Hyperkalaemia mimics pseudostemi infarct pattern
- 1 The Max Stern Yezreel Valley College, D.N. Emek Yezreel, 1930600, Emek Yezreel, Israel
- 2 Galilee Medical Center, Nahariya, Israel 22100, Nahariya, Israel
- Correspondence to Dr Nasra Idilbi; nasra612@hotmail.com
Abstract
Hyperkalaemia is an electrolyte abnormality that warrants urgent intervention and has well-recognised electrocardiographic changes. Peaking T wave is the most appreciated ECG sign, but hyperkalaemia manifesting electrocardiographically as acute ischemia with ST segment elevation is a very rare condition. We present a case of acute kidney injury, complicated by severe hyperkalaemia causing ST segment elevation changes in ECG simulating acute myocardial infarction. Rapid serum potassium level in arterial blood gases blood test guide treatment in this case saved the need for unnecessary activation of the catheterisation lab and more importantly, saved the patient from malignant dysthymia in case of treatment delay. Aggressive treatment of hyperkalaemia resulted in successful reduction of serum potassium level; ECG changes returned to baseline without any evidence of pseudoinfarction pattern. The medical staff should be aware of this condition in order to administer correct therapy and prevent unnecessary interventions and the associated risk of complications.
Background
Approximately 28 cases of severe hyperkalaemia mimicking acute ST segment elevation myocardial infarction (STEMI) have been described in the literature, all before 2017,1 probably because hyperkalaemia rarely produces abnormal ST segment elevation simulating an acute myocardial infarction.1–4 The mechanism for this ECG pattern may be due to the presence of hyperkalaemia as suggested in other studies.5 6 We present the case of a patient with acute kidney failure and hyperkalaemia whose initial ECG showed a ‘pseudoinfarction’ pattern.
Case presentation
An 80-year-old man with a medical history of diabetes mellitus type 2, HTN and prostatic cancer without any medical treatment or surgery presented to the emergency department with non-specific chest pain (the patient described it as a generalised chest pain, without radiation to arms or jaw and free of nausea), weakness and difficulty in walking in the previous 4 days. On arrival, the patient was in a wheelchair; primary vital signs were in the normal range, blood pressure (BP) 144/66, pulse 100, body temperature 37°C and pulse oximeter SaO2= 95%.
An ECG was done immediately on arrival, and showed inferior STEMI with reciprocal ST segment depression in led 1+AVL with total loss of P wave (figure 1), although the patient’s symptoms of chest pain were considered non-typical for acute coronary syndrome (ACS) as we mentioned above, The patient was given 300 mg of aspirin and an urgent cardiology consult was ordered out of concern for ACS and possible need for catheterisation according to ECG changes that suggested STEMI.
A 12-lead ECG of our patient on admission showing ST segment elevation in inferior lead with reciprocal changes in 1+AVL, absent of normal p wave and peaked T wave in lateral leads (K level=9.09 mmol/L).
While the medical staff attached the patient to full cardiac monitoring and prepared the setting in case of emergency transport to catheterisation lab, chemistry lab’s notification arrived promptly about concerning potassium level of 9.09 mmol/L in an arterial blood gases (ABG) test. Therefore, we initiated hyperkalaemia treatment protocol.
After 1 hour of treatment, our patient’s serum potassium level decreased to 7.58 mmol/L in ABG’s, and he reported an improvement in his symptoms. Another ECG was performed (figure 2), showing that the ST segment had returned to normal without any reciprocal changes and the P wave showed up again.
A 12-lead ECG after 1 hour of treatment, shows no ST segment elevation in inferior lead without significant reciprocal changes and p wave show up again (K level=7.58 mmol/L).
Repeat laboratory testing after primary treatment revealed several marked laboratory abnormalities (table 1), especially creatinine level of 12.23 mg/dL. Importantly, the troponin level was normal (29 ng/L, normal range <34 ng/L). Because of normalisation of ECG changes after hyperkalaemia treatment as well as the combination of atypical chest pain for ACS and low troponin level that did not support the case for STEMI, we decided to transfer our patient to emergency dialysis rather than to cardiac catheterisation.
