Cardiogenic shock medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammad Salih, MD. João André Alves Silva, M.D. [2]; Rim Halaby, M.D. [3] Syed Musadiq Ali M.B.B.S.[4] James Nasr[5]

Cardiogenic shock medical therapy

Overview

Cardiogenic shock is a medical emergency requiring simultaneous stabilization, diagnostic evaluation, treatment of the underlying cause, and prevention of progressive end-organ injury. Medical therapy includes early resuscitation, oxygenation and ventilatory support, vasoactive drugs, volume and congestion management, treatment of acute coronary syndrome when present, avoidance of medications that worsen shock physiology, selective temporary mechanical circulatory support, and transition to guideline-directed medical therapy during recovery.[1][2]

Medical therapy should be individualized according to shock phenotype, etiology, congestion, right- versus left-sided failure, arrhythmia burden, myocardial ischemia, renal function, and candidacy for temporary or durable mechanical circulatory support. Vasoactive agents should be used at the lowest effective dose for the shortest feasible duration.[1]

Initial stabilization

Resuscitation should begin immediately while the cause and hemodynamic phenotype of shock are being defined.[3][4]

Stabilization domain Practical approach
Monitoring Continuous telemetry, frequent blood pressure assessment, pulse oximetry, urine output, serial lactate, and early arterial line when vasoactive therapy is required.
Airway and oxygenation Correct hypoxemia promptly. Use noninvasive or invasive mechanical ventilation when respiratory failure, severe pulmonary edema, altered mental status, or high work of breathing is present.
Vascular access Obtain reliable peripheral access initially; use central venous access for vasoactive infusions and invasive monitoring when needed.
Electrolytes and acid-base status Correct clinically important hypokalemia, hypomagnesemia, severe acidosis, and other reversible contributors to arrhythmia or impaired contractility.
Glucose Monitor glucose and treat severe hyperglycemia while avoiding hypoglycemia.
Rhythm Treat ventricular arrhythmias, high-grade atrioventricular block, rapid atrial arrhythmias, or bradyarrhythmias when they contribute to hemodynamic compromise.
Acute coronary syndrome Give antithrombotic therapy according to acute coronary syndrome guidelines when ACS is suspected, recognizing that shock may impair oral drug absorption.[5]

Hemodynamic goals

No single blood pressure target has been proven superior in randomized cardiogenic shock trials. The 2021 AHA Scientific Statement on invasive management of AMI-related cardiogenic shock recommends using the minimum vasopressor dose needed to maintain mean arterial pressure above 65 mm Hg.[3] A trial comparing lower versus usual MAP targets in infarct-related cardiogenic shock is ongoing in the supplied evidence base.[2]

Commonly used treatment goals include:

  • Adequate mental status and peripheral perfusion
  • Improving or normalizing lactate
  • Urine output consistent with improving renal perfusion
  • MAP generally ≥65 mm Hg, individualized to chronic hypertension, end-organ perfusion, and mechanical support configuration
  • Cardiac index ≥2.2 L/min/m2 when invasively measured
  • Reduction of excessive right- or left-sided filling pressures when congestion is present

The 2022 AHA Scientific Statement on temporary mechanical circulatory support and 2024 JACC Heart Failure practical guidance include targets such as RAP 8-12 mm Hg, PCWP ≤15-18 mm Hg, and cardiac index ≥2.2 L/min/m2, but these targets should be individualized rather than applied mechanically.[6]

Vasoactive therapy

Principles

Vasoactive therapy is used to restore perfusion while definitive therapy is pursued. The 2022 AHA/ACC/HFSA guideline gives intravenous inotropic support a class 1, level B-NR recommendation in patients with cardiogenic shock to maintain systemic perfusion and preserve end-organ performance, despite limited randomized trial data guiding specific agent selection.[7] Excessive catecholamine exposure increases myocardial oxygen demand, arrhythmia risk, and afterload. Progressive escalation of vasoactive support is associated with worse outcomes, although this also reflects greater shock severity.[1]

