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  • Book
    Massimo Biondi, Massimo Pasquini, Lorenzo Tarsitani, editors.
    Summary: This book describes theory and techniques of empathic communication, normalization and de-escalation procedures for the management of aggressive or violent patients in clinical critical settings. Consisting of 9 chapters, it discusses in detail the self-regulation of empathy in potential dangerous interactions, as well as common mistakes and nonprofessional reactions. It also explores the basic concept of neurobiology of violence and aggression behaviour, such as brain circuitry and neuromodulators, and other rapid tranquillization guidelines. The final chapter focuses on the crucial topics of post-aggression debriefing. Based on the clinical experience of the editors and authors, who work in emergency psychiatry settings, the book offers practical key expressions to promote a normalization talk, to calm agitated individuals, and to prevent crises both for psychiatric patients and people without mental disorders. It is a useful tool to help readers gain confidence as mediators in critical circumstances and will be of interest for a wide range of practitioners in healthcare settings, from psychiatrists and psychologists, to nurses and other healthcare workers.

    Contents:
    Introduction: Meaning of the END Methods
    Psychomotor Agitation and Aggression
    Neurobiology of Aggression and Violence
    Empathy regulation in crisis scenario
    Normalization
    De-escalation techniques in various settings
    Rapid Tranquillisation
    Communication in psychiatric coercive treatment and patients' decisional capacity to consent
    Immediate post-aggression debrief.
    Digital Access Springer 2021
  • Article
    Hyman AL, Kadowitz PJ, Lands WE, Crawford CG, Fried J, Barton J.
    Proc Natl Acad Sci U S A. 1978 Jul;75(7):3522-6.
    The effects of a recently synthesized, stable prostacyclin (PGI2) analog, 13,14-dehydro-PGI2 methyl ester, and authentic PGI2 and several other prostanoids on the coronary circulation were investigated in the intact dog by using a new technique to measure coronary sinus blood flow. The PGI2 analog, PGI2, and prostaglandin (PG) E2 and D2 each increased coronary sinus blood flow in a dose-related fashion when injected into the left coronary artery. The analog and PGE2 had similar vasodilator activity while PGI2 was slightly more potent. PGD2 was a moderately active coronary vasodilator whereas PGF2alpha was inactive. The coronary vasodilator effects of PGI2, its analog, PGE2, and PGD2 occurred at doses that had little effect on aortic pressure, left ventricular pressure and its first derivative, or on cardiac output and heart rate. The prostaglandin precursor arachidonic acid and the endoperoxide intermediate PGH2 both increased coronary sinus blood flow in a dose-dependent manner. The effects of arachidonic acid were inhibited by indomethacin. These data show that PGE2, PGI2, and a stable PGI2 analog are potent vasodilators in the canine coronary vascular bed and suggest that the vasodilator effects of arachidonic acid and PGH2 may be due to the formation of PGE2, PGD2, or PGI2 in the dog heart.
    Digital Access Access Options