Cardiogenic shock pathophysiology: Difference between revisions

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__NOTOC__
__NOTOC__
{{Cardiogenic shock}}
{{Cardiogenic shock}}
{{CMG}}; {{AE}} {{JS}} {{sali}}
{{CMG}}; {{AE}} [[User:Mohammad Salih|Mohammad Salih, MD.]] {{JS}} {{sali}}


==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> Despite the many possible causes for the [[heart failure|cardiac failure]], the most common is [[left ventricular failure]] in the setting of [[myocardial infarction]].<ref name="HochmanBuller2000">{{cite journal|last1=Hochman|first1=Judith S|last2=Buller|first2=Christopher E|last3=Sleeper|first3=Lynn A|last4=Boland|first4=Jean|last5=Dzavik|first5=Vladimir|last6=Sanborn|first6=Timothy A|last7=Godfrey|first7=Emilie|last8=White|first8=Harvey D|last9=Lim|first9=John|last10=LeJemtel|first10=Thierry|title=Cardiogenic shock complicating acute myocardial infarction—etiologies, management and outcome: a report from the SHOCK Trial Registry|journal=Journal of the American College of Cardiology|volume=36|issue=3|year=2000|pages=1063–1070|issn=07351097|doi=10.1016/S0735-1097(00)00879-2}}</ref>
The pathophysiology of [[cardiogenic]] [[shock]] is complex and not fully understood. Ischemia to the [[myocardium]] causes derangement to both [[systolic]] and [[diastolic]] left ventricular function, resulting in a profound [[depression]] of [[myocardial contractility]]. This, in turn, leads to a potentially [[catastrophic]] and [[vicious]] spiral of reduced [[cardiac output]] and low [[blood pressure]], perpetuating further [[coronary ischemia]] and impairment of [[contractility]]. Several [[physiologic]] compensatory processes ensue. These include:The activation of the sympathetic system leading to peripheral [[vasoconstriction]] which may improve [[coronary]] perfusion at the cost of increased [[afterload]], and
In the presence of cardiogenic shock 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 [[RAAS|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 [[MI|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.<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><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>
[[Tachycardia]] which increases [[myocardial]] oxygen demand and subsequently worsens [[myocardial]] ischemia.These compensatory mechanisms are subsequently counteracted by [[pathologic]] [[vasodilation]] that occurs from the release of potent systemic [[inflammatory]] markers such as [[interleukin-1]], [[tumor necrosis factor]] a, and [[interleukin-6]]. Additionally, higher levels of [[nitric oxide]] and [[peroxynitrite]] are released, which also contribute to [[pathologic]] [[vasodilation]] and are known to be [[cardiotoxic]]. Unless interrupted by adequate treatment measures, this self-perpetuating cycle leads to global [[hypoperfusion]] and the inability to effectively meet the [[metabolic]] demands of the tissues, progressing to [[multiorgan]] failure and eventually [[death]].


==Pathophysiology==
==Pathophysiology==
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==The downward "Spiral" of Cardiogenic shock==
==The downward "Spiral" of Cardiogenic shock==


