I. Problem/Condition.

The normal QT interval is measured from the beginning of the QRS complex to the end of the T wave and represents the time required for both ventricular depolarization and repolarization. The upper limits of the normal QT interval are determined by the heart rate; as a result the QT corrected for heart rate, or QTc, is often used (QTc=QT/square root of the RR interval) as a reference point. In general the QT is less than 0.46 seconds, and intervals greater than this are defined as prolonged.

A prolonged QT interval may be seen in a variety of disease states and is of clinical concern as it predisposes patients to ventricular arrhythmias, in particular Polymorphic VT or Torsades de Pointes. Patients who have a prolonged QT in addition to polymorphic ventricular tachycardia are referred to as having Long QT Syndrome independent of etiology (LQTS).

Rarely patients may present with a shortened QT interval (QTc < 360ms). This may be seen in patients with an aquired derangement causing shortening of the QT (acidosis, hyperkalemia, hypercalcemia, hyperthermia, drug effect) or in short QT syndrome (SQTS) in which patients have an inherited chanellopathy predisposing them to atrial of ventricular arrythmias (see short QT syndrome).

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II. Diagnostic Approach.

A. What is the differential diagnosis for this problem?

Diagnostic Approach Qtc>= 0.46s

A prolonged QT interval may be due to an inherited mutation of a cardiac ion channel or acquired due to medication effect, electrolyte disturbance or bradycardia. The majority of drugs that cause lengthening of the QT interval do so by blocking the outward potassium current, thus prolonging the repolarization phase of the cardiac action potential. The effect of these medications on the cardiac action potential is exacerbated by hypokalemia or hypomagnesemia; both electrolyte disturbances that in themselves can prolong the QT interval. Occasionally patients diagnosed with acquired Long QT syndrome are found to have an underlying genetic predisposition.

Both congenital and acquired forms of Long QT Syndrome (LQTS) are associated with derangements in cardiac ion flow resulting in prolongation of the cardiac action potential and/or early afterdepolarizations. However, Polymorphic VT in the acquired form is more likely to be precipitated by a ventricular premature beat followed by a compensatory pause, and as a result long and short RR intervals may be seen on the EKG. Similarly, the acquired form may be associated with bradycardia and frequent pauses, and as a result acquired LQTS is often referred to as “pause dependant”. In contrast ventricular arrhythmias in patients with the inherited form are more likely associated with catecholamine release. However, these distinctions are not absolute, may depend on the genotypic variant ot LQTS and thus there is often overlap between the two clinical entities.

The differential for LQTS can be broken down into acquired and congenital forms:

1. Acquired:

Predisposing Metabolic Disorders:





Medication Induced/Associated:This list is not exhaustive and includes the drugs most commonly associated with QT abnormalities or those drugs frequently used in the hosptial setting. If a medication is suspected to be prolonging the QT, this can be verified via established drug references (www.torsades.org)

Antiarrhythmic Drugs:

Class IA (Quinidine)

Class II (Dofetilide, Sotalol, Ibutalide)

Antimicrobial drugs (Ketoconazole, Erythromycin, Clarithromycin, Voriconazole)


Psychiatric Drugs (Haldol*, Thorazine, Tricyclic Antidepressants, SSRI’s, Risperidone)

Gastric Motility Agents (Cisapride)

Other (Methadone, HIV Protease Inhibitors)

Evidence suggests that presence of these clinical variables in addition to treatment of Haldol increases the risk of developing Torsades associated with Haldol use. In addition, Haldol given intravenously or at doses larger than usual is thought to increase the risk of Torsades in patients given this medication.

Clinical Scenarios/Disease States Associated with Long QT Interval:



HIV infection


2. Congenital (see Congenital Long QT):

LQTS is due to mutations in cardiac ion channels. In modern day nomenclature these are classified as LQT1 through LQT 12. The most commone forms are LQT1 and LQT2 (mutations in cardiac potassium channels) and LQT3 (mutation in cardiac sodium channels).

B. Describe a diagnostic approach/method to the patient with this problem.

Prolongation of the QT interval in the hospitalized patient is a relatively common occurrence. In stable patients with asymptomatic prolongation of their QT interval historical information should be obtained to try and determine the etiology with concomitant correction of electrolyte disturbances and elimination of drugs which may further prolong the QT interval.

For patients with symptomatic Long QT (e.g., arrhythmia with hemodynamic instability) the immediate approach is towards stabilization of the patient based on ACLS guidelines. Secondary to this is determination of the etiology of prolongation of the QT.

1. Historical information important in the diagnosis of this problem.

Accurate history taking should look for both precipitants of Acquired Long QT and historical information in the patient’s History of Present Illness and family tree to elicit a possible genetic component to their presentation.

