Torsade de pointes is a variant of polymorphic VTach that occurs in patients with a baseline prolongation of the QT interval when measured while the patient is in normal sinus rhythm (Figure 33-2). The prolonged QT, and the clinical scenario in which the two arrhythmias occur, are the only identifiable differences between torsade de pointes and polymorphic VTach.
Figure 33-2 A patient with a prolonged QT interval has a premature ventricular contraction that triggers a run of torsade de pointes. The tachycardia has all of the morphologic characteristics of polymorphic VTach, including the flipping polarity from which the rhythm derives its name (turning of the points).
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The term torsade de pointes, from which the arrhythmia derives its name, means literally the “turning of the points.” The “turning” is a morphologic feature that is obvious on Figure 33-2. Notice how this strip is identical to Figure 33-1, except for the presence of the prolonged QT interval during the normal sinus segment of the strip.
The typical rates of torsade de pointes are between 200 and 250 BPM, although rates from 150 to 300 BPM have been documented. The complexes appear to be “grouped” just as in polymorphic VTach, with each group being composed of anywhere between 5 and 20 complexes each. Once again, the “grouping” occurs because of a twisting of the polarity around a central baseline. The morphologic appearance of each of the complexes will usually vary constantly throughout the strip.
CLINICAL PEARL
The causes of QT prolongation include:
1. AMI and ischemia
2. Hypocalcemia
3. Drugs: Class IA antiarrhythmics, amiodarone, phenothiazines, tricyclic antidepressants
4. Central nervous system events
5. Hypothermia
6. Hypothyroidism
7. Congenital or idiopathic prolonged QT syndromes
Be very careful administering medications that prolong the QT to someone who has a prolonged QT!
Just as we saw in polymorphic VTach, torsade de pointes is very dependent on the underlying rate of the patient prior to the development of the tachycardia. The rate frequently develops in patients with severe bradycardia or experiencing an AV block. The arrhythmia is usually suppressed if the baseline heart rate is increased. The arrhythmia can be terminated by speeding up the tachycardia either by drugs (e.g., isoproterenol) or by overdrive pacing.
The severity of symptoms is usually associated with the duration of the tachycardia. Torsade de pointes is usually self-limiting, but it can also break down into ventricular fibrillation.
Additional Information
Prolonged QT Interval and the QTc
Most of the problems that we encounter with the QT interval are related to a prolongation of the interval. Prolongation of the QT interval is different from prolongation of the PR interval. If the PR is prolonged, it is usually because of a diseased node or some pharmacologic agent. In general, a prolonged PR interval, when it occurs by itself, is not too clinically significant. QT prolongation, on the other hand, can be life threatening. Why? Because prolonged QT intervals have a tendency to break down into very bad arrhythmias, such as torsade de pointes. Take a look at the ECG strip in Figure 33-3.
Figure 33-3 QT prolongation. If you place your caliper pins as marked by ECG caliper A, you are measuring the QT interval of the complex. You should be able to walk the calipers over (side B) and still have the pin fall before the next QRS complex. If the caliper pin falls after the next QRS complex, the distance is more than half of the R-R interval and the QT interval is prolonged.
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DescriptionThe QT interval is dependent on the underlying rate of the patient. In general, the slower the heart rate, the longer the QT interval. The faster the heart rate, the shorter the QT interval. Because of these rate-related changes, a separate measure known as the QTc has been developed. The “c” stands for corrected; corrected for rate, that is. The QTc is considered prolonged if it is over 450 ms in men and 460 ms in women, and markedly prolonged if it is over 500 ms.
A good general rule is this: If the patient is not markedly tachycardic, the QT interval should not be more than half of the R-R interval. Let’s look at Figure 33-3. If we place our calipers over the QT interval and then walk them over, the caliper marked B should be before the next QRS complex. If it is after the next QRS, you can bet that the QT is prolonged.
(Normal and abnormal QT intervals are discussed in Chapter 4, Vectors and the Basic Beat.)
Due to the more frequent occurrence of torsade de pointes, compared with polymorphic VTach, and because they are essentially only clinical variants, torsade de pointes has literally “taken over” as the main terminology used to label this rhythm presentation. In essence, people preferentially use the term torsade de pointes to refer to either of the two rhythms and frequently use the terms interchangeably. For completeness, and because the therapeutic strategies can be different, you should be aware that they are two separate arrhythmias.
The keystone to treatment of the arrhythmia is to reverse the cause of the QT prolongation if possible. Intravenous magnesium sulfate can be very effective in terminating the arrhythmia and stabilizing cell membranes in many cases. Overdrive pacing or drugs to speed the tachycardia are also useful. If the patient is hemodynamically unstable, cardioversion or defibrillation should be attempted.
