View clinical trials related to Heart Arrest.
Filter by:The aim of the study is to describe the mechanisms of ultra-acute hyperglycemic response after return of spontaneous circulation (ROSC) in patients suffering out-of-hospital cardiac arrest. The investigators hypothesize that ischemia and reperfusion injury leads decreased secretion of insulin and glucose-like peptide 1 (GLP-1). Two blood samples will be drawn: (1.) Immediately after ROSC and (2.) 60 minutes after first sample. Concentrations of glucose, insulin, glucagon and GLP-1 will be compared between the samples. Metabolic profile will be compared between: (1.) diabetic and non-diabetic patients and (2.) survivors and non-survivors.
Background: Cardiac arrest is a life-threatening event. Intensivists are challenged with an increasing number of patients with uncertain neurological outcome following cardiopulmonary resuscitation (CPR). The prognostic value of current biomarkers for neurophysiologic long-term outcome is limited. Hypothesis: We hypothesize that specific brain-derived tissue leakage proteins can be identified to reveal novel, more reliable prognostic biomarkers for good neurological outcome. Methods: This translational study (n=100) is a combination of a prospective basic science study intended to reduce the number of potential plasma biomarker candidates by proteomic shotgun analyses in brain tissue autopsy samples and plasma samples from resuscitated patients (n=10) and a prospective clinical validation study in a large study population (n=90) by high-throughput analyses. Selection of proteomic markers and signature estimation will be performed to discriminate patients with good and poor outcome. Clinical perspective: A structured proteomic analysis approach might identify the best marker out of all proteins liberated during cellular damage.
This is a steering group approved substudy to the Target Temperature Management trial (TTM, ClinicalTrials.gov Identifier: NCT01020916). TTM compares the effect of two strictly controlled temperature regimes for survivors of out-of-hospital cardiac arrest. The primary aim of this sub-study is to compare the amount of cognitive impairment in cardiac arrest survivors treated with 33 degrees and 36 degrees and with a matched group of control patients with myocardial infarction. Our secondary aims are: - To investigate the impact of cognitive impairment on our patients' ability to participate in society and their health related quality of life. - To investigate the relationship between our patients cognitive impairments and their relatives/informants health related quality of life and feelings of burden. - To test the hypothesis that the simple cognitive screening battery used in the TTM main trial is sensitive enough to detect all patients with significant cognitive disability.
Current guidelines recommend the use of sedatives and neuromuscular blocking agents to avoid shivering during therapeutic hypothermia in cardiac arrest victims. Therefore, it is difficult to detect seizure and the frequent or continuous EEG monitoring is recommended. However, it is difficult to follow this recommendation in most clinical situations due to the lack of specialized devices and persons. The purpose of this study is whether SEDline (frontal 4-channel EEG device) has a diagnostic value to detect seizure during therapeutic hypothermia in cardiac arrest victims.
Out-of-hospital cardiac arrest (CA) is a leading public health problem causing nearly one third of a million deaths annually in the US, accounting for half of all cardiovascular deaths and surpassing deaths from stroke, heart failure, and breast and lung cancer combined. Twenty to fifty percent of CA patients (pts) can be resuscitated initially but many die before hospital discharge or suffer permanent neurologic damage. Therapeutic hypothermia (TH) improves survival and neurological outcomes. Despite aggressive, targeted post arrest management, including TH, approximately 50% of pts die before leaving the hospital due to global ischemia-reperfusion injury (IRI) known as the "post arrest syndrome", 1 which is a sepsis-like state characterized by elevated markers of cellular inflammation and injury. It is believed that TH works by decreasing the body's basal metabolic rate (BMR) and attenuating the systemic inflammatory response (SIR). However, specific triggers of the intense pro-inflammatory response are unclear. This "gap" in knowledge must be closed to identify targeted therapy to decrease IRI and improve outcomes. Blood flow to the gut is decreased markedly and intestinal tissue becomes ischemic during CA and CPR, particularly when vasoconstrictor drugs such as epinephrine, are given. IRI of the intestine increases intestinal permeability leading to intestinal microbial translocation and endotoxin release that can stimulate and perpetuate systemic inflammation and cause subsequent multi-organ dysfunction. Endotoxin also increases body temperature and energy expenditure and may attenuate TH induced reductions in BMR and hence, decrease efficacy. The purpose of this novel pilot study is to detect systemic endotoxin release following CA in humans and determine association with cytokine activation, and BMR alterations during TH.
This study must evaluate the benefit of a continuous audio guidance on the effectiveness of MCE directed by a volunteer. The evaluation of the MCE for this study is based on both quantitative criteria (based on the recommendations ERC 2010) - frequency - depth of chest compressions. This study compares two methods of continuous audio guide (one arm with an audio continuous guidance method by the regulator and second arm with an audio continuous guidance method by the controller relayed by an audio) to a method of incentive MCE based on a unique set made by the regulator(control arm).
Unlikely the other element for high quality chest compression during Cardiopulmonary resuscitation(i.e. compression rate, chest recoil, hand position), chest compression depth (CCD) is influenced by surface on which the patient is placed, especially in hospital. For solving this problem, to place the patient on rigid surface, use a backboard that might decrease the mattress compression, receive a feedback that reflects the mattress compression depth (MCD) using dual accelerometer or magnetic sensor have been proposed. As the other solution, we hypothesized that training of 6-7cm CCD for healthcare providers improve accurate CCD during cardiopulmonary resuscitation when manikin is placed on mattress in hospital.
The broad objective of this study is to test the association between hyperoxia exposure after resuscitation from cardiac arrest and outcome. Our overarching hypothesis is that hyperoxia after ROSC is associated with increased oxidative stress and worsened neurological and cognitive outcomes.
The main goal of this project is to help 9-1-1 emergency medical dispatchers save the lives of more cardiac arrest victims. The investigators will develop teaching tools to help the dispatchers recognize abnormal breathing that may indicate a victim as having a cardiac arrest. After training sessions, the investigators will see if dispatchers can get better at recognizing abnormal breathing, how often they give CPR instructions, and if use of the teaching tool will increase bystander CPR and the number of victims leaving the hospital alive.
The hypothesis is: In patients after an out of hospital cardiac arrest, treated with therapeutic hypothermia (33°C) will be found significantly more microcirculatory abnormalities, compared to the same group of patients treated with 36°C.