Cardiogenic shock differential diagnosis: Difference between revisions
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==Differential Diagnosis== | ==Differential Diagnosis== | ||
Depending on the author and the source used, there will be different ways of organizing the types of [[shock]]. Patients who present with [[signs]] and [[symptoms]] of [[hypoperfusion]] following a diagnosed or suspected [[myocardial infarction]], are commonly suffering a cardiogenic shock as a [[complication]] of the [[MI]]. However, other clinical scenarios, not related to acute [[MI]], may present similarly:<ref>{{Cite book | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages = }}</ref> | Depending on the author and the source used, there will be different ways of organizing the types of [[shock]]. The clinical presentation of [[shock]] is usually the result of a complexity of processes, such the [[sympathetic]] and [[endocrine]] response to [[hypoperfusion]] along with manifestations of [[organ failure]]. Patients who present with [[signs]] and [[symptoms]] of [[hypoperfusion]] following a diagnosed or suspected [[myocardial infarction]], are commonly suffering a cardiogenic shock as a [[complication]] of the [[MI]]. However, other clinical scenarios, not related to acute [[MI]], may present similarly:<ref>{{Cite book | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages = }}</ref> | ||
:*[[Hypovolemic shock]] - | :*[[Hypovolemic shock]] - | ||
:*[[Septic shock]] | :*[[Septic shock]] | ||
Revision as of 20:01, 18 May 2014
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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
Shock is a clinical syndrome resulting from the hypoperfusion of the tissues. Regardless of the underlying cause, this hypoperfusion leads to the failure to meet tissues' nutritional and oxygen needs, causing cellular dysfunction. The affected tissues lead to the production and release of inflammatory mediators that will further jeopardize perfusion through changes in the vasculature. The results of these changes are organ failure and death if treatment in not timely applied. According to the underlying cause, there will be different types of shock, which will have similar presentations. It is mandatory to determine the underlying cause of the condition so that proper treatment may be started.[1]
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.[2] 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.[3][4][5][6][7][8][9]
Differential Diagnosis
Depending on the author and the source used, there will be different ways of organizing the types of shock. The clinical presentation of shock is usually the result of a complexity of processes, such the sympathetic and endocrine response to hypoperfusion along with manifestations of organ failure. Patients who present with signs and symptoms of hypoperfusion following a diagnosed or suspected myocardial infarction, are commonly suffering a cardiogenic shock as a complication of the MI. However, other clinical scenarios, not related to acute MI, may present similarly:[10]
-
- Hyperdynamic -
- Hypodynamic -
- Traumatic shock -
- Distributive shock
- Neurogenic shock -
- Hypoadrenal shock -
References
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ 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.