The number of patients discharged alive from the ICU is increasing due to the remarkable progress of medical care. Nevertheless, a growing concern is that many ICU survivors subsequently develop mental health impairments. Recently, it has become clear that the memories formed during a patient's ICU stay are a risk factor for subsequent mental health impairment. Patient memories can be classified into memories of factual events, memories of feelings, and delusional memories. Delusional memories are reported by 26-73% of ICU survivors and can be difficult to forget. Delusional memories are also thought to be correlated with mental health impairment, such as anxiety, depression, posttraumatic stress disorder (PTSD), a lower QOL, and failure to return to work. To support the formation of beneficial memories in patients, clinicians should help patients to construct appropriate memories during their ICU stay, to restructure memories after their discharge from the ICU, and to avoid preserving delusional memories. However, further research is required in this field. Understanding how unpleasant memories can lead to long-term disturbances in patients, even if the memories are not factual, and providing follow-up opportunities for patients to talk about their experiences after they have left the ICU may be necessary.

Critically ill patients in intensive care units often manifest tachycardia induced by hyperactivity of the sympathetic nervous system, which has been shown to have deleterious effects in patients. As tachycardia has been recognized as a predictor of a poor prognosis, it is very important to suppress hyperactivity of the sympathetic nervous system. Beta blockers have often been used to control tachycardia in high-risk patients undergoing non-cardiac surgery or cardiac surgery, and those with acute myocardial infarction or acute heart failure; previous studies have demonstrated many beneficial effects of beta blocker therapy under these conditions. However, in accordance with advances in medical care, some recent studies have raised concerns about the effects of beta blocker therapy in some cases. It has been pointed out that cardiac dysfunction progresses in the early phase of sepsis, which is characterized by a dysregulated immune system associated with organ dysfunction induced by infection. Some recent animal studies have demonstrated cardioprotective effects of beta blocker therapy in cases of sepsis-induced cardiac dysfunction. Furthermore, these beneficial effects of beta blocker therapy in cases of sepsis were also shown in recent clinical randomized control trials. In this review article, based on the findings of recent studies, both beneficial and deleterious effects of beta blocker therapy in patients with pathophysiologies wherein beta blocker therapy was shown in previous studies to confer beneficial effects are described. The author hopes that future large clinical trials will elucidate the clinical conditions under which beta blocker therapy can confer maximal beneficial effects in critically ill patients.

A 37-year-old man was regularly administered medication by a physician for the treatment of epilepsy and personality disorder caused by childhood trauma-induced frontal lobe necrosis. One day before presentation, the patient overdosed on the prescription medication containing phenytoin for approximately 40 days and was delivered in an ambulance to our hospital on the following day for prolonged conscious disturbance. Upon arrival, the patient was comatose. We aspirated the stomach contents, intubated him, and started systemic management. On the morning of the 4th day, generalized convulsions, multiple ventricular arrhythmias, and ventricular tachycardia were observed, and his condition worsened to shock. Blood pressure increased with direct current and cardiotonic agent initiation; however, the left ventricular ejection fraction remained low at 30%. The phenytoin blood concentration increased to 40μg/mL or higher as compared to 24.6μg/mL at hospital admission. Thus, phenytoin was considered the primary cause of toxicity. After 12 hours, the patient developed refractory cardiac arrest (pulseless electrical activity, and ventricular fibrillation) from the shock state and thus veno arterial extracorporeal membrane oxygenation (VA-ECMO) was introduced. Direct hemoperfusion (DHP) was also started with the intent of lowering the concentration of phenytoin in the blood. Upon reduction of the phenytoin blood concentration, circulation became stable, and the VA-ECMO was withdrawn on the 8th day. The patient, now autonomous, was extubated and discharged home. This patient presents a rare case of cardiotoxicity, requiring VA-ECMO, due to late-onset phenytoin toxicity. And DHP may have had a critical role in lowering the phenytoin concentration in blood.