*Cardiac dysfunction in patients with cardiogenic shock is usually initiated by myocardial infarction or ischemia.  
*[[Cardiac dysfunction]] in patients with [[cardiogenic shock]] is usually initiated by [[myocardial infarction]] or [[ischemia]].  
*The myocardial dysfunction resulting from ischemia worsens that ischemia, creating a downward spiral.  
*The [[myocardial dysfunction]] resulting from [[ischemia]] worsens that ischemia, creating a downward spiral.  
*When a critical mass of left ventricular myocardium is ischemic or necrotic and fails to pump, stroke volume and cardiac output decrease.
*When a critical mass of [[left ventricular]] [[myocardium]] is [[ischemic]] or [[necrotic]] and fails to pump, [[stroke volume]] and [[cardiac output]] decrease.
*Myocardial perfusion, which depends on the pressure gradient between the coronary arterial system and the left ventricle.
*Myocardial perfusion, which depends on the pressure gradient between the [[coronary]] arterial system and the [[left ventricle]].
*The duration of diastole, is compromised by hypotension and tachycardia. Which in turn, exacerbates ischemia.  
*The duration of diastole, is compromised by hypotension and tachycardia. Which in turn, exacerbates ischemia.  
*The increased ventricular diastolic pressures caused by pump failure further reduce coronary perfusion pressure, and the additional wall stress elevates myocardial oxygen requirements, further worsening ischemia.  
*The increased [[ventricular diastolic pressures]] caused by pump failure further reduce [[coronary perfusion pressure]], and the additional wall stress elevates myocardial oxygen requirements, further worsening ischemia.  
*Decreased cardiac output also compromises systemic perfusion, which can lead to lactic acidosis and further compromise of systolic performance.
*Decreased cardiac output also compromises systemic perfusion, which can lead to lactic acidosis and further compromise of systolic performance.
*The pathologic process begins with [[myocardial]] [[ischemia]] leading to an abnormal function of the [[cardiac muscle]].  
*The pathologic process begins with [[myocardial]] [[ischemia]] leading to an abnormal function of the [[cardiac muscle]].  
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==Ventricular Septal and Free Wall Rupture==
==Ventricular Septal and Free Wall Rupture==
*[[Ventricular septal rupture]] and [[free wall rupture]], which constitute two entities of [[cardiac rupture]], represent the second most common cause of death in patients with acute [[myocardial infarction]], during hospital stay.<ref name="pmid19064683">{{cite journal| author=Figueras J, Alcalde O, Barrabés JA, Serra V, Alguersuari J, Cortadellas J et al.| title=Changes in hospital mortality rates in 425 patients with acute ST-elevation myocardial infarction and cardiac rupture over a 30-year period. | journal=Circulation | year= 2008 | volume= 118 | issue= 25 | pages= 2783-9 | pmid=19064683 | doi=10.1161/CIRCULATIONAHA.108.776690 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19064683  }} </ref><ref name="pmid8626938">{{cite journal| author=Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ et al.| title=A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. | journal=J Am Coll Cardiol | year= 1996 | volume= 27 | issue= 6 | pages= 1321-6 | pmid=8626938 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8626938  }} </ref><ref name="pmid9973029">{{cite journal| author=Becker RC, Hochman JS, Cannon CP, Spencer FA, Ball SP, Rizzo MJ et al.| title=Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9 Study. | journal=J Am Coll Cardiol | year= 1999 | volume= 33 | issue= 2 | pages= 479-87 | pmid=9973029 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9973029  }} </ref>
*[[Ventricular septal rupture]] and [[free wall rupture]], which constitute two entities of [[cardiac rupture]], represent the second most common cause of death in patients with acute [[myocardial infarction]], during hospital stay.<ref name="pmid19064683">{{cite journal| author=Figueras J, Alcalde O, Barrabés JA, Serra V, Alguersuari J, Cortadellas J et al.| title=Changes in hospital mortality rates in 425 patients with acute ST-elevation myocardial infarction and cardiac rupture over a 30-year period. | journal=Circulation | year= 2008 | volume= 118 | issue= 25 | pages= 2783-9 | pmid=19064683 | doi=10.1161/CIRCULATIONAHA.108.776690 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19064683  }} </ref><ref name="pmid8626938">{{cite journal| author=Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ et al.| title=A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. | journal=J Am Coll Cardiol | year= 1996 | volume= 27 | issue= 6 | pages= 1321-6 | pmid=8626938 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8626938  }} </ref><ref name="pmid9973029">{{cite journal| author=Becker RC, Hochman JS, Cannon CP, Spencer FA, Ball SP, Rizzo MJ et al.| title=Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9 Study. | journal=J Am Coll Cardiol | year= 1999 | volume= 33 | issue= 2 | pages= 479-87 | pmid=9973029 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9973029  }} </ref>
*Ventricular septal rupture in the SHOCK registry, it accounted for 4.6% of the cases of cardiogenic shock.<ref name="pmid10985706">{{cite journal| author=Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA et al.| title=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? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1063-70 | pmid=10985706 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985706  }} </ref>
*The most recent registries show that [[ventricular septal rupture]] generally develops within the first 16 to 24 hours post-[[MI]] and has the following characteristics:<ref name="pmid10985712">{{cite journal| author=Thompson CR, Buller CE, Sleeper LA, Antonelli TA, Webb JG, Jaber WA et al.| title=Cardiogenic shock due to acute severe mitral regurgitation complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we use emergently revascularize Occluded Coronaries in cardiogenic shocK? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1104-9 | pmid=10985712 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985712  }} </ref><ref name="pmid10618300">{{cite journal| author=Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS et al.| title=Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. | journal=Circulation | year= 2000 | volume= 101 | issue= 1 | pages= 27-32 | pmid=10618300 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10618300  }} </ref><ref name="pmid7020978">{{cite journal| author=Radford MJ, Johnson RA, Daggett WM, Fallon JT, Buckley MJ, Gold HK et al.| title=Ventricular septal rupture: a review of clinical and physiologic features and an analysis of survival. | journal=Circulation | year= 1981 | volume= 64 | issue= 3 | pages= 545-53 | pmid=7020978 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7020978  }} </ref><ref name="pmid2803872">{{cite journal| author=Skehan JD, Carey C, Norrell MS, de Belder M, Balcon R, Mills PG| title=Patterns of coronary artery disease in post-infarction ventricular septal rupture. | journal=Br Heart J | year= 1989 | volume= 62 | issue= 4 | pages= 268-72 | pmid=2803872 | doi= | pmc=PMC1277362 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2803872  }} </ref><ref name="pmid13836145">{{cite journal| author=SWITHINBANK JM| title=Perforation of the interventricular septum in myocardial infarction. | journal=Br Heart J | year= 1959 | volume= 21 | issue=  | pages= 562-6 | pmid=13836145 | doi= | pmc=PMC1017615 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13836145  }} </ref><ref name="NgYeghiazarians2011">{{cite journal|last1=Ng|first1=R.|last2=Yeghiazarians|first2=Y.|title=Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies|journal=Journal of Intensive Care Medicine|volume=28|issue=3|year=2011|pages=151–165|issn=0885-0666|doi=10.1177/0885066611411407}}</ref><ref>{{cite book | last = Cohn | first = Lawrence | title = Cardiac surgery in the adult | publisher = McGraw-Hill Medical | location = New York | year = 2012 | isbn = 978-0-07-163310-9 }}</ref><ref name="NgYeghiazarians2011">{{cite journal|last1=Ng|first1=R.|last2=Yeghiazarians|first2=Y.|title=Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies|journal=Journal of Intensive Care Medicine|volume=28|issue=3|year=2011|pages=151–165|issn=0885-0666|doi=10.1177/0885066611411407}}</ref><ref name="pmid8354804">{{cite journal| author=Oliva PB, Hammill SC, Edwards WD| title=Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. | journal=J Am Coll Cardiol | year= 1993 | volume= 22 | issue= 3 | pages= 720-6 | pmid=8354804 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8354804  }} </ref><ref name="pmid10985714">{{cite journal| author=Slater J, Brown RJ, Antonelli TA, Menon V, Boland J, Col J et al.| title=Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1117-22 | pmid=10985714 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985714  }} </ref>
*According to the SHOCK trial data, this type of rupture had 55% of [[mortality rate]] within the first 30 days.<ref name="pmid10985714">{{cite journal| author=Slater J, Brown RJ, Antonelli TA, Menon V, Boland J, Col J et al.| title=Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1117-22 | pmid=10985714 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985714  }} </ref> [[Free wall rupture]] may also be classified as ''simple'' or ''complex''. It may occur either on the anterior or the lateral and posterior [[left ventricular]] walls.<ref name="pmid10985714">{{cite journal| author=Slater J, Brown RJ, Antonelli TA, Menon V, Boland J, Col J et al.| title=Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1117-22 | pmid=10985714 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985714  }} </ref><ref name="pmid19064683">{{cite journal| author=Figueras J, Alcalde O, Barrabés JA, Serra V, Alguersuari J, Cortadellas J et al.| title=Changes in hospital mortality rates in 425 patients with acute ST-elevation myocardial infarction and cardiac rupture over a 30-year period. | journal=Circulation | year= 2008 | volume= 118 | issue= 25 | pages= 2783-9 | pmid=19064683 | doi=10.1161/CIRCULATIONAHA.108.776690 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19064683  }} </ref> These last two are thought to [[rupture]] easier, however, because of the higher proportion of anterior [[MI]]s, they are seen less frequently.<ref name="NgYeghiazarians2011">{{cite journal|last1=Ng|first1=R.|last2=Yeghiazarians|first2=Y.|title=Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies|journal=Journal of Intensive Care Medicine|volume=28|issue=3|year=2011|pages=151–165|issn=0885-0666|doi=10.1177/0885066611411407}}</ref>
*The [[rupture]] may present with different types of courses:
**''Acute'' - the patient generally feels acute onset of [[chest pain]], developing [[cardiac tamponade]], [[hemodynamic|hemodynamical]] collapse and [[sudden death]]. Because of the rapid course of this type, it is usually not controlled with current therapies.<ref name="pmid10768896">{{cite journal| author=Figueras J, Cortadellas J, Soler-Soler J| title=Left ventricular free wall rupture: clinical presentation and management. | journal=Heart | year= 2000 | volume= 83 | issue= 5 | pages= 499-504 | pmid=10768896 | doi= | pmc=PMC1760810 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10768896  }} </ref><ref>{{cite book | last = Cohn | first = Lawrence | title = Cardiac surgery in the adult | publisher = McGraw-Hill Medical | location = New York | year = 2012 | isbn = 007163312X }}</ref>
**''Subacute'' - this type generally results in smaller and contained [[rupture|ruptures]]. These may be stabilized by the formation of a [[clot]] or [[fibrinous]] [[pericardial]] [[adhesions]] for a short period of time. Therapeutical measures must be applied urgently.<ref>{{cite book | last = Cohn | first = Lawrence | title = Cardiac surgery in the adult | publisher = McGraw-Hill Medical | location = New York | year = 2012 | isbn = 007163312X }}</ref><ref name="pmid2803872">{{cite journal| author=Skehan JD, Carey C, Norrell MS, de Belder M, Balcon R, Mills PG| title=Patterns of coronary artery disease in post-infarction ventricular septal rupture. | journal=Br Heart J | year= 1989 | volume= 62 | issue= 4 | pages= 268-72 | pmid=2803872 | doi= | pmc=PMC1277362 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2803872  }} </ref>
**''Chronic'' - less frequently associated with cardiogenic shock.


