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Overview and Recommendations
Background
- •Cardiogenic shock (CS) represents the extreme end of the acute heart failure spectrum, where a primary cardiac insult—most commonly (AMI)—triggers a self-perpetuating downward spiral of reduced cardiac output, systemic hypotension, and coronary hypoperfusion.
- •The Society for Cardiovascular Angiography and Interventions (SCAI) staging system (Stages A–E) has replaced binary definitions, providing a dynamic framework that correlates with mortality risk, which ranges from ~3% in Stage A (At Risk) to >67% in Stage E (Extremis).
- •Ischemic etiologies (AMI-CS) account for the majority of cases, but heart failure-related shock (HF-CS) is increasing in prevalence; notably, the presence of concomitant right ventricular failure occurs in ~11% of patients and independently worsens prognosis across all stages.
- •Pathophysiology involves not only mechanical pump failure but also a systemic inflammatory response syndrome (SIRS) that can lead to a "mixed shock" phenotype, where low systemic vascular resistance (SVR) complicates the classic "cold and wet" presentation.
- •The paradigm of management has evolved from the 1999 SHOCK trial (establishing early revascularization) to the 2024 DanGer Shock trial, which provided the first randomized evidence that microaxial flow pumps ( CP) can reduce 180-day mortality in STEMI-related shock (NNT = 8).
Evaluation
- •Suspect cardiogenic shock in any patient with hypotension (SBP < 90 mmHg or MAP < 65 mmHg) who also exhibits signs of end-organ hypoperfusion, such as altered mental status, cool/mottled extremities, or oliguria (< 0.5 mL/kg/hr).
- •Perform an immediate bedside (POCUS) to assess left and right ventricular function, rule out mechanical complications (e.g., , acute ), and identify mimics like cardiac tamponade.
- •Order serial serum levels to quantify the depth of shock; a lactate > 2.0 mmol/L is a hallmark of Stage C shock, and a failure to clear lactate by > 10% within 6 hours of initiation of therapy is a strong predictor of 30-day mortality.
- •Assess for a narrow pulse pressure (< 25 mmHg), which often precedes overt hypotension in "normotensive" shock variants where high systemic vascular resistance temporarily masks low cardiac output.
- •Initiate invasive hemodynamic monitoring with a (PAC) to calculate the Cardiac Power Output (CPO = [MAP × CO] / 451); a CPO < 0.6 Watts is the most potent hemodynamic predictor of mortality in CS.
- •Evaluate right ventricular (RV) reserve using the Pulmonary Artery Pulsatility Index (PAPi = [sPAP - dPAP] / CVP); a PAPi < 1.0 suggests significant RV dysfunction that may require specific right-sided support.
- •Screen for mechanical complications of MI if a new holosystolic murmur is heard, as these patients require urgent surgical consultation and often benefit from immediate intra-aortic balloon pump (IABP) stabilization.
- •Differentiate between "cold and wet" (classic CS), "cold and dry" (hypovolemic CS requiring fluid challenge), and "warm and wet" (vasodilatory/mixed shock) phenotypes to tailor vasoactive therapy.
Management
- •Activate a multidisciplinary "Shock Team" (cardiology, cardiac surgery, critical care) immediately to coordinate rapid revascularization and potential mechanical support escalation.
- •Prioritize early revascularization in AMI-CS with a target door-to-catheterization (D2C) time of ≤ 39 minutes; use transradial access when possible, as it is associated with a > 50% reduction in mortality compared to femoral access.
- •Initiate (0.05–0.5 mcg/kg/min) as the first-line vasopressor to maintain a MAP of 65–70 mmHg; avoid due to a higher risk of arrhythmias and mortality.
- •Add an inotrope, such as (2.5–5 mcg/kg/min) or (0.125–0.25 mcg/kg/min), if signs of low cardiac output persist despite adequate MAP; milrinone may be preferred in patients on chronic beta-blockers.
- •Avoid as a first-line agent, as it is associated with increased rates of refractory shock and transient lactic acidosis (NNH = 4 for refractory shock).
- •Consider early insertion of a microaxial flow pump ( CP) in patients with STEMI-related shock (SCAI Stage C or D) to improve 180-day survival, while monitoring closely for major bleeding (BARC 3-5) and hemolysis.
- •Reserve venoarterial extracorporeal membrane oxygenation ( ) for patients in refractory shock (SCAI Stage E) or those with combined respiratory failure, ensuring proactive left ventricular unloading (e.g., with an IABP or Impella) to prevent pulmonary edema.
- •Perform culprit-only percutaneous coronary intervention (PCI) in the acute phase of shock for patients with multivessel disease, as immediate multivessel PCI increases the risk of death or renal failure (NNT = 11 to avoid these by choosing culprit-only).
- •Monitor renal function closely and initiate continuous renal replacement therapy ( ) early if volume overload or metabolic acidosis cannot be managed medically, especially in patients on tMCS.
- •Transition to guideline-directed medical therapy ( ), including beta-blockers and ACE inhibitors, only after the patient is weaned from all inotropic/vasopressor support and demonstrates hemodynamic stability.
Board Review — High Yield
- •SCAI Stage C — 'Classic' shock: hypotension + hypoperfusion requiring inotropes or MCS.
- •Cardiac Power Output (CPO) — (MAP x CO) / 451; < 0.6 Watts is the strongest predictor of mortality.
- •DanGer Shock Trial — First RCT to show mortality benefit for Impella CP in STEMI-CS (180-day mortality reduction).
- •CULPRIT-SHOCK Trial — Culprit-only PCI is superior to immediate multivessel PCI in the acute shock setting.
- •IABP-SHOCK II — Routine use of IABP in AMI-CS does not improve 30-day mortality.
- •PAPi — (sPAP - dPAP) / CVP; < 1.0 indicates right ventricular failure.
- •Norepinephrine vs Dopamine — Norepinephrine is superior due to fewer arrhythmic events and lower mortality in CS.
- •Mechanical Complications — Suspect VSD or papillary muscle rupture if a new murmur develops; IABP is indicated here.
Deep Dive — Evidence Details
Definition, Classification, and SCAI Staging
- ▸Cardiogenic shock is defined by primary cardiac dysfunction leading to systemic hypoperfusion and multiorgan failure.
- ▸The SCAI A-E staging system provides a validated, graded risk stratification tool with mortality rates ranging from 3% (Stage A) to over 67% (Stage E).
- ▸Serial reassessment of SCAI stage, particularly at 24 hours, is more prognostic than the initial admission stage.
Cardiogenic shock (CS) is a life-threatening clinical syndrome characterized by inadequate cardiac output to meet metabolic demands, resulting in systemic tissue hypoperfusion and subsequent multiorgan failure [1]A1c[5]D5[7]D5. This state of critical end-organ hypoperfusion is caused by primary cardiac dysfunction, which may be ischemic or non-ischemic in origin [5]D5[9]D5. CS remains the leading cause of in-hospital mortality following acute myocardial infarction, with mortality rates exceeding 40-50% in advanced stages [6]B2a[10]B3b.
Also Called / Synonyms:
- Cardiogenic shock (CS)
- with shock
- Pump failure
- AMI-CS (Acute myocardial infarction-related cardiogenic shock)
- HF-CS (Heart failure-related cardiogenic shock)
The SCAI Staging System
The Society for Cardiovascular Angiography and Interventions (SCAI) staging system provides a standardized, five-stage framework (A through E) to describe the severity of shock and predict mortality [1]A1c[6]B2a. This system replaces binary definitions with a dynamic spectrum that accounts for clinical, biochemical, and hemodynamic parameters [1]A1c[16]B2b.
- Stage A (At Risk): Patients with risk factors for CS (e.g., large MI, acute-on-chronic heart failure) who are currently hemodynamically stable [1]A1c[10]B3b.
- Stage B (Beginning): Compensated shock; patients exhibit clinical evidence of hypotension (SBP <90 mmHg or MAP <60 mmHg) or tachycardia without signs of hypoperfusion [1]A1c[4]B3b.
- Stage C (Classic): Decompensated shock; hypoperfusion is present (e.g., Lactate >2.0 mmol/L, cold extremities, oliguria) and requires intervention with inotropes, vasopressors, or mechanical circulatory support (MCS) [1]A1c[17]B3b.
- Stage D (Deteriorating): Failure of initial therapy; patients require escalating doses of vasopressors or additional MCS to maintain perfusion [1]A1c[16]B2b.
- Stage E (Extremis): Refractory shock; circulatory collapse or ongoing CPR [1]A1c[15]B3b.
Each stage is associated with a graded increase in mortality, ranging from approximately 3% in Stage A to over 67% in Stage E [10]B3b[15]B3b. The addition of a "(A)" modifier denotes the occurrence of cardiac arrest, which significantly worsens prognosis across all stages [1]A1c[3]B3b[18]B3b.
Phenotypes and Mixed Shock
Modern classification recognizes that CS is not a monolithic entity but a collection of distinct hemodynamic phenotypes [5]D5[13]B3b. While ischemic CS (AMI-CS) was historically the primary focus, heart failure-related CS (HF-CS) now accounts for a substantial proportion of cases [5]D5[11]B2b. Mixed shock occurs when CS is complicated by a secondary shock state, most commonly a systemic inflammatory response or sepsis, leading to a hybrid profile of low cardiac output and low systemic vascular resistance [5]D5. Identifying these phenotypes is critical, as they dictate the choice of pharmacological and mechanical support [9]D5[13]B3b.
Controversies and Guideline Disagreement
| Question | Position A (SCAI 2019) | Position B (CSWG/SCAI 2022) | Strength | Implication |
|---|---|---|---|---|
| Hypoperfusion Definition | Clinical signs or lactate >2.0 [1]A1c | Specific thresholds (Lactate >2.0, pH <7.25) [17]B3b | Moderate | Refines Stage C/D adjudication |
| Serial Reassessment | Not explicitly mandated [1]A1c | Reassessment at 24h is essential [16]B2b[19]B2b | Strong | 24h stage is more prognostic than admission stage |
Pearl: The SCAI staging system provides a dynamic framework for risk stratification, where a transition from Stage C to D identifies a critical window for therapeutic escalation before irreversible multiorgan failure occurs [1]A1c[16]B2b[19]B2b.
| Phenotype | Mechanism | Key Distinguishing Feature |
|---|---|---|
| Ischemic (AMI-CS) | Acute myocardial necrosis | ST-segment changes; elevated troponin [1]A1c |
| Non-Ischemic (HF-CS) | Chronic remodeling/decompensation | Low Cardiac Index; high filling pressures [11]B2b |
| Mixed Shock | Pump failure + Vasodilation | Low SVR; often triggered by sepsis/SIRS [5]D5 |
| Non-Cardiac CS | Extracardiac obstruction | PE, tamponade, or metabolic causes [7]D5 |
Epidemiology and Etiological Spectrum
- ▸AMI-CS mortality remains >50% despite early revascularization and MCS advances [42].
- ▸The etiological spectrum is diversifying, with increasing recognition of PPCM, TTS, and ICI-associated myocarditis as triggers for CS [31, 33, 36].
- ▸Concomitant right heart failure is a critical prognostic marker present in 11.3% of CS cases [40].
Mortality rates for acute myocardial infarction-related cardiogenic shock (AMI-CS) persistently exceed 50%, despite the widespread adoption of early revascularization and mechanical circulatory support (MCS) [42]B3b. While historically viewed as a complication of ST-segment elevation myocardial infarction (STEMI), the epidemiological landscape has shifted toward a more diverse etiological spectrum, including non-ST-segment elevation myocardial infarction (NSTEMI), acute decompensated heart failure (ADHF), and structural or inflammatory pathologies [34]B2a[40]B3b. In a large contemporary cohort of 348,919 patients with CS, the prevalence of concomitant right heart failure (RHF) was 11.3%, a finding independently associated with increased in-hospital mortality across all Society for Cardiovascular Angiography and Interventions (SCAI) stages [40]B3b.
Ischemic Etiologies: STEMI vs. NSTEMI
AMI remains the leading cause of CS, though the relative proportions of STEMI and NSTEMI are evolving. STEMI-CS patients frequently present with higher acuity; in the ECLS-SHOCK trial, 51.6% of patients were in SCAI stage C and 13.4% in stage D at admission [2]A1b. Early primary percutaneous coronary intervention (PPCI) within 60 minutes of randomization is associated with improved ST-segment resolution and lower 30-day composite outcomes of death and shock [23]A1b. Conversely, NSTEMI-CS often involves older patients with more extensive multi-vessel disease and comorbidities, leading to comparable or sometimes higher long-term mortality rates than STEMI-CS [34]B2a.
Non-Ischemic and Structural Spectrum
The etiological breadth of CS extends beyond coronary occlusion to include and mechanical complications. ADHF-related CS (often SCAI stage B) is characterized by progressive hemodynamic collapse in patients with known cardiomyopathy [26]A1b. Structural emergencies, such as (VSR), remain rare but catastrophic complications of MI, carrying extreme mortality risks despite modern MCS utilization [44]B2c. Acute valvular failure, including severe , may necessitate emergency transcatheter edge-to-edge repair (M-TEER) as a bridge to definitive surgery in selected high-risk patients [35]C4.
Special Populations and Rare Triggers
Specific clinical contexts present unique epidemiological profiles and challenges:
- (TTS): CS complicates a subset of TTS cases and can manifest either at admission or develop during hospitalization, with both timings significantly worsening the 1-year prognosis [31]B3b.
- (PPCM): The incidence of CS in PPCM is increasing; these patients often require combination therapies like levosimendan and bromocriptine or MCS to bridge to recovery [33]B3b[41]D5.
- Immune Checkpoint Inhibitor (ICI) : This rare immune-related adverse event can rapidly progress to fulminant CS, often requiring venoarterial extracorporeal membrane oxygenation (VA-ECMO) as a life-saving intervention [36]C4.
