Cardiogenic shock medical therapy: Difference between revisions

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


==Overview==
==Overview==
Cardiogenic shock is considered an [[emergency]] and irrespectively to the [[therapeutic]] approach, the target goal of any [[therapy]] is prompt [[revascularization]] of [[ischemic myocardium]]. This should be achieved in the shortest timespan possible. There are two major categories of treatment for cardiogenic shock, the ''medical/conservative approach'' and the ''interventional approach''. The ideal [[therapy|treatment]] combines both techniques, in which medical therapy, after restored filling pressures, allows [[hemodynamic|hemodynamical]] stabilization of the patient, until interventional methods, that contribute to the reversal of the process leading to the [[shock]] state, may performed. The interventional approach may include [[PCI]] or [[coronary artery bypass graft surgery]] ([[CABG]]) and in both techniques the goal is not only to reestablish [[perfusion]] of the occluded [[coronary artery]], but also to prevent [[coronary artery|vessel]] reoclusion. If there is no access to a [[cardiac catheterization]] facility, nor the possibility of transferring the patient to one within 90 minutes, then immediately [[thrombolytic therapy]] should be considered.<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> Other important factors to increase the chances of a better [[outcome]] are: [[mechanical ventilation]], in order to improve [[tissue]] [[oxygenation]], and close monitoring of the [[therapeutic]] dosages, particularly of [[vasoactive]] drugs, since these have been associated with excess [[mortality]] due to [[toxicity]] effects.<ref name="pmid17387132">{{cite journal| author=TRIUMPH Investigators. Alexander JH, Reynolds HR, Stebbins AL, Dzavik V, Harrington RA et al.| title=Effect of tilarginine acetate in patients with acute myocardial infarction and cardiogenic shock: the TRIUMPH randomized controlled trial. | journal=JAMA | year= 2007 | volume= 297 | issue= 15 | pages= 1657-66 | pmid=17387132 | doi=10.1001/jama.297.15.joc70035 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17387132  }} </ref><ref name="pmid16505643">{{cite journal| author=Sakr Y, Reinhart K, Vincent JL, Sprung CL, Moreno R, Ranieri VM et al.| title=Does dopamine administration in shock influence outcome? Results of the Sepsis Occurrence in Acutely Ill Patients (SOAP) Study. | journal=Crit Care Med | year= 2006 | volume= 34 | issue= 3 | pages= 589-97 | pmid=16505643 | doi=10.1097/01.CCM.0000201896.45809.E3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16505643 }} </ref> Also, it is recommended [[invasive]] [[hemodynamic]] monitoring, in order to monitor and guide the effects of the [[therapy]] as well as the overall status of the patient. The success of [[reperfusion]] is usually suggested by the relief of [[symptoms]], restoration of [[hemodynamic]] parameters and electrical stability, as well as the reduction of at least 50% in the [[ST-segment]] on the [[EKG]], in the case of a [[STEMI]].<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 = Hochman | first = Judith | title = Cardiogenic shock | publisher = Wiley-Blackwell | location = Chichester, West Sussex, UK Hoboken, NJ | year = 2009 | isbn = 9781405179263 }}</ref>
Cardiogenic shock is a medical emergency, rescusitive measures should be initiated immediately while the underlying etiology of the cardiogenic shock is promptly investigated.  [[Myocardial infarction]] (MI) is the most common cause of [[cardiogenic shock]], and when present, prompt [[revascularization]] should be performed. Other causes, such as [[free wall rupture]], [[acute valvular abnormality]], or [[left ventricular septum rupture]], may require more invasive interventions. The management plan of cardiogenic shock includes the initiation of resuscitation and general measures, optimization of the blood pressure (pharmacological therapy or mechanical therapy when [[hypotension]] is refractory to [[inotrope]] and [[vasopressors]]), [[reperfusion]] or [[revascularization]], and hemodynamic monitoring and stabilizationUrgent [[revascularization]] is a priority over [[hemodynamic]] monitoring in MI patients with [[cardiogenic shock]] and should not be delayed. The first line strategy for reperfusion is [[percutaneous coronary intervention]] which is preffered over [[coronary artery bypass graft]] ([[CABG]]), when [[PCI]] or [[CABG]] can not be perfomed, [[fibrinolytic therapy]] is indicated in the absence of any [[contraindications]].


==Medical Therapy==
==Medical Therapy==
Cardiogenic shock is a medical emergency, rescusitive measures should be initiated immediately while the underlying etiology of the cardiogenic shock is promptly investigated.  Myocardial infarction is the most common cause of cardiogenic shock, and when present, prompt revascularization should be performed.  Other causes, such as free wall rupture, acute valvular abnormality, or left ventricular septum rupture, may require more invasive interventions.


===Goals of Therapy===
===Goals of Therapy===
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* Improve systemic reperfusion
* Improve systemic reperfusion


The first line treatment to increase [[blood pressure]] in cardiogenic shock is the administration of pharmacological therapy with either ionotropes or vasopressors,<ref name="pmid15289388">{{cite journal| author=Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M et al.| title=ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). | journal=Circulation | year= 2004 | volume= 110 | issue= 5 | pages= 588-636 | pmid=15289388 | doi=10.1161/01.CIR.0000134791.68010.FA | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15289388  }} </ref> the main choices being [[dopamine]], [[dobutamine]], and [[norepinephrine]]. If pharmacological therapy fails to stabilize the patient's [[blood pressure]], mechanical support must be provided.
The first line treatment to increase [[blood pressure]] in cardiogenic shock is the administration of pharmacological therapy with either ionotropes or vasopressors.<ref name="pmid15289388">{{cite journal| author=Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M et al.| title=ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). | journal=Circulation | year= 2004 | volume= 110 | issue= 5 | pages= 588-636 | pmid=15289388 | doi=10.1161/01.CIR.0000134791.68010.FA | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15289388  }} </ref> If pharmacological therapy fails to stabilize the patient's [[blood pressure]], mechanical support must be provided.


