Torsade De Pointes, an atypical ventricular tachycardia.
- The American Journal of Cardiology 01/1979; 42(6):1054-6. · 3.21 Impact Factor
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ABSTRACT: Severe ventricular and supraventricular arrhythmias may be produced by inappropriate ventilation (hyperventilation or hypoventilation), hypoxemia or metabolic acidosis. Conventional therapy with antiarrhythmic drugs and precordial counter-shock is ineffective unless the underlying metabolic abnormalities are corrected. Nine representative patients are described and the physiologic determinants of hypoxemia and hyperventilation in the critically ill patient discussed.The American Journal of Medicine 05/1969; 46(4):495-505. · 4.77 Impact Factor
- Chest 06/1973; 63(5):661-5. · 5.85 Impact Factor
British HeartJ7ournal, 1976, 38, 117-120.
Torsade de pointes, an atypical
Dennis M. Kriklerl and Paul V. L. Curry'
'What's in a name? That which we call a rose
By any other name would smell as sweet'
W. Shakespeare, Romeo and Juliet, II, ii, 43
When defining a 'new' arrhythmia it is reasonable
to suppose that it may indeed have been recognized
many years previously. This applies to the disorder
now called torsade de pointes, whose features have
been so well worked out since it was characterized
by Dessertenne (1966, 1967). As the opening quota-
tion implies, why introduce a new name? The
poorly recognized in English and American reports
and the importance of principles relating to its
aetiology and management are so crucial that it
deserves to be better known; as its mechanism is
not yet quite clear a morphological name seems
more appropriate. Reference to a standard French-
English dictionary (Harrap's New Shorter French
andEnglish Dictionary, 1967) shows howwelltorsade
depointes describes theappearances:'torsade.,twisted
fringe, . . . twist, coil, . .
pointe, point (of pin, sword, etc.), tip, head (of
arrow, lance).. .'. Its use in French is much more
euphonious than translations like 'wave bursts'.
Though the electrocardiographic features were
first noted more than 50 years ago (MacWilliam,
(1954) described 'transient ventricular fibrillation
that its importance has been recognized. Neverthe-
less, the syndrome still receives inadequate atten-
tion: it is not mentioned in a recent otherwise
exelen edtoia on vetiua tahcri
axcellend N dioble,197)
andaNoble., 1975), and examples
under other guises in Anglo-American textbooks on
electrocardiography or arrhythmias.
we turn to the French literature for authoritative
reviews (Brochier, Motte, and Fauchier,
Slama et al., 1973; Puech, 1974), apparently obscure
difficult to classify become understandable (Bleifer
et al., 1974; Pilling and Nanton, 1974; Meijler,
am maticave bees
picted diagrammatically elsewhere (Krikler, 1974).
Thediagnosisis made from the electrocardiographic
and from any aetiological factors (Slama et al.,
multhe speous leadsarestaken
multiple simultaneous leads are taken) consist of
paroxysms of ventricular tachycardia in which the
QRS axis undulates over runs of 5 to 20 beats, with
definite changes in direction (Fig.). This has led
to the use of avarietyofdescriptiveterms for what
are clearly isolated examples of this disorder, in-
cluding 'paroxysmalventricular fibrillation' (Loeb
et al., 1968),'transient recurrent ventricular fibrilla-
tion' (Tamura et al., 1967) and 'cardiac ballet'
(Smirk and Ng, 1969). But these morphological
criteria can be deceptive, since torsade de pointes is
sometimesassociated with fairly long runs of uni-~
formQRS complexesand conventional ventricular
can be bidirectional (Slama
Attacks may be brief, consisting of only a few
complexes (when diagnosis may be difficult and be
thick bullion (of epaulet);
1929), it is only since Schwartz,
'Division of Cardiovascular Disease, Royal Postgraduate
Medical School, Hammersnith Hospital, London W12.
