Saturday, June 4, 2022

ECG Blog #310: A Special Hat Sign?

An acutely ill man in his 40s was admitted to the hospital. Suffice it to say that the patient was intubated — and that there was multi-organ involvement including effects from severe alcoholism, mental confusion, tenuous fluid balance — and significant ventricular dysfunction on Echo. His initial ECG is shown in Figure-1.
  • How would you interpret this initial tracing?

Figure-1: Initial ECG of an acutely ill man in his 40s with multi-organ involvement (See text).

MY Thoughts on the Initial ECG in Figure-1:
The rhythm in ECG #1 is sinus at a rate of 90-95/minute (ie, a small but definitely-present upright P wave is seen in lead II — and negative sinus P waves are consistently seen in leads V1 and V2).
  • Regarding Intervals: The PR interval is normal — and the QRS complex is narrow — but the QTc is markedly prolonged (especially in the lateral chest leads — the QT takes up ~2/3 of the R-R interval!).
  • The frontal plane axis in ECG #1 is normal (about +60 degrees).
  • There is no chamber enlargement.
  • Small (probably insignificant) q waves are seen in multiple leads (ie, leads I,II,III,aVF; V4,V5,V6). R wave progression is slightly delayed (Transition, where the R wave becomes taller than the S wave is deep — occurs between leads V4-to-V5).

  • ST-T wave appearance is remarkable, in that ST segments are coved (although not significantly elevated) in multiple leads — with diffuse, wide and extremely deep T wave inversion.
  • Especially in leads V4,V5,V6 (but also in several limb leads) — I found it difficult to determine where the baseline was!

My IMPRESSION of ECG #1: Sinus rhythm — a narrow QRS, but markedly prolonged QTc interval — diffuse ST segment coving (but probably not significant ST elevation) accompanied by wide and deep, symmetric T wave inversion — with a highly unusual picture in which it is difficult to determine where the baseline is.
  • Starting with what ECG #1 is "not" — I did not interpret this tracing as suggestive of acute infarction. 
  • Instead — the marked QTc prolongation — with diffuse ST-T wave abnormalities (ST coving; deep, wide and symmetric T wave inversion) that are not attributable to any specific anatomic area is highly suggestive of Takotsubo Cardiomyopathy (See ECG Blog #46for full discussion of this entity). The acutely ill state of today's patient, together with the report of significant ventricular dysfunction on Echo could certainly be consistent with Takotsubo (Clearly — specifics of the Echo would be needed to determine if the findings were or were not diagnostic of Takotsubo).

  • BOTTOM LINE: In addition to suspicion about Takotsubo Cardiomyopathy — I thought ECG #1 was strongly suggestive of the Spiked Helmet Sign.

Did YOU Recognize the Spiked Helmet Sign?
The common theme of today's case involving this patient with severe multi-system disease, with consideration of Takotsubo Cardiomyopathy and the Spiked Helmet Sign — is increased catecholamines!
  • First described by Littman in 2011 (Letter to Mayo Clin Proc86 (12): 1245, 2011) — the Spiked Helmet Sign ( = SHS) is an uncommon and unique electrocardiographic finding, that is seen in patients with acute critical illness (such as described in today's case). The sign is typically associated with a high mortality. In addition to extensive acute MI, Takotsubo Cardiomyopathy, and cardiac arrest — other conditions that have been associated with SHS include intracranial hemorrhage, sepsis, severe metabolic disorders. Many other critical care conditions will doubtlessly be added to this list — as recognition of this important ECG sign becomes more widespread.
  • As shown for the insert in the lower right part of Figure-2 — the name of this “dome-and-spike” pattern is derived from the Pickelhaube, a spiked helmet worn in the 19th and 20th centuries by Prussian and German soldiers, as well as by policemen and firemen. (The literal translation of “Pickelhaube” in German = “pointe” or “pickaxe” for Pickel — and “bonnet” for Haube.).

Figure-2: Features of SHS (Spiked Helmet Sign) that are seen in multiple leads from the initial tracing shown in ECG Blog #299. The insert with the spiked helmet is from Laszlo Littmann’s 2011 Letter to Mayo Clinic Proceedings. I have previously used this insert Figure to illustrate another case of SHS, in My Comment from the June 28, 2020 post of Dr. Smith's ECG Blog.

ECG Findings of Spiked Helmet:
  • As described by Crinion, Abdollah & Baranchuk (Circulation 141:2106  June 23, 2020) — the QRS-ST segment with the Spiked Helmet Sign is characterized by 3 specific components: i) Some elevation of the isoelectric line that begins before the QRS complex (ie, making up the first half of the helmet); ii) Then sharp ascent of the R wave (ie, the “spike” in the helmet); and finally; iii) Coved ST elevation of varying degree, that may mimic an acute ST elevation MI (ie, the second half of the helmet).
  • One, two, or all 3 of these components may be seen in one or more leads on the ECG. Although initial reports limited the occurrence of this finding to the inferior leads — any of the 12 leads on an ECG may be affected!

  • PEARL #1: The proposed mechanism of the Spiked Helmet Sign (SHS) is fascinating — namely, a hyperadrenergic state with adrenergically mediated prolongation of repolarization. The reason for elevation of the isoelectric line beginning before the QRS complex — may result from similar pathophysiology as is seen in conditions with marked QT (and/or QU) prolongation — with the late and enlarged T and U waves being superimposed on the initial portion of the QRS. Other features shared with excessive endogenous catecholamine states (such as long QT syndrome, Takotsubo Cardiomyopathy and CNS hemorrhage) — include Torsades de Pointes, T wave alternans, and pseudo-infarct ST elevation.

