Tuesday, April 19, 2022

ECG Blog #299 — Unresponsive and an Acute MI?

The ECG shown in Figure-1 is from a woman in her 60s. There was sudden loss of consciousness.

  • Should the cath lab be activated?
  • What is the rhythm?

Figure-1: The initial ECG in Today's Case (See text).


MY Thoughts on the ECG in Figure-1:

The patient was unresponsive at the time ECG #1 was recorded. I first looked at the rhythm. As per ECG Blog #185 — By the Ps, Qs, 3R approach:

  • The rhythm in the long lead II at the bottom of the tracing is fast and irregular.
  • Beats #7 and 16 are clearly wider and different-looking than the other beats on the tracing. These 2 beats are PVCs (Premature Ventricular Contractions).

  • Although I initially thought the QRS complex was wide everywhere — on closer inspection (except for beats #7 and 16) — the vertical dotted BLUE lines that I have added in simultaneously-recorded leads for each of the lead groups (in Figure-2) — verify that the QRS complex for all other beats on this tracing is narrow. Instead — it is the presence of marked "Shark-Fin" ST elevation that accounts for the mistaken appearance that the QRS is wide — when in fact the QRS is narrow (See ECG Blog #265for review of Shark Fin ST elevation).

  • By the Ps, Qs, 3R approach — this leaves us with having to account for atrial activity. Once again — my initial impression that P waves are present in front of many QRS complexes was not necessarily accurate. It is the presence of gross baseline artifact that makes rhythm assessment so difficult in this tracing (this artifact being most marked in leads III and aVF — but present to some extent throughout).

  • CONFESSION: I still am not certain what the rhythm in ECG #1 is. Certain beats (ie, beat #17especially if you look at this beat in simultaneously-recorded lead V1) — clearly look as if they are preceded by sinus P waves with a normal PR interval (The rhythm in lead V1 looks like a slightly irregular sinus tachycardia with a PVC for beat #16).
  • That said — the overall rhythm in the long lead II is clearly irregular — and coarse "fib waves" appear to be present during the post-ectopic pause between beats #7-to-8 (as well as in the shorter R-R intervals after beat #3 and after beat #17 in the long lead II rhythm strip). Additional coarse fib waves plus artifact appear to be present in lead III.

  • BOTTOM LINE: I suspect that the rhythm in ECG #1 is rapid AFib (Atrial Fibrillation). That said, even now — I am still not certain about the rhythm diagnosis. Clinically, however — the rhythm was less of a concern at the bedside than the marked "Shark-Fin" ST elevation that is present in multiple leads (ie, leads I, II, aVL; V2-thru-V6). Did the cath lab need to be activated?


Figure-2: I've labeled Figure-1 with vertical dotted BLUE lines in simultaneously-recorded leads, to clarify where the QRS complex ends.

CASE Follow-Up:
First priority in this case was to stabilize the patient. The patient was intubated, vital signs were stabilized — and the ECG was repeated (Figure-3). The patient remained unresponsive.

Figure-3: The repeat ECG that was obtained after the patient was intubated and stabilized (about 1 hour after ECG #1 had been done).

Comparison of the Repeat & Initial ECGs:
The repeat ECG in Figure-3 shows sinus rhythm at a much slower and regular heart rate (of ~70/minute). The PR interval is normal.
  • The QRS complex in ECG #2 is clearly of normal duration. This confirms the measurements I suggested for QRS duration by the dotted BLUE lines drawn in Figure-2. Of interest — except for a slight frontal plane axis shift and somewhat increased QRS amplitude in a number of leads — QRS morphology in ECG #2 is similar to QRS morphology in ECG #1.

  • The QTc is prolonged. One should measure intervals in whatever lead clearly shows the onset and offset of the interval, and in which the interval is longest. I measure the QT interval to be ~460 milliseconds in lead V2 of ECG #2 — which for a heart rate of ~70/minute — corrects for a QTc ~480 msec.

  • Otherwise — the axis in ECG #2 is normal (about +40 degrees) — and, there is now voltage for LVH (very tall R waves in the lateral chest leads). There is still J-point ST elevation in multiple leads, with straightening of the ST segment takeoff (if not ST segment coving i leads V2, V3). That said — the amount of ST elevation is markedly reduced in ECG #2 compared to what was seen in the initial ECG!

CASE Follow-Up:
Given the patient's sudden unresponsive state — a non-contrast Brain CT Scan was ordered — the results of which are shown in Figure-4:
  • The subarachnoid (or basal) cisterns are compartments within the subarachnoid space where the pia mater and arachnoid membrane are not in close contact with each other — such that CSF (CerebroSpinal Fluid) may "pool" in these spaces. As these cisterns are all interconnected — circulation of CSF depends on their patency. 
  • YELLOW arrows in Figure-4 highlight a few of the hyperdense (light gray) areas within the cisterns and other areas in the brain where there is blood in the subarachnoid space.

