Cardiogenic shock pathophysiology: Difference between revisions
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==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 results in the 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 do 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 this [[heart failure|cadiac 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> | '''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 results in the 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 do 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 this [[heart failure|cadiac 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> | ||
In the presence of cardiogenic shock develops a pathological cycle in which the [[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 [[heart]] [[sympathetic]] stimulation and activation of the [[Renin-angiotensin system|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]] muscle depression decreasing [[contractility]] and worsening [[hypotension]]. [[Lactic acidosis]] will also develop, resulting from the poor tissue perfusion, that causes a shift in the [[metabolism]] to [[glycolysis]], which will also 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> | In the presence of cardiogenic shock develops a pathological cycle in which the [[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 [[heart]] [[sympathetic]] stimulation and activation of the [[Renin-angiotensin system|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]] muscle depression decreasing [[contractility]] and worsening [[hypotension]]. [[Lactic acidosis]] will also develop, resulting from the poor [[tissue]] [[perfusion]], that causes a shift in the [[metabolism]] to [[glycolysis]], which will also 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> | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 14:19, 10 May 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Cardiogenic shock is a clinical condition, defined as a state of systemic hypoperfusion originated in cardiac failure, in the presence of adequate intravascular volume, typically followed by hypotension, which results in the insufficient ability to meet oxygen and nutrient demands of organs and other peripheral tissues.[1] It may range from mild to severe hypoperfusion and may be defined in terms of hemodynamic parameters, which according to most studies, means a state in which systolic blood pressure is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right ventricular filling pressures that do not respond to isolated fluid administration, is secondary to cardiac failure and occurs with signs of hypoperfusion (oliguria, cool extremities, cyanosis and altered mental status) or a cardiac index of < 2.2 L/min/m² (on inotropic, vasopressor or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg.[2][3][4][5][6][7][8] Despite the many possible causes for this cadiac failure, the most common is left ventricular failure in the setting of myocardial infarction.[9] In the presence of cardiogenic shock develops a pathological cycle in which the 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 heart sympathetic stimulation and activation of the renin/angiotensin/aldosterone system, trying to overcome the cardiac aggression, however, this will ultimately lead to a downward spiral worsening of the ischemia. Inflammatory mediators, originated in the infarcted area, will also intervene at some point causing myocardial muscle depression decreasing contractility and worsening hypotension. Lactic acidosis will also develop, resulting from the poor tissue perfusion, that causes a shift in the metabolism to glycolysis, which will also depress the myocardium, thereby worsening the clinical scenario.[10][11]
Pathophysiology
Basic Hemodynamic Derangements
Cardiogenic shock is due to inadequate forward output of the heart. This can be due to the following (either alone or often in combination):
- Systolic left ventricular dysfunction (e.g. acute MI, CHF, Cardiomyopathy, coronary artery bypass grafting, myocarditis, myocardial contusion,hypophosphatemia as can be seen in the refeeding syndrome). It is often said that 40% of the left ventricle must be infarcted to have cardogenic shock.
- Diastolic left ventricular dysfunction (e.g. ischemia)
- Obstruction of left ventricular outflow and increased after load (e.g. aortic stenosis, HOCM, coarctation of the aorta, malignant hypertension)
- Reversal of flow into the left ventricle (e.g. acute aortic insufficiency, endocarditis)
- Inadequate left ventricular filling due to mechanical causes (e.g. tamponade, pulmonary embolism). This has also been called obstructive shock in the past.
- Inadequate left ventricular filling due to inadequate filling time (e.g. tachycardia, tachycardia mediated cardiomyopathy)
- Conduction abnormalities (e.g. atrioventricular block, sinus bradycardia)
- A mechanical defect (e.g. a VSD, myocardial rupture of the left ventricular free wall)
- Right ventricular failure (e.g. Pulmonary embolism, hypoxic pulmonary vasoconstriction)
The Impact of Cardiogenic shock on the Pressure-Volume Loop
Cardiogenic shock shifts the pressure volume loop to the right: that is to say at a given pressure, the heart is able to eject less blood per heart beat, and stroke volume is reduced. Diastolic compliance is reduced, and left ventricular volumes are increased. This leads to the classic observation that an increased left ventricular end diastolic pressure is required to maintain adequate cardiac output. The rise in end diastolic pressure increases the wall stress and oxygen demands of the myocardium. These hemodynamic abnormalities contributes to the pathophysiologic spiral described below.
