Excerpt for Torsade De Pointes, A Simple Guide To The Condition, Diagnosis, Treatment And Related Conditions by , available in its entirety at Smashwords

Torsade De Pointes,





The Condition,




Related Conditions


Dr Kenneth Kee

M.B.,B.S. (Singapore)

Ph.D (Healthcare Administration)

Copyright Kenneth Kee 2018 Smashwords Edition

Published by Kenneth Kee at


This book is dedicated

To my wife Dorothy

And my children

Carolyn, Grace

And Kelvin

This book describes Torsade de pointes, Diagnosis and Treatment and Related Diseases which is seen in some of my patients in my Family Clinic.

(What The patient Need to Treat Torsade de pointes)

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Thank you for respecting the hard work of this author.


I have been writing medical articles for my blog (A Simple Guide to Medical Disorder) for the benefit of my patients since 2007.

My purpose in writing these simple guides was for the health education of my patients.

Health Education was also my dissertation for my Ph.D (Healthcare Administration).

I then wrote an autobiolographical account of his journey as a medical student to family doctor on his other blog

This autobiolographical account “A Family Doctor’s Tale” was combined with my early “A Simple Guide to Medical Disorders” into a new Wordpress Blog “A Family Doctor’s Tale” on

From which many free articles from the blog was taken and put together into 800 eBooks.

Some people have complained that the simple guides are too simple.

For their information they are made simple in order to educate the patients.

The later books go into more details of medical disorders.

The first chapter is always from my earlier blogs which unfortunately tends to have typos and spelling mistakes.

Since 2013, I have tried to improve my spelling and writing.

As I tried to bring the patient the latest information about a disorder or illness by reading the latest journals both online and offline, I find that I am learning more and improving on my own medical knowledge in diagnosis and treatment for my patients.

Just by writing all these simple guides I find that I have learned a lot from your reviews (good or bad), criticism and advice.

I am sorry for the repetitions in these simple guides as the second chapters onwards have new information as compared to my first chapter taken from my blog.

I also find repetition definitely help me and maybe some readers to remember the facts in the books more easily.

I apologize if these repetitions are irritating to some readers.

Chapter 1

Torsades de pointes

What is Torsades de pointes?

Torsades de pointes is a distinctive polymorphic ventricular tachycardia in which the QRS amplitude differs and the QRS complexes seem to twist around the baseline.

Torsades de pointes (French for “twisting of the points”) is linked with a prolonged QT interval, which may be congenital or acquired

Torsades de pointes is normally not sustained and ceases spontaneously but often returns unless the underlying cause is treated.

Torsades de pointes may deteriorate into sustained ventricular tachycardia or ventricular fibrillation.

Torsades is a life-threatening arrhythmia and may manifest as sudden cardiac death in patients with structurally normal hearts.

What is the cause of Torsades de pointes?


Torsades de pointes is one of several forms of life-threatening heart rhythm abnormalities.


In the case of torsades de pointes (TdP), the two lower chambers of the heart, called the ventricles, beat faster than and out of sync with the upper chambers, called the atria.

An abnormal heart rhythm is called an arrhythmia.

When the heart beats much faster than normal, the disorder is called tachycardia.

TdP is an abnormal type of tachycardia that occasionally recovers on its own, but can also become worse developing into a serious heart disorder called ventricular fibrillation.

Ventricular fibrillation can result in cardiac arrest, an event in which the heart suddenly stops.

Cardiac arrest is normally fatal.

Risk factors

1. Congenital long QT syndromes such as:

a. Jervell and Lange-Nielsen syndrome,

b. Romano-Ward syndrome.

2. Acquired long QT syndromes:

3. Acute myocardial infarction.

4. Drugs such as:

a. Anti-arrhythmic agents of classes Ia and III,

b. Erythromycin,

c. Ketoconazole,

d. Tricyclic antidepressants,

e. Methadone,

f. Antipsychotics

5. Electrolyte disturbances:

a. Hypo-kalemia,

b. Hypo-magnesemia,

c. Hypo-calcemia.