Dose ranges are approximate starting and titration ranges. The guiding principle is titration to clinical effect using the minimum dose needed to maintain systemic perfusion while definitive therapy, decongestion, revascularization, or mechanical support decisions are pursued.[1][3]

First-line vasopressor

Norepinephrine is a reasonable first-line vasopressor for most hypotensive patients with cardiogenic shock.[1] The 2021 AHA Scientific Statement on AMI-related cardiogenic shock recommends favoring norepinephrine as first-line therapy and using the minimum necessary dose to maintain MAP above 65 mm Hg.[3]

The SOAP II trial found more arrhythmic events with dopamine than norepinephrine in patients with shock. In the prespecified cardiogenic shock subgroup, dopamine was associated with nominally higher 28-day mortality, although the subgroup was not powered for mortality.[8] In the OptimaCC trial of AMI-related cardiogenic shock, epinephrine was associated with more refractory shock than norepinephrine, leading to early trial termination.[9]

Vasoactive agents used in cardiogenic shock

Class Agent Usual dosing range Hemodynamic profile Major cautions
Inopressor Norepinephrine 0.05-1 μg/kg/min Increases SVR and blood pressure with modest β1 inotropic effect Excessive afterload, arrhythmia, digital or splanchnic ischemia at high dose
Inopressor Epinephrine 0.01-0.5 μg/kg/min Increases contractility, heart rate, SVR, and blood pressure Tachyarrhythmia, increased lactate, higher refractory shock signal compared with norepinephrine in OptimaCC[9]
Inopressor Dopamine 2-20 μg/kg/min Dose-dependent dopaminergic, β1, and α1 activity; chronotropic effect More arrhythmias than norepinephrine; not preferred as first-line therapy in most cardiogenic shock patients[8]
Inodilator Dobutamine 2-20 μg/kg/min Increases contractility and cardiac output; may reduce SVR Hypotension, tachyarrhythmia, increased myocardial oxygen demand
Inodilator Milrinone 0.125-0.75 μg/kg/min; loading dose often omitted in shock PDE-3 inhibition; increases contractility and reduces pulmonary and systemic vascular resistance Hypotension, arrhythmia, accumulation in renal dysfunction
Vasopressor Vasopressin 0.01-0.04 U/min Increases SVR through V1 receptor activity; little direct chronotropy Ischemia at higher doses; usually adjunctive rather than sole first-line agent
Vasopressor Phenylephrine 40-180 μg/min Pure α1 vasoconstriction; increases SVR Reflex bradycardia and reduced cardiac output; discouraged as sole first-line continuous agent in cardiogenic shock except selected physiology such as dynamic LVOT obstruction[1]
Calcium sensitizer / inodilator Levosimendan 0.05-0.2 μg/kg/min Calcium sensitization and PDE-3 inhibition; increases cardiac output and reduces SVR Not FDA-approved in the United States; hypotension and arrhythmia risk

Agent selection by phenotype

Clinical scenario Preferred medical strategy Key caution
Hypotensive cardiogenic shock Norepinephrine as first-line vasopressor; add inotrope if cardiac output remains inadequate Avoid escalating vasopressors without reassessing phenotype, congestion, ischemia, and need for mechanical support.
Low-output shock without severe hypotension Dobutamine or milrinone may be considered, particularly when SVR is high Milrinone requires caution in renal dysfunction; both may worsen hypotension.
Bradycardia-mediated shock Chronotropic support such as dopamine or epinephrine may be used as a bridge to temporary pacing Correct reversible causes and do not delay pacing when indicated.
RV-dominant shock Optimize preload carefully, avoid hypoxemia and acidosis, consider inodilator support if blood pressure allows Excessive fluids can worsen septal shift and systemic congestion.
Dynamic LVOT obstruction Pure vasopressor support such as phenylephrine or vasopressin may be favored with volume repletion when appropriate Inotropes and inodilators may worsen obstruction.
Mixed cardiogenic-distributive shock Norepinephrine, often with adjunctive vasopressin if vasoplegia is prominent Reassess for sepsis, post-arrest vasoplegia, inflammatory shock, and inadequate cardiac output.

