Cardiogenic shock medical therapy: Difference between revisions

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__NOTOC__
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{{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 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==
==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, the main two choices being [[dopamine]] 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====
=====Systolic blood pressure (SBP) > 80 mm Hg=====
[[Dobutamine]] may be preferable over [[dopamine]] at this blood pressure. Dopamine increase contractility and heart rate and thereby increases myocardial oxygen demand. [[Dobutamine]] reduces the [[systemic vascular resistance]] and may not increase oxygen demands as much as dopamine, and is preferable at this systolic blood pressure. [[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. 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]].


=====Systolic blood pressure (SBP) < 80 mm Hg=====
=====''Systolic Blood Pressure (SBP) > 70 or 80 mm Hg''=====
At systolic blood pressures < 80 mm Hg dopamine should be initiated first.  The patient may not tolerate the vasodilating effects of dobutamine at this blood pressure. The initial dose of dopamine is 5 to 10 mcg/kg/min.
[[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


If the dopamine at doses of 20 mcg/kg/min does not achieve a MAP of 60-65 mm Hg, then norepinephrine can be added at an initial dose of 0.5 mcg/kg/min which can then be titrated up to 3.3 mcg/kg/min. Norepinephrine is avoided as a first line agent because of its adverse impact upon renal perfusion.
[[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


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]]
[[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''=====
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====
====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>
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'''
|-
|-
| '''Norepinephrine'''|| +++ || ++ || - || - ||  
| 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'''
|-
|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
Line 80: Line 91:
* 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
Line 88: Line 99:
* 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
Line 97: Line 108:
* 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
Line 105: Line 115:
* Consider ONLY in patients with [[bradyarrhythmia]] as a bridge to temporary [[pacemaker]]
* Consider ONLY in patients with [[bradyarrhythmia]] as a bridge to temporary [[pacemaker]]
|-
|-
| '''Phosphodiesterase inhibitors''' || || || || ||  
| 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
* Vasoconstriction
|-
| 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
* Increase myocardial contractility
|-
|}
 
Phosphodiesterase inhibitors (milrinone, amrinone):
* Potent ionotrope
* Potent ionotrope
* Potent chronotrope
* Potent chronotrope
* Vasodilation
* Vasodilation
* Increase myocardial contractility
* Increase myocardial contractility
|}
====Mechanical Therapy====
====Intra-aortic balloon placement====
In the setting of acute MI, the placement of an [[intra-aortic balloon pump]] (which reduces [[afterload|workload]] for the heart, and improves perfusion of the [[coronary arteries]]) should be considered. 
A meta-analysis of randomized trial data, however, challenges this common practice and class 1B recommendation.<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>  In a meta-analysis of seven randomized trials enrolling 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.
====Left ventricular assist device placement====
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.  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>
==Urgent Revascularization==
If the patient has an [[ST elevation myocardial infarction]], then [[primary angioplasty]] should be considered to restore flow to the culprit artery. Consideration should also be given to restoration of flow in the non-culprit territories in the setting of cardiogenic shock. 
Urgent revascularization can be achieved through one of the following:
* [[Percutaneous coronary intervention]] ([[PCI]])
* [[Coronary artery bypass graft]] ([[CABG]])
* [[Fibrinolytic therapy]]


Urgent revascularization is a priority over hemodynamic monitoring in MI patients and should not be delayed. [[PCI]] or [[CABG]] are indicated among MI patients with cardiogenic shock.  When [[PCI]] or [[CABG]] can not be perfomed, [[fibrinolytic therapy]] is indicated in the absence of any [[contraindications]].<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><ref name="Fath-OrdoubadiBeatt1994">{{cite journal|last1=Fath-Ordoubadi|first1=F.|last2=Beatt|first2=Kj|last3=Davis|first3=R.C.|last4=Carlsson|first4=Jörg|last5=Rahlf|first5=Günther|last6=Tebbe|first6=Ulrich|title=Fibrinolytic therapy in suspected acute myocardial infarction|journal=The Lancet|volume=343|issue=8902|year=1994|pages=912–913|issn=01406736|doi=10.1016/S0140-6736(94)90029-9}}</ref>
Vasopressin:
<ref name="MorrowAntman2000">{{cite journal|last1=Morrow|first1=D. A.|last2=Antman|first2=E. M.|last3=Charlesworth|first3=A.|last4=Cairns|first4=R.|last5=Murphy|first5=S. A.|last6=de Lemos|first6=J. A.|last7=Giugliano|first7=R. P.|last8=McCabe|first8=C. H.|last9=Braunwald|first9=E.|title=TIMI Risk Score for ST-Elevation Myocardial Infarction: A Convenient, Bedside, Clinical Score for Risk Assessment at Presentation : An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy|journal=Circulation|volume=102|issue=17|year=2000|pages=2031–2037|issn=0009-7322|doi=10.1161/01.CIR.102.17.2031}}</ref><ref name="pmid14597928">{{cite journal| author=French JK, Feldman HA, Assmann SF, Sanborn T, Palmeri ST, Miller D et al.| title=Influence of thrombolytic therapy, with or without intra-aortic balloon counterpulsation, on 12-month survival in the SHOCK trial. | journal=Am Heart J | year= 2003 | volume= 146 | issue= 5 | pages= 804-10 | pmid=14597928 | doi=10.1016/S0002-8703(03)00392-2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14597928  }} </ref>  Administration of [[streptokinase]] therapy to patients with cardiogenic shock has not been associated with an improvement in survival.<ref name="pmid2868337">{{cite journal |author= |title=Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) |journal=Lancet |volume=1 |issue=8478 |pages=397–402 |year=1986 |month=February |pmid=2868337 |doi= |url=}}</ref> Yet, these studies are old and limited by the infrequent use of [[adjunctive PCI]].  If a patient is not deemed a candidate for [[primary angioplasty]], then consideration should be given to fibrinolyitc administration.
* Act on V1 (vascular smooth muscle cells) and V2 (renal collecting duct system) receptors
* May cause cardiac ischemia
* Severe peripheral and splanchnic vasoconstriction


==Hemodynamic Monitoring and Stabilization==
Levosimendan:
* Used mainly in decompensated [[heart failure]]


===Hemodynamic Monitoring===
===Mechanical Therapy===
If hypotension persists despite adequate left ventricular filling pressures, then the addition of vasconstrictors and/or inotropes is suggested.  Hemodynamic monitoring is essential to assure that a target [[mean arterial pressure]] ([[MAP]]) of 60 to 65 mmHg is achieved to maintain perfusion to vital organs (brain, kidney, heart).
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 circulatory support: LV, RV, or biventricular and/or volume unloading
* Presence or absence of combined extracorporal membrane oxygenation (ECMO)


===Volume Management===
====Intra-Aortic Balloon Pump (IABP)====
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.   
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.
</ref>
* ↑ [[stroke volume]] and [[cardiac output]]
* ↑ systemic [[blood pressure]]
* ↑ coronary blood flow
* ↓ [[myocardial]] oxygen consumption
* ↓ [[pulmonary capillary wedge pressure]]