Risk Factors and Complications
Patient demographics in CS registries show a male predominance (72.3%) and a mean age ranging from 61.0 to 69.2 years [37]B2b[42]B3b. Beyond the primary cardiac insult, secondary complications significantly influence survival. Bleeding is a major risk factor, particularly with microaxial flow pumps (mAFP); in the DanGer Shock trial, BARC type 3-5 bleeding occurred in 26.3% (95% CI: 20.3%-33.2%) of mAFP patients compared to 15.3% in standard care [22]A1b. This represents an absolute risk increase of 11%, resulting in a NNH = 9 to cause one major bleeding event [22]A1b. Furthermore, antimicrobial use is high, with 55% of AMI-CS patients receiving therapy, although only 12.6% of blood cultures typically return positive [38]B3b.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| STEMI vs. NSTEMI Mortality | STEMI-CS has higher acute mortality due to sudden pump failure [2]A1b. | NSTEMI-CS has worse long-term outcomes due to comorbidities [34]B2a. | Moderate | Risk stratification must account for baseline frailty in NSTEMI. |
| ECMO Complications | Complications (bleeding, limb ischemia) drive mortality [22]A1b. | Complications are markers of severity but not independently causal for mortality [25]A1b. | Moderate | Focus on patient selection rather than just device safety. |
Pearl: The prevalence of right heart failure in cardiogenic shock is approximately 11.3%, and its presence significantly worsens mortality across all SCAI stages, necessitating early hemodynamic assessment of the right ventricle [40]B3b.
| Factor | Impact/Prevalence | Evidence Level |
|---|---|---|
| SCAI Stage D/E | Highest predictive metric for short-term mortality | 1b [2]A1b |
| Right Heart Failure | 11.3% prevalence; independently increases mortality | 3b [40]B3b |
| Age | Mean age 61–69; older age correlates with NSTEMI-CS | 3b [37]B2b[42]B3b |
| Major Bleeding | 26.3% incidence with mAFP; NNH = 9 | 1b [22]A1b |
| VSR | Rare but associated with near-universal mortality without surgery | 2c [44]B2c |
Pathophysiology and the Hemodynamic Spiral
- ▸The hemodynamic spiral is driven by a feedback loop where low diastolic pressure reduces coronary perfusion, further weakening the myocardium.
- ▸Mixed shock phenotypes, combining cardiogenic and distributive (inflammatory) elements, are increasingly prevalent and carry high mortality.
- ▸Cardiac Power Output (CPO) < 0.6 Watts is a critical threshold for identifying patients at the highest risk of death.
Myocardial dysfunction initiates a self-perpetuating cycle where declining cardiac output (CO) triggers systemic and coronary hypoperfusion, further compromising ventricular performance [52]D5[53]D5. This "downward spiral" is no longer viewed as a purely mechanistic pump failure but as a multifaceted syndrome involving a cascading inflammatory response and microcirculatory collapse [49]D5[57]D5. Rapid therapeutic intervention is required to "break" this spiral before end-organ sequelae become irreversible [55]D5.
The Classic Hemodynamic Spiral
The transition from acute myocardial injury to refractory shock follows a predictable sequence of physiological failures:
- Primary Myocardial Insult: A sudden loss of contractility—most commonly due to (AMI)—reduces stroke volume. In approximately 90% of AMI-related cases, the left ventricle is the primary site of dysfunction [53]D5.
- Pump Failure and Hypotension: Reduced CO leads to systemic hypotension and diminished mean arterial pressure (MAP) [48]D5[52]D5.
- Coronary Hypoperfusion: Unlike other organs, the heart is perfused primarily during diastole. Low diastolic blood pressure reduces coronary perfusion pressure (CPP = DBP - LVEDP), which exacerbates myocardial ischemia and further depresses contractility [61]D5.
- Neurohormonal Overdrive: To maintain MAP, the body activates the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). While compensatory, the resulting tachycardia and peripheral vasoconstriction increase myocardial oxygen demand and afterload, while fluid retention increases preload and pulmonary congestion [52]D5[61]D5.
- Metabolic Crisis: Persistent hypoperfusion leads to anaerobic metabolism, , and progressive multiorgan dysfunction [48]D5[57]D5.
Systemic Inflammation and the Mixed Shock Phenotype
Modern understanding of shock pathophysiology emphasizes that prolonged hypoperfusion triggers a systemic inflammatory response syndrome (SIRS) [49]D5. This inflammatory cascade involves the release of cytokines and nitric oxide, leading to pathological vasodilation and impaired oxygen extraction at the cellular level [61]D5.
This evolution often results in Mixed Cardiogenic Shock, defined as the presence of at least one additional shock state (typically distributive) alongside primary cardiac failure [5]D5. Mixed shock is now the second leading cause of shock in contemporary coronary intensive care units [5]D5. In these patients, the classic "cold and wet" profile may shift toward a "warm" phenotype due to low systemic vascular resistance (SVR), complicating the use of traditional vasopressors which may further impair microcirculatory flow [57]D5[61]D5.
The Rationale for Ventricular Unloading
Mechanical circulatory support (MCS), specifically microaxial flow pumps (mAFP), aims to interrupt the spiral by reducing the total intrinsic mechanical work of the heart [45]A1b. Unlike vasopressors, which increase afterload and myocardial oxygen demand, mAFPs augment CO while simultaneously "unloading" the left ventricle by reducing intraventricular pressure and volume [50]D5[58]D5. This reduction in wall stress improves the myocardial oxygen supply-demand balance and may facilitate ventricular recovery [58]D5. In the DanGer Shock trial, mAFP support was shown to improve survival in selected patients with STEMI-related shock (NNT not calculable from reported abstract data) [45]A1b[50]D5.
Microcirculatory Failure and Hemodynamic Metrics
Stabilizing macrocirculatory parameters (e.g., MAP and CO) does not always translate to improved tissue oxygenation. Microcirculatory impairment—characterized by reduced capillary density and heterogeneous flow—can persist despite normalized blood pressure, driving persistent tissue hypoxia and organ failure [57]D5.
To better capture this complexity, advanced hemodynamic markers are utilized for risk stratification. Cardiac Power Output (CPO), calculated as (MAP × CO) / 451, is a potent prognostic tool; values below 0.6 Watts are significantly associated with increased mortality [54]D5. Other markers, such as the Aortic Pulsatility Index (API) and the Pulmonary Artery Pulsatility Index (PAPi), provide insights into right ventricular reserve and the severity of the hemodynamic collapse [54]D5.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| Vasopressor Utility | First-line choice to maintain coronary perfusion [61]D5. | May worsen microcirculation and increase afterload [57]D5[61]D5. | Moderate | Shift toward early MCS to avoid high-dose vasopressors. |
| Unloading Strategy | Routine early mAFP in STEMI-CS improves survival [45]A1b[50]D5. | Evidence for IABP remains neutral; requires careful selection [53]D5[58]D5. | High | Differentiated patient selection is essential for benefit. |
Pearl: The transition from a purely low-output state to a systemic inflammatory syndrome marks the point of no return in the "downward spiral," where macrocirculatory stabilization often fails to reverse microcirculatory debt [49]D5[57]D5.
| Marker | Formula/Definition | Clinical Significance |
|---|---|---|
| Cardiac Power Output (CPO) | (MAP × CO) / 451 | Strongest predictor of mortality; threshold < 0.6 W [54]D5. |
| Aortic Pulsatility Index (API) | (SBP - DBP) / PCWP | Measures LV performance and filling pressures [54]D5. |
| PAPi | (PASP - PADP) / RAP | Predicts right ventricular failure [54]D5. |
| CPP | DBP - LVEDP | Determines the pressure gradient for coronary flow [61]D5. |
Clinical Presentation and Physical Examination
- ▸Cardiogenic shock is a dynamic state where end-organ hypoperfusion (e.g., lactate > 2.0 mmol/L, oliguria) often precedes overt hypotension.
- ▸The 'Cold and Wet' phenotype remains most common, but 'Mixed Shock' (cardiac failure + vasodilation) is increasingly recognized in contemporary intensive care.
- ▸Diastolic Perfusion Pressure (DPP) and Blood Pressure Response Index (BPRI) are emerging bedside metrics that better predict mortality and treatment response than systolic blood pressure alone.
End-organ hypoperfusion serves as the clinical pivot, often preceding the overt hypotension that defines late-stage collapse [71]D5[73]D5. While the classic presentation involves a patient who is "cold and wet," the clinical spectrum is broad, ranging from compensated states with preserved blood pressure to refractory multiorgan failure [1]A1c[72]D5. Early recognition is hampered by the "point of no return," where hemodynamic dysregulation becomes irreversible despite escalating support [73]D5.
Presenting Symptoms
Patients typically present with a combination of low-output symptoms and signs of pulmonary or systemic congestion. Dyspnea is the most frequent complaint, often progressing rapidly from exertional intolerance to orthopnea and paroxysmal nocturnal dyspnea. Chest pain may be present in the setting of , but its absence does not exclude the diagnosis, particularly in elderly or diabetic populations [68]A1c. Symptoms often progress over hours to days, though in chronic heart failure patients, the transition to shock may be a more insidious decline over weeks [73]D5. Fatigue, profound weakness, and a sense of impending doom are common subjective markers of severely reduced .
Neurological Examination Findings
Cerebral hypoperfusion manifests as a spectrum of encephalopathy, often serving as the earliest sign of SCAI Stage C shock [1]A1c. Initial findings include agitation, restlessness, or a "clouded" sensorium. As perfusion worsens, this progresses to somnolence, obtundation, and eventually coma. The neurological exam must distinguish between primary cardiogenic encephalopathy and secondary insults such as post-cardiac arrest hypoxic-ischemic brain injury [59]D5. Autonomic instability may manifest as diaphoresis and peripheral vasoconstriction, though these may be absent in patients with a "mixed" shock phenotype involving systemic vasodilation [5]D5.
Phenotypic Variants
Modern phenotyping moves beyond the binary "shock vs. no shock" to categorize patients by volume status and peripheral perfusion [72]D5[75]D5.
| Variant | Key Features | Frequency |
|---|---|---|
| Cold and Wet | Classic CS; low CI, high PCWP; cool skin, crackles, JVD | ~70–80% |
| Cold and Dry | Euvolumic or hypovolemic CS; low CI, low/normal PCWP; requires fluid challenge | ~10–15% |
| Warm and Wet | "Normotensive" shock; high SVR masks low CO; pulmonary edema with peripheral perfusion | ~5–10% |
| Mixed Shock | CS plus systemic inflammatory response (e.g., sepsis or post-arrest); low SVR and low CO [5]D5 | Increasing |
Red Flags
Immediate escalation is required when bedside markers suggest a failure of compensatory mechanisms. A narrow pulse pressure < 25 mmHg or a systolic blood pressure < 90 mmHg for >30 minutes are traditional triggers, but clinicians must prioritize signs of metabolic failure. Urine output < 0.5 mL/kg/hr for two consecutive hours and a serum lactate > 2.0 mmol/L are critical thresholds for Stage C shock [1]A1c[75]D5. The presence of an S3 gallop, new-onset holosystolic murmurs (suggesting papillary muscle rupture or VSD), and cold, mottled extremities (Livedo reticularis) indicate a high risk of imminent hemodynamic collapse [71]D5[72]D5.
Atypical Presentations
Normotensive cardiogenic shock is a frequent diagnostic pitfall where the patient maintains a "normal" blood pressure through extreme systemic vascular resistance (SVR) at the expense of organ perfusion [72]D5. In these cases, the Diastolic Perfusion Pressure (DPP = DBP - RAP) may be more predictive; a lower DPP is associated with a limited response to vasoactive drugs and higher mortality [65]B2b. Right ventricular (RV) shock presents atypically with clear lung fields despite high central venous pressure and profound hypotension [71]D5. Additionally, the Blood Pressure Response Index (BPRI) can help identify patients with a poor dose-effect response to vasopressors, signaling a higher risk of in-hospital mortality [70]B3b.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| Definition of Shock | Requires SBP < 90 mmHg or MAP drop > 30 mmHg [68]A1c. | Focuses on hypoperfusion markers (lactate, organ injury) regardless of BP [1]A1c[59]D5. | Moderate | Affects trial inclusion and timing of MCS [59]D5. |
| Role of Hypothermia | Moderate hypothermia (33-34°C) may improve cardiac performance [64]D5. | Meta-analysis shows no significant mortality benefit in CS without arrest [67]A1a. | High | Routine use not recommended outside of post-arrest [67]A1a. |
Pearl: The absence of hypotension does not rule out cardiogenic shock; bedside markers of hypoperfusion like a narrow pulse pressure and oliguria are more sensitive indicators of the "normotensive" shock variant [65]B2b[72]D5.
| Phenotype | Perfusion (CI) | Congestion (PCWP) | Clinical Findings |
|---|---|---|---|
| Classic (Cold/Wet) | Low (< 2.2) | High (> 18) | Edema, crackles, cool skin, JVD |
| Euvolemic (Cold/Dry) | Low (< 2.2) | Low/Normal (≤ 15) | Clear lungs, cool skin, flat neck veins |
| Vasodilatory (Warm/Wet) | Low (< 2.2) | High (> 18) | Edema, warm skin (low SVR), often mixed etiology |
| RV Shock | Low (< 2.2) | Low/Normal | Clear lungs, high JVD, prominent V-waves |
Diagnostic Workup and Hemodynamic Monitoring
- ▸Pulmonary artery catheterization (PAC) is essential for calculating Cardiac Power Output (CPO) and Pulmonary Artery Pulsatility Index (PAPi), which guide MCS selection.
- ▸Lactate clearance of >10% within the first 6 hours is a critical prognostic marker for 30-day survival in patients receiving mechanical support.
- ▸Echocardiographic RVOT VTI is the most accurate non-invasive surrogate for stroke volume in ischemic cardiogenic shock.
Invasive and point-of-care ultrasonography (POCUS) serve as the dual pillars of modern , transforming the diagnostic process from a static clinical assessment into a dynamic, longitudinal evaluation of tissue perfusion and ventricular-arterial coupling [71]D5[98]D5. While clinical signs of hypoperfusion—such as cold extremities, oliguria, and altered mentation—initiate the workup, they are often insensitive to early-stage shock (SCAI stage B) [71]D5[100]D5. Clinicians prioritize rapid metabolic and hemodynamic phenotyping to differentiate between ischemic and non-ischemic etiologies and to identify mechanical complications that require urgent surgical or transcatheter intervention [91]D5[94]D5.