Dobutamine versus milrinone

The DOREMI trial found no significant difference between dobutamine and milrinone for a composite endpoint including in-hospital death, resuscitated cardiac arrest, cardiac transplantation or mechanical circulatory support, nonfatal myocardial infarction, transient ischemic attack or stroke, or renal replacement therapy. Selection between agents should be based on blood pressure, pulmonary vascular resistance, renal function, arrhythmia risk, β-blocker exposure, and clinician familiarity.[1][5]

Milrinone has a longer half-life and renal clearance, so hypotension or arrhythmias may be more difficult to reverse in patients with renal dysfunction.[1] CAPITAL DOREMI 2 is evaluating dobutamine or milrinone versus placebo in SCAI C-D cardiogenic shock in the supplied evidence base.[5]

Levosimendan

Levosimendan is not approved in the United States. The SURVIVE trial did not show significant survival advantage compared with dobutamine, and ongoing studies are evaluating its role in cardiogenic shock.[5]

Volume and congestion management

Volume management should be guided by clinical examination, echocardiography, invasive hemodynamics when available, and pulmonary congestion. Empiric large-volume resuscitation can worsen pulmonary edema and ventricular dilation in LV-dominant shock. A cautious volume challenge may be appropriate in selected patients with suspected hypovolemia, RV infarction, low filling pressures, or dynamic LVOT obstruction.[4]

When a congestive phenotype is present, decongestion is a treatment priority. The 2025 ACC Expert Consensus Statement emphasizes IV loop diuretics, thiazide-type diuretic augmentation, and renal replacement therapy for ultrafiltration when congestion is refractory to medical therapy.[1]

Elevated central venous pressure can impair renal perfusion despite apparently adequate MAP. Transrenal perfusion pressure, conceptualized as MAP minus CVP, may help explain persistent renal dysfunction in congestive shock.[1]

Emergency revascularization

In acute coronary syndrome-related cardiogenic shock, definitive therapy is revascularization when feasible. The 2025 ACC/AHA/ACEP/NAEMSP/SCAI acute coronary syndromes guideline gives emergency culprit-vessel revascularization by PCI or CABG a class 1, level B-R recommendation in patients with ACS and cardiogenic shock or hemodynamic instability, irrespective of time from symptom onset.[10]

The SHOCK trial established long-term survival benefit with emergency revascularization compared with initial medical stabilization in acute myocardial infarction complicated by cardiogenic shock.[2][10]

Culprit-lesion-only PCI

In patients with AMI-related cardiogenic shock and multivessel coronary disease, the CULPRIT-SHOCK trial showed that culprit-lesion-only PCI with an option for staged revascularization reduced 30-day death or renal replacement therapy compared with immediate multivessel PCI. The 2025 ACS guideline gives routine PCI of a non-infarct-related artery during the index primary PCI a class 3: Harm, level B-R recommendation in cardiogenic shock.[10][2]

Detailed revascularization strategy, procedural selection, staged PCI, and CABG considerations are addressed in the procedural therapy microchapter.

Fibrinolytic therapy

When PCI or CABG cannot be performed in STEMI-related cardiogenic shock and there are no contraindications, fibrinolytic therapy is indicated. A pharmacoinvasive approach may be considered when prolonged interhospital transport would delay PCI.[10][2]

Temporary mechanical circulatory support

Temporary mechanical circulatory support may be used when pharmacologic therapy and definitive treatment are insufficient, but routine use in all patients with cardiogenic shock is discouraged. Device selection should be based on shock severity, hemodynamic phenotype, respiratory failure, vascular access, institutional expertise, complication risk, anticoagulation and bleeding risk, and exit strategy.[1]

Most temporary mechanical circulatory support devices require systemic anticoagulation or device-specific anticoagulation strategies. Anticoagulation monitoring and device-specific targets are addressed in the procedural therapy microchapter, but bleeding risk should be incorporated into medical decision-making when tMCS is considered.[6]

