Nurse Empowerment a Key Factor in Cardiac Arrest Survival of Hospitalized Patients

Background: Studies suggest that blood lactate differs between survivors and non-survivors of out-of-hospital cardiac arrest who are transported to hospital. The prognostic role of lactate taken during out-of-hospital cardiac arrest remains unexplored. Aims: To measure the association between lactate taken during out-of-hospital cardiac arrest, survival to hospital and 30-day mortality. Methods: This is a feasibility, single-centre, prospective cohort study. Eligible for inclusion are patients aged ≥18 years suffering out-of-hospital cardiac arrest, receiving cardiopulmonary resuscitation, in the catchment of Newcastle or Gateshead hospitals, who are attended to by a study-trained specialist paramedic. Exclusions are known/apparent pregnancy, blunt or penetrating injury as primary cause of out-of-hospital cardiac arrest and an absence of intravenous access. Between February 2020 and March 2021, 100 participants will be enrolled. Primary outcome is survival to hospital; secondary outcomes are return of spontaneous circulation at any time and 30-day mortality.

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Abstract 249: The Effect of Response Time on Out-Of-Hospital Cardiac Arrest Survival Varies by Patient Subpopulation

Circulation ◽

10.1161/circ.138.suppl_2.249 ◽

2018 ◽

Vol 138 (Suppl_2) ◽

Author(s):

Clara Stoesser ◽

Justin Boutilier ◽

Christopher L Sun ◽

Katie N Dainty ◽

Steve Lin ◽

...

Keyword(s):

Cardiac Arrest ◽

Regression Analysis ◽

Response Time ◽

Time Interval ◽

Probability Of Survival ◽

Subgroup Analyses ◽

Impact On Survival ◽

The Impact ◽

Cardiac Arrest Survival ◽

Hospital Cardiac Arrest

Itroduction: Previous research has quantified the impact of EMS response time on the probability of survival from OHCA, but the impact on different subpopulations is currently unknown. Aim: To investigate how response time affects OHCA survival for different patient subpopulations. Methods: We conducted a logistic regression analysis on non-EMS witnessed OHCAs of presumed cardiac etiology from the Toronto Regional RescuNet between January 1, 2007 and December 31, 2016. We predicted survival using age, sex, public location, presenting rhythm, bystander witnessed, bystander resuscitation, and response time, defined as the time interval from 911 call to EMS arrival at the patient. We conducted subgroup analyses to quantify the effect of response time on survival for eight different subpopulations: public, private, bystander resuscitation, no bystander resuscitation, patients ≥65, patients <65, witnessed, and unwitnessed OHCA. We also quantified the effect of response time on survival for pairwise intersections of the subpopulations. We compared our results to Valenzuela et al. (1997), which suggests survival odds decrease by 10% for each minute delay in response time. Results: We identified 22,988 OHCAs. Overall, a one-minute delay in EMS response time was associated with a 13.2% reduction in the odds of survival. The reduction varied by subpopulation, ranging from a 7.2% reduction in survival odds for unwitnessed arrests to a 16.4% reduction in survival odds for arrests with bystander resuscitation. Response time had the largest impact on survival for the subpopulation of OHCAs that were both witnessed and received bystander resuscitation (17.4% reduction in survival odds). Conclusion: The effect of a one-minute delay in EMS response on the odds of survival from OHCA can be as low as a 7.2% reduction and as high as a 17.4% reduction. This variability contrasts with the currently accepted 10% rule that is assumed across the entire population.

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Abstract 67: Cardiac Arrest and Surgical Case Volume, Household Income and Availability of Trauma and Cardiac Surgery Are Associated with Higher Risk-Standardized Survival After Cardiac Arrest Among University Hospital Consortium Institutions in 2012

Circulation ◽

10.1161/circ.130.suppl_2.67 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Michael C Kurz ◽

John P Donnelly ◽

Henry E Wang

Keyword(s):