History and Physical
Clinicians must rapidly assess the timeline of symptom evolution, as acute-onset shock often suggests (AMI) or a mechanical complication, whereas gradual decompensation is more typical of chronic heart failure (HF-CS) [93]B3b[100]D5. Physical examination focuses on identifying the "wet and cold" phenotype, though up to 20% of patients may present with a "dry and cold" profile due to profound volume depletion or prior diuretic use [71]D5. Red flags include a new holosystolic murmur, which may indicate ventricular septal rupture or acute [94]D5. In cases of suspected calcium channel antagonist toxicity, POCUS is essential to differentiate between vasoplegia and cardiogenic collapse [79]C4.
Gold-Standard Test: Invasive Hemodynamic Assessment
Invasive hemodynamic assessment via pulmonary artery catheterization (PAC) remains the gold standard for phenotyping and guiding the escalation of (MCS) [71]D5[98]D5. PAC provides direct measurements of central venous pressure (CVP), pulmonary artery pressure (PAP), and pulmonary capillary wedge pressure (PCWP), allowing for the calculation of critical indices [11]B2b[98]D5.
- Cardiac Power Output (CPO): Calculated as (Mean Arterial Pressure × Cardiac Output) / 451. A CPO <0.6 W is a powerful predictor of mortality in CS [11]B2b.
- Pulmonary Artery Pulsatility Index (PAPi): Calculated as (Systolic PAP - Diastolic PAP) / CVP. A PAPi <1.0 suggests significant right ventricular (RV) dysfunction [11]B2b.
- Aortic Pulsatility Index (API): Integrates ventricular output with filling pressures; non-invasive "echo-API" is a feasible surrogate in patients on tMCS [102]C4.
Laboratory Studies
Metabolic markers provide a quantitative measure of the depth of shock and the adequacy of resuscitation. Serum lactate >2.0 mmol/L is the primary marker of anaerobic metabolism; however, lactate clearance is more prognostic than a single peak value [78]B3b. A failure to achieve >10% lactate clearance within 6 hours of initiating therapy is associated with significantly higher 30-day mortality [78]B3b.
| Test | Finding in CS | Clinical Significance |
|---|---|---|
| Serum Lactate | >2.0 mmol/L | Marker of tissue hypoperfusion and anaerobic metabolism [78]B3b. |
| Glycemic Gap | Elevated | Superior to blood glucose for identifying stress-induced hyperglycemia [77]B3b. |
| Creatinine/LFTs | Elevated | Indicates multiorgan dysfunction syndrome (MODS) [71]D5[87]B2c. |
| NT-proBNP | Elevated | Reflects ventricular wall stress and filling pressures [71]D5. |
Imaging and "Echodynamics"
Transthoracic echocardiography (TTE) is the first-line imaging modality for identifying the underlying cause of shock, such as severe bicuspid or SARS-CoV-2-related fulminant [82]C4[83]C4. Beyond ejection fraction, Doppler-derived parameters provide a non-invasive hemodynamic profile, a concept termed "echodynamics" [11]B2b. RV outflow tract velocity time integral (RVOT VTI) is the strongest echocardiographic correlate of stroke volume (r=0.78) [76]B3b. Furthermore, Global Longitudinal Strain (GLS) ≤5.0% (Quartile 4) is associated with the highest risk of in-hospital mortality (NNT not calculable from reported data) [88]B3b.
Echocardiography is also indispensable for monitoring patients on tMCS, ensuring optimal device positioning and assessing for cardiac recovery [85]D5[90]D5. For patients on V-A ECMO, parameters such as the Pressure-Strain Product (PSP) and total isovolumic time (t-IVT) are emerging as predictors of successful weaning [89]B2b[90]D5. In cases of AMI-CS, TTE must be performed immediately to rule out mechanical complications like papillary muscle rupture, which may require emergency mitral transcatheter edge-to-edge repair (M-TEER) as a bridge to surgery [35]C4[80]C4[94]D5.
Diagnostic Algorithm
- Step 1: Clinical Screening. Identify SCAI stage (A-E) based on physical signs of hypoperfusion and hypotension [71]D5.
- Step 2: Bedside POCUS/TTE. Assess LV/RV function, rule out mimics (e.g., LVOTO), and screen for mechanical complications [92]C4[95]B2b.
- Step 3: Metabolic Profiling. Obtain arterial blood gas, lactate, and glycemic gap [77]B3b[78]B3b.
- Step 4: Invasive Hemodynamics. Place PAC to calculate CPO and PAPi, especially if the patient is refractory to initial inotropes or requires MCS [11]B2b[98]D5.
- Step 5: Longitudinal Re-evaluation. Monitor lactate clearance and use the W score or similar tools to predict successful tMCS liberation [78]B3b[86]B3b.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| Routine PAC Use | Routine use in all CS patients to guide therapy [98]D5. | Selective use in refractory or complex cases [71]D5. | Moderate | PAC resurgence is driven by the need for precise MCS titration. |
| LVEF vs. Doppler | LVEF remains the standard for defining shock severity [71]D5. | Doppler parameters (CPO, VTI) are superior for risk stratification [97]B3b. | Emerging | Shift toward functional rather than structural assessment. |
Pearl: Early invasive hemodynamic phenotyping using pulmonary artery catheters, combined with serial lactate clearance monitoring, reduces diagnostic uncertainty and facilitates the timely escalation of mechanical circulatory support [71]D5[78]B3b[98]D5.
| Parameter | Threshold | Clinical Interpretation |
|---|---|---|
| Cardiac Power Output (CPO) | <0.6 W | High risk of mortality; suggests inadequate pump function [11]B2b. |
| PAPi | <1.0 | Suggests predominant right ventricular failure [11]B2b. |
| PCWP | >15 mmHg | Indicates left-sided congestion and elevated filling pressures [11]B2b. |
| RVOT VTI | <10 cm | Correlates with severely reduced stroke volume [76]B3b. |
Pharmacological Management: Inotropes and Vasopressors
- ▸Norepinephrine is superior to dopamine in cardiogenic shock, reducing arrhythmic events and mortality (RR 0.89).
- ▸The DOREMI trial established that milrinone and dobutamine are equivalent regarding in-hospital mortality and major clinical outcomes.
- ▸Epinephrine increases the risk of refractory shock and metabolic distress (NNH = 4) compared to norepinephrine.
Norepinephrine reduces the risk of arrhythmic events and 28-day mortality compared to dopamine (RR 0.89, 95% CI 0.81–0.98), establishing it as the first-line vasopressor for maintaining perfusion [115]A1a (1a). While vasoactive agents are essential for immediate stabilization, they function as a double-edged sword by increasing myocardial oxygen demand and potentially exacerbating the hemodynamic spiral. Clinicians must balance the necessity of maintaining a Mean Arterial Pressure (MAP) ≥ 65–70 mmHg against the risks of catecholamine-induced toxicity and metabolic distress [104]B2b[114]C4 (2b, 4).
Vasopressor Selection and MAP Targets
Norepinephrine is the preferred agent for achieving hemodynamic stability because it provides potent alpha-1 agonism with minimal beta-1-mediated chronotropy compared to dopamine [111]A1a[115]A1a (1a). In the SOAP II trial and subsequent meta-analyses, dopamine was associated with a significantly higher incidence of arrhythmias and increased mortality in the cardiogenic shock (CS) subgroup [115]A1a (1a). Epinephrine should generally be avoided as a first-line agent; the OptimaCC trial demonstrated that epinephrine increases the risk of refractory shock (37% vs 7%, p=0.002) and induces transient and tachycardia compared to norepinephrine [107]A1b (1b). This "metabolic distress" signal suggests an NNH of 4 for epinephrine to cause refractory shock compared to norepinephrine [107]A1b.
Targeting a MAP ≥ 70 mmHg may be superior to the traditional 65 mmHg threshold. A post hoc analysis of the DOREMI trial found that patients maintaining an average MAP < 70 mmHg over the first 36 hours had significantly higher in-hospital mortality (60% vs 44%; OR 2.09, 95% CI 1.05–4.14), suggesting an NNT of 7 to maintain the higher target to prevent one death [104]B2b (2b). However, uptitrating norepinephrine to a MAP of 85 mmHg does not appear to improve microcirculatory tissue oxygenation or lactate levels, indicating a ceiling effect for vasopressor benefit [114]C4 (4).
Inotropic Support: Dobutamine vs. Milrinone
Selection between and depends more on patient-specific factors than on a difference in primary efficacy. The landmark DOREMI trial (N=192) found no significant difference between the two agents regarding a composite of death, cardiac arrest, or need for mechanical support (49% milrinone vs 54% dobutamine; HR 0.90, 95% CI 0.70–1.17) [106]A1b (1b). Milrinone, a phosphodiesterase-3 (PDE3) inhibitor, may be preferred in patients with chronic use, as its mechanism is independent of the beta-receptor [105]B2b (2b). However, milrinone requires dose adjustment in renal impairment and can cause prolonged hypotension due to its longer half-life and vasodilatory properties [106]A1b[122]D5. Dobutamine remains the standard for rapid titration but is limited by dose-dependent tachycardia and increased myocardial oxygen consumption [117]A1a[118]A1a (1a).
Refractory and Mixed Shock States
In cases of refractory vasoplegia or mixed cardiogenic-septic shock, is frequently utilized as a catecholamine-sparing agent [123]B2c[124]B2b (2c, 2b). Retrospective data suggest that adding vasopressin may be associated with higher mortality in unselected CS patients (OR 1.65, 95% CI 1.06–2.57), likely reflecting its use in more severe, end-stage shock [126]B3b (3b). In patients supported by VA-ECMO, the timing of vasopressin initiation may influence renal outcomes, though high-quality RCT data are lacking [121]B3b (3b). Lactate clearance serves as the primary laboratory surrogate for therapeutic success; failing to achieve >10% clearance within 24 hours is independently associated with a three-fold increase in mortality (OR 3.26, 95% CI 1.54–6.90) [103]B2b (2b).
Step-by-Step Pharmacological Protocol
- Establish MAP Target: Aim for ≥65–70 mmHg initially [104]B2b.
- Initiate Vasopressor: Start Norepinephrine 0.05–0.5 mcg/kg/min to achieve the MAP target [115]A1a.
- Add Inotrope: If signs of low cardiac output persist (e.g., cold extremities, oliguria, rising lactate), initiate Dobutamine 2.5–5 mcg/kg/min or Milrinone 0.125–0.25 mcg/kg/min [106]A1b.
- Monitor and Titrate: Assess response via lactate clearance every 4–6 hours and bedside echocardiography or (PAC) [103]B2b[127]B3b.
- Escalate or Wean: If shock is refractory to dual therapy, consider early escalation to mechanical circulatory support (MCS) rather than further catecholamine uptitration [112]D5[113]D5.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| Optimal MAP Target | DOREMI Analysis — Suggests MAP ≥ 70 mmHg reduces mortality [104]B2b | Standard Guidelines — Often recommend MAP ≥ 65 mmHg as the default | Moderate | Higher targets may improve organ perfusion but increase vasopressor load. |
| Inotrope Choice in BB Users | Theoretical Benefit — Milrinone bypasses beta-receptors, suggesting superiority | DOREMI Subgroup — No clinical difference in outcomes between milrinone and dobutamine [105]B2b | Moderate | Clinicians may still favor milrinone in BB users despite lack of RCT-proven mortality benefit. |
Pearl: Norepinephrine is the first-line vasopressor to minimize arrhythmias, while dobutamine and milrinone are clinically equivalent inotropes; prioritize lactate clearance >10% in the first 24 hours as a key marker of therapeutic success [103]B2b[106]A1b[115]A1a.
| Drug | Starting Dose | Max Dose | Key Considerations | Evidence Level |
|---|---|---|---|---|
| Norepinephrine | 0.05 mcg/kg/min | 1.0 mcg/kg/min | First-line vasopressor; lower arrhythmia risk than dopamine. | 1a [115]A1a |
| Dobutamine | 2.5 mcg/kg/min | 20 mcg/kg/min | Rapid titration; risk of tachycardia and increased MVO2. | 1b [106]A1b |
| Milrinone | 0.125 mcg/kg/min | 0.75 mcg/kg/min | PDE3 inhibitor; requires renal adjustment; preferred in BB users. | 1b [106]A1b |
| Vasopressin | 0.01 units/min | 0.04 units/min | Catecholamine-sparing; used in mixed vasoplegic shock. | 3b [126]B3b |
| Epinephrine | 0.05 mcg/kg/min | 0.5 mcg/kg/min | Avoid as first-line; causes lactic acidosis and refractory shock. | 1b [107]A1b |
Temporary Mechanical Circulatory Support (tMCS)
- ▸The DanGer Shock trial established a 180-day survival benefit for Impella CP in STEMI-related cardiogenic shock, though at the cost of increased major bleeding.
- ▸Routine VA-ECMO does not improve 30-day mortality in AMI-CS (ECLS-SHOCK trial), necessitating a shift toward highly selective use and proactive left ventricular unloading.
- ▸The Aortic Pulsatility Index (API) and ELSO-score are validated tools for predicting native recovery and in-hospital mortality, respectively, in patients on mechanical support.
Escalation to temporary mechanical circulatory support (tMCS) is indicated when pharmacological therapy fails to maintain a cardiac index >2.2 L/min/m² or when SCAI stage C shock rapidly progresses toward stage E [71]D5[133]D5. The primary goal of tMCS is to provide a bridge to recovery, bridge to decision, or bridge to a durable device by maintaining end-organ perfusion while reducing myocardial oxygen demand [48]D5[135]B3b. Early activation of a multidisciplinary shock team is essential to navigate the complex selection of devices, as each modality offers distinct hemodynamic profiles and complication risks [71]D5[132]D5.
Intra-aortic Balloon Pump (IABP)
The IABP remains the most widely utilized tMCS due to its rapid insertion and low complication rate, despite the lack of a routine mortality benefit in infarct-related cardiogenic shock (AMI-CS) [133]D5[143]B3b. It functions via counterpulsation, inflating during diastole to augment coronary perfusion and deflating during systole to reduce afterload by approximately 10% to 20% [138]C4. While the IABP-SHOCK II trial established that routine use does not improve 30-day mortality, the device remains a reliable pillar for patients with mechanical complications or those requiring modest support [133]D5. The Aortic Pulsatility Index (API)—calculated as (systolic blood pressure – diastolic blood pressure) / pulmonary capillary wedge pressure—serves as a potent predictor of native heart recovery in patients supported by IABP [144]B3b.