Trial or evidence base Device or strategy Population Key finding
IABP-SHOCK II Intra-aortic balloon pump AMI-related cardiogenic shock undergoing early revascularization 30-day all-cause mortality was 39.7% vs 41.3% (P=0.69); no benefit was observed at 6-year follow-up (HR 1.01; 95% CI 0.82-1.24).[11]
ECLS-SHOCK Early VA-ECMO strategy AMI-related cardiogenic shock with planned early revascularization 30-day all-cause mortality was 47.8% in the ECLS group vs 49.0% in the control group (RR 0.98; 95% CI 0.80-1.19; P=0.81). Moderate/severe bleeding and peripheral vascular complications were higher with ECLS.[12]
DanGer Shock Impella CP microaxial flow pump Selected STEMI-related cardiogenic shock without anoxic brain injury at experienced centers 180-day mortality was 45.8% vs 58.5% (HR 0.74; 95% CI 0.55-0.99; P=0.04). Composite safety endpoint events occurred in 24.0% vs 6.2% (RR 4.74); moderate/severe bleeding occurred in 21.8% vs 11.9%, and limb ischemia in 5.6% vs 1.1%.[13]
Altshock-2 Early intra-aortic balloon support Heart failure-related cardiogenic shock (SCAI stages B-D; n=117) Early IABP did not improve survival or successful bridge at 60 days compared with standard care.[14]

The 2025 ACS guideline states that, in selected patients with STEMI and severe or refractory cardiogenic shock, insertion of a microaxial intravascular flow pump is reasonable to reduce death. Short-term mechanical circulatory support is also reasonable as a bridge to surgery in mechanical complications of ACS. Routine use of IABP or VA-ECMO in AMI-related cardiogenic shock is not recommended due to lack of survival benefit.[10]

The DanGer Shock population was narrowly selected: STEMI-related cardiogenic shock, systolic blood pressure below 100 mm Hg or vasoactive support requirement, lactate elevation, exclusion of comatose patients after cardiac arrest, enrollment within 24 hours, and treatment in experienced centers. A hemodynamic substudy showed that Impella CP reduced vasoactive-inotropic scores during the first 12 hours and achieved lactate normalization approximately 12 hours earlier than standard care.[15]

An individual patient data meta-analysis of randomized tMCS trials with 6-month follow-up suggested that patients with STEMI-related cardiogenic shock without risk of hypoxic brain injury had a reduction in mortality after tMCS use, inclusive of VA-ECMO, providing broader context for the DanGer Shock findings.[16]

Medications to avoid during active shock

Medication or class Reason to avoid during active cardiogenic shock Recovery-phase consideration
Beta blockers Negative inotropy and chronotropy may worsen low-output state, hypotension, or decompensated heart failure. Consider after euvolemia, perfusion recovery, and discontinuation of inotropes and vasopressors.
ACE inhibitors, ARBs, or ARNIs May worsen hypotension, renal dysfunction, or hyperkalemia during active shock. Start or restart when blood pressure, renal function, and potassium are stable.
Negative inotropic calcium channel blockers Verapamil and diltiazem may worsen contractility and hypotension. Avoid in HFrEF; use only if a separate indication and hemodynamic tolerance are clear.
Negative inotropic antiarrhythmics Disopyramide, flecainide, and propafenone may worsen myocardial depression or proarrhythmia risk. Avoid in structural heart disease and low-output states unless specialist-directed.
Nesiritide Vasodilatory effect may worsen hypotension. Not used for active cardiogenic shock.