Laboratory studies on admission
| Lab data | Normal range | Result |
| Glucose (mg/dL) | 70–100 | 169.60 |
| Potassium (mmol/L) | 3.5–5.10 | 9.09 |
| Sodium (mmol/L) | 136–145 | 135 |
| Chloride (mmol/L) | 98–107 | 103 |
| eGFR (CKD-EPI) | 90 | 3 |
| BUN (mg/dL) | 8.4–25.70 | 109.60 |
| Creatinine (mg/dL) | 0.7–1.25 | 12.23 |
| Troponin (ng/L) | <34 | 29 |
| PH | 7.35–7.45 | 7.100 |
| HCo3 (mmol/L) | 22–29 | 9.2 |
| Ionised calcium (mmol/L) | 1.12–1.32 | 1.20 |
| HGB (g/dL) | 13–18 | 13 |
| WCC (x106/µL) | 4.00–10.00 | 12.91 |
| Platelet (x103/µL) | 130.00–400.00 | 247.00 |
While the patient was in the emergency department, urine catheter inserted with 2000 cc urine rest and non-contrast CT (NCCT) was done in order to investigate a possible cause of acute kidney injury (AKI). The NCCT showed bilateral hydronephrosis without kidney or urethral stones or prostatic enlargement.
After emergency dialysis the patient was admitted to the Nephrology Unit for further investigation and observation. During hospitalisation, serial troponin levels were taken but no further elevation was seen, creatinine levels returned to baseline range 1.2 mg/dL, and above all, there was significant clinical improvement in the patient’s symptoms without any further elevation in potassium levels.
Medical investigation in reference to blood workout, radiologic exams and clinical picture led us to conclude that post-renal obstruction due to prostatic enlargement led to AKI, causing elevation in potassium level.
The patient was discharged from hospital with urine catheter and directed to resume treatment at the oncourology outpatient clinic.
Written informed consent was obtained from the patient for publication of this case report and accompanying images.
Investigations
Measurement of vital markers, BP, pulse, body temperature, number of breaths, pain and stasis additionally taken blood gases (ABG) test. An ECG was done immediately on arrival, and showed inferior STEMI with reciprocal ST segment depression in led 1+AVL with total loss of P wave.
In addition, a repeat ECG was performed after treatment for hyperkalaemia
Differential diagnosis
Myocardial infarction especially due to ST segment elevation. Soon after activation of the cath lab, minutes before transport from the Emergency Department, the chemistry lab notified us of concerning potassium levels. After urgent treatment for hyperkalaemia the patient’s ECG returned to baseline, his symptoms improved and serial troponin levels showed no elevation (troponin was taken three times during the first 24 hours after admission).
Treatment
The patient was started immediately on a hyperkalaemia treatment protocol, including 20 cc of calcium gluconate 10%, 20 units of regular insulin plus Dextrose 125 cc 20%, and 10 mg inhaled β2 agonist. Our patient was sent to emergency dialysis and observation in the inpatient renal unit.
Outcome and follow-up
After urgent dialysis and further investigation and observation in renal unit in-hospital, the patient was diagnosed with AKI secondary to post-renal obstruction due to prostatic enlargement. The patient’s creatinine and serum potassium levels returned to baseline after a single haemodialysis treatment and insertion of urinary catheter without any further complications. We also excluded the presence of ACS by taking serial troponins during hospitalisation, normal ECG and absence of chest pain.
The patient was discharged to outpatient clinics without current need for renal replacement therapy (RRT).
