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4 results

  • A Novel Algorithm for Improving the Prehospital Diagnostic Accuracy of ST-Segment Elevation Myocardial Infarction

  • Mat Goebel, Lauren M. Westafer, Stephanie A. Ayala, El Ragone, Scott J. Chapman, Masood R. Mohammed, Marc R. Cohen, James T. Niemann, Marc Eckstein, Stephen Sanko, Nichole Bosson
  • Journal:
    Prehospital and Disaster Medicine / Volume 39 / Issue 1 / February 2024
    Published online by Cambridge University Press:
    04 December 2023, pp. 37-44
    Print publication:
    February 2024
    • Article
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  • Introduction:

    Early detection of ST-segment elevation myocardial infarction (STEMI) on the prehospital electrocardiogram (ECG) improves patient outcomes. Current software algorithms optimize sensitivity but have a high false-positive rate. The authors propose an algorithm to improve the specificity of STEMI diagnosis in the prehospital setting.

    Methods:

    A dataset of prehospital ECGs with verified outcomes was used to validate an algorithm to identify true and false-positive software interpretations of STEMI. Four criteria implicated in prior research to differentiate STEMI true positives were applied: heart rate <130, QRS <100, verification of ST-segment elevation, and absence of artifact. The test characteristics were calculated and regression analysis was used to examine the association between the number of criteria included and test characteristics.

    Results:

    There were 44,611 cases available. Of these, 1,193 were identified as STEMI by the software interpretation. Applying all four criteria had the highest positive likelihood ratio of 353 (95% CI, 201-595) and specificity of 99.96% (95% CI, 99.93-99.98), but the lowest sensitivity (14%; 95% CI, 11-17) and worst negative likelihood ratio (0.86; 95% CI, 0.84-0.89). There was a strong correlation between increased positive likelihood ratio (r2 = 0.90) and specificity (r2 = 0.85) with increasing number of criteria.

    Conclusions:

    Prehospital ECGs with a high probability of true STEMI can be accurately identified using these four criteria: heart rate <130, QRS <100, verification of ST-segment elevation, and absence of artifact. Applying these criteria to prehospital ECGs with software interpretations of STEMI could decrease false-positive field activations, while also reducing the need to rely on transmission for physician over-read. This can have significant clinical and quality implications for Emergency Medical Services (EMS) systems.

  • Weekly Checks Improve Real-Time Prehospital ECG Transmission in Suspected STEMI

  • Nicole T. D’Arcy, Nichole Bosson, Amy H. Kaji, Quang T. Bui, William J. French, Joseph L. Thomas, Yvonne Elizarraraz, Natalia Gonzalez, Jose Garcia, James T. Niemann
  • Journal:
    Prehospital and Disaster Medicine / Volume 33 / Issue 3 / June 2018
    Published online by Cambridge University Press:
    30 April 2018, pp. 245-249
    Print publication:
    June 2018
  • Introduction

    Field identification of ST-elevation myocardial infarction (STEMI) and advanced hospital notification decreases first-medical-contact-to-balloon (FMC2B) time. A recent study in this system found that electrocardiogram (ECG) transmission following a STEMI alert was frequently unsuccessful.

    Hypothesis

    Instituting weekly test ECG transmissions from paramedic units to the hospital would increase successful transmission of ECGs and decrease FMC2B and door-to-balloon (D2B) times.

    Methods

    This was a natural experiment of consecutive patients with field-identified STEMI transported to a single percutaneous coronary intervention (PCI)-capable hospital in a regional STEMI system before and after implementation of scheduled test ECG transmissions. In November 2014, paramedic units began weekly test transmissions. The mobile intensive care nurse (MICN) confirmed the transmission, or if not received, contacted the paramedic unit and the department’s nurse educator to identify and resolve the problem. Per system-wide protocol, paramedics transmit all ECGs with interpretation of STEMI. Receiving hospitals submit patient data to a single registry as part of ongoing system quality improvement. The frequency of successful ECG transmission and time to intervention (FMC2B and D2B times) in the 18 months following implementation was compared to the 10 months prior. Post-implementation, the time the ECG transmission was received was also collected to determine the transmission gap time (time from ECG acquisition to ECG transmission received) and the advanced notification time (time from ECG transmission received to patient arrival).

    Results

    There were 388 patients with field ECG interpretations of STEMI, 131 pre-intervention and 257 post-intervention. The frequency of successful transmission post-intervention was 73% compared to 64% prior; risk difference (RD)=9%; 95% CI, 1-18%. In the post-intervention period, the median FMC2B time was 79 minutes (inter-quartile range [IQR]=68-102) versus 86 minutes (IQR=71-108) pre-intervention (P=.3) and the median D2B time was 59 minutes (IQR=44-74) versus 60 minutes (IQR=53-88) pre-intervention (P=.2). The median transmission gap was three minutes (IQR=1-8) and median advanced notification time was 16 minutes (IQR=10-25).

    Conclusion

    Implementation of weekly test ECG transmissions was associated with improvement in successful real-time transmissions from field to hospital, which provided a median advanced notification time of 16 minutes, but no decrease in FMC2B or D2B times.

