Authors: Lloyd Tannenbaum, MD (EM Attending Physician, APD, Geisinger Wyoming Valley, PA); Christian Daniello, MD (Staff Physician, Geisinger Wyoming Valley) // Reviewer: Brit Long, MD (@long_brit)
Hello and welcome back to ECG Pointers, a series designed to make you more confident in your ECG interpretations. This week, we feature a post from Dr. Tannenbaum’s ECG Teaching Cases, a free ECG resource. Please check it out. Without further ado, let’s look at some ECGs!
“This is Medic 929 coming in Priority 1, Hospital, do you copy? Over.”
You and the charge nurse look at each other and race over to the EMS radio. “Go ahead Medic 929, this is the hospital”
“Hey Doc, we’re about 7 minutes out from your location with an 87-year-old male coming in with weakness and on-and-off syncope for the past 3 hours. According to family, he’s been in and out of consciousness and they were having trouble keeping him awake. We just got vital signs and they are as follows: heart rate is 32, blood pressure is 70/30, SpO2 89% on room air, respiratory rate is 12, and he’s afebrile. We’ll see you in less than 5; be ready for us, he’s a sick one.” Click.
Ok, so much for that coffee run. You and the charge nurse look at each other and wonder where exactly you’re going to put another patient in an ED that is bursting at the seams. Well, if we move that patient over to a hallway bed and shuffle these 8 other people, maybe we can make it work. Oops. That’s the EMS door buzzer; we’re just going to have to figure it out on the fly.
“Hey doc, we got Mr. Williams over here, he’s still bradycardic and hypotensive. Moving him over to your bed and monitors now, good luck!” You and your team get him hooked up as quickly as you can and then the tech hands you this ECG:
Rate: Slow. Low 40s at best
Rhythm: No p waves, not sinus bradycardia
Axis: Left axis
Intervals: No P waves, No PR interval, Narrow QRS Complexes, reasonable looking QTc.
Morphology: Some nonspecific ST-T wave changes, but nothing terrible.
Final read: This is a slow, regular, narrow complex rhythm consistent with junctional bradycardia.
Let’s take a second and review what happens when the SA node decides that it’s had enough and stops pacing the heart.
Remember, the SA node likes to pace between 60-100 bpm. When the SA node decides that it wants a break or just gives up entirely, another pacemaker cell of the heart will take over. The atria can pace at 60-80 beats per minute (bpm). The AV node wants to pace around 40-60 bpm and the ventricles can pace around 20-40 bpm.
The ECG can tell you where the electrical impulses are originating from. If you see sinus rhythm, then the SA node is in control of the heart.
An atrial escape rhythm will still show P waves and a narrow QRS complex. The rate will be probably around 60-70 bpm and your tip off that this isn’t sinus is that the p waves will look different from the “normal” p waves when the patient was in sinus. These are usually seen on a rhythm strip where the patient’s normal sinus rhythm will pause and you’ll see a few “weird p waves” and then the SA node will take back over.
Let’s say the atria are out to lunch. They don’t want to pace the heart. Who steps in next? Well, the AV node would be next up for pacing. The AV node will still produce a narrow QRS complex but it will be slow and there won’t be any P waves. An AV node-produced rhythm is also called a Junctional Rhythm.
Oops. Now the AV node is broken. So, we have no SA node, no working atrial cells, and no AV node to pace. Is this game over? Well. No, but almost. The ventricles can pace! They pace SUPER SLOWLY. Think rates in the 20s to maybe the 40s on a good day. Also, since it’s a ventricular rhythm, it will produce a wide complex QRS and still won’t have any P waves. If the ventricles are running the show, it’s not really a good day for the heart.
Mr. William’s ECG above shows a junctional rhythm (Remember, no p waves and a narrow QRS complex). For completeness, I’ve included an example of a ventricular escape rhythm below:
Rate: Only 3 beats in the whole strip! That’s 18 beats per minute. That’s very very slow.
Rhythm: There is definitely a block present. Notice that there are multiple p waves, and they don’t match up 1:1 with the QRS complexes. Not sinus rhythm.
Axis: Probably left axis but also there are more important things to worry about right now.
Intervals: No PR interval, WIDE QRS complexes, QTc looks ok.
Morphology: The ST segments are appropriately discordant, so probably wouldn’t activate the cath lab over this ECG. There are also non-conducted P waves on the strip (P waves that don’t produce a QRS complex).
Final read: This is an extremely bradycardic ECG showing a ventricular escape rhythm. The patient is probably in third degree heart block, but there’s a good bit of baseline artifact so it’s tough to be 100% sure. I would make sure that there are crash cart pads on this patient. If they aren’t hypotensive yet, they likely will be shortly.
“Hey doc, I love that you’re having a really good academic discussion about that ECG in your head, but any chance you could snap out of it and give us a hand here???”
