ESICM LIVES Physiology 2026

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Arthur Guyton changed our understanding of the circulation by shifting focus from the heart as the sole driver of flow to an integrated system where venous return, stressed volume, and vascular capacity play central roles. In this lecture, Jukka Takala will revisit the core principles of Guytonian haemodynamics, explaining how pressure–flow relationships, cardiac function curves, and systemic vascular dynamics interact to determine perfusion and demonstrate how these concepts remain crucial for guiding therapy in critically ill patients.

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Introduction Emergency ultrasound has become fundamental for the management of critically ill patients. POCUS is commonly used in the emergency department (ED) because it allows rapid bedside diagnosis. Its utilization is increasing during cardiopulmonary resuscitation (CPR) and has the potential to improve Advanced Life Support (ALS) outcomes. Meanwhile, transesophageal echocardiography (TEE) has gained importance in critical care and may benefit the resuscitation of cardiac arrest for several reasons. Future research is warranted to confirm the added value of TEE in ALS and its clinical feasibility during CPR. Case presentation A 68-year-old man was admitted to our ED after out-of-hospital cardiac arrest. After breakfast and taking his antihypertensive medication, he developed sudden severe chest pain and collapsed when the Emergency Medical Services arrived. The first ECG showed pulseless electrical activity. ROSC was not achieved at home and the patient was intubated and transferred to hospital under mechanical chest compression device (“LUCAS”) and norepinephrine infusion. Bedside POCUS was inconclusive due to technical limitations and poor image quality, but raised suspicion for pericardial effusion. TEE was performed because the patient had a history of ascending aortic aneurysm. The mid-esophageal 2-chamber view demonstrated a severe (> 20 mm) loculated pericardial effusion along the anterior wall of the left ventricle (Figure 1A). The mid-esophageal long-axis view showed an intimal flap in the proximal ascending aorta, consistent with a Stanford Type A dissection (Figure 1B). Unfortunately, we only observed agonal twitching with no organized cardiac activity on ultrasound. Finally, considering persistent pulseless electrical activity with cardiac standstill, we decided to discontinue resuscitation efforts. Discussion Emergency ultrasound represents a fundamental skill in the current practice of emergency medicine. Recommendations for education, training experience and quality improvement in the emergency setting are well described in the literature. POCUS can reliably be used to identify reversible causes of CA [1]. However, POCUS use during cardiac arrest management may be associated with prolonged CPR pauses [2]. TEE could be used to diagnose reversible causes of collapse, optimize the quality of chest compressions, guide therapies, and identify cardiac activity [3]. Despite potential advantages during resuscitation, TEE is not currently widely adopted in the routine practice of ED. As described in the « 2025 European Resuscitation Council Guidelines », further studies are needed to better define the diagnostic value of TEE in identifying reversible pathology and myocardial contractility in cardiac arrest patients [4]. Development of a comprehensive guide is also essential to define the minimum training requirement for an effective implementation of TEE into emergency medicine practice. In the meantime, developing local CPR protocols in collaboration with TEE-proficient specialists may offer crucial information to physicians involved in cardiac arrest management (Figure 2). Conclusion Focused cardiac ultrasound during resuscitation represents an increasingly important skill for the modern critical care physician. Understanding cellular physiology and its integration into the management of cardiac arrest may facilitate decision-making during resuscitation. Our experience demonstrates that point-of-care TEE can be instrumental in the diagnosis and treatment guidance of cardiac arrest and acute aortic syndrome. Further studies are required to validate the clinical benefit and feasibility of implementing TEE during CPR.