===Volume Management===
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.<ref name="pmid12912817">{{cite journal |author=Chen EW, Canto JG, Parsons LS, ''et al'' |title=Relation between hospital intra-aortic balloon counterpulsation volume and mortality in acute myocardial infarction complicated by cardiogenic shock |journal=Circulation |volume=108 |issue=8 |pages=951–7 |year=2003 |month=August |pmid=12912817 |doi=10.1161/01.CIR.0000085068.59734.E4 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=12912817}}</ref> 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.<ref name="pmid21764661">{{cite journal| author=Zeymer U, Bauer T, Hamm C, Zahn R, Weidinger F, Seabra-Gomes R et al.| title=Use and impact of intra-aortic balloon pump on mortality in patients with acute myocardial infarction complicated by cardiogenic shock: results of the Euro Heart Survey on PCI. | journal=EuroIntervention | year= 2011 | volume= 7 | issue= 4 | pages= 437-41 | pmid=21764661 | doi=10.4244/EIJV7I4A72 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21764661 }} </ref>
Even though, by definition cardiogenic shock's etiology resides in a [[heart]] problem with adequate [[intravascular]] volume, fluid administration should be considered in patients with CS following [[acute MI]], since these are often [[diaphoretic]] and relative [[hypovolemia]] may be present.<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref><ref name="pmid16088508">{{cite journal| author=Hollenberg SM| title=Recognition and treatment of cardiogenic shock. | journal=Semin Respir Crit Care Med | year= 2004 | volume= 25 | issue= 6 | pages= 661-71 | pmid=16088508 | doi=10.1055/s-2004-860980 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16088508 }} </ref> The goal of managing the patient with cardiogenic shock is to optimize the filling of the [[left ventricle]] so that the [[starling relationship]], mechanical performance and [[contractility]] of the [[heart]] are 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 [[LV]] function.


There are different approaches to volume management, yet some critical elements should be present in every one of them, such as: constant deliverance of [[oxygen]], thereby ensuring adequate [[arterial oxygen saturation]] at all times; [[titration]] of the treatment to specific clinical endpoints of volume repletion and therapy guided by parameters that represent tissue and organ [[perfusion]].<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</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>


===Pharmacologic Hemodynamic Support===
====Left Ventricular Assist Device (LVAD)====
According to the recommendations of the [[AHA]]/[[ACC]] guidelines, in the case of cardiogenic shock complicating [[acute MI]], the most common cause of [[cardiogenic shock|CS]], [[pharmacological]] therapy with [[vasopressor]] and [[inotropic]] [[drugs]], stands as a mainstay in the management of these patients.<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> [[Hemodynamic]] monitoring is essential to assure that a target [[mean arterial pressure]] ([[MAP]]) of 60 to 65 mmHg is achieved, in order to maintain [[perfusion]] of [[vital organ]]s, such as the [[brain]], [[kidney]] and [[heart]], as well as to monitor and guide the effects and [[doses]] of the treatment [[drugs]]. The main purpose of this [[hemodynamic]] therapy is to restore adequate [[tissue]] [[perfusion]] and to normalize the [[cellular metabolism]].<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref> However, due to the significant [[toxicity]] of these [[drugs]], they should be given in [[doses]] as minimal as possible. This [[toxicity]] may be translated into short and long-term [[adverse effects]], such as activation of pro-[[apoptotic]] signaling cascades, [[mitochondrial]] damage or [[membrane]] disruption and [[necrosis]], following increases of already elevated [[cytosolic]] [[calcium]] levels in [[ischemia|postischemic]] [[cardiac myocytes]], after administration of [[dopamine]].<ref name="pmid12354748">{{cite journal| author=Stamm C, Friehs I, Cowan DB, Cao-Danh H, Choi YH, Duebener LF et al.| title=Dopamine treatment of postischemic contractile dysfunction rapidly induces calcium-dependent pro-apoptotic signaling. | journal=Circulation | year= 2002 | volume= 106 | issue= 12 Suppl 1 | pages= I290-8 | pmid=12354748 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12354748  }} </ref> When choosing the [[dose|dosages]] and [[medications]] to use, it is better to choose combinations of moderate [[doses]] of different [[medications]], than to use 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>
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>


Although a definitive approach to evaluate the adequacy of global [[perfusion]] and determine the adequate administration and [[titration]] of certain [[vasoactive]] [[medications]], and proper volume manipulation, are yet to be established, this evaluation may be done by targeting:<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><ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</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>
:*a particular [[MAP]]
* ↑ [[cardiac output]]
:*an increase in [[cardiac output]]
* ↑ mean arterial pressure
:*bed-side clinical assessment by evaluating indices of organ [[perfusion]], such as [[urine]] output and [[lactate]] levels while maintaining adequate [[oxygenation]]
* ↓ [[pulmonary capillary wedge pressure]]
* ↓ central venous pressure
* ↓ pulmonary arterial pressure
* ↓ filling pressures in the [[left ventricle|left]] and [[right ventricle]]
* ↓ myocardial oxygen demand


*'''Selection of a Vasopressor or an Inotrope''' - In the clinical setting, patients are usually treated with a combination of [[vasopressors]] and [[inotropes]]. However, generally and according to the [[AHA]]/[[ACC]] guidelines:<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>
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>
:*''Low-Output Syndrome without Shock'' - Patients presenting in this setting should be started on an [[inotrope]], such as [[dobutamine]].
:*''Low-Output Syndrome with Shock'' - Patients presenting in this setting should be started on a [[vasopressor]], such as [[dopamine]], or in case of [[systolic blood pressure]] inferior to 70 mm Hg, [[norepinephrine]] should be started instead.
Attending to the fact that many [[vasoactive]] [[drugs]] have both [[inotropic]] and [[vasopressor]] actions, the selection of the adequate [[drug]] will depend on the target parameters to approach in each patient, since different [[drugs]] will work on different [[receptors]] and locations, therefore resulting in different actions. [[Vasoconstrictive]] [[drugs]] commonly aim at restoration of adequate [[arterial pressure]], while [[inotropic]] [[drugs]] aim at increasing the [[cardiac output]]. The individual patient scenario is of extreme importance, since for instance: tissue [[hypoperfusion]] may occur in different settings, such as abnormal [[shunting]] of [[blood]] within organs, decreased [[perfusion]] or inability to deliver substrates to peripheral [[cells]], which may justify the failure of certain therapies that aim for global [[hemodynamics]].<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref><ref>{{Cite book  | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages =  }}</ref><ref name="pmid10446833">{{cite journal| author=Ince C, Sinaasappel M| title=Microcirculatory oxygenation and shunting in sepsis and shock. | journal=Crit Care Med | year= 1999 | volume= 27 | issue= 7 | pages= 1369-77 | pmid=10446833 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10446833 }} </ref><ref name="pmid12493070">{{cite journal| author=Fink MP| title=Bench-to-bedside review: Cytopathic hypoxia. | journal=Crit Care | year= 2002 | volume= 6 | issue= 6 | pages= 491-9 | pmid=12493070 | doi= | pmc=PMC153437 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12493070 }} </ref>


