“Unstable v-tach.”
“What is your plan?” I ask
“Unstables get the cables, man.” He smirks as he hits the button and starts charging the monitor… “I’m going to shock’em.”
I give him a quizzical look, like he is forgetting something. “ I mean, synchronized cardiovert…” as he pokes the sync button, I nod in agreement with a grin.
“Nice catch. Do your thing, man.”
Fast-forward to the debrief. He has the correct impression, a sound treatment plan, and executes it well.
What more could an instructor ask for? He is going to be a fine paramedic. Time to push him.
“Hey, what would you do if that blood pressure was 110/62?” I ask.
“150 of amio over ten minutes. Since they’re stable.”
“That is what I was afraid you would say…”
Stop and think… If unstable gets the cable, what should stable get?
What should we do for “stable” wide complex tachycardias?
Are antiarrhythmics really the next best/safest thing to do?
Here is how the protocol he has memorized is written:
Unstable, in fact does get synchronized cardioversion, but the interesting thing is the box under “No” indicating that the patient is hemodynamically stable: “Treat underlying non-cardiac causes, if present.” What are some non-cardiac causes of wide complex tachycardia (WCT) and how can we test for them?
It may be a fool’s errand to simply rely on the 12-lead EKG to differentiate non-cardiac causes of WCT. But we do not have a way to look at things like electrolytes or blood gasses (generally) at the scene. So, unless it is blatantly obvious (like on an EKG), we can assume a non-cardiac cause is not present and drive on with an amiodarone infusion. Right? It will convert the rhythm, and it is the recommended action by the AHA in our ACLS classes.
At first glance it does seem like amiodarone or even lidocaine are great alternatives to synchronized cardioversion in a well-tolerated wide complex tachycardia. But what if it was not ventricular tachycardia? What else looks like a VT but is actually more dangerous and sinister? What is the harm anyway?
Unstable, in fact does get synchronized cardioversion, but the interesting thing is the box under “No” indicating that the patient is hemodynamically stable: “Treat underlying non-cardiac causes, if present.” What are some non-cardiac causes of wide complex tachycardia (WCT) and how can we test for them?
It may be a fool’s errand to simply rely on the 12-lead EKG to differentiate non-cardiac causes of WCT. But we do not have a way to look at things like electrolytes or blood gasses (generally) at the scene. So, unless it is blatantly obvious (like on an EKG), we can assume a non-cardiac cause is not present and drive on with an amiodarone infusion. Right? It will convert the rhythm, and it is the recommended action by the AHA in our ACLS classes.
At first glance it does seem like amiodarone or even lidocaine are great alternatives to synchronized cardioversion in a well-tolerated wide complex tachycardia. But what if it was not ventricular tachycardia? What else looks like a VT but is actually more dangerous and sinister? What is the harm anyway?
At the risk of being redundant, here is a little bit of depth for each of Dr. Mattu’s examples:
Hyperkalemia : The really wide and bizarre (in some cases) appearing QRS complexes are due to alteration in the electrical conduction of cardiac cells, specifically, the speed at which the electrical impulse travels through the myocardium. This is happening because the sodium/potassium pump function of the cardiac cells is being altered due to a change in the extracellular / intracellular gradients of sodium and potassium (there is normally less K+ extracellularly and higher NA+). The altered electrochemical gradient leads toslower movement of electrical impulses through the myocardium, hence a wider QRS duration.
If we jog by hyperkalemia on the differentials list and reach for the antiarrhythmics, we will supercharge the problem. Lidocaine and Amiodarone both further alter the sodium action and slows conduction through the ventricles even more! You can be left with heart blocks, pulseless VF/VT, or asystole. This is a lethal error.
Metabolic Problems: Metabolic issues, specifically acidosis, can also cause a wide QRS. As hydrogen ions begin to take up residence inside the cells, potassium gets moved out of the cells, creating a relative hyperkalemia. As expected, the collection of extracellular potassium alters the sodium/potassium pump function that the cardiac cells use to generate electrical impulses. The result is the same slow and sluggish movement of the electrical impulse through the myocardium that is observed in true hyperkalemia.
Misdiagnosing acidosis as VT can be as lethal an error as doing so with hyperkalemia. “Unstable gets the cable” may be the initial response to this, and it should be no shock (see what I did there) that cardioversion will not be effective in converting the rhythm. Moreover, amiodarone and lidocaine can be detrimental by, again, altering the sodium/potassium pump action and further slowing the conduction through the ventricles and reducing the efficacy of all other mechanisms of cardiac compensation (inotropy..). What was once a wide complex tachycardia will soon become asystole.
The priority is treating the cause of the acidosis. Are they in severe septic shock? DKA? Resuscitate as you differentiate, but you must maintain awareness of the situation you are in to avoid making things worse.
Toxicologic Examples : Sodium channel blockade (SCB) should be near the top of the differentials list when dealing with a wide complex tachycardia. Patients may be exposed to sodium channel blockers most commonly via antiarrhythmics or tricyclic antidepressants (TCA). SCB overdose results in the inability of sodium to move into the cell as part of normal cellular depolarization. The result of which is dangerously slow electrical conduction through the myocardium. The slower the conduction through the myocardium, the weaker the force of contraction, and the worse the cardiac output will be.
A wide complex tachycardia from SCB or TCA overdose will be difficult to differentiate from VT unless the clinician has lab values available to them OR is astute during the assessment and is able to make a connection between the presentation, medical history, medication list, and the EKG. Amiodarone or lidocaine in this case will super charge the problem and the effect will be the exact opposite of what is intended when those medications are administered.
What Does Stable Get? Treat the Patient, Not the Monitor
Treat the patient, not the monitor… One of the oldest adages in the EMS world. It is meant to prevent this very problem of just reacting to what we see on the monitor. What does “treat the patient” mean in this case?
Dr. Mattu’s YouTube talk gives some sound advice for this in the setting of WCT (or more specifically really wide complex tachycardia as he calls it). His advice is to give some sodium bicarb and calcium…and wait. If the QRS narrows, then it is not VT, it is a metabolic/tox problem (likely hyperkalemia). At this point you have differentiated this WCT from VT, and you know amiodarone or lidocaine are NOT going to be beneficial. If the QRS does not narrow, then the bicarb and calcium will not have hurt them, and you are left with the conclusion that you are likely dealing with VT. At this point you can move on down the rest of the algorithm.
Close Out
Some lessons you just learn the hard way. Thankfully, a lot of lessons have already been learned and it warrants a periodic revisiting to keep these lessons fresh. This topic has been covered ad nauseum by just about everyone with a blog, podcast, or education platform, and this addition to the mountain of reviews is mostly for the instructor who is helping a burgeoning young paramedic student avoid relying on the nursery rhymes, understanding the physiology and pharmacology that informs the guidelines, and how to THINK through problems.
References:
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