Ventricular Rhythms

• Ventricular Tachycardia

  • Characteristics:

    • Rate: 100-200  bpm

    • Regular waveform

    • Dissociation from atrial rate {no correlation with "P" wave}

    • Variable P:QRS relationship

    • No apparent PR interval

    • QRS waveform features: Wide, unusual

    • No dropped beats or groupings

  

  courtesy of  Frank G.Yanowitz, M.D. &  The Alan E. Lindsey  ECG Learning Center, used with permission; http://medstat.med.utah.edu/kw/ecg/index.html "The main features of this wide QRS tachycardia that indicate its ventricular origin is the condordance of QRS's in the precordial leads (all QRS's are in the same direction)." The above example describes "uniform" ventricular tachycardia, in which the waveforms are very similar in shape; these forms are in contrast to "polymorphic" ventricular tachycardia in which the waveforms differ in shape.

• Ventricular tachycardia Example below: 

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• Definition: Sustained ventricular tachycardia, usually symptomatic; hemodynamic insufficiency and/or evidence of cardiac ischemia

  • Duration > 30 seconds OR

  • Requires termination secondary to hemodynamic collapse

• Causes:

  • Primary reason -- secondary to chronic ischemic cardiac disease, usually subsequent to a previous myocardial infarction

    • Other associations:

      1. cardiomyopathies

      2. "prolonged Q-T syndrome"

      3. metabolic disorders

  • Anatomical abnormalities are likely responsible for most recurrent episodes of sustained uniform ventricular tachycardia

  • Acute ischemic episodes may predisposed transition from stable ventricular tachycardia intraventricular fibrillation or initiation of non-uniform (polymorphic) ventricular tachycardia

  •  Ventricular fibrillation rhythm usually begins with ventricular tachycardia

• ECG features/onset:

  • Wide-complex QRS tachycardia

  • Rate > 100 bpm

  •  Uniform shape (monomorphic) or polymorphic {beat to beat variation in shape}

  • Rate  is typically regular (may be slightly irregular)

  • Atrial activity typically associated from ventricular rhythm (atria could be depolarized subsequent to retrograde transmission)

  • Onset characteristics -- typically abrupt; Paroxysmal ventricular tachycardia is typically induced by a PVC

• Differential Diagnostic Issues:

  • Ventricular tachycardia vs. Supraventricular tachycardia with abnormal intraventricular conduction 

    • Most important clinical indicator:  presence of significant cardiovascular disease (favors ventricular tachycardia diagnosis), i.e. structural myocardial  disease

    • Presence of cannon a waves in the CVP waveform

    • 

      • The a wave occurs following atrial contraction  with attendant increase in atrial pressure and, as a consequence, large veins [No valves between veins & atrium] {image courtesy of the Committee for Advancement of University Teaching, Christian Narkowicz and Stewart Nicol, Department of Physiology, University of Tasmania, with cooperation from Carl Moller, Cardiac Unit, Royal Hobart Hospital, used with permission]

      • Large or Cannon a waves may be observed in the jugular venous pulse suggests ventricular tachycardia with AV dissociation. With AV dissociation, atrial contractions may occur against a closed tricuspid valve those producing a large retrograde ulceration.  These cannon a waves would occur irregularly as a result those dissociation between atrial and ventricular contractions.  The presence of cannon a waves suggests ventricular tachycardia

      • Hemodynamic instability -- suggestive of ventricular tachycardia

      • "Variable intensity of the S1 heart sound at the apex (mitral closure)

        •  again this is seen when there is AV dissociation resulting in varying position of the mitral valve leaflets depending on the timing of atrial and ventricular systole"--Frank G.Yanowitz, M.D.
          

      • Review -- S1 heart sound: Ventricular contraction with mitral valve & tricuspid valve closure produce the S1 heart sound More rapid development of left ventricular pressure gradients cause mitral valve to close in advance of tricuspid valve closure sometimes allowing resolution of S1 splitting. S1. Significant S1 splitting may be caused by myocardial disease. http://www.monroecc.edu/depts/pstc/parasss1.htm   

      • 

      • Specific ECG evidence supporting the diagnosis of ventricular tachycardia:

        • Rhythm regularity; sustained monomorphic QRS tachycardia (R-R equal intervals) {note that on irregularly irregular rhythm would suggest aberrant atrial fibrillation or WPW preexcitation.

        • AV dissociation-strong suggestion of ventricular tachycardia;may only occur again about 50% of cases-the remainder have retrograde atrial capture or "V-A" association.  Also it is difficult to recognize AV dissociation unless the tachycardic rate is < 150 bpm since faster rates obscure P wave identification.

        • "Bizarre" frontal-plane QRS axis (from +150^o to -90^o or NW quadrant)

        • QRS wave form similar to PVCs

        • If QRS complexes exhibit the same polarity from V1 to V6, ventricular tachycardia is likely

      • Reference for ventricular tachycardia discrimination indices:Frank G.Yanowitz, M.D. &  The Alan E. Lindsey  ECG Learning Center

    • Fusion and Capture beats

      • During ventricular tachycardia, a sinus beat may propagate to the ventricle resulting in a fusion beat which exhibits a morphology between a normal QRS complex and the abnormal ventricular form-- this phenomenon, which results from two pacemakers, is a characteristic of ventricular tachycardia

      • Similarly, critical timing allows an occasional normal SA nodal depolarization propagate normally through the AV node, producing a normal appearing QRS complex.

      • Both fusion and capture beats would be expected in ventricular tachycardia.

    • Brugada's sign: The interval from the R wave to the bottom of the S ways = 0.10 sec---characteristic ventricular tachycardia

    • Josephson's sign: a small notching near the low point of the S wave = an indicator of ventricular tachycardia

    • 

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