Microaxial Flow Pumps (mAFP)
Microaxial flow pumps, such as the Impella series, provide active non-pulsatile support by continuous blood aspiration from the left ventricle (LV) into the ascending aorta [27]A1a[140]B2b. The DanGer Shock trial demonstrated that the Impella CP reduces 180-day mortality in STEMI-related cardiogenic shock compared to standard care (45.8% vs 58.5%; HR 0.74, 95% CI 0.55-0.99); NNT = 8 to prevent one death at 6 months [22]A1b. However, this benefit is offset by a significant increase in BARC type 3-5 bleeding (26.3% vs 15.3%; NNH = 9) and vascular complications [22]A1b.
High-capacity devices like the Impella 5.5 (surgically implanted) provide up to 5.5 L/min of flow and are increasingly used to bridge patients to durable LVADs or heart transplantation [135]B3b[140]B2b. To mitigate vascular injury, a sheathless femoral technique for Impella CP has shown feasibility in patients with small or diseased arteries [137]C4. Clinicians must also monitor for device-associated valvular complications, such as aortic or mitral valve injury, which may require surgical intervention [130]C4.
Venoarterial Extracorporeal Membrane Oxygenation (VA-ECMO)
VA-ECMO provides the highest level of support, offering full biventricular and respiratory bypass for patients in refractory shock (SCAI stage D or E) [25]A1b[134]B2c. Despite its potency, the ECLS-SHOCK trial found that routine VA-ECMO did not reduce 30-day mortality in AMI-CS compared to medical therapy alone (47.8% vs 49.0%, p=0.70) [25]A1b[2]A1b. This equipoise may be due to the increased afterload VA-ECMO imposes on the LV, which can lead to pulmonary edema and impaired myocardial recovery [131]B2a[138]C4.
Prognostication on VA-ECMO is guided by the ELSO-score, which utilizes pre-ECMO variables to predict in-hospital mortality [134]B2c. Acid-base status at 24 hours post-initiation—specifically pH, bicarbonate, and PaCO2—is also strongly associated with survival [136]B3b. For weaning, the LEVOECMO trial investigated levosimendan (0.2 µg/kg/min for 24 hours) but found it did not significantly reduce the time to successful weaning or improve 30-day survival [24]A1b.
Left Ventricular Unloading and Combined Strategies
Active LV unloading is often required during VA-ECMO to counteract retrograde flow and reduce LV wall tension [131]B2a[138]C4. Combining VA-ECMO with an IABP or Impella (often termed "ECMELLA" or "ECMO-pella") has been shown to improve cardiac energetics and modulate cardioprotective signaling pathways [138]C4. A meta-analysis of 2,117 patients suggests that early unloading (within 12 hours of ECMO initiation) is associated with lower mortality compared to late or no unloading [131]B2a.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| Routine VA-ECMO in AMI-CS | Recommended for rapid stabilization in all refractory cases. | Not recommended routinely; no mortality benefit in ECLS-SHOCK [25]A1b. | High (RCT) | Reserve for highly selected, refractory SCAI E patients. |
| Routine mAFP in STEMI-CS | Use early to improve 180-day survival (DanGer Shock [22]A1b). | Avoid routine use due to high bleeding and cost (older meta-analyses). | Moderate (RCT) | Favor use in STEMI-CS but strictly monitor for BARC 3-5 bleeding. |
| LV Unloading Timing | Proactive unloading at the time of ECMO insertion [131]B2a. | Reactive unloading only if signs of LV distention appear. | Moderate (Meta-analysis) | Growing evidence favors early, proactive unloading. |
Pearl: The survival benefit of the Impella CP in STEMI-CS (NNT = 8) is the first RCT evidence of a mortality reduction for tMCS in decades, but it requires vigilant of its high bleeding risk (NNH = 9) [22]A1b.
| Device | Flow (L/min) | Primary Effect | Common Complications | Evidence Level |
|---|---|---|---|---|
| IABP | 0.5–1.0 | ↑ Coronary perfusion, ↓ Afterload | Limb ischemia, Thrombocytopenia | Class IIa/IIb [133]D5 |
| Impella CP | Up to 4.3 | ↑ Systemic flow, ↓ LV work | Bleeding (26%), Hemolysis, Vascular injury | Class I (STEMI-CS) [22]A1b |
| Impella 5.5 | Up to 5.5 | Full LV support, ↓ LV work | Bleeding, Infection (surgical site) | Class IIa [140]B2b |
| VA-ECMO | Up to 7.0 | Biventricular & Respiratory support | ↑ LV afterload, AKI, Stroke | Class IIb (Refractory) [25]A1b |
| VP ECLS | Variable | Right ventricular support | Bleeding, Cannula malposition | Emerging [141]B3b |
Revascularization and Definitive Interventions
- ▸Early revascularization (D2C ≤39 min) is the primary determinant of survival in AMI-CS, a target more easily achieved with cardiologist-led first contact [157].
- ▸Transradial access (TRA) reduces in-hospital mortality by 55% compared to transfemoral access in patients undergoing PCI for cardiogenic shock [148].
- ▸Multidisciplinary Advanced Cardiogenic-Shock Teams (ACT) and protocolized care are essential to reduce treatment delays and address persistent health disparities [153, 154].
Rapid restoration of coronary blood flow remains the cornerstone of for infarct-related cardiogenic shock (AMI-CS), as every minute of delay correlates with increased myocardial loss and worsening systemic hypoperfusion [133]D5[157]B3b. Achieving a door-to-cardiac catheterization laboratory (D2C) time of ≤39 minutes is associated with improved survival, a target more frequently met when a cardiologist is the first point of medical contact [157]B3b. Despite the established benefit of early revascularization, significant disparities persist; women and racial minorities are 20% to 40% less likely to receive guideline-recommended interventions or mechanical circulatory support (MCS) [154]D5.
Percutaneous Coronary Intervention (PCI) Strategy
Transradial access (TRA) is the preferred approach for PCI in AMI-CS due to its superior safety profile compared to transfemoral access (TFA). A meta-analysis of 33,311 individuals demonstrated that TRA reduces the odds of in-hospital mortality by 55% (OR 0.45, 95% CI 0.30-0.67); (NNT not calculable from reported data) [148]B2a. While TFA remains necessary for large-bore MCS insertion, a sheathless femoral technique for CP can mitigate vascular and bleeding complications in patients with small or diseased vessels [137]C4.
Culprit-only revascularization remains the standard of care for patients with multivessel disease (MVD) to minimize procedure time and contrast-induced nephropathy [128]A1c[158]B2c. However, approximately 50% of AMI-CS patients present with MVD, and recent evidence suggests that complete revascularization may be considered in selected patients, particularly those with adequate hemodynamic support [145]B2b[158]B2c. The integration of microaxial flow pumps, such as the Impella CP, has shown a reduction in 180-day all-cause mortality in STEMI-related shock, though only 30.5% of real-world patients may meet the strict eligibility criteria used in pivotal trials like DanGer Shock [149]D5[156]B3b.
Pharmacological Adjuncts and Surgical Options
Intravenous antiplatelet agents provide rapid, predictable inhibition in patients with impaired oral absorption due to shock or therapeutic hypothermia [43]B3b[151]B2a. Agents such as are increasingly utilized due to their organ-independent metabolism and rapid offset, which is critical if urgent surgery is required [151]B2a. In the ACTION-SHOCK cohort, intravenous antiplatelet therapy was not associated with a significant increase in major bleeding while providing potent platelet inhibition during the critical early phase of shock [43]B3b.
Surgical revascularization ( ) is indicated for patients with complex multivessel disease not amenable to PCI or those with mechanical complications [147]A1c[155]B2c. Between 2011 and 2022, over 34,000 AMI-CS patients underwent CABG, with a trend toward increased preoperative use of temporary MCS to stabilize patients before the operating room [155]B2c. High-capacity MCS devices (e.g., Impella 5.0/5.5) may offer superior survival compared to low-capacity versions (e.g., Impella 2.5/CP) in this surgical population [27]A1a.
Mechanical Complications
Mechanical complications, including ventricular septal rupture (VSR) and papillary muscle rupture leading to acute , carry a mortality rate often exceeding 50% [147]A1c[150]B2a. Expert consensus recommends early surgical or percutaneous repair, as medical management alone is almost universally fatal [147]A1c. Percutaneous VSR closure or edge-to-edge mitral repair serves as a viable alternative for patients deemed too high-risk for traditional surgery, with some patients achieving long-term survival exceeding 12 years despite an initially futile prognosis [152]C4.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| Multivessel PCI in AMI-CS | Culprit-only revascularization is the default to minimize procedure time [128]A1c[158]B2c. | Complete revascularization may be considered in stable patients or those with MCS [145]B2b[158]B2c. | Moderate | Individualized approach based on SCAI stage and support. |
| Access Site with ECLS | Radial access is preferred to reduce bleeding [148]B2a. | Femoral access is often mandatory for ECLS/MCS cannulation [146]B2b. | Moderate | Access site must balance bleeding risk with MCS requirements. |
Pearl: Early revascularization with a target D2C time of ≤39 minutes and the use of transradial access (OR 0.45 for mortality) are the most critical modifiable factors for improving survival in AMI-CS [148]B2a[157]B3b.
| Strategy | Clinical Action | Evidence/Outcome |
|---|---|---|
| Access Site | Transradial (TRA) preferred over Transfemoral (TFA) | 55% reduction in mortality odds [148]B2a |
| PCI Timing | Door-to-Cath Lab (D2C) ≤39 minutes | Improved in-hospital survival [157]B3b |
| PCI Extent | Culprit-only revascularization (Standard) | Minimizes contrast and procedure time [128]A1c[158]B2c |
| Antiplatelets | IV Cangrelor or GPIIb/IIIa inhibitors | Rapid inhibition; organ-independent metabolism [151]B2a |
| Mechanical Repair | Early surgical or percutaneous intervention | Essential for VSR or papillary muscle rupture [147]A1c |
Multiorgan Dysfunction and Supportive Care
- ▸AKI affects up to 80% of CS patients and is a major predictor of mortality, often requiring CRRT for fluid and metabolic management.
- ▸Mechanical circulatory support with mAFPs (Impella) reduces mortality but increases the incidence of RRT compared to standard care.
- ▸Therapeutic hypothermia (33–34°C) does not provide a survival benefit in patients with cardiogenic shock on VA-ECMO.
Acute kidney injury (AKI) complicates up to 80% of cardiogenic shock (CS) cases, serving as a primary driver of mortality and a hallmark of the transition from isolated cardiac failure to systemic multiorgan dysfunction [168]D5. This systemic phase, often termed the "hemodynamic spiral," involves a complex interplay of impaired perfusion, venous congestion, and a profound inflammatory response that necessitates a comprehensive ICU-based supportive care strategy [168]D5[169]D5.
Renal and Replacement Therapy
Renal dysfunction in CS is multifactorial, driven by reduced arterial inflow (low cardiac output) and increased venous backpressure (congestive nephropathy) [168]D5. In the DanGer Shock trial, the use of a microaxial flow pump (mAFP) significantly reduced 180-day mortality (45.8% vs 58.5%; NNT = 8) but at the cost of a higher requirement for renal replacement therapy (RRT) (41.9% vs 26.7%; NNH = 7) [160]A1b. When AKI occurs, continuous renal replacement therapy (CRRT) is the preferred modality in hemodynamically unstable patients to allow for gradual fluid removal and metabolic control [168]D5. Notably, early renal recovery (within 7 days) is possible in approximately 43% of patients rescued by venoarterial extracorporeal membrane oxygenation (VA-ECMO), particularly those with reversible primary cardiac pathology [167]B3b.
Respiratory Support and Monitoring
Mechanical ventilation (MV) is frequently required to reduce the work of breathing and optimize oxygenation, yet it must be tailored to the patient's specific hemodynamic profile [170]D5. High positive end-expiratory pressure (PEEP) can be detrimental in preload-dependent states by decreasing venous return and further reducing cardiac output [170]D5. While mild hypercapnia (PaCO2 50–55 mmHg) has been studied to improve cerebral perfusion after cardiac arrest, it does not significantly reduce the incidence of AKI in patients with post-resuscitation CS [159]A1b.
Supportive Care and ICU Complications
Supportive care focuses on preventing secondary insults that exacerbate the primary shock state. This includes aggressive prophylaxis against venous thromboembolism and hospital-acquired infections.
- DVT/PE Prophylaxis: 40 mg SC daily or 5000 units SC TID is standard, though dosing must be adjusted for renal function [label].
- Pain Management: is typically achieved with (25–50 mcg IV) or (2–5 mg IV), with careful monitoring for respiratory depression and hypotension.
- Autonomic and Metabolic Stability: Arrhythmias and blood pressure instability are common; however, adjunctive therapies like high-dose selenium have not shown benefit in reducing the duration of mechanical support or mortality in post-cardiotomy CS [162]B2b.
- Temperature Management: Unlike its role in isolated cardiac arrest, early moderate hypothermia (33–34°C) does not improve 30-day mortality in CS patients receiving VA-ECMO compared to strict normothermia (RR 1.16, 95% CI 0.91–1.48) [163]A1b[67]A1a.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| Therapeutic Hypothermia in CS | ESC/AHA: Consider in post-arrest CS [67]A1a. | LEVOECMO/Trial Data: No benefit in mortality or organ recovery [163]A1b. | Moderate | Routine use in CS without arrest is not supported. |
| Levosimendan in ECMO | Use to facilitate weaning [24]A1b. | Standard inotropic support without levosimendan. | Emerging | LEVOECMO trial suggests potential for faster weaning [24]A1b. |
Pearl: Survival in cardiogenic shock is frequently determined by the severity of acute kidney injury; while mechanical support like mAFPs improves survival (NNT = 8), it significantly increases the risk of requiring RRT (NNH = 7) [160]A1b[168]D5.
| Parameter | Threshold/Criteria | Clinical Action |
|---|---|---|
| Intubation Trigger | PaO2/FiO2 < 150 or RR > 30 | Initiate Mechanical Ventilation |
| FVC Threshold | < 15 mL/kg | Consider ventilatory fatigue/failure |
| PEEP Setting | 5–10 cm H2O | Titrate to avoid preload compromise |
| PaCO2 Target | 35–45 mmHg | Avoid hypercapnia-induced AKI [159]A1b |
| Complication | Frequency | Prevention | Management |
|---|---|---|---|
| Acute Kidney Injury | 13–80% [168]D5 | Optimize MAP; avoid congestion | CRRT; avoid nephrotoxins |
| Shock Liver | ~20% | Maintain systemic perfusion | Supportive; monitor INR/Bili |
| VAP | 10–20% | Head of bed >30°; oral care | Targeted antibiotics |
| Pressure Injury | ~15% | Frequent turning; specialized beds | Wound care; nutrition |
Landmark Trials and Evidence-Based Evolution
- ▸Early revascularization remains the only intervention with a long-term mortality benefit established for over two decades (SHOCK trial).