Transition to guideline-directed medical therapy

Survivors of cardiogenic shock with reduced ejection fraction should be transitioned to guideline-directed medical therapy during recovery when tolerated. This includes beta blockers, renin-angiotensin system inhibition or ARNI therapy, mineralocorticoid receptor antagonists, and SGLT2 inhibitors when blood pressure, renal function, potassium, perfusion, and congestion status permit.[17][18]

In the FRENSHOCK registry of cardiogenic shock survivors, discharge triple therapy with beta blocker, renin-angiotensin system inhibitor, and mineralocorticoid receptor antagonist was associated with lower 1-year all-cause mortality. Mortality decreased stepwise as the number of heart failure drug classes increased.[19]

Practical medical therapy approach

  1. Stabilize airway, oxygenation, rhythm, perfusion, electrolytes, and acid-base abnormalities immediately.
  2. Identify the dominant shock phenotype using clinical examination, echocardiography, laboratory markers, and invasive hemodynamics when needed.
  3. Use norepinephrine as the usual first-line vasopressor in hypotensive cardiogenic shock.
  4. Add dobutamine or milrinone when forward flow remains inadequate and blood pressure permits.
  5. Avoid dopamine as routine first-line therapy because of arrhythmia and adverse outcome signals.
  6. Avoid phenylephrine as a sole first-line continuous agent except selected physiology such as dynamic LVOT obstruction.
  7. Treat congestion with IV diuretics and adjunctive strategies when a congestive phenotype is present.
  8. Avoid empiric large-volume fluids unless low filling pressure, RV infarction, dynamic LVOT obstruction, or hypovolemia is suspected.
  9. Revascularize culprit vessel urgently in ACS-related cardiogenic shock.
  10. Avoid routine immediate multivessel PCI during primary PCI for AMI-related cardiogenic shock.
  11. Consider temporary mechanical circulatory support for severe or refractory shock using phenotype, severity, expertise, complication risk, anticoagulation/bleeding risk, and exit strategy.
  12. Initiate or restart guideline-directed medical therapy before discharge when hemodynamically tolerated.

Common pitfalls

  • Using dopamine as a routine first-line vasopressor instead of norepinephrine
  • Escalating catecholamines without reassessing shock phenotype or need for mechanical support
  • Treating MAP alone while ignoring cardiac output, lactate, urine output, congestion, and filling pressures
  • Giving large-volume IV fluids to patients with pulmonary edema or high left-sided filling pressures
  • Failing to decongest patients with wet cardiogenic shock
  • Initiating inotropes in dynamic LVOT obstruction
  • Applying DanGer Shock results to all cardiogenic shock populations regardless of etiology, neurologic status after cardiac arrest, or center experience
  • Performing routine immediate multivessel PCI in AMI-related cardiogenic shock
  • Placing IABP or VA-ECMO routinely without individualized assessment
  • Continuing or initiating beta blockers, RAAS inhibitors, or negative inotropic calcium channel blockers during active shock with hypotension
  • Failing to transition survivors with reduced ejection fraction to guideline-directed medical therapy before discharge when tolerated

Historical note: The following 2013 ACCF/AHA guideline recommendations are retained for historical reference only because this legacy source section is marked "DO NOT EDIT." They have been superseded by the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Key changes include: routine IABP use in AMI-related cardiogenic shock is now classified as no benefit; microaxial flow pump use is reasonable in selected patients with STEMI and severe or refractory cardiogenic shock; and routine VA-ECMO use is not recommended due to lack of survival benefit.[10]

2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)[20]

General and Specific Considerations (DO NOT EDIT)[20][21]

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.[22][23][24] (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)[20]

