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A previously healthy patient presented to the emergency department with acute dyspnoea preceded by 2 days’ history of cough and chest pain. The patient was diagnosed with moderate COVID-19 pneumonia based on the chest X-ray findings and positive nasal swab for SARS-CoV-2. Three days later, his condition deteriorated with progressive renal failure and development of acute right cerebellar infarction, low GCS and desaturation requiring mechanical ventilation.
Clinically, the patient was sedated, on mechanical ventilation and anuric; had a blood pressure of 157/80 mmHg and a heart rate of 116 beats/min; and maintained saturation at FiO2 of 60%.
Laboratory investigations showed elevated inflammatory markers, ferritin, dimer and cardiac troponin. His creatinine was 8 mg/dL; urea was 369 mg/dL; and potassium was 6.2 mmol/L.
He was referred to the cardiology team for an abnormal ECG (Figure 1) and an episode of ventricular tachycardia.
Based on the ECG, which of the following is most appropriate next step?
Emergent percutaneous coronary intervention.
Non-contrast CT of the brain.
Response to ECG challenge
The patient’s ECG showed sinus tachycardia, prolonged PR interval, flattening of P wave, wide bizarre-looking QRS complex combined with hyperacute T in a ‘pseudo-infarction pattern’ indicating changes due to severe hyperkalaemia. Repeat testing showed that the patient had a potassium of 7.1 mmol/L; after initiation of antihyperkalaemic measures and dialysis, the follow-up potassium level decreased to 5.2 mmol/L and his follow-up ECG (Figure 2) showed resolution of the pseudo-infarction pattern and development of atrial fibrillation that was managed by antiarrhythmic medications.
The differential diagnosis of ST elevation is many, including acute myocardial infarction, myocarditis, left bundle branch block, early repolarisation and ventricular hypertrophy, Brugada syndrome, left ventricular aneurysm, Takotsubo cardiomyopathy, traumatic brain injury (intracerebral hemorrhage) and hyperkalaemia.1
Electrocardiographic changes due to hyperkalaemia are characterised by early development of P-wave flattening and disappearance with tall tented bifid T waves associated with wide QRS complex and PR prolongation. The so called ‘pseudo-infraction’ pattern is rare and resulted from the fusion of tall T waves with the widened QRS.2
The distribution of the hyperkalaemic ST elevation pattern on ECG can mimic the Brugada and De-Winter patterns. However, other distributions are reported especially in critically ill patients. In our patient, the reverse stick sign of Brugada was present in anteroseptal and inferior leads.3 4
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Contributors All authors have equal contribution to the article.
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.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.
Provenance and peer review Not commissioned; internally peer reviewed.
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