====Vasopressors====
====Extracorporeal Membrane Oxygenation (ECMO)====
The main goal of [[vasopressors|vasopressor therapy]] is to reach an adequate [[arterial pressure]] in order to maintain [[perfusion]] to vital organs, when in the presence of severe [[hypotension]] with [[shock]]. It is important to notice that [[hypotension]] alone may not require [[vasopressors|vasopressor therapy]]. Treatment should be initiated once fluid administration is shown to be insufficient to reach adequate [[blood pressure|pressures]].<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref><ref name="pmid15343024">{{cite journal| author=Hollenberg SM, Ahrens TS, Annane D, Astiz ME, Chalfin DB, Dasta JF et al.| title=Practice parameters for hemodynamic support of sepsis in adult patients: 2004 update. | journal=Crit Care Med | year= 2004 | volume= 32 | issue= 9 | pages= 1928-48 | pmid=15343024 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15343024  }} </ref> [[Vasopressors]] have different funtions in the different types of [[shock]], however, in the cardiogenic type, since [[hypotension]] may exacerbate the underlying [[myocardial ischemia]], [[vasopressors]] should be administered in order to maintain capable [[coronary]] [[perfusion pressure]]. <ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref> Potential [[vasopressors|vasopressor drugs]] include:
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>
*'''[[Vasopressin]]''' - a [[peptide hormone]] synthesized in the [[hypothalamus]] and stored in the [[pituitary gland]] that is released in response to low [[blood volume]] or increased [[plasma osmolarity]]. Under [[physiological]] conditions, normal values of [[vasopressin]] do not have a great impact on [[blood pressure]], yet, in cases of [[hypovolemia]] and/or [[shock]], it helps in the maintenance of [[blood pressure]] and in the recovery of impaired [[hemodynamic]] mechanisms, as well as in the inhibition of pathological [[vascular]] responses.<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref><ref name="pmid11555538">{{cite journal| author=Holmes CL, Patel BM, Russell JA, Walley KR| title=Physiology of vasopressin relevant to management of septic shock. | journal=Chest | year= 2001 | volume= 120 | issue= 3 | pages= 989-1002 | pmid=11555538 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11555538  }} </ref><ref name="pmid16436769">{{cite journal| author=Barrett BJ, Parfrey PS| title=Clinical practice. Preventing nephropathy induced by contrast medium. | journal=N Engl J Med | year= 2006 | volume= 354 | issue= 4 | pages= 379-86 | pmid=16436769 | doi=10.1056/NEJMcp050801 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16436769  }} </ref><ref name="pmid2242439">{{cite journal| author=Abboud FM, Floras JS, Aylward PE, Guo GB, Gupta BN, Schmid PG| title=Role of vasopressin in cardiovascular and blood pressure regulation. | journal=Blood Vessels | year= 1990 | volume= 27 | issue= 2-5 | pages= 106-15 | pmid=2242439 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2242439  }} </ref> It acts by: stimulating directly V1 [[receptors]], thereby inducing [[constriction]] of [[vascular smooth muscle]], increasing the responsiveness of [[blood vessels]] to [[catecholamines]]; and by inhibiting [[nitric oxide]] production in [[vascular smooth muscle]] and k1-ATP channels.<ref name="pmid11555538">{{cite journal| author=Holmes CL, Patel BM, Russell JA, Walley KR| title=Physiology of vasopressin relevant to management of septic shock. | journal=Chest | year= 2001 | volume= 120 | issue= 3 | pages= 989-1002 | pmid=11555538 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11555538  }} </ref><ref name="pmid16436769">{{cite journal| author=Barrett BJ, Parfrey PS| title=Clinical practice. Preventing nephropathy induced by contrast medium. | journal=N Engl J Med | year= 2006 | volume= 354 | issue= 4 | pages= 379-86 | pmid=16436769 | doi=10.1056/NEJMcp050801 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16436769  }} </ref> This increased responsiveness to [[catecholamines]] is useful in the way that initiation of [[vasopressin]] leads to a decrease in the dosage of [[catecholamines]] needed to achieve the same or a better [[blood pressure]] control.<ref name="pmid11873030">{{cite journal| author=Patel BM, Chittock DR, Russell JA, Walley KR| title=Beneficial effects of short-term vasopressin infusion during severe septic shock. | journal=Anesthesiology | year= 2002 | volume= 96 | issue= 3 | pages= 576-82 | pmid=11873030 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11873030  }} </ref><ref name="pmid12732600">{{cite journal| author=Dünser MW, Mayr AJ, Ulmer H, Knotzer H, Sumann G, Pajk W et al.| title=Arginine vasopressin in advanced vasodilatory shock: a prospective, randomized, controlled study. | journal=Circulation | year= 2003 | volume= 107 | issue= 18 | pages= 2313-9 | pmid=12732600 | doi=10.1161/01.CIR.0000066692.71008.BB | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12732600 }} </ref>
* ↓ [[left ventricular]] preload
*'''[[Phenylephrine]]''' - a short-acting and rapid onset α1-[[adrenerghic agonist]]. Its primary [[vasoactive]] effects, increasing [[blood pressure]], make it valuable in the management of [[hypotension]], however, its potential effect to reduce [[cardiac output]] may limit its use. Although some studies indicate [[phenylephrine]] to be of use in raising [[blood pressure]] of fluid-resuscitated patients, the lack of studies to confirm and understand its effects make it a second-line [[drug]]. Another potential benefit of [[phenylephrine]] is that it can be used patients suffering from [[tachyarrhythmias]] due to other [[vasopressor]] use, either in addition or as an alternative [[drug]].<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref>
* ↑ [[left ventricular]] afterload
*'''[[Epinephrine]]''' - an [[hormone]] produced in the [[chromaffin cells]] of the [[adrenal medulla|medulla]] of the [[adrenal glands]] that works as a strong α and β [[adrenergic]] agent. It increases the [[arterial pressure]] by working both on [[vascular]] tone and [[cardiac index]], increasing them. It also increases [[oxygen]] delivery, nevertheless, the increase in [[muscular]] activity may also lead to an increased [[oxygen]] consumption and [[lactate]] production.<ref name="pmid2012297">{{cite journal| author=Lipman J, Roux A, Kraus P| title=Vasoconstrictor effects of adrenaline in human septic shock. | journal=Anaesth Intensive Care | year= 1991 | volume= 19 | issue= 1 | pages= 61-5 | pmid=2012297 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2012297  }} </ref><ref name="pmid1463175">{{cite journal| author=Wilson W, Lipman J, Scribante J, Kobilski S, Lee C, Krause P et al.| title=Septic shock: does adrenaline have a role as a first-line inotropic agent? | journal=Anaesth Intensive Care | year= 1992 | volume= 20 | issue= 4 | pages= 470-4 | pmid=1463175 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1463175  }} </ref><ref name="pmid8420733">{{cite journal| author=Moran JL, O'Fathartaigh MS, Peisach AR, Chapman MJ, Leppard P| title=Epinephrine as an inotropic agent in septic shock: a dose-profile analysis. | journal=Crit Care Med | year= 1993 | volume= 21 | issue= 1 | pages= 70-7 | pmid=8420733 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8420733  }} </ref><ref name="pmid2037723">{{cite journal| author=Mackenzie SJ, Kapadia F, Nimmo GR, Armstrong IR, Grant IS| title=Adrenaline in treatment of septic shock: effects on haemodynamics and oxygen transport. | journal=Intensive Care Med | year= 1991 | volume= 17 | issue= 1 | pages= 36-9 | pmid=2037723 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2037723  }} </ref><ref name="pmid9255647">{{cite journal| author=Le Tulzo Y, Seguin P, Gacouin A, Camus C, Suprin E, Jouannic I et al.| title=Effects of epinephrine on right ventricular function in patients with severe septic shock and right ventricular failure: a preliminary descriptive study. | journal=Intensive Care Med | year= 1997 | volume= 23 | issue= 6 | pages= 664-70 | pmid=9255647 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9255647  }} </ref><ref name="pmid8684198">{{cite journal| author=Day NP, Phu NH, Bethell DP, Mai NT, Chau TT, Hien TT et al.| title=The effects of dopamine and adrenaline infusions on acid-base balance and systemic haemodynamics in severe infection. | journal=Lancet | year= 1996 | volume= 348 | issue= 9022 | pages= 219-23 | pmid=8684198 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8684198  }} </ref> Even though [[epinephrine]] is able to increase [[blood pressure]] in patients unresponsive to other drugs, it has the potential to induce [[ischemia]], [[tachyarrhythmias]] and [[hypoglycemia]]. These conditions, together with its tendency to increase [[lactate]] levels and its effects in [[gastric]] [[blood flow]] make this [[drug]] a second line therapy.<ref name="pmid15343024">{{cite journal| author=Hollenberg SM, Ahrens TS, Annane D, Astiz ME, Chalfin DB, Dasta JF et al.| title=Practice parameters for hemodynamic support of sepsis in adult patients: 2004 update. | journal=Crit Care Med | year= 2004 | volume= 32 | issue= 9 | pages= 1928-48 | pmid=15343024 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15343024  }} </ref>