- ▸Culprit-lesion-only PCI is superior to immediate multivessel PCI in reducing the composite of death and renal failure (CULPRIT-SHOCK).
- ▸Routine use of VA-ECMO and IABP has failed to show a mortality benefit in unselected cardiogenic shock patients, shifting focus toward protocolized, hemodynamic-driven care.
Survival rates for infarct-related cardiogenic shock (AMICS) remained stagnant for decades until the SHOCK trial established early revascularization as the definitive therapeutic cornerstone [172]A1c. This landmark evidence shifted the paradigm from passive medical stabilization to aggressive invasive intervention, yet mortality rates have plateaued at approximately 40% to 50% despite widespread adoption of this strategy [172]A1c. Modern evidence now focuses on refining revascularization techniques and defining the role of temporary mechanical circulatory support (tMCS) through rigorous randomized controlled trials (RCTs).
SHOCK: The Revascularization Mandate
Design: RCT | N: 302 | Population: AMICS due to left ventricular failure. Intervention: Emergency revascularization (PCI or ) vs. initial medical stabilization. Primary Outcome: 30-day all-cause mortality. Key Result: While 30-day mortality did not differ significantly, the 6-month mortality was significantly lower in the revascularization group (50.3% vs. 63.1%, p=0.027); NNT = 8 to prevent one death at 6 months [172]A1c. Clinical Impact: Established early revascularization as a Class I recommendation, regardless of the time delay from MI onset [172]A1c.
IABP-SHOCK II: The De-escalation of Counterpulsation
Design: RCT | N: 600 | Population: AMICS undergoing early revascularization. Intervention: Intra-aortic balloon pump (IABP) vs. medical therapy. Primary Outcome: 30-day all-cause mortality. Key Result: No difference in 30-day mortality (39.7% vs. 41.3%, p=0.69) or long-term survival [174]B3b. Clinical Impact: Led to the downgrading of routine IABP use in guidelines (ESC Class III, AHA/ACC Class IIb), as it failed to improve hemodynamics or outcomes in unselected patients [172]A1c[174]B3b.
CULPRIT-SHOCK: Simplifying the PCI Strategy
Design: RCT | N: 706 | Population: AMICS with multivessel coronary artery disease. Intervention: Culprit-lesion-only PCI vs. immediate multivessel PCI. Primary Outcome: Composite of death or severe renal failure requiring renal replacement therapy (RRT) at 30 days. Key Result: Culprit-only PCI reduced the primary endpoint (45.9% vs. 55.4%; RR 0.83, 95% CI 0.71-0.96); NNT = 11 to prevent one death or RRT event [171]A1b. Clinical Impact: Established culprit-only PCI as the standard of care in the acute phase of shock. Sub-analyses confirmed that women, who generally face higher shock mortality, derive the same benefit from this simplified strategy as men [171]A1b.
ECLS-SHOCK and the ECMO Paradox
Design: RCT | N: 420 | Population: AMICS with planned early revascularization. Intervention: Routine VA-ECMO plus medical therapy vs. medical therapy alone. Primary Outcome: 30-day all-cause mortality. Key Result: No significant difference in mortality (47.8% vs. 49.0%, p=0.81), but VA-ECMO was associated with higher rates of major bleeding and vascular complications [173]D5. Clinical Impact: Challenged the routine use of VA-ECMO in AMICS. While trials like ARREST and PRAGUE OHCA suggested benefit in refractory out-of-hospital cardiac arrest, the INCEPTION trial and ECLS-SHOCK indicate that routine initiation in standard shock does not improve survival [173]D5.
DanGer Shock: The Microaxial Flow Pump Breakthrough
Design: RCT | N: 355 | Population: STEMI-related cardiogenic shock. Intervention: Microaxial flow pump (mAFP; Impella CP) vs. standard care. Primary Outcome: 180-day all-cause mortality. Key Result: mAFP significantly reduced 180-day mortality (45.8% vs. 58.5%; HR 0.74, 95% CI 0.55-0.99); NNT = 8 to prevent one death [160]A1b. However, mAFP increased the risk of RRT (41.9% vs. 26.7%; NNH = 7) and major bleeding [160]A1b. Clinical Impact: The first RCT to show a survival benefit for a percutaneous MCS device in AMICS. It highlights a critical trade-off: improved systemic perfusion and survival at the cost of increased device-related complications and acute kidney injury [160]A1b.
National Cardiogenic Shock Initiative (NCSI)
Design: Single-arm prospective multicenter study | N: 171 | Population: AMICS treated with PCI. Intervention: Standardized protocol emphasizing early mAFP (pre-PCI) and invasive . Key Result: Survival to discharge was 72%, significantly higher than historical benchmarks [175]B2b. Clinical Impact: Demonstrated that protocolized care—prioritizing rapid MCS initiation and hemodynamic-guided management—may be more critical than the choice of device alone [172]A1c[175]B2b.
Controversies and Guideline Disagreement
| Question | Position A (AHA/ACC) | Position B (ESC) | Strength | Implication |
|---|---|---|---|---|
| Routine IABP Use | Class IIb: May be considered in specific subsets [172]A1c. | Class III: Not recommended for routine use [174]B3b. | Moderate | IABP is largely reserved for mechanical complications. |
| Routine VA-ECMO | Class IIb: Considered for refractory shock [172]A1c. | Class IIb: Short-term support may be considered [173]D5. | Weak | ECLS-SHOCK has made routine use highly controversial. |
| Multivessel PCI | Class III: Harmful in the acute setting [172]A1c. | Class III: Not recommended during the index procedure [171]A1b. | Strong | Staged revascularization is preferred. |
Pearl: The DanGer Shock trial provides the first high-level evidence that microaxial flow pumps reduce 180-day mortality in STEMI-related shock (NNT = 8), though clinicians must weigh this against a significant increase in renal replacement therapy (NNH = 7) [160]A1b.
| Trial | Year | N | Intervention | Key Finding |
|---|---|---|---|---|
| SHOCK | 1999 | 302 | Early Revascularization | Reduced 6-month mortality (50% vs 63%) [172]A1c |
| IABP-SHOCK II | 2012 | 600 | IABP | No mortality benefit at 30 days or 1 year [174]B3b |
| CULPRIT-SHOCK | 2017 | 706 | Culprit-only PCI | Reduced death/RRT compared to multivessel PCI [171]A1b |
| ECLS-SHOCK | 2023 | 420 | VA-ECMO | No mortality benefit; increased complications [173]D5 |
| DanGer Shock | 2024 | 355 | Impella CP | Reduced 180-day mortality; increased RRT [160]A1b |
Prognostication and Long-term Outcomes
- ▸In-hospital mortality for cardiogenic shock remains approximately 40–50%, with SCAI Stage E representing the highest risk cohort [2, 180].
- ▸The CS4P protein-based score and machine learning nomograms provide superior predictive accuracy over traditional clinical-only models [21, 183].
- ▸Early initiation of GDMT (score ≥ 4) before ICU discharge is a critical determinant of 6-month survival and functional recovery [32].
Survival rates in acute myocardial infarction-related cardiogenic shock (AMICS) have plateaued near 40–50%, necessitating precise risk stratification to guide resource-intensive therapies [177]B2a[180]A1a. While in-hospital mortality remains high, survivors who reach discharge often achieve significant functional recovery, provided that early revascularization and appropriate hemodynamic support are maintained [32]B3b[180]A1a. Prognostication relies on a combination of validated clinical scores, biochemical markers, and the dynamic assessment of the Society for Cardiovascular Angiography and Interventions (SCAI) shock stages [2]A1b[4]B3b.
Validated Risk Scores and Biomarkers
The SCAI staging system serves as a primary prognostic framework, where mortality increases progressively from Stage A to Stage E [2]A1b[4]B3b. In the ECLS-SHOCK trial sub-study, Stage E was associated with the highest risk, and the initiation of extracorporeal life support (ECLS) did not significantly alter the mortality trajectory across different stages [2]A1b. Beyond clinical staging, the Cardiogenic Shock 4 Proteins (CS4P) score—utilizing a biomarker-based approach—demonstrates superior predictive performance compared to traditional clinical scores in both STEMI and NSTEMI cohorts [21]B2b. Machine learning models and nomograms have also emerged, showing high accuracy in predicting 30-day in-hospital mortality by integrating variables such as age, lactate, and renal function [183]B3b.
Clinical and Procedural Predictors
Procedural choices significantly impact short-term survival. Transradial access (TRA) for percutaneous coronary intervention (PCI) is associated with a 55% reduction in in-hospital mortality compared to transfemoral access (OR 0.45, 95% CI 0.30–0.67; NNT not calculable from reported data) [148]B2a. Additionally, the use of a microaxial flow pump (mAFP) in STEMI-CS improves survival but increases the risk of Bleeding Academic Research Consortium (BARC) type 3–5 events to 26.3% (vs. 15.3% in standard care); NNH = 9 to cause one major bleeding event [22]A1b. Physiological indices such as high glycemic variability (GV) and a low Blood Pressure Response Index (BPRI)—reflecting poor cardiovascular reserve—are independent predictors of all-cause mortality in the intensive care unit [70]B3b[181]B3b.
Long-term Recovery and GDMT
Survivors of the acute phase require aggressive secondary prevention to mitigate the risk of recurrent heart failure and death. Initiating guideline-directed medical therapy (GDMT) early during the ICU stay is associated with improved 6-month clinical outcomes [32]B3b. A GDMT score ≥ 4 at discharge (incorporating beta-blockers, ACE inhibitors/ARBs, and mineralocorticoid receptor antagonists) correlates with reduced composite endpoints of mortality and heart failure hospitalization [32]B3b. Long-term sequelae often include persistent fatigue and psychological impact, though approximately 80% of survivors can walk independently by 6 months post-event [180]A1a.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| PCI Strategy in Multivessel Disease | Culprit-only PCI is preferred in the acute phase [145]B2b. | Immediate multivessel PCI may be considered in selected cases [145]B2b. | Moderate | Avoidance of non-culprit PCI reduces procedural risk in unstable patients. |
| Timing of LV Unloading | Early unloading (e.g., within 12h of VA-ECMO) improves survival [131]B2a[177]B2a. | Delayed unloading is acceptable if hemodynamics are stable [131]B2a. | Low | Shift toward proactive venting to prevent pulmonary edema. |
Pearl: Precise prognostication requires integrating SCAI staging with dynamic markers like lactate and BPRI; notably, transradial PCI reduces mortality by over 50% compared to transfemoral access [70]B3b[148]B2a.
| Factor | Good Prognosis | Poor Prognosis |
|---|---|---|
| SCAI Stage | Stage A or B [2]A1b[4]B3b | Stage D or E [2]A1b[4]B3b |
| Lactate | Rapid clearance < 2 mmol/L | Persistent elevation > 4 mmol/L |
| Access Site | Transradial (OR 0.45 for death) [148]B2a | Transfemoral [148]B2a |
| Glycemic Control | Low variability [181]B3b | High glycemic variability [181]B3b |
| BPRI | High response index [70]B3b | Low response index [70]B3b |
| Medical History | No prior heart failure | History of preeclampsia (in women) [182]B2b |
Guidelines and Management Algorithms
- ▸SCAI staging (A-E) is the foundational tool for risk stratification and clinical communication in cardiogenic shock [1].
- ▸Early revascularization remains the cornerstone of management for infarct-related shock, supported by international S3 and AATS guidelines [147, 189].
- ▸Escalation to temporary mechanical circulatory support (tMCS) should be considered early (SCAI Stage C/D) rather than as a last resort in Stage E [187].
SCAI staging (A through E) provides the standardized framework for rapid triage and escalation in the modern cardiac intensive care unit [1]A1c (1c). This classification system, endorsed by the ACC, AHA, and SCCM, allows clinicians to communicate severity and trajectory, moving from Stage A (At Risk) to Stage E (Extremis) [1]A1c. algorithms now emphasize early multidisciplinary "Shock Team" activation and the rapid transition from pharmacological support to temporary mechanical circulatory support (tMCS) when initial measures fail [186]A1c[187]A1c.
Step-by-Step Management Protocol
- Initial Triage and Severity Classification: Assign a SCAI stage immediately upon presentation. Patients in SCAI Stage C (Classic) or higher require intensive care admission and invasive [1]A1c[190]D5.
- First-line Pharmacological Support: Initiate Norepinephrine 0.01–1.0 µg/kg/min IV as the preferred vasopressor to maintain a mean arterial pressure (MAP) >65 mmHg [128]A1c[191]D5. Add Dobutamine 2.5–20 µg/kg/min IV or Milrinone 0.125–0.75 µg/kg/min IV if cardiac output remains inadequate despite adequate filling pressures [128]A1c[191]D5.
- Immediate Revascularization: For infarct-related shock (AMI-CS), perform immediate percutaneous coronary intervention (PCI) or ( ) regardless of time from symptom onset [147]A1c[189]A1c. The German-Austrian S3 guideline emphasizes that early revascularization is the only intervention with a proven mortality benefit [189]A1c (1c).
- Escalation to tMCS: If hemodynamic stability is not achieved within 30–60 minutes of initiating inotropes, or if SCAI Stage D/E is present, initiate tMCS (e.g., Impella, VA-ECMO, or TandemHeart) [186]A1c[187]A1c. The POQI/ERAS 2025 consensus recommends tMCS initiation before the onset of profound multiorgan dysfunction [187]A1c (1c).
- Monitoring and De-escalation: Reassess support requirements every 12–24 hours. Weaning from tMCS should only be considered when the underlying etiology is reversed, vasopressor requirements are minimal, and the patient demonstrates intrinsic cardiac recovery (e.g., cardiac index >2.2 L/min/m² off support) [187]A1c.
