top of page
  • David Didlake


David Didlake

Firefighter / Paramedic

Acute Care Nurse Practitioner


Peer review provided by Dr. Steve Smith


An adult female called 911 for chest discomfort and difficulty breathing. EMS found her acutely ill, mottled, dry mucous membranes, modestly hypotensive, and lethargic. She reported a history of IDDM, but denied any known ischemic heart disease. A finger-stick glucose resulted 551 mg/dL, and the following ECG was recorded.

The attending crews were concerned for SVT with corresponding ischemic hyperacute T waves (HATW) and subsequently activated STEMI pre-hospital.

By pure technicality, this is an SVT, however not the AV nodal reentrant kind that would benefit from Adenosine administration. Closer inspection will show that it is Sinus, after all. Here I have isolated the augmented leads with emphasis (blue arrows) on repetitious P wave activity.

Are the T waves truly hyperacute, though? They are definitely high in amplitude and, intermittently, appear to disproportionately tower over the respective QRS. If hyperacute, then – as we have seen in previous posts – this would classify as Grade I in the Sclarovsky-Birnbaum ischemic triage for occlusive MI. This grading system is the time sensitive prelude to Q-wave (irreversible transmural scar) formation, as demonstrated in the image below. [1]

In their publication, Sclarovsky and Birnbaum discovered that with each grading escalation there is less salvageable myocardium and higher likelihood of heart failure at hospital discharge (an inversely proportional relationship). This is critical for the EMS provider, or ED clinician, as identification of Grade I ischemia (aka, HATW’s) addresses the culprit lesion at the earliest opportunity with excellent downstream prognosis for the patient. [2]

But there is also Sinus Tachycardia! This makes occlusive MI (in isolation) less likely and merits further investigation, as well as intensified ECG scrutiny – specifically, the T waves. HATW’s are traditionally wide at the base, whereas these T waves are narrow at the base. Such a finding is most dramatic in Lead I, reproduced here.

This ECG is pathognomonic for hyperkalemia.

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. In today’s case the patient is suffering from diabetic ketoacidosis, which facilitates hydrogen ion 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. [3]

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. [4]

The relative 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. [5]

The attached image provides a visual of the RMP and TP millivolt changes with respect to hyper- and hypokalemia. [6]

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.

No calcium was administered during pre-hospital transport. The following ECG was captured upon arrival at the receiving ED.

Cardiology was consulted, who advised to surveil a metabolic process as this did not strike them as acute coronary syndrome. The serum K returned 8.7, along with a pH 6.94, and an HCO3 of 5. Unfortunately, no ECG was captured after resuscitation.

Thankfully, the patient experienced an uncomplicated ICU stay and subsequently made a full recovery. A deceptive feature about this case, however, is the perception that time is somewhat leisurely on our side to verify ECG changes of hyperkalemia on chemistry panels. For example, at the point of initial EMS contact to hospital arrival (interspersed with cardiology consultation) to, finally, serum potassium result was 68 minutes. But surreptitious unpredictability (with lethal downstream sequelae) mandates that we instantly recognize the hyperkalemic ECG and act immediately with therapeutic measures, lest we find ourselves in a frantically reactive state, as demonstrated by the two examples below.

Example 1

EMS is called to the residence of an elderly male experiencing profound weakness. An ECG is recorded.

This was interpreted as RBBB. Then, six minutes later…

Calcium and Bicarb were administered as part of the respective agency’s PEA Arrest protocol, followed by ROSC. The ED resulted an 8.7 potassium value.

The first ECG is undeniably pathognomonic for hyperkalemia and manifests itself in a Sinoventricular rhythm. Perhaps a grossly wide QRS is the key to foreshadowing imminent arrest, as opposed to an otherwise preserved QRS duration. Can sudden death occur just as quickly when the QRS is more narrow?


Example 2

EMS responds to the residence of an elderly female who is experiencing intense abdominal discomfort and fatigue. An ECG is recorded.

The T waves are pinched at the tip, and narrow at the base. This is pathognomonic for hyperkalemia, but the attending crews were uncertain because the respective T waves are not tall. There is QRS prolongation, to the point of modest IVCD, but certainly not to the degree as that seen in Example 1. The patient was alert and oriented, and thus created a false sense of security that waiting for ED chemistry panel validation of suspected hyperkalemia – as opposed to empirical therapy – was acceptable.

Then, four minutes later…

She became unconscious and unresponsive. Then, three minutes later…

Crews activated STEMI as she deteriorated into PEA arrest. Bicarb was administered per local protocol, however calcium was not. Resuscitation was unsuccessful and she was pronounced in the ED. The only acquired lab test was a Covid swab, which resulted positive.

Hyperkalemia is both vicious and deadly. When pathognomonic on the ECG, empiric therapy is emergently warranted. The DKA patient in today’s case was fortunate enough (even lucky, perhaps) to maintain myocardial electrical stability over the course of 68 minutes before resuscitation commenced. The patients in the other two examples, however, demonstrate that time is not always in the clinician’s favor.

Moreover, the hyperkalemic ECG does not require a grossly prolonged QRS before onset of precipitous clinical decline. Even the preserved QRS duration is at risk of imminent death.

Do not miss this fantastic tutorial from Dr. Jesse McLaren!


[1] Strauss, D. G. & Schocken, D. D. (2021). Marriott’s Practical Electrocardiography (13th ed). Chapter 6: Introduction to Myocardial Ischemia and Infarction. Wolters-Kluwer: Philadelphia, PA.

[2] Birnbaum, Y., et al. (2004). Refinement and interobserver agreement for the electrocardiographic Sclarovsky-Birnbaum ischemia grading system. Journal of Electrocardiology, 37(3), 149-156.

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

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

[5] 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.

[6]. 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

Screen Shot 2021-06-19 at 9.28.50 AM.png

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.

Posts Archive

bottom of page