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Introduction: Intravenous bicarbonate is a commonly used agent in the management of acute metabolic acidosis. However, it’s clinical benefit and safety is largely uncertain. We summarized the existing randomized controlled data and examined whether the use of intravenous bicarbonate, as compared to control or an alternate type of fluid without bicarbonate, leads to improvements in patient-important outcomes in those hospitalized with acute metabolic acidosis. Methods: We searched Ovid MEDLINE, Embase, the Cochrane library, and Clinicaltrials.gov, from inception until Jan 2nd 2026 and included randomized controlled trials of hospitalized adult participants who received intravenous bicarbonate, as compared to control or an alternate type of fluid without bicarbonate, for metabolic acidosis. We excluded studies examining oral bicarbonate. We pooled data using a random-effects model and present risk ratios (RRs) or mean differences (MDs), along with 95% confidence intervals (CIs). We assessed individual study risk of bias using the modified Cochrane tool, and certainty of evidence using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. Results: Of 1066 citations, we included 9 RCTs (n = 1331 patients), three of which focused on patients exclusively with severe diabetic ketoacidosis, with initial pH values ranging from 7.00 -7.06. Pooled analysis showed that bicarbonate may be associated with decreased mortality (RR 0.93, 95% CI: 0.82–1.05, low certainty), and decreased need for renal replacement therapy (RR 0.69, 95% CI 0.60 to 0.80, low certainty) compared to not using bicarbonate. Bicarbonate may have no effect on length of hospital stay (MD of 0.41 days longer, 95% CI 3.54 fewer to 4.36 days longer, low certainty). Conclusion: Bicarbonate may reduce mortality and need for renal replacement therapy in hospitalized patients with metabolic acidosis, but further data is needed to increase precision in effect estimates and further assess the impact of bicarbonate on other patient-important outcomes.

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Introduction Mechanical circulatory support devices have become an integral component of modern cardiac intensive care, significantly improving survival in advanced heart failure. Implantation of a biventricular assist device (BiVAD) profoundly alters cardiovascular physiology, creating a state of device-dependent circulation in which pump flow, rather than intrinsic myocardial performance, determines cardiac output. With Frank–Starling mechanism no longer functioning adequately, and the presence of concomitant autonomic and endothelial dysfunction, the heart’s capacity to respond to physiological stressors is substantially compromised. In this context, the onset of septic shock may generate metabolic and hemodynamic demands that exceed the adaptive capacity of device-supported circulation. Methods We analyzed the pathophysiological mechanisms underlying septic shock in BiVAD supported patient, with particular focus on hemodynamic responses to pump flow adjustments and on laboratory parameters reflecting tissue perfusion, inflammation, and organ dysfunction. In order to respond to the higher metabolic needs and improve the systemic perfusion an echocardiography-guided optimization of BiVAD pump parameters was performed. Results In BiVAD-supported patients, the increased metabolic and circulatory demands associated with sepsis cannot be adequately met due to limited or absent native cardiac reserve. Compensatory mechanisms as tachycardia and enhanced myocardial contractility are absent or markedly blunted. Moreover, the absence of pulsatile blood flow leads to impaired regulation of vascular tone. This results in a dissociation between pump flow, arterial pressure, and tissue perfusion. Sepsis-induced systemic vasodilation further aggravates the imbalance between fixed or semi-fixed cardiac output and reduced systemic vascular resistance, creating a complex hemodynamic state characterized by features of both cardiogenic and distributive shock. Even though an integrated therapeutic approach incorporating pump flow optimization and multimodal organ support in this case was associated with favorable clinical outcome, the treatment is significantly prolonged. Conclusion The coexistence of constrained cardiac output and sepsis-induced vasodilation in a patient supported with BiVAD produces a mixed form of cardiogenic and distributive shock with impaired compensatory mechanisms. Recognition of this unique hemodynamic profile is essential for appropriate monitoring and therapeutic strategies. To achieve a hyperdynamic response, a multimodal management strategy is required, in which pump flow may be adjusted, with careful consideration of the associated risk of suction events.