Controversies and Guideline Disagreement
| Question | Position A | Position B | Strength | Implication |
|---|---|---|---|---|
| Timing of tMCS Initiation | POQI/ERAS 2025 — Recommend early initiation in SCAI Stage C/D to prevent multiorgan failure [187]A1c | French Expert Consensus — Suggest a more conservative approach, reserving tMCS for refractory cases after inotrope failure [128]A1c | Moderate | Practice varies by center; early use may prevent SIRS but increases vascular complications. |
| Sex-based Management | SCAI/EAPCI 2025 — Highlights significant disparities; women receive tMCS and revascularization less frequently [185]D5 | Standard Guidelines — Do not currently provide sex-specific treatment thresholds [1]A1c[189]A1c | Moderate | Clinicians must be vigilant for implicit bias; women often present with non-ischemic etiologies [185]D5. |
What NOT to Do
- Do NOT rely on the intra-aortic balloon pump (IABP) as the primary support device in AMI-CS unless mechanical complications (e.g., VSD) are present [147]A1c[191]D5.
- Do NOT delay revascularization in AMI-CS to wait for hemodynamic stabilization; the procedure itself is the stabilization [188]B2c[189]A1c.
- Do NOT maintain high-dose catecholamines (e.g., Dobutamine >20 µg/kg/min) for prolonged periods due to increased myocardial oxygen demand and arrhythmogenic risk [191]D5.
Pearl: Utilize the SCAI staging system to trigger early "Shock Team" involvement; delaying tMCS until SCAI Stage E (Extremis) is associated with significantly higher mortality compared to intervention at Stage C or D [1]A1c[187]A1c.
| Drug | Starting Dose | Target / Max Dose | Key Monitoring | Evidence Level |
|---|---|---|---|---|
| Norepinephrine | 0.05 µg/kg/min | 1.0 µg/kg/min | MAP, peripheral perfusion | 1c [128]A1c |
| Dobutamine | 2.5 µg/kg/min | 20 µg/kg/min | Heart rate, arrhythmias | 1c [191]D5 |
| Milrinone | 0.125 µg/kg/min | 0.75 µg/kg/min | Blood pressure (vasodilation) | 1c [191]D5 |
| Vasopressin | 0.01 U/min | 0.04 U/min | SVR, skin ischemia | 5 [128]A1c |
References
- [1]
Baran DA, Grines CL, Bailey S et al.. “SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2019). PMID: 31104355 ↗
L1GUIDELINECited in: Definition, Classification, and SCAI Staging, Clinical Presentation and Physical Examination, Guidelines and Management Algorithms - [2]
Pöss J, Jentzer J, Desch S et al.. “Prognostic impact of SCAI shock severity classes in AMI-related cardiogenic shock: A sub-study of the ECLS-SHOCK Trial.” ESC heart failure (2025). PMID: 41083288 ↗
L1RCTCited in: Definition, Classification, and SCAI Staging, Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS), Prognostication and Long-term Outcomes - [3]
Linde L, Beske RP, Meyer MAS et al.. “Hemodynamic Characteristics and Prognostic Implication of Modified Society for Cardiovascular Angiography and Interventions Shock Classification in Comatose Patients With Out-of-Hospital Cardiac Arrest.” Journal of the American Heart Association (2025). PMID: 39704227 ↗
L3RCTCited in: Definition, Classification, and SCAI Staging - [4]
Becher T, Hahn L, Britsch M et al.. “Consistency and Risk Stratification Performance of 4 Society for Cardiovascular Angiography and Interventions SHOCK Stage Definitions: A Retrospective Study.” Journal of the American Heart Association (2025). PMID: 40847509 ↗
L3COHORTCited in: Definition, Classification, and SCAI Staging, Prognostication and Long-term Outcomes - [5]
van Diepen S, Pöss J, Senaratne JM et al.. “Mixed Cardiogenic Shock: A Proposal for Standardized Classification, a Hemodynamic Definition, and Framework for Management.” Circulation (2024). PMID: 39466889 ↗
L5REVIEW_NARRATIVECited in: Definition, Classification, and SCAI Staging, Pathophysiology and the Hemodynamic Spiral, Clinical Presentation and Physical Examination - [6]
Hill KL, Rustin MA, Asche MA et al.. “Cardiogenic Shock Classification and Associated Mortality Risk.” Mayo Clinic proceedings (2023). PMID: 37028976 ↗
L2REVIEW_NARRATIVECited in: Definition, Classification, and SCAI Staging - [7]
Yuen T, Senaratne JM. “Definition, Classification, and Management of Primary Noncardiac Causes of Cardiogenic Shock.” The Canadian journal of cardiology (2025). PMID: 39675467 ↗
L5REVIEW_NARRATIVECited in: Definition, Classification, and SCAI Staging - [8]
Britsch S, Britsch M, Hahn L et al.. “Prognostic performance of the SCAI shock classification at admission and during ICU treatment: A retrospective, observational cohort study.” Heart & lung : the journal of critical care (2024). PMID: 38924856 ↗
L3COHORTCited in: Definition, Classification, and SCAI Staging - [9]
Dutt DP, Pinney SP. “Clinical variability within the INTERMACS 1 profile: implications for treatment options.” Current opinion in cardiology (2014). PMID: 24694386 ↗
L5REVIEW_NARRATIVECited in: Definition, Classification, and SCAI Staging - [10]
Jentzer JC, van Diepen S, Barsness GW et al.. “Cardiogenic Shock Classification to Predict Mortality in the Cardiac Intensive Care Unit.” Journal of the American College of Cardiology (2019). PMID: 31548097 ↗
L3OTHERCited in: Definition, Classification, and SCAI Staging - [11]
Frea S, Gravinese C, Boretto P et al.. “Comprehensive non-invasive haemodynamic assessment in acute decompensated heart failure-related cardiogenic shock: a step towards echodynamics.” European heart journal. Acute cardiovascular care (2024). PMID: 39012797 ↗
L2OTHERCited in: Definition, Classification, and SCAI Staging, Diagnostic Workup and Hemodynamic Monitoring - [12]
Rueda F, Borràs E, García-García C et al.. “Protein-based cardiogenic shock patient classifier.” European heart journal (2019). PMID: 31204432 ↗
L2OTHERCited in: Definition, Classification, and SCAI Staging - [13]
Zweck E, Ton VK, Kanwar M et al.. “CSWG-SCAI Stages Combined With Machine Learning-Based Phenotypes for Serial Risk Stratification in Cardiogenic Shock.” JACC. Heart failure (2025). PMID: 40840206 ↗
L3OTHERCited in: Definition, Classification, and SCAI Staging - [14]
Jentzer JC, Senghavi D, Patel PC et al.. “Shock Severity Classification and Mortality in Adults With Cardiac, Medical, Surgical, and Neurological Critical Illness.” Mayo Clinic proceedings (2024). PMID: 37815781 ↗
L3OTHERCited in: Definition, Classification, and SCAI Staging - [15]
Jentzer JC, Baran DA, Kyle Bohman J et al.. “Cardiogenic shock severity and mortality in patients receiving venoarterial extracorporeal membrane oxygenator support.” European heart journal. Acute cardiovascular care (2022). PMID: 36173885 ↗
L3OTHERCited in: Definition, Classification, and SCAI Staging - [16]
Baran DA, Long A, Badiye AP et al.. “Prospective validation of the SCAI shock classification: Single center analysis.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2020). PMID: 33026155 ↗
L2OTHERCited in: Definition, Classification, and SCAI Staging - [17]
Scott M, Kyriakopoulos CP, Sheffield E et al.. “Application of the Updated Cardiogenic Shock Working Group SCAI Classification for Cardiogenic Shock: A Single-Centre Analysis.” The Canadian journal of cardiology (2025). PMID: 40311672 ↗
L3OTHERCited in: Definition, Classification, and SCAI Staging - [18]
Sarma D, Tabi M, Jentzer JC. “Society for cardiovascular angiography and intervention shock classification predicts mortality after out-of-hospital cardiac arrest.” Resuscitation (2022). PMID: 35122891 ↗
L3OTHERCited in: Definition, Classification, and SCAI Staging - [19]
Morici N, Frea S, Bertaina M et al.. “SCAI stage reclassification at 24 h predicts outcome of cardiogenic shock: Insights from the Altshock-2 registry.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2023). PMID: 36378673 ↗
L2OTHERCited in: Definition, Classification, and SCAI Staging - [20]
Oyabu K, Hattori H, Kikuchi N et al.. “Cardiogenic shock severity predicts bleeding events in patients with temporary mechanical circulatory support.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2024). PMID: 39219443 ↗
L3OTHERCited in: Definition, Classification, and SCAI Staging - [21]
Obradovic D, Schulz L, Loncar G et al.. “Prognostic performance of cardiogenic shock 4 proteins prediction model in infarct-related cardiogenic shock.” ESC heart failure (2026). PMID: 41711227 ↗
L2RCTCited in: Epidemiology and Etiological Spectrum, Prognostication and Long-term Outcomes - [22]
Sørensen R, Møller JE, Vandenbriele C et al.. “Bleeding in Patients With Infarct-Related Cardiogenic Shock: A DanGer Shock Substudy.” JACC. Cardiovascular interventions (2026). PMID: 41672689 ↗
L1RCTCited in: Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS), Prognostication and Long-term Outcomes - [23]
Armstrong PW, Zheng Y, Welsh RC et al.. “Primary percutaneous coronary intervention within the first hour: Insights from early-treated patients with ST-elevation myocardial infarction.” American heart journal (2026). PMID: 41619999 ↗
L1RCTCited in: Epidemiology and Etiological Spectrum - [24]
Combes A, Saura O, Nesseler N et al.. “Levosimendan to Facilitate Weaning From ECMO in Patients With Severe Cardiogenic Shock: The LEVOECMO Randomized Clinical Trial.” JAMA (2026). PMID: 41324946 ↗
L1RCTCited in: Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS), Multiorgan Dysfunction and Supportive Care - [25]
Thevathasan T, Alyahoud M, Freund A et al.. “Extracorporeal Membrane Oxygenation Complications Are Not Causal for Mortality in Patients With Infarct-Related Cardiogenic Shock: A Mediation Analysis of the Extracorporeal Life Support in Infarct-Related Cardiogenic Shock (ECLS-SHOCK) Trial.” Critical care medicine (2025). PMID: 41114622 ↗
L1RCTCited in: Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS) - [26]
Pagnesi M, Cotter G, Davison B et al.. “Haemodynamic effects of istaroxime in SCAI stage B HF-related cardiogenic shock: Insights from the SEISMiC trial.” ESC heart failure (2025). PMID: 41085472 ↗
L1RCTCited in: Epidemiology and Etiological Spectrum - [27]
Haberman D, Verma B, Abusnina W et al.. “Low- Versus High-capacity Impella for CS After AMI: A Systematic Review and Pooled Data Analysis.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2026). PMID: 41507087 ↗
L1SR_OBSCited in: Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS), Revascularization and Definitive Interventions - [28]
Parlow S, Jung RG, Almoosawy SA et al.. “Prognostic Factors Among Patients Receiving Microaxial Flow Pump for Acute Myocardial Infarction-Related Cardiogenic Shock: A Systematic Review and Meta-Analysis.” Critical care medicine (2026). PMID: 41504526 ↗
L1SR_OBSCited in: Epidemiology and Etiological Spectrum - [29]
Scquizzato T, Grunau B, Fernando SM et al.. “Temporary mechanical circulatory support after return of spontaneous circulation following cardiac arrest: a systematic review and meta-analysis.” Resuscitation (2025). PMID: 41232590 ↗
L1SR_OBSCited in: Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS) - [30]
Ng GWY, Low CJW, Ng KJ et al.. “Predictive Models for Mortality in Cardiogenic Shock: A Systematic Review and Meta-Analysis.” Critical care medicine (2026). PMID: 41212048 ↗
L1SR_OBSCited in: Epidemiology and Etiological Spectrum, Prognostication and Long-term Outcomes - [31]
Sans-Roselló J, Fernández-Peregrina E, Kuku KO et al.. “Timing of cardiogenic shock and clinical outcomes in takotsubo syndrome: A multicenter cohort study.” International journal of cardiology (2026). PMID: 41765143 ↗
L3COHORTCited in: Epidemiology and Etiological Spectrum - [32]
Yokawa J, Nishikawa T, Shimojima M et al.. “Early initiation of guideline-directed medical therapy in patients with cardiogenic shock supported with Impella®: a two-center retrospective study.” BMC cardiovascular disorders (2025). PMID: 41257682 ↗
L3COHORTCited in: Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS), Prognostication and Long-term Outcomes - [33]
Hyder SA, Shirwany H, Parcha V et al.. “Clinical Outcomes in Peripartum Cardiomyopathy Complicated by Cardiogenic Shock: A Retrospective Multicenter Cohort Study.” The American journal of cardiology (2026). PMID: 41253240 ↗
L3COHORTCited in: Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS) - [34]
Sheng Z, Chen B. “Differences in the characteristics and outcomes of STEMI versus NSTEMI cardiogenic shock: A systematic review and meta-analysis.” Medicine (2025). PMID: 41189239 ↗
L2SR_OBSCited in: Epidemiology and Etiological Spectrum - [35]
Besnard A, Djebbar M, Akodad M et al.. “Emergency Mitral Transcatheter Edge-to-Edge Repair as a Bridge to Surgical Mitral Valve Replacement in Cardiogenic Shock: A Case Report.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2026). PMID: 41881834 ↗
L4CASE_REPORTCited in: Epidemiology and Etiological Spectrum, Diagnostic Workup and Hemodynamic Monitoring - [36]
Zhang Y, Li R, Jiang Y et al.. “Successful ECMO support for cardiogenic shock induced by immune checkpoint inhibitor-associated myocarditis: a case report and literature review.” Frontiers in immunology (2025). PMID: 41438754 ↗
L4CASE_REPORTCited in: Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS) - [37]
Pesce F, Dini CS, Righini FM et al.. “Optimizing cardiogenic shock outcomes: A system-based network approach.” International journal of cardiology (2026). PMID: 42082006 ↗
L2OTHERCited in: Epidemiology and Etiological Spectrum - [38]
