Severe Hyperkalemia: Electrocardiographic Tips for Early Recognition Based on a Case Report

Background: Rapid correction of severe hyperkalemia is mandatory to survival due to its induction of fatal cardiac arrhythmias. The electrocardiogram serves as the diagnostic tool that can provide insight into such fatal arrhythmias. We present two relevant alterations seen in an 84-year-old female patient with previous anterior myocardial infarction, angioplasty of the circumflex coronary artery, left ventricular ejection fraction of 35%, hypertension, dyslipidemia, paroxysmal atrial fibrillation


Introduction
Hyperkalemia is a potentially lethal electrolyte disturbance which needs urgent care as it could led to fatal cardiac arrhythmias.The kidneys (with the capacity to handle high amounts of potassium) play the most important role in the maintenance of normal concentrations of this electrolyte, 1 and consequently renal failure is one of the most prevalent causes for this disorder.
The 12-lead electrocardiogram constitutes a valuable tool for rapid diagnosis and shows a wide spectrum of alterations: 2 (i) peaked high-amplitude and narrow-based T-waves (usually later replaced by broad-based T-waves and widening of the QRS), (ii) decreased amplitude or absence of the P-wave, (iii) conduction disturbances, (iv) ST-segment elevation, (v) absence of STsegment and merging with the wide QRS, (vi) pulseless electrical activity, (vii) non-shockable ventricular tachycardia and (viii) ventricular fibrillation.
A case of severe hyperkalemia and typical electrocardiographic changes constitutes the subject of our presentation.

The Case
An 84-year-old woman presented to the emergency room with 96-hour evolution of asthenia, adynamia, and dyspnea.She had prior history of an anterior myocardial infarction treated with angioplasty of the circumflex artery, severe depression of the left ventricular systolic function (ejection fraction 35%), hypothyroidism, chronic obstructive pulmonary disease, arterial hypertension, paroxysmal atrial fibrillation, dyslipidemia, and non-insulin dependent diabetes mellitus type 2. The patient was on inhaled budesonide, bisoprolol, amiodarone, enalapril, aspirin, rosuvastatin and metformin.Anticoagulation was not indicated because of frailty and low compliance.The patient lived by herself and her income was limited.Her mother (deceased) had suffered hypertension and she ignored the medical history of her father.

Highlights:
• Critical importance of early electrocardiographic recognition in severe hyperkalemia through a patient case.
• Urgency of treatment for hyperkalemia exceeding 7.0 mEq/liter to prevent fatal arrhythmias.
• Challenges in managing complex cases with delayed presentation, underscoring the need for rapid diagnostic and therapeutic interventions.
Her vital signs on admission: Blood pressure 100/60 mmHg, heart rate 50 per minute, oxygen saturation 87%, and temperature 36°C.Auscultation of the heart and lung fields revealed normal sounds and absence of murmurs, with bilateral lung base rales.There was lividity in the lower limbs.
The patient was awake and disoriented in person, place, time and situation.She had no fever or chills.Abdominal palpation revealed soft and mildly tender abdomen, with no guarding or peritoneal signs.
An anteroposterior chest X-ray showed no evidence of acute lung disease (Figure 1).
Lab work was performed including cell counts, metabolic and urinary profiles, and cardiac biomarkers.Renal panel showed markedly elevated urea (228 mg/dl) and creatinine (3.75 mg/dl).
There was severe hyperkalemia (7 mEq/liter) and severe metabolic acidosis, with a pH of 7.11 and bicarbonate of 11 mmol/liter (Table ).Hematologic investigations (cell counts, INR) were normal, as well as CPK, while ultra-sensitive troponin was elevated (81.3 ng/liter for a normal value <19 ng/liter).Initial urinalysis was not suggestive of urinary tract infection The patient was diagnosed with hyperkalemia (7.9 mEq/liter) secondary to acute renal failure.The 12-lead ECG showed regular rhythm with a cycle length of 920-950 ms without discernible P-waves, marked widening of the QRS complex (200 ms) and absence of STsegment (Figure 2).In the emergency room, IV insulin was started at 10 units/hour and IV dextrose (5% in 500 ml for 8 hours) to prevent hypoglycemia.Treatment was complemented with 0.9% sodium chloride, bicarbonate and ASA diuretics.
Two hours after hospital admission, she suffered a cardiorespiratory arrest which required advanced resuscitation maneuvers followed by rapid sequence intubation for mechanical respiratory assistance with O2 at 50% and hemodynamic support with vasoactive drugs (dopamine).Three hours later, a lab work showed K+ of 6.1 mEq/liter, and initial normalization of the 12lead ECG (Figure 3).
The patient´s decompensation and persistent hypotension progressed gradually despite the increase in the dose of dopamine and the addition of noradrenaline.The marked hypotension and progressive decompensation precluded dialysis, and she died 15 hours post-admission.