====Pharmacological Therapy====
===Pharmacological Therapy===
The appropriate choice of an [[inotrope]] or [[vasopressor]] requires the assessment of the balance between its desired and undesired effects:
The appropriate choice of an [[inotrope]] or [[vasopressor]] requires the assessment of the balance between its desired and undesired effects:
* Desired effects:  ↑ [[cardiac output]] and ↓ left ventricular pressure
* Desired effects:  ↑ [[cardiac output]] and ↓ left ventricular pressure
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All [[inotrope]]s and [[vasopressor]]s increase myocardial oxygen consumption to a certain extent.  However, the benefit of their administration in the setting of a cardiogenic shock is achieved through counteracting the deleterious effects of hypotension.  In cardiogenic shock, hypotension decreases myocardial perfusion and leads to compensatory elevation in [[LV]] filling pressure which in turn increases myocardial energy consumption.  Therefore, the balance between desired and undesired effects of these agents necessitate their administration at the minimum efficacious dose.<ref name="pmid18765387">{{cite journal| author=Overgaard CB, Dzavík V| title=Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease. | journal=Circulation | year= 2008 | volume= 118 | issue= 10 | pages= 1047-56 | pmid=18765387 | doi=10.1161/CIRCULATIONAHA.107.728840 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18765387  }} </ref>  There is no robust data that compares the efficacy of inotropes and vasopressors in improvement of cardiovascular outcomes and reduction in mortality.<ref name="pmid24385385">{{cite journal| author=Unverzagt S, Wachsmuth L, Hirsch K, Thiele H, Buerke M, Haerting J et al.| title=Inotropic agents and vasodilator strategies for acute myocardial infarction complicated by cardiogenic shock or low cardiac output syndrome. | journal=Cochrane Database Syst Rev | year= 2014 | volume= 1 | issue=  | pages= CD009669 | pmid=24385385 | doi=10.1002/14651858.CD009669.pub2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24385385  }} </ref>
All [[inotrope]]s and [[vasopressor]]s increase myocardial oxygen consumption to a certain extent.  However, the benefit of their administration in the setting of a cardiogenic shock is achieved through counteracting the deleterious effects of hypotension.  In cardiogenic shock, hypotension decreases myocardial perfusion and leads to compensatory elevation in [[LV]] filling pressure which in turn increases myocardial energy consumption.  Therefore, the balance between desired and undesired effects of these agents necessitate their administration at the minimum efficacious dose.<ref name="pmid18765387">{{cite journal| author=Overgaard CB, Dzavík V| title=Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease. | journal=Circulation | year= 2008 | volume= 118 | issue= 10 | pages= 1047-56 | pmid=18765387 | doi=10.1161/CIRCULATIONAHA.107.728840 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18765387  }} </ref>  There is no robust data that compares the efficacy of inotropes and vasopressors in improvement of cardiovascular outcomes and reduction in mortality.<ref name="pmid24385385">{{cite journal| author=Unverzagt S, Wachsmuth L, Hirsch K, Thiele H, Buerke M, Haerting J et al.| title=Inotropic agents and vasodilator strategies for acute myocardial infarction complicated by cardiogenic shock or low cardiac output syndrome. | journal=Cochrane Database Syst Rev | year= 2014 | volume= 1 | issue=  | pages= CD009669 | pmid=24385385 | doi=10.1002/14651858.CD009669.pub2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24385385  }} </ref>


The two main agents used to optimize the blood pressure are:
The two main agents used to optimize the blood pressure are [[Dopamine]], [[dobutamine]] (mainly among non-sick patients), and [[norepinephrine]] (mainly among patients with severe [[hypotension]]).  Alternative agents include [[phosphodiesterase]] inhibitors ([[amrinone]] or [[milrinone]]) and [[levosimendan]].  The choices of pharmacological agents is guided by the blood pressure and clinical status of the patient.  There is no clear cut regarding the choice of the agents, combinations of moderate [[doses]] of different [[medications]] are commonly used instead of the administration of the maximal [[dose]] of any individual [[drug]].<ref name="pmid6821904">{{cite journal| author=Richard C, Ricome JL, Rimailho A, Bottineau G, Auzepy P| title=Combined hemodynamic effects of dopamine and dobutamine in cardiogenic shock. | journal=Circulation | year= 1983 | volume= 67 | issue= 3 | pages= 620-6 | pmid=6821904 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6821904  }} </ref>
* [[Dopamine]]
* [[Norepinephrine]]: Norepinephrine is mainly used among patients with severe [[hypotension]].


Alternative agents include [[dobutamine]] (mainly in non-sick patients) and [[phosphodiesterase]] inhibitors ([[amrinone]] or [[milrinone]]).  
====Low Output without Shock====
[[Dobutamine]] is the treatment of choice among non-sick patients with low output and preserved [[systolic blood pressure]].


====Selection of a Vasopressor or an Inotrope====
====Low Output with Shock====
The choices of pharmacological agents is guided by the blood pressure and clinical status of the patient.  There is no clear cut regarding the choice of the agents, combinations of moderate [[doses]] of different [[medications]] are commonly used instead of the administration of the maximal [[dose]] of any individual [[drug]].<ref name="pmid6821904">{{cite journal| author=Richard C, Ricome JL, Rimailho A, Bottineau G, Auzepy P| title=Combined hemodynamic effects of dopamine and dobutamine in cardiogenic shock. | journal=Circulation | year= 1983 | volume= 67 | issue= 3 | pages= 620-6 | pmid=6821904 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6821904  }} </ref>


===== Low Output without Shock=====
=====''Systolic Blood Pressure (SBP) > 70 or 80 mm Hg''=====
[[Dobutamine]] is the treatment of choice among patients with low output and preserved systolic blood pressure.
 
=====Low Output with Shock=====
 
=====Systolic blood pressure (SBP) > 70 or 80 mm Hg=====
[[Dobutamine]] is preferred over [[dopamine]] when the patient does not have symptoms:  
[[Dobutamine]] is preferred over [[dopamine]] when the patient does not have symptoms:  
* Usual dose: 2.0–20 μg/kg/min
* Usual dose: 2.0–20 μg/kg/min
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[[Phosphodiesterase inhibitors]] ([[PDI]]s) such as [[milrinone]] and [[inamrinone]] (formerly known as [[amrinone]]) are not dependent upon the adrenoreceptor activity and patients may not develop tolerance, and they may be less likely to increase myocardial oxygen demands and risks of arrhythmia. However, the addition of a vasopressor is often required as these agents reduce [[preload]] and [[afterload]].  PDIs are more likely to be associated with [[tachyarrhythmias]] than [[dobutamine]], significant vasodilation and [[hypotension]].
[[Phosphodiesterase inhibitors]] ([[PDI]]s) such as [[milrinone]] and [[inamrinone]] (formerly known as [[amrinone]]) are not dependent upon the adrenoreceptor activity and patients may not develop tolerance, and they may be less likely to increase myocardial oxygen demands and risks of arrhythmia. However, the addition of a vasopressor is often required as these agents reduce [[preload]] and [[afterload]].  PDIs are more likely to be associated with [[tachyarrhythmias]] than [[dobutamine]], significant vasodilation and [[hypotension]].


=====Systolic blood pressure (SBP) < 70 or 80 mm Hg=====
=====''Systolic Blood Pressure (SBP) < 70 or 80 mm Hg''=====
Norepinephrine is indicated among patients with severe hypotension:
Norepinephrine is indicated among patients with severe hypotension:
* Initial dose: 0.5–1.0 μg/min
* Initial dose: 0.5–1.0 μg/min
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* Titrate to [[SBP]] >90 mm Hg
* Titrate to [[SBP]] >90 mm Hg


If norepinephrine does not generate a MAP of 60 mm Hg, then epinephrine can be added. Epinephrine increases both the [[stroke volume]] and [[heart rate]], but is associated with [[lactic acidosis]]
If [[norepinephrine]] does not generate a MAP of 60 mm Hg, then epinephrine can be added. Epinephrine increases both the [[stroke volume]] and [[heart rate]], but is associated with an increased rate of [[lactic acidosis]].