In the case of '''''ventricular septal rupture''''', in the SHOCK registry, it accounted for 4.6% of the cases of cardiogenic shock.<ref name="pmid10985706">{{cite journal| author=Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA et al.| title=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? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1063-70 | pmid=10985706 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985706  }} </ref> The most recent registries show that [[ventricular septal rupture]] generally develops within the first 16 to 24 hours post-[[MI]] and has the following characteristics:<ref name="pmid10985712">{{cite journal| author=Thompson CR, Buller CE, Sleeper LA, Antonelli TA, Webb JG, Jaber WA et al.| title=Cardiogenic shock due to acute severe mitral regurgitation complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we use emergently revascularize Occluded Coronaries in cardiogenic shocK? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1104-9 | pmid=10985712 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985712  }} </ref><ref name="pmid10618300">{{cite journal| author=Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS et al.| title=Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. | journal=Circulation | year= 2000 | volume= 101 | issue= 1 | pages= 27-32 | pmid=10618300 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10618300  }} </ref>
==Inflammation and Hemodynamics==
:*most common in the setting of transmural [[myocardial infarction]], generally associated with [[Anterior myocardial infarction|anterior]] or anterolateral [[infarction]], with about 60% of cases being related to [[left anterior descending coronary artery]] [[occlusion]];<ref name="pmid7020978">{{cite journal| author=Radford MJ, Johnson RA, Daggett WM, Fallon JT, Buckley MJ, Gold HK et al.| title=Ventricular septal rupture: a review of clinical and physiologic features and an analysis of survival. | journal=Circulation | year= 1981 | volume= 64 | issue= 3 | pages= 545-53 | pmid=7020978 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7020978  }} </ref><ref name="pmid2803872">{{cite journal| author=Skehan JD, Carey C, Norrell MS, de Belder M, Balcon R, Mills PG| title=Patterns of coronary artery disease in post-infarction ventricular septal rupture. | journal=Br Heart J | year= 1989 | volume= 62 | issue= 4 | pages= 268-72 | pmid=2803872 | doi= | pmc=PMC1277362 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2803872  }} </ref>
*Studies like the ''SHOCK trial'' show that not all patients follow this classic paradigm, since:<ref name="pmid10460813">{{cite journal| author=Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD et al.| title=Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. | journal=N Engl J Med | year= 1999 | volume= 341 | issue= 9 | pages= 625-34 | pmid=10460813 | doi=10.1056/NEJM199908263410901 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10460813  }} </ref><ref name="pmid12538428">{{cite journal| author=Picard MH, Davidoff R, Sleeper LA, Mendes LA, Thompson CR, Dzavik V et al.| title=Echocardiographic predictors of survival and response to early revascularization in cardiogenic shock. | journal=Circulation | year= 2003 | volume= 107 | issue= 2 | pages= 279-84 | pmid=12538428 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12538428  }} </ref><ref name="pmid16043684">{{cite journal| author=Kohsaka S, Menon V, Lowe AM, Lange M, Dzavik V, Sleeper LA et al.| title=Systemic inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock. | journal=Arch Intern Med | year= 2005 | volume= 165 | issue= 14 | pages= 1643-50 | pmid=16043684 | doi=10.1001/archinte.165.14.1643 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16043684  }} </ref>
:*20 to 40% of cases are associated with inferior [[ventricular septal rupture]] and are related to [[coronary artery dominance|dominant right coronary artery]], or less frequently, [[coronary artery dominance|dominant left circumflex coronary artery]] [[occlusion]];<ref name="pmid13836145">{{cite journal| author=SWITHINBANK JM| title=Perforation of the interventricular septum in myocardial infarction. | journal=Br Heart J | year= 1959 | volume= 21 | issue=  | pages= 562-6 | pmid=13836145 | doi= | pmc=PMC1017615 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13836145  }} </ref>
:*can be classified as:<ref name="NgYeghiazarians2011">{{cite journal|last1=Ng|first1=R.|last2=Yeghiazarians|first2=Y.|title=Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies|journal=Journal of Intensive Care Medicine|volume=28|issue=3|year=2011|pages=151–165|issn=0885-0666|doi=10.1177/0885066611411407}}</ref><ref>{{cite book | last = Cohn | first = Lawrence | title = Cardiac surgery in the adult | publisher = McGraw-Hill Medical | location = New York | year = 2012 | isbn = 978-0-07-163310-9 }}</ref>
::*''simple'' - "direct through-and-through any defect", generally an anterior defect;
::*''complex'' - a serpigenous [[dissection]] tract radiating from the primary [[ventricular septal rupture]] site, generally an inferior defect.
The [[rupture]] of the [[ventricular septum]] leads to the formation of a "[[left-to-right shunt]]", which precipitates [[hemodynamic]] decompensation and [[congestive heart failure]].<ref name="NgYeghiazarians2011">{{cite journal|last1=Ng|first1=R.|last2=Yeghiazarians|first2=Y.|title=Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies|journal=Journal of Intensive Care Medicine|volume=28|issue=3|year=2011|pages=151–165|issn=0885-0666|doi=10.1177/0885066611411407}}</ref>
 