Poster ke stažení

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Introduction: Severe aortic stenosis (AS) is a recognized risk factor for sudden cardiac death (SCD). While ventricular tachyarrhythmias are the most common immediate cause of SCD, the majority of cases of SCD in patients with severe AS exhibited bradyarrhythmia as the primary rhythm. Enhanced activation of left ventricular baroreceptors (Bezold-Jarisch reflex) has been implicated in the pathogenesis of syncope in patients with AS. However, the precise mechanism by which an otherwise benign circulatory syncope can progress to cardiac arrest in severe AS remains unclear. We propose a hemodynamic-energetic mechanism to explain this progression and demonstrate its plausibility using a mathematical model of cardiac hemodynamics and energetics. Methods: The mathematical model of cardiac hemodynamics and energetics developed in this work is based on the two-element Windkessel model of arterial hemodynamics, the ventriculoarterial coupling model, and ventricular energetics model. The model quantifies energy delivered to the heart by the coronary circulation and energy expenditure of the heart. Under physiological conditions, energy delivery is higher than energy expenditure. Using the model, we examined whether and under which circumstances the opposite situation can arise where energy expenditure is higher than energy delivery. Such a situation does not allow more than very short-term cardiac function and leads inevitably to cardiac arrest. To analyze the model, the influence of individual independent model variables on energies, pressures and stroke volume was assessed, and global sensitivity analysis was performed using Sobol indices. Simulations of syncopal episodes were performed for individuals with a normal aortic valve and with severe AS. Four scenarios were assessed: resting state, isolated pronounced reduction in total peripheral resistance (TPR), TPR reduction with compensatory response, and TPR reduction with concomitant bradycardia. The model was validated against published clinical data to ensure physiological plausibility and consistency. Results: The model identifies states of cardiac energetic imbalance, wherein the energy expenditure of the heart exceeds the energy delivered to it. Analysis of individual independent variable influence indicates that an energy imbalance in AS is precipitated by low aortic valve area (Sao), low TPR, high left ventricular end-diastolic volume (EDV), high end-systolic elastance, high heart rate (HR), low arterial compliance and high coronary vascular resistance (Rcor). Global sensitivity analysis shows that in normal aortic valve or non-severe AS, energy balance is primarily determined by Rcor, TPR and HR, with Rcor being dominant. In severe AS with preserved coronary vasodilatory reserve, Rcor remains most influential, while TPR, Sao and EDV also contribute significantly. When coronary vasodilation is impaired in severe AS, Rcor loses relevance, and energy balance depends mainly on Sao, EDV, and TPR. Other variables have minimal impact. The results of simulation of syncopal episode reveal that in an individual with a normal aortic valve, an isolated profound reduction in TPR results in energy destabilization. However, the compensatory response as well as the concomitant bradycardia serve to reverse this imbalance. In contrast, only the resting situation is energetically stable in case of AS. As in the normal case, an isolated profound reduction in TPR results in energy destabilization. However, neither compensatory response nor concomitant bradycardia can reverse the imbalance. Conclusions: This study proposes a hemodynamic-energetic mechanism to explain how otherwise benign circulatory syncope can progress to cardiac arrest in patients with severe AS and demonstrates the plausibility of this concept. In individuals with a normal aortic valve, compensatory mechanisms can restore energetic balance during syncope. In contrast, only resting state is energetically stable in severe AS; all conditions involving low TPR are energetically unstable, regardless of compensatory response. As energy imbalance is incompatible with sustained cardiac function, it inevitably leads to death. The proposed mechanism does not require an exaggerated Bezold-Jarisch reflex, although this reflex likely acts as a trigger of syncope. Reference: Dvoulety, M. and Sitina, M. (2026), Haemodynamic-energetic mechanism of sudden cardiac death in severe aortic stenosis: A modelling study. J Physiol. https://doi.org/10.1113/JP288423

