Sunday, January 13, 2019

What will you do for this altered and bradycardic patient?

Written by Pendell Meyers

A female in her 60s with COPD, DM, hypothyroidism, CAD, and severe bladder cancer presented from a nursing home with altered mental status, hypotension, hypoxia, and bradycardia.

Here is her initial ECG (no prior for comparison):
What do you think?

Here is another ECG minutes later:
There is a regular wide complex bradycardia.
There are P-waves at a rate of approximately 100bpm with no clear relationship to the QRS complexes, diagnostic of complete heart block (see correction below!).
The QRS morphology is wide (computer QRS duration 179 msec) but it does not fit any clear bundle branch block pattern (it is similar to LBBB but not truly LBBB).
The T-waves in the precordial leads are peaked. Overall this is highly concerning, if not diagnostic, for hyperkalemia.

Important correction by Dr. K Wang:
"By the way, it's not complete AV block right away because the QRSs do not occur regularly.  In complete AV block, the QRSs occur regularly whether its junctional or ventricular escape rhythm. In this case, actually QRSs have a P wave in front of them with an identical PR interval, revealing 3:1 ,4:1 or higher degree AV conduction ratio. Regardless, the most important thing clinically in this patient is to recognize  that the T wave of the V3 in the first tracing is tented, pointed, highly suggestive of hyperkalemia, a life threatening condition, which it turned out to be. Yes, the pacemaker induced QRSs are very wide and the T waves are very tall, again making one to suspect hyperkalemia."

Heart block (of some sort) was recognized, but hyperkalemia was not initially. She was given push dose epinephrine and atropine with no change. External pacing was attempted but failed.

A transvenous pacemaker was then placed, with capture obtained:
Ventricular paced rhythm. 
Computerized QRS duration 192ms, but it appears to be ~200 msec in several leads. 
It is unusual for any patient with any conduction pattern to reach 190-200 msec in the absence of hyperkalemia or other sodium channel blockade. 
The J-point is not easy to find, but there is excessively discordant ST deviation in many leads (this is why we excluded hyperkalemic patients in our ventricular paced rhythm study of acute coronary occlusion using the modified Sgarbossa criteria!). 

The first potassium level was reported to be hemolyzed by the laboratory.

She was placed on an epinephrine drip. Her mentation improved after pacing and epinephrine drip.

The second potassium then returned at 8.1 mEq/L. Labs confirmed new renal failure.

Around this time the patient's family arrived and explained that the patient's goals of care were palliative. Comfort care was instituted. The patient expired.

Learning Points:

Hyperkalemia is an important cause of bradycardia and heart blocks.

Never place a transvenous pacemaker without considering hyperkalemia and a trial of IV calcium.

Comment by KEN GRAUER, MD (1/13/2019):
Superb case with essential teaching points by Dr. Pendell Meyers that have been emphasized many times on Dr. Smith’s blog, but which never cease to be insightful and instructive. As stressed by Dr. Meyers — HyperKalemia is an important cause of bradycardia and heart blocks! It needs to be given high priority whenever clinical circumstances are potentially consistent with this diagnosis.
  • The goal of My Comment is to illustrate some advanced pointers in clinical arrhythmia interpretation. Although none of these pointers were “needed” for the essentials of diagnosis and management of this case — awareness of these ECG & Arrhythmia PEARLS may prove invaluable in evaluation and management of other cases.
  • For clarity — I’ve labeled the first 2 tracings in this case (Figure-1):

Figure-1: The first 2 ECGs in this case (See text).

