Cardiogenic shock natural history, complications and prognosis: Difference between revisions
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===Pulmonary=== | ===Pulmonary=== | ||
Revision as of 20:05, 16 May 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Zaghw, M.D. [2] João André Alves Silva, M.D. [3]
Overview
Cardiogenic shock (CS) 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] Despite the many possible causes for the cardiac failure, the most common is left ventricular failure in the setting of myocardial infarction.[9] In the presence of CS, a pathological cycle develops in which ischemia, the initial aggression, leads to myocardial dysfunction. This will affect parameters like the cardiac output, stroke volume and myocardial perfusion thereby worsening the ischemia. The body will then initiate a series of compensatory mechanisms, such as sympathetic stimulation of the heart and activation of the renin/angiotensin/aldosterone system, trying to overcome the cardiac aggression, however, this will ultimately lead to a downward spiral worsening of the ischemia. Inflammatory mediators, originated in the infarcted area, will also intervene at some point causing myocardial depression, decreasing contractility and worsening hypotension. Lactic acidosis will also develop, resulting from the poor tissue perfusion, that is responsible for a shift in metabolism to glycolysis, which will further depress the myocardium, thereby worsening the clinical scenario.[10][11] CS has several risk factors which will contribute to the progression of the condition. Depending on these underlying factors and in concordance to the pathological mechanism responsible for the development of CS, the patient will have higher or lower probability of developing complications, of which the most common are cardiac, renal and pulmonary. The presence of certain risk factors and the etiology behind the shock will dictate the outcome of the condition. Despite the decreasing incidence and mortality rate seen throughout recent years, CS is still associated with a poor prognosis, particularly in elderly patients.
Natural History
Complications
Complications of cardiogenic shock include:
Cardiac
- A downward spiral of hypotension leading to reduced coronary perfusion leading to hypotension and further reduction in coronary and peripheral tissue perfusion
- Heart block[12]
- Ventricular septal rupture[13]
- Ventricular free wall rupture[13]
- Valvular abnormalities[13]
Neurologic
Renal
Pulmonary
Cardiogenic pulmonary edema
Prognosis
The prognosis of cardiogenic shock (CS) will be dictated by several factors, including: the underlying condition precipitating the progression into shock, the risk factors owned by the patient; the severity of the hemodynamic disorder; along with the possible emergence of complications during the process of the disease. To better help in the prediction of the evolution of the cardiogenic shock along with the prognosis of the patient, some important facts are relevant to underline:
- CS occurs in 8% of hospitalized STEMI patients, with a mortality rate of 50-60% within 30 days.[14]
- CS carries a very poor prognosis, particularly in the elderly. In the GUSTO 1 trial, the following were identified as correlates of higher mortality among patients with CS:[15]
- Older age
- Prior MI
- Signs of hypoperfusion including cold and clammy skin
- Altered mental state
- Oliguria
- CS is associated with more severe lesions of the coronary territories, with 53% of patients in the SHOCK trial suffering from disease in three coronary arteries and 16% with predominant left main coronary artery disease.[16]
- The mortality rate in CS is significantly higher when the culprit lesion is located in the left main coronary artery or saphenous vein graft, compared to those with lesions located in the circumflex, left anterior descending, or right coronary artery.[17]
- Among the causes of CS following MI, ventricular septal rupture has one of the highest mortality rates post-MI, around 87.3%[18]
- The prognosis is in part dictated by the amount of myocardium affected and the ability to reperfuse the ischemic myocardium. The sooner the ischemia is treated, better chances of a good outcome there will be[13]
- There is no difference between the mortality rate of CS complicating STEMI or CS complicating NSTEMI.[19]
- The left ventricular ejection fraction (LVEF) and the severity of mitral regurgitation (MR) are good echocardiographic predictors for the mortality rate of CS.[20]
- The only way to prevent CS and to improve the outcome, is by early reperfusion therapy of MI. Early revascularization therapy, particularly by PCI, has shown global improvement in echocardiographic indicators, such as the LVEF and MR grade and therefore in the outcome and prognosis of these patients.[20]
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.
