PROLONGED QT INTERVAL
- CARDIAC ELECTROPHYSIOLOGY
- Heart muscle cells are negatively charged at rest. When the heart's electrical system is activated, a positive wave of electricity (depolarization) passes through the heart. The wave causes
positive ions (Na+ and Ca++) to rush into muscle cells, and they contract (see cardiac conduction).
- After contraction, the muscle cells must regain their negative charge (repolarization). One way they accomplish this is by opening potassium channels (K+) so that positively-charged potassium ions will leave the cell.
- The QT interval begins at the very start of the QRS complex and ends at the end of the T-wave
- The QT interval encompasses ventricular depolarization and repolarization
- Measuring the QT interval
- The length of the QT interval varies depending on the heart rate; it is shorter at faster rates
and longer at slower rates. Because of this variability, the QT interval is often "corrected" for the heart rate. The corrected QT interval is abbreviated as QTc.
- The Bazett formula (see below) is the most widely used method for calculating the QTc, but it has been criticized for being inaccurate at faster heart rates. Modern ECG machines typically calculate and report the QTc automatically.
- A normal QTc is ≤ 400 ms, and a prolonged QTc is > 500 ms
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- A normal QTc is ≤ 440 ms, and a markedly prolonged QTc is > 500 ms.
- QT prolongation occurs when the ventricles are unable to repolarize normally, and its causes may be congenital or acquired
- Risk factors for prolonged QT interval
- Older age
- Female sex
- Low left ventricular ejection fraction
- Left ventricular hypertrophy
- Cardiac ischemia
- Slow heart rate
- Energy drinks 
- Hypocalcemia 
- Physiology of QT prolongation
- QT interval prolongation occurs when potassium channels that facilitate repolarization are abnormal or blocked. Genetic defects may cause irregular channels that slow repolarization (congenital long-QT syndrome), medications may block the channels, or a combination of the two may be present. No matter the cause, when repolarization is slowed, there is an increased risk of arrhythmia, specifically torsades de pointes which can be deadly (see torsades de pointes).
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- Torsades de pointes is a heart arrhythmia classified as a polymorphic ventricular tachycardia. Its name is derived from its distinctive appearance on an ECG; torsades de pointes is French for "twisting of points." The exact mechanism of torsades de pointes is not completely understood, but it is thought to occur when QT prolongation leaves heart muscle vulnerable to reentrant tachycardias that cause waves of depolarization traveling in a circular path.
- Medications and torsades de pointes
- As more studies have evaluated the effects of drugs on the QT interval, QT prolongation warnings have become a common alert from drug interaction checkers. Unfortunately, there is not a lot of definitive guidance on handling these warnings, and it can be difficult to determine which ones are relevant. Two websites that provide information on medication-induced QT prolongation are provided below.
- CredibleMeds - database of medications that have been associated with QT prolongation along with recommendations for their use
- MedSafety Scan - app that provides QT prolongation information based on patient history and medication list
- 1 - PMID 12709470 - JAMA review
- 2 - PMID 14999113 - NEJM review
- 3 - PMID 31137991 - Impact of High Volume Energy Drink Consumption on Electrocardiographic and Blood Pressure Parameters: A Randomized Trial. J Am Heart Assoc (2019)