In the case of '''''free wall rupture''''', some studies show that half of the cases occur in the first 5 days after [[myocardial infarction]], with about 90% happening within the first 2 weeks.<ref name="pmid8354804">{{cite journal| author=Oliva PB, Hammill SC, Edwards WD| title=Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. | journal=J Am Coll Cardiol | year= 1993 | volume= 22 | issue= 3 | pages= 720-6 | pmid=8354804 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8354804  }} </ref><ref name="pmid10985714">{{cite journal| author=Slater J, Brown RJ, Antonelli TA, Menon V, Boland J, Col J et al.| title=Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1117-22 | pmid=10985714 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985714  }} </ref> According to the SHOCK trial data, this type of rupture had 55% of [[mortality rate]] within the first 30 days.<ref name="pmid10985714">{{cite journal| author=Slater J, Brown RJ, Antonelli TA, Menon V, Boland J, Col J et al.| title=Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1117-22 | pmid=10985714 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985714  }} </ref> [[Free wall rupture]] may also be classified as ''simple'' or ''complex''. It may occur either on the anterior or the lateral and posterior [[left ventricular]] walls.<ref name="pmid10985714">{{cite journal| author=Slater J, Brown RJ, Antonelli TA, Menon V, Boland J, Col J et al.| title=Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 3 Suppl A | pages= 1117-22 | pmid=10985714 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10985714  }} </ref><ref name="pmid19064683">{{cite journal| author=Figueras J, Alcalde O, Barrabés JA, Serra V, Alguersuari J, Cortadellas J et al.| title=Changes in hospital mortality rates in 425 patients with acute ST-elevation myocardial infarction and cardiac rupture over a 30-year period. | journal=Circulation | year= 2008 | volume= 118 | issue= 25 | pages= 2783-9 | pmid=19064683 | doi=10.1161/CIRCULATIONAHA.108.776690 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19064683  }} </ref> These last two are thought to [[rupture]] easier, however, because of the higher proportion of anterior [[MI]]s, they are seen less frequently.<ref name="NgYeghiazarians2011">{{cite journal|last1=Ng|first1=R.|last2=Yeghiazarians|first2=Y.|title=Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies|journal=Journal of Intensive Care Medicine|volume=28|issue=3|year=2011|pages=151–165|issn=0885-0666|doi=10.1177/0885066611411407}}</ref> The [[rupture]] may present with different types of courses:
*''Acute'' - the patient generally feels acute onset of [[chest pain]], developing [[cardiac tamponade]], [[hemodynamic|hemodynamical]] collapse and [[sudden death]]. Because of the rapid course of this type, it is usually not controlled with current therapies.<ref name="pmid10768896">{{cite journal| author=Figueras J, Cortadellas J, Soler-Soler J| title=Left ventricular free wall rupture: clinical presentation and management. | journal=Heart | year= 2000 | volume= 83 | issue= 5 | pages= 499-504 | pmid=10768896 | doi= | pmc=PMC1760810 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10768896  }} </ref><ref>{{cite book | last = Cohn | first = Lawrence | title = Cardiac surgery in the adult | publisher = McGraw-Hill Medical | location = New York | year = 2012 | isbn = 007163312X }}</ref>
*''Subacute'' - this type generally results in smaller and contained [[rupture|ruptures]]. These may be stabilized by the formation of a [[clot]] or [[fibrinous]] [[pericardial]] [[adhesions]] for a short period of time. Therapeutical measures must be applied urgently.<ref>{{cite book | last = Cohn | first = Lawrence | title = Cardiac surgery in the adult | publisher = McGraw-Hill Medical | location = New York | year = 2012 | isbn = 007163312X }}</ref><ref name="pmid2803872">{{cite journal| author=Skehan JD, Carey C, Norrell MS, de Belder M, Balcon R, Mills PG| title=Patterns of coronary artery disease in post-infarction ventricular septal rupture. | journal=Br Heart J | year= 1989 | volume= 62 | issue= 4 | pages= 268-72 | pmid=2803872 | doi= | pmc=PMC1277362 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2803872  }} </ref>
*''Chronic'' - less frequently associated with cardiogenic shock.
 
===Inflammation and Hemodynamics===
Studies like the ''SHOCK trial'' show that not all patients follow this classic paradigm, since:<ref name="pmid10460813">{{cite journal| author=Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD et al.| title=Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. | journal=N Engl J Med | year= 1999 | volume= 341 | issue= 9 | pages= 625-34 | pmid=10460813 | doi=10.1056/NEJM199908263410901 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10460813  }} </ref><ref name="pmid12538428">{{cite journal| author=Picard MH, Davidoff R, Sleeper LA, Mendes LA, Thompson CR, Dzavik V et al.| title=Echocardiographic predictors of survival and response to early revascularization in cardiogenic shock. | journal=Circulation | year= 2003 | volume= 107 | issue= 2 | pages= 279-84 | pmid=12538428 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12538428  }} </ref><ref name="pmid16043684">{{cite journal| author=Kohsaka S, Menon V, Lowe AM, Lange M, Dzavik V, Sleeper LA et al.| title=Systemic inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock. | journal=Arch Intern Med | year= 2005 | volume= 165 | issue= 14 | pages= 1643-50 | pmid=16043684 | doi=10.1001/archinte.165.14.1643 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16043684  }} </ref>
*The range of elevation of [[systemic vascular resistance]] in this trial was wide, suggesting that the compensatory [[vasoconstriction]] wasn't a rule in every patient;
*The range of elevation of [[systemic vascular resistance]] in this trial was wide, suggesting that the compensatory [[vasoconstriction]] wasn't a rule in every patient;
*The mean [[ejection fraction]] was also moderately decreased in this trial, showing that other mechanisms besides [[cardiac failure]] were present;
*The mean [[ejection fraction]] was also moderately decreased in this trial, showing that other mechanisms besides [[cardiac failure]] were present;
*Some of the patients had [[leukocytosis]] and [[fever]], which along with the decreased [[systemic vascular resistance]] suggested [[SIRS]].
*Some of the patients had [[leukocytosis]] and [[fever]], which along with the decreased [[systemic vascular resistance]] suggested [[SIRS]].
These facts have introduced the concept that [[myocardial infarction]] may cause [[SIRS]] and that [[inflammation]] plays an important part in the development and persistence of cardiogenic shock, contributing to [[myocardial]] dysfunction and [[vasodilation]]. The possibility of developing [[SIRS]] raises with the increasing permanence in cardiogenic shock.<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 name="Hochman2003">{{cite journal|last1=Hochman|first1=J. S.|title=Cardiogenic Shock Complicating Acute Myocardial Infarction: Expanding the Paradigm|journal=Circulation|volume=107|issue=24|year=2003|pages=2998–3002|issn=0009-7322|doi=10.1161/01.CIR.0000075927.67673.F2}}</ref><ref name="pmid10636626">{{cite journal| author=Brunkhorst FM, Clark AL, Forycki ZF, Anker SD| title=Pyrexia, procalcitonin, immune activation and survival in cardiogenic shock: the potential importance of bacterial translocation. | journal=Int J Cardiol | year= 1999 | volume= 72 | issue= 1 | pages= 3-10 | pmid=10636626 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10636626  }} </ref>
*These facts have introduced the concept that [[myocardial infarction]] may cause [[SIRS]] and that [[inflammation]] plays an important part in the development and persistence of cardiogenic shock, contributing to [[myocardial]] dysfunction and [[vasodilation]].  
 