====Mechanism of Action of Ionotropes and Vasopressors====
====Mechanism of Action of Ionotropes and Vasopressors====
Shown below is a table summarizing the different inotrope or vasopressor agents used in the setting of cardiogenic shock.<ref name="pmid24530672">{{cite journal| author=Francis GS, Bartos JA, Adatya S| title=Inotropes. | journal=J Am Coll Cardiol | year= 2014 | volume= 63 | issue= 20 | pages= 2069-78 | pmid=24530672 | doi=10.1016/j.jacc.2014.01.016 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24530672 }} </ref><ref name="pmid18765387">{{cite journal| author=Overgaard CB, Dzavík V| title=Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease. | journal=Circulation | year= 2008 | volume= 118 | issue= 10 | pages= 1047-56 | pmid=18765387 | doi=10.1161/CIRCULATIONAHA.107.728840 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18765387 }} </ref>
Shown below is a table summarizing the different inotrope or vasopressor agents used in the setting of cardiogenic shock.<ref name="pmid18765387">{{cite journal| author=Overgaard CB, Dzavík V| title=Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease. | journal=Circulation | year= 2008 | volume= 118 | issue= 10 | pages= 1047-56 | pmid=18765387 | doi=10.1161/CIRCULATIONAHA.107.728840 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18765387 }} </ref><ref name="pmid24530672">{{cite journal| author=Francis GS, Bartos JA, Adatya S| title=Inotropes. | journal=J Am Coll Cardiol | year= 2014 | volume= 63 | issue= 20 | pages= 2069-78 | pmid=24530672 | doi=10.1016/j.jacc.2014.01.016 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24530672 }} </ref>


{|
{| style="cellpadding=0; cellspacing= 0; width: 1000px;"
| '''Drug''' || '''Alpha 1''' || '''Beta 1''' || '''Beta 2''' || '''Dopamine'''|| '''Effects'''
|-
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Drug''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Alpha 1''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Beta 1''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Beta 2''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Dopamine'''|| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Effects'''
|-
|-
| '''Norepinephrine'''|| +++ || ++ || + || - ||  
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | '''Norepinephrine'''|| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left| +++ || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left| ++ ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | + || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left| - || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
* Minimal to moderate inotropic effect
* Minimal to moderate inotropic effect
* Minimal chronotropic effect
* Minimal chronotropic effect
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* Increase coronary blood flow (increase diastolic BP)
* Increase coronary blood flow (increase diastolic BP)
|-
|-
| '''Dopamine (dose---)''' || ++ || ++ || - || ++ ||
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | '''Dopamine (dose---)''' || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |++ ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | ++ || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |- || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |++ ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
* Increase CO
* Increase CO
* Increase BP and SVR
* Increase BP and SVR
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* Increases PCWP
* Increases PCWP
|-
|-
| '''Dobutamine''' || + || +++|| ++ || -||
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Dobutamine''' || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |+ ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | +++|| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |++ ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | - ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
* Increase CO  
* Increase CO  
* Increase myocardial contractility
* Increase myocardial contractility
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* Less arrythmogenic
* Less arrythmogenic
|-
|-
| '''Isoprotenerol''' || - || +++ || +++ || - ||  
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Isoprotenerol''' || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | - || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | +++ || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | +++ ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | - || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |* Positive inotrope
* Positive inotrope
* Positive chronotrope
* Positive chronotrope
* Decrease coronary reperfusion
* Decrease coronary reperfusion
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* Consider ONLY in patients with [[bradyarrhythmia]] as a bridge to temporary [[pacemaker]]
* Consider ONLY in patients with [[bradyarrhythmia]] as a bridge to temporary [[pacemaker]]
|-
|-
| '''Phenylephrine''' || +++ || -|| -|| - ||  
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Phenylephrine''' ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | +++ ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | -||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | -||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | - ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
* Reflex bradycardia
* Reflex bradycardia
* Vasoconstriction
* Vasoconstriction
|-
|-
| '''Epinephrine''' || +++ ||+++|| ++|| - ||  
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Epinephrine''' ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | +++ ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |+++||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | ++||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | - || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |* Arrythmogenic
* Arrythmogenic
* Increase myocardial contractility
* Increase myocardial contractility
|-
|-
|}
|}


Phosphodiesterase inhibitors (milrinone, amrinone)
Phosphodiesterase inhibitors (milrinone, amrinone):
* Potent ionotrope
* Potent ionotrope
* Potent chronotrope
* Potent chronotrope
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Levosimendan:
Levosimendan:
* Ussed in decompensated heart failure
* Used mainly in decompensated [[heart failure]]


====Mechanical Therapy====
===Mechanical Therapy===
Mechanical therapy for cardiac shock involves the use of circulatory assist systems, which are different by:<ref name="pmid24014384">{{cite journal| author=Werdan K, Gielen S, Ebelt H, Hochman JS| title=Mechanical circulatory support in cardiogenic shock. | journal=Eur Heart J | year= 2014 | volume= 35 | issue= 3 | pages= 156-67 | pmid=24014384 | doi=10.1093/eurheartj/eht248 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24014384  }} </ref>
Mechanical therapy for cardiac shock involves the use of circulatory assist systems, which are different by:<ref name="pmid24014384">{{cite journal| author=Werdan K, Gielen S, Ebelt H, Hochman JS| title=Mechanical circulatory support in cardiogenic shock. | journal=Eur Heart J | year= 2014 | volume= 35 | issue= 3 | pages= 156-67 | pmid=24014384 | doi=10.1093/eurheartj/eht248 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24014384  }} </ref>
* Mode of placement: percutaneous vs. surgical
* Mode of placement: percutaneous vs. surgical
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* Presence or absence of combined extracorporal membrane oxygenation (ECMO)
* Presence or absence of combined extracorporal membrane oxygenation (ECMO)


====Intra-aortic Balloon Placement====
====Intra-Aortic Balloon Pump (IABP)====
As per the recommendation of the 2013 [[AHA]]/[[ACC]] guidelines, in the setting of acute MI complicated by cardiogenic shock refractory to pharmacological therapy, the placement of an [[intra-aortic balloon pump]] ([[IABP]]) (which reduces [[afterload|workload]] for the heart, and improves perfusion of the [[coronary arteries]]) should be considered.<ref name="pmid23247303">{{cite journal| author=O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA et al.| title=2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 4 | pages= 529-55 | pmid=23247303 | doi=10.1161/CIR.0b013e3182742c84 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23247303  }} </ref>
As per the recommendation of the 2013 [[AHA]]/[[ACC]] guidelines, in the setting of acute MI complicated by cardiogenic shock refractory to pharmacological therapy, the placement of an [[intra-aortic balloon pump]] ([[IABP]]) (which reduces [[afterload|workload]] for the heart, and improves perfusion of the [[coronary arteries]]) should be considered (Class IIa, level of evidence B).<ref name="pmid23247303">{{cite journal| author=O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA et al.| title=2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 4 | pages= 529-55 | pmid=23247303 | doi=10.1161/CIR.0b013e3182742c84 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23247303  }} </ref>