    D’ArcyNT, BossonN, KajiAH, BuiQT, FrenchWJ, ThomasJL, ElizarrarazY, GonzalezN, GarciaJ, NiemannJT. Weekly Checks Improve Real-Time Prehospital ECG Transmission in Suspected STEMI. Prehosp Disaster Med. 2018;33(3):245–249.

  • 8 - Inflammatory and Immunologic responses to ischemia and reperfusion

  • from Part II - Basic science
    • By Jason S. Haukoos, Department of Emergency Medicine, Denver Health Medical Center, Department of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, CO, USA, Ronald J. Korthuis, Department of Medical Pharmacology & Physiology and, The Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA, James T. Niemann, Department of Emergency Medicine, Harbor-UCLA Medical Center, Torrance, CA, USA, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
  • Edited by Norman A. Paradis, University of Colorado, Denver, Henry R. Halperin, The Johns Hopkins University School of Medicine, Karl B. Kern, University of Arizona, Volker Wenzel, Douglas A. Chamberlain, Cardiff University
  • Book:
    Cardiac Arrest
    Published online:
    06 January 2010
    Print publication:
    18 October 2007, pp 163-178

  • Summary

    Introduction

    Despite advances in the treatment of cardiac arrest, the development of organ dysfunction following return of spontaneous circulation causes considerable morbidity and mortality. The complex pathophysiologic mechanisms underlying this postresuscitation syndrome likely result from global ischemia, reperfusion, and the triggering of a profound systemic inflammatory response syndrome. To understand such mechanisms and to improve therapy for victims of cardiac arrest, it is essential to identify the principal mediators that contribute to this disease process, and to identify their roles in the development of organ dysfunction. By understanding the roles of key inflammatory and immunologic mediators during the resuscitation and postresuscitation periods, it may be possible to improve understanding of the whole-body response to ischemia and reperfusion, and to develop effective therapeutic strategies for patients who suffer cardiac arrest and for those who achieve return of spontaneous circulation.

    Systemic inflammatory response

    The pathophysiology of cardiac arrest is complex and, like sepsis, induces a profound systemic inflammatory response syndrome. Unlike sepsis, however, the systemic inflammatory response syndrome following cardiac arrest results from whole-body ischemia (i.e., low or noflow) and reperfusion (i.e., restoration of flow following ischemia). The development of a systemic inflammatory response syndrome has been divided into three stages. The first stage occurs in response to an insult, resulting in a local cytokine response primarily intended to evoke an inflammatory response to promote local cellular repair by recruiting cells from the reticuloendothelial and immune systems. The second stage involves release of small quantities of cytokines into the systemic circulation in order to enhance, or magnify, this local response. This acute-phase response is usually tightly controlled by endogenous proinflammatory antagonists, and cytokines and immunologic mediators are kept in check by specific downregulation and antagonism.

  • 18 - Coronary perfusion pressure during cardiopulmonary resuscitation

  • from Part III - The pathophysiology of global ischemia and reperfusion
    • By Karl B. Kern, University of Arizona Sarver Heart Center, Tucson, AZ, USA, James T. Niemann, Department of Emergency Medicine, Harbor-UCLA Medical Center, Torrance CA, USA, Stig Steen, Department of Cardiothoracic Surgery, University Hospital of Lund, Sweden
  • Edited by Norman A. Paradis, University of Colorado, Denver, Henry R. Halperin, The Johns Hopkins University School of Medicine, Karl B. Kern, University of Arizona, Volker Wenzel, Douglas A. Chamberlain, Cardiff University
  • Book:
    Cardiac Arrest
    Published online:
    06 January 2010
    Print publication:
    18 October 2007, pp 369-388

  • Summary

    Introduction

    The resurgence of resuscitation research in the 1970s and 1980s initially focused on the physiological mechanisms for systemic blood flow during closed chest resuscitation for cardiac arrest. At the same time, the importance of both myocardial and cerebral blood flow during cardiopulmonary resuscitation (CPR) became evident. Using contemporary, state-of-art techniques, investigators found that regional perfusion of vital organs occurs with closed chest compression CPR, but at substantially lower rates than that measured during normal sinus rhythm. Such studies have shown that standard anteroposterior chest compressions can, at best, provide 30% to 40% of normal cerebral blood flow levels. Myocardial blood flow achieved with external chest compressions is often even lower, typically between 10% and 30% of normal. Peripheral perfusion is almost non-existent during CPR. Nevertheless, good CPR efforts can temporarily provide at least some perfusion to the myocardium and cerebrum until more definitive treatment (i.e., defibrillation) can be accomplished.

    Myocardial perfusion during cardiac arrest can be estimated by measuring “coronary perfusion pressure” during the resuscitation effort. This perfusion pressure gradient correlates well with resultant myocardial blood flow generated with CPR and with the subsequent possibility of successful defibrillation. The critical importance of coronary perfusion pressure during CPR has been confirmed in both laboratory and clinical studies of resuscitation. This part of the chapter focuses on coronary perfusion pressure during CPR: its generation and impact.

    Determinants of coronary perfusion pressure during cardiopulmonary resuscitation

    AoD pressure during CPR

    The importance of anadequate perfusion pressure for resuscitation from cardiac arrest was first noted by Crile and Dolley in 1906.