6. Acute kidney injury

7. Liver failure.

8. Metabolic:

a. Hypothyroidism,

b. Anorexia nervosa,

c. Malnutrition.

9. Bradycardia:

a. Sinoatrial disease,

b. Atrioventricular (AV) block.

10. Toxins:

a. Heavy metals,

b. Insecticides.


TdP can be an after effect of a rare disorder called long QT syndrome.

Most people with long QT syndrome are born with it, though the patient can get it later in life.

Q and T are two of the five waves tracked in an ECG.

The electrical activity in the heart that happens between the Q and T waves is called the QT interval.

A QT interval is measured from the start of the Q wave through the end of the T wave.

If this interval is abnormally long, the patient is at a higher risk for ventricular tachycardia and TdP.

Researchers could find only 46 reported cases of TdP between 1978 and 2011.

In nearly all of these cases, TdP coincided with a long QT interval.

These were peri-operative TdP cases, meaning they were evident before someone went through heart surgery.

In some instances, heart surgery can result in arrhythmias.

TdP episodes may be precipitated by the usage of certain drugs.

These drugs are certain antibiotics and antipsychotics in addition to other medications.

Tricyclic antidepressants may also put the patient at higher risk of TdP.

Certain anti-arrhythmia drugs, which are planned to restore a healthy heart rhythm for people with arrhythmias, are also linked with TdP.

Some of these anti-arrhythmic drugs are:

1. Quinidine

2 .Procainamide

3. Disopyramide

The patient may also be at a higher risk for TdP if the patient is low in potassium or magnesium or have liver or kidney disease.


The corrected QT interval is longer in the white population than in the black population, and longer in females than males.

Torsades de pointes is more frequent in white races and in females

Torsades happens at any age.

If it happens at an early age, the cause is normally due to congenital long QT syndrome.

In later years, the cause is normally because of acquired long QT syndrome.

What are the symptoms of Torsades de pointes?


TdP can appear without warning.

The patient may rapidly feel the heart beating faster than normal, even when the patient is at rest.

In some TdP episodes, the patient may feel light-headed and faint.

In the most severe cases, TdP can induce cardiac arrest or sudden cardiac death.

It is also possible have an event (or more than one) that recovers quickly.

This form of ventricular tachycardia is known as “unsustained.”

“Sustained” ventricular tachycardia interrupts the normal functioning of the heart.

Events of torsades in patients with congenital long QT syndromes may be precipitated by stress, fear or physical exertion.

Patients with torsades normally manifest with repeat occurrence of episodes of palpitations, dizziness, and syncope.

Sudden cardiac death can happen with the first episode.

Some symptoms happening are:

1. Nausea,

2. Pallor,

3. Cold sweats,

4. Shortness of breath and

5. Chest pain

A history of congenital deafness or a family history of sudden death may suggest a long QT syndrome.

Physical findings are dependent on:

1. The rate and duration of tachycardia and

2. The degree of cerebral hypo-perfusion.

Findings are:

1. Rapid pulse,

2. Low or normal blood pressure, and

3. Transient or prolonged loss of consciousness.

Other physical signs depend on the cause - e.g., features of a congenital disorder.

How is Torsades de pointes diagnosed?


Diagnosis starts with a medical history and physical examination.


An electrocardiogram (ECG) measures the heart’s electrical activity.

The heartbeat is regulated by electrical signals that start at the top of the heart and travel down to the ventricles.

Along the way, the heart contracts and pumps blood out to the body.

An electrocardiograph tracks the electrical signals all the way through this process and then displays them as wavy lines on an ECG.

If the patient has TdP, the lines look like row after row of twisted ribbon.

1. ECG:

a. Paroxysms of 5-20 beats, with a heart rate faster than 200 beats per minute.

Sustained episodes are occasionally seen.

b. Progressive change in polarity of QRS about the isoelectric line occurs with complete 180° twist of QRS complexes in 10-12 beats.

c. Usually, a prolonged QT interval and pathological U waves are present.

