, ventricular incision
    5. Repaired Tetrology of Fallot (Batista) - scar related reentry
    6. ARVD is arrhythmogenic right ventricular dysplasia, a congenital cardiomyopathy [31]
  6. Diagnosis [1]
    1. Careful history with evaluation of prior events which might suggest arrhythmia
    2. Family history also important, as arrhythmias can have a genetic component
    3. Echocardiography is very important to evaluate cardiac structure
    4. Stress echocardiogram or nuclear study for patients with suspected ischemia
    5. Electrocardiogram (ECG) may identify at risk patients (long QTc, bundle branch blocks)
    6. Holter monitoring for patients with frequent events
    7. Ambulatory ECG monitoring with telephonic continuous loop monitors very helpful [4]
    8. Assess serum electrolyte levels, especially potassium, magnesium, and calcium
    9. Suggestions of arrhythmia may prompt physician to electrophysiologic testing (EPS)
  7. VT versus Superventricular Tachycardia (SVT) with Aberrancy [5]
    1. Setting of arrhythmia most helpful
    2. For example, post-MI arrhythmias are usually VTach
    3. AV dissociation nearly always implies VTach
    4. Rate of VT usually <240bpm (typically 150-220)
    5. Flipped axis, severe Left axis deviation usually VTach
    6. Absence of RS complex in all precordial leads suggests VTach
    7. Axis similar in V1-V6 usually VTach
    8. QRS usually > 140ms with VTach; if RS in precordium >100ms, then likely VTach
  8. Treatment Overview [1]
    [Figure] "Ventricular Arrhythmia Treatment"
    1. Etiology is important here
    2. Monomorphic foci should be ablated with radiofrequency methods whenever possible
    3. Children with high risk WPW should probably be treated with radiofrequency ablation [12]
    4. Implantable Cardioverter-Defibrillators (ICD) can be placed percutaneously [23]
    5. ICD are generally first line for symptomatic VTach or VF
    6. ICD is more effective than amiodarone [7,8]
    7. Amiodarone (400mg / day, high dose) may be added to ICD if frequent events occur
    8. Intravenous amiodarone (150mg IV load, 1mg/min x 6 hours) is rapidly effective [4]
    9. Amiodarone bolus 150mg may be repeated and is effective for incessant VTach [28]
    10. Amiodarone may be combined with ICD in very high risk patients
    11. Sotalol may be used in patients with EF ~35% or greater
    12. Type I anti-arrhythmics and combinations have also been used (but not recommended)
  9. Overview of ICD [23,30]
    1. ICD are highly programmable, record rhythms, and deliver 10-30J shock to heart
    2. ICD are available with dual, sensing pacing mechanisms
    3. Thus, ICD can deliver a short burst of rapid ventricular pacing that can terminate some types of VTach
    4. ICD is strongly recommended in patients with recurrent VTach or VF [6,7]
    5. ICD has been shown to reduce mortality in patients at high risk for VTach or VF
    6. Indicated for patients with reduced LV ejection fraction (LVEF <35-40%) due to CAD and who have nonsustained VTach [23]
    7. Indicated for patients with unexplained cardiac arrest or syncope with inducible VTach on electrophysiological testing
    8. ICD is as or more effective than amiodarone in essentially all settings [7,8]
    9. ICD particularly more effective than anti-arrhythmic agents with LVEF <35%
    10. Backup pacing for ICD in patients with LVEF <40% should be VVI rather than DDD [25]
    11. ICD is effective in both primary and secondary arrhythmia prevention [26]
    12. Combinations of amiodarone or sotalol with ICD will
  10. Indications for ICD Therapy [1,9,23,30]
    1. Cardiac arrest due to VF or VTach, not due to transient or reversible causes
    2. Spontaenous sustained VTach
    3. Syncope of undetermined origin with clinically relevant VTach or VF on EPS
    4. Nonsustained VTach with coronary artery disease, LV dysfunction
    5. Nonsustained VTach with EPS inducible VF or sustained VTach not suppressed by drug
  11. Infections of ICD [10]
    1. Complete device removal required
    2. Treatment with systemic antimicrobial agents
    3. Reimplantation at a remote anatomic site is effective and safe

B. Torsade de Pontes (TDP) [11]navigator

  1. Characteristics [27]
    1. Means "twisting of the points"
    2. Swinging polarity of QRS complexes change + / - from baseline
    3. Polymorphic VT usually preceded by marked QT prolongation
    4. Interspersed sinus beats usually have long QT interval
    5. QTc >0.5 seconds associated with greatly increased risk of TDP
    6. QTc = QT interval / (Square Root of the preceding RR interval)
  2. Precipitated by Prolongation of QTc Interval [27]
    1. Electrolyte abnormalities: low serum Mg2+, K+, Ca2+
    2. Tricyclic Antidepressants
    3. Type Ia Anti-arrhythmics and sotalol
    4. Amiodarone also lengthens QTc, oral has low risk of TDP; intravenous has higher risk
    5. Phenothiazines
    6. Bradycardia with atrioventricular (AV) block
    7. Congenital QT elongation
    8. Digitalis toxicity
    9. Removed from Market: Cisapride (Propulsid®), Terfenadine (Seldane®), Astemizole (Hismanal®)
  3. Women appear to be at higher risk than men for development of TDP
  4. Treatment
    1. Give 4 amps Magnesium intravenously immediately
    2. Replete potassium (caution not to cause hyperkalemia)
    3. Consider Calcium Gluconate, 2amps iv stat
    4. Overdrive pacing (ventricular or atrial) increases heart rate, prevents spells [13]
    5. ß-blockers and pacing may be useful for congenital prolonged QT syndromes
    6. Consider phenytoin (Dilantin®), which shortens QT interval
    7. Cardioversion if decompensating (200J initially)
    8. Stop (potentially) offending agents

