So I’ll be recertifying my Advanced Life Cardiac Support (ACLS) soon.
And so before my upcoming ACLS course, I’ll be reviewing my past posts relevant to ACLS and other resources relevant to Advanced Cardiac Life Support.
First I’ll review some excerpts on the diagnosis of Torsade from emedicine.medscape.com on this page.
And then on page 2 of this post I’ll review some excerpts on acute management of Torsade from Dr. Josh Farkas post, PulmCrit- A better approach to Torsade de Pointes July 2, 2018.
Here are excerpts of Torsade de Pointes from emedicine.medscape.com.
Torsade de pointes is an uncommon and distinctive form of polymorphic ventricular tachycardia (VT) characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line. Torsade de pointes, often referred to as torsade, is associated with a prolonged QT interval, which may be congenital or acquired. Torsade usually terminates spontaneously but frequently recurs and may degenerate into ventricular fibrillation.
In torsade, the morphology of the QRS complexes varies from beat to beat. The ventricular rate can range from 150 beats per minute (bpm) to 250 bpm.
This was symbolically termed torsade de pointes, or “twisting of the point” about the isoelectric axis, because it reminded the authors of the torsade de pointes movement in ballet. Most cases exhibit polymorphism, but the axis changes may not have regularity.
The definition also requires that the QT interval be increased markedly (often to ≥600 msec). Cases of polymorphous ventricular tachycardia in which the QT interval is not prolonged are treated as generic ventricular tachycardia. Torsade usually occurs in bursts that are not sustained; thus, the rhythm strip usually shows the patient’s baseline QT prolongation.
The etiology and management of torsade are, in general, quite different from those of garden-variety VT. In particular, the use of group IA antidysrhythmic drugs, which tend to prolong the QT interval, can have disastrous consequences in torsade. Differentiating between these entities, therefore, is critically important.
The association between torsade and a prolonged QT interval has long been known, but the mechanisms involved at the cellular and ionic levels have been made clearer in approximately the last decade. The abnormality underlying both acquired and congenital long QT syndromes is in the ionic current flow during repolarization, which affects the QT interval.
Six genetic variants underlying torsade are currently recognized. Genotypes LQT1 and LQT2 have slow potassium channels, while LQT3 shows defects in the sodium channels. Treatment modalities soon may be based on the genotype of the individual.
Prolongation of the QT interval may be congenital, as seen in the Jervell and Lange-Nielsen syndrome (ie, congenitally long QT associated with congenital deafness) and the Romano Ward syndrome (ie, isolated prolongation of QT interval). Both of these syndromes are associated with sudden death due to either primary ventricular fibrillation or torsade that degenerates into ventricular fibrillation.
Brugada syndrome is characterized by a coved ST segment in the right precordial leads. The syndrome may cause sudden death due to polymorphic VT resembling torsade.
Takotsubo cardiomyopathy (stress-induced cardiomyopathy) causes a predisposition to torsade. [2, 3]
The acquired conditions that predispose one to torsade either decrease the outward potassium current or interfere with the inward sodium and calcium currents, or fluxes.
Patients with torsade usually present with recurrent episodes of palpitations, dizziness, and syncope that correspond to arrhythmia episodes; however, sudden cardiac death can occur with the first episode. Nausea, cold sweats, shortness of breath, and chest pain also may occur but are nonspecific and can be produced by any form of tachyarrhythmia.
In a young patient with torsade, a diagnosis of congenital long QT syndrome should be considered, especially if a family history of sudden cardiac death or sudden infant death syndrome is present. In these patients, episodes of torsade are triggered by adrenergic stimulation such as stress, fear, or physical exertion, [17] but other predisposing factors also should be considered. See Long QT Syndrome and Long QT Syndrome Workup.
Differential Diagnosis for Torsade
[See link above for this section]
Frequent ECG monitoring is indicated for patients who are at risk due to chronic conditions or drug therapy. When the patient is in sinus rhythm, examine the QT interval. Usually, a prolonged QT interval and pathological U waves are present, reflecting abnormal ventricular repolarization. The most consistent indicator of QT prolongation is a QT of 0.60 s or longer or a QTc (corrected for heart rate) of 0.45 s or longer.
Other electrocardiographic features helpful in diagnosing torsade include its typical mode of onset and its morphology, as follows:
Patients have paroxysms of 5-20 beats at a rate faster than 200 bpm; sustained episodes occasionally can be seen
Progressive change in polarity of QRS about the isoelectric line occurs
Complete 180° twist of QRS complexes in 10-12 beats is present
A short-long-short sequence between the R-R intervals occurs before the trigger response.
Patients may revert spontaneously or convert to a nonpolymorphic ventricular tachycardia or ventricular fibrillation
- Occasionally, T-wave alternans may be seen before torsade
Torsade occurring in the setting of acquired long QT syndrome is preceded by pauses in almost all cases. In congenital long QT syndrome (adrenergic-dependent), pause dependence is found in most of the adult cases, whereas onset of torsade is not pause-dependent in children.
Failure to identify this rhythm may occur for various reasons. During very short runs of torsade, the typical twisting of the QRS complexes around the isoelectric line may not be apparent. Early events usually are short-lived. In the case of a single-lead recording, the typical morphology of torsade may not be obvious.
The diagnosis of torsade should be considered in any patient with pause-dependent ventricular tachycardia, and ventricular bigeminy in a patient with long QT interval may be a sign of an impending torsade.
Findings from electrophysiological studies usually are negative in torsade.
Check for hypoglycemia, hypokalemia, hypomagnesemia, and hypocalcemia.
Rule out myocardial ischemia, especially in patients without QT prolongation.
Chest radiographs and echocardiography should be performed to rule out structural heart disease, if any clinical suggestion is present.
Other tests should be ordered depending on the etiological factors being considered (see the section Etiology of Torsade)
Acute management
Treatment can be divided into short-term and long-term management. Short-term management of torsade is the same in both acquired and congenital long QT syndrome, except that beta1-adrenergic stimulation may be tried in the acquired form but is contraindicated in the congenital form.
In an otherwise stable patient, direct current (DC) cardioversion is kept as a last resort, because torsade is paroxysmal in nature and is characterized by its frequent recurrences following cardioversion. Although torsade frequently is self-terminating, it may degenerate into ventricular fibrillation, which requires DC defibrillation.
Any offending agent should be withdrawn. Predisposing conditions such as hypokalemia, hypomagnesemia, and bradycardia should be identified and corrected.
Long-term treatment
Beta-adrenergic antagonists at maximally tolerated doses are used as a first-line long-term therapy in congenital long QT syndrome. Propranolol is used most extensively, but other agents such as esmolol or nadolol also can be used. Beta-blockers should be avoided in those congenital cases in which bradycardia is a prominent feature. Beta-blockers are contraindicated in acquired long QT syndrome because bradycardia produced by these agents can precipitate torsade. One approach to assess the adequacy of beta-blockade is by exercise testing. One investigator recommends aiming for at least a 20% reduction in maximum heart rate compared to that of the baseline (pre-beta blocker therapy). Another approach is to check the blood levels of beta blockers (eg, propranolol) when possible. [21]
Pharmacologic therapy
Magnesium is the drug of choice for suppressing early afterdepolarizations (EADs) and terminating the arrhythmia. Magnesium achieves this by decreasing the influx of calcium, thus lowering the amplitude of EADs. [19]
And now on to Page 2 for excerpts from Dr. Farkas’ post PulmCrit- A better approach to Torsade de Pointes July 2, 2018.
