Many emergency practitioners and even many cardiologists are unsure of what to do with the QT interval on an ECG. This recommendation is a prime example of the confusion: “Potassium ion repletion to 4.5 to 5 mmol/L may be reasonable for patients who take QT-prolonging drugs and present with few episodes of torsades de pointes in whom the QT remains long. Level of Evidence: C.”
That's from the “Guidelines for Management of Patients with Ventricular Arrhythmias and Prevention of Sudden Death.” (J Am Coll Cardiol 2006;48:e247; http://bit.ly/2PdxLNi.)
The authors here performed a feat of equivocation rarely attempted even in the committee-based guideline competition. Authors unsure of what to recommend will say that some action is reasonable or can be considered. That's the verbal equivalent of a shrug. But to say that something may be reasonable increases the confusion, that the authors are uncertain about their uncertainty. This befuddlement is also based on the lowest quality of evidence.
What to do with a long QT interval is not unimportant. We know that a prolonged QT will increase the risk of polymorphic ventricular tachycardia (torsades de pointes) and sudden cardiac death.
Let's say a healthy young man overdosed on an unknown medication. His vital signs are unremarkable except for a heart rate of 120 bpm. How do we assess the QT interval on his ECG and determine if intervention is needed? This is complicated by a lack of standardization in measurement, correction for heart rate, and a cut-off above which the interval is considered abnormal. (Clin Toxicol 2015;53:189.)
Measurement: I was taught that a prolonged QT could be determined by eyeballing the ECG to see if it was more than half the associated RR interval. This was never adequately tested and lacks scientific validity. A small study showed that this rule was unreliable, lacking sensitivity and specificity especially when the heart rate is extremely fast or slow. (Acad Emerg Med 2015;22:1139.) Many clinicians will read the QT interval off the computerized ECG report, but these results are also unreliable. The most accurate way to determine the QT interval is probably manually, but this may involve measuring the interval in multiple leads and averaging the results, a cumbersome procedure rarely done in practice.
The QT interval is measured from the beginning of the QRS complex to the end of the T wave, the full cycle of cardiac depolarization and repolarization. (Figure.) It is most frequently measured in leads I, II, V5, and V6. Where unusual morphology makes it difficult to determine the true end of the T wave, a tangent can be drawn along the steepest slope of the terminal T wave; the end of the QT interval is where that tangent intercepts the isoelectric line. Studies have shown that interobserver agreement is poor and the results vary significantly when cardiologists determine QT intervals.
Correction: The duration of the QT interval is inversely related to heart rate; it will increase with bradycardia and decrease with tachycardia. When determining if the QT is prolonged, the measured interval is often corrected to a standard heart rate of 60 bpm.
There is no agreement on the best way to make that correction. The most common method is Bazett's, in which the corrected QT interval equals the measured QT divided by the square root of the preceding RR in seconds. This method is also used by many ECG machines and medical calculation apps. Bazett's, however, undercorrects in bradycardia (missing many abnormally prolonged QTs) and overcorrects in tachycardia (identifying normal QT intervals as worrisome.) It is only accurate when the heart rate is close to 60 bpm, in which case the QTc roughly equals the measured QT.
Cut-Off: There is also no agreement about what constitutes a prolonged QT interval. When the measured interval is corrected for heart rate, none of the common formulas has demonstrated acceptable sensitivity and specificity in large trials. A QT nomogram, popular in Australia but not validated in a large prospective study, plots the uncorrected QT interval against the pulse rate to separate abnormal from normal QT intervals. (Clin Toxicol 2015;53:189.)
Torsades de pointes (TdP) is rare in acute intoxication, and there is no agreement about what intervention if any is required even if the QT interval is prolonged. Administering magnesium will tend to suppress recurrent TdP without decreasing the QT interval, but no good data support using magnesium empirically to prevent TdP. Supplementing potassium to a serum level in the high normal range (4.5-5.0 mEq/L) would be reasonable in an acutely intoxicated patient who presents with a prolonged QT interval, but surveys of toxicologists show absolutely no consensus on it.
Paying careful attention to the QT interval is essential if a patient's presentation is consistent with TdP—unexplained syncope, seizures, or cardiac arrest, for example. Supplementing magnesium and potassium if necessary is important if there is any suspicion that the QT may be prolonged, as is reviewing the patient's medications to see if they are contributing to the ECG abnormality.
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