C. Brugada Syndrome [33,34]navigator

  1. Two Types
    1. Type 1: alpha subunit of sodium channel (SCN5a) mutations, decreased Na+ current
    2. Type 2: mapped to chromosome 3p22-25, unknown ion channel dysfunction
    3. Much more common in men than women, usually presents in 3rd-4th decade
  2. ECG Changes
    1. Right bundle branch block (RBBB)
    2. J point ST segment elevation >2cm in right precordial leads (V1, V2, or V3)
    3. Slowly descending ST segments with flat or negative T waves in V1-V3
    4. ECG changes vary in individuals
    5. Sympathetic stimulation reduce findings
    6. Patients may have normal ECG at rest
    7. Administration of Type 1a (sodium blocker) anti-arrhythmic agent can precipitate ECG
  3. High incidence of sudden cardiac death (SCD)
    1. Most due to ventricular fibrillation (VF)
    2. Polymorphic VTach can also occur
    3. Usually at rest or asleep
    4. Worsening of arrhythmia with use of Na+ channel blocking agents
  4. Elevated Risk of SCD
    1. Previous episode of VTach or VF
    2. Male sex
    3. Presence of ECG changes at rest
    4. Potential to induce ventricular arrhythmias with electrical stimulation (probably)
  5. Prognosis
    1. Mortality up to 10% per year mortality in patients with previous episode
    2. ICD is treatment of choice and may reduce mortality
    3. ß-blockers and amiodarone are not effective

D. Accelerated Idioventricular Rhythm (AIVR)
[Figure] "AIVR" navigator

  1. Regular, automatic ectopic ventricular firing at 50-100 bpm
  2. Occurs due to ventricular ectopy, though not an escape rhythm (> 45 bpm)
  3. Slower than true Tachycardia
  4. Widened QRS (that is, ventricular origin) with inverted T waves
  5. Seen in digitalis intoxication and inferior myocardial infarction (MI)
  6. Most commonly seen in reperfusion following thrombolytic therapy

E. Ventricular Fibrillation (VF) navigator

  1. Zigzagging baseline; heart is a useless pump
  2. Risk Factors
    1. Atherosclerosis / Coronary Artery Disease
    2. Myocardial infarction
    3. Cardiomyopathy: any type
    4. Arrhythmias: Ventricular Tachycardia, TDP and Wolff-Parkinson-White
    5. Early repolarization on ECG in ~30% with idiopathic VFib versus 5% control subjects [35]
  3. Cardiac emergency due to very low output
  4. Cardiogenic shock immediately ensues
  5. New guidelines for use of epinephrine, vasopressin, amiodarone issued [14]
  6. Amiodarone 5mg/kg for shock resistant VF gave nearly 2X increase in survival to hospital admission compared with lidocaine []

F. Agonal Rhythmnavigator

  1. Grossly widened QRS, bizarre shape degenerates to VTach or VF
  2. Should be treated as asystole or EMD
  3. Epinephrine should be given
  4. Prognosis is very poor

G. Sudden Cardiac Death (SCD) [7] navigator

  1. SCD accounts for ~50% of all cardiovascular deaths
  2. In general, VTach or VF are believed to be major pre-morbid arrhythmias
  3. Causes
    1. Most cases occur in patients with acute MI within first 72 hours
    2. Many cases occur in patients with previous MI and scar tissue
    3. 10-15% of cases in hypertrophic or dilated cardiomyopathy
    4. Other genetic syndromes associated with VTach or VF in <5% [15]
    5. Blunt impact (including sports, violence injuries) may predisopse to SCD [16]
    6. Earthquake may also trigger SCD [13]
    7. Neuro-cardiac interactions may play a role in some cases
  4. High blood levels of long chain N-3 fatty acids associated with >70% reduced risk of sudden cardiac death in men with no prior history of cardiovascular disease [24]
  5. Anti-Hypertensive Therapy and SCD
    1. Non-potassium sparing diuretics appear to increase risk of SCD [17,18]
    2. This occurs more frequently within 1 year of initiating therapy than subsequently
    3. May be related to potassium and/or magnesium depletion
    4. ß-Blockers may increase risk of SCD in patients without coronary artery disease (CAD)
    5. However, ß-blockers protect from diuretic (and CAD) associated SCD [10]
  6. Prevention of Sudden Cardiac Death in Patients with CAD [7]
    1. Patients at risk for arrhythmias should be evaluated for arrhythmia potential
    2. Electrophysiology study should be performed to guide therapy
    3. Microvolt T-wave alternans testing (T wave analysis during stress) may identify patients at high risk for VTach or VF with low ejection fraction (EF) [29]
    4. Patients with CAD and low EF with positive T wave alternans tests had ~15% event rate versus 0% of negative T wave alternans patients at 2 years [29]
    5. ß-Adrenergic blockers are the most effective post-MI preventive therapy available [19]
    6. In general, implantable cardioverter defibrillator (ICD) is preferred therapy and may particularly useful in patients with T wave alternans
    7. Amiodarone and ICD may have similar efficacy in primary prevention of SCD in patients with ventricular arrhythmia [20]
    8. Other anti-arrhythmic agents do not substantially prevent post-MI arrhythmias
    9. Antiarrhythmic agents (except for ß-blockers and amiodarone) are associated with increased events in EPS-inducible patients who have CAD [21]
    10. No anti-arrhythmic agent (including ß-blockers and amiodarone) prevent recurrence of life-threatening arrhythmic events
    11. Only ICD have prevented recurrence of life-threatening arrhythmic events
    12. High fish oil intake associated with increased arrhythmias in patients with ICDs [32]

Resources navigator

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References navigator

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