Electrocardiogram alterations in non-traumatic brain injury: a systematic review.

The presence of abnormal electrocardiograms in individuals without known organic heart disease is one of the most common manifestations of cardiac dysfunction occurring during acute non traumatic brain injury. The primary goal of the present review is to provide an overview of the available data and literature regarding the presence of new-onset electrocardiographic (ECG) alterations in acute non traumatic brain injury. The secondary aim is to identify the incidence of ECG alterations and consider the prognostic significance of new-onset ECG changes in this setting. To do so, English language articles from January 2000 to January 2022 were included from PubMed using the following keywords: "electrocardiogram and subarachnoid hemorrhage", "electrocardiogram and intracranial hemorrhage", "Q-T interval and subarachnoid hemorrhage ", "Q-T interval and intracranial bleeding ", "Q-T interval and intracranial hemorrhage", and "brain and heart- interaction in stroke". Of 3162 papers, 27 original trials looking at electrocardiogram alterations in acute brain injury were included following the PRISMA guideline. ECG abnormalities associated with acute brain injury could potentially predict poor patient outcomes. They could even herald the future development of neurogenic pulmonary edema (NPE), delayed cerebral ischemia (DCI), and even in-hospital death. In particular, patients with SAH are at increased risk of having severe ventricular dysrhythmias. These may contribute to a high mortality rate and to poor functional outcome at 3 months. The current data on ECG QT dispersion and mortality appear less clearly associated. While some patients demonstrated poor outcomes, others showed no relationship with poor outcomes or increased in-hospital mortality. Observing ECG alterations carefully after cerebral damage is important in the critical care of these patients as it can expose preexisting myocardial disease and change prognosis.

Electroencephalographic monitoring of brain activity during cardiac arrest: a narrative review.

BACKGROUND: To date cardiac arrest (CA) remains a frequent cause of morbidity and mortality: despite advances in cardiopulmonary resuscitation (CPR), survival is still burdened by hypoxic-ischemic brain injury (HIBI), and poor neurological outcome, eventually leading to withdrawal of life sustaining treatment (WLST). The aim of CPR is cardiac pump support to preserve organ perfusion, until normal cardiac function is restored. However, clinical parameters of target organ end-perfusion during CPR, particularly brain perfusion, are still to be identified. In this context, electroencephalography (EEG) and its derivatives, such as processed EEG, could be used to assess brain function during CA. OBJECTIVES: We aimed to review literature regarding the feasibility of EEG and processed or raw EEG monitoring during CPR. METHODS: A review of the available literature was performed and consisted of mostly case reports and observational studies in both humans and animals, for a total number of 22 relevant studies. RESULTS: The research strategy identified 22 unique articles. 4 observational studies were included and 6 animal testing studies in swine models. The remaining studies were case reports. Literature regarding this topic consists of conflicting results, containing studies where the feasibility of EEG during CPR was positive, and others where the authors reached opposite conclusions. Furthermore, the level of evidence, in general, remains low. DISCUSSION: EEG may represent a useful tool to assess CPR effectiveness. A multimodal approach including other non-invasive tools such as, quantitative infrared pupillometry and transcranial Doppler, could help to optimize the quality of resuscitation maneuvers.

Excessive Sedation as a Risk Factor for Delirium: A Comparison between Two Cohorts of ARDS Critically Ill Patients with and without COVID-19.