The hemodynamic effects of IABP are:<ref>Marco Tubaro, Nicolas Danchin, Gerasimos Filippatos, Patrick Goldstein, Pascal Vranckx, Doron Zahger, Werdan K, Ruß M, Buerke M, Marco Tubaro, Nicolas Danchin, Gerasimos Filippatos, Patrick Goldstein, Pascal Vranckx, Doron Zahger, editors. The intra-aortic balloon pump. The ESC Textbook of Intensive and Acute Cardiac Care. Oxford: Oxford University Press; 2011. p. 277-288.
The hemodynamic effects of IABP are:<ref>Marco Tubaro, Nicolas Danchin, Gerasimos Filippatos, Patrick Goldstein, Pascal Vranckx, Doron Zahger, Werdan K, Ruß M, Buerke M, Marco Tubaro, Nicolas Danchin, Gerasimos Filippatos, Patrick Goldstein, Pascal Vranckx, Doron Zahger, editors. The intra-aortic balloon pump. The ESC Textbook of Intensive and Acute Cardiac Care. Oxford: Oxford University Press; 2011. p. 277-288.
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Clinical outcome studies also demonstrate conflicting results regarding the use of IABP and improved survival.  In a Cochrane database systematic review among 190 patients, the use of IABP was not associated with a reduction in all-cause 30-day mortality (HR=1.04; 95% confidence interval 0.62–1.73).<ref name="pmid21735410">{{cite journal| author=Unverzagt S, Machemer MT, Solms A, Thiele H, Burkhoff D, Seyfarth M et al.| title=Intra-aortic balloon pump counterpulsation (IABP) for myocardial infarction complicated by cardiogenic shock. | journal=Cochrane Database Syst Rev | year= 2011 | volume=  | issue= 7 | pages= CD007398 | pmid=21735410 | doi=10.1002/14651858.CD007398.pub2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21735410  }} </ref> In another meta-analysis of 9 cohorts (n = 10529), the use of IABP was associated with 18% decrease (p<0.0001) and and 6% increase (p<0.0008) in 30-day mortality among STEMI patients with cardiogenic shock treated with [[fibrinolytic therapy]] and those undergoing primary [[PCI]], respectively. <ref name="pmid19168529">{{cite journal| author=Sjauw KD, Engström AE, Vis MM, van der Schaaf RJ, Baan J, Koch KT et al.| title=A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 4 | pages= 459-68 | pmid=19168529 | doi=10.1093/eurheartj/ehn602 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19168529  }} </ref>  In a meta-analysis of seven randomized trials among 1009 patient, IABP placement in STEMI was not associated with an improvement in mortality or in left ventricular function but was associated with a higher rate of stroke and bleeding.  When data from non-randomized cohort studies were evaluated in a meta-analysis (n=10,529 STEMI patients with cardiogenic shock), IABP placement was associated with an 18% relative risk reduction in 30 day mortality among patients treated with a fibrinolytic agent. This particular analysis is confounded by the fact that those patients in whom an [[IABP]] was placed underwent [[adjunctive percutaneous intervention]] (PCI) more frequently. In this non-randomized cohort analysis, [[IABP]] placement in patients undergoing [[primary angioplasty]] was associated with a 6% relative increase in mortality (p<0.0008).  Thus, neither randomized nor observational data support IABP placement in the setting of [[primary PCI]] for cardiogenic shock, and careful consideration should be given to the risk of [[stroke]] and bleeding  prior to [[IABP]] placement in this population.<ref name="pmid19168529">{{cite journal |author=Sjauw KD, Engström AE, Vis MM, van der Schaaf RJ, Baan J, Koch KT, de Winter RJ, Piek JJ, Tijssen JG, Henriques JP |title=A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? |journal=European Heart Journal |volume=30 |issue=4 |pages=459–68 |year=2009 |month=February |pmid=19168529 |doi=10.1093/eurheartj/ehn602 |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=19168529}}</ref>
Clinical outcome studies also demonstrate conflicting results regarding the use of IABP and improved survival.  In a Cochrane database systematic review among 190 patients, the use of IABP was not associated with a reduction in all-cause 30-day mortality (HR=1.04; 95% confidence interval 0.62–1.73).<ref name="pmid21735410">{{cite journal| author=Unverzagt S, Machemer MT, Solms A, Thiele H, Burkhoff D, Seyfarth M et al.| title=Intra-aortic balloon pump counterpulsation (IABP) for myocardial infarction complicated by cardiogenic shock. | journal=Cochrane Database Syst Rev | year= 2011 | volume=  | issue= 7 | pages= CD007398 | pmid=21735410 | doi=10.1002/14651858.CD007398.pub2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21735410  }} </ref> In another meta-analysis of 9 cohorts (n = 10529), the use of IABP was associated with 18% decrease (p<0.0001) and and 6% increase (p<0.0008) in 30-day mortality among STEMI patients with cardiogenic shock treated with [[fibrinolytic therapy]] and those undergoing primary [[PCI]], respectively. <ref name="pmid19168529">{{cite journal| author=Sjauw KD, Engström AE, Vis MM, van der Schaaf RJ, Baan J, Koch KT et al.| title=A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 4 | pages= 459-68 | pmid=19168529 | doi=10.1093/eurheartj/ehn602 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19168529  }} </ref>  In a meta-analysis of seven randomized trials among 1009 patient, IABP placement in STEMI was not associated with an improvement in mortality or in left ventricular function but was associated with a higher rate of stroke and bleeding.  When data from non-randomized cohort studies were evaluated in a meta-analysis (n=10,529 STEMI patients with cardiogenic shock), IABP placement was associated with an 18% relative risk reduction in 30 day mortality among patients treated with a fibrinolytic agent. This particular analysis is confounded by the fact that those patients in whom an [[IABP]] was placed underwent [[adjunctive percutaneous intervention]] (PCI) more frequently. In this non-randomized cohort analysis, [[IABP]] placement in patients undergoing [[primary angioplasty]] was associated with a 6% relative increase in mortality (p<0.0008).  Thus, neither randomized nor observational data support IABP placement in the setting of [[primary PCI]] for cardiogenic shock, and careful consideration should be given to the risk of [[stroke]] and bleeding  prior to [[IABP]] placement in this population.<ref name="pmid19168529">{{cite journal |author=Sjauw KD, Engström AE, Vis MM, van der Schaaf RJ, Baan J, Koch KT, de Winter RJ, Piek JJ, Tijssen JG, Henriques JP |title=A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? |journal=European Heart Journal |volume=30 |issue=4 |pages=459–68 |year=2009 |month=February |pmid=19168529 |doi=10.1093/eurheartj/ehn602 |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=19168529}}</ref>


