Tuesday, December 11, 2018

Found comatose with prehospital ECG showing "bigeminal PVCs" and "Tachycardia at a rate of 156"

This patient with a history diabetes was found with a GCS of 4.

Prehospital EKG and strips (not shown) had "heart rate 156" (according to the computer interpretation) and "Bigeminal PVCs"

The prehospital 12-lead looked just like the first ED ECG:
What do you think?





















Answer: The "bigeminal PVCs" is really a QRS followed by a very narrow peaked T-wave, which was so narrow that it was mistaken for a separate QRS.  The heart rate is 78, not 156.  Notice also the very long ST segment, most easily seen in inferior leads.

This ECG is pathognomonic for severe hyperK, and the long ST segment is all but pathognomonic for hypocalcemia. So I knew immediately that the patient needed a lot of IV calcium, and, based on the prehospital ECG, we gave 6 grams of calcium gluconate before even drawing blood for lab values.

When we did get a chem back (drawn after 6 g Ca gluconate), the K was 9.0 mEq/L and the ionized calcium was not reported because it was too low.

The patient had a glucose of 1400, was severely dehydrated, and after receiving 4 liters of fluid, albuterol, and insulin, the K had dropped precipitously to 5.8 and the ECG improved:




The Calcium AFTER 6 g of treatment was 8.2 mg/dL.

Cr was 8.0 (previous was normal).  The patient had hyperK due to acute renal failure.

Learning Points:

1. Learn all the different pathognomonic ECGs of severe, life threatening hyperK.
2. A long ST segment is typical of hypocalcemia
3. Immediate treatment of HyperK is calcium. It is safe even when there is no hypocalcemia, but is particularly safe if there is hypocalcemia, which you can infer from a long ST segment.


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Comment by KEN GRAUER, MD (12/11/2018):
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I love this case — because it brings home 3 of my favorite teaching points about electrolyte disorders and ECG interpretation. For illustrative purposes — I’ve put both tracings in this case together in Figure-1.
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Figure-1: The 2 ECGs in this case (See text). 
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Teaching Point #1: You can sometimes make the diagnosis of acute DKA (Diabetic KetoAcidosisfrom an ECG, even before blood values come back! If the clinical setting is “right” (ie, an acutely ill patient with a history of diabetes, or impaired mentation with Kussmaul respiration) — and, the initial ECG suggests marked hyperkalemia — then acute DKA should be immediately considered.There just aren’t that many clinical conditions that cause hyperkalemia. Among the most common entities are:
  • Renal failure (acute or chronic).
  • Severe acidosis.
  • Use of K+-retaining medications or K+ supplementation (especially if the patient has underlying renal impairment).
  • Severe dehydration.
  • Addison’s disease (adrenal insufficiency) — which is not common ...
  • Destruction of red blood cells due to trauma, severe injury or burns.
COMMENT — An ECG can often be obtained in the ED before lab values come back. If the tracing suggests significant hyperkalemia — then think of the above entities as you correlate clinically to the patient in front of you in your search for a cause. Considering that acute DKA often presents with 3 of the above causes of hyperkalemia (ie, severe acidosis, renal impairment, and dehydration) — acute DKA should be high on your list unless another etiology is obvious.
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Teaching Point #2: The typical ECG picture of hypocalcemia is a long, relatively normal (and typically isoelectric) ST segment — at the end of which is a relatively normal T wave (unless the T wave is altered by another disorder, such as hyperkalemia).
  • Although the ST segment manifests abnormal coving in multiple leads in ECG #1 (Figure-1) — ST segments are strikingly prolonged without obvious elevation or depression — and only then … comes the T wave. As per Dr. Smith, the pointedness and narrow base of T waves in virtually every lead in ECG #1 is the result of hyperkalemia.
COMMENT — Hyperkalemia and hypocalcemia often occur together in renal failure. This makes it easier to suspect associated hypocalcemia when a hyperkalemic-looking ECG shows an unexpectedly prolonged ST segment prior to the peaked T waves.
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Teaching Point #3: There is a REASON why the initial ECG ( = ECG #1 in Figure-1in this case looks highly unusual! By this I mean that although T waves are clearly pointed and peaked with a narrow base — we don’t usually see biphasic T waves in hyperkalemia, as are present in leads V1-thru-V6!

QUESTION: Why do the T waves in ECG #1 look so strange that they were mistaken for PVCs?

