What lies beneath this month's column are the foundations of what we know and how we build with bricks the ideas of which we are sure and of what we are convinced. And to take us there is the ECG, that insistent, pounding song-sheet of the living. This technology, virtually unchanged since Einthoven got the bright idea of it in 1895, is a straightforward, easily understandable set of waves depicting the activity of the heart. Or is it?
Let us talk about cerebral T waves. What causes them? It's an unusual hill to die on, sure, but these always trouble me deeply. Every year or so while teaching our trainees in the warrens of our hospital, I will ask somebody the question, “What causes the unrivalled majesty of these beasts? The plunging symmetrical inverted Ts seen in raised intracranial pressure, in particular, subarachnoid hemorrhage.” I ask because I do not know.
Uniformly I will be told: It is caused by a sympathetic storm, resulting in subendocardial ischemia. This, of course, does not make sense, and I may, on occasion, sigh dramatically and point this out. We will then parry a little and try to leap across the logic gap. We see sympathetic surges in other conditions, such as acute severe trauma and uncommon autonomic dystonia, yet these deep T waves are not routinely seen. And on the flip side, subendocardial ischemia, a result of metabolic demand mismatch, such as in type 2 acute myocardial infarction, usually results in ST depression. Yes, it can be widespread, but those cavernous T waves are nowhere to be seen.
I can hardly blame our juniors. A quick scout through current textbooks gives us little intellectual succor. If the cause of them is mentioned at all (which it rarely is), the pat line is repeated—sympathetic outflow, subendocardial ischemia.
Reviewing the literature doesn't propel us a whole lot further. UpToDate agrees acute neurologic events have myriad cardiac complications: Left ventricle (LV) regional wall abnormalities and transient LV dysfunction (a breed of Takotsubo cardiomyopathy), troponin leaks, and a smorgasbord of repolarization abnormalities. (June 26, 2018; http://bit.ly/31sXLKa.) True cerebral T waves, however, don't make the cut.
In one of the largest series—800 patients with a primary diagnosis of acute ischemic or hemorrhagic stroke—only 2.1 percent showed cerebral T waves (and all of these events were ischemic). (Am J Cardiol. 2018;121:120.) But we know that it is the severe subarachnoid hemorrhage most likely to manifest these ECG changes. So, we have to venture further down the rabbit hole to 1998 and a paper by Munoz, et al., which focused on subarachnoid hemorrhages, demonstrating that 11 of 14 patients had ECG changes, with five having left ventricle dysfunction. (Med Clin [Barc]. 1998;111:6.) But the ECG changes were protean, and it is unclear how many were true, distinctive cerebral Ts. There is some evidence for unilaterality in cardiac manifestations of neurologic disease, with left insular area involvement having greater arrhythmogenesis than the right (which is very cool).
Animal models direct us down another corridor into this unexpected theory, that right hypothalamic stimulation markedly increases T wave amplitude while left-sided stimulation decreases it. (Crit Care Med. 1973;1:192; http://bit.ly/31rnXoB.)
Current theories are, thankfully, being hotly debated. Autopsies of patients with these electrocardiographic findings sometimes show contraction band necrosis, and a current working theory is that catecholamines may be released from intramyocardial nerve endings rather than a systemic splurge in some of these patients when the hypothalamus is tickled with blood. (Heart-Brain Interactions. Berlin: Springer-Verlag; 1992.) Some theories propose a genetic disposition. MRI examination suggests endomyocardial edema. It all amounts to the fact that we are not yet sure what causes the specific pattern.
What matters? Almost nothing.
Does having these ECG changes with a severe intracranial event change management? Not really. A small proportion will have LV dysfunction, and there may be an increased risk of arrhythmias, but these patients are usually managed in critical care anyway.
So, we're really just talking irrelevant minutiae. Or are we?
The point is the unqualified proliferation of sureties. In this era of #FakeNews, Cambridge Analytica, lies that travel halfway around the world before the truth has a chance to pull up its pants (incorrectly attributed to Winston Churchill, then further relegated, also incorrectly, to Mark Twain. Thank you, internet), it is we in the scientific fields who have a responsibility to ensure we can verify information as true, as best as we are able, before we propagate it. And if we can't, it is appropriate that we admit it.
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Dr. Johnstonis a board-certified emergency physician, thus the same as you but with a weird accent. She works in a trauma center situated down the unfashionable end of Perth, Western Australia. She is the author of the novel Dustfall, available on her website, http://michellejohnston.com.au/. She also contributes regularly to the blog, Life in the Fast Lane, https://lifeinthefastlane.com. Follow her on Twitter @Eleytherius, and read her past columns at http://bit.ly/EMN-WhatLiesBeneath.Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.