The most consistent indicator of QT prolongation is a QT of 0.60 seconds or longer or a QTc (corrected for heart rate) of 0.45 seconds or longer.

QTc = QT interval divided by the square root of the interval (in seconds) between the onset of each QRS complex (Bazett's formula).

d. A short-long-short sequence between the R-R interval occurs before the trigger response.

2. Electrolytes; hypo-kalemia, hypo-magnesemia and hypo-calcemia.

3. Cardiac enzymes; assessment for myocardial ischemia.

4. CXR and echocardiography, to rule out structural heart disease.

What is the treatment of Torsades de pointes?


Short-term treatment

1. Resuscitation

2. Defibrillation:

While torsades is often self-terminating, it may develop into ventricular fibrillation, which requires defibrillation

In an otherwise stable patient, direct current (DC) cardioversion is normally a last resort

This is because torsades is paroxysmal in nature and often recurs after cardioversion.

There should be a discontinuation of any offending agent (stop all QT-prolonging drugs) and correction of any underlying cause such as:

1. Hypo-kalemia,

2. Hypo-magnesemia and

3. Bradycardia.

Intravenous magnesium is the drug of choice for torsades de pointes.

Magnesium is effective even in patients with normal magnesium levels.

Acceleration of the heart rate can be achieved by using beta 1-adrenergic agonists such as isoprenaline or overdrive electrical pacing.

Isoprenaline is used as an interim treatment until overdrive pacing can be started:

1. Isoprenaline accelerates AV conduction and decreases the QT interval.

2. It can be used in bradycardia-dependent torsades that is usually associated with acquired long QT syndrome.

3. Isoprenaline is given as a continuous intravenous infusion to keep the heart rate faster than 90 beats per minute.

4. Beta-adrenergic agonists are contra-indicated in the congenital form of long QT syndrome.

Temporary transvenous pacing:

Pacing can be effective in stopping torsades by increasing the heart rate and so reducing the QT interval.

Atrial pacing is the preferred mode because it preserves the atrial contribution to ventricular filling.

In patients with AV block, ventricular pacing can be used to suppress torsades.

Long-term treatment

Patients without syncope, ventricular tachyarrhythmia or a family history of sudden cardiac death can be observed without starting any treatment.

Congenital long QT syndrome:

Beta-adrenergic antagonists are used as a first-line long-term therapy in congenital long QT syndrome.

Propranolol is has been the most extensively used.

Beta-blockers are contra-indicated in acquired cases because bradycardia produced by these agents can precipitate torsades.

They should also not be used in those congenital cases in which bradycardia are a main feature.

Permanent pacing benefits patients who remain symptomatic in spite of receiving the maximally tolerated dose of beta-blockers

It can be used in addition to beta-blockers.

High left thoracic sympathectomy is effective in patients who remain refractory to beta-blockade and pacing.

Implantable cardioverter-defibrillators (ICDs) are useful in rare instances when torsades still persists in spite of all of these treatments.

Beta-blockers should be used along with ICDs because shock can further precipitate torsades by adrenergic stimulation.

Acquired long QT syndrome:

Long-term treatment in acquired cases is normally not needed because the QT interval returns to normal once the predisposing factor has been treated.

Pacemaker implantation is effective in cases that are linked with heart block or bradycardia.

ICDs are indicated in cases that cannot be treated by avoidance of any specific precipitating factor.

If the patient is diagnosed with TdP, the doctor will examine the potassium, magnesium, and calcium levels.

If they are low, the patient will be given these supplements to get the levels up into the healthy range.

The patient will also undergo ECG monitoring until the heart returns to a normal rhythm.

The doctor may prescribe anti-arrhythmic drugs to help resolve the present TdP episode and to prevent future events.

If the doctor decides that the patient is at high risk for more TdP episodes, they may advise the patient to have a pacemaker implanted in the chest.

This will help keep the heart beating at a safe rhythm.

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