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ANSWER: The effect of hyperkalemia on the ECG is additive to (superimposed onhowever the baseline ECG looked! This fundamental point is all-too-often ignored!
  • IF the baseline ECG is relatively normal — then development of severe hyperkalemia will produce a picture of tall, peaked and pointed T waves with a narrow base — ultimately resulting in loss of P wave amplitude, bradyarrhythmias, and QRS widening.
  • BUT — IF the baseline ECG is abnormal, with preexisting ST-T wave depression — then the degree of T wave peaking from hyperkalemia may be significantly attenuated.
  • FINALLY — IF the patient presenting with hyperkalemia is also acutely ischemic — these ischemic ECG changes may not be recognizable until serum K+ is normalized and the ECG is repeated.
COMMENT — The ECG after treatment in this case is the bottom tracing in Figure-1 ( = ECG #2). It should be emphasized that serum K+ was not yet normal at the time ECG #2 was recorded (serum K+ = 5.8 mEq/L) — so we are not privilege to a true “baseline” tracing for this patient. That said, it is clear that fairly deep, symmetric T wave inversion is present in leads V3, V4 and V5 of ECG #2 — with at least suggestion of abnormal ST segment coving in these leads. Whether these ST-T wave abnormalities in ECG #2 are new (and whether they might be even more pronounced if the ECG was repeated after complete resolution of electrolyte disorders) is uncertain. BOTTOM LINE: Seeing ECG #2 explains the highly unusual picture of ST segment coving with biphasic T waves that was seen in the initial ECG ( = ECG #1) when serum K+ = 9.0 mEq/L.
  • P.S.  Did you notice that the QRS complex in ECG #1 is wide? (ie, it appears to be at least 0.12 second in duration in leads V2,V3,V4). That this QRS widening in ECG #1 is real, and is the result of marked hyperkalemia is verified by the presence of a decidedly more narrow QRS complex in ECG #2 after treatment.
  • P.P.S.  Did you notice that in addition to QRS widening — there is also a marked axis shift between the initial ECG ( = ECG #1) and the post-treatment tracing ( = ECG #2). Given the adverse effect hyperkalemia has on conduction — the presence of an unusual frontal plane axis and/or marked axis shift from the patient's baseline tracing are additional indicators from the ECG suggesting the degree of hyperkalemia is severe!
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Final NOTE: Did you recognize that the rhythm in ECG #2 is not simply sinus? If not — then you weren’t systematic in your interpretation.
  • PEARL  The easiest way to never overlook a non-sinus rhythm — is to always begin your interpretation of any ECG by spending a quick 2-3 seconds surveying every beat in the long lead II rhythm strip. If you do not see an upright P wave with fixed PR interval preceding each QRS complex — then the rhythm is not strictly sinus. The only 2 exceptions to this rule are lead misplacement and dextrocardia.
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QUESTION: What then is the rhythm in ECG #2 of Figure-1?

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ANSWER: The rhythm in ECG #2 is complex. The important point — is to recognize that because the initial beats in the long lead II rhythm strip are not preceded by an upright P wave (BLUE arrows in Figure-2) — this can’t be a sinus rhythm (assuming no dextrocardia or lead misplacement).
  • Admittedly, assessment of the rhythm in ECG #2 is complicated by baseline artifact and the low amplitude of atrial activity. That said — there should be NO doubt that the P wave preceding the first 9 beats is negative in lead II (BLUE arrows), as well as in the other inferior leads. A small upright P wave does appear to be present in front of the QRS in lead I. This suggest this is a coronary sinus rhythm.
  • Beat #10 is early. It is a PAC.
  • Sinus rhythm clearly resumes for the last 4 beats on this tracing (ie, beats #13-16) — as each of these beats is preceded by a small-but-clearly-upright P wave with a fixed and normal PR interval (RED arrows).
  • Sinus P waves also appear to precede beats #11 and 12 (RED arrows) — but the PR interval preceding these 2 beats is short, suggesting they are junctional escape beats.
Figure-2: We have labeled ECG #2 to explain the rhythm (See text).
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Clinically — Brief appearance of a coronary sinus rhythm until a PAC reset the sinus pacemaker did not affect outcome in this case. My purpose in discussing the rhythm in ECG #2 was simply to highlight how easy it is to overlook subtle arrhythmias if one is not meticulous and systematic. Failure to do so may affect clinical outcome in other cases ...



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