Cardiogenic shock and Inflammatory Mediators
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.
The Pathophysiologic "Spiral" of Cardiogenic shock
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.
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.
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 vasodilators and venodilators may further reduce cardiac output and accelerate or trigger such a spiral.
Pathophysiologic Mechanisms to Compensate for Cardiogenic shock
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.
Pathophysiology of Multiorgan Failure
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.
References
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hochman, Judith (2009). Cardiogenic shock. Chichester, West Sussex, UK Hoboken, NJ: Wiley-Blackwell. ISBN 1405179260.
- ↑ Goldberg, Robert J.; Gore, Joel M.; Alpert, Joseph S.; Osganian, Voula; de Groot, Jacques; Bade, Jurgen; Chen, Zuoyao; Frid, David; Dalen, James E. (1991). "Cardiogenic Shock after Acute Myocardial Infarction". New England Journal of Medicine. 325 (16): 1117–1122. doi:10.1056/NEJM199110173251601. ISSN 0028-4793.
- ↑ Goldberg, Robert J.; Samad, Navid A.; Yarzebski, Jorge; Gurwitz, Jerry; Bigelow, Carol; Gore, Joel M. (1999). "Temporal Trends in Cardiogenic Shock Complicating Acute Myocardial Infarction". New England Journal of Medicine. 340 (15): 1162–1168. doi:10.1056/NEJM199904153401504. ISSN 0028-4793.
- ↑ Menon, V.; Slater, JN.; White, HD.; Sleeper, LA.; Cocke, T.; Hochman, JS. (2000). "Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: report of the SHOCK trial registry". Am J Med. 108 (5): 374–80. PMID 10759093. Unknown parameter
|month=ignored (help) - ↑ Hasdai, D.; Holmes, DR.; Califf, RM.; Thompson, TD.; Hochman, JS.; Pfisterer, M.; Topol, EJ. (1999). "Cardiogenic shock complicating acute myocardial infarction: predictors of death. GUSTO Investigators. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries". Am Heart J. 138 (1 Pt 1): 21–31. PMID 10385759. Unknown parameter
|month=ignored (help) - ↑ Fincke, R.; Hochman, JS.; Lowe, AM.; Menon, V.; Slater, JN.; Webb, JG.; LeJemtel, TH.; Cotter, G. (2004). "Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry". J Am Coll Cardiol. 44 (2): 340–8. doi:10.1016/j.jacc.2004.03.060. PMID 15261929. Unknown parameter
|month=ignored (help) - ↑ Dzavik, V.; Cotter, G.; Reynolds, H. R.; Alexander, J. H.; Ramanathan, K.; Stebbins, A. L.; Hathaway, D.; Farkouh, M. E.; Ohman, E. M.; Baran, D. A.; Prondzinsky, R.; Panza, J. A.; Cantor, W. J.; Vered, Z.; Buller, C. E.; Kleiman, N. S.; Webb, J. G.; Holmes, D. R.; Parrillo, J. E.; Hazen, S. L.; Gross, S. S.; Harrington, R. A.; Hochman, J. S. (2007). "Effect of nitric oxide synthase inhibition on haemodynamics and outcome of patients with persistent cardiogenic shock complicating acute myocardial infarction: a phase II dose-ranging study". European Heart Journal. 28 (9): 1109–1116. doi:10.1093/eurheartj/ehm075. ISSN 0195-668X.
- ↑ Hochman, Judith S; Buller, Christopher E; Sleeper, Lynn A; Boland, Jean; Dzavik, Vladimir; Sanborn, Timothy A; Godfrey, Emilie; White, Harvey D; Lim, John; LeJemtel, Thierry (2000). "Cardiogenic shock complicating acute myocardial infarction—etiologies, management and outcome: a report from the SHOCK Trial Registry". Journal of the American College of Cardiology. 36 (3): 1063–1070. doi:10.1016/S0735-1097(00)00879-2. ISSN 0735-1097.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hollenberg SM, Kavinsky CJ, Parrillo JE (1999). "Cardiogenic shock". Ann Intern Med. 131 (1): 47–59. PMID 10391815.