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| ==Pathophysiology== | | ==HIV-TB Coinfection== |
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| ===Right Ventricle Myocardial Infarction===
| | Recommendations for the treatment of tuberculosis in [[HIV]]-infected adults: |
| Accounts for about 5% of the cases but represents as high [[mortality rate]] as [[left ventricle]] shock. The [[right ventricular]] regions more commonly affected by [[infarction]] are the inferior and inferior-posterior walls. The [[coronary arteries]] frequently occluded in this setting are the [[right coronary artery]], or the [[left circumflex coronary artery]], in a [[coronary artery dominance|left dominant system]].<ref name="pmid153103">{{cite journal| author=Isner JM, Roberts WC| title=Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease. Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction. | journal=Am J Cardiol | year= 1978 | volume= 42 | issue= 6 | pages= 885-94 | pmid=153103 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=153103 }} </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> Patients with [[right coronary artery]] [[occlusion]], in a [[coronary artery dominance|right dominant system]], are at higher risk of developing [[papillary muscle rupture]] and therefore undergoing [[valvular heart disease]], such as [[mitral regurgitation]].<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="pmid7643642">{{cite journal| author=Reeder GS| title=Identification and treatment of complications of myocardial infarction. | journal=Mayo Clin Proc | year= 1995 | volume= 70 | issue= 9 | pages= 880-4 | pmid=7643642 | doi=10.1016/S0025-6196(11)63946-3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7643642 }} </ref><ref name="pmid2190052">{{cite journal| author=Lavie CJ, Gersh BJ| title=Mechanical and electrical complications of acute myocardial infarction. | journal=Mayo Clin Proc | year= 1990 | volume= 65 | issue= 5 | pages= 709-30 | pmid=2190052 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2190052 }} </ref>
| | The recommended treatment of TB disease in HIV-infected adults (when the disease is caused by organisms that are known or presumed to be susceptible to first-line drugs) is a 6-month regimen consisting of: |
| | *For the first 2 months: An initial phase of [[isoniazid]] (INH), a [[rifamycin]], [[pyrazinamide]] (PZA), and [[ethambutol]] (EMB). |
| | *For the last 4 months: A continuation phase of INH and a rifamycin. |
| | *Patients with advanced HIV (CD4 counts < 100/µl) should be treated with daily or three-times-weekly therapy in both the initial and the continuation phases. |
| | *Twice weekly therapy may be considered in patients with less-advanced immunosuppression (CD4 counts ≥ 100/µl). |
| | *Once-weekly INH/rifapentine in the continuation phase should not be used in any HIV-infected patient. |
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| [[Right ventricle]] failure may affect [[left ventricular]] performance by several means:<ref name="pmid12706920">{{cite journal| author=Jacobs AK, Leopold JA, Bates E, Mendes LA, Sleeper LA, White H et al.| title=Cardiogenic shock caused by right ventricular infarction: a report from the SHOCK registry. | journal=J Am Coll Cardiol | year= 2003 | volume= 41 | issue= 8 | pages= 1273-9 | pmid=12706920 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12706920 }} </ref><ref name="BrookesRavn1999">{{cite journal|last1=Brookes|first1=C.|last2=Ravn|first2=H.|last3=White|first3=P.|last4=Moeldrup|first4=U.|last5=Oldershaw|first5=P.|last6=Redington|first6=A.|title=Acute Right Ventricular Dilatation in Response to Ischemia Significantly Impairs Left Ventricular Systolic Performance|journal=Circulation|volume=100|issue=7|year=1999|pages=761–767|issn=0009-7322|doi=10.1161/01.CIR.100.7.761}}</ref> | | Recommendations for the treatment of tuberculosis in [[HIV]]-infected adults are, with a few exceptions, the same as those for HIV-uninfected adults. The [[INH]]--[[rifapentine]] once weekly continuation phase is contraindicated in HIV-infected patients because of an unacceptably high rate of relapse, frequently with organisms that have acquired resistance to [[rifamycin]]s. The development of acquired [[rifampin]] [[drug resistance|resistance]] has also been noted among HIV-infected patients with advanced [[immunosuppression]] treated with twice weekly rifampin- or [[rifabutin]]-based regimens. Consequently, patients with [[CD4]]+ cell counts <100/µl should receive daily or three times weekly treatment. DOT and other adherence-promoting strategies are especially important for patients with HIV-related tuberculosis. |
| *Decrease in [[right ventricle]] output leading to a decrease in [[left ventricle]] filling thereby affecting [[cardiac output]];
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| *Increased [[right ventricle]] telediastolic pressure, leading to shifting of the [[interventricular septum]] into the [[left ventricle]] therefore jeopardizing [[left ventricle]] filling and [[systolic]] function.
