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Editorials |

Cardiogenic Shock: What Has Changed?

Vinod K. Puri
Author and Funding Information

Affiliations: Southfield, MI
 ,  Dr. Puri is Director of Critical Care Services, Providence Hospital and Medical Center.

Correspondence to: Vinod K. Puri, MD, Director Critical Care Services, Providence Hospital and Medical Center, 16001 West Nine Mile Rd, Southfield, MI 48037-2043; e-mail: vinodpuri@providencehospital.org



Chest. 2003;124(5):1634-1636. doi:10.1378/chest.124.5.1634
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The oft-repeated adage that we have gained the ability to keep critically ill patients alive longer is valid for the complication of cardiogenic shock. So the next question is, has the disease state changed in the last 40 years? The breathtaking advances in cardiology that have focused on reperfusion of the myocardium after an infarct are supplemented by intensive care to preserve the myocardium. The exhaustive review by Hollenberg and colleagues1 estimated the incidence of cardiogenic shock at 5 to 10% after myocardial infarction, a value that has remained stable in other studies since 1975.2 The reviewers emphasized that myocardial dysfunction due to ischemia worsens the ischemia that creates the “downward spiral.”1 The study by Lim and associates in this issue (see page 1885) seems to suggest that the pathophysiology of cardiogenic shock may have changed in some patients. They present a provocative idea that a group of patients who were significantly younger and were kept alive for 4 to 5 days actually may have experienced a distributive form of shock. Their hypothesis is based on data from nine nonsurvivors in whom cardiac index (CI) levels were restored to > 2.2 L/min/m2. These patients had no clinical or bacteriologic evidence of sepsis, including nosocomial infections. In comparison, patients with low CI values died rapidly from either the classic downward spiral or malignant arrhythmias. They speculate from an analysis of a subgroup of patients in the retrospective study about the role of cytokines, tissue mediators, and nitric oxide in cardiogenic shock. These authors, interestingly, do not consider the important role of myocardial stunning or hibernation that contribute to the pathogenesis of cardiogenic shock.,1

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