Extreme brady with strange rhythm

[kataraang, BSN]

Background: patient in for a pacemaker. He has complete heart block as well. Elderly, in his 90's (that's all I knew). I work in a telemetry unit.

It wasn't my patient but I was by the monitors when I noticed a patient's HR in the 40s. It was heart block, as we knew already from the ED report (he had just arrived on unit). As I watched a moment longer, it dropped into the 30s, and then it was 28. I quickly walked into the room where I saw a conscious man sitting up in bed, in no apparent distress getting his vitals taken by another nurse. I asked, "are you feeling okay?". He told me yes. I said, "nothing is bothering you at all?" He said he was fine. I just couldn't believe that a man with a HR in 20's felt "fine". I verified the HR (now in 30's) by taking his pulse.

There was a doctor in the room at this point. I stepped outside to the hallway monitor again and saw a QRS complex with a period of v-fib looking activity before the next QRS. It was not artifact, because it was very clearly defined. Was it a-fib? Below is a google image search of the closest thing I could find:

I'm used to very high ventricular rates in a-fib. A-flutter, then? Sorry if it's a dumb question. I'm still learning the difference between textbook and real life for many concepts.

I now very quickly returned to the room. He was still alert and conversing. A rapid had been called by this point, but I was just baffled by how he presented given his vital signs/heart rhythm.

Any ideas? Have you seen a patient with a HR so low that was asymptomatic? I'm a new nurse 5 months into my first job, so I haven't gained enough experience to know these things. He was sent to CCU externally paced before he could get his implanted.

[Penelope_Pitstop, BSN, RN]

I'm rusty on my dysrhythmia zebras (if ya don't use it you'll lose it with that one!) as I've been out of acute care for 2 1/2 years. It has a flutter look to me but this is just my guess without pulling out calipers and and a book and whatnot.

I can answer your other question, though.

When I was in clinical, there was a patient on the floor who lived in the 30s, asymptomatic; in fact, he would be screaming and carrying on and his heart rate did not once hit 40. I saw him drop to 25 asymptomatically. I don't know anything about his history but I've never seen anything like it.

[MunoRN, RN]

The atrial rhythm you've posted appears to be a coorifice atrial flutter, which could have been the underlying atrial rhythm you observed in a patient in complete heart block. Keep in mind a patient in complete heart block has two rhythms; their atrial rhythm and (hopefully) their ventricular escape rhythm since conduction between the atria and ventricles is completely blocked. The escape rhythm could be junctional or ventricular depending on where the block is. Rhythms that originate at the junction and particularly those that originate in the ventricles tend to be slow, causing a slow ventricular rate, which is the main problem with complete heart block. When there is atrial to ventricular conduction, A-fib and A-flutter often cause rapid ventricular rates, but that's because the high rate of conduction impulses being sent to the ventricles by the atria will produce a rapid ventricular rate, in complete heart block none of that conduction is making it through to the ventricles, so it has no effect on the ventricular rate.

It's not all that unusual for someone to tolerate a HR in the 30's at rest just fine, in the ICU we wouldn't normally externally pace someone who is otherwise WNL and sitting there watching TV just because they have a ventricular rate of 30. We would have atropine quickly available, and often have pacing pads already on and maybe even hooked up to a defib/pacer all ready to go, but to continuously externally pace for an extended period of time would morally require a level of sedation that would also require being vented, so there has to be strong justification for doing so.

[Julius Seizure]

It's not all that unusual for someone to tolerate a HR in the 30's at rest just fine, in the ICU we wouldn't normally externally pace someone who is otherwise WNL and sitting there watching TV just because they have a ventricular rate of 30. We would have atropine quickly available, and often have pacing pads already on and maybe even hooked up to a defib/pacer all ready to go, but to continuously externally pace for an extended period of time would morally require a level of sedation that would also require being vented, so there has to be strong justification for doing so.

Atropine wouldn't be useful in this patient, though, because they have complete heart block, correct? If I remember correctly, atropine works on the SA node...so its not going to change this patients ventricular rate.

[Greenclip]

That looks like coorifice flutter to me. Yes, I've had at least two patients who had rates in the 30s and were completely asymptomatic. Both men.

Good for you for being curious and asking questions!

[calivianya, BSN, RN]

I had a patient flip from normal sinus into a-fib with slow ventricular response once. She had the characteristic fib wiggles, but the ventricular rate was hanging out between 27-33. Couldn't tell how she felt about it because she was vented and sedated.

I got an order to start dopamine for HR. I was worried that it would cause more arrythmias, but started it anyway because I didn't like the HRs in the 20s... and the dopamine sent her into V-tach. I cut off the dopamine and the HR started dropping again. Fortunately, at this point, it was the end of my shift, so whatever happened next ended up being a day shift problem. I did what I could, and I've never been happier to get the heck out of dodge.

[MunoRN, RN]

Atropine wouldn't be useful in this patient, though, because they have complete heart block, correct? If I remember correctly, atropine works on the SA node...so its not going to change this patients ventricular rate.

I was speaking generally about whether or not we would externally pace a patient overnight in the ICU for completely asymptomatic bradycardia, regardless of the cause, but actually atropine can still work in complete AV block depending where exactly the block is. I had always been under the same impression, that atropine won't do anything for complete AV block, then I had a patient that the cardiologist (an EP) ordered atropine for and it worked very well, which led to a long-winded explanation by the cardiologist about conduction pathway anatomy. The short version is that if they still have a narrow QRS, then there's a reasonable chance atropine will work.

Atropine primarily works by numbing the vagus nerve, which innervates both the SA node and AV node and even down into the bundle, as long as the origin of the escape rhythm below the block is innervated by the vagus nerve, then atropine will work. If the escape rhythm running the ventricles has a narrow QRS, then it originates at or near the AV node.

Someone in complete AV block is who is asymptomatic or minimally symptomatic typically has a junctional escape rhythm, someone who's escape rhythm originates in the ventricles is usually going to have a slower rate and with floppy, ineffective contractions and usually require external pacing followed by a more permanent solution.

[Julius Seizure]

I was speaking generally about whether or not we would externally pace a patient overnight in the ICU for completely asymptomatic bradycardia, regardless of the cause, but actually atropine can still work in complete AV block depending where exactly the block is. I had always been under the same impression, that atropine won't do anything for complete AV block, then I had a patient that the cardiologist (an EP) ordered atropine for and it worked very well, which led to a long-winded explanation by the cardiologist about conduction pathway anatomy. The short version is that if they still have a narrow QRS, then there's a reasonable chance atropine will work.

Atropine primarily works by numbing the vagus nerve, which innervates both the SA node and AV node and even down into the bundle, as long as the origin of the escape rhythm below the block is innervated by the vagus nerve, then atropine will work. If the escape rhythm running the ventricles has a narrow QRS, then it originates at or near the AV node.

Someone in complete AV block is who is asymptomatic or minimally symptomatic typically has a junctional escape rhythm, someone who's escape rhythm originates in the ventricles is usually going to have a slower rate and with floppy, ineffective contractions and usually require external pacing followed by a more permanent solution.

Interesting! Thanks for the explanation. Makes total sense now that you said it.

[CKPM2RN, ASN, EMT-P]

I've seen lower rates in A-flutter. I once had a patient with a heart rate and matching pulse of below 30, we are supposed to start CPR, right? Well he had a systolic BP over 140 and was alert, oriented and had a complaint only of feeling strange. So obviously there's no perfusion problem. We just watched him and waited for the cardiology consult to figure it out. Weird things can happen out there.