Discussion
Sir Humphrey Davy was the first to isolate potassium (K+) by electrolyzing plant ashes "soaked in pots of water" (the term "pots" gives origin to the name of the electrolyte), as Weiss et al. point out in an interesting review. 3The largest amount of potassium in our bodies (98%) is intracellular, with a significant gradient in relation with the extracellular space.An increase in the serum concentration of potassium (above 5.5 mEq/liter) leads to electrophysiological disturbances mainly characterized by shortening of the action potential and slow conduction.With increasing values, the electrocardiographic manifestations aggravate and may trigger malignant arrhythmias and death. 4  The 12-lead ECG is a readily available tool and helps establishing the potential risks better than the mere potassium level, which in fact should be considered in conjunction with the rate of increase and the duration of the elevated values. 4In a study from a single institution, 5 the electrocardiograms recorded within one hour of potassium determination in 188 patients with concentration of the electrolyte >6.5 mEq/L were reviewed and the correlation between the electrocardiographic abnormalities and the occurrence of adverse events (symptomatic bradycardia, ventricular tachycardia or fibrillation, necessity of resuscitation maneuvers or death) was analyzed.The authors found adverse events in 15% and all occurred before calcium administration and all but one prior to interventions to lower potassium.Three electrocardiographic alterations were associated (alone or in combination) with adverse events: wide QRS (relative risk [RR] 4.74), bradycardia <50 beats/min (RR 12.29) and junctional rhythm (RR 7.46).Despite the need for a rapid intervention, the diagnosis may be challenging, especially in the presence of the so-called "dialyzable current of injury", as some electrocardiographic changes seen in hyperkalemia may resemble pericarditis, STEMI (ST-elevation myocardial infarction) 6 or type I Brugada pattern. 7o Signs are Characteristic of Severe Hyperkalemia 1) Junctional Rhythm: The regular rhythm (Figure 2) with a cycle length of 920-950 ms may have a junctional or ventricular origin as P waves were not discernible.][10] This would have been definitively proved in case the P-wave appeared at a similar rate once the electrolyte disturbance had been solved, but in this patient we may only mention the existence of the phenomenon as P-waves cannot be seen (in Figure 3 the underlying rhythm was atrial fibrillation once the potassium level had been lowered).
2) Sine-Wave Morphology: Our case, with a potassium level of 7.9 mEq/liter, shows the typical sine-wave morphology: (i) markedly wide QRS due to reduced influx of sodium and slower rise of the action potential, 2 and (ii) absence of ST-segment and broadly based T-wave (which differs from the "tenting" T-waves of high amplitude and narrow base seen in less pronounced hyperkalemia).Early recognition of this pattern may result in saving the life of a patient, as it correlates with hyperkalemia exceeding 7.0 mEq/liter.
In conclusion, electrocardiographic patterns present in this patient are characteristic of severe hyperkalemia and must prompt measures to lower potassium concentration and prevent death.

Figure 1 .
Figure 1.Antero-Posterior Chest X-Ray Showing Cardiomegaly and Features of Interstitial Pulmonary Edema.