Krikler and Curry
showing torsade de pointes. Sinus rhythm is shown in thefirst, and in the last three, beats in
which the QT appears prolonged; precise measurement is impossible because the succeeding P
waves are merged with the preceding T waves. The first four beats of the arrhythmia show
tachycardia, bidirectional in leads II and III, succeeded by a run of tachycardia with wide
QRS complexes in which the QRS axis rotates, in an undulating fashion, the differences being
well shown by comparison ofthe three leads. The last runoftorsade depointes isprolonged, and
the QRS complex is more uniform, with a closer resemblance to classical ventricular tachycardia,
the arrhythmia terminating with another change in axisfor the lastfour beats.
Simultaneous recording of leads I, II, and III from a patient with Conn's syndrome
aided by identification of the underlying features),
or prolonged, as in the Figure, when syncope may
result. When an attack stops spontaneously it is
often with a ventricular complex intermediateinAeilg
form between the QRS of the basic tracing andthatAeilg
seen intachycardia, though sometimes the final beat
is identical to the initiating ventricular extrasystole.
Some cases do, however, progress to ventricular
fibrillation, and death is an ever-present risk in
untreated torsade de pointes.
The start of the tatchycardia is of both diagnostic
and pathogenetic importance. Whereas ventricular
tachycardia may follow an early ventricular extra-
systole falling on the T wave of the preceding sinus
beat (Smirk, 1949),in torsade depointes theinitiating
extrasystole is usually late, and if, as is often the
case, the QT interval is prolonged there is a longer
periodinwhichasynchronyof cardiac activity exists
(Pick and Katz, 1963). It is tempting to describe
the appearances as indicating chaotic cardiac action
but, as Dessertenne (1973) points out, the features
reflect a well-organized electrical process: clearly
there is mechanical inefficiency leading to poor
cardiac output, often with syncope. We have noted
the initiation of torsade de pointes in four patients
as a result of intracardiac
(Evans et al., 1976)., and think that this supports
deductions-that can be made from the morpho-
logical appearances and the fact that there is usually
underlying evidence of impaired repolarization-
that the arrhythmia is due to a re-entry mechanism
(Raynaud et al., 1969).
A cardinalaspect of torsade depointesis theunderly-
ing aetiological situation, which can often be seen or
suspected in the basic electrocardiogram of the
patient (Table). Of major importance are brady-
cardias, very often high-grade atrioventricular or
sinoatrial block. While the precise mechanism is
unclear, it has been suggested that this favours
desynchronization of cardiac activation (Han and
Moe, 1964; Han et al., 1966; Motte' et al., 1970):
the occurrence ofventriculartachycardia in apatient
suffering from heart block suggests that it is torsade
de pointes. Hypokalaemia may also provide electro-
cardiographic clues and should be excluded in all
cases of torsade de pointes; retrospective analysis of
hypokalaemia-induced ventricular arrhythmias may
show them to have been caused by torsade de
pointes (Tamura et al., 1967), and we have recently
found torsade depointes causedby Conn's syndrome
and familial periodic paralysis (Krikler et al., 1976).
While hypomagnesaemia is much less common-
and certainly less often looked for-it has been
identified as a cause of torsade de pointes (Loeb
et al., 1968).
Ventricular tachycardia is clearly a major cause of
death in patients with the congenital syndromes in
Torsade de pointes
Recognized causes of torsade de pointessubstituted, the interval returning to normal when
all psychotropic agents were stopped.
Torsade de pointes is aknown but rare complication
Kravitz, 1967), occurring so seldom perhaps be-
cause of lack of associated asynchrony ofrepolariza-
tion (Puech, 1974), but it has been recognized
during the course of so-called Prinzmetal (variant)
angina. When this is associated with paroxysmal
atrioventricular block (Chiche, Haiat, and Steff,
1974) the pathogenesis could be that of atrioven-
tricular block of any cause, but its occurrence in
this disorder in the absence of heart block (Benaim
et al., 1975) implies the presence of subtle factors
encouraging re-entry. Histologically-proven myo-
carditis has been incriminated in a single patient
(W. Somerville, 1975, personal communication), and
we are aware of anotherunpublished case.