Torsade de pointes is also triggered by a PVC in most cases. However, due to the prolonged QT intervals present in the baseline rhythm, the chances of the PVC being triggered during the relative refractory period are greater in these patients (Figure 33-4). As you can imagine, if the interval is longer, the chances of having an R-on-T phenomenon are much greater than they are in a patient with a normal QT interval.
Figure 33-4 A premature ventricular contraction appearing at a fixed coupling interval will not fall on the relative refractory period of a patient with a normal QT interval. However, a premature ventricular contraction occurring with the same coupling interval would fall within the relative refractory period of a patient with a prolonged QT. This R-on-T type of phenomenon will increase the likelihood of developing torsade de pointes in these patients.
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DescriptionThere is also a strong association between bigeminy in a patient with a prolonged QT interval and the development of torsade de pointes. Once again, the chances of an R-on-T phenomenon are greater in these patients.
In this section, we will spend some time going over the actual “turning of the points” that develops in these patients due to a constant change in the polarity of the complexes. First, let’s go over the actual appearance on the ECG and why we get such a strange pattern of grouping. Then, we will go into why these changes in polarity occur.
At this point in our lives, we should all be familiar with party streamers. Let’s imagine that we had a party streamer with a different color on each side, and a long, uninterrupted episode of VTach recorded on it (Figure 33-5). How do we hang party streamers? Well, we usually twist them around to create a spiral or helical appearance. This is exactly what happens in torsade de pointes. In essence, the vectors are twisting in the heart. The ECG is just simply recording the spiral effect and this spiraling gives rise to the appearance of the “twisting of the points” and the grouping.
Figure 33-5 A party streamer with a different color on each side and an episode of uninterrupted ventricular tachycardia imprinted on it. If we were to take that streamer and twist it along a horizontal axis, we would create a spiral appearance with the two colors showing at regular intervals. In addition, the tracing would be upright in some sections and inverted in the others, depending on the length of the spiral.
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This gives you a general idea of why the ECG tracings appear the way they do in patients with polymorphic VTach and torsade de pointes. Now let’s turn our attention to the actual cause of the “twisting.”
As you know, the ECG tracing is only a graphical representation of the vectors occurring in the heart. The mechanisms causing torsade de pointes are complex and are still being examined closely. They are beyond the scope of this text. But, we can use another analogy to help us understand the twisting a little better. Imagine you had a ventricular vector placed as the arrow of a game wheel (Figure 33-6). As you spin the vector, the electrical lead recording the vector would at first see the vector coming at it, then it would see it going away from it, then coming at it, and so forth.
Figure 33-6 Imagine the main electrical axis of the heart (blue and pink vector) sitting on top of a big game wheel on the surface of the heart. An electrode recording the spinning motion that Vanna placed on this vector would record an undulating pattern on the paper, depending on the orientation of the vector in relation to the electrode; in this case, it is lead II. Since the orientation of the vector is constantly changing as it spins, the pattern on the ECG undulates.
When the vector points directly at the electrode, the QRS complexes will be the tallest and in a positive direction. When the vector points directly away from the electrode, the QRS complexes will be their deepest and in a negative direction. When the vectors are facing 90 degrees to the electrode, the complexes will be the smallest.
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DescriptionA vector heading toward an electrode is recorded as a positive QRS complex. The QRS is the most positive when it is pointing directly toward the electrode. A vector heading away from an electrode is recorded as a negative QRS complex. The QRS is most negative when it is pointing directly away from the electrode. Vectors headed at a 90-degree angle from the electrode are isoelectric. Vectors falling anywhere in between these points give rise to complexes of varying sizes and polarities. It is this constant changing of the orientation of the electrical vectors in the heart that leads to the twisting pattern found in polymorphic VTach and torsade de pointes.
Remember, the picture created on the ECG or rhythm strip by each lead is different. The helical nature of the twisting in torsade de pointes can be seen in some leads but may not be evident in others. Whenever you have a very rapid wide tachycardia, and you have the time, you should try to obtain a full 12-lead ECG to evaluate the rhythm further. An irregular wide-complex rhythm at this rate could be atrial fibrillation that is completely out of control (possibly in a patient with WPW syndrome or an accessory pathway), or it could be torsade de pointes. The 12-lead ECG is a very important tool in deciding between these two possibilities. If you cannot obtain a full 12-lead ECG because the patient is unstable, then trying several different leads may also give you the information you need to make your decision.
There are quite a large number of predisposing factors that can lead to torsade. In this section, we will list them individually and give a short description of the problem. These lists are not intended to be all-inclusive, but rather to point out the most common causes.
Slow Heart Rates
Torsade de pointes is more likely to occur in patients with severe bradycardia or in patients with severe AV blocks. There appears to be a regional repolarization abnormality found in susceptible patients who develop the arrhythmia when they are bradycardic. The bradycardia in these patients is usually associated with prolongation of the QT interval.
