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Part of the book series: Update in Intensive Care and Emergency Medicine ((UICMSOFT,volume 44))

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Conclusion

Myocardial dysfunction is an important component in the hemodynamic collapse induced by sepsis and septic shock. A series of inflammatory cascades triggered by the inciting infection generate circulatory myocardial depressant substances, including TNF-α, IL-1β, PAF and lysozyme. Current evidence suggests that septic myocardial depression in humans is characterized by reversible biventricular dilatation, decreased systolic contractile function, and decreased response to both fluid resuscitation and catecholamine stimulation, all in the presence of an overall hyperdynamic circulation. This phenomenon is linked to the presence of a circulating myocardial depressant substance or substances which probably represents low concentrations of pro-inflammatory cytokines including TNF-α, IL-1β and perhaps IL-6 acting in synergy. These effects are mediated through mechanisms that include but are not limited to NO and cGMP generation. The mechanism through which NO depresses cardiac contractility is largely unknown. Recent data suggest that pre-apoptotic signaling involving transcription factors STAT1, IRF1 and NF-κB leading to apoptotic pathways may play a role in septic myocardial depression related to inflammatory cytokines circulating during septic shock. Links between this response and NO generation are postulated but have not been fully delineated.

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Kumar, A., Parrillo, J.E. (2007). Myocardial Depression in Sepsis and Septic Shock. In: Abraham, E., Singer, M. (eds) Mechanisms of Sepsis-Induced Organ Dysfunction and Recovery. Update in Intensive Care and Emergency Medicine, vol 44. Springer, Berlin, Heidelberg . https://doi.org/10.1007/3-540-30328-6_30

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