  • PEARL #2: As noted above, the Spiked Helmet Sign (SHS) may produce ST elevation that might easily be mistaken for an acute STEMI. However, distinction from a STEMI can often be made by recognizing the upward shift of the isoelectric line that begins before the QRS complex — and which often comes close to “lining up” with the ST elevation seen after the QRS. This distinguishing feature is best illustrated within the PURPLE rectangle in the Spiked Helmet insert in the lower right part of Figure-2
  • Further support that the ST elevation pattern of SHS is not the result of acute infarction may be forthcoming from: i) Atypical distribution of the QRS-ST segment changes on the 12-lead ECG; and, ii)lack of the typical evolutionary pattern of ECG changes seen with true STEMI.

  • The tracing seen in the upper portion of Figure-2 is from ECG Blog #299. I've outlined in RED the features of the Spiked Helmet Sign that are seen in several leads of this ECG. Although the pre-QRS elevation component of SHS is admittedly subtle — Isn't the picture of pointed spikes with associated marked ST elevation and coving seen in multiple leads striking?

The Spiked Helmet Sign in Today's CASE:
For clarity in Figure-3 — I've put the initial ECG in today's case together with a follow-up ECG done 3 days later on this patient. The patient's clinical condition was improved at the time ECG #2 was obtained, although he was still extremely ill.
  • WHICH leads in the initial ECG ( = ECG #1) — best show the Spiked Helmet Sign?
  • What difference do you see in Figure-3 between the initial ECG — and ECG #2, that was obtained 3 days later when the patient showed signs of clinical improvement?

Figure-3: Comparison between the initial ECG — and a follow-up ECG does 3 days later after some clinical improvement.

  • In the initial ECG — the Spiked Helmet Sign is BEST seen in the lateral chest leads (leads V4,V5,V6) — but it is also suggested in leads II and aVF. The "mirror-image" of this sign is seen in lead aVR.
  • For clarity — I've outlined in RED the 3 Components of the Spiked Helmet in lead V5 of ECG #1: i) Elevation of the isoelectric line that begins before the QRS complex (1st PURPLE arrow — making up the first half of the helmet); ii) Sharp ascent of the R wave (ie, the "spike" in the helmet); and, iii) Coved ST elevation after the QRS (ie, 2nd PURPLE arrow — making up the second half of the helmet). Note that the onset of the ST elevation almost "lines up" with the top point of the pre-QRS elevation.

  • In the follow-up ECG (ie, ECG #2, done 3 days later) — the heart rate, frontal plane axis, and QRS morphology in virtually all leads is similar (with exception of the flat line in lead V3 due to a lost lead connection). The markedly long QTc, ST segment coving and diffuse wide, deep T wave inversion persist — but the isoelectric baseline is returning! As a result — a clear Spiked Helmet Sign is no longer present in ECG #2

FINAL Tracing in Today's CASE:
What I found most interesting about the ECGs in today's case — was how quickly the ECG manifestations in ECG #1 developed.
  • The patient had been seen 10 days earlier for a less severe illness. An ECG was done at that time ( = ECG #3 in Figure-4). What do YOU think?

Figure-4: Comparison of the initial ECG in today's case — with a "baseline" tracing done 10 days earlier for a less severe illness.

MY Thoughts on Figure-4:
The lead V3 electrode in the "baseline" tracing done 10 days earlier — is probably malpositioned (ie, the abrupt R wave increase from lead V2-to-V3 — followed by an equally abrupt decrease in R wave amplitude from V3-to-V4 does not make physiologic sense). That said — comparison of the frontal plane axis and QRS morphology in other leads is similar between the 2 tracings. But everything else is different!
  • The rhythm in ECG #3 — shows marked sinus bradycardia and arrhythmia, with a PAC toward the end of the tracing.
  • Given how slow the rate is — the QTc is probably no more than minimally prolonged.
  • ST-T waves are diffusely flat — with no T wave inversion.
  • The isoelectric baseline is flat throughout the entire tracing.

Today's CASE: Putting It All Together:
Seeing the "baseline" tracing from 10 day's earlier is highly insightful.
  • The "theme" for the ECG changes in today's case is "catecholamine surge"! With the space of 10 days — this patient's ECG evolved in dramatic fashion from presumed catecholamine excess due to severe acute illness (with multi-organ involvement and need for prolonged mechanical ventilation) — including alcohol withdrawal, mental confusion with suspected Wernicke encephalopathy — and probable Takotsubo (ie, "Stress") Cardiomyopathy.
  • The 1st ECG manifestation of catecholamine excess — is the significant increase in heart rate compared to the bradycardia in the earlier tracing.

  • Take-Home PEARL: The ECG picture in the initial tracing (ECG #1 in Figure-4) — shows marked QTc prolongation and diffuse ST coving with wide, deep T wave inversion, but without specific anatomic distribution. This ECG picture should immediately suggest the possibility of Takotsubo Cardiomyopathy. Loss of the isoelectric baseline in multiple leads should facilitate recognition of the 3 components of the Spiked Helmet Sign (outlined in RED in lead V5 of Figure-3). The common "theme" for the increase in heart rate and these ECG findings is catecholamine surge — which is completely consistent with the clinical presentation of today's patient.


Acknowledgment: My appreciation to Jean Max Figueiredo (from Nova Iguaçu, Brazil) for the case and this tracing.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205).

  • ECG Blog #299 — Reviews a case of Shark Fin ST Elevation with the Spiked Helmet Sign — as a result of a CNS Catastrophe (subarchnoid hemorrhage).

  • ECG Blog #46 — Reviews a case (and the KEY ECG findings) of Takotsubo Cardiomyopathy.

  • ECG Blog #59 — Reviews a case of Giant T Waves.

No comments:

Post a Comment