Really a listener answer.
Kelly and Ron,
As an avid listener of the show, I can’t help but comment on some of what was said on the last podcast.
Firstly, any automated reading algorithm is prone to incorrectly measure the QT interval when the t wave is low voltage or biphasic. It’s important to manually check if the T wave ends past the mid-point between R waves (for heart rates about 60-100 bpm). It’s usually at this point that the QT becomes clinically significant.
Secondly, the risk of torsades with prolonged QT is exaggerated. While all patient who go into torsades have a long QT, most patients with a long QT will not go into torsades. (see 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; and Droperidol, QT prolongation, and sudden death: what is the evidence? Kao LW, Kirk MA, Evers SJ, Rosenfeld SH. Ann Emerg Med. 2003 Apr;41(4):546-58. Review. PMID: 12658255)
Third, the function of a pacemaker magnet is to turn off any sensing functions and cause it to pace at a fixed rate. This used to be how the battery was checked (the pacing rate with magnet correlated to battery charge). If the patient has an underlying rhythm, this can be dangerous because it creates the potential for an r on t. The pacer magnet is most often used when attempting to diagnose a pacemaker mediated tachycardia in an atrial sensing pacer. When the magnet is placed on a device configured as ICD only, any anti-tachycardia pacing and cardioversion functions are disabled.
Pacemaker mediated tachycardia has two common causes. The first occurs in a pacemaker that is configured to trigger the ventricles when it senses an atrial beat. A ventricular paced beat has retrograde atrial capture, which is sensed by the pacemaker as an atrial beat, so it triggers a ventricular beat that causes another retrograde atrial beat, which is sensed by the pacemaker, etc etc etc. The second occurs when the device is set for rate modulation. Some devices are configured to increase the rate of pacing when an accelerometer senses movement (eg going up stairs). If the patient is shaking from anxiety or is having muscle spasms, it can trigger the pacer to fire too fast. This theory can be tested with a pacer magnet, and treated with your favourite benzo.
—
Mat Goebel, NREMT-P
ED-EKG Liaison
Intermountain Heart Institute EKG
Intermountain Medical Center

Matt asks:

First of all, I follow both of you on Twitter and saw that Ron passed his final, so congratulations!

I have three questions for y’all:

1) How do you tell the difference between Biot’s and Cheyne-Stokes respirations? All the definitions I’ve seen describe them as being very similar, other than the causes.

2) Do you know why Atropine when given in small doses or very slow can cause paradoxical bradycardia? I’ve asked my Paramedic instructor (who Kelly writes occasionally with for EMS World) and he didn’t know, but said he has seen it happen before. I’m fortunate enough to attend an University with a Medical School on campus and I went to their library to do some research but didn’t come up with much more information than I already knew.

The only think I could come up with, and this is purely a guess is that maybe with small dosages/slow administration of the Atropine there isn’t enough atropine (either in the total dose or concentrations of it in the blood) to fully inhibit the vagus nerve stimulation, thus lowering the HR. If y’all are interested I can send some PDF files of the studies that I read on the subject.