Figure-4: Non-contrast CT scan showed multiple areas of hyperdensity (light gray areas) — reflecting a large amount of blood in the subarachnoid space (YELLOW arrows highlight a few of these hyperdense areas).

ECG Changes in SAH (SubArachnoid Hemorrhage):
There has long been literature documentation of ECG abnormalities with CNS catastrophes — which are often particularly marked in association with SAH (ChatterjeeNeth Heart J 19:31-34, 2011) — (Saritemur et alAm J Emerg Med 31:271.e5, 2013) — (Park et al Clin Exp Emerg Med 2:260-263, 2015).
  • ECG abnormalities encompass QTc prolongation — development of large U wavesplusST elevation and/or T wave inversion that on occasion may be accompanied by reciprocal ST depression in leads opposite the ST elevation. 

  • Cardiac arrhythmias are also common with SAH — including bradycardiaAFibfrequent PVCsVT/VFib — and Torsade de Pointes (especially if the QTc is significantly prolonged).

  • Among the proposed mechanisms accounting for ECG abnormalities associated with SAH are: i) Hypothalamic stimulation; and, ii) Autonomic dysfunction with resultant catecholamine surge.

  • NOTE: ECG abnormalities associated with SAH tend to be most marked within the first 48-72 hours after onset of this neurologic event. Troponin may be elevated with SAH (usually not by a large amount — but enough to confuse the issue) — and regional wall motion abnormalities may be seen due to neurogenic stunned myocardium.

  • Clinical implications for being aware of SAH as an important cause of "Pseudo-Infarction Patterns" to consider, are obvious from today's case — in which consideration was initially given to activating the cath lab. Doing so would not only subject the patient to an unnecessary invasive procedure — but would further delay diagnosis of the real cause of ECG abnormalities (ie, SAH). Cardiac cath was not done given the patient's overall clinical condition.

  • SAH is not uncommonly associated with out-of-hospital cardiac arrest. In such cases — the patient will most often still be unresponsive on arrival in the Emergency Department. It is easy to imagine how confusion as to the cause of patient collapse might arise when the initial ECG shows a pseudo-infarction pattern from unsuspected SAH.

  • Take-Home Message: In an unresponsive, resuscitated patient — SAH should be considered as a possible cause of cardiac arrest regardless of whether or not the ECG suggests an acute STEMI.

Did YOU Recognize the Spiked Helmet Sign?
The final interesting ECG sign seen in today's case is the Spiked Helmet Sign (See Figure-5).
  • 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 the sudden loss of consciousness, as occurred in this 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 righ part of Figure-5 — 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.).

  • 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!

  • The proposed mechanism 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 — 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-5
  • Further support that the ST elevation pattern of SHS is not the result of acute infarction may be forthcoming from atypical distribution of the QRS-ST segment changes on the 12-lead ECG — and lack of the typical evolutionary pattern of ECG changes seen with true STEMI.

  • Returning to the initial ECG in today's case — I've outlined in RED in Figure-5 the features of the Spiked Helmet Sign that are seen in a number of leads in ECG #1. Although the pre-QRS elevation component of SHS is admittedly subtle — Isn't the pointed spikes with associated marked ST elevation and coving seen in multiple leads striking?

Figure-5: Features of the Spiked Helmet Sign that are seen in multiple leads in the initial ECG from today's case. The insert with the spiked helmet is from Laszlo Littmann’s 2011 Letter to Mayo Clinic Proceedings (See text). 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.


Acknowledgment: My appreciation to 陳俊宏 (Chun-Hung Chen from Taichung City, Taiwan) 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 #265 — which reviews in detail a case of "Shark Fin" ST elevation due to ischemia/infarction from CO poisoning.
  • The November 22, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was cardiac arrest, ischemic Osborn waves, with massive Shark Fin ST deviation from acute STEMI.
  • The June 11, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LPHB), in addition to Shark Fin ST elevation & depression. 
  • The January 24, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LAHB), in addition to Shark Fin ST elevation & depression — followed by progressive Low Voltage due to Myocardial Stunning from the huge infarct.


  1. Hi Prof, This is a great great Post. SuBarachnoid Haemorrhage and MORE, My colleagues and students love this and there is much to learn and treasure as gems, thanks

    1. @ Plus Ultra — THANK YOU so much for the positive feedback. Glad this was helpful! — :)