- ↑ Hochman, Judith S; Buller, Christopher E; Sleeper, Lynn A; Boland, Jean; Dzavik, Vladimir; Sanborn, Timothy A; Godfrey, Emilie; White, Harvey D; Lim, John; LeJemtel, Thierry (2000). "Cardiogenic shock complicating acute myocardial infarction—etiologies, management and outcome: a report from the SHOCK Trial Registry". Journal of the American College of Cardiology. 36 (3): 1063–1070. doi:10.1016/S0735-1097(00)00879-2. ISSN 0735-1097.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hollenberg SM, Kavinsky CJ, Parrillo JE (1999). "Cardiogenic shock". Ann Intern Med. 131 (1): 47–59. PMID 10391815.
- ↑ Braat SH, de Zwaan C, Brugada P, Coenegracht JM, Wellens HJ (1984). "Right ventricular involvement with acute inferior wall myocardial infarction identifies high risk of developing atrioventricular nodal conduction disturbances". Am Heart J. 107 (6): 1183–7. PMID 6326559.
- ↑ 13.0 13.1 13.2 13.3 Ng, R.; Yeghiazarians, Y. (2011). "Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies". Journal of Intensive Care Medicine. 28 (3): 151–165. doi:10.1177/0885066611411407. ISSN 0885-0666.
- ↑ Antman, EM.; Hand, M.; Armstrong, PW.; Bates, ER.; Green, LA.; Halasyamani, LK.; Hochman, JS.; Krumholz, HM.; Lamas, GA. (2008). "2007 focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". J Am Coll Cardiol. 51 (2): 210–47. doi:10.1016/j.jacc.2007.10.001. PMID 18191746. Unknown parameter
|month=ignored (help) - ↑ Hasdai D, Califf RM, Thompson TD, et al. Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction. J Am Coll Cardiol. Jan 2000;35(1):136-43.
- ↑ Wong, SC.; Sanborn, T.; Sleeper, LA.; Webb, JG.; Pilchik, R.; Hart, D.; Mejnartowicz, S.; Antonelli, TA.; Lange, R. (2000). "Angiographic findings and clinical correlates in patients with cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?". J Am Coll Cardiol. 36 (3 Suppl A): 1077–83. PMID 10985708. Unknown parameter
|month=ignored (help) - ↑ Sanborn, TA.; Sleeper, LA.; Webb, JG.; French, JK.; Bergman, G.; Parikh, M.; Wong, SC.; Boland, J.; Pfisterer, M. (2003). "Correlates of one-year survival inpatients with cardiogenic shock complicating acute myocardial infarction: angiographic findings from the SHOCK trial". J Am Coll Cardiol. 42 (8): 1373–9. PMID 14563577. Unknown parameter
|month=ignored (help) - ↑ Menon V, Webb JG, Hillis LD, Sleeper LA, Abboud R, Dzavik V; et al. (2000). "Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK?". J Am Coll Cardiol. 36 (3 Suppl A): 1110–6. PMID 10985713.
- ↑ Holmes, DR.; Berger, PB.; Hochman, JS.; Granger, CB.; Thompson, TD.; Califf, RM.; Vahanian, A.; Bates, ER.; Topol, EJ. (1999). "Cardiogenic shock in patients with acute ischemic syndromes with and without ST-segment elevation". Circulation. 100 (20): 2067–73. PMID 10562262. Unknown parameter
|month=ignored (help) - ↑ 20.0 20.1 Picard, MH.; Davidoff, R.; Sleeper, LA.; Mendes, LA.; Thompson, CR.; Dzavik, V.; Steingart, R.; Gin, K.; White, HD. (2003). "Echocardiographic predictors of survival and response to early revascularization in cardiogenic shock". Circulation. 107 (2): 279–84. PMID 12538428. Unknown parameter
|month=ignored (help)