* ↑ myocardial oxygen demand
*'''[[Dopamine]]''' - [[precursor]] [[catecholamine]] of [[norepinephrine]] and [[epinephrine]], increases [[cardiac output]] and [[arterial pressure]], particularly due to the increase in [[stroke volume]].<ref name="pmid7933396">{{cite journal| author=Marik PE, Mohedin M| title=The contrasting effects of dopamine and norepinephrine on systemic and splanchnic oxygen utilization in hyperdynamic sepsis. | journal=JAMA | year= 1994 | volume= 272 | issue= 17 | pages= 1354-7 | pmid=7933396 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7933396  }} </ref><ref name="pmid8370292">{{cite journal| author=Ruokonen E, Takala J, Kari A, Saxén H, Mertsola J, Hansen EJ| title=Regional blood flow and oxygen transport in septic shock. | journal=Crit Care Med | year= 1993 | volume= 21 | issue= 9 | pages= 1296-303 | pmid=8370292 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8370292  }} </ref><ref name="pmid8404107">{{cite journal| author=Martin C, Papazian L, Perrin G, Saux P, Gouin F| title=Norepinephrine or dopamine for the treatment of hyperdynamic septic shock? | journal=Chest | year= 1993 | volume= 103 | issue= 6 | pages= 1826-31 | pmid=8404107 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8404107  }} </ref> It has the characteristic of having distinct [[pharmacological]] effects according to the [[dose]]:
:*< 5 mg/kg/minute - [[vasodilation]] in [[mesenteric]] and [[renal]] regions<ref name="pmid9468162">{{cite journal| author=Hoogenberg K, Smit AJ, Girbes AR| title=Effects of low-dose dopamine on renal and systemic hemodynamics during incremental norepinephrine infusion in healthy volunteers. | journal=Crit Care Med | year= 1998 | volume= 26 | issue= 2 | pages= 260-5 | pmid=9468162 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9468162  }} </ref>
:*≥ 5 and ≤ 10 mg/kg/minute - increase in [[cardiac contractility]] and [[heart rate]]
:*≥ 10 mg/kg/minute -  [[arterial]] [[vasoconstriction]] and increase in [[blood pressure]]
However, especially in critically ill patients, these effects may overlap. Other adverse effects include: [[immunosuppression]] from [[lymphocyte]] [[apoptosis]]; common [[arrhythmic]] effects of [[catecholamines]] that appear to be more prominent with the use of [[dopamine]]; and potential decrease in [[prolactin]] release.<ref name="pmid8797634">{{cite journal| author=Van den Berghe G, de Zegher F| title=Anterior pituitary function during critical illness and dopamine treatment. | journal=Crit Care Med | year= 1996 | volume= 24 | issue= 9 | pages= 1580-90 | pmid=8797634 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8797634  }} </ref><ref name="pmid16583219">{{cite journal| author=Oberbeck R, Schmitz D, Wilsenack K, Schüler M, Husain B, Schedlowski M et al.| title=Dopamine affects cellular immune functions during polymicrobial sepsis. | journal=Intensive Care Med | year= 2006 | volume= 32 | issue= 5 | pages= 731-9 | pmid=16583219 | doi=10.1007/s00134-006-0084-y | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16583219  }} </ref>
*'''[[Norepinephrine]]''' - a strong α [[agonist]] and less pronounced β [[agonist]], that increases [[arterial pressure]] mainly by [[vasoconstriction]], with a lesser contribution from [[cardiac output]] (10-15%), without causing deterioration of [[cardiac function]].<ref name="pmid2520533">{{cite journal| author=Desjars P, Pinaud M, Bugnon D, Tasseau F| title=Norepinephrine therapy has no deleterious renal effects in human septic shock. | journal=Crit Care Med | year= 1989 | volume= 17 | issue= 5 | pages= 426-9 | pmid=2520533 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2520533  }} </ref><ref name="pmid2389659">{{cite journal| author=Martin C, Saux P, Eon B, Aknin P, Gouin F| title=Septic shock: a goal-directed therapy using volume loading, dobutamine and/or norepinephrine. | journal=Acta Anaesthesiol Scand | year= 1990 | volume= 34 | issue= 5 | pages= 413-7 | pmid=2389659 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2389659  }} </ref> It is considered a first-line [[vasopressor]] in the treatment of patients with [[shock]]. The required dosages for the desired effect may vary greatly, possibly because of a downregulation of [[α-receptors]] in some tissues.<ref name="pmid2389659">{{cite journal| author=Martin C, Saux P, Eon B, Aknin P, Gouin F| title=Septic shock: a goal-directed therapy using volume loading, dobutamine and/or norepinephrine. | journal=Acta Anaesthesiol Scand | year= 1990 | volume= 34 | issue= 5 | pages= 413-7 | pmid=2389659 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2389659  }} </ref><ref name="pmid2721267">{{cite journal| author=Schreuder WO, Schneider AJ, Groeneveld AB, Thijs LG| title=Effect of dopamine vs norepinephrine on hemodynamics in septic shock. Emphasis on right ventricular performance. | journal=Chest | year= 1989 | volume= 95 | issue= 6 | pages= 1282-8 | pmid=2721267 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2721267  }} </ref><ref name="pmid8315122">{{cite journal| author=Redl-Wenzl EM, Armbruster C, Edelmann G, Fischl E, Kolacny M, Wechsler-Fördös A et al.| title=The effects of norepinephrine on hemodynamics and renal function in severe septic shock states. | journal=Intensive Care Med | year= 1993 | volume= 19 | issue= 3 | pages= 151-4 | pmid=8315122 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8315122  }} </ref><ref name="pmid8370292">{{cite journal| author=Ruokonen E, Takala J, Kari A, Saxén H, Mertsola J, Hansen EJ| title=Regional blood flow and oxygen transport in septic shock. | journal=Crit Care Med | year= 1993 | volume= 21 | issue= 9 | pages= 1296-303 | pmid=8370292 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8370292  }} </ref><ref name="pmid9083230">{{cite journal| author=Levy B, Bollaert PE, Charpentier C, Nace L, Audibert G, Bauer P et al.| title=Comparison of norepinephrine and dobutamine to epinephrine for hemodynamics, lactate metabolism, and gastric tonometric variables in septic shock: a prospective, randomized study. | journal=Intensive Care Med | year= 1997 | volume= 23 | issue= 3 | pages= 282-7 | pmid=9083230 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9083230  }} </ref><ref name="pmid3004777">{{cite journal| author=Chernow B, Roth BL| title=Pharmacologic manipulation of the peripheral vasculature in shock: clinical and experimental approaches. | journal=Circ Shock | year= 1986 | volume= 18 | issue= 2 | pages= 141-55 | pmid=3004777 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3004777  }} </ref><ref name="pmid10966247">{{cite journal| author=Martin C, Viviand X, Leone M, Thirion X| title=Effect of norepinephrine on the outcome of septic shock. | journal=Crit Care Med | year= 2000 | volume= 28 | issue= 8 | pages= 2758-65 | pmid=10966247 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10966247  }} </ref><ref name="pmid12794401">{{cite journal| author=De Backer D, Creteur J, Silva E, Vincent JL| title=Effects of dopamine, norepinephrine, and epinephrine on the splanchnic circulation in septic shock: which is best? | journal=Crit Care Med | year= 2003 | volume= 31 | issue= 6 | pages= 1659-67 | pmid=12794401 | doi=10.1097/01.CCM.0000063045.77339.B6 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12794401  }} </ref> In a prespecified analysis of patients, according to the origin of [[shock]], the [[mortality rate]] with [[norepinephrine]] was lower in the subgroup of patients with cardiogenic shock than with [[dopamine]].<ref name="pmid20200382">{{cite journal| author=De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C et al.| title=Comparison of dopamine and norepinephrine in the treatment of shock. | journal=N Engl J Med | year= 2010 | volume= 362 | issue= 9 | pages= 779-89 | pmid=20200382 | doi=10.1056/NEJMoa0907118 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20200382  }} </ref>


