Unconscious + STEMI criteria: activate the cath lab?

Case submitted and written by Dr. Mazen El-Baba and Dr. Evelyn Dell, with edits from Jesse McLaren

EMS brought a John Doe, in his 30s, who was found in an urban forest near a homeless encampment on a cool fall day. There were no signs of trauma on scene or on the patient. EMS reported an initial GCS of 8 with pupils equal and reactive. The patient had a witnessed generalized tonic-clonic seizure leading to GCS 4. Vitals: HR 45; systolic BP was 110-120; irregular respiratory rate; oxygen saturation was normal; tympanic temperature 30; glucose was 6. In the resuscitation room, the patient had another seizure that stopped after IV Lorazepam. ECG met STEMI criteria and was labeled STEMI by computer interpretation. What is your ECG interpretation, and would you activate the cath lab?

What do you think?

This ECG shows a sinus bradycardia with a normal conduction pattern (normal PR, normal QRS, and normal QTc), normal axis, normal R-wave progression, normal voltages. There’s ST elevation inferolaterally, with reciprocal ST depression in aVL. But it has an atypical morphology, followed by almost no T wave, and preceded by J waves. 

 

J waves (the small deflection at the R-ST junction) on the baseline ECG are often associated with normal variant ST elevation. While traditionally described as “benign early repolarization”, they have been associated with J wave syndromes along with Brugada syndrome, causing ventricular arrhythmias (1, 2). Acute and reversible J waves are called "Osborn waves" and are often associated with hypothermia which can also induce ventricular arrhythmias (3), where their size correlates with colder temperatures and resolves with warming (5). J waves can also be induced by Occlusion MI (5), STEMI mimics including takotsubo and myocarditis complicated by ventricular arrhythmias (6, 7), and subarachnoid hemorrhage with VF (8). 

Clinical questions:

1. Is this an occlusion myocardial infarction and does the patient need the cath lab?

While meeting STEMI criteria, the morphology is atypical for OMI and therefore could be false positive STEMI, especially with the presentation of unconsciousness, seizure, and a perfusing rhythm. 

2. Is this takotsubo?

This can produce bizarre ST elevation that mimics STEMI, and can be caused by intracranial catastrophes that would fit the presentation. 

3. Could anything else produce this ECG pattern and clinical presentation?

Hypothermia can also produce bradycardia and J waves, with a pseudo-STEMI pattern. An esophageal thermometer was placed that read 28 degrees celsius (82.4F)! 

So rather than activating the cath lab, the patient had a stat CT head and was rewarmed.

ECG findings expected in hypothermia include: SLOWED mnemonic: 

1. Shivering artfacts 

2. Low voltages

3. Osborn waves: + deflection at the J-point in precordial and limb leads and usually a reciprocal negative deflection in aVR and V1. Osborn waves are the most specific ECG sign of hypothermia and the amplitude of the J-wave is directly correlated with the degree of hypothermia (4)

4. Wide intervals (PR, QRS, QT, RR) 

1. Including bradyarrhythmias

1. Sinus

2. Atrial fibrillation with slow ventricular response 

3. Slow junctional rhythms 

4. AV blocks 

5. Ectopy 

1. Ventricular ectopics

6. Dead (cardiac arrest due to VT, VF, or asystole) 

Case continued:

Initial blood work showed the following: mild respiratory acidosis (prior to intubation) on VBG with a lactate of 3 and pCO2 68 and a negative troponin (4 ng/L). Electrolytes and an extended electrolytes panel were normal. CT head showed traumatic SAH and small SDH with a traumatic occipital fracture. Metabolic panel including cortisol and TSH was still pending.

Active rewarming continued: patient was infused with 2L of warmed normal saline and a bear hugger was applied. His body core temperature was very resistant to change, increasing our suspicion that the cause of his hypothermia was not environmental, but due to a metabolic versus central cause.

TSH came back as 45. T3 was almost undetectable. STAT endocrine consult was made and T3/T4 infusion and IV synthroid was administered. 

Approximately 24 hours later, the patient began rewarming and his core temperature was 34.7C (94.5F). Another ECG was obtained showing the following:

Normal sinus rhythm, normal rate, normal electrical conduction (PR, QRS, QTc), normal axis, borderline low voltages, normalized ST/T with disappearance of J waves. 

Take home: 

• Not all STEs are STEMIs or OMIs. Always have a broad differential diagnosis and approach to STEs on an ECG, applied in clinical context.

• J waves can be seen with normal variant ST elevation but also Occlusion MI (see these cases of J waves with and without OMI) and its mimics including takotsubo and myocarditis.