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Abstract Background: Hyponatremia is a common feature of severe hyperglycemia in diabetic patients. We studied whether it is due to plasma dilution, a sodium deficit, or both. Methods: In 17 patients with diabetes-induced severe hyperglycemia, blood hemoglobin and the concentrations of glucose, sodium, and other electrolytes in plasma and urine were measured during and after an intravenous infusion of 1 L of 0.9% saline over 30 min on two consecutive days. Fluid volume and electrolyte kinetics were applied to study relationships between the glucose and electrolyte levels and to estimate the sizes of the body fluid compartments. Results: There was a statistically significant inverse linear relationship between plasma glucose (highest value 53 mmol/L) and plasma sodium (lowest 120 mmol/L). The correction factor was 1.6 or 2.2 depending on how the comparison was made. The hyperglycemia on admission corresponded to a fluid shift from the intracellular space of 350 mL, which was sufficient to explain the difference in baseline plasma sodium between the two study days. However, this dilution co-existed with a 20% reduction of the plasma and extracellular fluid volumes, and the body contents of sodium and chloride were 26% and 30% below normal, corresponding to deficits of 400 mmol. Restoration of the acid-base balance and the kidney function, rather than decreasing plasma glucose levels, seemed to drive the normalization of plasma sodium. Conclusions: Hyponatremia in severe diabetic hyperglycemia can be explained both by dilution and a sodium deficit. The medical treatment should consider both factors. Keywords: Dehydration, diagnosis, urine, physiopathology, diabetes mellitus, physiology; normal saline; pharmacokinetics.

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Background: There is growing evidence of microcirculatory dysfunction being a major factor in determining the extent of multiorgan failure and, thus, the outcome of critically ill patients. Quick acidification of a bicarbonate anion (HCO₃⁻)-containing solution causes carbon dioxide (CO₂) supersaturation-triggered gas bubble formation in that solution. Blood is an HCO₃⁻-containing solution as well. Accordingly, we believe that the rapid occurrence of profound metabolic acidosis could result in gas bubble formation in the critically ill. Gas bubbles form due to CO₂ supersaturation at first, then other gases diffuse into bubbles in proportional amounts. Gas bubble-blood interface-triggered platelet adhesion and activation with consequent capillary occlusion could explain microcirculatory dysfunction. Methods: With a retrospective observational study including all admitted patients to our ICU in 2020, we investigated if there exists a correlation between the severity of metabolic acidosis in patients upon their admission to the ICU and their platelet count trend in the following two days. Base excess (BE) from blood gas analysis with the lowest pH around ICU admission was used as a marker of the severity of metabolic acidosis. Platelet counts in patients upon admission and lowest platelet count on their second day were used to calculate patients' relative platelet count decline after ICU admission; delta P = ((P2−P0)/P0) x 100. Results: Comparison of delta P in all six groups of BE showed a statistically significant difference (Kruskal–Wallis test; p < 0.001). Patients from groups with more negative BE values tend to have more negative delta P. Conclusions: Patients with more profound metabolic acidosis upon their ICU admission tend to have larger relative platelet count decline in the following days. Although in a very indirect way, these findings support our theory of gas bubble-blood interface-triggered platelet consumption with resulting microcirculatory dysfunction in most severely ill ICU patients. References: 1. Tachon G, Harrois A, Tanaka S, Kato H, Huet O, Pottecher J, Vicaut E, Duranteau J. Microcirculatory alterations in traumatic hemorrhagic shock. Crit Care Med. 2014;42(6):1433-41. doi: 10.1097/CCM.0000000000000223. 2. Merdji H, Levy B, Jung C, Ince C, Siegemund M, Meziani F. Microcirculatory dysfunction in cardiogenic shock. Ann Intensive Care. 2023;13(1):38. doi: 10.1186/s13613-023-01130-z. 3. den Uil CA, Lagrand WK, van der Ent M, Jewbali LS, Cheng JM, Spronk PE, et al. Impaired microcirculation predicts poor outcome of patients with acute myocardial infarction complicated by cardiogenic shock. Eur Heart J. 2010;31(24):3032-9. doi: 10.1093/eurheartj/ehq324. 4. Damiani E, Carsetti A, Casarotta E, Domizi R, Scorcella C, Donati A, et al. Microcirculation guided resuscitation in sepsis: the next frontier? Front Med (Lausanne). 2023;10:1212321. doi: 10.3389/fmed.2023.1212321. 5. De Backer D, Orbegozo Cortes D, Donadello K, Vincent JL. Pathophysiology of microcirculatory dysfunction and the pathogenesis of septic shock. Virulence. 2014;5(1):73-9. doi: 10.4161/viru.26482. 6. De Backer D, Donadello K, Sakr Y, Ospina-Tascon G, Salgado D, Scolletta S, et al. Microcirculatory alterations in patients with severe sepsis: impact of time of assessment and relationship with outcome. Crit Care Med. 2013;41(3):791-9. doi: 10.1097/CCM.0b013e3182742e8b. 7. Scardina P, Edwards MA. Prediction and measurement of bubble formation in water treatment. Journal of Environmental Engineering. 2001;127(11):968-73. 8. Levi M, Opal SM. Coagulation abnormalities in critically ill patients. Crit Care. 2006;10(4):222. doi: 10.1186/cc4975. 9. Pontier JM, Blatteau JE, Vallée N. Blood platelet count and severity of decompression sickness in rats after a provocative dive. Aviat Space Environ Med. 2008;79(8):761-4. doi: 10.3357/asem.2299.2008. 10. Pontier JM, Jimenez C, Blatteau JE. Blood platelet count and bubble formation after a dive to 30 msw for 30 min. Aviat Space Environ Med. 2008;79(12):1096-9. doi: 10.3357/asem.2352.2008. 11. Pontier JM, Vallée N, Bourdon L. Bubble-induced platelet aggregation in a rat model of decompression sickness. J Appl Physiol. 2009;107:1825-9. doi:10.1152/japplphysiol.91644.2008.