====Left Ventricular Assist Device Placement====
====Left Ventricular Assist Device (LVAD)====
As per the recommendation of the 2013 [[AHA]]/[[ACC]] guidelines, in the setting of pronounced [[hypotension]] despite medical therapy and IABP placement, placement of a left [[ventricular assist device]] (which augments the pump-function of the heart) should be considered.<ref name="pmid23247303">{{cite journal| author=O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA et al.| title=2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 4 | pages= 529-55 | pmid=23247303 | doi=10.1161/CIR.0b013e3182742c84 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23247303  }} </ref>  A ventricular assist device should only be placed in those patients in whom the cardiogenic shock is deemed to be reversible or if it is being used as a bridge option. <ref>Farrar DJ, Lawson JH, Litwak P, Cederwall G. Thoratec VAD system as a bridge to heart transplantation. J Heart Transplant. Jul-Aug 1990;9(4):415-22; discussion 422-3.</ref>
As per the recommendation of the 2013 [[AHA]]/[[ACC]] guidelines, in the setting of pronounced [[hypotension]] refractory to medical therapy and IABP placement, placement of a left [[ventricular assist device]] (LVAD) should be considered.<ref name="pmid23247303">{{cite journal| author=O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA et al.| title=2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 4 | pages= 529-55 | pmid=23247303 | doi=10.1161/CIR.0b013e3182742c84 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23247303  }} </ref>  A ventricular assist device should only be placed in those patients in whom the cardiogenic shock is deemed to be reversible or if it is being used as a bridge option.<ref>Farrar DJ, Lawson JH, Litwak P, Cederwall G. Thoratec VAD system as a bridge to heart transplantation. J Heart Transplant. Jul-Aug 1990;9(4):415-22; discussion 422-3.</ref>
 
The hemodynamic effects of [[LVAD]] are superior to those of [[IABP]]:<ref name="pmid24014384">{{cite journal| author=Werdan K, Gielen S, Ebelt H, Hochman JS| title=Mechanical circulatory support in cardiogenic shock. | journal=Eur Heart J | year= 2014 | volume= 35 | issue= 3 | pages= 156-67 | pmid=24014384 | doi=10.1093/eurheartj/eht248 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24014384  }} </ref>
* ↑ [[cardiac output]]
* ↑ mean arterial pressure
* ↓ [[pulmonary capillary wedge pressure]]
* ↓ central venous pressure
* ↓ pulmonary arterial pressure
* ↓ filling pressures in the [[left ventricle|left]] and [[right ventricle]]
* ↓ myocardial oxygen demand


====ECMO====
Despite the superiority of hemodynamic support of LVAD compared to IABP, the use of [[LVAD]] is limited by the high risk of complications (such as bleeding), the complexity of insertion, and the absence of data regarding survival benefit.<ref name="pmid24014384">{{cite journal| author=Werdan K, Gielen S, Ebelt H, Hochman JS| title=Mechanical circulatory support in cardiogenic shock. | journal=Eur Heart J | year= 2014 | volume= 35 | issue= 3 | pages= 156-67 | pmid=24014384 | doi=10.1093/eurheartj/eht248 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24014384  }} </ref>  According to a metanalysis of 3 controlled trials (two trials on the TandemHeart and one trial on the Impella device), the use of LVAD was associated with a superior hemodynamic support without a reduction in 30-day mortality (RR=1.06, 95% CI 0.68–1.66).<ref name="pmid19617601">{{cite journal| author=Cheng JM, den Uil CA, Hoeks SE, van der Ent M, Jewbali LS, van Domburg RT et al.| title=Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta-analysis of controlled trials. | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 17 | pages= 2102-8 | pmid=19617601 | doi=10.1093/eurheartj/ehp292 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19617601  }} </ref>
 
====Extracorporeal Membrane Oxygenation (ECMO)====
Hemodynamic effects of extracorporeal membrane oxygenation (ECMO):<ref name="pmid24014384">{{cite journal| author=Werdan K, Gielen S, Ebelt H, Hochman JS| title=Mechanical circulatory support in cardiogenic shock. | journal=Eur Heart J | year= 2014 | volume= 35 | issue= 3 | pages= 156-67 | pmid=24014384 | doi=10.1093/eurheartj/eht248 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24014384  }} </ref>
* ↓ [[left ventricular]] preload
* ↑ [[left ventricular]] afterload
* ↑ myocardial oxygen demand
 
ECMO use is associated with complications such as [[bleeding]], [[renal failure]], and [[systemic inflammatory response syndrome]].<ref name="pmid24014384">{{cite journal| author=Werdan K, Gielen S, Ebelt H, Hochman JS| title=Mechanical circulatory support in cardiogenic shock. | journal=Eur Heart J | year= 2014 | volume= 35 | issue= 3 | pages= 156-67 | pmid=24014384 | doi=10.1093/eurheartj/eht248 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24014384  }} </ref>


==Urgent Revascularization==
==Urgent Revascularization==
Line 186: Line 194:


===Hemodynamic Monitoring===
===Hemodynamic Monitoring===
The aims of [[hemodynamic]] monitoring are:
The aim of [[hemodynamic]] monitoring is to assess the response to treatment and monitor and guide the [[doses]] of the [[inotrope]]s and [[vasopressor]]s.
* To make sure that a target [[mean arterial pressure]] ([[MAP]]) of 60 to 65 mmHg is achieved to maintain perfusion to vital organs (brain, kidney, heart)
* To monitor and guide the effects and [[doses]] of the [[ionotrope]] and [[vasopressor]]s


The response to the treatment is determined through the assessment of whether the [[mean arterial pressure]] reached the target value, an increase in [[blood pressure]], and bed-side clinical assessment by evaluating indices of organ [[perfusion]], such as physical exam, [[urine]] output, and [[lactate]] levels,
Target endpoints are:
* [[Mean arterial pressure]] ([[MAP]]) of 60 to 65 mmHg
* SaO2 >92%
* SvO2 >60%
* ScvO2 >70%
* Urine output >0.5 mL/kg/h
* Lactate <2.2 mM/L
* Hematocrit ≥30%


Target endpoints:
Shown below is a table summarizing the different parameters of hemodynamic monitoring, their target goals, and action items needed to achieve these goals.
SaO2 >92%
<ref name="isbn1616690003">{{cite book | author = | authorlink = | editor = | others = | title = Handbook of Emergency Cardiovascular Care for Healthcare Providers | edition = | language = | publisher = | location = | year = | origyear = | pages = | quote = | isbn = 1616690003 | oclc = | doi = | url = | accessdate = }}</ref><ref name="-2000">{{Cite journal  | title = Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 7: the era of reperfusion: section 1: acute coronary syndromes (acute myocardial infarction). The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. | journal = Circulation | volume = 102 | issue = 8 Suppl | pages = I172-203 | month = Aug | year = 2000 | doi =  | PMID = 10966673 }}</ref>
SvO2 >60%
{| style="cellpadding=0; cellspacing= 0; width: 1000px;"
ScvO2 >70%
|-
Urine output >0.5 mL/kg/h
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Preload'''
Lactate <2.2 mM/L
|colspan="3" style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center|'''Afterload''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Cardiac index'''
Hematocrit ≥30%
|-
 
|style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align=center| '''Goal: PCWP 15–18 mm Hg, CVP 8–12 cm H2O''' ||colspan="3" style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align=center|'''Goal: MAP >65 mm Hg, SVR 800–1200 dyn·s·cm−5'''|| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align=center|'''Goal: CI >2.2 L/min/m2'''
====Preload====
|-
 