*The possibility of developing [[SIRS]] raises with the increasing permanence in cardiogenic shock.<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 name="Hochman2003">{{cite journal|last1=Hochman|first1=J. S.|title=Cardiogenic Shock Complicating Acute Myocardial Infarction: Expanding the Paradigm|journal=Circulation|volume=107|issue=24|year=2003|pages=2998–3002|issn=0009-7322|doi=10.1161/01.CIR.0000075927.67673.F2}}</ref><ref name="pmid10636626">{{cite journal| author=Brunkhorst FM, Clark AL, Forycki ZF, Anker SD| title=Pyrexia, procalcitonin, immune activation and survival in cardiogenic shock: the potential importance of bacterial translocation. | journal=Int J Cardiol | year= 1999 | volume= 72 | issue= 1 | pages= 3-10 | pmid=10636626 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10636626  }} </ref>
At the time of the [[cardiac]] injury, the [[myocardium]] releases into [[circulation]] [[cytokines]], particularly during the first 24 to 72 hours after the [[MI]], these will induce the [[enzyme]] [[nitric oxide synthase]], thereby increasing the level of [[nitric oxide]], which will be responsible for [[vasodilation]] and worsening of [[hypotension]], further jeopardizing [[left ventricle]] performance.<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><ref name="NeumannOtt1995">{{cite journal|last1=Neumann|first1=F.-J.|last2=Ott|first2=I.|last3=Gawaz|first3=M.|last4=Richardt|first4=G.|last5=Holzapfel|first5=H.|last6=Jochum|first6=M.|last7=Schomig|first7=A.|title=Cardiac Release of Cytokines and Inflammatory Responses in Acute Myocardial Infarction|journal=Circulation|volume=92|issue=4|year=1995|pages=748–755|issn=0009-7322|doi=10.1161/01.CIR.92.4.748}}</ref><ref name="Shah2000">{{cite journal|last1=Shah|first1=A|title=Inducible nitric oxide synthase and cardiovascular disease|journal=Cardiovascular Research|volume=45|issue=1|year=2000|pages=148–155|issn=00086363|doi=10.1016/S0008-6363(99)00316-8}}</ref><ref name="pmid11489778">{{cite journal| author=Feng Q, Lu X, Jones DL, Shen J, Arnold JM| title=Increased inducible nitric oxide synthase expression contributes to myocardial dysfunction and higher mortality after myocardial infarction in mice. | journal=Circulation | year= 2001 | volume= 104 | issue= 6 | pages= 700-4 | pmid=11489778 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11489778  }} </ref><ref name="pmid10736276">{{cite journal| author=Cotter G, Kaluski E, Blatt A, Milovanov O, Moshkovitz Y, Zaidenstein R et al.| title=L-NMMA (a nitric oxide synthase inhibitor) is effective in the treatment of cardiogenic shock. | journal=Circulation | year= 2000 | volume= 101 | issue= 12 | pages= 1358-61 | pmid=10736276 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10736276  }} </ref><ref name="pmid17133844">{{cite journal| author=Kaluski E, Hendler A, Blatt A, Uriel N| title=Nitric oxide synthase inhibitors in post-myocardial infarction cardiogenic shock--an update. | journal=Clin Cardiol | year= 2006 | volume= 29 | issue= 11 | pages= 482-8 | pmid=17133844 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17133844  }} </ref> [[NO]] may also form a toxic radical, called [[peroxynitrite]], when combined with [[superoxide]], affecting [[myocardial]] [[contractility]].<ref name="pmid10926876">{{cite journal| author=Ferdinandy P, Danial H, Ambrus I, Rothery RA, Schulz R| title=Peroxynitrite is a major contributor to cytokine-induced myocardial contractile failure. | journal=Circ Res | year= 2000 | volume= 87 | issue= 3 | pages= 241-7 | pmid=10926876 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10926876  }} </ref> Among these released [[cytokines]] during cardiogenic shock, are [[interleukin-6]] and [[tumor necrosis factor]]. In the case of [[IL-6]], this specific [[cytokine]] is correlated with the degree of [[organ failure]] and therefore [[mortality]].<ref name="pmid16775569">{{cite journal| author=Geppert A, Dorninger A, Delle-Karth G, Zorn G, Heinz G, Huber K| title=Plasma concentrations of interleukin-6, organ failure, vasopressor support, and successful coronary revascularization in predicting 30-day mortality of patients with cardiogenic shock complicating acute myocardial infarction. | journal=Crit Care Med | year= 2006 | volume= 34 | issue= 8 | pages= 2035-42 | pmid=16775569 | doi=10.1097/01.CCM.0000228919.33620.D9 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16775569  }} </ref> These [[inflammatory]] mediators, among other actions, are responsible for the release of [[BNP]], which makes the levels of [[BNP]] good markers, not only for the level of [[inflammation]], but also to evaluate [[hemodynamic]] decompensation.<ref name="pmid16763507">{{cite journal| author=Rudiger A, Gasser S, Fischler M, Hornemann T, von Eckardstein A, Maggiorini M| title=Comparable increase of B-type natriuretic peptide and amino-terminal pro-B-type natriuretic peptide levels in patients with severe sepsis, septic shock, and acute heart failure. | journal=Crit Care Med | year= 2006 | volume= 34 | issue= 8 | pages= 2140-4 | pmid=16763507 | doi=10.1097/01.CCM.0000229144.97624.90 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16763507  }} </ref>
*At the time of the [[cardiac]] injury, the [[myocardium]] releases into [[circulation]] [[cytokines]], particularly during the first 24 to 72 hours after the [[MI]]. *These will induce the [[enzyme]] [[nitric oxide synthase]], thereby increasing the level of [[nitric oxide]], which will be responsible for [[vasodilation]] and worsening of [[hypotension]], further jeopardizing [[left ventricle]] performance.<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><ref name="NeumannOtt1995">{{cite journal|last1=Neumann|first1=F.-J.|last2=Ott|first2=I.|last3=Gawaz|first3=M.|last4=Richardt|first4=G.|last5=Holzapfel|first5=H.|last6=Jochum|first6=M.|last7=Schomig|first7=A.|title=Cardiac Release of Cytokines and Inflammatory Responses in Acute Myocardial Infarction|journal=Circulation|volume=92|issue=4|year=1995|pages=748–755|issn=0009-7322|doi=10.1161/01.CIR.92.4.748}}</ref><ref name="Shah2000">{{cite journal|last1=Shah|first1=A|title=Inducible nitric oxide synthase and cardiovascular disease|journal=Cardiovascular Research|volume=45|issue=1|year=2000|pages=148–155|issn=00086363|doi=10.1016/S0008-6363(99)00316-8}}</ref><ref name="pmid11489778">{{cite journal| author=Feng Q, Lu X, Jones DL, Shen J, Arnold JM| title=Increased inducible nitric oxide synthase expression contributes to myocardial dysfunction and higher mortality after myocardial infarction in mice. | journal=Circulation | year= 2001 | volume= 104 | issue= 6 | pages= 700-4 | pmid=11489778 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11489778  }} </ref><ref name="pmid10736276">{{cite journal| author=Cotter G, Kaluski E, Blatt A, Milovanov O, Moshkovitz Y, Zaidenstein R et al.| title=L-NMMA (a nitric oxide synthase inhibitor) is effective in the treatment of cardiogenic shock. | journal=Circulation | year= 2000 | volume= 101 | issue= 12 | pages= 1358-61 | pmid=10736276 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10736276  }} </ref><ref name="pmid17133844">{{cite journal| author=Kaluski E, Hendler A, Blatt A, Uriel N| title=Nitric oxide synthase inhibitors in post-myocardial infarction cardiogenic shock--an update. | journal=Clin Cardiol | year= 2006 | volume= 29 | issue= 11 | pages= 482-8 | pmid=17133844 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17133844  }} </ref> [[NO]] may also form a toxic radical, called [[peroxynitrite]], when combined with [[superoxide]], affecting [[myocardial]] [[contractility]].<ref name="pmid10926876">{{cite journal| author=Ferdinandy P, Danial H, Ambrus I, Rothery RA, Schulz R| title=Peroxynitrite is a major contributor to cytokine-induced myocardial contractile failure. | journal=Circ Res | year= 2000 | volume= 87 | issue= 3 | pages= 241-7 | pmid=10926876 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10926876  }} </ref>  