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| ===Ventricular Septal and Free Wall Rupture===
| | Management of HIV-related tuberculosis is complex and requires expertise in the management of both HIV disease and tuberculosis. Because HIV-infected patients are often taking numerous medications, some of which interact with antituberculosis medications, it is strongly encouraged that experts in the treatment of HIV-related tuberculosis be consulted. A particular concern is the interaction of [[rifamycin]]s with [[antiretroviral agent]]s and other antiinfective drugs. [[Rifampin]] can be used for the treatment of tuberculosis with certain combinations of antiretroviral agents. [[Rifabutin]], which has fewer problematic drug interactions, may also be used in place of rifampin and appears to be equally effective although the doses of rifabutin and antiretroviral agents may require adjustment. As new antiretroviral agents and more pharmacokinetic data become available, these recommendations are likely to be modified. |
| [[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> | |
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| 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>
| | On occasion, patients with HIV-related tuberculosis may experience a temporary exacerbation of symptoms, signs, or radiographic manifestations of tuberculosis while receiving antituberculosis treatment. This clinical or radiographic worsening (paradoxical reaction) occurs in HIV-infected patients with active tuberculosis and is thought to be the result of immune reconstitution as a consequence of effective [[antiretroviral therapy]]. Symptoms and signs may include high [[fever]]s, [[lymphadenopathy]], expanding [[central nervous system]] lesions, and worsening of [[chest radiographic]] findings. The diagnosis of a paradoxical reaction should be made only after a thorough evaluation has excluded other [[etiologies]], particularly tuberculosis treatment failure. [[Nonsteroidal antiinflammatory agent]]s may be useful for symptomatic relief. For severe paradoxical reactions, [[prednisone]] (1--2 mg/kg per day for 1--2 weeks, then in gradually decreasing doses) may be used, although there are no data from controlled trials to support this approach. |
| :*most common in the setting of transmural [[myocardial infarction]], generally associated with 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>
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| :*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>
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| :*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>
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| ::*''simple'' - "direct through-and-through any defect", generally an anterior defect;
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| ::*''complex'' - a serpigenous [[dissection]] tract radiating from the primary [[ventricular septal rupture]] site, generally an inferior defect.
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| 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>
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| 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 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:
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| *''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>
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| *''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.<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>
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| *''Chronic'' - less frequently associated with cardiogenic shock.
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| ===Inflammation and Hemodynamics===
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| 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>
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| *The the range of elevation of [[systemic vascular resistance]] in this trial was wide, suggesting that the compensatory [[vasoconstriction]] wan't a rule in every patient
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| *The mean [[ejection fraction]] was also moderately decreased in this trial, showing that other mechanisms besides [[cardiac failure]] were present
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| *Some of the patients had [[leukocytosis]] and [[fever]], which along with the decreased [[systemic vascular resistance]] suggested [[SIRS]]
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| These facts have introduced the concept that [[myocardial infarction]] may cause [[SIRS]] and that [[inflammation]] plays a 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>
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| 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]], by combining 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>
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| 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>
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| | |
| ===Iatrogenic Cardiogenic Shock===
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| 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>
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| *[[Beta-blockers]]
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| *[[ACE inhibitor]]s
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| *[[Morphine]]
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| *[[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.
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| *Excess fluid administration, in the case of [[right ventricular myocardial infarction]], the excess volume loading in these patients may also lead or contribute to the development of [[shock]].
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| ===Pathology===
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| ====Myocardium====
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| *INFARCT EXTENSION AND EXPANSION
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| *REMOTE ISCHEMIA
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| *DIASTOLIC DYSFUNCTION
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| *VALVULAR ABNORMALITIES - (page 155 article #2)
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| ====Cellular====
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| *ENERGY METABOLISM
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| *ION PUMPS
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| *NECROSIS
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| *APOPTOSIS
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| ===Myocardial dysfunction===
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| *STUNNING
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| *HIBERNATING
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| ===Reperfusion Injury===
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| +++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
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| ===Cardiogenic shock and Inflammatory Mediators===
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| Myocardial infarction or ischemia lead to production of superoxide radicals which combine with nitrous oxide to form perioxinitrite which in turn causes myocardial depression and [[hypotension]].
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| [[Image:Cardiogenic_shock.JPG|center|500px]]
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| ===The Pathophysiologic "Spiral" of Cardiogenic shock===
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| Among patients with acute MI, there is often a downward spiral of hypoperfusion leading to further ischemia which leads to a further reduction in cardiac output and further hypoperfusion. The [[lactic acidosis]] that develops as a result of poor systemic perfusion can further reduce cardiac contractility. Reduced cardiac output leads to activation of the sympathetic nervous system, and the ensuing [[tachycardia]] that develops further exacerbates the myocardial ischemia. The increased left ventricular end diastolic pressures is associated with a rise in wall stress which results in further myocardial ischemia. [[Hypotension]] reduces epicardial perfusion pressure which in turn further increases myocardial ischemia.