Direct Drug Effects
Many drugs used to treat arrhythmias prolong the QT interval and cause repolarization abnormalities. These include the class IA antiarrhythmics (quinidine, procainamide, and disopyramide), adenosine, and class III drugs (sotalol, amiodarone, ibutilide). Some of the psychotropics (e.g., phenothiazines and tricyclic antidepressants) have been known to prolong the QT and lead to torsade. Intravenous haloperidol has been associated with QT prolongation. There have been many case reports for other medications, and many others have an effect on the QT interval. All of those drugs should be used with caution in patients with prolonged QT intervals at baseline.
Of the drugs listed previously that commonly cause torsade, quinidine appears to be the one that causes the most cases and amiodarone appears to have the least effect. The clinician needs to keep in mind the possible QT-prolonging effects of these drugs and assess and monitor patients accordingly.
Drug Combinations
In addition to direct effects, many drugs have been found to cause QT prolongation and an increased risk for torsade when used in combination with others. The major drugs that cause QT prolongation as a consequence of a drug-drug interaction include the antifungals (ketoconazole, fluconazole) and the macrolide antibiotics (erythromycin, clarithromycin). Two drugs that especially cause interactions with these are terfenadine and cispride.
These drugs should be used cautiously, if at all, in patients with prolonged QT intervals. The dangerous combinations mentioned previously should not be used under any circumstances, if possible.
Electrolyte Imbalances
Hypokalemia is the biggest culprit in this bunch. Hypokalemia is frequently associated with prolongation of the QT interval and the prevalence of large U waves. These findings are due to the repolarization abnormalities that are occurring in the ventricles due to the electrolyte imbalance. The repolarization abnormalities, in turn, lead to an increased propensity for torsade de pointes.
Hypomagnesemia and hypocalcemia are also associated with an increased chance of developing torsade, although they both remain a rare cause of the arrhythmia. Both prolong the QT interval and cause repolarization abnormalities.
Congenital Long QT Syndromes
There are some genetic disorders that are related to a familial predisposition to the development of sudden cardiac death due to an underlying prolongation of the QT interval. The sudden cardiac death in these cases has been caused by either torsade de pointes or ventricular fibrillation. The genetic defects in these disorders are being isolated down to the level of the ionic channels on the cell membranes.
Prolongation of the QT interval, torsade de pointes, or sudden death, and the presence of familial deafness are the key characteristics of Jervell and Lange-Nielsen syndrome. The Romano-Ward syndrome has the same prolongation of the QT interval and an association with torsade and sudden death, but these patients have normal hearing.
Clinical presentation of individual patients is variable and there are many differences among patients in the age of onset, presenting symptoms, and severity of symptoms. Syncope is a common presenting symptom for many of these patients. We have personally treated patients with these syndromes who were misdiagnosed all their lives and considered either to have psychological issues for their syncope or thought to be simply faking their symptoms. Always check the QT interval on any patient with syncope!
Acute Myocardial Infarction
Severe ischemia and AMI are associated with an increased risk of both polymorphic VTach and torsade de pointes.
Metabolic Disorders
Various metabolic disorders have been associated with the development of torsade de pointes. These include hypothyroidism, “liquid protein” or fad dieting, starvation, anorexia nervosa, intracranial hemorrhages, large strokes, and encephalitis. Finally, with the increased focus on terrorism, we should mention that poisoning with organophosphates can cause torsade de pointes.
A final word: Always keep in mind the various causes of an arrhythmia. In most cases, focused treatment of the source of the problem will help terminate the arrhythmia or will be instrumental in preventing future episodes from occurring. These principles apply to torsade, just as much as they apply to every other rhythm abnormality in this text.
Additional Information
T-Wave Alternans
There is one electrocardiographic morphologic abnormality that is rarely found in patients with torsade de pointes. We say rarely because it is rarely found on a plain surface rhythm strip or even a 12-lead ECG. However, digital or computerized signal averaging techniques are finding that micro-events of this nature are more common than expected in patients with proven torsade de pointes. That electrocardiographic morphologic abnormality is known as T-wave alternans (Figure 33-7).
Figure 33-7 T-wave alternans.
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The main point to keep in mind with T-wave alternans is that the patient will be at greater risk of developing torsade de pointes, especially if the underlying QT interval is prolonged. Close observation and a consultation with a cardiologist or an electrophysiologist are strongly encouraged.
ARRHYTHMIA RECOGNITION
Torsade de Pointes
Don’t forget: Torsade de pointes is associated with a prolonged QT interval!
| Rate: | 150 to 300 BPM |
| Regularity: | Irregular |
| P wave:
Morphology: Upright in II, III, and aVF: |
None
None None |
| P:QRS ratio: | None |
| PR interval: | None |
| QRS width: | Wide |
| Grouping: | 5 to 20 ventricular complexes |
| Dropped beats: | None |
DIFFERENTIAL DIAGNOSIS
Torsade de Pointes
This list is not inclusive but reflects the most common causes of the arrhythmia.