Discussion
Potassium (K+) is the most abundant cation in the body, with only 2% of total body potassium found in the extracellular fluid. The acceptable normal value regulated between 3.5 and 5 mmol/L, the kidney is the primary organ to balance and maintain the normal range of potassium, with excretion accounting for 90% of daily potassium loss. Another 5%–10% of potassium is regulated by the gut in people with normal kidney function.7
The gut can also be the major mechanism for up to 25% of potassium elimination in patients with impaired kidney function such as end-stage renal failure.7 Hyperkalaemia is the most fatal electrolyte disorder associated with malignant arrhythmia and cardiopulmonary arrestوrrest diopulmonay olyte disorder assiociated with malignant arrythmia, and its severity may be classified according to blood concentration: mild (5.0–5.9 mmol/L), moderate (6.0–6.4 mmol/L) and severe hyperkalaemia (k≥6.5 mmol/L).7 A serum level of 10 mmol/L is usually fatal; however, survival cases have been reported in concentrations of 14 mmol/L.7
Symptoms
In severe cases the patient may present with weakness, flaccid paralysis, paraesthesia, depressed deep tendon reflexes and respiratory difficulties.7 The symptoms are not specific to hyperkalaemia and may be masked by primary illness precipitating hyperkalaemia.7
Hyperkalaemia can be also asymptomatic, with patients complaining occassionally of palpitations, nausea or muscle pain.8 Because of the non-specific presentation of hyperkalaemia, the examination and investigation should be systematic and always include assessment of cardiac function, and renal and neurological evaluation.8
ECG changes in hyperkalaemia
The ECG changes depend on two major factors: absolute serum potassium and the rate of increase.7 However, changes in ECG mostly appear in patients with a serum potassium level above 6.7 mmol/L7; cases of extreme hyperkalamia without evidence of ECG changes should raise the possibility of pseudohyperkalaemia (especially in paediatric mechanical haemolysis, samples with lymphocytosis and thrombocytosis8).
As serum potassium rises above 5.5–6.5 mmol/L, the classic sign of peaked T-waves appear in only 20% of hyperkalaemic patients.7 As a serum potassium level rises to 6.5–7.5 mmol/L, the PR interval becomes prolonged and the P wave becomes flattened and is eventually lost, followed by prolongation of QRS complex when the serum potassium reaches 7.0–8.0 mmol/L. If left untreated, the QRS complex merges with the T wave to form a sine-wave pattern with impending cardiac arrest.7
In our case presentation, the ECG changes mimicking STEMI are not usually seen in the setting of hyperkalaemia as we discussed earlier in this section. Moreover, in many of the case reports that include ‘pseudoinfarction’,1 3–5 the ECG shows ST segment elevation with visible P wave in all 12-Led. Thus, to the best of our knowledge, this case report may be a uniquely documented case that shows ST segment elevation with reciprocal changes without visible P wave.
We conclude that ST segment elevation can be considered a rare manifestation of hyperkalaemia. In the currently-described case, we did not find any primary cardiac pathology (eg, coronary artery spasm or plaque), but rather, the ECG changes induced were due to a metabolic state of severe hyperkalaemia secondary to AKI, especially since ECG changes returned to baseline after hyperkalaemia treatment without any elevation in troponin level in serial exams.
The ECG changes in our case are not recognised as common even in cases of severe hyperkalaemia.6–9 Interestingly, we noticed in other cases of hyperkalaemia mimicking STEMI where the patients suffered from abnormal kidney function in initial blood tests, that the creatinine level ranged from 2.26 mg/dL-19.1mg/dL,1 2 4 5 10 and serum potassium level ≥7.2 mmol/L.
The mechanism for these ECG changes is unclear but may be related to a shortening of the repolarisation phase of action potential.1
Learning points
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A patient with chest pain and ECG changes with ST segment elevation myocardial infarction should have a potassium test.
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Arterial blood gases analyser in the emergency department is a quick test for changes in patient markers.
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This test can prevent unnecessary cardiac catheterisation and patient complications.
Ethics statements
Patient consent for publication
Footnotes
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Contributors MZ wrote the first draft and gathered the scientific and laboratory data. He followed the case from start to finish. NI wrote the final manuscript and was also responsible for data gathering. Both agreed on sending the manuscript to BMJ case reports and both are responsible for the integrity of the manuscript.
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Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
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Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
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Competing interests None declared.
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Provenance and peer review Not commissioned; externally peer reviewed.
- © BMJ Publishing Group Limited 2022. No commercial re-use. See rights and permissions. Published by BMJ.
References
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