A 61-year-old Japanese man with impaired consciousness was transported to our hospital. He had a history of type 2 diabetes mellitus, old myocardial infarction, angina pectoris, and chronic kidney disease (CKD). On initial evaluation, he had shock with cool peripheries, blood pressure of 79/68 mmHg, heart rate of 78 beats per minute, Glasgow Coma Scale score of 3/15, and axillary temperature of 31 °C. Additionally, transthoracic echocardiography (TTE) revealed diffuse left ventricular wall dyskinesia, with a visual ejection fraction (EF) of 20–30% (originally 47% with posterolateral wall hypokinesia/akinesia). Electrocardiography revealed widespread ST depression with ST elevation in the aVR lead. Laboratory findings showed leukocytosis, acute kidney injury (AKI), metabolic acidosis, anemia, hypoglycemia, and elevated high-sensitivity cardiac troponin I (hs-cTnI) level. Chest computed tomography revealed bilateral consolidation. We consulted a cardiologist because of the extremely high hs-cTnI level (54,138 ng/L), but the cardiologist considered AMI unlikely. The patient was diagnosed as having pneumonia (sputum culture grew Streptococcus pneumoniae) and septic shock, and acute upper gastrointestinal bleeding. The Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores were 54 and 12, respectively. In the emergency department, orotracheal intubation was performed, and antimicrobial administration, fluid resuscitation, vasopressor agent administration, and blood transfusion were started. After admission to the intensive care unit, continuous hemodiafiltration (CHDF) was also started for AKI. On the first day of admission, he had a pulseless electrical activity (PEA) twice, but the return of spontaneous circulation was achieved at both times with a 1 g adrenaline dose. CHDF was terminated on the second day, and vasopressors/inotropic agent administration was terminated on the third day. The patient was weaned off from the ventilator on the seventh day and transferred to the hospital for rehabilitation on the 23rd day. After the transfer, he had no problems and was discharged. Nevertheless, his hs-cTnI level continued to be extremely high during admission. It was > 500,000, 193,309, 29,357, and 4747 ng/L on the second, third, 13th, and 20th days, respectively. On the 17th day, TTE was performed, no new asynergy was found, and the EF improved to 38%. On the 21st day, myocardial perfusion scintigraphy was performed under the care of a cardiologist, and no new myocardial necrosis was observed.