Other [[circulatory]] factors, such as [[procalcitonin]], [[complement]] and [[CRP]], have been reported in some studies to contribute to the development of [[SIRS]] in cardiogenic shock.<ref name="pmid12925454">{{cite journal| author=Granger CB, Mahaffey KW, Weaver WD, Theroux P, Hochman JS, Filloon TG et al.| title=Pexelizumab, an anti-C5 complement antibody, as adjunctive therapy to primary percutaneous coronary intervention in acute myocardial infarction: the COMplement inhibition in Myocardial infarction treated with Angioplasty (COMMA) trial. | journal=Circulation | year= 2003 | volume= 108 | issue= 10 | pages= 1184-90 | pmid=12925454 | doi=10.1161/01.CIR.0000087447.12918.85 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12925454  }} </ref><ref name="pmid17200474">{{cite journal| author=APEX AMI Investigators. Armstrong PW, Granger CB, Adams PX, Hamm C, Holmes D et al.| title=Pexelizumab for acute ST-elevation myocardial infarction in patients undergoing primary percutaneous coronary intervention: a randomized controlled trial. | journal=JAMA | year= 2007 | volume= 297 | issue= 1 | pages= 43-51 | pmid=17200474 | doi=10.1001/jama.297.1.43 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17200474  }} </ref>
*Among these released [[cytokines]] during cardiogenic shock, are [[interleukin-6]] and [[tumor necrosis factor]].  
Besides the aforementioned macrocirculatory changes in cardiogenic shock, which may also be seen in [[septic shock]], it is important to mention that [[microcirculation|microcirculatory]] abnormalities, caused in part by the [[inflammatory]] cascades, play an important part in the [[pathogenesis]] of [[organ failure]] as well.<ref name="pmid14691425">{{cite journal| author=De Backer D, Creteur J, Dubois MJ, Sakr Y, Vincent JL| title=Microvascular alterations in patients with acute severe heart failure and cardiogenic shock. | journal=Am Heart J | year= 2004 | volume= 147 | issue= 1 | pages= 91-9 | pmid=14691425 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14691425  }} </ref><ref name="pmid12091178">{{cite journal| author=De Backer D, Creteur J, Preiser JC, Dubois MJ, Vincent JL| title=Microvascular blood flow is altered in patients with sepsis. | journal=Am J Respir Crit Care Med | year= 2002 | volume= 166 | issue= 1 | pages= 98-104 | pmid=12091178 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12091178  }} </ref><ref name="pmid17095120">{{cite journal| author=Trzeciak S, Dellinger RP, Parrillo JE, Guglielmi M, Bajaj J, Abate NL et al.| title=Early microcirculatory perfusion derangements in patients with severe sepsis and septic shock: relationship to hemodynamics, oxygen transport, and survival. | journal=Ann Emerg Med | year= 2007 | volume= 49 | issue= 1 | pages= 88-98, 98.e1-2 | pmid=17095120 | doi=10.1016/j.annemergmed.2006.08.021 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17095120  }} </ref>
*[[IL-6]],is specific [[cytokine]] is correlated with the degree of [[organ failure]] and therefore [[mortality]].<ref name="pmid16775569">{{cite journal| author=Geppert A, Dorninger A, Delle-Karth G, Zorn G, Heinz G, Huber K| title=Plasma concentrations of interleukin-6, organ failure, vasopressor support, and successful coronary revascularization in predicting 30-day mortality of patients with cardiogenic shock complicating acute myocardial infarction. | journal=Crit Care Med | year= 2006 | volume= 34 | issue= 8 | pages= 2035-42 | pmid=16775569 | doi=10.1097/01.CCM.0000228919.33620.D9 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16775569  }} </ref>  
*These [[inflammatory]] mediators, among other actions, are responsible for the release of [[BNP]], which makes the levels of [[BNP]] good markers, not only for the level of [[inflammation]], but also to evaluate [[hemodynamic]] decompensation.<ref name="pmid16763507">{{cite journal| author=Rudiger A, Gasser S, Fischler M, Hornemann T, von Eckardstein A, Maggiorini M| title=Comparable increase of B-type natriuretic peptide and amino-terminal pro-B-type natriuretic peptide levels in patients with severe sepsis, septic shock, and acute heart failure. | journal=Crit Care Med | year= 2006 | volume= 34 | issue= 8 | pages= 2140-4 | pmid=16763507 | doi=10.1097/01.CCM.0000229144.97624.90 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16763507  }} </ref>
*Other [[circulatory]] factors, such as [[procalcitonin]], [[complement]] and [[CRP]], have been reported in some studies to contribute to the development of [[SIRS]] in cardiogenic shock.<ref name="pmid12925454">{{cite journal| author=Granger CB, Mahaffey KW, Weaver WD, Theroux P, Hochman JS, Filloon TG et al.| title=Pexelizumab, an anti-C5 complement antibody, as adjunctive therapy to primary percutaneous coronary intervention in acute myocardial infarction: the COMplement inhibition in Myocardial infarction treated with Angioplasty (COMMA) trial. | journal=Circulation | year= 2003 | volume= 108 | issue= 10 | pages= 1184-90 | pmid=12925454 | doi=10.1161/01.CIR.0000087447.12918.85 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12925454  }} </ref><ref name="pmid17200474">{{cite journal| author=APEX AMI Investigators. Armstrong PW, Granger CB, Adams PX, Hamm C, Holmes D et al.| title=Pexelizumab for acute ST-elevation myocardial infarction in patients undergoing primary percutaneous coronary intervention: a randomized controlled trial. | journal=JAMA | year= 2007 | volume= 297 | issue= 1 | pages= 43-51 | pmid=17200474 | doi=10.1001/jama.297.1.43 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17200474  }} </ref>
*Besides the aforementioned macrocirculatory changes in cardiogenic shock, which may also be seen in [[septic shock]], it is important to mention that [[microcirculation|microcirculatory]] abnormalities, caused in part by the [[inflammatory]] cascades, play an important part in the [[pathogenesis]] of [[organ failure]] as well.<ref name="pmid14691425">{{cite journal| author=De Backer D, Creteur J, Dubois MJ, Sakr Y, Vincent JL| title=Microvascular alterations in patients with acute severe heart failure and cardiogenic shock. | journal=Am Heart J | year= 2004 | volume= 147 | issue= 1 | pages= 91-9 | pmid=14691425 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14691425  }} </ref><ref name="pmid12091178">{{cite journal| author=De Backer D, Creteur J, Preiser JC, Dubois MJ, Vincent JL| title=Microvascular blood flow is altered in patients with sepsis. | journal=Am J Respir Crit Care Med | year= 2002 | volume= 166 | issue= 1 | pages= 98-104 | pmid=12091178 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12091178  }} </ref><ref name="pmid17095120">{{cite journal| author=Trzeciak S, Dellinger RP, Parrillo JE, Guglielmi M, Bajaj J, Abate NL et al.| title=Early microcirculatory perfusion derangements in patients with severe sepsis and septic shock: relationship to hemodynamics, oxygen transport, and survival. | journal=Ann Emerg Med | year= 2007 | volume= 49 | issue= 1 | pages= 88-98, 98.e1-2 | pmid=17095120 | doi=10.1016/j.annemergmed.2006.08.021 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17095120  }} </ref>