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
Goal: PCWP 15–18 mm Hg, CVP 8–12 cm H2O
* Fluid challenge protocol ("TROL")
* Fluid challenge protocol ("TROL")
* ± Correct pulmonary congestion
* ± Correct [[pulmonary congestion]]
** Furosemide
** [[Furosemide]]
*** Usual dose: 40 mg slow IV injection
*** Usual dose: 40 mg slow IV injection
*** May increase dose to 80 mg after 1 hour as needed
*** May increase dose to 80 mg after 1 hour as needed
** Morphine
** [[Morphine]]
*** Usual dose: 2–4 mg slow IV injection
*** Usual dose: 2–4 mg slow IV injection
*** May repeat dose every 5–30 minutes as needed
*** May repeat dose every 5–30 minutes as needed
 
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''''If ↑ MAP & ↑ SVR:''''' <br>
====Afterload====
 
Goal: MAP >65 mm Hg, SVR 800–1200 dyn·s·cm−5
 
If ↑ MAP & ↑ SVR:
 
* Taper vasopressor
* Taper vasopressor
* ± Vasodilator
* ± Vasodilator
** Nitroglycerin
** [[Nitroglycerin]]
*** Initial dose: 5.0 μg/min
*** Initial dose: 5.0 μg/min
*** Titrate by 10–20 μg/min q 3–5 min
*** Titrate by 10–20 μg/min q 3–5 min
** Nitroprusside
** [[Nitroprusside]]
*** Initial dose: 0.3 μg/kg/min
*** Initial dose: 0.3 μg/kg/min
*** Usual dose: 3.0–5.0 μg/kg/min
*** Usual dose: 3.0–5.0 μg/kg/min
*** Maximum dose: 10 μg/kg/min
*** Maximum dose: 10 μg/kg/min
 
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''''If ↓ MAP & ↓ SVR:''''' <br>
If ↓ MAP & ↓ SVR:
* [[Vasopressor]]
* Vasopressor
** [[Norepinephrine]]
** Norepinephrine
*** Initial dose: 0.5–1.0 μg/min
*** Initial dose: 0.5–1.0 μg/min
*** Maximum dose: 30–40 μg/min
*** Maximum dose: 30–40 μg/min
*** Titrate to SBP >90 mm Hg
*** Titrate to SBP >90 mm Hg
** Dopamine
** [[Dopamine]]
*** Cardiac dose: 5.0–10 μg/kg/min
*** Cardiac dose: 5.0–10 μg/kg/min
*** Pressor dose: 10–20 μg/kg/min
*** Pressor dose: 10–20 μg/kg/min
*** Maximum dose: 20–50 μg/kg/min
*** Maximum dose: 20–50 μg/kg/min
** Phenylephrine
** [[Phenylephrine]]
*** Initial dose: 100–180 μg/min
*** Initial dose: 100–180 μg/min
*** Maintenance dose: 40–60 μg/min
*** Maintenance dose: 40–60 μg/min
** ± Vasopressin
** ± Vasopressin
*** Adjunctive therapy to norepinephrine or dopamine
*** Adjunctive therapy to [[norepinephrine]] or [[dopamine]]
*** Usual dose: 0.01–0.03 U/min
*** Usual dose: 0.01–0.03 U/min
*** Maximum dose: 0.04 U/min
*** Maximum dose: 0.04 U/min
 
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''''If ↓ MAP & ↑ SVR:''''' <br>
If ↓ MAP & ↑ SVR:
* Continue [[vasopressor]]
* Continue vasopressor
* Optimize [[cardiac output]] with inotropic agent
* Optimize cardiac output with inotropic agent
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
 
* [[Dobutamine]]
====Cardiac index====
 
Goal: CI >2.2 L/min/m2
 
* Dobutamine
** Usual dose: 2.0–20 μg/kg/min
** Usual dose: 2.0–20 μg/kg/min
** Maximum dose: 40 μg/kg/min
** Maximum dose: 40 μg/kg/min
** Avoid ↑ HR by >10% of baseline
** Avoid ↑ HR by >10% of baseline
* Milrinone
* [[Milrinone]]
** Loading dose: 50 μg/kg (slowly over 10 minutes)
** Loading dose: 50 μg/kg (slowly over 10 minutes)
** Maintenance dose: 0.375–0.75 μg/kg/min
** Maintenance dose: 0.375–0.75 μg/kg/min
|}


===Volume Management===
===Volume Management===

Latest revision as of 23:04, 11 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]; Rim Halaby, M.D. [3] Syed Musadiq Ali M.B.B.S.[4]

Overview

Cardiogenic shock is a medical emergency, rescusitive measures should be initiated immediately while the underlying etiology of the cardiogenic shock is promptly investigated. Myocardial infarction (MI) is the most common cause of cardiogenic shock, and when present, prompt revascularization should be performed. Other causes, such as free wall rupture, acute valvular abnormality, or left ventricular septum rupture, may require more invasive interventions. The management plan of cardiogenic shock includes the initiation of resuscitation and general measures, optimization of the blood pressure (pharmacological therapy or mechanical therapy when hypotension is refractory to inotrope and vasopressors), reperfusion or revascularization, and hemodynamic monitoring and stabilization. Urgent revascularization is a priority over hemodynamic monitoring in MI patients with cardiogenic shock and should not be delayed. The first line strategy for reperfusion is percutaneous coronary intervention which is preffered over coronary artery bypass graft (CABG), when PCI or CABG can not be perfomed, fibrinolytic therapy is indicated in the absence of any contraindications.

Medical Therapy

Goals of Therapy

Cardiogenic shock is characterized by low cardiac output, high left ventricular filling pressure, and decreased blood pressure with organ hypoperfusion. Goals of therapy:

  • Increase coronary blood flow
  • Decrease myocardial energy consumption
  • Increase systemic blood flow

Management Plan

  • Resuscitation and general measures
  • Optimization of the blood pressure
    • Pharmacological therapy
    • Mechanical therapy
  • Reperfusion or revascularization
  • Hemodynamic monitoring and stabilization

Resuscitation and General Measures

Resuscitation measures should be IMMEDIATELY initiated:

Optimization of the Blood Pressure

The goal of blood pressure optimization are to:

  • Improve coronary blood flow
  • Improve systemic reperfusion

The first line treatment to increase blood pressure in cardiogenic shock is the administration of pharmacological therapy with either ionotropes or vasopressors.[1] If pharmacological therapy fails to stabilize the patient's blood pressure, mechanical support must be provided.

Pharmacological Therapy

The appropriate choice of an inotrope or vasopressor requires the assessment of the balance between its desired and undesired effects:

  • Desired effects: ↑ cardiac output and ↓ left ventricular pressure
  • Undesired effects: ↑ myocardial energy consumption

All inotropes and vasopressors increase myocardial oxygen consumption to a certain extent. However, the benefit of their administration in the setting of a cardiogenic shock is achieved through counteracting the deleterious effects of hypotension. In cardiogenic shock, hypotension decreases myocardial perfusion and leads to compensatory elevation in LV filling pressure which in turn increases myocardial energy consumption. Therefore, the balance between desired and undesired effects of these agents necessitate their administration at the minimum efficacious dose.[2] There is no robust data that compares the efficacy of inotropes and vasopressors in improvement of cardiovascular outcomes and reduction in mortality.[3]

The two main agents used to optimize the blood pressure are Dopamine, dobutamine (mainly among non-sick patients), and norepinephrine (mainly among patients with severe hypotension). Alternative agents include phosphodiesterase inhibitors (amrinone or milrinone) and levosimendan. The choices of pharmacological agents is guided by the blood pressure and clinical status of the patient. There is no clear cut regarding the choice of the agents, combinations of moderate doses of different medications are commonly used instead of the administration of the maximal dose of any individual drug.[4]

Low Output without Shock

Dobutamine is the treatment of choice among non-sick patients with low output and preserved systolic blood pressure.