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Background: Ventilator-induced lung injury (VILI) remains a major challenge associated with mechanical ventilation. A primary mechanism underlying VILI is cyclic alveolar recruitment and derecruitment (R/D) (atelectrauma). To minimise its development, ventilator settings, such as Positive End-Expiratory Pressure (PEEP), must be carefully optimised for each patient. Despite this need for personalisation, current bedside techniques cannot continuously measure local alveolar dynamics. Consequently, clinicians must rely on global parameters, which may not fully capture the heterogeneity of regional lung behaviour. In silico modelling offers a promising solution by linking local alveolar mechanics with global lung function. We sought to investigate whether our in silico modelling framework could simulate the effect of an impaired lung on R/D behaviour. Methods: This work leverages a lumped-parameter model presented in [1], which estimates patient-specific regional elastance and recruitment information derived from dual-volume CT in a mechanically ventilated ARDS patient. The model was used to simulate mechanical ventilation during an incremental PEEP trial consisting of 30-second steps at 5, 10, and 15 cmH2O. Next, the mean critical pressures were shifted by +5cmH2O to mimic a severe lung injury, and the trial was repeated. Results: The shifted-critical-pressures trial demanded higher PEEP to maintain alveolar aeration throughout the respiratory cycle. It was observed that tidal recruitment remained high and unstable at 10cmH2O and was significantly reduced only at the higher PEEP of 15cmH2O, while it was already reduced at 10cmH2O in the control simulation. Conclusion: In this study we utilised a methodology that infers local lung properties derived from dual-volume CT. A proof-of-concept simulation shows that the model can reproduce the effect of conventional changes in ventilator settings, such as PEEP, as well as can simulate an impaired lung with worsening biomechanics. As such, this scalable strategy provides a mechanistic foundation for future personalised ventilator optimisation to reduce atelectrauma. References [1] Quicken et al., ESB 2025 conference.