Historical questions to aid in the diagnosis:

  • 1. What medications are you currently taking? Are any new?

  • 2. Have you ever experienced palpitations, near loss of consciousness or a sudden loss of consciousness?

  • 3. Has anyone in your family died unexpectedly or without clear explanation? Any family history of deaths in pools or during sleep?

  • 4. Do you or does anyone in your family suffer from deafness since childhood (seen in some patients with inherited potassium channel disorders)?

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

The physical examination in a patient with long QT generally adds little diagnostic information. When suspected, clinical exam maneuvers looking for hypothyroidism (e.g., prolonged relaxation of deep tendon reflexes) or looking for a congenital syndrome (e.g., deafness associated with Jervell and Lange Nielsen Syndrome) may be warranted.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

Laboratory testing to identify electrolyte disturbance with a basic metabolic profile in all patients with a prolonged QT is appropriate. In a select cases as suggested by patient history laboratory testing for HIV or hypothyroidism may be warranted.

In specific cases when congenitial LQTS is suspected genetic tests to esablish the diagnosis may be appropriate (see Congenital long QT).

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

The diagnosis of QT abnormality is based on measurement of the QTc interval. The QTc may be influenced by a variety of factors including: overall autonomic state, time of day and gender. In addition, accurate measurement of the QT interval may be hindered by determination of the end of the T wave, beat to beat variability (especially in states where this is exacerbated such as atrial fibrillation), prolongation of the QRS and respiratory variation. As a result, it is reccomended that:

1. The QT interval is measured over several successive beats and averaged when calculating the QTc for any individual EKG.

2. The QTc is calculated on several EKG’s in a patient in whom the QT is thought to be prolonged.

As a baseline rule for generalists, the QTC should be between 0.4 -0.46 ms.

LQTS is diagnosed in patients with a baseline long QT (acquired or congenital) with associated Polymorphic Ventricular Tachycardia or Torsades de Pontes. For patients in whom an inherited form of LQTS is suspected, additional diagnostic tests may be required (assessment of T wave alternans, QT dispersion, exercise testing, provocative testing and allocation of a LQTS score). These patients should be referred to and followed by a cardiac specialist with expertise in congenital LQTS.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

Laboratory testing outside of a basic metabolic profile should be guided by patient history (see diagnosis above).

III. Management while the Diagnostic Process is Proceeding.

A. Management of Clinical Problem QT Interval Abnormalities.

The management of Long QT depends on the clinical scenario and can be divided into:

Acute Management of Prolonged QT Associated with Ventricular Arrhythmia

(see ACLS algorithims at http://www.acls.net/aclsalg.htm):

In this setting the goal is to stabilize the patient; any evidence of hemodynamic instabillity requires defibrillation according to ACLS guidelines. Patients who do not yet manifest hemodynamic instability but have Torsades may be appropriate for intervention prior to defibrillation:

Hemodynamically unstable >>> Defibrillate

VT with stable BP>>> Brief trial of IV Magnesium (2 g IV bolus over 1-2 minutes followed by repeat dosing in 15 minutes if needed) >>> if no response and still hemodynamically stable >>> temporary overdrive pacing or administration of Isoproterenol to increase heart rate

Management of Prolonged QT in Patient Without Evidence of Associated Arrhythmia

Due to Acquired Cause: The management is based on the severity of the QT prolongation and the underlying etiology. In almost all situations correction of electrolyte abnormalities is warranted. Management of QT prolonging drugs may depend on the underlying need for the pharmacologic intervention and the overall risk of Torsades as a result of the prolonged QT. In some cases, QT prolonging drugs may be continued with close medical observation when there is no evidence of existing or previous arrhythmias and the overall risk of Torsades is thought to be acceptably low. Conversely, many medical situations occur in which the appropriate intervention is to stop any medications thought to prolong the QT.

Due to Inherited LQTS (see Congential Long QT)

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem.


IV. What's the evidence?

“Goldberger: Clinical Electrocardiography: A Simplified Approach”. Basic ECG Measurements and Some Normal Values. 2011.

Roden, DM.. “Drug-Induced Prolongation of the QT Interval”. NEJM. vol. 350. 2004. pp. 1013-1020.

Birati, EY, Belhassen, B, Bardai, A, Wilde, AA, Viskin, S.. “The site of origin of torsade de points”. Heart. vol. 97. 2011. pp. 1650-1654.

Haddad, PM, Anderson, IM.. “Antipsychotic-related QTc prolongationtorsade de pointessudden death”. Drugs. vol. 62. 2002. pp. 1649-1671..