VENTRICULAR TACHYCARDIA

    DEFINITION

    Ventricular tachycardia (VT) is a wide complex cardiac rhythm
    originating in the ventricles. The rate is usually between 150 and 200
    beats/minute and regular. There is dissociation between atrial and
    ventricular activity. The rapid rate and A-V dissociation may lead to
    reduced cardiac filling and low cardiac output, hypotension, and
    cardiac arrest. 

     Atypical ventricular tachycardia (also known as polymorphous VT or
    torsade de pointes) is a particular type of VT associated with QT
    interval prolongation.

    TOXIC CAUSES

    Many toxic substances cause ventricular tachycardia. Individuals with
    underling ischaemic heart disease are special risk.  

    Important examples include:

          Ventricular tachycardia:
         Aconite (found in certain Chinese herbal preparations)
         Amphetamines and related stimulants
         Aromatic and halogenated petroleum distillates
         Caffeine 
         Cardiac glycosides (digoxin, digitoxin)
         Chloral hydrate
         Chlorinated fluorocarbons
         Cocaine
         Quinidine and other type 1a antiarrhythmics
         Quinine
         Theophylline
         Tricyclic antidepressants

          Atypical Ventricular Tachycardia (Torsades de Pointes):
         Amiodarone
         Antihistamines (terfenadine and astemizole)
         Arsenic 
         Fluoride
         Quinidine and other type 1a antiarrhythmics
         Thioridazine

    NON-TOXIC CAUSES

    Acute myocardial infarction or ischaemia
    Congestive heart failure
    Intrinsic conduction system disease
    Hypokalaemia
    Hypocalcaemia
    Congenital long QT syndromes

    CLINICAL FEATURES

    The clinical features of ventricular tachycardia vary across a wide
    spectrum according to the cardiac output and end-organ perfusion.  The
    features of cardiorespiratory arrest may be observed, or the patient
    may be in shock with hypotension, diaphoresis, confusion or syncope. 
    Occasionally, especially in young otherwise healthy individuals, the
    patient may be virtually asymptomatic.  

    In the case of atypical VT, patients may present with abrupt onset of
    episodic dizziness, weakness, or syncope.  

    DIFFERENTIAL DIAGNOSIS

    Sinus or supraventricular tachycardia accompanied by a wide QRS
    complex

    A number of toxins may cause wide QRS complexes including:

         Chloroquine and related drugs
         Diphenhydramine
         Phenothiazines (especially thioridazine)
         Propoxyphene
         Quinidine and other type 1a and 1c antiarrhythmics
         Quinine
         Tricyclic antidepressants

    RELEVANT INVESTIGATIONS

    A cardiac monitor is essential to determine the electrical activity of
    the heart and should be applied immediately and followed continuously.

    ECG

    Serum electrolytes (including potassium, calcium and magnesium)
    Arterial blood gases
    Pulse oximetry
    Cardiac enzymes

    TREATMENT

    The patient must be treated immediately.  The priorities in management
    are as follows:

         a)   Establish a secure airway, if necessary, initially by
              positioning and suctioning, then with definitive measures
              such as endotracheal intubation.

         b)   Support breathing, if necessary, by assisting ventilation
              with a bag-valve mask device followed by mechanical
              ventilation. Administer supplemental oxygen to all patients.

         c)   Obtain intravenous access by the most rapid means possible
              and commence continuous cardiac monitoring.  If pulses are
              impalpable, assist the circulation with closed chest
              compressions until spontaneous cardiac output is
              re-established.  Direct current cardioversion of toxic
              ventricular dysrhythmias is seldom successful and should not
              take precedence over correction of hypoxia, external cardiac
              compression and administration of specific antidotes.

         d)   Other specific interventions:

              1.   Administer specific antidotes if indicated (see below)
              2.   Restore electrolyte balance.
              3.   For  Atypical or  Polymorphous VT, give intravenous
                   magnesium sulphate 5 to 10 mmol (1 to 2 g) or attempt
                   overdrive pacing.

    Note that standard antiarrhythmics are seldom effective in VT of toxic
    origin.  In fact, they usually detrimental in that they increase the
    proarrhythmic effect of the toxic compound already present. 

    Specific antidotes:

         Caffeine                      Beta blockers
         Chloral hydrate               Beta blockers
         Digitalis glycosides          Digoxin-specific Fab antibodies
         Fluoride                      Calcium
         Petroleum distillates         Beta blockers
         Quinidine and other           Sodium bicarbonate
           Type Ia/Ic agents
         Tricyclic antidepressants     Sodium bicarbonate

    CLINICAL COURSE AND MONITORING

    The prognosis for VT of toxic origin is generally more favourable than
    that of VT from other causes, provided the circulation can be
    supported through the acute phase.  Efforts at cardiopulmonary
    resuscitation, especially in young otherwise healthy individuals
    should be continued for a long period. The overall clinical course is
    dependent on the underlying agent.  Intensive monitoring and support
    of cardiorespiratory function is necessary until toxicity resolves.

    LONG TERM COMPLICATIONS

    Hypoxic brain injury

    AUTHOR(S)/REVIEWERS

    Author:        Kent R. Olson, MD, University of California,
                   San Francisco, USA.

    Peer Review:   London 3/98: T. Meredith, L. Murray, A. Nantel,
                   T. della Puppa, J. Pronczuk.
                   Geneva 8/98: D. Jacobsen, L. Murray, J. Pronczuk.