- The QT interval predominately represents ventricular repolarization, as well as the much-shorter depolarization (QRS wave.)
- The primary concern regarding a prolonged QT interval is the potential risk for the rare life-threatening arrhythmia, Torsades de Pointes.
- The QT nomogram assesses the actual QT interval versus the heart rate from the EKG to better determine risk for TdP.
Many medications can prolong the QT interval, but how should we respond clinically?
On the EKG, the QRS wave represents ventricular depolarization; the QT interval also incorporates the longer repolarization time. Repolarization occurs by means of flux through potassium channels. It occurs more quickly as the heart rate increases, because there is less time in a shorter cardiac cycle to restore the membrane potential. This is seen as a shorter QT interval. Conversely, the QT interval lengthens at lower heart rates. When potassium channel function is impeded or delayed by certain medications, it takes longer to repolarize the ventricles and the QT interval is prolonged. The primary concern regarding QT prolongation is the potential risk of the life-threatening arrhythmia, Torsades de Pointes (TdP, “twisting of the points”). This effect is extremely rare.
QT VS. QTC – WHAT IS THE DIFFERENCE?
Most clinicians assess the QT interval based on the corrected interval that is obtained from the EKG software (i.e., the QTc interval). This “corrected” interval attempts to normalize the actual QT interval to a standard heart rate using a population-based correction factor. The correction factor can vary based on the software of the machine.
Recent investigations have shown that this may actually lead to an overcorrection of the QT interval at faster heart rates which misrepresents the risk for TdP. Overstating the risk for Torsades can lead to longer hospital stays and costly and unnecessary extra monitoring in an ICU. The researchers suggest an alternative method to evaluate the risk of TdP, which is use of the QT nomogram.1 This nomogram uses the actual QT interval and the heart rate from the same EKG as coordinates on a graph. (See nomogram below.) If the QT/HR pair plots on or above the risk line, the patient is at risk for TdP; below the line is not considered at risk. In the portion of the graph where the risk line is broken (heart rate above 110) there were insufficient data points to validate the nomogram. Tachycardia protects against Torsades. If the nomogram is not available, a QTc interval > 500 can be substituted to estimate risk. Although the nomogram was initially validated in cases of overdose from antipsychotic drugs, it is showing clinical utility for a wide range of pharmacologic agents as well as various disease states that can impact the heart.
MANAGEMENT OF A PROLONGED QT INTERVAL
If the patient is at risk for TdP, continue to monitor and repeat the EKG in 2-4 hours. Since other risk factors for Torsades are low serum potassium and magnesium, these electrolytes should be checked and maintained in the high-normal range. If TdP develops, treatment includes IV magnesium, cardiac overdrive pacing, and other interventions as appropriate (lidocaine, atropine, cardioversion).
Note: DO NOT USE sodium bicarbonate for a prolonged QT interval; it could paradoxically make repolarization time worse. Sodium bicarbonate is treatment for a wide QRS (>120 msec), which represents impaired function of the sodium (not potassium) channels.
There are many drugs that can cause a prolonged QT and this can be difficult to assess and manage. Our advice to you is to call the Missouri Poison Center. Our specially trained nurses, pharmacists and medical toxicologist can provide you with the most uptodate treatment advice.
Isbister GK. Risk assessment of drug-induced QT prolongation Aust Prescr. 2015 Feb;38(1):20-4