QT interval

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Schematic representation of normal ECG trace (sinus rhythm), with waves, segments, and intervals labeled.

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Overview

In medicine, specifically cardiology, the QT interval is a measure of the time between the start of the Q wave and the end of the T wave in the heart's electrical cycle. The QT interval is dependent on the heart rate in an obvious way (the faster the heart rate, the shorter the QT interval) and has to be adjusted to aid interpretation.

The standard clinical correction is to use Bazett's formula,^[1] named after physiologist Henry Cuthbert Bazett, calculating the heartrate-corrected QT interval QTc.

The formula is as follows:

,

where QTc is the QT interval corrected for rate, and RR is the interval from the onset of one QRS complex to the onset of the next QRS complex, measured in seconds. However, this formula tends to not be accurate, and over-corrects at high heart rates and under-corrects at low heart rates.

In the same year, Fridericia ^[1] published an alternative adjustment:

.

There are several other methods, but a regression based approach is the most accurate according to the current knowledge. An example of the regression-based approach is that developed by Sagie et al.,^[1] as follows:

QT_S = QT + 0.154(1 − RR).

Normal values for the QT interval are between 0.30 and 0.44 (0.45 for women) seconds. QT interval can be measured by different methods such as the threshold method in which the end of the T wave is determined by the point at which the component of the T wave merges with the isoelectric baseline or the tangent method in which the end of the T wave is determined by the intersection of a line extrapolated from the isoelectric baseline and the tangent line which touches the terminal part of the T wave at the point of maximium downslope.^[1]

Abnormal intervals

If abnormally prolonged or shortened, there is a risk of developing ventricular arrhythmias.

Genetic causes

An abnormal prolonged QT interval could be due to Long QT syndrome, whereas an abnormal shortened QT interval could be due to Short QT syndrome.

Due to adverse drug reactions

Prolongation of the QT interval may be due to an adverse drug reaction.^[1] Many drugs such as haloperidol^[1] can prolong the QT interval.

Prolongation of the QT Interval:

1. Represents an excess time required for completion of ventricular depolarization and repolarization.
2. Abnormal when the QTc is > 0.44 seconds.

Differential Diagnosis:

• Idiopathic long QT syndrome

1. Jervell and Lange-Nielsen syndrome
   • is associated with congenital deafness, syncope, and sudden death.
   • autosomal recessive inheritance
   • heterozygotes may be normal or have a slightly prolonged QT interval
   • incidence among deaf mute children is .25%
2. Romano-Ward syndrome
   • clinically similar to the Jervell and Lange-Nielsen syndrome except the hearing is normal
   • autosomal dominant
   • heterozygotes and homozygotes persons may have similar symptoms
3. Sporadic long QT syndrome
   • females:males = 2:1
   • 57% had a history of syncope
   • there was a strong association between syncopal episodes and emotions, vigorous activities and loud noises.
4. Pathogenesis
   • imbalance between various components of the cardiac sympathetic innervation.
5. Treatment to shorten the QT syndrome:
   • left stellate ganglion block
   • right stellate ganglion stimulation
   • the administration of propranolol ^[1]

Short QT Intervals:

Differential Diagnosis:

1. Digoxin therapy
2. Hypercalcemia
3. Secondary (acquired) types of QT prolongation

• Coronary artery disease: Ischemia, infarction
• MVP, cardiomyopathy
• CNS disease, especially hemorrhage
• Autonomic nervous system dysfunction secondary to radical neck dissection, carotid endarterectomy, transabdominal truncal vagotomy.
• Metabolic disturbances. Electrolyte imbalance (such as hypocalcemia), liquid protein diet, intracoronary injection of contrast agents.
• Cardiac medications: Quinidine, PCA, disopyramide, encainide, flecainide, propafenone, amiodarone.
• Psychotropic drugs. Phenothiazines, tricyclic antidepressants.
• Miscellaneous. Severe bradycardia, high degree AV block, post Stokes-Adams attacks, hypothyroidism, hypothermia, pheochromocytoma, organophosphate poisoning.

References

Additional resources

• ECGpedia: Course for interpretation of ECG
• The whole ECG - A basic ECG primer
• 12-lead ECG library
• Simulation tool to demonstrate and study the relation between the electric activity of the heart and the ECG
• ECG information from Children's Hospital Heart Center, Seattle
• ECG Challenge from the ACC D2B Initiative
• National Heart, Lung, and Blood Institute, Diseases and Conditions Index
• A history of electrocardiography
• EKG Interpretations in infants and children

See also

• Electrocardiogram
• Long QT syndrome.
• Short QT syndrome.

External links

Cardiac safety section in the Biopharmaceutical network

de:Elektrokardiogramm fr:Électrocardiographie he:אלקטרוקרדיוגרם lb:Elektrokardiogramm nl:Elektrocardiogram ja:心電図sv:EKG

Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .