Showing posts with label long ST segment. Show all posts
Showing posts with label long ST segment. Show all posts

Saturday, June 15, 2019

Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer.

I was handed this ECG of a patient with dyspnea:

What do you think?

Computer interpretation: Normal EKG
Physician Overread (Final interpretation): Normal EKG





















The ST segment is very flat, with a sudden rise to the peak of the T-wave.  This makes the base of the T-wave look very narrow.  A narrow-based T-wave is nearly pathognomonic for hyperkalemia.  My diagnosis was hyperkalemia.

The resident I showed it to saw nothing.  I explained all this to the resident, then went to see the patient.

Turns out he is a dialysis patient.

Later, the ECG computer interpretation was overread by another physician, and that physician thought it was normal, but took the step to compare with the most recent previous ECG.  There was no change, so that physician concluded that it was indeed normal and entered "Normal EKG" as the final diagnosis.

However, I looked a bit more in depth, and the previous ECG had also been recorded during hyperkalemia.

The K returned at 6.3 mEq/L.

Let's look at a couple previous ones from 2 years prior:

This was recorded when this patient presented with diaphoresis and muscle cramps:
The formal read was normal except for "possible old lateral MI"
QTc was measured at 484 ms which appears to be accurate, but the statement did not say "long QT"

There are definitely peaked T waves, and a long flat ST segment with an abrupt rise to the peak of the T-waves.

The K was 6.6 mEq/L

What else do you suspect?

This ECG was recorded a few hours later after bringing down the K to 4.8 mEq/L.:
These are now normal T-waves.
Can you see the difference between these and the T-waves in the 1st 2 ECGs?


Computer interpretation AND physician overread:
Normal except for long QT (486 ms)

The other thing you might have suspected is hypocalcemia, as the long QT is long because of a long ST segment (not because of a wide T-wave). 
The (not ionized) Ca on these 2 ECGs was 6.4 mg/dL (very low)
On the first ECG above, the QTc was 402 ms and the Calcium was normal.

The diagnosis was fluid overload and hyperkalemia.  Dialysis fixed both.

Learning Points:

1. Peaking of T-waves can be very subtle
2. Comparison with previous must be done with a previous that is recorded in the presence of a normal K.
3.  Peaked Ts are not necessarily large or tall.  They have a narrow base, and a sharp upstroke.  Often they look as though they would puncture you if you sat on them.
4.  Early repolarization and even LVH can have T-waves that mimic hyperK.
5. Having the physician read every EKG, whether the computer calls it normal or not, is of course only useful if the physician can recognize the abnormality

If you miss hyperK T-waves, your patient may have an unexpected cardiac arrest:

Here is a really interesting post, in which a patient with very subtly peaked T-waves, which are misinterpreted as early repolarization, has a ventricular fibrillation arrest before the K returns high:

HyperKalemia with Cardiac Arrest. 

Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia



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Comment by KEN GRAUER, MD (6/15/2019):
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Instructive case! I focus My Comments on ECG #1 = the initial ECG obtained in the ED (Figure-1). In my opinion, rather than calling this ECG “normal” (as did 2 clinicians and the computer) — there are ECG findings that should be noted: iProlonged QTc; iiLVH, clearly by voltage; iiiST segment straightening in multiple leads; andivTall, peaked (and pointed) T waves with a narrow base in at least 4 of the 6 chest leads. 
  • While I fully acknowledge that some of these ECG findings are subtle — I submit that recognition that this ECG is not “normal” would not have been overlooked IF interpreters had used a Systematic Approach (For “My Take” on how routine use of a Systematic Approach not only improves accuracy, but also speeds you up — See Dr. Smith’s May 7, 2019 Blog).
Figure-1: The initial ECG done in the ED (See text).

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Beginning with Descriptive Analysis:
  • There is baseline artifact in ECG #1 — which is most marked in the limb leads. That said, this does not prevent accurate interpretation of the key findings.
  • Rate & Rhythm — The rhythm is sinus at ~85/minute. Intervals  The PR interval is normal. The QRS complex is not wide. However, the QTc is somewhat prolonged. I measure the QT = 400 msec (See markings in lead V3). Correcting for the heart rate of 85/minute — I estimate a QTc ~470-480 msec (which is clearly above the upper expected range ~440 msec).
  • Axis  The frontal plane QRS axis is normal (about +30 degrees).
  • Chamber Enlargement — There is no atrial abnormality, and no RVH. But voltage criteria for LVH are definitely satisfied! I have reviewed “My Take” on a user-friendly approach to ECG diagnosis of LVH in Dr. Smith’s April 27, 2019 Blog. For ease of recall — I’ve excerpted the user-friendly criteria I favor in Figure-2. ECG #1 is an example in which the most commonly helpful criteria (35 & 12 — as per Figure-2) are negative — but both Cornell Criteria (R in aVL + S in V3 ≥28 for a manand especially Peguero Criteria (deepest S + S in V4 ≥28mm for a manare met. NOTE: Short, horizontal BLUE lines in leads V4 and V5 indicate the limits for R wave and S wave amplitude in these leads, in which overlap of complexes makes assessment a bit challenging.
  • Q-R-S-T Changes  There are small, narrow Q waves in leads V5 and V6 (most probably normal septal q waves). R Wave Progression — shows slightly delayed transition (the R becomes taller than the S wave is deep between lead V4-to-V5). ST-T Waves — show ST segment straightening (short PURPLE lines in leads V4,V5,V6) and frank ST flattening (PURPLE lines) in leads V2 and V3. This is not normal — as the ST segment should normally be gently upsloping (Please see My Comment in Dr. Smith’s June 9, 2019 Blog). And, there is even a hint of ST depression in leads V5 and V6.
  • As noted by Dr. Smith — it is because of this ST segment straightening and flattening in multiple chest leads — that the abnormal shape of the T waves in leads V2-thru-V6 should be noted. As a memory aid — the shape of the Eiffel Tower (= tall and rising to a point at the top, but with a surprisingly narrow base) — should recall the shape of typical hyerkalemic waves (See Figure-1).
Putting this Together to formulate your Clinical Impression:
  • After looking at the ECG in Figure-1 — my thoughts were that we needed to know more about this patient! I saw sinus rhythm — a prolonged QTc — definite LVH by voltage — and, ST segment straightening + flattening (and slight ST depression) T waves in multiple leads that strongly suggested hyperkalemia.
  • The fact that the QTc is prolonged in association with hyperkalemia should suggest that there may also be hypocalcemia (these 2 electrolyte abnormalities in patients with renal disease so often go hand-in-hand). Although sensitivity and specificity of the ECG is far from optimal for detection of hypocalcemia — the morphologic picture we see here (ie, with fairly straightened but not elevated ST segments, at the end of which appears a hyperkalemia-looking T wave) should strongly suggest this possibility, especially in a patient with severe renal disease.
  • NOTE  Marked LVH is very common in chronic dialysis patients. The reason why T waves in ECG #1 are not all that tall in multiple leads — and why ST-T wave changes typical for LV “strain” are not seen — might be that these 2 conditions are each attenuating ST-T wave effects of the other (ie, IF on a “baseline” of marked LVH + “strain”, serum K+ then becomes markedly elevated — then you might see exactly the ST-T wave pattern we see here in Figure-1in which there is diffuse ST straightening with slight lateral ST depression + relatively modest T wave height in most leads given the high K+ value = 6.3 mEq/L).
  • P.S.  Very important point emphasized by Dr. Smith! — when going back in the patient’s chart to look for prior tracings — BE SURE (as best you can) to determine the patient’s clinical status athe time the baseline” tracing was done. This is why peaked and pointed T waves looked “unchanged” from the first prior tracing in this case — when the patient’s serum K+ was also high ( = 6.6 mEq/L) at that time.

Figure-2: The user-friendly criteria I favor for ECG diagnosisof LVH (For my source —  CLICK HERE).



Tuesday, March 19, 2019

A Pathognomonic ECG. What is it?


This patient presented with weakness, decreased urine output, and vomiting:
What is the ECG diagnosis?




















There is a very long QT (computer says the QTc is 525 ms) due to a long ST segment.  This is pathognomonic for hypocalcemia.  The ionized Ca was 2.34 mg/dL (normal is 4.4-5.2)

The Cr was 12.1 indicating (new onset) of renal failure.

Calcium was given without much change.

The next AM the non-ionized Ca was 5.7 mg/dL (normal: 8.6-12.0).

Here was a repeat ECG:
QTc 523.  Long ST segment remains.

Although the QT is very long, long QT due to hypocalcemia is rarely associated with Torsades de Pointes.





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Comment by KEN GRAUER, MD (3/19/2019):
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There are a number of ECG patterns that should immediately suggest a clinical diagnosis. This is one of them! The value of recognizing this particular ECG pattern — is that it may expedite your clinical diagnosis even before laboratory results return.
  • To my reading — both of the ECGs in this case looked similar. I chose the 1st ECG — and for clarity, I’ve put it together with a user-friendly method I devised many years ago to rapidly estimate the QTc (Figure-1).

Figure-1: The initial ECG in this case — and a rapid method for estimating the QTc (See text).


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COMMENT: I wanted to discuss a number of interesting aspects regarding the ECG in Figure-1. As per Dr. Smith — our attention is immediately captured by the very long QTc interval in ECG #1. Measurement of intervals is one of the tasks that the computerized ECG interpretation is usually very accurate with. The computer calculated a QTc 525 ms for the ECG #1.
  • I like the eyeball method” to tell at a glance if the QTc is likely to be prolonged. Assuming the heart rate is not too rapid (this method works less well with heart rates >90-100/minute) — one may suspect that the QTc will be long if the longest QT interval that you can clearly see on the tracing is more than half the R-R interval.
  • To quickly estimate a numerical value for the QTc — I developed a Correction Factor that has been surprisingly accurate for me in assessing too-numerous-to-count QTc values that I’ve estimated over the past 3+ decades.  As per the text under the ECG in Figure-1 — you only need to remember 3 values (ie, 1.1 for a rate ~75/min; 1.2 for ~85/min; and 1.3 for ~100/minute). With a little practice using this method — you can estimate the QTc within seconds.
  • Applying my method to the case at hand — the rhythm in ECG #1 is regular, with an R-R interval just under large boxes. Thus, the heart rate is just a bit over 75/minute (ie, 300÷4). I selected lead V3 as one of the leads where we can clearly define the onset and offset of the QT interval. I measure the QT in this lead to be ~2.4 large boxes = 480 msec. Using a correction factor of 1.1 (since the heart rate ~75/minute) — I estimate the QTc = 480 + [480 X .1 = 48) = 480 + 48 ~528 msec. For speed and ease of calculation — I usually round off values (it’s all an estimate anyway! ) — but I’ve enjoyed being able to get very close to computer-calculated QTc values by this simple correction factor method.

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When the QTc is Prolonged:  Assuming there is no bundle branch block, ischemia or infarction — I suggest remembering the following short LIST whenever you recognize QTc Prolongation. Think ofiDrugs (many drugs prolong the QT interval — and combinations of drugs may result in marked prolongation)iiLytes” (ie, Think of low K+ — low Mg++  and/or — low Ca++)andiiiCNS Catastrophe (ie, stroke, bleed, coma, seizure, trauma, brain tumor).
  • Clinical correlation will typically suggest which one or more of these 3 causes of a prolonged QTc is operative for the case at hand. The patient in the case presented here had new-onset renal failure — so, assuming normal mentation and no potentially QT-altering drugs — electrolyte disturbance should be strongly suspected.

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ECG Findings of HypoCalcemia:  Hypocalcemia generally prolongs the QT interval. It is therefore one of the entities on our short LIST to immediately think of whenever you recognize QT prolongation.
  • PEARL #1: In theory — pure hypocalcemia does not affect the T wave! As a result — the characteristic ECG picture of hypocalcemia is that of a flat and prolonged ST segment, at the end of which occurs a surprisingly normal-looking T wave.
  • PEARL #2: Hypocalcemia and hyperkalemia may occur together in patients with renal failure. Clinically — this combined electrolyte disorder may occasionally be suspected by the ECG finding of peaked T waves with narrow base that occur at the end of a long and flat ST segment that produces a prolonged QT interval.

Final THOUGHT: We were not told what the serum K+ value was in this case. Given the very long QT interval in ECG #1 the remarkably flat ST segment in most leads the peaked and relatively narrow base for many T waves that look taller-than-they-should-be in leads II, III, aVF, and V2-V4 — I suspect combined Hypocalcemia and Hyperkalemia in this case.






Thursday, March 24, 2016

A Pathognomonic ECG

This was sent to me by Mauro Cassazza from Italy:
What do you see?

















Analysis

It is tempting to think that the waves before the QRS are large P-waves, but in fact one can discern P-waves within these large waves (see V2 in particular).

Thus, these are very late T-waves.   Thus the QT interval is very long.

I measure the QT interval at about 520 ms.  Since the RR interval is about 560 ms, then the Bazett-corrected QTc is about 690 ms (very long).  

What part of the QT interval is long?   Is the T-wave itself very wide?  Is the time from T-wave peak to T-wave end (T-peak to T-end, or TpTe, long)?  No!  

TpTe is perhaps the best predictor of Torsade de Pointe (TdP).

The long QT is due to a very long ST segment.   This is pathognomonic of hypocalcemia.  The fact that hypocalcemia affects the ST segment and not the TpTe interval may account for the fact that TdP from long QT due to hypocalcemia is exceedingly rare, with only a few case reports (in which the etiologic link to low calcium is not even definitely established).  

In hypocalcemia (long ST, but NOT a wide T-wave, not a long TpTe), depolarization has a long duration, but repolarization occurs relatively quickly.  

The ionized calcium was 1.08 mg/dL.  I do not have information on the etiology.


Clinical history

This was an elderly woman who presented with altered mental status.  Vital signs were normal except for an oxygen saturation of 91% and temperature of 35C.
Exam had peripheral vasoconstriction, but otherwise normal
Bedside US: normal
Chest x-ray: normal
No tetany!
Calcium gluconate was given.


After the Ca was replenished to 4.09 mg/dL, this ECG was recorded:
The T-waves are somewhat flat, but you can see that the QT interval is now about 370 ms, QTc about 460 ms, and a normal ST segment.


The patient's mental status normalized.
The etiology of the hypocalcemia was not investigated.

Learning Points:

1. Hypocalcemia causes a long QT by lengthening the ST segment.
2. The T-wave duration, specifically the TpTe does not lengthen
3. It is a long TpTe which is most responsible for Torsades in long QT
4. Thus, long QT in hypocalcemia does not appear to have nearly the risk of long QT from other etiologies.




T-Peak to T-end (TpTe)
This comes from a manuscript that Dr. Ken Dodd and I have written.  Ken was my primary co-author on the derivation of the Modified Sgarbossa Criteria. 

"In patients with normal conduction, the TpTe interval has been noted to prolong during myocardial ischemia and correct after reperfusion [1, 2]. It has also been claimed to predict mortality after myocardial infarction and has been called the best determinant of TdP development in the setting of acquired bradydysrhythmias [3]. In patients with LBBB, prolongation of the TpTe has been shown to be independently associated with sudden cardiac death [4]."

[1]     Eslami V, Safi M, Taherkhani M, Adibi A, Movahed MR. Evaluation of QT, QT dispersion, and T-wave peak to end time changes after primary percutaneous coronary intervention in patients presenting with acute ST-elevation myocardial infarction. J Invasive Cardiol 2013;25:232–4.

[2]     Gupta P, Patel C, Patel H, Narayanaswamy S, Malhotra B, Green JT, et al. T(p-e)/QT ratio as an index of arrhythmogenesis. J Electrocardiol 2008;41:567–74. doi:10.1016/j.jelectrocard.2008.07.016.

[3]     Topilski I, Rogowski O, Rosso R, Justo D, Copperman Y, Glikson M, et al. The morphology of the QT interval predicts torsade de pointes during acquired bradyarrhythmias. J Am Coll Cardiol 2007;49:320–8. doi:10.1016/j.jacc.2006.08.058.

[4]     Panikkath R, Reinier K, Uy-Evanado A, Teodorescu C, Hattenhauer J, Mariani R, et al. Prolonged Tpeak-to-tend interval on the resting ECG is associated with increased risk of sudden cardiac death. Circ Arrhythm Electrophysiol 2011;4:441–7. doi:10.1161/CIRCEP.110.960658.

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