Cardiogenic Shock by Judith S. Hochman, E. Magnus Ohman MD

By Judith S. Hochman, E. Magnus Ohman MD

* A complete resource of data at the administration of cardiogenic surprise * a part of the AHA medical sequence released together with the yank center organization * specializes in high-interest and rising subject matters in heart problems designated to cardiologists and different healthcare prone * a great tool for investigating, comparing and treating essentially the most vital lingering demanding situations in acute cardiovascular care

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Cardiogenic Shock

* A entire resource of data at the administration of cardiogenic surprise * a part of the AHA medical sequence released along with the yank middle organization * makes a speciality of high-interest and rising themes in heart problems specific to cardiologists and different healthcare services * a great tool for investigating, comparing and treating the most vital lingering demanding situations in acute cardiovascular care

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Remote ischemia Pump failure in cardiogenic shock need not result only from infarcted myocardium; myocardial ischemia can contribute significantly to systolic dysfunction. Ischemia remote from the infarct zone may be particularly important in this respect [29,30]. Patients with cardiogenic shock usually have multivessel coronary artery disease [1,21], with limited vasodilator reserve, impaired autoregulation, and consequent pressure-dependent coronary flow in several perfusion territories [31].

During ischemia, energy depletion impairs outward sodium pumps and intracellular sodium increases, but sodium–calcium exchange is inhibited by concomitant acidosis. With reperfusion, the acidosis reverses more quickly than the sodium overload, and the reactivated sodium–calcium exchange causes transient calcium overload [48]; reactive oxygen species may contribute to calcium overload as well [49]. Such overload can activate calcium-dependent proteases, termed calpains. Although calcium transients are normal in stunned myocardial cells, responsiveness of the contractile apparatus to calcium is decreased.

Ongoing apoptosis could also be an important factor in late remodeling after acute infarction as well. What is most important about the notion that apoptotic cell death contributes to myocyte loss in acute infarction, however, is that apoptosis is a potential therapeutic target. Inhibitors of apoptosis have been found to attenuate myocardial injury in animal models of postischemic reperfusion [40]. Such inhibitors may P1: SFK/UKS 9781405179263 P2: SFK/UKS QC: SFK/UKS BLBK160-Hochman T1: SFK February 13, 2009 11:24 36 Cardiogenic Shock also have therapeutic potential for myocyte salvage after large infarctions, but both a deeper understanding of the magnitude and mechanisms of apoptosis after infarction as well as appropriate clinical trials will be needed [39].

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