Cardiogenic shock medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Cardiogenic shock is 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 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.[2][3] 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.[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:

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,[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:

Alternative agents include dobutamine (mainly in non-sick patients) and phosphodiesterase inhibitors (amrinone or milrinone).

Selection of a Vasopressor or an Inotrope

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

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

Low Output with Shock
Systolic blood pressure (SBP) > 70 or 80 mm Hg

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

  • 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 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]

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:

  • Ussed in decompensated heart failure

Mechanical Therapy

Mechanical therapy for cardiac shock involves the use of circulatory assist systems, which are different by:[10]

  • 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).[11]

The hemodynamic effects of IABP are:[12]

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.[13] 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.[14]

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).[15] 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. [16] 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.[16]

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.[11] 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.[17]

The hemodynamic effects of LVAD are superior to those of IABP:[10]

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.[10] 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).[18]

Extracorporeal Membrane Oxygenation (ECMO)

Hemodynamic effects of extracorporeal membrane oxygenation (ECMO):[10]

ECMO use is associated with complications such as bleeding, renal failure, and systemic inflammatory response syndrome.[10]

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).[11] 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).[11][19] 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.[11][20][21][22]

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.

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
      • Adjunctive therapy to norepinephrine or dopamine
      • Usual dose: 0.01–0.03 U/min
      • Maximum dose: 0.04 U/min
 If ↓ MAP & ↑ SVR:
  • Continue vasopressor
  • Optimize cardiac output with inotropic agent
  • 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.[23][24]

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)[11]

General and Specific Considerations (DO NOT EDIT)[11][25]

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.[26][27][28] (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)[11]

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.[26][29][30] (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.[31][32][20] (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.[33][13][34][16][35] (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. ↑ 1.0 1.1 Ng, 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. ISSN 0885-0666.
  2. ↑ TRIUMPH Investigators. Alexander JH, Reynolds HR, Stebbins AL, Dzavik V, Harrington RA; et al. (2007). "Effect of tilarginine acetate in patients with acute myocardial infarction and cardiogenic shock: the TRIUMPH randomized controlled trial". JAMA. 297 (15): 1657–66. doi:10.1001/jama.297.15.joc70035. PMID 17387132.
  3. ↑ Sakr Y, Reinhart K, Vincent JL, Sprung CL, Moreno R, Ranieri VM; et al. (2006). "Does dopamine administration in shock influence outcome? Results of the Sepsis Occurrence in Acutely Ill Patients (SOAP) Study". Crit Care Med. 34 (3): 589–97. doi:10.1097/01.CCM.0000201896.45809.E3. PMID 16505643.
  4. ↑ Hochman, Judith (2009). Cardiogenic shock. Chichester, West Sussex, UK Hoboken, NJ: Wiley-Blackwell. ISBN 9781405179263.
  5. ↑ 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.
  6. ↑ 6.0 6.1 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.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 10.0 10.1 10.2 10.3 10.4 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.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 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.
  12. ↑ 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.
  13. ↑ 13.0 13.1 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)
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ 16.0 16.1 16.2 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.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ 20.0 20.1 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.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ 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.
  25. ↑ 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)
  26. ↑ 26.0 26.1 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)
  27. ↑ 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)
  28. ↑ 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)
  29. ↑ 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)
  30. ↑ 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)
  31. ↑ "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)
  32. ↑ 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)
  33. ↑ 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)
  34. ↑ 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)
  35. ↑ 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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