===Iatrogenic Cardiogenic Shock===
===Iatrogenic Cardiogenic Shock===
An important number of patients in cardiogenic shock complicating [[myocardial infarction]] (around 3/4), develop it after hospital admission.<ref name="pmid16046651">{{cite journal| author=Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS et al.| title=Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. | journal=JAMA | year= 2005 | volume= 294 | issue= 4 | pages= 448-54 | pmid=16046651 | doi=10.1001/jama.294.4.448 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16046651  }} </ref><ref name="Jeger2006">{{cite journal|last1=Jeger|first1=R. V.|title=Emergency revascularization in patients with cardiogenic shock on admission: a report from the SHOCK trial and registry|journal=European Heart Journal|volume=27|issue=6|year=2006|pages=664–670|issn=0195-668X|doi=10.1093/eurheartj/ehi729}}</ref> In some of these patients, it is reported that the development of [[shock]], particularly in high risk patients, is related to the use of certain classes of medications, used to treat the [[MI]]. These include:<ref name="pmid15976786">{{cite journal| author=Meine TJ, Roe MT, Chen AY, Patel MR, Washam JB, Ohman EM et al.| title=Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. | journal=Am Heart J | year= 2005 | volume= 149 | issue= 6 | pages= 1043-9 | pmid=15976786 | doi=10.1016/j.ahj.2005.02.010 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15976786  }} </ref><ref name="pmid7661937">{{cite journal| author=| title=ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. | journal=Lancet | year= 1995 | volume= 345 | issue= 8951 | pages= 669-85 | pmid=7661937 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7661937  }} </ref><ref name="pmid9631869">{{cite journal| author=| title=Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systematic overview of individual data from 100,000 patients in randomized trials. ACE Inhibitor Myocardial Infarction Collaborative Group. | journal=Circulation | year= 1998 | volume= 97 | issue= 22 | pages= 2202-12 | pmid=9631869 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9631869  }} </ref><ref name="pmid16271643">{{cite journal| author=Chen ZM, Pan HC, Chen YP, Peto R, Collins R, Jiang LX et al.| title=Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. | journal=Lancet | year= 2005 | volume= 366 | issue= 9497 | pages= 1622-32 | pmid=16271643 | doi=10.1016/S0140-6736(05)67661-1 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16271643  }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16646603 Review in: ACP J Club. 2006 May-Jun;144(3):58-9]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17213104 Review in: Evid Based Med. 2006 Jun;11(3):82-3] </ref>
*An important number of patients in cardiogenic shock complicating [[myocardial infarction]] (around 3/4), develop it after hospital admission.<ref name="pmid16046651">{{cite journal| author=Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS et al.| title=Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. | journal=JAMA | year= 2005 | volume= 294 | issue= 4 | pages= 448-54 | pmid=16046651 | doi=10.1001/jama.294.4.448 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16046651  }} </ref><ref name="Jeger2006">{{cite journal|last1=Jeger|first1=R. V.|title=Emergency revascularization in patients with cardiogenic shock on admission: a report from the SHOCK trial and registry|journal=European Heart Journal|volume=27|issue=6|year=2006|pages=664–670|issn=0195-668X|doi=10.1093/eurheartj/ehi729}}</ref>  
*In some of these patients, it is reported that the development of [[shock]], particularly in high risk patients, is related to the use of certain classes of medications, used to treat the [[MI]]. These include:<ref name="pmid15976786">{{cite journal| author=Meine TJ, Roe MT, Chen AY, Patel MR, Washam JB, Ohman EM et al.| title=Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. | journal=Am Heart J | year= 2005 | volume= 149 | issue= 6 | pages= 1043-9 | pmid=15976786 | doi=10.1016/j.ahj.2005.02.010 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15976786  }} </ref><ref name="pmid7661937">{{cite journal| author=| title=ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. | journal=Lancet | year= 1995 | volume= 345 | issue= 8951 | pages= 669-85 | pmid=7661937 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7661937  }} </ref><ref name="pmid9631869">{{cite journal| author=| title=Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systematic overview of individual data from 100,000 patients in randomized trials. ACE Inhibitor Myocardial Infarction Collaborative Group. | journal=Circulation | year= 1998 | volume= 97 | issue= 22 | pages= 2202-12 | pmid=9631869 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9631869  }} </ref><ref name="pmid16271643">{{cite journal| author=Chen ZM, Pan HC, Chen YP, Peto R, Collins R, Jiang LX et al.| title=Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. | journal=Lancet | year= 2005 | volume= 366 | issue= 9497 | pages= 1622-32 | pmid=16271643 | doi=10.1016/S0140-6736(05)67661-1 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16271643  }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16646603 Review in: ACP J Club. 2006 May-Jun;144(3):58-9]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17213104 Review in: Evid Based Med. 2006 Jun;11(3):82-3] </ref>
*[[Beta-blockers]]
*[[Beta-blockers]]
*[[ACE inhibitor]]s
*[[ACE inhibitor]]s
*[[Morphine]]
*[[Morphine]]
*[[Diuretics]] (As a cause or aggravating factor. This is due to the fact that [[pulmonary edema]] is a common [[complication]] of cardiogenic shock, leading to a decrease of circulating [[plasma]] volume, particularly in patients with prior [[heart failure]]. After the administration of high-dose [[diuretics]], the [[plasma]] volume will further decline)
*[[Diuretics]] (As a cause or aggravating factor. This is due to the fact that [[pulmonary edema]] is a common [[complication]] of cardiogenic shock, leading to a decrease of circulating [[plasma]] volume, particularly in patients with prior [[heart failure]].  
*After the administration of high-dose [[diuretics]], the [[plasma]] volume will further decline)
*Excess fluid administration (In the case of [[right ventricular myocardial infarction]], the excess volume loading in these patients may also contribute to the development of [[shock]])
*Excess fluid administration (In the case of [[right ventricular myocardial infarction]], the excess volume loading in these patients may also contribute to the development of [[shock]])
==Histopathological Findings Of myocardial infarction and plaque rupture==
http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
<div align="left">
<gallery heights="175" widths="175">
Image:Plaque rupture 1.jpg|Coronary artery: Atherosclerosis: Micro H&E med mag; A good example of plaque rupture with thrombosis.
Image:Plaque rupture 2.jpg|Right coronary artery: Ruptured Plaque: Micro low mag H&E; Ruptured plaque with foam cell lesion (near rupture site).
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Plaque rupture 3.jpg|Right coronary artery: Atherosclerosis Plaque Ruptured with Thrombus: Micro low mag H&E; an excellent view of ruptured plaque with thrombus and some old fibrin in it.
Image:Plaque rupture 4.jpg|Right coronary artery: Atherosclerosis Plaque Ruptured with Thrombus: Micro low mag trichrome.
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Plaque rupture 5.jpg|Right coronary artery: Atherosclerosis Plaque Ruptured: Micro low mag H&E; large plaque with hemorrhage; (an excellent example of hemorrhage).
Image:Plaque 1.jpg|Coronary artery: Atherosclerosis: Micro H&E low mag injected artery fairly typical uncomplicated atheromatous plaque
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Plaque 2.jpg|Coronary artery: Atherosclerosis: Micro H&E low mag, injected artery has typical fibrous plaque with small hemorrhage in atheroma.
Image:Plaque 3.jpg|Coronary artery: Atherosclerosis: Micro H&E low mag, injected artery is a very good example of marked lumen stenosis due to typical fibrous plaque with calcification
</gallery>
</div>