====Inotropes====
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>
[[Inotropic]] therapy targets the improvement of [[myocardial]] [[contractility]] and therefore the increase of [[cardiac output]]. The best way to monitor its effect is to evaluate the changes in [[cardiac output]], following a certain dosage of the [[drug]]. It is important to notice that many [[catecholamines]] have both [[inotropic]] and [[vasopressor]] effects. In the particular case of cardiogenic shock, [[hypoperfusion]] of peripheral tissues is a consequence of impaired [[cardiac output]], therefore [[inotropic]] treatment should only be given once the etiology of [[shock]] has been established. It may be necessary to use a [[vasopressor]] [[drug]] in order to insure adequate [[coronary]] [[perfusion]] pressure.<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref>
*'''[[Levosimendan]]''' - new drug with both inotropic and vasodilatory properties that has the benefit of not increasing myocardial oxygen consumption. This is achieved by an increase of cardiac muscle calcium responsiveness, as well as the opening of ATP-dependent K<sup>+</sup> channels. It has the possible adverse effect of causing hypotension, hence it should be carefully used in cardiogenic shock patients.<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref>


*'''[[Phosphodiesterase inhibitors]]''' - of which [[milrinone]] is an example, increase the [[intracellular]] quantity of [[cAMP]], thus having [[inotropic]] effects, that are not related to β-receptors. Despite having less arrhythmic and [[chronotropic]] effects that [[catecholamines]], [[phosphodiesterase inhibitors]], because of the increase in [[cAMP]] in [[vascular]] [[muscle]], may lead to the development of [[hypotension]], which may further jeopardize the [[shock]] condition.<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref>
==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).<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> 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).<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><ref name="pmid11176812">{{cite journal| author=Hochman JS, Sleeper LA, White HD, Dzavik V, Wong SC, Menon V et al.| title=One-year survival following early revascularization for cardiogenic shock. | journal=JAMA | year= 2001 | volume= 285 | issue= 2 | pages= 190-2 | pmid=11176812 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11176812  }} </ref> Urgent revascularization is a priority over hemodynamic monitoring in MI patients with cardiogenic shock and should not be delayed.
*'''[[Dobutamine]]''' - a mixture of two [[isomers]] whose predominate function is due to stimulation of β1 [[receptors]]. It increases [[cardiac output]] by increasing [[heart rate]] and [[contractility]], having a variable effect on [[blood pressure]].<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref>


===Mechanical Support===
Urgent revascularization can be achieved through one of the following:
====Intra-aortic Balloon Placement====
* [[Percutaneous coronary intervention]] ([[PCI]])
According to the [[AHA]]/[[ACC]] guidelines, [[IABP]] may be indicated in patients [[left ventricular failure]], following [[STEMI]], complicated by cardiogenic shock ''(under a level of evidence B)'' who fail to respond to [[pharmacological]] therapy.<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> In the setting of [[acute MI]], the placement of an [[IABP]] (which reduces [[afterload|workload]] for the [[heart]] and improves [[perfusion]] of the [[coronary arteries]]) should be considered. 
* [[Coronary artery bypass graft]] ([[CABG]])
* [[Fibrinolytic therapy]]


A recent [[meta-analysis]] of [[randomized trial]] data, however, challenges this common practice and class 1B recommendation.<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> In a [[meta-analysis]] of seven [[randomized trial]]s enrolling 1009 patients, [[IABP]] placement in [[STEMI]] patients was not associated with a decrease in [[mortality]] nor improvement 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|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 studies|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.
[[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]].<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><ref name="pmid14597928">{{cite journal| author=French JK, Feldman HA, Assmann SF, Sanborn T, Palmeri ST, Miller D et al.| title=Influence of thrombolytic therapy, with or without intra-aortic balloon counterpulsation, on 12-month survival in the SHOCK trial. | journal=Am Heart J | year= 2003 | volume= 146 | issue= 5 | pages= 804-10 | pmid=14597928 | doi=10.1016/S0002-8703(03)00392-2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14597928  }} </ref><ref name="Fath-OrdoubadiBeatt1994">{{cite journal|last1=Fath-Ordoubadi|first1=F.|last2=Beatt|first2=Kj|last3=Davis|first3=R.C.|last4=Carlsson|first4=Jörg|last5=Rahlf|first5=Günther|last6=Tebbe|first6=Ulrich|title=Fibrinolytic therapy in suspected acute myocardial infarction|journal=The Lancet|volume=343|issue=8902|year=1994|pages=912–913|issn=01406736|doi=10.1016/S0140-6736(94)90029-9}}</ref><ref name="MorrowAntman2000">{{cite journal|last1=Morrow|first1=D. A.|last2=Antman|first2=E. M.|last3=Charlesworth|first3=A.|last4=Cairns|first4=R.|last5=Murphy|first5=S. A.|last6=de Lemos|first6=J. A.|last7=Giugliano|first7=R. P.|last8=McCabe|first8=C. H.|last9=Braunwald|first9=E.|title=TIMI Risk Score for ST-Elevation Myocardial Infarction: A Convenient, Bedside, Clinical Score for Risk Assessment at Presentation : An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy|journal=Circulation|volume=102|issue=17|year=2000|pages=2031–2037|issn=0009-7322|doi=10.1161/01.CIR.102.17.2031}}</ref>


