Long QT Syndrome (LQTS) is a condition purely diagnosed by an electrocardiogram (ECG). This condition is represented by a long QT interval, hints the name. This represents delayed ventricular repolarization. This condition can be genetic or induced by certain prescribed medications.
How do I detect it?
Easy, as the name implies, measure the QT/QTc interval. The image below shows that the QT interval begins at the very end of the PR Interval, where your isoelectric line will begin another positive or negative deflection, and it ends at the very end of the T wave. Lead II is generally a good place to make your measurement. This may change depending on the R axis.
Normal QT intervals are between 300 & 450ms (0.30 - 0.45 seconds)
An easier way to measure is by looking at your 12-lead diagnostics. While rhythm interpretation may not always be up to par with your monitor; the measurements are usually pretty accurate.
What is the difference between QT & QTc?
The c in QTc stands for corrected. The QTc is the QT interval with a formulated correction based on the patient's heart rate (HR). The faster the HR the shorter the QT interval. The QTc may not always be accurate, but is commonly used for diagnostic purposes. Bazett's formula is used to determine QTc (well according to wikipedia it is).
Why is LQTS bad?
Remember the term refractory period?
Here is your refresher:
The absolute refractory period is the interval during which a second action potential absolutely cannot be initiated, no matter how large a stimulus is applied.
The relative refractory period is the interval immediately following during which initiation of a second action potential is inhibited but not impossible.[1]
Well people with LQTS have a prolonged refractory period, this includes a prolonged relative refractory period. As the definition explains, the relative refractory period tries not to but may invite pre-excitation. What this means is that another beat, from another part of the heart, may occur.
One example of aberrancy due to abnormal refractory period is Ashman's phenomenon. This is an arrhythmia with what is called a "long-short cycle". In atrial fibrillation, you may see a string of QRS complexes with longer R-R intervals (long cycle) followed by a PVC or a run of what looks to be PVCs. This will be followed by QRS complexes with shorter R-R intervals (short cycle). This is caused by pre-excitation during the relative refractory period, and the "PVC" is actually an aberrantly conducted supraventricular complex (bundle branch block pattern). The conduction was delayed due to a busy electrical pathway. Picture a traffic jam in the hearts one lane electrical highway. Below is an example, look at the R-R intervals pre & post premature beat.
Another complication of a longer refractory period is what is known as R on T Phenomenon. This condition may be more severe because it may interfere with hemodynamic stability. A premature complex finds it's home on the tail end of a supraventricular complex and takes over. While the ventricles are attempting to repolarize another focus decides he wants to take over. The best way to do this is by depolarizing while the other pacemaker is repolarizing. Like attacking a sleeping enemy. Below is another image stolen from Google. Those complexes are ventricular in origin.
Another risk associated with LQTS is sudden cardiac arrest. That one doesn't need much explanation. The cause is most likely an arrhythmia brought on by the R on T phenomenon.
More on LQTS to come. If any information I have provided is thought to be inaccurate, please let me know (Tom). I have no problem with being wrong, there is a first time for everything (hopefully sarcasm was detected).
*Once again, all images stolen from Google searches.
3 comments:
Adam -
You're doing fine. I would just add that any lead that shows an unambiguous onset of the QRS and termination of the T wave is a good lead to measure the QT interval.
My main concern with a prolonged QT interval (right or wrong) is Torsades de Pointes degenerating into VF. I've never really investigated whether or not the TdP is preceded by R-on-T.
So how long is too long? I teach that a QTc > 460 ms is prolonged (that the upper range of normal for females).
Prolongation of the QT interval is one of the most common reasons the FDA gives a medication a "black box" warning.
Hypokalemia is also a common cause of prolonged QT interval, and unless you correct the underlying electrolyte imbalance, Torsades is likely to come back (which is sometimes a reason for multiple shocks by an ICD).
The first drug of choice is magnesium sulfate, but what if it doesn't work? Do you give amiodarone, which is known to prolong the QT interval? Or do you use lidocaine, which is known to shorten the QT interval?
It's also worth mentioning that you should not attempt synchronized cardioversion for Torsades de Pointes. It's polymorphic, so use an unsynchronized shock (defibrillation) for the unstable patient.
Tom
My main concern with a prolonged QT interval (right or wrong) is Torsades de Pointes degenerating into VF. I've never really investigated whether or not the TdP is preceded by R-on-T.
Way to blow the surprise. This is a topic planned for my next post, since it is the most common and lethal arrhythmia related to LQTS.
I'm not quite sure if the torsades is caused by the R on T either. The arrhythmia statement I made was based on an assumption. I will research R on T as it relates to torsades specifically though.
I don't want to get too deep into the physiology, since the medic mentality is often "what will that change?". I really do want to stress the danger of LQTS though and hopefully keep people reading enough to get that.
So how long is too long? I teach that a QTc > 460 ms is prolonged (that the upper range of normal for females).
I didn't mention that females have slightly longer QTs, good point.
> 460ms is generally accepted as prolonged. However I would be cautious with any patient that presented with symptoms of LQTS around 450 ms. We are just prompting preparation for an arrhythmia anyhow, not initiating treatments.
Hypokalemia is also a common cause of prolonged QT interval, and unless you correct the underlying electrolyte imbalance, Torsades is likely to come back (which is sometimes a reason for multiple shocks by an ICD).
The first drug of choice is magnesium sulfate, but what if it doesn't work? Do you give amiodarone, which is known to prolong the QT interval? Or do you use lidocaine, which is known to shorten the QT interval?
It's also worth mentioning that you should not attempt synchronized cardioversion for Torsades de Pointes. It's polymorphic, so use an unsynchronized shock (defibrillation) for the unstable patient.
You have just given me some great stuff to mention in the next post. Part 3 will cover Torsades, sudden cardiac arrest associated with LQTS, Hypokalemia, and the role of the paramedic when it comes to LQTS (I will cover the dysrythmics & cardioversion with this).
Is there a maximum HR up to which LQTS can be detected? It would seem that after a certain point the complexes would be too close to detect any meaningful elongation. Is LQTS something that is paroxysmal, or present with all complexes ?
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