Cardiogenic shock natural history, complications and prognosis: Difference between revisions
Joao Silva (talk | contribs) |
Joao Silva (talk | contribs) |
||
| Line 9: | Line 9: | ||
==Natural History== | ==Natural History== | ||
As the name implies, cardiogenic shock (CS) consists of a [[shock]] of [[cardiac]] origin, with adequate [[intravascular]] volume (therefore ruling out [[hypovolemic]] cause), with [[hypoperfusion]] of [[myocardium]] and peripheral tissues. There are different possible causes for this condition, of which the [[left ventricular]] [[myocardial infarction]] is the most common. There is also the possibility of mechanical [[complications]], arising from the [[myocardial infarction]], leading to the [[pump failure]] that is underneath CS, such as [[mitral regurgitation]] and [[ventricular septal defect]].<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> The common basic mechanism underneath CS is the [[ischemia]]. Because of it, the [[myocardium]] fails to contract properly, thereby affecting [[cardiac output]]. This abnormality worsens the initial [[ischemia]], which then deteriorates even further the [[ventricular function]], creating the so called ''"downward spiral"''.<ref name="pmid10391815">{{cite journal| author=Hollenberg SM, Kavinsky CJ, Parrillo JE| title=Cardiogenic shock. | journal=Ann Intern Med | year= 1999 | volume= 131 | issue= 1 | pages= 47-59 | pmid=10391815 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10391815 }} </ref> When [[ischemia]] reaches a point that the [[left ventricular]] [[myocardium]] fails to pump properly, parameters like [[stroke volume]] and [[cardiac output]] will therefore decrease. The [[pressure]] gradient produced between the [[pressure]] within the [[coronary arteries]] and the [[left ventricle]], along with the duration of the [[diastole]], dictate [[myocardial]] [[perfusion]]. This will be compromised by the [[hypotension]] and the [[tachycardia]], worsening the [[myocardial]] [[ischemia]] and the [[perfusion]] of other vital organs. The fact that the [[heart]] is the only organ that benefits from a low [[blood pressure]], as [[afterload]] decreases, makes these [[hemodynamic|hemodynamical]] changes both beneficial and detrimental. The [[pump failure]] will then decrease the ability to push the [[blood]] out of the [[ventricle]], thereby increasing the [[ventricular]] [[diastolic pressure|diastolic pressures]]. This will not only reduce the [[coronary]] [[perfusion pressure]], as it will also increase the [[ventricle]] wall stress, so that the [[myocardial]] [[oxygen]] requirements will also raise, consequently propagating the [[ischemia]].<ref name="pmid10391815">{{cite journal| author=Hollenberg SM, Kavinsky CJ, Parrillo JE| title=Cardiogenic shock. | journal=Ann Intern Med | year= 1999 | volume= 131 | issue= 1 | pages= 47-59 | pmid=10391815 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10391815 }} </ref><ref name="ReynoldsHochman2008">{{cite journal|last1=Reynolds|first1=H. R.|last2=Hochman|first2=J. S.|title=Cardiogenic Shock: Current Concepts and Improving Outcomes|journal=Circulation|volume=117|issue=5|year=2008|pages=686–697|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.106.613596}}</ref><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> | |||
The [[hypoperfusion]] of the peripheral tissues leads to the release of [[catecholamines]], such as [[norepinephrine]], which will increase the [[heart]]'s [[contractility]] and peripheral [[blood flow]], by causing constriction of [[arterioles]], together with [[angiotensin II]], to maintain [[perfusion]]. However, this mechanism will also increase the [[heart]]'s [[oxygen]] demand and have proarrhythmic and [[cardiotoxic|myocardiotoxic]] consequences. The increased [[SVR]] coupled with the low [[cardiac output]] will lead to an even more pronounced reduction of tissue perfusion.<ref name="ReynoldsHochman2008">{{cite journal|last1=Reynolds|first1=H. R.|last2=Hochman|first2=J. S.|title=Cardiogenic Shock: Current Concepts and Improving Outcomes|journal=Circulation|volume=117|issue=5|year=2008|pages=686–697|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.106.613596}}</ref> | |||
The [[ischemia]] generated by all these processes increases the [[diastolic]] stiffness of the [[ventricle]] wall and this, along with the [[left ventricular dysfunction]], will increase the [[left atrial]] pressure. The increased [[left atrial]] pressure will propagate through the [[pulmonary veins]], generating [[pulmonary congestion]], which by decreasing [[oxygen]] exchanges, leads to [[hypoxia]]. The [[hypoxia]] will further worsen the [[ischemia]] of the [[myocardium]] and the [[pulmonary congestion]] will propagate its effect through the [[pulmonary arteries]] to the [[right ventricle]], hence jeopardizing its performance. Once [[myocardial]] function is affected, the body will put in motion compensatory mechanisms to try to increase the [[cardiac output]]. These include:<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> | |||