• When faced with a hypothermic patient, think of the SLOWED mnemonic to anticipate ECG changes. 

• J waves in hypothermia (including from myxedema) are inversely related to temperature, improves with warming, and can be associated with other hypothermic changes – consider the SLOWED mnemonic: Shivering artifact, Low voltage, Osborn waves, Wide intervals, Ectopy and Deadly arrhythmias

References

1. Osborn waves: history and significance. Indian Pacing Electrophysiol J 2004

2. Antzelevitch C, Yan G.  J wave syndromes. Heart Rhythm 2010

3. Hudzik B, Gasior M. J-waves in hypothermia. CMAJ 2017

4. Vassallo SU, Delaney KA, Hoffman RS, et al. A prospective evaluation of the electrocardiographic manifestations of hypothermia. Acad Emerg Med 1999

5. Rituparna S, Suresh S, Chandrashekhar M, et al. Occurrence of “J Waves” in 12-Lead ECG as a Marker of Acute Ischemia and Their Cellular Basis. Pacing Clin Electrophysiol 2008

6. Choi SH, Lee OH, Yoon G-S, et al. The relationship between J wave and ventricular tachycardia during Takotsubo cardiomyopathy. Internat J Arrhyth 2020

7. Uesako H, Fukikawa H, Hashimoto S, et al. Prominent J waves and ventricular fibrillation caused by myocarditis and pericarditis after BNT162b2 mRNA COVID-19 vaccination. Can J Cardiol 2022

8. Kukla P, Jastrezebski M, Praefort W. J-wave-associated ventricular fibrillation in a patient with a subarachnoid haemorrhage. Europace 2012

9. Shinde R, Shinde S, Makhale C, Grant P, Sathe S, Durairaj M, Lokhandwala Y, Di Diego J, Antzelevitch C. Occurrence of "J waves" in 12-lead ECG as a marker of acute ischemia and their cellular basis. Pacing Clin Electrophysiol. 2007 
   

   10. Maruyama M, Kobayashi Y, Kodani E, Hirayama Y, Atarashi H, Katoh T, Takano T Osborn waves: history and significance. Indian Pacing Electrophysiol J. 2004 

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My Comment by KEN GRAUER, MD (1/21/2023):

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I thought today's case by Drs. El-Baba, Dell and McLaren to be intriguing for a series of important concepts that it raises — as well as for a number of equally intriguing unanswered questions.

• I'll add the following points to the detailed discussion by Drs. El-Baba, Dell and McLaren.

ECG Signs of Hypothermia:

As per the above discussion — the "SLOWED" mnemonic facilitates recall of the many ECG findings associated with hypothermia. I'd suggest slight alteration of this mnemonic:

• Instead of "E" for "Ectopy" — I'd use the "E" for "Elevation" — as it is common for hypothermia to produce ST elevation, sometimes in multiple leads (as was seen in today's case).
• The final letter in the SLOWED mnemonic is "D" for "Dead" (resulting from VT/VF or asystolic cardiac arrest). In a sense — frequent ventricular ectopy is already included in this "D" (which frees use of the "E" to prompt recall of ST elevation that may be seen with hypothermia, and which is not the result of acute OMI).

Large Osborn Waves:

We've discussed Osborn Waves (both ischemic and hypothermic) — on a number of occasions in Dr. Smith's ECG Blog (Please check out My Comment at the bottom of the page in the February 8, 2022 post). When due to ischemia — Osborn waves may be associated with high risk of developing malignant ventricular arrhythmias (My Comment in the September 23, 2020 post). When due to hypothermia — there is a correlation (as noted by Drs. El-Baba, Dell and McLaren) between severity of hypothermia and the size of Osborn Waves.

• Although present in a number of leads in today's initial tracing (See Figure-2 below) — despite the low esophageal thermometer reading of 84°C ( = 82.4°F) — the Osborn Waves in today's case are relatively small.
• For illustrative purposes, contrast the size of the Osborn Waves in today's case — with the truly huge Osborn Waves in Figure-1, which I've taken from the February 8, 2022 case (RED arrows in Figure-1). It should be noted that on presentation to the ED — the patient whose ECG is shown in Figure-1 had a much lower core temperature than the 31°C shown in the label of Figure-1 — which tells us that after the appearance of Osborn Waves — there may be a "lag time" for these exaggerated J waves to resolve. But the point is to appreciate the potential variability in Osborn Wave size, with awareness of how large they can sometimes become!

Figure-1: RED arrows highlight huge Osborn Waves in multiple leads. (This is the 2nd ECG from the February 8, 2022 post in Dr. Smith's ECG Blog).

