Cardiogenic shock classification
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Cardiogenic shock is a clinical condition, defined as a state of systemic hypoperfusion originated in cardiac failure, in the presence of adequate intravascular volume, typically followed by hypotension, which leads to insufficient ability to meet oxygen and nutrient demands of organs and other peripheral tissues.[1] It may range from mild to severe hypoperfusion and may be defined in terms of hemodynamic parameters, which according to most studies, means a state in which systolic blood pressure is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right ventricular filling pressures that does not respond to isolated fluid administration, is secondary to cardiac failure and occurs with signs of hypoperfusion (oliguria, cool extremities, cyanosis and altered mental status) or a cardiac index of < 2.2 L/min/m² (on inotropic, vasopressor or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg. There are different causes explaining the development of cardiogenic shock, these may be grouped into two major categories: intrinsic and compressive.[2][3][4][5][6][7][8]
Classification
In cardiogenic shock, the root abnormality is the inability of the heart to pump out enough blood to maintain normal organ perfusion and blood pressure. However, this failure may be due to different factors, which allow us to classify cardiogenic shock into two categories:[9][10]
- Intrinsic - this includes the conditions affecting the heart or the structures that allow it to function properly. In this category, the affected structures may be: the myocardial muscle, responsible to pump out the blood; the heart valves allowing the blood in and out of the heart chambers; the conduction system, responsible for the transmission of the electrical signals that allow the myocardium to contract in a coordinated fashion or, a combination of the previous. Examples of such factors are: myocardial infarction, mitral regurgitation and electrolyte imbalances.
- Compressive - this includes the conditions in which an otherwise "healthy heart" is prevented from working properly and pumping the blood through the vascular system, by a mechanism not related to it. The degree of impact that an extrinsic factor must have on the heart will depend on the overall "health status" of this last one. An "healthy heart" might take a more aggressive outside influence without compromising its function, while a heart already weakened by another disease, such as atherosclerosis, might fail more promptly. An example of such factor is cardiac tamponade.
Often times both factors are affecting the heart's ability to perform its function, at which times it might be hard to identify clearly the underlying mechanism of the cardiogenic shock.[11]
References
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hochman, Judith (2009). Cardiogenic shock. Chichester, West Sussex, UK Hoboken, NJ: Wiley-Blackwell. ISBN 1405179260.
- ↑ Goldberg, Robert J.; Gore, Joel M.; Alpert, Joseph S.; Osganian, Voula; de Groot, Jacques; Bade, Jurgen; Chen, Zuoyao; Frid, David; Dalen, James E. (1991). "Cardiogenic Shock after Acute Myocardial Infarction". New England Journal of Medicine. 325 (16): 1117–1122. doi:10.1056/NEJM199110173251601. ISSN 0028-4793.
- ↑ Goldberg, Robert J.; Samad, Navid A.; Yarzebski, Jorge; Gurwitz, Jerry; Bigelow, Carol; Gore, Joel M. (1999). "Temporal Trends in Cardiogenic Shock Complicating Acute Myocardial Infarction". New England Journal of Medicine. 340 (15): 1162–1168. doi:10.1056/NEJM199904153401504. ISSN 0028-4793.
- ↑ Menon, V.; Slater, JN.; White, HD.; Sleeper, LA.; Cocke, T.; Hochman, JS. (2000). "Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: report of the SHOCK trial registry". Am J Med. 108 (5): 374–80. PMID 10759093. Unknown parameter
|month=ignored (help) - ↑ Hasdai, D.; Holmes, DR.; Califf, RM.; Thompson, TD.; Hochman, JS.; Pfisterer, M.; Topol, EJ. (1999). "Cardiogenic shock complicating acute myocardial infarction: predictors of death. GUSTO Investigators. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries". Am Heart J. 138 (1 Pt 1): 21–31. PMID 10385759. Unknown parameter
|month=ignored (help) - ↑ Fincke, R.; Hochman, JS.; Lowe, AM.; Menon, V.; Slater, JN.; Webb, JG.; LeJemtel, TH.; Cotter, G. (2004). "Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry". J Am Coll Cardiol. 44 (2): 340–8. doi:10.1016/j.jacc.2004.03.060. PMID 15261929. Unknown parameter
|month=ignored (help) - ↑ Dzavik, V.; Cotter, G.; Reynolds, H. R.; Alexander, J. H.; Ramanathan, K.; Stebbins, A. L.; Hathaway, D.; Farkouh, M. E.; Ohman, E. M.; Baran, D. A.; Prondzinsky, R.; Panza, J. A.; Cantor, W. J.; Vered, Z.; Buller, C. E.; Kleiman, N. S.; Webb, J. G.; Holmes, D. R.; Parrillo, J. E.; Hazen, S. L.; Gross, S. S.; Harrington, R. A.; Hochman, J. S. (2007). "Effect of nitric oxide synthase inhibition on haemodynamics and outcome of patients with persistent cardiogenic shock complicating acute myocardial infarction: a phase II dose-ranging study". European Heart Journal. 28 (9): 1109–1116. doi:10.1093/eurheartj/ehm075. ISSN 0195-668X.
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ Myers, Jeffrey (2002). Principles of pathophysiology and emergency medical care. Albany: Delmar/Thomson Learning. ISBN 978-0766825482.
- ↑ Myers, Jeffrey (2002). Principles of pathophysiology and emergency medical care. Albany: Delmar/Thomson Learning. ISBN 978-0766825482.