====Left Ventricular Assist Device Placement====
==Hemodynamic Monitoring and Stabilization==
According to the [[AHA]]/[[ACC]] guidelines, alternative [[Ventricular assist device|LV assist devices]] may be indicated in patients with [[refractory]] cardiogenic shock for [[circulatory]] support ''(under a level of evidence C)''.<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> In the setting of pronounced [[hypotension]], despite [[medical treatment|medical therapy]] and [[IABP]] placement, [[Ventricular assist device|LV assist devices]], which augment the pump-function of the [[heart]], should be considered. A [[ventricular assist device]] should only be placed in those patients in whom 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>


[[Percutaneous]] [[Ventricular assist device|LV assist devices]] (PLVADs) such as Tandem heart, Impella, [[ECMO]] may be used until [[cardiac]] recovery occurs, as a temporary procedure during high-risk [[coronary]] interventions, or as a bridge to definitive therapy, such as heart [[transplant]], left [[ventricular assist device]] ([[LVAD]]) or decision making. They provide improved [[hemodynamics]] in patients with cardiogenic shock.<ref name="pmid16878609">{{cite journal| author=Kar B, Adkins LE, Civitello AB, Loyalka P, Palanichamy N, Gemmato CJ et al.| title=Clinical experience with the TandemHeart percutaneous ventricular assist device. | journal=Tex Heart Inst J | year= 2006 | volume= 33 | issue= 2 | pages= 111-5 | pmid=16878609 | doi= | pmc=PMC1524679 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16878609  }} </ref>
===Hemodynamic Monitoring===
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.


====Coronary Artery Bypass Graft (CABG) Placement====
Target endpoints are:
[[CABG]] in this setting is associated with high rates of [[mortality]] and [[morbidity]], therefore if [[primary angioplasty]] can be performed successfully, [[CABG]] is preferably avoided.
* [[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%


===Mechanical Ventilation===
Shown below is a table summarizing the different parameters of hemodynamic monitoring, their target goals, and action items needed to achieve these goals.
[[Mechanical ventilation]] is often required in patients with cardiogenic shock to assure adequate oxygenation.
<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>
{| style="cellpadding=0; cellspacing= 0; width: 1000px;"
|-
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Preload'''
|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'''
|-
|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'''
|-
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
* 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
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''''If ↑ MAP & ↑ SVR:''''' <br>
* 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
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''''If ↓ MAP & ↓ SVR:''''' <br>
* [[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
*** Adjunctive therapy to [[norepinephrine]] or [[dopamine]]
*** Usual dose: 0.01–0.03 U/min
*** Maximum dose: 0.04 U/min
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''''If ↓ MAP & ↑ SVR:''''' <br>
* Continue [[vasopressor]]
* Optimize [[cardiac output]] with inotropic agent
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
* [[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
|}


===Invasive Hemodynamic Monitoring===
===Volume Management===
Considering the importance of proper [[blood pressure]] assessment in patients in [[shock]], along with the fact that peripheral [[vasoconstriction]] may jeopardize [[blood pressure]] assessment through common manual [[sphygmomanometry]], all patients should have an indwelling [[arterial pressure]] [[catheter]] placed in order to gather more accurate measurements.<ref>{{cite book | last = Parrillo | first = Joseph | title = Critical care medicine principles of diagnosis and management in the adult | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2013 | isbn = 0323089291 }}</ref><ref name="pmid5336422">{{cite journal| author=Cohn JN| title=Blood pressure measurement in shock. Mechanism of inaccuracy in ausculatory and palpatory methods. | journal=JAMA | year= 1967 | volume= 199 | issue= 13 | pages= 118-22 | pmid=5336422 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5336422  }} </ref> This method not only supplies continuous [[hemodynamic]] data, therefore allowing a beat-to-beat analysis, useful in evaluating the response to therapy, unlike other manual methods, but also allows for the collection of [[arterial blood gas]] samples.<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref><ref>{{Cite book | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages =  }}</ref> The most commonly used [[catheter]] is the ''flow-directed balloon-tipped [[pulmonary artery catheter]]'', which not only allows for [[cardiac output]] determination, as it is a good method for [[hemodynamic]] assessment of these patients, as well as continuous monitoring of [[pulmonary artery]] and [[central venous pressure]] and waveforms.<ref>{{cite book | last = Parrillo | first = Joseph | title = Critical care medicine principles of diagnosis and management in the adult | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2013 | isbn = 0323089291 }}</ref> With this device it is also possible to collect [[blood]] from the [[pulmonary artery]], therefore enabling determination of MVO<sub>2</sub>, in order to evaluate [[oxygen]] delivery to peripheral tissues and at the same time also helping in the [[diagnosis]] of [[left-to-right shunt]]s, usually associated with [[anatomic]] abnormalities. All these features make the ''flow-directed balloon-tipped [[pulmonary artery catheter]]'' a good tool for [[diagnosis]], management and monitoring of [[therapy]] of cardiogenic shock patients.<ref>{{cite book | last = Parrillo | first = Joseph | title = Critical care medicine principles of diagnosis and management in the adult | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2013 | isbn = 0323089291 }}</ref>
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.
 
Other monitoring techniques include:<ref>{{cite book | last = Parrillo | first = Joseph | title = Critical care medicine principles of diagnosis and management in the adult | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2013 | isbn = 0323089291 }}</ref>
 
*'''Oxymetry''' - although a useful tool in theory, since [[oxygen]] delivery will be directly affected by [[arterial oxygen saturation]], it has some limitations, such as affected results from ambient lights, [[hypothermia]] and dyshemoglobinemias. Also, motion artifacts, [[vasoconstriction]] and [[hypoperfusion]] in the [[shock]] state will jeopardize the readings.<ref name="pmid2024749">{{cite journal| author=Ralston AC, Webb RK, Runciman WB| title=Potential errors in pulse oximetry. III: Effects of interferences, dyes, dyshaemoglobins and other pigments. | journal=Anaesthesia | year= 1991 | volume= 46 | issue= 4 | pages= 291-5 | pmid=2024749 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2024749 }} </ref><ref name="pmid3688400">{{cite journal| author=Norley I| title=Erroneous actuation of the pulse oximeter. | journal=Anaesthesia | year= 1987 | volume= 42 | issue= 10 | pages= 1116 | pmid=3688400 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3688400  }} </ref><ref name="pmid2909323">{{cite journal| author=Pälve H, Vuori A| title=Pulse oximetry during low cardiac output and hypothermia states immediately after open heart surgery. | journal=Crit Care Med | year= 1989 | volume= 17 | issue= 1 | pages= 66-9 | pmid=2909323 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2909323  }} </ref>