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.[22][25][26] (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.[27][28][29] (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.[30][31][32][33][34] (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. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 Sinha SS, Morrow DA, Kapur NK, Kataria R, Roswell RO (2025). "2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock". Journal of the American College of Cardiology. 85 (16): 1618–1641. doi:10.1016/j.jacc.2025.02.018.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Thiele H, Hassager C (2026). "Cardiogenic Shock". The New England Journal of Medicine. 394 (1): 62–77. doi:10.1056/NEJMra2312086.
  3. ↑ 3.0 3.1 3.2 3.3 Henry TD, Tomey MI, Tamis-Holland JE; et al. (2021). "Invasive Management of Acute Myocardial Infarction Complicated by Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 143 (15): e815–e829. doi:10.1161/CIR.0000000000000959.
  4. ↑ 4.0 4.1 van Diepen S, Katz JN, Albert NM; et al. (2017). "Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 136 (16): e232–e268. doi:10.1161/CIR.0000000000000525.
  5. ↑ 5.0 5.1 5.2 5.3 Lüsebrink E, Binzenhöfer L, Adamo M; et al. (2024). "Cardiogenic Shock". Lancet. 404 (10466): 2006–2020. doi:10.1016/S0140-6736(24)01818-X.
  6. ↑ 6.0 6.1 Geller BJ, Sinha SS, Kapur NK; et al. (2022). "Escalating and De-Escalating Temporary Mechanical Circulatory Support in Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 146 (6): e50–e68. doi:10.1161/CIR.0000000000001076.
  7. ↑ Heidenreich PA, Bozkurt B, Aguilar D; et al. (2022). "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure". Journal of the American College of Cardiology. 79 (17): e263–e421. doi:10.1016/j.jacc.2021.12.012.
  8. ↑ 8.0 8.1 Zampieri FG, Bagshaw SM, Njimi H, Vincent JL, DeBacker D (2024). "Exploration of Different Statistical Approaches in the Comparison of Dopamine and Norepinephrine in the Treatment of Shock: SOAP II". Critical Care. 28 (1): 299. doi:10.1186/s13054-024-05016-9.
  9. ↑ 9.0 9.1 Levy B, Clere-Jehl R, Legras A; et al. (2018). "Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction". Journal of the American College of Cardiology. 72 (2): 173–182. doi:10.1016/j.jacc.2018.04.051.
  10. ↑ 10.0 10.1 10.2 10.3 10.4 10.5 Rao SV, O'Donoghue ML, Ruel M; et al. (2025). "2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes". Journal of the American College of Cardiology. doi:10.1016/j.jacc.2024.11.009.
  11. ↑ Thiele H, Zeymer U, Thelemann N; et al. (2019). "Intraaortic Balloon Pump in Cardiogenic Shock Complicating Acute Myocardial Infarction: Long-Term 6-Year Outcome of the Randomized IABP-SHOCK II Trial". Circulation. 139 (3): 395–403. doi:10.1161/CIRCULATIONAHA.118.038201.
  12. ↑ Thiele H, Zeymer U, Akin I; et al. (2023). "Extracorporeal Life Support in Infarct-Related Cardiogenic Shock". The New England Journal of Medicine. 389 (14): 1286–1297. doi:10.1056/NEJMoa2307227.
  13. ↑ Møller JE, Engstrøm T, Jensen LO; et al. (2024). "Microaxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock". The New England Journal of Medicine. 390 (15): 1382–1393. doi:10.1056/NEJMoa2312572.
  14. ↑ Morici N, Sacco A, Frea S; et al. (2025). "Early Intra-Aortic Balloon Support for Heart Failure-Related Cardiogenic Shock: A Randomized Clinical Trial". Journal of the American College of Cardiology. 85 (16): 1587–1597. doi:10.1016/j.jacc.2025.03.003.
  15. ↑ Udesen NLJ, Beske RP, Hassager C; et al. (2025). "Microaxial Flow Pump Hemodynamic and Metabolic Effects in Infarct-Related Cardiogenic Shock". JAMA Cardiology. 10 (1): 9–16. doi:10.1001/jamacardio.2024.4197.
  16. ↑ Thiele H, Møller JE, Henriques JPS; et al. (2024). "Temporary Mechanical Circulatory Support in Infarct-Related Cardiogenic Shock: An Individual Patient Data Meta-Analysis of Randomised Trials With 6-Month Follow-Up". Lancet. 404 (10457): 1019–1028. doi:10.1016/S0140-6736(24)01448-X.
