Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

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How Dangerous is a Long QT Segment on the ECG

Also posted over at Paramedicine 101 (now at EMS Blogs) and at Research Blogging. Go check out the excellent material at these sites.

There are many things that will lengthen the QT segment, but how much should we worry when the patient has a long QT segment, or when giving the patient a treatment that lengthens the QT segment? Are there some things that, even though they may lengthen the QT segment, may protect the heart from arrhythmia at the same time?

This prospective study was conducted to evaluate the frequency of malignant arrhythmias and to analyse the possible effect of hypothermia on the QTc interval using a continuous Holter ECG during MTH treatment.[1]

Mild therapeutic hypothermia (MTH in the paper) is one of condition these authors wanted to investigate to find out if it really does cause QT prolongation and if that QT prolongation might be dangerous. Torsades is the arrhythmia that is the main concern. It is potentially lethal, but often responds to magnesium and/or defibrillation. Cardioversion cam be used, if we can get the monitor to synchronize on the spiraling QRS complex, which is not as difficult as some would have us believe.

Torsades. Image credit. This is from a discussion of wide complex tachycardias at EMS 12 Lead.

During the inclusion period between April 2009 and December 2009 a total number of 34 patients were analysed. All patients received mild therapeutic hypothermia treatment after resuscitation according to the current guidelines and regardless of the initial rhythm.[1]

Out-of-hospital and initial in-hospital treatments were not altered for the study.

The target temperature of 33° C was maintained for 24 h. Intravenous sedation and analgesia were induced in all patients by a combination of midazolam (0.125 mg/kg/h) and fentanyl (0.002 mg/kg/h) with dose adjustment as needed. Muscle relaxation with repetitive administration of pancuronium (0.1 mg/kg) in order to prevent shivering was induced if necessary.[1]

The interesting part is what they did when they saw these dramatically prolonged QT segments.

They did nothing. We need to learn to be a little less interventionist, when it comes to stable ventricular rhythms.

Post-resuscitation care was uninfluenced by the Holter ECG results and the ICU physicians followed the standard operating procedure for cardiac arrest patients. All patients completed the cooling procedure and survived the first 48 h. Overcooling (central body temperature lower than 32° C) did not occur in any case, potassium serum levels were closely monitored and supplemented to stay within normal range and to avoid hypokalemia.[1]

They did keep the potassium in the normal range, which is not something that patients always do outside of the hospital. This is one advantage these patients have over patients being treated for excited delirium, but this is what should be expected with admitted patients.

It isn’t clear if the doctors were blinded to the Holter results, or just did not act on anything they saw. I am interested in which it was.

The number of patients with at least one VT (ventricular tachycardia) was three (8.8%) during MTH and were non-sustained without any additional treatment. Torsade de pointes were not detected.[1]

In spite of the very long QTc (median 564.47 ms), there were no cases of torsades. There were three cases of VT (≥ 30 seconds of ventricular ectopic beats), but all of these resolved spontaneously.

What happened to the good old days of having to panic and give the antiarrhythmic before the arrhythmia had a chance to go away on its own?

In one patient a maximum of 673.52 ms of QTc interval prolongation was reached after 12 h of 33° C as the highest recorded value without any additional drug treatment causing a QTc prolongation.[1]

After 24 hours at 33°, the median QTc was 564.47 ms. A QTc longer than 450 is considered prolonged, but some will be comfortable well beyond that.

17 patients (50%) were discharged with a favourable neurological outcome (CPC 1–2) whereas 50% had an unfavourable outcome (CPC 3–5). The overall mortality rate was 38.2%,[1]

An unfavorable outcome included both death and unfavorable neurological outcomes, so only 11.8% were discharged alive with unfavorable neurological outcomes.

Experimental data showed a stabilization of cell membranes during hypothermia and a higher likelihood of successful defibrillation with a better ROSC rate in a swine model due to hypothermic conditions.9,10 This indicates that MTH lowers the incidence of arrhythmias rather than raising it. One should keep in mind that more profound hypothermia <30° will increase the risk and therefore temperature should be closely monitored in patients undergoing MTH.[1]

Hypothermia does appear to protect against arrhythmia, but probably only when the hypothermia is mild.

The green line is at 450 ms, beyond which is considered to be a prolonged QTc.

The blue line is at 550 ms – a level that, if we are to believe those who are most concerned about QTc, is just begging for torsades. The patients’ rhythms should have changed to torsades long before they got to a QTc of 550 ms.

However, a QTc prolongation in elderly emergency patients (QTc ≥450 ms) has been observed in almost 544/1558 patients (35%) in a study by Seftchick et al. The most common comorbidities in this study were structural heart disease, renal failure, and stroke.14 Five percent of the patients with QTc prolongation died in the emergency department or during hospitalization but none had QTc prolongation or Torsade de pointes listed as a cause of death. Therefore a delay of repolarisation per se seems not necessarily torsadogenic.11[1]

Will a prolonged QT segment cause torsades?

Maybe, but don’t bet on it, because thaere appear to be many more factors involved, than just the QTc.


[1] Severe QTc prolongation under mild hypothermia treatment and incidence of arrhythmias after cardiac arrest–a prospective study in 34 survivors with continuous Holter ECG.
Storm C, Hasper D, Nee J, Joerres A, Schefold JC, Kaufmann J, Roser M.
Resuscitation. 2011 Jul;82(7):859-62. Epub 2011 Mar 15.
PMID: 21482009 [PubMed – in process]

Storm C, Hasper D, Nee J, Joerres A, Schefold JC, Kaufmann J, & Roser M (2011). Severe QTc prolongation under mild hypothermia treatment and incidence of arrhythmias after cardiac arrest–a prospective study in 34 survivors with continuous Holter ECG. Resuscitation, 82 (7), 859-62 PMID: 21482009



  1. Man I just wanted an excuse to say torsadogenic.

  2. if the cardiac arrest occurs due to hypothermia , and patient in persistent asystole,to get back the ROSC what should be done, like how rapidly we can correct the hypothermia and in what ways it can be corrected?

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