*'''Near Infrared Spectroscopy (NIRS)''' - an innovative technique that allows for monitoring of tissue [[oxygenation]] by measuring regional tissue [[blood flow]], [[oxygen]] delivery and utilization. The near-infrared light passes through [[biological tissues]], such as [[muscle]] and [[skin]], and is absorbed by chromophores that is has passed through. The chromophores known to absorb the near-infrared light wavelength are [[cytochrome]] aa3, [[hemoglobin]] and [[myoglobin]], depending on the level of [[oxygenation]]. Since peripheral [[tissue]] [[hypoperfusion]] is a good marker of [[cardiovascular]] stress, NIRS presents itself as a good method to assess, in real-time, [[tissue]] [[perfusion]] throughout the evaluation and treatment periods, as well as during [[resuscitation]].<ref name="pmid11303156">{{cite journal| author=Cohn SM, Varela JE, Giannotti G, Dolich MO, Brown M, Feinstein A et al.| title=Splanchnic perfusion evaluation during hemorrhage and resuscitation with gastric near-infrared spectroscopy. | journal=J Trauma | year= 2001 | volume= 50 | issue= 4 | pages= 629-34; discussion 634-5 | pmid=11303156 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11303156  }} </ref><ref name="pmid10485597">{{cite journal| author=Beilman GJ, Groehler KE, Lazaron V, Ortner JP| title=Near-infrared spectroscopy measurement of regional tissue oxyhemoglobin saturation during hemorrhagic shock. | journal=Shock | year= 1999 | volume= 12 | issue= 3 | pages= 196-200 | pmid=10485597 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10485597  }} </ref><ref name="pmid10780595">{{cite journal| author=McKinley BA, Marvin RG, Cocanour CS, Moore FA| title=Tissue hemoglobin O2 saturation during resuscitation of traumatic shock monitored using near infrared spectrometry. | journal=J Trauma | year= 2000 | volume= 48 | issue= 4 | pages= 637-42 | pmid=10780595 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10780595  }} </ref><ref name="pmid8989194">{{cite journal| author=Rhee P, Langdale L, Mock C, Gentilello LM| title=Near-infrared spectroscopy: continuous measurement of cytochrome oxidation during hemorrhagic shock. | journal=Crit Care Med | year= 1997 | volume= 25 | issue= 1 | pages= 166-70 | pmid=8989194 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8989194  }} </ref><ref name="pmid9095123">{{cite journal| author=Cairns CB, Moore FA, Haenel JB, Gallea BL, Ortner JP, Rose SJ et al.| title=Evidence for early supply independent mitochondrial dysfunction in patients developing multiple organ failure after trauma. | journal=J Trauma | year= 1997 | volume= 42 | issue= 3 | pages= 532-6 | pmid=9095123 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9095123  }} </ref><ref name="pmid9932678">{{cite journal| author=Puyana JC, Soller BR, Zhang S, Heard SO| title=Continuous measurement of gut pH with near-infrared spectroscopy during hemorrhagic shock. | journal=J Trauma | year= 1999 | volume= 46 | issue= 1 | pages= 9-15 | pmid=9932678 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9932678  }} </ref>
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]].<ref name="Hollenberg2011">{{cite journal|last1=Hollenberg|first1=Steven M.|title=Vasoactive Drugs in Circulatory Shock|journal=American Journal of Respiratory and Critical Care Medicine|volume=183|issue=7|year=2011|pages=847–855|issn=1073-449X|doi=10.1164/rccm.201006-0972CI}}</ref><ref name="pmid16088508">{{cite journal| author=Hollenberg SM| title=Recognition and treatment of cardiogenic shock. | journal=Semin Respir Crit Care Med | year= 2004 | volume= 25 | issue= 6 | pages= 661-71 | pmid=16088508 | doi=10.1055/s-2004-860980 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16088508 }} </ref>
*'''Advanced echocardiography in the ICU''' - particularly with the development of more advanced [[echocardiographic]] techniques, such as [[TEE]] and [[contrast]] [[echocardiography]], the inclusion of this [[noninvasive]] method in [[ICU]] has allowed for the decreased of more [[invasive]] techniques, such as [[pulmonary artery catheterization]]. This replacement has been seen due to the vast amount of important data that this method provides, such as assessment of of [[hemodynamic]] stability, [[cardiac output]], [[stroke volume]], [[preload]], detection of [[anatomic]] abnormalities, [[intravascular]] [[volume status]], [[pulmonary artery]] pressures, [[diagnosis]] of hemodynamically significant [[pulmonary embolism]], among others.<ref name="pmid8902376">{{cite journal| author=Porembka DT| title=Transesophageal echocardiography. | journal=Crit Care Clin | year= 1996 | volume= 12 | issue= 4 | pages= 875-918 | pmid=8902376 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8902376  }} </ref><ref name="pmid15302640">{{cite journal| author=ten Wolde M, Söhne M, Quak E, Mac Gillavry MR, Büller HR| title=Prognostic value of echocardiographically assessed right ventricular dysfunction in patients with pulmonary embolism. | journal=Arch Intern Med | year= 2004 | volume= 164 | issue= 15 | pages= 1685-9 | pmid=15302640 | doi=10.1001/archinte.164.15.1685 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15302640 }} </ref>


==Contraindicated Medications==
==Contraindicated Medications==

Latest revision as of 23:04, 11 March 2020

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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)"