…Oops. Ok, game time. So, to recap, we have a patient having repeated episodes of syncope with a heart rate in the 40s and a blood pressure in the 70s systolic. This is a clear indication for pacing the patient. We can try transcutaneous pacing (which is usually not well tolerated) or we can place a (hopefully quick) right IJ and float a transvenous pacer. There are also some meds to consider in bradycardic patients.
For medications in critically ill bradycardic patients, I consulted my pharmacist friend, Scott, who was apparently feeling a bit snarky this week. Here were his thoughts:
What about meds? Well, Lloyd, I’m not really sure why we’re talking about meds for a hypotensive bradycardic patient when you really should be pacing them, but if you insist, I’ll indulge you.
You’re welcome to try atropine, but in a high degree heart block, it’s extremely unlikely that it’ll work at all. Remember, atropine is a muscarinic blocker. It decreases vagal tone. So, it makes the SA node fire faster and increase conduction through the AV node. In a high degree AV block, the block is usually below the AV node. So, the SA node can fire as much as it wants and the AV node can let as many impulses through as it wants, but the impulses run into that block, the conduction stops. Don’t delay starting pacing in a hypotensive patient because you’re waiting for the atropine to kick in. It won’t. It may even make it worse. Wait. What? Atropine can make bradycardic patients worse?
Yes, you read that right. At low doses, atropine blocks M1 acetylcholine receptors in the parasympathetic ganglion controlling the SA node. This decreases heart rate.
At higher doses, atropine also blocks M2 acetylcholine receptors on the myocardium itself. This blocks parasympathetic effects on the heart, increasing the heart rate.
Atropine doses below 0.5 mg should be avoided, because sub-therapeutic atropine levels can cause bradycardia. At higher doses, the dominant effect of atropine is usually to increase the heart rate hence the updated algorithm utilizing 1 mg as a first dose in the 2020 ACA ACLS guidelines. Historically the maximum dose for atropine is 3 mg (0.04 mg/kg) as atropine is still an anticholinergic agent and we want to avoid toxicity.
Now you are standing at the bedside and right before you push the atropine, I’ll ask you “Just double checking, the patient hasn’t had a heart transplant, right?” Why would that matter right now?
Atropine has an unpredictable effect on heart transplant patients and can actually worsen the heart block. The mechanism is not fully understood but is related to vagal denervation during the transplant process. That, and I like to distract you, right as you push vasoactive meds on critical patients. It’s why we work so well together.
How about pressors? Well, you have two to reach for here, Epinephrine or Dopamine. If you’re out of those for some reason, isoproterenol or dobutamine can be considered as a backup. So why are these agents specifically called out as opposed to the wide array of other adrenergic agents? Once again, we find ourselves focusing back on the receptor affinity. Both epinephrine and dopamine will exert significant β1 activity at lower doses! Dobutamine and isoproterenol are entirely focused on beta activity but come with their own challenges including tachyphylaxis risk for dobutamine and risk of worsening hypotension with isoproterenol. So maybe we go back to the original plan of putting in a temporary pacer while the EP team sets up to place a permanent pacemaker?
Also, before I go back to my drugs, remember, push dose epi can help you if you’re in a pinch. It’s 1 cc of code dose epi in a 10-cc syringe of NS. Squirt out 1 cc from the saline syringe. Replace that 1 cc of NS with 1 cc from the code dose epi box. That makes a syringe of 10 mcg of epi per ml. You can use 1-2 mL of the push dose epi (10-20 mcg) to give the patient’s BP a little bump while you set up pacing.
Thanks Scott! After a quick discussion with Cardiology and Electrophysiology, they ask you to start the patient on dopamine and place a temporary transvenous pacer while they get set up to take the patient to the EP lab for pacemaker placement. The patient’s blood pressure comes up slightly with the dopamine but really responds well to pacing. Right as you stabilize the patient, EP comes and rushes him away.
Ok, let’s recap before we wrap up:
- For bradycardic, hypotensive patients, always consider pacing sooner rather than later.
- If the SA node decides it’s not going to pace anymore, there are some backups in place:
- Atrial pacing (rates 60s-80s), look for “weird” p waves that look different from the sinus p waves.
- AV nodal pacing (rates 40s-60s), look for NO p waves and a NARROW QRS.
- Ventricular pacing (rates 20s-40s), look for NO p waves and a WIDE QRS.
- If, for some reason, pacing is contraindicated or you can’t pace the patient, consider Dopamine or Epinephrine as first line pressors.
- Don’t be surprised if atropine doesn’t work and AVOID low doses of atropine (anything less than 0.5 mg), as it may worsen the bradycardia.
- Also avoid atropine in heart transplant patients.
- Someone get Scott a Snickers.