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| Patients with cardiogenic shock in the setting of [[STEMI]] more often have multivessel disease, and myocardial ischemia may be present in multiple territories. It is for this reason that multivessel angioplasty may be of benefit in the patient with cardiogenic shock. Non-culprit or remote territories may also exhibit [[myocardial stunning]] in response to an ischemic insult which further reduces myocardial function. The pathophysiology of myocardial stunning is multifactorial and involves calcium overload in the sarcolemma and "stone heart" or [[diastolic dysfunction]] as well as the release of myocardial depressant substances. Areas of stunned myocardium may remain stunned after revascularization, but these regions do respond to inotropic stimulation. In contrast to stunned myocardium, [[hibernating myocardium]] does respond earlier to revascularization.
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| The multifactorial nature of cardiogenic shock can also be operative in the patient with critical [[aortic stenosis]] who has "spiraled": There is impairment of left ventricular outflow, with a drop in [[cardiac output]] there is greater [[subendocardial]] ischemia and poorer flow in the coronary arteries, this leads to further [[left ventricular systolic dysfunction]], given the subendocardial ischemia, the left ventricle develops [[diastolic dysfunction]] and becomes harder to fill. Inadvertent administration of [[vasodilator]]s and [[venodilator]]s may further reduce cardiac output and accelerate or trigger such a spiral.
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| ===Pathophysiologic Mechanisms to Compensate for Cardiogenic shock===
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| [[Cardiac output]] is the product of [[stroke volume]] and heart rate. In order to compensate for a reduction in stroke volume, there is a rise in the heart rate in patients with cardiogenic shock. As a result of the reduction in [[cardiac output]], peripheral tissues extract more oxygen from the limited blood that does flow to them, and this leaves the blood deoxygenated when it returns to the right heart resulting in a fall in the mixed venous oxygen saturation.
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| ===Pathophysiology of Multiorgan Failure===
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| The poor perfusion of organs results in [[hypoxia]] and [[metabolic acidosis]]. Inadequate perfusion to meet the metabolic demands of the brain, kidneys and heart leads to multiorgan failure.
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| ++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
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| Differential Diagnosis
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| {| style="border: 2px solid #A8A8A8; font-size: 70%;" align="center"
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| |+ <SMALL>''Classification of shock based on hemodynamic parameters.'' (CO, cardiac output; CVP; central venous pressure; PAD, pulmonary artery diastolic pressure; PAS, pulmonary artery systolic pressure; RVD, right ventricular diastolic pressure; RVS, right ventricular systolic pressure; SVO2, systemic venous oxygen saturation; SVR, systemic vascular resistance.)<ref name="isbn0-683-06754-0">{{Cite book | last1 = Parrillo | first1 = Joseph E. | last2 = Ayres | first2 = Stephen M. | title = Major issues in critical care medicine | date = 1984 | publisher = William Wilkins | location = Baltimore | isbn = 0-683-06754-0 | pages = }}</ref><ref name="isbn9781405179263">{{cite book | author = Judith S. Hochman, E. Magnus Ohman | authorlink = | editor = | others = | title = Cardiogenic Shock | edition = | language = | publisher = Wiley-Blackwell | location = | year = 2009 | origyear = | pages = | quote = | isbn = 9781405179263 | oclc = | doi = | url = | accessdate = }}</ref></SMALL>
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| | align="center" style="background: #A8A8A8; width: 100px;"| '''Type of Shock'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''Etiology'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''CO'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''SVR'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''PCWP'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''CVP'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''SVO2'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''RVS'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''RVD'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''PAS'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''PAD'''
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| |-
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC; width: 80px;" align=center rowspan=4 | '''Cardiogenic'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC; width: 20%;" | '''[[Ventricular septal defect|Acute Ventricular Septal Defect]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑ — ↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| |-
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[Mitral regurgitation|Acute Mitral Regurgitation]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑ — ↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| |-
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[Myocardium|Myocardial Dysfunction]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| |-
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[RV infarction|Right Ventricular Infarction]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↑
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| |-
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" rowspan=2 align=center | '''Obstructive'''
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" | '''[[Pulmonary embolism|Pulmonary Embolism]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↓
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓ — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓ — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓ — ↑
| |
| |-
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" |'''[[Cardiac tamponade|Cardiac Tamponade]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓ — ↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↑
| |
| |-
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" rowspan=2 align=center | '''Distributive'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[Septic shock|Septic Shock]]'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑ — ↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
| |
| |-
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[Anaphylactic shock|Anaphylactic Shock]]'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑ — ↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
| |
| |-
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" rowspan=1 align=center | '''Hypovolemic'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" | '''[[Volume depletion|Volume Depletion]]'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
| |
| |}
| |
| | |
| ==References==
| |
| {{Reflist|2}}
| |