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INTRODUCTION: Acute right ventricular (RV) failure is a challenging condition in critical care associated with significant morbidity. Portopulmonary hypertension, a severe and under-recognized complication of liver cirrhosis, is an important cause of right-sided heart failure in chronic liver disease. We present the case of a 69-year-old female with cirrhosis who developed cardiac arrest secondary to acute decompensated right ventricular (RV) failure likely due to underlying portopulmonary hypertension. CASE REPORT: A 69-year-old female with Child Pugh B7 Hepatitis B cirrhosis and recurrent hepatic hydrothorax presented with syncope and exertional dyspnea. Imaging demonstrated a massive right pleural effusion, which was drained uneventfully. Computed tomography pulmonary angiography excluded pulmonary embolism but revealed right heart strain. The following day, while straining during defecation, she developed sinus bradycardia progressing to pulseless electrical activity arrest. Return of spontaneous circulation was achieved after 14 minutes. Bedside echocardiography demonstrated severe RV dilation with impaired systolic function (TAPSE 11 mm), septal flattening with left ventricular cavity obliteration, severe tricuspid regurgitation, and (estimated) elevated pulmonary vascular resistance. Lactate exceeded 10 mmol/L despite a preserved indirect Fick cardiac index, consistent with acute RV failure and mixed shock physiology. Acute decompensated RV failure, likely secondary to portopulmonary hypertension, was diagnosed. She required escalating vasopressor support and developed multi-system organ failure. Management targeted RV physiology: preload reduction with continuous renal replacement therapy, inotropic agents, pulmonary vasodilators, preferential vasopressin use, and ventilatory strategies avoiding high PEEP and hypercapnia. Despite transient echocardiographic improvement, she experienced recurrent arrests. Care was subsequently re-directed to palliation. CONCLUSION: This case underscores the importance of early recognition of RV-predominant shock physiology in cirrhosis and reinforces the need for timely identification of portopulmonary hypertension to mitigate the risk of acute decompensation.

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Introduction: Recovery processes in intensive care units (ICUs) interact with patients’ cultural values, belief systems, and lifestyles. The increase in global migration and multicultural societies has heightened the importance of culturally sensitive care practices in ICUs. This narrative review aims to examine the effects of cultural practices on physiological parameters in critically ill patients. Methodology: In this narrative review, studies indexed in the Web of Science and Scopus databases between January 2016 and February 2026 were systematically examined. The search strategy incorporated keywords related to cultural care ("cultural care," "spiritual care," "family-centered care"), intensive care settings ("intensive care unit," "ICU," "critical care"), and physiological outcomes ("vital signs," "hemodynamic parameters," "cortisol"). Results: The findings were structured into three main categories corresponding to patients’ cultural frameworks, including family-based, spiritual/religious, and mind–body interventions. Flexible visiting policies have been shown to reduce blood pressure and heart rate while stabilizing respiratory rates and improving oxygen saturation. Additionally, the involvement of family members in supportive care practices, such as touch and massage, improves vital signs, shortens weaning duration, reduces reintubation rates, and decreases adverse events associated with physiological fluctuations. Spiritual interventions, including listening to the Holy Qur’an, prayer, and structured spiritual care practices, have been reported to suppress sympathetic activity, thereby reducing respiratory rate, blood pressure, and pulse, lowering mean arterial pressure, increasing oxygen saturation, and producing a significant reduction in cortisol levels. Guided meditation, a mind–body intervention originating from Eastern traditions, has also been reported to support hemodynamic stability by increasing parasympathetic activity. Conclusion: Current evidence suggests that culturally sensitive interventions may be associated with measurable physiological parameters in critically ill patients. However, well-designed studies are needed to clarify the underlying causal mechanisms and to support their integration into clinical practice. Keywords: Cultural care, Family-centered care; Intensive care unit; Mind–body interventions; Physiological outcomes, Spiritual care.