My thoughts ( = my opinions) are the following:
  • As per Dr. Meyers — the rhythm in the initial ECG (ECG #1) is slow and irregular at a rate between 30-40/minute. The QRS is very wide. Baseline artifact prevents reliable recognition of atrial activity. I think it important to recognize when artifact impedes identification of the rhythm — and to state this in your written interpretation.
  • Under normal circumstances (ie, when the patient is not markedly hyperkalemic) — one of the most helpful hints for recognizing that a rhythm is not complete AV block, is if the ventricular response is not regular. Very often — beats that occur earlier-than-expected in an otherwise regular rhythm are conducted. That said, I’ve found that this general rule does not hold true well when there is marked metabolic abnormality, as is the case here. Therefore, given the absence of reliable atrial activity in ECG #1 — I don’t believe any conclusion can be reached regarding the rhythm beyond stating there is a marked, somewhat irregular slow rhythm with a wide QRS.
  • To highlight the point Dr. Meyers made regarding T wave morphology — I’ve enclosed within RED dotted rectangles the QRS complexes in leads V3 and V4 of ECG #1. Note that the T waves of these 2 QRS complexes are exceeding thin, pointed at their peak, and display a narrow base. It is these 2 T waves that should immediately heighten your suspicion of hyperkalemia. T waves elsewhere on both of these tracings show more-than-you-might-expect T wave peaking — but none are as dramatically suggestive of hyperkalemia as the T waves within the RED dotted rectangles.
  • QRS morphology in ECG #1 is potentially consistent with LBBB — because there is an all upright QRS complex in lead I — there is predominant negativity with fairly steep S wave downslope in anterior leads — and there is a positive (albeit small) QRS in lead V6. Some patients with LBBB do not transition to an all-positive R wave until leads V7 or V8 — so the pattern in ECG #1 is consistent with LBBB.
  • Atrial activity is clearly present in ECG #2! Although there is still significant baseline artifact — RED arrows across the long lead V1 rhythm strip show a fairly regular atrial rhythm at a rate just over 100/minute. I’ve placed a GREEN arrow at the point in the long lead V1 strip where a P wave is not seen in lead V1 — but — we know that a regular P wave does occur at this point, because we can clearly see it in simultaneously-recorded leads aVL and aVF (vertical BLUE lines). PEARL — If you are not already doing so, LEARN to use simultaneously-recorded leads in assessment of challenging arrhythmias!
  • There are only 3 QRS complexes in the long lead V1 rhythm strip of ECG #2. That said, the PR interval (horizontal thick PURPLE line) is the SAME for each of these 3 beats. Whether this is by chance … — or whether it indicates conduction of these 3 beats can not be determined from this single tracing. But IF a longer period of monitoring were to confirm that the PR interval in front of each QRS complex that appears is identical to that seen in ECG #2 — then the rhythm would be Mobitz II, 2nd-Degree AV Block (and not complete AV Block). And if the rhythm in ECG #2 is Mobitz II — then we are seeing a manifestation of why Mobitz II is a potentially lethal rhythm, because there is no QRS complex at all for the last 3 seconds of this ECG!
  • NOTE: As I said at the outset — determination of the precise rhythm in these 2 tracings is not clinically essential, because regardless of what the rhythm may be, this patient has life-threatening bradycardia with some form of AV block as a result of potentially treatable hyperkalemia. My point is simply to illustrate how we can not distinguish between an irregular idioventricular rhythm vs some form of AV block in ECG #1 — and, how we can not distinguish between high-grade Mobitz II vs something else in ECG #2.
  • QRS morphology in ECG #2 remains potentially consistent with LBBB. I’ve drawn in vertical BLACK lines to illustrate the point of lead change. Note that beat #1 in ECG #2 occurs right at the point of the first lead change — and that the QRS is all positive in lead I (PURPLE arrow). The QRS manifests a qR pattern in lead aVL in ECG #2, which is also consistent with LBBB — there is again predominant negativity in anterior leads, with steep S wave descent (which is consistent with LBBB) — and no QRS complex at all occurs in leads V4,V5,V6. Whether or not this patient has underlying LBBB vs a pattern of QRS widening solely from hyperkalemia can only be determined if a repeat ECG is done after K+ has normalized.


  1. Is that a 2. Av block high degree ? Because pr interval is fixed, not changed? Thank you for advise

    1. You're correct,thanks! See the correction above which was also noted by Dr. K Wang.

  2. In all these cases I order a stat VBG and will get in 5 - 10 minutes K levels and acid/base, lactate, HB...

  3. She also very likely improved on the epinephrine because of epinephrine's known effect on potassium levels. Driving K+ intracellularly likely helped with both cardiac contractility and ability to capture. I am curious as to the timing of the push-dose epinephrine administration (and dosage), the epinephrine drip, and the K+ lab draws.

    1. Agreed that epinephrine likely helped temporize the situation.

      I do not have access to the details on the push dose epi adminsitration, sorry. There was only 1 K+ recorded (first one "hemolyzed", second 8.1, no more measured as pt was made comfort care).


  4. Another interesting teaching case as usual.
    By the way, it's not complete AV block right away because the QRSs do not occur regularly. In complete AV block, they occur regularly whether it is the junction or the ventricle escaping. In this case, actually the QRSs have a P wave in front of them with identical PR interval, revealing 3:1, 4:1 and higher degree AV conduction ratio. Regardless, the most important thing clinically in this patient is to recognize that the T wave in V3 in the first tracing is tented and pointed, highly suggestive of hyperkalemia, a life threatening condition, which it turned out to be. Yes, the pacemaker induced QRSs are very wide and the T waves are very tall, again making one to suspect hyperkalemia.


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