Cardiac Axis

This blog is essentially the transcript of our most recent Podcast 04.08 "Is the AHA Wrong: Cardiac Axis"

Cardiac Axis

How many times have you read a 12-lead that says sinus bradycardia with left axis deviation or right axis deviation and you’ve just thought.. “Okay”.. I wasn’t taught that in medic school so it must be unimportant. Let’s explore that and I’ll let you come to your own conclusion whether cardiac axis is an important item on your differentials list.

What is cardiac axis?

-       Direction the electricity is travelling throughout the heart

-       We all know the normal conduction pathways in the heart, the SA node is located just right of your sternum at the 3rd or 4th rib. The apex of your hear is left of your sternum around the 6th rib. If you draw a line from the SA node to the apex it would essentially be straight line from the middle of your right clavicle to your left hip.

-       Every single heart beat, the electricity should start there (top right) and travel continuously until it reaches the purkinje fibers (heading in a downward and left direction)

-       What if the electricity doesn’t quite follow that path? What does that mean for our patient?

That’s where determining the cardiac axis comes into play. For our purposes today, I’m not going to get deep into the weeds regarding physiologic vs pathologic axis deviation, as I don’t know that it’s all that important to our practice. We’ll keep it simple.

What we have to understand when we’re looking at an EKG is that we’re looking at three things simultaneously on the tracing.

-       The first is the obvious one, and what most people learn: the waves we see are caused by the movement of electrolytes in (or out of) the cardiac cells and that causes a change to the electrical charge in the area. Thus the EKG is literally just a voltage tester and is visually showing us the electrical charge of the membranes.

-       Second: we are seeing the passage of time. For some reason this escapes people even though it is really obvious. If the QRS complex is wide, it simply means the electrical took “longer” to get from the bundle of HIS to the purkinje fibers. Could it be a block in the bundle branches so the electricity simply takes longer to reach the purkinje fibers? Sure. Could it be an electrolyte abnormality that is causing a reduction in the dromotropy? Also sure. We cannot forget that. If the waveforms are wider than they should be, its because they’re taking too much time.

-       The third thing we’re seeing on the ECG is the physical flow of electricity heading toward or away from a camera. We can essentially think of each lead on the ECG like it’s a stationary camera on the roadway (like a traffic camera). Now imagine a heartbeat like a solo car on the road. If the car is heading toward the camera, this would be represented by an ECG tracing that is above the baseline (or positively deflected). If the car is heading away from the camera, the QRS will be face-down or deflected in a negative manner.

This concept is incredibly useful because we know a few things definitively.

-       First, we know exactly how the electricity should be travelling through the heart in a normal person.

-       Second, we know exactly where all the cameras are located.

-       This means that we actually know exactly what all the tracings on each lead should look like.

While we should only be using a 12-lead to interpret cardiac axis, we can certainly use a 3-lead as a poor-mans alternative and I’ll show you how to use both.

To understand cardiac axis, we just need to understand where the cameras are. If you already know where all the leads are (meaning what all the leads are looking at) on a 12-lead, then this will be super easy. If you don’t, don’t worry. It’s pretty easy to remember.

-       First we’ll look at einthovens triangle (this is what makes leads I, II, and III)

o   Explain the triangle and where the cameras are

-       Next, we need to look at the augmented voltage leads aVL, aVR, aVF

Walk through a normal cardiac conduction

-       So lead I should be positive, and lead AVF should be positive as well. That is a normal cardiac axis.

What is the lead I is down and lead AVF is up?

-       This is called right axis deviation

-       Right “reaches”

-       When we see right axis deviation we should be thinking about three possibilities:

o   Right heart or pulmonary problems (making the axis deviate to the right because of a bloated right ventricle)

o   Toxicological problems (like a sodium channel blockade – cocaine, propranolol, TCA’s)

o   Potassium problems

What if lead I is up and lead AVF is down?