Low Output with Shock

Systolic Blood Pressure (SBP) > 70 or 80 mm Hg

Dobutamine is preferred over dopamine when the patient does not have symptoms:

  • Usual dose: 2.0–20 μg/kg/min
  • Maximum dose: 40 μg/kg/min
  • Avoid ↑ HR by >10% of baseline

Dopamine should be administered among symptomatic patients:

  • Cardiac dose: 5.0–10 μg/kg/min
  • Pressor dose: 10–20 μg/kg/min
  • Maximum dose: 20–50 μg/kg/min

Phosphodiesterase inhibitors (PDIs) such as milrinone and inamrinone (formerly known as amrinone) are not dependent upon the adrenoreceptor activity and patients may not develop tolerance, and they may be less likely to increase myocardial oxygen demands and risks of arrhythmia. However, the addition of a vasopressor is often required as these agents reduce preload and afterload. PDIs are more likely to be associated with tachyarrhythmias than dobutamine, significant vasodilation and hypotension.

Systolic Blood Pressure (SBP) < 70 or 80 mm Hg

Norepinephrine is indicated among patients with severe hypotension:

  • Initial dose: 0.5–1.0 μg/min
  • Maximum dose: 30–40 μg/min
  • Titrate to SBP >90 mm Hg

If norepinephrine does not generate a MAP of 60 mm Hg, then epinephrine can be added. Epinephrine increases both the stroke volume and heart rate, but is associated with an increased rate of lactic acidosis.

Mechanism of Action of Ionotropes and Vasopressors

Shown below is a table summarizing the different inotrope or vasopressor agents used in the setting of cardiogenic shock.[2][5]

Drug Alpha 1 Beta 1 Beta 2 Dopamine Effects
Norepinephrine +++ ++ + -
  • Minimal to moderate inotropic effect
  • Minimal chronotropic effect
  • Increase systolic and diastolic BP
  • Minimal impact on CO
  • Potent vasoconstriction
  • Increase coronary blood flow (increase diastolic BP)
Dopamine (dose---) ++ ++ - ++
  • Increase CO
  • Increase BP and SVR
  • Increase myocardial consumption
  • Increase renal perfusion and urine output
  • Peripheral vasoconstriction
  • Increases PCWP
Dobutamine + +++ ++ -
  • Increase CO
  • Increase myocardial contractility
  • Decrease LV filling pressure
  • Increase coronary flow during diastole
  • Increase collateral blood flow to ischemic regions
  • Vasoconstriction
  • Less arrythmogenic
Isoprotenerol - +++ +++ - * Positive inotrope
  • Positive chronotrope
  • Decrease coronary reperfusion
  • No effect of CO
  • Arrhythmogenic
  • Consider ONLY in patients with bradyarrhythmia as a bridge to temporary pacemaker
Phenylephrine +++ - - -
  • Reflex bradycardia
  • Vasoconstriction
Epinephrine +++ +++ ++ - * Arrythmogenic
  • Increase myocardial contractility

Phosphodiesterase inhibitors (milrinone, amrinone):

  • Potent ionotrope
  • Potent chronotrope
  • Vasodilation
  • Increase myocardial contractility

Vasopressin:

  • Act on V1 (vascular smooth muscle cells) and V2 (renal collecting duct system) receptors
  • May cause cardiac ischemia
  • Severe peripheral and splanchnic vasoconstriction

Levosimendan:

Mechanical Therapy

Mechanical therapy for cardiac shock involves the use of circulatory assist systems, which are different by:[6]

  • Mode of placement: percutaneous vs. surgical
  • Mode of circulatory support: LV, RV, or biventricular and/or volume unloading
  • Presence or absence of combined extracorporal membrane oxygenation (ECMO)

Intra-Aortic Balloon Pump (IABP)

As per the recommendation of the 2013 AHA/ACC guidelines, in the setting of acute MI complicated by cardiogenic shock refractory to pharmacological therapy, the placement of an intra-aortic balloon pump (IABP) (which reduces workload for the heart, and improves perfusion of the coronary arteries) should be considered (Class IIa, level of evidence B).[7]

The hemodynamic effects of IABP are:[8]

Despite IABP's favorable hemodymaic benefits, the survival benefit associated with the use of IABP is controversial. An analysis from the National Registry of Myocardial Infarction (NRMI) database indicates that in-hospital mortality rates are decreased at hospitals with higher rates of IABP insertion for cardiogenic shock complicating STEMI. The raw mortality was 65.4% at hopsitals in the lowest volume tertile (3.4 IABPs/year); 54.1% at hopsitals with intermediate volume (12.7 IABPs/year); and 50.6% for hospitals with the highest volume (37.4 IABPs/yr)(P for trend <0.001). This difference in mortality would yield 150 fewer deaths per 1000 patients treated at the high IABP hospitals. Even in a multivariate analysis, hospitals with the highest IABP volume had the lowest mortality (OR=0.71, 95% CI=0.56 to 0.90), independent of baseline patient characteristics, hospital factors, treatment, and procedures such as PTCA.[9] In the Euro Heart Survey on PCI among 654 MI patients with cardiogenic shock, the use of IABP was associated with non-statistically significant reduction in mortality.[10]

Clinical outcome studies also demonstrate conflicting results regarding the use of IABP and improved survival. In a Cochrane database systematic review among 190 patients, the use of IABP was not associated with a reduction in all-cause 30-day mortality (HR=1.04; 95% confidence interval 0.62–1.73).[11] In another meta-analysis of 9 cohorts (n = 10529), the use of IABP was associated with 18% decrease (p<0.0001) and and 6% increase (p<0.0008) in 30-day mortality among STEMI patients with cardiogenic shock treated with fibrinolytic therapy and those undergoing primary PCI, respectively. [12] In a meta-analysis of seven randomized trials among 1009 patient, IABP placement in STEMI was not associated with an improvement in mortality or in left ventricular function but was associated with a higher rate of stroke and bleeding. When data from non-randomized cohort studies were evaluated in a meta-analysis (n=10,529 STEMI patients with cardiogenic shock), IABP placement was associated with an 18% relative risk reduction in 30 day mortality among patients treated with a fibrinolytic agent. This particular analysis is confounded by the fact that those patients in whom an IABP was placed underwent adjunctive percutaneous intervention (PCI) more frequently. In this non-randomized cohort analysis, IABP placement in patients undergoing primary angioplasty was associated with a 6% relative increase in mortality (p<0.0008). Thus, neither randomized nor observational data support IABP placement in the setting of primary PCI for cardiogenic shock, and careful consideration should be given to the risk of stroke and bleeding prior to IABP placement in this population.[12]