Excessive sedation is associated with poor outcome in critically ill acute respiratory distress syndrome (ARDS) patients. Whether this prognostic effect varies among ARDS patients with and without COVID-19 has yet to be determined. We compared the prognostic value of excessive sedation­in terms of delirium, length of stay in intensive care unit (ICU-LOS) and ICU mortality­between COVID-19 and non-COVID-19 critically ill ARDS patients. This was a second analysis of prospectively collected data in four European academic centers pertaining to 101 adult critically ill ARDS patients with and without COVID-19 disease. Depth of sedation (DOS) and delirium were monitored through processed electroencephalogram (EEG) and the Confusion Assessment Method for ICU (CAM-ICU). Our main exposure was excessive sedation and how it relates to the presence of delirium, ICU-LOS and ICU mortality. The criterion for excessive sedation was met in 73 (72.3%) patients; of these, 15 (82.2%) and 58 (69.1%) were in non-COVID-19 and COVID-19 ARDS groups, respectively. The criteria of delirium were met in 44 patients (60.3%). Moreover, excessive sedation was present in 38 (86.4%) patients with delirium (p < 0.001). ICU death was ascertained in 41 out of 101 (41.0%) patients; of these, 37 (90.2%) had excessive sedation (p < 0.001). The distribution of ICU-LOS among excessive-sedated and non-sedated patients was 22 (16−27) vs. 14 (10.5−19.5) days (p < 0.001), respectively. In a multivariable framework, excessive sedation was independently associated with the development of delirium (p = 0.001), increased ICU mortality (p = 0.009) and longer ICU-LOS (p = 0.000), but only in COVID-19 ARDS patients. Independent of age and gender, excessive sedation might represent a risk factor for delirium in COVID-19 ARDS patients. Similarly, excessive sedation shows to be an independent predictor of ICU-LOS and ICU mortality. The use of continuous EEG-based depth of sedation (DOS) monitoring and delirium assessment in critically ill COVID-19 patients is warranted.

Are you Ernest Shackleton, the polar explorer? Refining the criteria for delirium and brain dysfunction in sepsis.

The Third International Consensus Definitions for Sepsis and Septic Shock has recently defined sepsis as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Organ dysfunctions in this consensus definition were identified as an organ-specific Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score ≥ 2 points. The quick SOFA (qSOFA) considers altered mentation indicating brain dysfunction when the Glasgow Coma Scale (GCS) score is ≤13 or ≤14. However, concern has been expressed that the revised criteria may lead to a failure in recognizing the signs of potentially lethal organ dysfunction and thus sepsis. Patients with delirium have a fluctuating course, and GCS can be normal or only slightly reduced at the time when signs of delirium are already present. We here report an illustrative case showing how an acute, initially unrecognized, urinary tract infection caused acute brain dysfunction with profound behavioral and cognitive dysfunction despite normal GCS, hence not meeting the criteria for sepsis.

Are optimal cerebral perfusion pressure and cerebrovascular autoregulation related to long-term outcome in patients with aneurysmal subarachnoid hemorrhage?

BACKGROUND AND OBJECTIVES: Continuous assessment of the cerebrovascular autoregulation (CVA) through use of the pressure reactivity index (PRx), a moving linear correlation coefficient between mean arterial blood pressure and intracranial pressure, has been effective in optimizing cerebral perfusion pressure (CPPopt) in traumatic brain injured (TBI) patients. This study investigates the feasibility of measuring CPPopt in patients with aneurysmal subarachnoid hemorrhage (aSAH) by continuously assessing the CVA. METHODS: Twenty-nine aSAH patients were enrolled, and data from CVA status, CPPopt, and periods when CPP was below, within, or above CPPopt were computed daily. Outcome was assessed at 6 months with the Glasgow Outcome Scale. Mann-Whitney U test was used to analyze differences in the duration of impaired CVA and duration of CPP below CPPopt in patients with good and poor outcomes. Multivariable logistic regression analysis was used to identify independent predictors of outcome. RESULTS: CVA monitoring data were available for all 29 patients with a total monitoring time of 2757 h. The duration of impaired CVA was 36.5% (interquartile range: 24.6 to 49.8) of the total monitoring time in 15 patients with good outcome and 71.6% of the total monitoring time (51.2 to 80.0) in 14 patients with poor outcome (Mann-Whitney U test 3.295, P=0.0010). PRx-based CPPopt could be identified in 26 patients (89.6%) with a total monitoring time of 2691 h. The duration of CPP below the CPPopt range was 28.0% (interquartile range: 18.0 to 47.0) of the total monitoring time in patients with good outcome and 76.0% (48.5 to 82.5) in patients with poor outcome (Mann-Whitney U test 2.779, P=0.0054). Glasgow Coma Scale score and duration of impaired CVA were independently associated with 6-month outcome (Glasgow Coma Scale score odds ratio: 1.95, 95% confidence interval: 1.01-3.75; duration of impaired CVA odds ratio: 0.88, 95% confidence interval: 0.78-0.99). CONCLUSIONS: The assessment of CVA and CPPopt is feasible in aSAH patients and may provide important information regarding long-term outcome. A PRx above the 0.2 threshold and a CPP below the CPPopt range are associated with worse outcome.