The ECGs in Today's Case:

For clarity and ease of comparison — I've put both ECGs from today's case together in Figure-2.

• RED arrows show modest J-point notching (Osborn Waves) in ECG #1.
• There is marked sinus bradycardia.
• As per Drs. El-Baba, Dell and McLaren — although there is inferolateral ST elevation (that technically satisfies "STEMI" critieria) — the morphology of this elevation is atypical for OMI. It just doesn't "look" acute. Even the subtle ST depression in lead aVL looks less like a reciprocal change — and more like a nonspecific longterm finding.
• There also are narrow Q waves in several inferolateral leads that manifest ST elevation — which I interpreted to be of uncertain significance (possibly just normal septal q waves).
• 
  
• Comparison of ECG #1 with the repeat tracing done ~1 day later after partial rewarming shows resolution of all ECG signs of hypothermia. Specifically — the heart rate has normalized — all intervals (PR, QRS, QTc) have narrowed — Osborn Waves have vanished — the small and narrow inferolateral "normal septal q waves" remain — and there is no longer ST elevation nor reciprocal ST depression. Instead, flat T waves in a number of leads were beginning to regain some of their normal amplitude.

Figure-2: Comparison between the 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

Questions Raised by Today's Case:

Today's patient presented with marked hypothermia in an uncommunicative state, with an initial GCS recorded by EMS personnel on the scene = 8, consistent with severe neurologic impairment. Although there were "no signs of trauma on scene or on the patient" — Head CT revealed an occipital fracture, with traumatic SAH and a small SDH. Seizure activity was witnessed in the ED. Other lab pertinent to today's case included:

• TSH = 45
• T3 = almost undetectable ...
• Normal serum electrolytes; Normal troponin.
• Glucose = 6

Core rewarming took longer than anticipated ...

• Since the patient was non-communicative — details of his history were unknown. 
• A TSH = 45 is markedly elevated (although not to the extremes of patients with the most severe forms of hypothyroidism). How long this patient had been hypothyroid, and how severe his symptoms had been before this hypothermic and traumatic episode — was therefore uncertain. Did he have very-slow onset, therefore previously undetected hypothyroidism that had left him functioning — but for which the homeostasis that had been maintained was interrupted by one or more "precipitating" factors (ie, cold exposure — neurologic trauma)? — OR — Was this myxedema coma? (See Wiersinga on Myxedema/Severe Hypothyroidism).
• 
  
• Given the absence of signs of trauma at the scene and on the patient — How did he sustain an occipital fracture with traumatic SAH?
• What happened first? How much interaction was there between hypothermia — hypothyroidism — and neurologic injuries — in terms of exacerbating the other conditions? (ie, temperature regulation may be impaired with severe hypothyroidism or neurologic trauma — cold exposure may aggravate thyroid function, etc.). 

Additional Learning Points:

I informally consulted my favorite endocrinologist about this case. He offered the following suggestions re optimal management.

• "Sick Euthyroid Syndrome" may be seen in acutely ill patients — in whom T3 and T4 may be markedly decreased because of the patient's illness. But in such cases — the TSH remains normal. The fact that the TSH = 45 in today's case indicates definite (and significant) hypothyroidism. 
• T3 levels are most useful when assessing hyperthyroidism (especially Graves' disease). That said — the "almost undetectable" T3 level in today's case does not add to our understanding about the state of this patient's hypothyroidism (ie, many factors may cause T3 to drop). Instead — a free T4 level would be the test of choice to complement TSH in the assessment of hypothyroidism.
• The fact that today's patient's serum glucose was extremely depressed is relevant — because this is not a typical sign associated with hypothyroidism. Instead — it is commonly seen in Addison's disease, which is part of polyglandular failure and autoimmune endocrine disease. Hypothyroid patients are at higher risk of autoimmune adrenal failure (especially when glucose values are so low in such patients). As a result — one should not give IV T4 without also administering IV cortisol (to cover for the possibility of associated adrenal failure). This is because the catabolism of cortisol is enhanced by treating the low T4. This further lowers cortisol levels — and may be harmful if associated undetected adrenal failure is present.
• Don't forget to test for adrenal failure (with an ACTH level).
• True myxedema coma is rare. That said — simple hypothyroidism + some other potential precipitating factor (ie, hypothermia, neurologic injury) — can severely aggravate the endocrine situation and mimic the presentation of myxedema coma. Unfortunately — uncertainty resides in today's case until we can learn more about what precipitated this patient's condition (and about what his state of health and function had been prior to these events).