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Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction

Authors
Judith S Hochman, MD
Alex Reyentovich, MD
Section Editor
Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Deputy Editor
Gordon M Saperia, MD, FACC

INTRODUCTION

Cardiogenic shock is a clinical condition of inadequate tissue (end-organ) perfusion due to the inability of the heart to pump an adequate amount of blood. The reduction in tissue perfusion results in decreased oxygen and nutrient delivery to the tissues and, if prolonged, potentially end-organ damage and multi-system failure. (See "Definition, classification, etiology, and pathophysiology of shock in adults", section on 'Introduction'.)  

Acute myocardial infarction (MI) is the most common cause of cardiogenic shock and is defined as a clinical event consequent to the death of cardiac myocytes (myocardial necrosis) that is caused by ischemia (as opposed to other etiologies such as myocarditis or trauma). (See "Criteria for the diagnosis of acute myocardial infarction", section on 'Acute MI'.)

Cardiogenic shock is the leading cause of death in patients with acute MI, with hospital mortality rates approaching 50 percent [1]. Short-term prognosis is directly related to the severity of the hemodynamic disorder. The clinical manifestations and diagnosis of cardiogenic shock in acute MI will be reviewed here. The prognosis and treatment are discussed separately. (See "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)

An overview of the types of shock in adults and the diagnostic approach to such patients is presented separately. (See "Definition, classification, etiology, and pathophysiology of shock in adults".)

PATHOPHYSIOLOGY

All forms of shock, including hypovolemic and distributive, are characterized by relatively low blood pressure and manifestations of end-organ hypoperfusion, such as poor mentation or low urine output. Patients with cardiogenic shock have a low cardiac index (<2.2 L/min/m2), elevated filling pressures of the left, right, or both ventricles, and a decreased mixed venous oxygen saturation (table 1) [2-4]. The systemic vascular resistance is often high, but it may be in the normal or low range. Individuals with normal or low range of systemic vascular resistance represent a group of patients with more profound hypoperfusion and inflammatory response and associated worse prognosis [4].

               

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Literature review current through: Nov 2016. | This topic last updated: Wed Nov 25 00:00:00 GMT+00:00 2015.
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References
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  1. Fox KA, Steg PG, Eagle KA, et al. Decline in rates of death and heart failure in acute coronary syndromes, 1999-2006. JAMA 2007; 297:1892.
  2. Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation 2008; 117:686.
  3. Hochman JS. Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm. Circulation 2003; 107:2998.
  4. Kohsaka S, Menon V, Lowe AM, et al. Systemic inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock. Arch Intern Med 2005; 165:1643.
  5. Hollenberg SM, Kavinsky CJ, Parrillo JE. Cardiogenic shock. Ann Intern Med 1999; 131:47.
  6. Califf RM, Bengtson JR. Cardiogenic shock. N Engl J Med 1994; 330:1724.
  7. Stegman BM, Newby LK, Hochman JS, Ohman EM. Post-myocardial infarction cardiogenic shock is a systemic illness in need of systemic treatment: is therapeutic hypothermia one possibility? J Am Coll Cardiol 2012; 59:644.
  8. Picard MH, Davidoff R, Sleeper LA, et al. Echocardiographic predictors of survival and response to early revascularization in cardiogenic shock. Circulation 2003; 107:279.
  9. Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovasc Res 2002; 53:31.
  10. Neumann FJ, Ott I, Gawaz M, et al. Cardiac release of cytokines and inflammatory responses in acute myocardial infarction. Circulation 1995; 92:748.
  11. Wildhirt SM, Dudek RR, Suzuki H, Bing RJ. Involvement of inducible nitric oxide synthase in the inflammatory process of myocardial infarction. Int J Cardiol 1995; 50:253.
  12. Babaev A, Frederick PD, Pasta DJ, et al. Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA 2005; 294:448.
  13. Holmes DR Jr, Bates ER, Kleiman NS, et al. Contemporary reperfusion therapy for cardiogenic shock: the GUSTO-I trial experience. The GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol 1995; 26:668.
  14. Hands ME, Rutherford JD, Muller JE, et al. The in-hospital development of cardiogenic shock after myocardial infarction: incidence, predictors of occurrence, outcome and prognostic factors. The MILIS Study Group. J Am Coll Cardiol 1989; 14:40.
  15. Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med 1999; 340:1162.
  16. Jeger RV, Radovanovic D, Hunziker PR, et al. Ten-year trends in the incidence and treatment of cardiogenic shock. Ann Intern Med 2008; 149:618.
  17. Goldberg RJ, Spencer FA, Gore JM, et al. Thirty-year trends (1975 to 2005) in the magnitude of, management of, and hospital death rates associated with cardiogenic shock in patients with acute myocardial infarction: a population-based perspective. Circulation 2009; 119:1211.
  18. Aissaoui N, Puymirat E, Tabone X, et al. Improved outcome of cardiogenic shock at the acute stage of myocardial infarction: a report from the USIK 1995, USIC 2000, and FAST-MI French nationwide registries. Eur Heart J 2012; 33:2535.
  19. Hochman JS, Boland J, Sleeper LA, et al. Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Results of an International Registry. SHOCK Registry Investigators. Circulation 1995; 91:873.
  20. Holmes DR Jr, Berger PB, Hochman JS, et al. Cardiogenic shock in patients with acute ischemic syndromes with and without ST-segment elevation. Circulation 1999; 100:2067.
  21. Hasdai D, Harrington RA, Hochman JS, et al. Platelet glycoprotein IIb/IIIa blockade and outcome of cardiogenic shock complicating acute coronary syndromes without persistent ST-segment elevation. J Am Coll Cardiol 2000; 36:685.
  22. Alonso DR, Scheidt S, Post M, Killip T. Pathophysiology of cardiogenic shock. Quantification of myocardial necrosis, clinical, pathologic and electrocardiographic correlations. Circulation 1973; 48:588.
  23. Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating acute myocardial infarction--etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol 2000; 36:1063.
  24. Chockalingam A, Tejwani L, Aggarwal K, Dellsperger KC. Dynamic left ventricular outflow tract obstruction in acute myocardial infarction with shock: cause, effect, and coincidence. Circulation 2007; 116:e110.
  25. Hasdai D, Califf RM, Thompson TD, et al. Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction. J Am Coll Cardiol 2000; 35:136.
  26. Menon V, Slater JN, White HD, et al. Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: report of the SHOCK trial registry. Am J Med 2000; 108:374.
  27. Menon V, White H, LeJemtel T, et al. The clinical profile of patients with suspected cardiogenic shock due to predominant left ventricular failure: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol 2000; 36:1071.
  28. Webb JG, Sleeper LA, Buller CE, et al. Implications of the timing of onset of cardiogenic shock after acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol 2000; 36:1084.
  29. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. www.acc.org/qualityandscience/clinical/statements.htm (Accessed on August 24, 2006).
  30. Mueller HS, Chatterjee K, Davis KB, et al. ACC expert consensus document. Present use of bedside right heart catheterization in patients with cardiac disease. American College of Cardiology. J Am Coll Cardiol 1998; 32:840.
  31. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med 1999; 341:625.