1) Slow basic rhythm
a) Sinoatrial depression/disease
b) High-degree AV block
2) Electrolyte deficit(s)
3) Congenital QT prolongation syndromes
a) Overt, with deafness
b) Forme fruste
a) Cardioactive agents: quinidine, lignocaine, procaln-
amide, prenylamine, etc.
b) Psychotropic agents: phenothiazines, *tricyclic anti-
depressants, ? other major tranquillizers
5) Cardiac ischaemia
which the QT interval is prolonged, whether with
(Jervell and Lange-Nielsen,
without (Romano, Gemme, and Pongiglione, 1963;
Ward, 1964); indeed it may be present as a forme
fruste, with QT prolongation only apparent after
exercise (Von Bernuth et al., 1973). In at least some
of these cases the ventricular arrhythmia appears to
be torsade de tointes (Motte et al., 1970).
For many years ventricular tachyarrhythmias
have been known as a complication of quinidine
therapy (Levy, 1922), and as this drug acts in part
by prolonging repolarization it is not surprising that
torsade de pointes should be seen (Acierno and
Gubner, 1951; Rainier-Pope et al., 1962), more
often as a result of overdosage than idiosyncrasy
(Brochier et al., 1972). Though other drugs with an
action resembling that of quinidine were not noted
as causes of torsade de pointes by Brochier et al.
(1972), we have seen it twice (a new observation,
overdose of lignocaine (unpublished observations).
Several cases of the arrhythmia have been caused by
prenylamine, possibly because of its quinidine-like
effects (Bens et al., 1973). In its own right digitalis
has not been incriminated, and we would not expect
it to cause torsade de pointes as it shortens the
repolarization time. If it occurs attention should be
focussed on any concomitant medications-for
example, potassium-losing diuretics or quinidine.
Among non-cardiac drugs that may induce torsade
de pointes are phenothiazines, notably thioridazine
(Schoonmaker, Osteen, and Greenfield, 1966), and
tricyclic antidepressants. We have seen torsade de
pointes followed by ventricular fibrillation after an
overdose of amitryptiline (unpublished observa-
tions): in sinus rhythm the QT had been pro-
longed, and this persisted when haloperidol was
Certain of the aetiological factors provide important
clues to the therapy of torsade de pointes. It is
absolutely vital not to interpret the appearances as
representing ventricular hyperexcitability, for quini-
dine and similar agents given on this assumption
may disastrously aggravate the arrhythmia (Brochier
et al., 1972). We have on two occasions had to use
direct-current countershock when torsade de pointes
led to ventricular fibrillation (Krikler et al., 1976;
Evans et al., 1976), but this has only a temporary
effect. Clearly the underlying situation must be
corrected-for example, potassium should be re-
placed and quinidine or other drugs withdrawn-
but urgent action is needed upon diagnosis. The
first step should be to infuse isoprenaline intra-
venously to shorten repolarization time and thus
avoid a state of asynchronous depolarization; while
this is being done cardiac pacing may be instituted.
When heart block is the underlying cause of the
arrhythmia this is the definitive therapy; when other
causes are present it helps while such corrective
measures as are feasible-for example, potassium
infusion-are undertaken. Right atrial pacing at
100 to 120 beats a minute usually suffices, the
increased rate shortening repolarization and pro-
viding less opportunity for re-entry (Brochier et al.,
1972); if there is AV block the ventricle must of
course be paced.
Torsade de pointes can thus be seen to constitute a
definable arrhythmia with important aetiological,
pathogenetic, diagnostic, and therapeutic features:
its recognition is not an academic matter because it
requires urgent treatment quite different from that
of classical ventricular tachycardia.
it less than coincidence) after an
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