*[[Tachycardia]] and increased [[contractility]] through [[sympathetic]] stimulation | |||
*Activation of the [[RAAS|renin/angiotensin/aldosterone system]], leading to fluid retention and consequently increased [[preload]] | |||
However, these compensatory mechanisms eventually become maladaptive seeing that:<ref name="ReynoldsHochman2008">{{cite journal|last1=Reynolds|first1=H. R.|last2=Hochman|first2=J. S.|title=Cardiogenic Shock: Current Concepts and Improving Outcomes|journal=Circulation|volume=117|issue=5|year=2008|pages=686–697|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.106.613596}}</ref><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> | |||
*[[Tachycardia]] and increased [[contractility]] will increase [[myocardium|cardiac muscle]] [[oxygen]] demand, thereby exacerbating the initial [[ischemia]]; | |||
*[[Vasoconstriction]], as a response to impaired [[cardiac output]], in order to try to maintain [[coronary artery]] [[perfusion]] and systemic [[blood pressure]] ([[SVR]]) increases [[myocardial]] [[afterload]], leading to an impairment in [[myocardial]] performance and an increase in its [[oxygen]] demand, worsening [[ischemia]]; | |||
*The activation of the neurohormonal cascade will promote retention of [[water retention|water]] and [[sodium]], in order to compensate for the [[hypotension]] and improve [[perfusion]], yet this will also exacerbate [[pulmonary edema]]. | |||
The prolonged systemic [[hypoperfusion]] and [[hypoxia]] will cause a shift in [[cellular metabolism]], prioritizing [[glycolysis]], leading to a state of [[lactic acidosis]], which jeopardizes [[contractility]] and [[systolic]] performance, thereby affecting the previously described system. | |||
On the case of [[right ventricular infarction]], the underlying mechanism of disease is similar to the one described for [[left ventricular]] [[infarction]], with the particularity that it usually evolves to affect left ventricular function as well. | |||
All these factors affecting [[oxygen]] demand and [[cardiac]] performance create a vicious cycle that if not interrupted, may eventually lead to death.<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> | |||
==Complications== | ==Complications== | ||
Revision as of 01:28, 17 May 2014
|
Cardiogenic Shock Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Cardiogenic shock natural history, complications and prognosis On the Web |
|
American Roentgen Ray Society Images of Cardiogenic shock natural history, complications and prognosis |
|
FDA on Cardiogenic shock natural history, complications and prognosis |
|
CDC on Cardiogenic shock natural history, complications and prognosis |
|
Cardiogenic shock natural history, complications and prognosis in the news |
|
Blogs on Cardiogenic shock natural history, complications and prognosis |
|
Risk calculators and risk factors for Cardiogenic shock natural history, complications and prognosis |
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
As the name implies, cardiogenic shock (CS) consists of a shock of cardiac origin, with adequate intravascular volume (therefore ruling out hypovolemic cause), with hypoperfusion of myocardium and peripheral tissues. There are different possible causes for this condition, of which the left ventricular myocardial infarction is the most common. There is also the possibility of mechanical complications, arising from the myocardial infarction, leading to the pump failure that is underneath CS, such as mitral regurgitation and ventricular septal defect.[12] The common basic mechanism underneath CS is the ischemia. Because of it, the myocardium fails to contract properly, thereby affecting cardiac output. This abnormality worsens the initial ischemia, which then deteriorates even further the ventricular function, creating the so called "downward spiral".[11] When ischemia reaches a point that the left ventricular myocardium fails to pump properly, parameters like stroke volume and cardiac output will therefore decrease. The pressure gradient produced between the pressure within the coronary arteries and the left ventricle, along with the duration of the diastole, dictate myocardial perfusion. This will be compromised by the hypotension and the tachycardia, worsening the myocardial ischemia and the perfusion of other vital organs. The fact that the heart is the only organ that benefits from a low blood pressure, as afterload decreases, makes these hemodynamical changes both beneficial and detrimental. The pump failure will then decrease the ability to push the blood out of the ventricle, thereby increasing the ventricular diastolic pressures. This will not only reduce the coronary perfusion pressure, as it will also increase the ventricle wall stress, so that the myocardial oxygen requirements will also raise, consequently propagating the ischemia.