• David Didlake

50 Shades of T

David Didlake, NRP, APRN, ACNP-BC


This case is provided by C. Madden, Paramedic. Many thanks for sharing!


A 48 y/o Male called 911 after experiencing sudden onset chest discomfort while performing yard work. He presented to EMS with extreme pallor, Levine sign, diaphoresis, bilateral arm pain, and an apprehensive sense of doom. Past medical history included HTN, HLD, and MI 10 years prior.


It should be emphasized here that this is a presentation of high-pretest probability for Acute Coronary Syndrome (ACS). Factors consistently manifesting as such, in addition to chest pain, include, diaphoresis, vomiting, radiation of pain (most alarming when inclusive of both arms), and pain aggravated by exertion. [1]


Vitals

  • BP 160/110

  • HR 90 (trend)

  • RR 24 (BBS CTA)

  • SaO2 92% RA

Attached is the Patient's ECG.


There is mixed overlap of ST-segment elevation (STE), ST-segment depression (STD), Hyperacute T waves (HATW), and deWinter pattern (which the ACC regards as a STEMI-equivalent but is better suited under the blanket of OMI). The overall distribution of findings suggests that this LAD is a Type III, or "Wraparound", that traverses around the myocardial apex.


For a detailed review of deWinter OMI visit this post--

https://www.ems12lead.com/post/the-dewinter-debacle


Dr. Stephen Smith provides an academic hypothesis concerning the true underlying physiology of deWinter occlusion here--

https://hqmeded-ecg.blogspot.com/2014/07/is-lad-really-completely-occluded-when.html


The clinical significance of HATW's can be found here--

https://www.ems12lead.com/post/the-hyperacute-t-wave


Crews administered 324 mg of ASA and a total of 0.12 mg of SL NTG, along with a total of 100 mcg of Fentanyl with little to no change in symptoms. Here are the ECG changes after this therapy.



The nearest PCI center was activated but ultimately denied by Cardiology. Troponin I returned 80 ng/mL, and the Cath Lab was then reactivated where a 100% LAD occlusion was found and stented.


An interesting comment provided by Paramedic Madden is that a few team members initially interpreted the T wave presentation as hyperkalemia, as opposed to occlusive hyperacuity. The T waves of hyperkalemia can be just as dramatic, intimidating, and downright frightening, as HATW's, but there are distinctive characteristics that help differentiate between the two.


A brief review of the pathophysiology of hyperkalemia will help set the stage for the ECG changes inherent therein. Predisposition to hyperkalemia is complex, but in general, patients with renal disease, or those taking medications that yield potassium retention (e.g. ACE inhibitors, or potassium-sparing diuretics), are particularly susceptible. Other causes include metabolic acidosis, in which hydrogen ions shift into the cells in exchange for potassium.


Potassium is most concentrated in the intracellular space, and in doses of relative paucity along the cell exterior. Conversely, the distribution of sodium is the exact opposite -- that is, its concentration is most significant extracellularly with very little intracellular presence. These two extremes of sodium and potassium concentrations produce an electrical potential across the cell membrane, all of which is maintained by the sodium-potassium pump (aka, Na-K ATPase). The resting membrane potential (RMP) for the cardiac myocyte is classically measured at -90mv. [2]


It should be emphasized that potassium is the most important component in RMP stability. Thus, as extracellular potassium rises (due to various reasons listed above) the RMP becomes less negative and drifts closer to threshold potential (TP). TP is the moment in which depolarization is self-sustained, even irreversible, and gives rise to the upstroke of the action potential -- the point at which the cell does work: contraction, in the case of the cardiac myocyte. Different texts provide varying measures of TP, but usually in the range of -70mv to -60mv. [3]


The critical difference between the RMP and the TP is roughly 30mv.


Sodium channels are key players in the action potential, and their function is directly proportional to the RMP. Thus, if the RMP becomes less negative and drifts closer to TP (as in the case of hyperkalemia) sodium channels begin to fail, the byproduct of which is reduced impulse conduction through the myocardium. This is manifested on the ECG as reduced P wave amplitude, increased PR interval, prolongation of the QRS duration, and peaked T waves. [4]


The attached image provides a visual of the RMP and TP millivolt changes with respect to hyper- and hypokalemia. [5]



This image simultaneously shows the clinical benefits of calcium administration during potassium burden. Calcium provides membrane stabilization, specifically in that it adjusts the TP to a less negative value amidst RMP drift. Ultimately, this shifting restores the roughly 30mv critical difference needed between RMP and TP for the action potential to optimally peak.


It is common knowledge in the world of emergency medicine that hyperkalemia is the syphilis of ECG's because it can manifest as just about anything, even OMI. The full spectrum of ECG hyperkalemic changes is beyond the scope of this post. Rather, we will focus primarily on the T wave (as previously mentioned) and its distinction in circumstances of potassium overload versus occlusive hyperacuity.


Let's revisit the deWinter occlusion provided by Paramedic Madden.

The T waves are tall and symmetrical, which is not very helpful distinguishing HATW's and hyperkalemic T waves because both can have this. But HATW's are usually blunted at the tip, whereas hyperkalemic T waves are pinched. Moreover, HATW's are wide at the base, whereas hyperkalemic T waves are narrow.


Below is an example of a patient in DKA whose respective serum potassium resulted 8.1 mEq/L. The T waves here are tall (even masquerading as hyperacute) and sometimes symmetrical. But they are also pinched at the tip and narrow at the base. The most striking lead to display this signature pattern is Lead I.

ECG's are difficult. ACS and hyperkalemia both have lethal downstream consequences, so it is imperative for the clinician to acclimate to the presentation, or developing, features of each. In the case of ACS, the ECG can rapidly change from this...

To this...

In the case of undetected hyperkalemia, the ECG can rapidly deteriorate from this...

To this...

Use the below link as a resource for more details on various ECG changes in hyperkalemia. From there you can link to other great websites (including Dr. Smith's ECG Blog) that provide multiple case studies of both subtle and overt hyperkalemia.


https://litfl.com/hyperkalaemia-ecg-library/


[1] Zachary et al. (2017). Utility of the history and physical examination in the detection of Acute Coronary Syndromes in emergency department patients. Western Journal of Emergency Medicine, 18 (4), 752-760.


[2] Costanzo, L. S. (2018). Physiology. Chapter 4: Cardiovascular Physiology. Elsevier: Philadelphia, PA.


[3] Parham, W. A. et al. (2006). Hyperkalemia revisited. Texas Heart Institute Journal, 33 (1), 40-47.


[4] Surawicz, B. & Knilans, T. K. (2008). Chou's Electrocardiography in Clinical Practice, 6th ed. Chapter 22: Electrolytes, Temperature, Central Nervous System Disease, and Miscellaneous Effects. Elsevier-Saunders: Philadelphia, PA.


[5]. McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The Biological Basis for Disease in Adults and Children. Chapter 3: The Cellular Envrionment, Fluids and Electrollytes, Acids and Bases. Elsevier: St Louis, MO.

About Me

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I am the Battalion Chief of EMS for Hilton Head Island Fire Rescue and obsessed with all things process improvement, system performance, human factors, crew resource management, and evidence-based performance measures for time-sensitive diagnoses.

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