-       This is called left axis deviation

-       Left “leaves”

-       When we see left axis deviation we should think about three things as well:

o   Left heart problems (like an MI)

o   12-lead STEMI disqualifiers (LBBB, LVH, pacing)

o   WPW

We could spend all day talking about the 12-lead findings for each of the aforementioned things and this format would not be a good place for that. If you’re interested, we have a 12-lead course on our website that goes over all that stuff.

Let’s review.

-       If leads I and AVF are both up, that’s normal

-       If leads I and AVF are reaching for eachother, that’s right axis deviation (think about right heart, tox, and K)

-       If leads I and AVF are leaving eachother, that’s left axis deviation. (think about left heart, disqualifiers, and WPW)

-       If both are down, that’s extreme right axis deviation and is only present when a patient is in VT.

That’s the final point we’ll make regarding cardiac axis. In the ACLS algorithm, for stable patients in monomorphic VT, the AHA tells you to give adenosine. If it doesn’t work, then start an antiarrhythmic. Wait a minute… everything I learned about adenosine growing up what that it only works on the SA and AV nodal cells and that it doesn’t work on the ventricles. That is almost completely true, as the ventricles and the purkinje fibers of the heart don’t have a1 receptors so there’s nowhere for the adenosine to attach and suppress the release of cAMP. (that’s a little beyond the scope of this talk). However, there have been cases where VT was terminated by adenosine if the VT was cAMP dependent (which is uncommon). So why then would we waste a med, cause the patient to feel like they’re dying if the med isn’t going to work.

Well friends, it’s because pulsing VT is actually pretty uncommon. In 2020 Havakuk and colleagues looked at wide complex monomorphic tach in 168 patients and found that only 59 of them were actual VT, while the remainder were in SVT. Remember, in SVT with a bundle branch block, the SVT will appear wide. In antidromic AVRT (which is a form of SVT) the rhythm will appear wide. Not all SVTs are narrow and not all VT’s are wide. Jerónimo Farré and his collegues published a case review in 2022 showing that many post MI VT’s can have a narrow QRS.

What’s my point in all this…. Regardless of what the width of the qrs is, it can be either VT or SVT. However, all VTs will have a extreme right axis deviation. Meaning the points of the R wave will be face down (below the isoelectric line) in both leads I and AVF. SVT can have normal, right, or left axis, but never an extreme right axis. So yes, the AHA is not being dumb when they say you should treat monomorphic VT with adenosine before doing an AMI drip as about 65% of the time, you’re actually looking at a wide SVT. But also consider that when you’ve given adenosine to a wide-ish SVT a couple times without conversion, it may be VT (especially if they’ve had a recent MI). If you just run a 12-lead before giving the meds, you can forego the unsureness of your decision and you’ll know you’re giving the appropriate med.

Before, we’re done, I promised that you could also use the 3-lead instead of a 12-lead in a pinch. That’s true. Insead of using lead I and AVF, just use lead I and III instead. It’s not as accurate, but it’s good enough for most situations.

References:

B Garner J, M Miller J. Wide Complex Tachycardia - Ventricular Tachycardia or Not Ventricular Tachycardia, That Remains the Question. Arrhythm Electrophysiol Rev. 2013 Apr;2(1):23-9. doi: 10.15420/aer.2013.2.1.23. PMID: 26835036; PMCID: PMC4711501.

Gupta PN, Kumar A, Namboodiri N, Balachandran A. What is this? VT versus SVT. BMJ Case Rep. 2013 Sep 23;2013:bcr2013200806. doi: 10.1136/bcr-2013-200806. PMID: 24064403; PMCID: PMC3794232.

Sundhu M, Yildiz M, Gul S, Syed M, Azher I, Mosteller R. Narrow Complex Ventricular Tachycardia. Cureus. 2017 Jul 4;9(7):e1423. doi: 10.7759/cureus.1423. PMID: 28875096; PMCID: PMC5580969.