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Introduction: Obesity-associated neuroinflammation is characterized by increased levels of saturated fatty acids (SFAs) and other lipids, along with the recruitment and activation of astrocytes and microglia, which actively contribute to the initiation and spread of the inflammatory response. Among the therapeutic strategies for obesity, glucagon-like peptide-1 (GLP-1) analogs have gained attention due to their anti-inflammatory, antidiabetic, and anti-obesity properties. This study aimed to investigate the effects of peripheral liraglutide treatment on lipid metabolism, mitochondrial function, and hypothalamic neuroinflammation induced by a high-fat diet (HFD). Methods: Male C57BL/6 mice were fed with either standard chow or HFD for 14 weeks. At the end of this period, the animals received daily injection of liraglutide(200 μg/kg, sc) for ten consecutive days. Body composition was assessed using the MiniSPEC NMR system before and after the treatment period. For histological analyses, immunofluorescence to detect hypothalamic and brainstem astrocyte activation through glial fibrillary acidic protein (GFAP) expression. The hypothalamic lipid profile was determined by high-performance liquid chromatography coupled with tandem mass spectrometry (LC–MS/MS), and mitochondrial function was assessed by high-resolution respirometry using the Oroboros O2k Oxygraph. Results: Liraglutide treatment significantly reduced food intake, body weight, fasting glucose levels, plasma triglycerides, total cholesterol, and leptin levels in HFD-fed mice (p < 0.05). In addition, liraglutide decreased both fat and lean mass (p < 0.05) and reduced GFAP expression in the hypothalamus and nucleus tractus solitarius (NTS). Furthermore, peripheral liraglutide administration altered the hypothalamic lipid profile and improved mitochondrial respiratory capacity (OXPHOS) in obese mice (p < 0.05; R²= 0.42). Conclusion: In conclusion, peripheral liraglutide treatment improves metabolic parameters, modulates hypothalamic lipid composition, enhances mitochondrial function, and attenuates hypothalamic neuroinflammation in diet-induced obese mice.

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Introduction: Post-Hypoxic Myoclonus (PHM) can present early after cardiac arrest and indicates poor neurologic outcome. Its management may be challenging and EEG may aid to guide clinical management. We present the management of a patient suffering from acute, persistent PHΜ in absence of bedside EEG. Methodology: This is the case of a 46 year old man who survived after cardiac arrest due to a STEMI. After primary PCI the patient was initially admitted in the Coronary Care Unit, intubated under sedation with propofol infusion. Shortly after cessation of the sedative medication he developed bilateral asymmetrical (right prominent side) myoclonus of the limbs which was treated with levetiracetam. A brain CT was performed which revealed diffuse brain edema and then at day 4 the patient was transferred to the ICU for further management under sedation with propofol, fentanyl and midazolam continuous infusion. Mannitol was also administered and sedation was withheld after 48 h to allow for assessment of the neurologic status. Myoclonus was evident within 15 minutes, sedation was reinitiated and valproic acid as a continuous infusion was added along with an increase of levetiracetam. The following days as guided by neurologic consultation, antiepileptic medication had to be titrated until day 23 due to persistent myoclonus activity up to levetiracetam 6g, valproic acid 4g, clonazepam 3mg, lacosamide 200mg and perampanel 8mg. He also received continuous infusion of 1.5mg/kg/h ketamine for 24 hours to allow for therapeutic levels of the accompanying treatment. Management of antiepileptic medication was based on clinical manifestations of myoclonus due to lack of portable EEG. Results: On day 23 of hospitalisation the patient status allowed for his transfer to the EEG laboratory where despite demonstrating myoclonus, this was not associated with epileptiform abnormalities in the EEG. The EEG performed was asymmetrical, with θ waves in the left hemisphere, lack of basal activity was recorded in the other hemisphere and myoclonic status epilepticus of cortical origin was excluded. Gradually, the frequency of myoclonus decreased and antiepileptic treatment was reduced to 2.4g valproic acid, lacosamide 100mg, clonazepam 1mg, perampanel 8mg and levetiracetam 4g. No ECG changes were recorded during the course of treatment. The patient died after 58 days of hospitalisation due to complications of sepsis. Conclusion: PHM can be a challenging phenomenon that occurs after cardiac arrest. EEG data may not be indicative of clinical manifestations while thorough, step by step titration is necessary to manage such demanding and persistent cases.