Adi A, Jain R, Guru S et al.. “Antimicrobial Use in Acute Myocardial Infarction-Related Cardiogenic Shock.” Journal of the American Heart Association (2026). PMID: 41904804 ↗
L3OTHERCited in: Epidemiology and Etiological Spectrum - [39]
Suzuki T, Asano T, Shinozaki T et al.. “Prognostic Implications of Bleeding and Ischemic Complications in Acute Myocardial Infarction-Related Cardiogenic Shock Managed With Microaxial Flow Pump.” Circulation. Cardiovascular interventions (2026). PMID: 41904791 ↗
L3OTHERCited in: Epidemiology and Etiological Spectrum - [40]
Lapetina Arroyo R, Khosla P, Caraballo C et al.. “Impact of right heart failure in patients with cardiogenic shock.” European heart journal. Acute cardiovascular care (2026). PMID: 41863824 ↗
L3OTHERCited in: Epidemiology and Etiological Spectrum - [41]
Pfeffer TJ, Matinmehr F, Radocaj A et al.. “Cardiogenic shock complicating peripartum cardiomyopathy benefits from combination therapy with levosimendan and bromocriptine.” European journal of heart failure (2026). PMID: 41771115 ↗
L5OTHERCited in: Epidemiology and Etiological Spectrum - [42]
Wybraniec MT, Sufryd A, Cichoń M et al.. “Cardiogenic shock in the course of myocardial infarction: the results of the Shock-POL registry.” ESC heart failure (2026). PMID: 41746839 ↗
L3OTHERCited in: Epidemiology and Etiological Spectrum, Temporary Mechanical Circulatory Support (tMCS), Revascularization and Definitive Interventions - [43]
Elhadad A, El Zouhayri O, Silvain J et al.. “Efficacy and Safety of Intravenous Antiplatelet Therapy in Acute Myocardial Infarction With Cardiogenic Shock.” JACC. Cardiovascular interventions (2026). PMID: 41672691 ↗
L3OTHERCited in: Epidemiology and Etiological Spectrum, Revascularization and Definitive Interventions - [44]
Fernandez J, Khan N, Rubens M et al.. “Incidence and In-Hospital Mortality of Ventricular Septal Rupture Following Acute Myocardial Infarction.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2026). PMID: 41656944 ↗
L2OTHERCited in: Epidemiology and Etiological Spectrum - [45]
Møller JE, Beske RP, Jensen LO et al.. “Effect of Microaxial Flow Pump on Hemodynamics in STEMI-Related Cardiogenic Shock.” Journal of the American College of Cardiology (2025). PMID: 40562510 ↗
L1RCTCited in: Pathophysiology and the Hemodynamic Spiral - [46]
Biegus J, Mebazaa A, Metra M et al.. “Safety and efficacy intravenous istaroxime up to 60 hours for patients with pre-cardiogenic shock.” The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation (2025). PMID: 40451596 ↗
L1RCTCited in: Pathophysiology and the Hemodynamic Spiral - [47]
Fukushima N, Tatsumi E, Seguchi O et al.. “Assessment of Safety and Effectiveness of the Extracorporeal Continuous-Flow Ventricular Assist Device (BR16010) Use as a Bridge-to-Decision Therapy for Severe Heart Failure or Refractory Cardiogenic Shock: Study Protocol for Single-Arm Non-randomized, Uncontrolled, and Investigator-Initiated Clinical Trial.” Cardiovascular drugs and therapy (2018). PMID: 29948739 ↗
L5TRIAL_NONRANDOMCited in: Pathophysiology and the Hemodynamic Spiral - [48]
Spaeth LD, Rahim M, Kochar A et al.. “Cardiogenic Shock and Temporary Mechanical Circulatory Support.” The Medical clinics of North America (2025). PMID: 41136064 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral, Temporary Mechanical Circulatory Support (tMCS) - [49]
Théry G, Aissaoui N, Hamzaoui O. “Cardiac and systemic inflammation in cardiogenic shock.” Current opinion in critical care (2025). PMID: 40522922 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [50]
Krause TT, Werner N, Leick J. “Microaxial flow-pump support in patients with cardiogenic shock: a review of the literature.” Current opinion in critical care (2025). PMID: 40522088 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [51]
Germinario L, Catena D, Ott S et al.. “Iron deficiency in patients with cardiogenic shock: protocol for a scoping review.” BMJ open (2025). PMID: 40254303 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [52]
Randhawa VK, Baran DA, Kanwar MK et al.. “The Comparative Epidemiology, Pathophysiology and Management of Cardiogenic Shock Associated With Acute Myocardial Infarction and Advanced Heart Failure.” The Canadian journal of cardiology (2025). PMID: 39892612 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [53]
Moller JE, Thiele H, Zeymer U et al.. “Mechanical circulatory support for patients with infarct-related cardiogenic shock: a state-of-the-art review.” Heart (British Cardiac Society) (2025). PMID: 39819613 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [54]
Sideris K, Kyriakopoulos CP, Brinker L et al.. “Advanced Markers for Hemodynamic Monitoring in Cardiogenic Shock and End-Stage Heart Failure: A Mini Review.” Heart failure reviews (2025). PMID: 39808367 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [55]
Brahmbhatt DH, Kalra S, Luk A et al.. “From Escalate to Elevate: A New Paradigm for Comprehensive Cardiogenic Shock Management.” The Canadian journal of cardiology (2025). PMID: 39798668 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [56]
Maigrot JA, Wakefield BJ, Donaldson CM et al.. “Tailored Approach to Temporary Mechanical Circulatory Support for Cardiogenic Shock: Strategies to Facilitate Patient Mobilization.” Current cardiology reports (2025). PMID: 39792281 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [57]
Schemmelmann M, Kelm M, Jung C. “The microcirculation in cardiogenic shock.” European heart journal. Acute cardiovascular care (2024). PMID: 39506546 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [58]
Besch L, Schrage B. “Unloading in cardiogenic shock: the rationale and current evidence.” Current opinion in critical care (2024). PMID: 38841993 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [59]
Ostadal P, Belohlavek J. “What is cardiogenic shock? New clinical criteria urgently needed.” Current opinion in critical care (2024). PMID: 38841985 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral, Clinical Presentation and Physical Examination - [60]
Tehrani BN, Truesdell AG, Psotka MA et al.. “A Standardized and Comprehensive Approach to the Management of Cardiogenic Shock.” JACC. Heart failure (2020). PMID: 33121700 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [61]
Squara P, Hollenberg S, Payen D. “Reconsidering Vasopressors for Cardiogenic Shock: Everything Should Be Made as Simple as Possible, but Not Simpler.” Chest (2019). PMID: 30935893 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [62]
Chakravarthy M, Tsukashita M, Murali S. “A Targeted Management Approach to Cardiogenic Shock.” Critical care clinics (2018). PMID: 29907274 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and the Hemodynamic Spiral - [63]
Uribarri A, Guillen-Del Castillo A, Belahnech Y et al.. “Cardiogenic shock in systemic sclerosis: a retrospective study of acute ventricular dysfunction.” Rheumatology international (2025). PMID: 40285931 ↗
L4COHORTCited in: Pathophysiology and the Hemodynamic Spiral - [64]
Jacquot A, Lepage X, Merckle L et al.. “Protocol for a multicentre randomised controlled trial evaluating the effects of moderate hypothermia versus normothermia on mortality in patients with refractory cardiogenic shock rescued by venoarterial extracorporeal membrane oxygenation (VA-ECMO) (HYPO-ECMO study).” BMJ open (2019). PMID: 31615800 ↗
L5TRIAL_NONRANDOMCited in: Clinical Presentation and Physical Examination - [65]
Lim HS, Vondrakova D, Belohlavek J et al.. “Diastolic Perfusion Pressure Predicts Response to Inotropes and Vasopressors and Benefit From Mechanical Circulatory Support in Cardiogenic Shock.” Circulation. Heart failure (2025). PMID: 40365681 ↗
L2RCTCited in: Clinical Presentation and Physical Examination - [66]
Takagi K, Blet A, Levy B et al.. “Circulating dipeptidyl peptidase 3 and alteration in haemodynamics in cardiogenic shock: results from the OptimaCC trial.” European journal of heart failure (2020). PMID: 31472039 ↗
L2RCTCited in: Clinical Presentation and Physical Examination - [67]
Mhanna M, Al-Abdouh A, Sauer MC et al.. “Hypothermia as an Adjunctive Therapy in Cardiogenic Shock: A Systematic Review and Meta-Analysis.” Therapeutic hypothermia and temperature management (2023). PMID: 37074118 ↗
L1SR_OBSCited in: Clinical Presentation and Physical Examination, Multiorgan Dysfunction and Supportive Care - [68]
Werdan K, Buerke M, Geppert A et al.. “Infarction-Related Cardiogenic Shock- Diagnosis, Monitoring and Therapy–A German-Austrian S3 Guideline.” Deutsches Arzteblatt international (2021). PMID: 33827749 ↗
L1GUIDELINECited in: Clinical Presentation and Physical Examination - [69]
Shaffer A, Sheikh O, Prasad A. “Cardiogenic Shock: A Systematic Review of Clinical Trials Registered With ClinicalTrials.gov.” The Journal of invasive cardiology (2020). PMID: 32240097 ↗
L5TRIAL_NONRANDOMCited in: Clinical Presentation and Physical Examination - [70]
You X, Zhu Y, Zhang Z et al.. “Blood Pressure Response Index and Mortality in Patients With Cardiogenic Shock: A Multicenter Retrospective Cohort Study.” Journal of the American Heart Association (2025). PMID: 40879024 ↗
L3COHORTCited in: Clinical Presentation and Physical Examination, Prognostication and Long-term Outcomes - [71]
Es-Saad O, Ng W, Messina A et al.. “Current perspectives in cardiogenic shock.” Journal of critical care (2026). PMID: 41655405 ↗
L5REVIEW_NARRATIVECited in: Clinical Presentation and Physical Examination, Diagnostic Workup and Hemodynamic Monitoring, Temporary Mechanical Circulatory Support (tMCS) - [72]
Møller JE, Hassager C, Proudfoot A et al.. “Cardiogenic shock: diagnosis, phenotyping and management.” Intensive care medicine (2025). PMID: 40768067 ↗
L5REVIEW_NARRATIVECited in: Clinical Presentation and Physical Examination - [73]
Galusko V, Wenzl FA, Vandenbriele C et al.. “Current and novel biomarkers in cardiogenic shock.” European journal of heart failure (2025). PMID: 39822053 ↗
L5REVIEW_NARRATIVECited in: Clinical Presentation and Physical Examination - [74]
Damluji AA, Tehrani B, Sinha SS et al.. “Position Statement on Vascular Access Safety for Percutaneous Devices in AMI Complicated by Cardiogenic Shock.” JACC. Cardiovascular interventions (2022). PMID: 36265932 ↗
L5REVIEW_NARRATIVECited in: Clinical Presentation and Physical Examination - [75]
Sciaccaluga C, Mandoli GE, Ghionzoli N et al.. “Risk stratification in cardiogenic shock: a focus on the available evidence.” Heart failure reviews (2022). PMID: 34263413 ↗
L5REVIEW_NARRATIVECited in: Clinical Presentation and Physical Examination - [76]
Lashin H, Olusanya O, Smith A et al.. “Right ventricular echocardiographic parameters and prediction of stroke volume in ischemic cardiogenic shock: A retrospective study.” Journal of critical care (2023). PMID: 36494258 ↗
L3COHORTCited in: Diagnostic Workup and Hemodynamic Monitoring - [77]
Xu Q, Wang J, Lin Z et al.. “The glycemic gap as a prognostic indicator in cardiogenic shock: a retrospective cohort study.” BMC cardiovascular disorders (2024). PMID: 39223451 ↗
L3COHORTCited in: Diagnostic Workup and Hemodynamic Monitoring - [78]
Scolari FL, Schneider D, Fogazzi DV et al.. “Association between serum lactate levels and mortality in patients with cardiogenic shock receiving mechanical circulatory support: a multicenter retrospective cohort study.” BMC cardiovascular disorders (2020). PMID: 33234107 ↗
L3COHORTCited in: Diagnostic Workup and Hemodynamic Monitoring - [79]
Anderson J, Rushton WF, Burleson SL et al.. “Calcium channel antagonists and point-of-care ultrasound: A case series.” The American journal of emergency medicine (2026). PMID: 41349276 ↗
L4CASE_REPORTCited in: Diagnostic Workup and Hemodynamic Monitoring, Temporary Mechanical Circulatory Support (tMCS) - [80]
Licciardi M, Sanna F, Melis M et al.. “Transcatheter Edge to Edge Repair as a Bridge to Recovery in Patient With Severe Mitral Regurgitation, Advanced Left Ventricular Dysfunction and ECMO Support: A Case Report.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2025). PMID: 40421705 ↗
L4CASE_REPORTCited in: Diagnostic Workup and Hemodynamic Monitoring - [81]
Lochy S, Galloo X, Droogmans S et al.. “Paravalvular leak closure of a native aortic valve for cardiogenic shock post valvular surgery.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2024). PMID: 38971970 ↗
L4CASE_REPORTCited in: Diagnostic Workup and Hemodynamic Monitoring - [82]
Blusztein D, Teng P, Deuse T et al.. “Shock, Thrombus, TAVR: A Challenging TAVR With Large Left-Ventricular Thrombus.” The Canadian journal of cardiology (2021). PMID: 34139300 ↗
L4CASE_REPORTCited in: Diagnostic Workup and Hemodynamic Monitoring - [83]
Garau G, Joachim S, Duliere GL et al.. “Sudden cardiogenic shock mimicking fulminant myocarditis in a surviving teenager affected by severe acute respiratory syndrome coronavirus 2 infection.” ESC heart failure (2021). PMID: 33190387 ↗
L4CASE_REPORTCited in: Diagnostic Workup and Hemodynamic Monitoring - [84]
Sharif S, Wang K, Basmaji J et al.. “Critical Care Ultrasonography for Cardiogenic Shock: A Scoping Review.” Critical care explorations (2026). PMID: 41817314 ↗
L5REVIEW_NARRATIVECited in: Diagnostic Workup and Hemodynamic Monitoring - [85]
Saura O, Hekimian G, Schmidt M. “Echography monitoring in patients with temporary mechanical circulatory support.” Current opinion in critical care (2025). PMID: 40079507 ↗