  17. ↑ Maddox TM, Januzzi JL, Allen LA; et al. (2024). "2024 ACC Expert Consensus Decision Pathway for Treatment of Heart Failure With Reduced Ejection Fraction". Journal of the American College of Cardiology. 83 (15): 1444–1488. doi:10.1016/j.jacc.2023.12.024.
  18. ↑ Blumer V, Sinha SS, Carnicelli AP; et al. (2026). "Cardiogenic Shock Survivorship: A Multidisciplinary Approach Across the Continuum of Care". Journal of the American College of Cardiology. doi:10.1016/j.jacc.2026.02.5080.
  19. ↑ Matsushita K, Delmas C, Marchandot B; et al. (2024). "Optimal Heart Failure Medical Therapy and Mortality in Survivors of Cardiogenic Shock: Insights From the FRENSHOCK Registry". Journal of the American Heart Association. 13 (5): e030975. doi:10.1161/JAHA.123.030975.
  20. ↑ 20.0 20.1 20.2 O'Gara PT, Kushner FG, Ascheim DD; et al. (2012). "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. doi:10.1161/CIR.0b013e3182742c84. PMID 23247303. Unknown parameter |month= ignored (help)
  21. ↑ 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 and ACC/AHA/SCAI guidelines on percutaneous coronary intervention". Journal of the American College of Cardiology. 54 (23): 2205–2241. doi:10.1016/j.jacc.2009.10.015. PMID 19942100. Retrieved 2011-12-06. Unknown parameter |month= ignored (help)
  22. ↑ 22.0 22.1 Hochman JS, Sleeper LA, Webb JG; et al. (1999). "Early revascularization in acute myocardial infarction complicated by cardiogenic shock". The New England Journal of Medicine. 341 (9): 625–634. doi:10.1056/NEJM199908263410901. PMID 10460813. Unknown parameter |month= ignored (help)
  23. ↑ Hochman JS, Lamas GA, Buller CE; et al. (2006). "Coronary intervention for persistent occlusion after myocardial infarction". The New England Journal of Medicine. 355 (23): 2395–2407. doi:10.1056/NEJMoa066139. PMC 1995554. PMID 17105759. Unknown parameter |month= ignored (help)
  24. ↑ 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): 2017–2021. doi:10.1161/CIRCULATIONAHA.105.558676. PMID 16186438. Unknown parameter |month= ignored (help)
  25. ↑ 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): 448–454. doi:10.1001/jama.294.4.448. PMID 16046651. Unknown parameter |month= ignored (help)
  26. ↑ 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): 2511–2515. doi:10.1001/jama.295.21.2511. PMC 1782030. PMID 16757723. Unknown parameter |month= ignored (help)
  27. ↑ "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' Collaborative Group". Lancet. 343 (8893): 311–322. 1994. PMID 7905143. Unknown parameter |month= ignored (help)
  28. ↑ 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". Circulation. 102 (17): 2031–2037. PMID 11044416. Unknown parameter |month= ignored (help)
  29. ↑ French JK, Feldman HA, Assmann SF; et al. (2003). "Influence of thrombolytic therapy, with or without intra-aortic balloon counterpulsation, on 12-month survival in the SHOCK trial". American Heart Journal. 146 (5): 804–810. doi:10.1016/S0002-8703(03)00392-2. PMID 14597928. Unknown parameter |month= ignored (help)
  30. ↑ 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". American Heart Journal. 141 (6): 933–939. doi:10.1067/mhj.2001.115295. PMID 11376306. Unknown parameter |month= ignored (help)
  31. ↑ 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): 951–957. doi:10.1161/01.CIR.0000085068.59734.E4. PMID 12912817. Unknown parameter |month= ignored (help)
  32. ↑ Sanborn TA, Sleeper LA, Bates ER; et al. (2000). "Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction". Journal of the American College of Cardiology. 36 (3 Suppl A): 1123–1129. PMID 10985715. Unknown parameter |month= ignored (help)
  33. ↑ Sjauw KD, Engström AE, Vis MM; 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?". European Heart Journal. 30 (4): 459–468. doi:10.1093/eurheartj/ehn602. PMID 19168529. Unknown parameter |month= ignored (help)
  34. ↑ 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". Journal of Thrombosis and Thrombolysis. 19 (1): 33–39. doi:10.1007/s11239-005-0938-0. PMID 15976965. Unknown parameter |month= ignored (help)
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