Abstract
Septic shock in the course of overwhelming bacterial infection carries a mortality rate of about 50% [1]. Even though late mortality from septic shock after initially successful resuscitation is mainly due to failure of multiple organ systems, septic shock can be rapidly fatal because of irreversible hypotension. It has been a matter of debate whether this hypotension is primarily caused by cardiac failure or not. Classically, the hemodynamic alterations in septic shock have been described to consist of two phases: an early hyperdynamic phase in which cardiac output is elevated, particularly after initial fluid resuscitation, and a late phase in which cardiac output is low, possibly as a result of myocardial depression and ultimately leading to demise. However, the clinical evidence for this bi-phasic hemodynamic pattern and the prognostic importance thereof, is not certain. After describing the recent insights into the global hemodynamic changes of septic shock and their relation to outcome in more detail, we will discuss the evidence for myocardial dysfunction, the mechanisms involved, methods for diagnosis at the bedside, and the prognostic and therapeutic implications.
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© 1991 Springer-Verlag Berlin, Heidelberg
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Groeneveld, A.B.J., Schneider, A.J., Thijs, L.G. (1991). Cardiac Alterations in Septic Shock: Pathophysiology, Diagnosis, Prognostic, and Therapeutic Implications. In: Vincent, J.L. (eds) Update 1991. Update in Intensive Care and Emergency Medicine, vol 14. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84423-2_15
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DOI: https://doi.org/10.1007/978-3-642-84423-2_15
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