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.
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]].<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>
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>
-------
===Volume Management===
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>
===Pharmacologic Hemodynamic Support===
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>
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>
:*a particular [[MAP]]
:*an increase in [[cardiac output]]
:*bed-side clinical assessment by evaluating indices of organ [[perfusion]], such as [[urine]] output and [[lactate]] levels while maintaining adequate [[oxygenation]]
*'''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>
:*''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====
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:
*'''[[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>
*'''[[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>
*'''[[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>
*'''[[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====
[[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>
*'''[[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===
====Intra-aortic Balloon Placement====
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.
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.
====Left Ventricular Assist Device Placement====
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>
[[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.
===Mechanical Ventilation===
[[Mechanical ventilation]] is often required in patients with cardiogenic shock to assure adequate oxygenation.
===Invasive Hemodynamic Monitoring===
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>
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>
*'''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>
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 treatment combines both techniques, in which medical therapy, after restored filling pressures, allows 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 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.[1] Other important factors to increase the chances of a better outcome are: mechanical ventilation, in order to improve tissueoxygenation, and close monitoring of the therapeutic dosages, particularly of vasoactive drugs, since these have been associated with excess mortality due to toxicity effects.[2][3] Also, it is recommended invasivehemodynamic 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.[1][4]
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
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:
Correct hypoxia and ensure optimal oxygenation and ventilation support (mechanical ventilation is often required in patients with cardiogenic shock to assure adequate oxygenation.)
The first line treatment to increase blood pressure in cardiogenic shock is the administration of pharmacological therapy with either ionotropes or vasopressors,[5] the main choices being dopamine, dobutamine, and norepinephrine. 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.[6] There is no robust data that compares the efficacy of inotropes and vasopressors in improvement of cardiovascular outcomes and reduction in mortality.[7]
The two main agents used to optimize the blood pressure are:
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.[8]
Low Output without Shock
Patients presenting in this setting should be started on an inotrope, such as dobutamine.
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. 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) < 70 or 80 mm Hg
Norepinephrine is indicated among patients with severe hypotension:
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
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.[9][6]
A meta-analysis of randomized trial data, however, challenges this common practice and class 1B recommendation.[11] 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
As per the recommendation of the 2013 AHA/ACC guidelines, in the setting of pronounced hypotension despite medical therapy and IABP placement, placement of a left ventricular assist device (which augments the pump-function of the heart) should be considered.[10] 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. [12]
ECMO
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:
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.[10][13][14][15] Administration of streptokinase therapy to patients with cardiogenic shock has not been associated with an improvement in survival.[16] 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. 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.
The response to the treatment is determined through the assessment of whether the mean arterial pressure reached the target value, an increase in blood pressure, and bed-side clinical assessment by evaluating indices of organ perfusion, such as physical exam, urine output, and lactate levels,
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.[17][18]
Contraindicated Medications
Cardiogenic shock is considered an absolute contraindication to the use of the following medications:
"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)"
"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)[10]
"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.[25][26][15](Level of Evidence: B)"
"1. Alternative left ventricular (LV) assist devices for circulatory support may be considered in patients with refractory cardiogenic shock. (Level of Evidence: C)"
References
↑ 1.01.1Ng, R.; Yeghiazarians, Y. (2011). "Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies". Journal of Intensive Care Medicine. 28 (3): 151–165. doi:10.1177/0885066611411407. ISSN0885-0666.
↑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.
↑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. ISSN0009-7322.
↑"Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI)". Lancet. 1 (8478): 397–402. 1986. PMID2868337. Unknown parameter |month= ignored (help)
↑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. ISSN1073-449X.
↑ 20.020.1Hochman 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. PMID10460813. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑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. PMID16186438. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑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. PMID16046651. Unknown parameter |month= ignored (help)CS1 maint: Multiple names: authors list (link)
↑"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. PMID7905143. Unknown parameter |month= ignored (help)
↑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. PMID11044416. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑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. PMID11376306. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑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. PMID12912817. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑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. PMID10985715. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑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. PMID15976965. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)