Cardiac Arrest ◽

Cardiac Surgery ◽

Household Income ◽

University Hospital ◽

Individual Risk ◽

P Value ◽

Case Volume ◽

Surgical Case ◽

Catchment Areas ◽

Cardiac Arrest Survival

Objective: Wide variation exists in cardiac arrest survival. Historically cardiac arrest research has focused upon clinical pre-arrest and intra-arrest factors to explain this variation in outcomes. In-hospital post-arrest care is increasingly recognized as an important aspect of survival. We sought to identify hospital characteristics associated with improved cardiac arrest survival. Methods: We examined all participating hospitals in the University Hospital Consortium (UHC) clinical database with more than 25 adult cardiac arrests in 2012. Cases were identified using International Classification of Diseases, 9th Edition, code 427.5 (cardiac arrest) or 99.60 (CPR), excluding prisoners, pregnant patients, transfers, and hospice patients. We estimated hospital-specific risk-standardized survival rates (RSSRs) using hierarchical logistic regression, adjusting for individual risk of mortality. Institutions in the highest RSSR quartile were compared with those in the lowest three quartiles using Pearson chi-square tests of association. Results: UHC institutions admitted 3,686,296 patients in 2012, of which 33,700 patients experienced cardiac arrest. Overall survival was 42.3% (95% CI 41.8-42.9) with median RSSR of 42.7% (IQR 35.5-50.8). Hospitals in the highest quartile of RSSR had higher cardiac arrest volume (median 193 vs. 150, p-value 0.019), higher annual surgical operation volume (21,177 vs. 14,122, 0.007), cared for patients from catchment areas with higher household income ($60,753 vs. $56,424, 0.027), and were more likely to be a trauma (79% vs 59%, 0.024) or cardiac surgery center (91% vs 70%, 0.007). In addition, hospital size (477 vs 415 beds, 0.060) and teaching status (77% vs. 62%, 0.067) demonstrated a trend toward association with higher RSSR. Conclusion: Among hospitals in the UHC, those with higher cardiac arrest and surgical case volume, patient household income, and availability of trauma and cardiac surgery were associated with improved RSSR.

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Abstract 216: Tat Delivery of a Pten Peptide Inhibitor Has Direct Cardioprotective Effects and Improves Outcomes in Rodent Models of Cardiac Arrest

Circulation ◽

10.1161/circ.142.suppl_4.216 ◽

2020 ◽

Vol 142 (Suppl_4) ◽

Author(s):

Xiangdong Zhu ◽

Jing Li ◽

Huashan Wang ◽

Filip Gasior ◽

Chunpei Lee ◽

...

Keyword(s):

Cardiac Arrest ◽

Mouse Model ◽

Pyruvate Dehydrogenase ◽

Contractile Function ◽

Heart Function ◽

Isolated Heart ◽

Lactate Production ◽

Polyol Pathway ◽

Protective Effects ◽

Cardiac Arrest Survival

Introduction: We have recently shown that pharmacologic inhibition of PTEN significantly increases cardiac arrest survival in a mouse model, however, this protection required pretreatment 30 min prior to the arrest. To improve the onset of PTEN inhibition during cardiac arrest treatment, we have designed a TAT fused cell-permeable peptide (TAT-PTEN9c) for rapid tissue delivery and protection. Hypothesis: We hypothesized that TAT-PTEN9c interferes with the endogenous PTEN binding to its regulatory proteins, resulting in reduced PTEN activity, improved mouse survival and cardiac functional recovery. The improved survival is in part due to enhanced glycolysis and reduced shunting to polyol pathway and osmotic injury in heart and brain. Methods: TAT-PTEN9c (7.5 mg/kg) was given intravenously after CA in mouse to determine protective effects of the treatment on survival and heart function. Western blot was used to determine the efficacy of TAT-PTEN9c for enhancing Akt and PDH E1α activity. The effect of TAT-PTEN9c on sorbitol accumulation in tissues was measured by spectrophotometer using NAD as substrate. Direct effect of TAT-PTEN9c treatment on cardiac function were also measured in Langendorff model of isolated rat heart. Results: In the mouse model of cardiac arrest, survival was significantly increased in the TAT-PTEN9c treated group compared to saline controls at 4 h after CPR. The treated mice had increased Akt phosphorylation and pyruvate dehydrogenase dephosphorylation at R30 min in heart tissues with significantly decreased sorbitol content and reduced release of taurine and glutamate into blood, suggesting improved metabolic recovery and glucose utilization. For the isolated heart model, RPP was reduced by 25% for non-treatment groups following arrest. With TAT-PTEN9c treatment, cardiac contractile function was completely recovered. TAT-PTEN9c significantly increased lactate production at 20 min of reperfusion, indicating increased glycolysis. Conclusion: TAT-PTEN9c enhances Akt and pyruvate dehydrogenase activity and decrease glucose shunting to the polyol pathway in critical organs, preventing osmotic injury and early cardiovascular collapse and death.

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