Cardiogenic shock differential diagnosis: Difference between revisions
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==Overview== | ==Overview== | ||
'''Cardiogenic shock''' is a clinical condition, defined as a state of systemic [[hypoperfusion]] originated in [[heart failure|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.<ref>{{Cite book | last1 = Hasdai | first1 = David. | title = Cardiogenic shock : diagnosis and treatmen | date = 2002 | publisher = Humana Press | location = Totowa, N.J. | isbn = 1-58829-025-5 | pages = }}</ref> 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 [[heart failure|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.<ref>{{cite book | last = Hochman | first = Judith | title = Cardiogenic shock | publisher = Wiley-Blackwell | location = Chichester, West Sussex, UK Hoboken, NJ | year = 2009 | isbn = 1405179260 }}</ref><ref name="GoldbergGore1991">{{cite journal|last1=Goldberg|first1=Robert J.|last2=Gore|first2=Joel M.|last3=Alpert|first3=Joseph S.|last4=Osganian|first4=Voula|last5=de Groot|first5=Jacques|last6=Bade|first6=Jurgen|last7=Chen|first7=Zuoyao|last8=Frid|first8=David|last9=Dalen|first9=James E.|title=Cardiogenic Shock after Acute Myocardial Infarction|journal=New England Journal of Medicine|volume=325|issue=16|year=1991|pages=1117–1122|issn=0028-4793|doi=10.1056/NEJM199110173251601}}</ref><ref name="GoldbergSamad1999">{{cite journal|last1=Goldberg|first1=Robert J.|last2=Samad|first2=Navid A.|last3=Yarzebski|first3=Jorge|last4=Gurwitz|first4=Jerry|last5=Bigelow|first5=Carol|last6=Gore|first6=Joel M.|title=Temporal Trends in Cardiogenic Shock Complicating Acute Myocardial Infarction|journal=New England Journal of Medicine|volume=340|issue=15|year=1999|pages=1162–1168|issn=0028-4793|doi=10.1056/NEJM199904153401504}}</ref><ref>{{Cite journal | last1 = Menon | first1 = V. | last2 = Slater | first2 = JN. | last3 = White | first3 = HD. | last4 = Sleeper | first4 = LA. | last5 = Cocke | first5 = T. | last6 = Hochman | first6 = JS. | title = Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: report of the SHOCK trial registry. | journal = Am J Med | volume = 108 | issue = 5 | pages = 374-80 | month = Apr | year = 2000 | doi = | PMID = 10759093 }}</ref><ref name="Hasdai-1999">{{Cite journal | last1 = Hasdai | first1 = D. | last2 = Holmes | first2 = DR. | last3 = Califf | first3 = RM. | last4 = Thompson | first4 = TD. | last5 = Hochman | first5 = JS. | last6 = Pfisterer | first6 = M. | last7 = Topol | first7 = EJ. | title = Cardiogenic shock complicating acute myocardial infarction: predictors of death. GUSTO Investigators. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries. | journal = Am Heart J | volume = 138 | issue = 1 Pt 1 | pages = 21-31 | month = Jul | year = 1999 | doi = | PMID = 10385759 }}</ref><ref name="Fincke-2004">{{Cite journal | last1 = Fincke | first1 = R. | last2 = Hochman | first2 = JS. | last3 = Lowe | first3 = AM. | last4 = Menon | first4 = V. | last5 = Slater | first5 = JN. | last6 = Webb | first6 = JG. | last7 = LeJemtel | first7 = TH. | last8 = Cotter | first8 = G. | title = Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. | journal = J Am Coll Cardiol | volume = 44 | issue = 2 | pages = 340-8 | month = Jul | year = 2004 | doi = 10.1016/j.jacc.2004.03.060 | PMID = 15261929 }}</ref><ref name="DzavikCotter2007">{{cite journal|last1=Dzavik|first1=V.|last2=Cotter|first2=G.|last3=Reynolds|first3=H. R.|last4=Alexander|first4=J. H.|last5=Ramanathan|first5=K.|last6=Stebbins|first6=A. L.|last7=Hathaway|first7=D.|last8=Farkouh|first8=M. E.|last9=Ohman|first9=E. M.|last10=Baran|first10=D. A.|last11=Prondzinsky|first11=R.|last12=Panza|first12=J. A.|last13=Cantor|first13=W. J.|last14=Vered|first14=Z.|last15=Buller|first15=C. E.|last16=Kleiman|first16=N. S.|last17=Webb|first17=J. G.|last18=Holmes|first18=D. R.|last19=Parrillo|first19=J. E.|last20=Hazen|first20=S. L.|last21=Gross|first21=S. S.|last22=Harrington|first22=R. A.|last23=Hochman|first23=J. S.|title=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|journal=European Heart Journal|volume=28|issue=9|year=2007|pages=1109–1116|issn=0195-668X|doi=10.1093/eurheartj/ehm075}}</ref> | |||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
Revision as of 02:33, 17 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
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.[2][3][4][5][6][7][8]
Differential Diagnosis
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. These may be classified in two categories, according to the mechanism at its genesis:
- 1. Acute myocardial infarction with shock of non-cardiac etiology:
- Sepsis from indwelling catheter
- Hypovolemia following overaggressive diuresis
- 2. Cardiovascular disease in which the acute myocardial infarction is not the primary problem:[9]
- Stress-induced cardiomyopathy or Takotsubo cardiomyopathy
- Hypertrophic cardiomyopathy
- Acute myopericarditis
- Pulmonary embolism
- Acute regurgitant valvular heart disease
- Acute MI from ascending aortic dissection
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.
- ↑ Hollenberg SM, Kavinsky CJ, Parrillo JE (1999). "Cardiogenic shock". Ann Intern Med. 131 (1): 47–59. PMID 10391815.