[11][13][14] The hypoperfusion of the peripheral tissues leads to the release of catecholamines, such as norepinephrine, which will increase the heart's contractility and peripheral blood flow, by causing constriction of arterioles, together with angiotensin II, to maintain perfusion. However, this mechanism will also increase the heart's oxygen demand and have proarrhythmic and myocardiotoxic consequences. The increased SVR coupled with the low cardiac output will lead to an even more pronounced reduction of tissue perfusion.[13]
The ischemia generated by all these processes increases the diastolic stiffness of the ventricle wall and this, along with the left ventricular dysfunction, will increase the left atrial pressure. The increased left atrial pressure will propagate through the pulmonary veins, generating pulmonary congestion, which by decreasing oxygen exchanges, leads to hypoxia. The hypoxia will further worsen the ischemia of the myocardium and the pulmonary congestion will propagate its effect through the pulmonary arteries to the right ventricle, hence jeopardizing its performance. Once myocardial function is affected, the body will put in motion compensatory mechanisms to try to increase the cardiac output. These include:[15]
- Tachycardia and increased contractility through sympathetic stimulation
- Activation of the renin/angiotensin/aldosterone system, leading to fluid retention and consequently increased preload
However, these compensatory mechanisms eventually become maladaptive seeing that:[13][16]
- Tachycardia and increased contractility will increase cardiac muscle oxygen demand, thereby exacerbating the initial ischemia;
- Vasoconstriction, as a response to impaired cardiac output, in order to try to maintain coronary artery perfusion and systemic blood pressure (SVR) increases myocardial afterload, leading to an impairment in myocardial performance and an increase in its oxygen demand, worsening ischemia;
- The activation of the neurohormonal cascade will promote retention of water and sodium, in order to compensate for the hypotension and improve perfusion, yet this will also exacerbate pulmonary edema.
The prolonged systemic hypoperfusion and hypoxia will cause a shift in cellular metabolism, prioritizing glycolysis, leading to a state of lactic acidosis, which jeopardizes contractility and systolic performance, thereby affecting the previously described system. On the case of right ventricular infarction, the underlying mechanism of disease is similar to the one described for left ventricular infarction, with the particularity that it usually evolves to affect left ventricular function as well. All these factors affecting oxygen demand and cardiac performance create a vicious cycle that if not interrupted, may eventually lead to death.[17]
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[18]
- Ventricular septal rupture[19]
- Ventricular free wall rupture[19]
- Valvular abnormalities[19]
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.[20]
- 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:[21]
- 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.[22]
- 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.[23]
- Among the causes of CS following MI, ventricular septal rupture has one of the highest mortality rates post-MI, around 87.3%[24]
- 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[19]
- There is no difference between the mortality rate of CS complicating STEMI or CS complicating NSTEMI.[25]
- The left ventricular ejection fraction (LVEF) and the severity of mitral regurgitation (MR) are good echocardiographic predictors for the mortality rate of CS.[26]
- 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.[26]
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.
- ↑ 11.0 11.1 11.2 Hollenberg SM, Kavinsky CJ, Parrillo JE (1999). "Cardiogenic shock". Ann Intern Med. 131 (1): 47–59. PMID 10391815.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ 13.0 13.1 13.2 Reynolds, H. R.; Hochman, J. S. (2008). "Cardiogenic Shock: Current Concepts and Improving Outcomes". Circulation. 117 (5): 686–697. doi:10.1161/CIRCULATIONAHA.106.613596. ISSN 0009-7322.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ 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.
- ↑ 19.0 19.1 19.2 19.3 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) - ↑ 26.0 26.1 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)