References

  1. ↑ Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M; et al. (2004). "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)". Circulation. 110 (5): 588–636. doi:10.1161/01.CIR.0000134791.68010.FA. PMID 15289388.
  2. ↑ 2.0 2.1 Overgaard CB, Dzavík V (2008). "Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease". Circulation. 118 (10): 1047–56. doi:10.1161/CIRCULATIONAHA.107.728840. PMID 18765387.
  3. ↑ Unverzagt S, Wachsmuth L, Hirsch K, Thiele H, Buerke M, Haerting J; et al. (2014). "Inotropic agents and vasodilator strategies for acute myocardial infarction complicated by cardiogenic shock or low cardiac output syndrome". Cochrane Database Syst Rev. 1: CD009669. doi:10.1002/14651858.CD009669.pub2. PMID 24385385.
  4. ↑ Richard C, Ricome JL, Rimailho A, Bottineau G, Auzepy P (1983). "Combined hemodynamic effects of dopamine and dobutamine in cardiogenic shock". Circulation. 67 (3): 620–6. PMID 6821904.
  5. ↑ Francis GS, Bartos JA, Adatya S (2014). "Inotropes". J Am Coll Cardiol. 63 (20): 2069–78. doi:10.1016/j.jacc.2014.01.016. PMID 24530672.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 Werdan K, Gielen S, Ebelt H, Hochman JS (2014). "Mechanical circulatory support in cardiogenic shock". Eur Heart J. 35 (3): 156–67. doi:10.1093/eurheartj/eht248. PMID 24014384.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA; et al. (2013). "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". Circulation. 127 (4): 529–55. doi:10.1161/CIR.0b013e3182742c84. PMID 23247303.
  8. ↑ 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.
  9. ↑ 9.0 9.1 Chen EW, Canto JG, Parsons LS; et al. (2003). "Relation between hospital intra-aortic balloon counterpulsation volume and mortality in acute myocardial infarction complicated by cardiogenic shock". Circulation. 108 (8): 951–7. doi:10.1161/01.CIR.0000085068.59734.E4. PMID 12912817. Unknown parameter |month= ignored (help)
  10. ↑ Zeymer U, Bauer T, Hamm C, Zahn R, Weidinger F, Seabra-Gomes R; et al. (2011). "Use and impact of intra-aortic balloon pump on mortality in patients with acute myocardial infarction complicated by cardiogenic shock: results of the Euro Heart Survey on PCI". EuroIntervention. 7 (4): 437–41. doi:10.4244/EIJV7I4A72. PMID 21764661.
  11. ↑ Unverzagt S, Machemer MT, Solms A, Thiele H, Burkhoff D, Seyfarth M; et al. (2011). "Intra-aortic balloon pump counterpulsation (IABP) for myocardial infarction complicated by cardiogenic shock". Cochrane Database Syst Rev (7): CD007398. doi:10.1002/14651858.CD007398.pub2. PMID 21735410.
  12. ↑ 12.0 12.1 12.2 Sjauw KD, Engström AE, Vis MM, van der Schaaf RJ, Baan J, Koch KT; et al. (2009). "A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines?". Eur Heart J. 30 (4): 459–68. doi:10.1093/eurheartj/ehn602. PMID 19168529.
  13. ↑ 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.
  14. ↑ Cheng JM, den Uil CA, Hoeks SE, van der Ent M, Jewbali LS, van Domburg RT; et al. (2009). "Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta-analysis of controlled trials". Eur Heart J. 30 (17): 2102–8. doi:10.1093/eurheartj/ehp292. PMID 19617601.
  15. ↑ Hochman JS, Sleeper LA, White HD, Dzavik V, Wong SC, Menon V; et al. (2001). "One-year survival following early revascularization for cardiogenic shock". JAMA. 285 (2): 190–2. PMID 11176812.
  16. ↑ 16.0 16.1 French JK, Feldman HA, Assmann SF, Sanborn T, Palmeri ST, Miller D; et al. (2003). "Influence of thrombolytic therapy, with or without intra-aortic balloon counterpulsation, on 12-month survival in the SHOCK trial". Am Heart J. 146 (5): 804–10. doi:10.1016/S0002-8703(03)00392-2. PMID 14597928.
  17. ↑ Fath-Ordoubadi, F.; Beatt, Kj; Davis, R.C.; Carlsson, Jörg; Rahlf, Günther; Tebbe, Ulrich (1994). "Fibrinolytic therapy in suspected acute myocardial infarction". The Lancet. 343 (8902): 912–913. doi:10.1016/S0140-6736(94)90029-9. ISSN 0140-6736.
  18. ↑ Morrow, D. A.; Antman, E. M.; Charlesworth, A.; Cairns, R.; Murphy, S. A.; de Lemos, J. A.; Giugliano, R. P.; McCabe, C. H.; Braunwald, E. (2000). "TIMI Risk Score for ST-Elevation Myocardial Infarction: A Convenient, Bedside, Clinical Score for Risk Assessment at Presentation : An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy". Circulation. 102 (17): 2031–2037. doi:10.1161/01.CIR.102.17.2031. ISSN 0009-7322.
  19. ↑ Handbook of Emergency Cardiovascular Care for Healthcare Providers. ISBN 1616690003.
  20. ↑ "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". Circulation. 102 (8 Suppl): I172–203. 2000. PMID 10966673. Unknown parameter |month= ignored (help)
  21. ↑ Hollenberg, Steven M. (2011). "Vasoactive Drugs in Circulatory Shock". American Journal of Respiratory and Critical Care Medicine. 183 (7): 847–855. doi:10.1164/rccm.201006-0972CI. ISSN 1073-449X.
  22. ↑ Hollenberg SM (2004). "Recognition and treatment of cardiogenic shock". Semin Respir Crit Care Med. 25 (6): 661–71. doi:10.1055/s-2004-860980. PMID 16088508.
  23. ↑ Kushner FG, Hand M, Smith SC, King SB, Anderson JL, Antman EM, Bailey SR, Bates ER, Blankenship JC, Casey DE, Green LA, Hochman JS, Jacobs AK, Krumholz HM, Morrison DA, Ornato JP, Pearle DL, Peterson ED, Sloan MA, Whitlow PL, Williams DO (2009). "2009 focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update) a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Journal of the American College of Cardiology. 54 (23): 2205–41. doi:10.1016/j.jacc.2009.10.015. PMID 19942100. Retrieved 2011-12-06. Unknown parameter |month= ignored (help)
  24. ↑ 24.0 24.1 Hochman JS, Sleeper LA, Webb JG; et al. (1999). "Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock". N. Engl. J. Med. 341 (9): 625–34. doi:10.1056/NEJM199908263410901. PMID 10460813. Unknown parameter |month= ignored (help)
  25. ↑ Hochman JS, Lamas GA, Buller CE; et al. (2006). "Coronary intervention for persistent occlusion after myocardial infarction". N. Engl. J. Med. 355 (23): 2395–407. doi:10.1056/NEJMoa066139. PMC 1995554. PMID 17105759. Unknown parameter |month= ignored (help)
  26. ↑ Thune JJ, Hoefsten DE, Lindholm MG; et al. (2005). "Simple risk stratification at admission to identify patients with reduced mortality from primary angioplasty". Circulation. 112 (13): 2017–21. doi:10.1161/CIRCULATIONAHA.105.558676. PMID 16186438. Unknown parameter |month= ignored (help)
  27. ↑ Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS (2005). "Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock". JAMA. 294 (4): 448–54. doi:10.1001/jama.294.4.448. PMID 16046651. Unknown parameter |month= ignored (help)
  28. ↑ Hochman JS, Sleeper LA, Webb JG; et al. (2006). "Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction". JAMA. 295 (21): 2511–5. doi:10.1001/jama.295.21.2511. PMC 1782030. PMID 16757723. Unknown parameter |month= ignored (help)
  29. ↑ "Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group". Lancet. 343 (8893): 311–22. 1994. PMID 7905143. Unknown parameter |month= ignored (help)
  30. ↑ Morrow DA, Antman EM, Charlesworth A; et al. (2000). "TIMI risk score for ST-elevation myocardial infarction: A convenient, bedside, clinical score for risk assessment at presentation: An intravenous nPA for treatment of infarcting myocardium early II trial substudy". Circulation. 102 (17): 2031–7. PMID 11044416. Unknown parameter |month= ignored (help)
  31. ↑ Barron HV, Every NR, Parsons LS; et al. (2001). "The use of intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating acute myocardial infarction: data from the National Registry of Myocardial Infarction 2". Am. Heart J. 141 (6): 933–9. doi:10.1067/mhj.2001.115295. PMID 11376306. Unknown parameter |month= ignored (help)
  32. ↑ Sanborn TA, Sleeper LA, Bates ER; et al. (2000). "Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?". J. Am. Coll. Cardiol. 36 (3 Suppl A): 1123–9. PMID 10985715. Unknown parameter |month= ignored (help)
  33. ↑ Ohman EM, Nanas J, Stomel RJ; et al. (2005). "Thrombolysis and counterpulsation to improve survival in myocardial infarction complicated by hypotension and suspected cardiogenic shock or heart failure: results of the TACTICS Trial". J. Thromb. Thrombolysis. 19 (1): 33–9. doi:10.1007/s11239-005-0938-0. PMID 15976965. Unknown parameter |month= ignored (help)


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