==References==
==References==

Latest revision as of 00:57, 12 March 2020

Cardiogenic Shock Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammad Salih, MD. João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

Overview

The pathophysiology of cardiogenic shock is complex and not fully understood. Ischemia to the myocardium causes derangement to both systolic and diastolic left ventricular function, resulting in a profound depression of myocardial contractility. This, in turn, leads to a potentially catastrophic and vicious spiral of reduced cardiac output and low blood pressure, perpetuating further coronary ischemia and impairment of contractility. Several physiologic compensatory processes ensue. These include:The activation of the sympathetic system leading to peripheral vasoconstriction which may improve coronary perfusion at the cost of increased afterload, and Tachycardia which increases myocardial oxygen demand and subsequently worsens myocardial ischemia.These compensatory mechanisms are subsequently counteracted by pathologic vasodilation that occurs from the release of potent systemic inflammatory markers such as interleukin-1, tumor necrosis factor a, and interleukin-6. Additionally, higher levels of nitric oxide and peroxynitrite are released, which also contribute to pathologic vasodilation and are known to be cardiotoxic. Unless interrupted by adequate treatment measures, this self-perpetuating cycle leads to global hypoperfusion and the inability to effectively meet the metabolic demands of the tissues, progressing to multiorgan failure and eventually death.

Pathophysiology

The downward "Spiral" of Cardiogenic shock

Right Ventricle Myocardial Infarction

Ventricular Septal and Free Wall Rupture

Inflammation and Hemodynamics

Iatrogenic Cardiogenic Shock

Histopathological Findings Of myocardial infarction and plaque rupture

http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]

References

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