Left Ventricular Assist Device (LVAD)

As per the recommendation of the 2013 AHA/ACC guidelines, in the setting of pronounced hypotension refractory to medical therapy and IABP placement, placement of a left ventricular assist device (LVAD) should be considered.[7] A ventricular assist device should only be placed in those patients in whom the cardiogenic shock is deemed to be reversible or if it is being used as a bridge option.[13]

The hemodynamic effects of LVAD are superior to those of IABP:[6]

Despite the superiority of hemodynamic support of LVAD compared to IABP, the use of LVAD is limited by the high risk of complications (such as bleeding), the complexity of insertion, and the absence of data regarding survival benefit.[6] According to a metanalysis of 3 controlled trials (two trials on the TandemHeart and one trial on the Impella device), the use of LVAD was associated with a superior hemodynamic support without a reduction in 30-day mortality (RR=1.06, 95% CI 0.68–1.66).[14]

Extracorporeal Membrane Oxygenation (ECMO)

Hemodynamic effects of extracorporeal membrane oxygenation (ECMO):[6]

ECMO use is associated with complications such as bleeding, renal failure, and systemic inflammatory response syndrome.[6]

Urgent Revascularization

If the patient has an ST elevation myocardial infarction complicated by cardiogenic shock, then primary angioplasty should be performed to restore flow to the culprit artery irrespective of time delay since the onset of symptoms (Class I, level of evidence B).[7] Consideration should also be given to restoration of flow in the non-culprit territories in the setting of cardiogenic shock. Patients with MI complicated by cardiogenic shock who initially present to a hospital where PCI is not available should be urgently transferred to another PCI-capable healthcare facility (Class I, level of evidence B).[7][15] Urgent revascularization is a priority over hemodynamic monitoring in MI patients with cardiogenic shock and should not be delayed.

Urgent revascularization can be achieved through one of the following:

PCI is the first line revascularization strategy among MI patients with cardiogenic shock. CABG in the setting of cardiogenic shock is associated with high rates of mortality and morbidity, therefore if primary angioplasty can be performed successfully, CABG is preferably avoided. When PCI or CABG can not be perfomed, fibrinolytic therapy is indicated in the absence of any contraindications.[7][16][17][18]

Hemodynamic Monitoring and Stabilization

Hemodynamic Monitoring

The aim of hemodynamic monitoring is to assess the response to treatment and monitor and guide the doses of the inotropes and vasopressors.

Target endpoints are:

  • Mean arterial pressure (MAP) of 60 to 65 mmHg
  • SaO2 >92%
  • SvO2 >60%
  • ScvO2 >70%
  • Urine output >0.5 mL/kg/h
  • Lactate <2.2 mM/L
  • Hematocrit ≥30%

Shown below is a table summarizing the different parameters of hemodynamic monitoring, their target goals, and action items needed to achieve these goals. [19][20]

Preload Afterload Cardiac index
Goal: PCWP 15–18 mm Hg, CVP 8–12 cm H2O Goal: MAP >65 mm Hg, SVR 800–1200 dyn·s·cm−5 Goal: CI >2.2 L/min/m2
  • Fluid challenge protocol ("TROL")
  • ± Correct pulmonary congestion
    • Furosemide
      • Usual dose: 40 mg slow IV injection
      • May increase dose to 80 mg after 1 hour as needed
    • Morphine
      • Usual dose: 2–4 mg slow IV injection
      • May repeat dose every 5–30 minutes as needed
If ↑ MAP & ↑ SVR:
  • Taper vasopressor
  • ± Vasodilator
    • Nitroglycerin
      • Initial dose: 5.0 μg/min
      • Titrate by 10–20 μg/min q 3–5 min
    • Nitroprusside
      • Initial dose: 0.3 μg/kg/min
      • Usual dose: 3.0–5.0 μg/kg/min
      • Maximum dose: 10 μg/kg/min
If ↓ MAP & ↓ SVR:
  • Vasopressor
    • Norepinephrine
      • Initial dose: 0.5–1.0 μg/min
      • Maximum dose: 30–40 μg/min
      • Titrate to SBP >90 mm Hg
    • Dopamine
      • Cardiac dose: 5.0–10 μg/kg/min
      • Pressor dose: 10–20 μg/kg/min
      • Maximum dose: 20–50 μg/kg/min
    • Phenylephrine
      • Initial dose: 100–180 μg/min
      • Maintenance dose: 40–60 μg/min
    • ± Vasopressin
If ↓ MAP & ↑ SVR:
  • Dobutamine
    • Usual dose: 2.0–20 μg/kg/min
    • Maximum dose: 40 μg/kg/min
    • Avoid ↑ HR by >10% of baseline
  • Milrinone
    • Loading dose: 50 μg/kg (slowly over 10 minutes)
    • Maintenance dose: 0.375–0.75 μg/kg/min

Volume Management

The goal of managing the patient with cardiogenic shock is to optimize the filling of the left ventricle so that the Starling relationship and mechanical performance and contractility of the heart is optimized. In the setting of acute MI, a pulmonary capillary wedge pressure of 18 to 20 mm Hg may optimize left ventricular filling. Filling pressures higher than this may lead to LV dilation, and poorer left ventricular function.

Even though, there is adequate intravascular volume in cardiogenic shock, fluid administration should be considered in patients with cardiogenic shock following acute MI because patients are often diaphoretic with subsequent relative hypovolemia.[21][22]

Contraindicated Medications

Cardiogenic shock is considered an absolute contraindication to the use of the following medications:

2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)[7]

General and Specific Considerations (DO NOT EDIT)[7][23]

Class I
"1. Primary PCI should be performed for patients less than 75 years old with ST elevation or presumably new left bundle-branch block who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock, unless further support is futile because of the patient’s wishes or contraindications/unsuitability for further invasive care. (Level of Evidence: A)"
"7. Primary PCI should be performed in patients with STEMI and cardiogenic shock or acute severe HF, irrespective of time delay from myocardial infarction (MI) onset.[24][25][26] (Level of Evidence: B)"


Class IIa
"1. Primary PCI is reasonable for selected patients 75 years or older with ST elevation or left bundle-branch block or who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock. Patients with good prior functional status who are suitable for revascularization and agree to invasive care may be selected for such an invasive strategy. (Level of Evidence: B)"

Treatment of Cardiogenic Shock in Patients with STEMI (DO NOT EDIT)[7]

Class I
"1. Emergency revascularization with either PCI or CABG is recommended in suitable patients with cardiogenic shock due to pump failure after STEMI irrespective of the time delay from MI onset.[24][27][28] (Level of Evidence: B)"
"2. In the absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI and cardiogenic shock who are unsuitable candidates for either PCI or CABG.[29][30][16] (Level of Evidence: B)"
Class IIa
"1. The use of intra-aortic balloon pump counterpulsation can be useful for patients with cardiogenic shock after STEMI who do not quickly stabilize with pharmacological therapy.[31][9][32][12][33] (Level of Evidence: B)"
Class IIb
"1. Alternative left ventricular (LV) assist devices for circulatory support may be considered in patients with refractory cardiogenic shock. (Level of Evidence: C)"

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