L5REVIEW_NARRATIVECited in: Diagnostic Workup and Hemodynamic Monitoring - [86]
Sacchi S, Venuti A, Gobbi FM et al.. “Clinical Prediction Score for Successful Liberation from Temporary Mechanical Circulatory Support in Cardiogenic Shock Patients.” The Canadian journal of cardiology (2025). PMID: 39947458 ↗
L3OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [87]
Wang X, Fan X, Wu T et al.. “A CLINICAL PREDICTION MODEL FOR SHORT-TERM PROGNOSIS IN PATIENTS WITH NON-ACUTE MYOCARDIAL INFARCTION-RELATED CARDIOGENIC SHOCK.” Shock (Augusta, Ga.) (2025). PMID: 39665474 ↗
L2OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [88]
Berg-Hansen K, Ito S, Oh J et al.. “Global longitudinal strain is a predictor of mortality in patients with cardiogenic shock.” European heart journal. Cardiovascular Imaging (2025). PMID: 39657586 ↗
L3OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [89]
Tavazzi G, Colombo CNJ, Klersy C et al.. “Echocardiographic parameters for weaning from extracorporeal membrane oxygenation-the role of longitudinal function and cardiac time intervals.” European heart journal. Cardiovascular Imaging (2025). PMID: 39441992 ↗
L2OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [90]
Sato K, Heinsar S, Chan J et al.. “A novel echocardiographic parameter considering left ventricular afterload during V-A ECMO support.” European journal of clinical investigation (2024). PMID: 38849326 ↗
L5OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [91]
Tavazzi G, Corradi F, Vandenbriele C et al.. “Multimodality imaging in cardiogenic shock: state-of-the art.” Current opinion in critical care (2023). PMID: 37395328 ↗
L5REVIEW_NARRATIVECited in: Diagnostic Workup and Hemodynamic Monitoring - [92]
Harrington J, Aron J, Lashin H. “The Role of Focused 2-Dimensional Echocardiography in Managing Left Ventricular Outflow Tract Obstruction Mimicking Cardiogenic Shock.” Journal of intensive care medicine (2023). PMID: 37287244 ↗
L4REVIEW_NARRATIVECited in: Diagnostic Workup and Hemodynamic Monitoring - [93]
Singam NSV, Tabi M, Wiley B et al.. “Echocardiographic findings in cardiogenic shock due to acute myocardial infarction versus heart failure.” International journal of cardiology (2023). PMID: 37116757 ↗
L3OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [94]
Murphy A, Goldberg S. “Mechanical Complications of Myocardial Infarction.” The American journal of medicine (2022). PMID: 36075485 ↗
L5REVIEW_NARRATIVECited in: Diagnostic Workup and Hemodynamic Monitoring - [95]
Ramadan A, Abdallah T, Abdelsalam H et al.. “Accuracy of echocardiography and ultrasound protocol to identify shock etiology in emergency department.” BMC emergency medicine (2022). PMID: 35768775 ↗
L2OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [96]
Tabi M, Singam NSV, Wiley B et al.. “Echocardiographic Characteristics of Cardiogenic Shock Patients with and Without Cardiac Arrest.” Journal of intensive care medicine (2023). PMID: 35656768 ↗
L3OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [97]
Jentzer JC, Tabi M, Wiley BM et al.. “Echocardiographic Correlates of Mortality Among Cardiac Intensive Care Unit Patients With Cardiogenic Shock.” Shock (Augusta, Ga.) (2022). PMID: 34710882 ↗
L3OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [98]
VanDyck TJ, Pinsky MR. “Hemodynamic monitoring in cardiogenic shock.” Current opinion in critical care (2021). PMID: 33967209 ↗
L5REVIEW_NARRATIVECited in: Diagnostic Workup and Hemodynamic Monitoring - [99]
Kim D, Jang WJ, Park TK et al.. “Echocardiographic Predictors of Successful Extracorporeal Membrane Oxygenation Weaning After Refractory Cardiogenic Shock.” Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography (2021). PMID: 33321165 ↗
L3OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [100]
Daly M, Long B, Koyfman A et al.. “Identifying cardiogenic shock in the emergency department.” The American journal of emergency medicine (2020). PMID: 33039227 ↗
L5REVIEW_NARRATIVECited in: Diagnostic Workup and Hemodynamic Monitoring - [101]
Chiu MH, Howlett JG, Sharma NC. “Initiation of ivabradine in cardiogenic shock.” ESC heart failure (2019). PMID: 31332966 ↗
L5OTHERCited in: Diagnostic Workup and Hemodynamic Monitoring - [102]
Pandompatam G, Goswami R. “Noninvasive Echocardiographic Hemodynamics in Patients on Mechanical Circulatory Support: A Case Series.” ASAIO journal (American Society for Artificial Internal Organs : 1992) (2026). PMID: 40934345 ↗
L4CASE_REPORTCited in: Diagnostic Workup and Hemodynamic Monitoring - [103]
Marbach JA, Di Santo P, Kapur NK et al.. “Lactate Clearance as a Surrogate for Mortality in Cardiogenic Shock: Insights From the DOREMI Trial.” Journal of the American Heart Association (2022). PMID: 35261289 ↗
L2RCTCited in: Pharmacological Management: Inotropes and Vasopressors - [104]
Parlow S, Di Santo P, Mathew R et al.. “The association between mean arterial pressure and outcomes in patients with cardiogenic shock: insights from the DOREMI trial.” European heart journal. Acute cardiovascular care (2021). PMID: 34382063 ↗
L2RCTCited in: Pharmacological Management: Inotropes and Vasopressors - [105]
Di Santo P, Mathew R, Jung RG et al.. “Impact of baseline beta-blocker use on inotrope response and clinical outcomes in cardiogenic shock: a subgroup analysis of the DOREMI trial.” Critical care (London, England) (2021). PMID: 34376218 ↗
L2RCTCited in: Pharmacological Management: Inotropes and Vasopressors - [106]
Mathew R, Di Santo P, Jung RG et al.. “Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock.” The New England journal of medicine (2021). PMID: 34347952 ↗
L1RCTCited in: Pharmacological Management: Inotropes and Vasopressors - [107]
Levy B, Clere-Jehl R, Legras A et al.. “Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction.” Journal of the American College of Cardiology (2018). PMID: 29976291 ↗
L1RCTCited in: Pharmacological Management: Inotropes and Vasopressors - [108]
Lawson CK, Faine BA, Rech MA et al.. “Norepinephrine versus epinephrine for hemodynamic support in post-cardiac arrest shock: A systematic review.” The American journal of emergency medicine (2024). PMID: 38150986 ↗
L2SR_OBSCited in: Pharmacological Management: Inotropes and Vasopressors - [109]
Léopold V, Gayat E, Pirracchio R et al.. “Epinephrine and short-term survival in cardiogenic shock: an individual data meta-analysis of 2583 patients.” Intensive care medicine (2018). PMID: 29858926 ↗
L2SR_OBSCited in: Pharmacological Management: Inotropes and Vasopressors - [110]
Skoog CA, Engebretsen KM. “Are vasopressors useful in toxin-induced cardiogenic shock?” Clinical toxicology (Philadelphia, Pa.) (2017). PMID: 28152638 ↗
L1SR_OBSCited in: Pharmacological Management: Inotropes and Vasopressors - [111]
Liao X, Qian L, Zhang S et al.. “Network Meta-Analysis of the Safety of Drug Therapy for Cardiogenic Shock.” Journal of healthcare engineering (2020). PMID: 32802302 ↗
L1SR_OBSCited in: Pharmacological Management: Inotropes and Vasopressors - [112]
Bloom JE, Ball J, Okyere D et al.. “Design and rationale of a multicenter paramedic randomized trial of noradrenaline versus adrenaline in the initial management of patients with cardiogenic shock-The PANDA trial.” American heart journal (2026). PMID: 41679570 ↗
L5TRIAL_NONRANDOMCited in: Pharmacological Management: Inotropes and Vasopressors - [113]
Parlow S, Santo PD, Sterling LH et al.. “Inotrope versus placebo therapy in cardiogenic shock: Rationale and study design of the CAPITAL DOREMI2 trial.” American heart journal (2023). PMID: 37094667 ↗
L5TRIAL_NONRANDOMCited in: Pharmacological Management: Inotropes and Vasopressors - [114]
Perez P, Kimmoun A, Blime V et al.. “Increasing mean arterial pressure in cardiogenic shock secondary to myocardial infarction: effects on hemodynamics and tissue oxygenation.” Shock (Augusta, Ga.) (2014). PMID: 24509521 ↗
L4TRIAL_NONRANDOMCited in: Pharmacological Management: Inotropes and Vasopressors - [115]
Rui Q, Jiang Y, Chen M et al.. “Dopamine versus norepinephrine in the treatment of cardiogenic shock: A PRISMA-compliant meta-analysis.” Medicine (2017). PMID: 29069037 ↗
L1SR_OBSCited in: Pharmacological Management: Inotropes and Vasopressors - [116]
Beyls C, Hanquiez T, Mollet N et al.. “The Effect of Vasopressin on 90-Day Mortality in Patients With Cardiogenic Shock: A Retrospective Cohort Study Using Propensity Score-Weighted Analysis.” Cardiovascular therapeutics (2025). PMID: 40469854 ↗
L3COHORTCited in: Pharmacological Management: Inotropes and Vasopressors, Prognostication and Long-term Outcomes - [117]
Biswas S, Malik AH, Bandyopadhyay D et al.. “Meta-analysis Comparing the Efficacy of Dobutamine Versus Milrinone in Acute Decompensated Heart Failure and Cardiogenic Shock.” Current problems in cardiology (2023). PMID: 35545181 ↗
L1SR_OBSCited in: Pharmacological Management: Inotropes and Vasopressors - [118]
Uhlig K, Efremov L, Tongers J et al.. “Inotropic agents and vasodilator strategies for the treatment of cardiogenic shock or low cardiac output syndrome.” The Cochrane database of systematic reviews (2020). PMID: 33152122 ↗
L1SR_OBSCited in: Pharmacological Management: Inotropes and Vasopressors - [119]
Schumann J, Henrich EC, Strobl H et al.. “Inotropic agents and vasodilator strategies for the treatment of cardiogenic shock or low cardiac output syndrome.” The Cochrane database of systematic reviews (2018). PMID: 29376560 ↗
L1SR_OBSCited in: Pharmacological Management: Inotropes and Vasopressors - [120]
Unverzagt S, Wachsmuth L, Hirsch K et al.. “Inotropic agents and vasodilator strategies for acute myocardial infarction complicated by cardiogenic shock or low cardiac output syndrome.” The Cochrane database of systematic reviews (2014). PMID: 24385385 ↗
L1SR_OBSCited in: Pharmacological Management: Inotropes and Vasopressors - [121]
Guinot PG, Nguyen M, Berthoud V et al.. “Timing of vasopressin initiation influences renal outcomes in mixed cardiogenic-vasodilatory shock supported by VA-ECMO.” Anaesthesia, critical care & pain medicine (2026). PMID: 41207377 ↗
L3OTHERCited in: Pharmacological Management: Inotropes and Vasopressors - [122]
Manoeuvrier F, Recher M, Grimaud M et al.. “Use of milrinone in pediatric intensive care units: a multicenter survey of French-speaking countries.” European journal of pediatrics (2025). PMID: 41186722 ↗
L5OTHERCited in: Pharmacological Management: Inotropes and Vasopressors - [123]
Patel SM, Berg DD, Bohula EA et al.. “Contemporary Practice Patterns of Vasoactive Use in Cardiogenic Shock in the American Heart Association Cardiogenic Shock Registry.” Journal of the American Heart Association (2025). PMID: 41147380 ↗
L2OTHERCited in: Pharmacological Management: Inotropes and Vasopressors - [124]
Li B, Gershengorn HB, Vail EA et al.. “Inotrope selection in mixed cardiogenic shock with sepsis: a comparative analysis between milrinone and dobutamine.” Annals of the American Thoracic Society (2026). PMID: 40960311 ↗
L2OTHERCited in: Pharmacological Management: Inotropes and Vasopressors - [125]
Ten Berg S, Bogerd M, Peters EJ et al.. “Milrinone versus dobutamine in acute myocardial infarction-related cardiogenic shock; a propensity score matched analysis.” Clinical research in cardiology : official journal of the German Cardiac Society (2025). PMID: 40900181 ↗
L2OTHERCited in: Pharmacological Management: Inotropes and Vasopressors - [126]
Sarma D, Smith R, Padkins M et al.. “Association between vasopressin administration and mortality in patients with cardiogenic shock.” American heart journal (2025). PMID: 40120706 ↗
L3OTHERCited in: Pharmacological Management: Inotropes and Vasopressors - [127]
Ortega-Hernández JA, González-Pacheco H, García-Ruiz M et al.. “Effect of pulmonary artery catheter, type & combination of vasoactives for optimizing lactate clearance in acute myocardial infarction complicated by cardiogenic shock.” Journal of critical care (2025). PMID: 39667287 ↗
L3OTHERCited in: Pharmacological Management: Inotropes and Vasopressors - [128]
Aissaoui N, Delmas C, Merdji H et al.. “Experts' recommendations for the management of adult patients with cardiogenic shock.” Archives of cardiovascular diseases (2026). PMID: 41876324 ↗
L1GUIDELINECited in: Temporary Mechanical Circulatory Support (tMCS), Revascularization and Definitive Interventions, Guidelines and Management Algorithms - [129]
Papakonstantinou NA, Antonopoulos CN. “Extracorporeal Membrane Oxygenation Following Acute Type A Aortic Dissection Repair: A Systematic Review and Meta-Analysis.” ASAIO journal (American Society for Artificial Internal Organs : 1992) (2026). PMID: 41736226 ↗
L2SR_OBSCited in: Temporary Mechanical Circulatory Support (tMCS) - [130]
Nolan GP, Hammond MC, Rahimov D et al.. “Valvular Complications Related to Microaxial Assist Device Use: A Case-Level Systematic Review.” Artificial organs (2026). PMID: 41410269 ↗
L4SR_OBSCited in: Temporary Mechanical Circulatory Support (tMCS) - [131]
Peng S, Li Z, Wang S et al.. “Impact of left ventricular unloading timing on clinical outcomes in venoarterial extracorporeal membrane oxygenation: an updated systematic review and meta-analysis.” BMC cardiovascular disorders (2025). PMID: 41126042 ↗
L2SR_OBSCited in: Temporary Mechanical Circulatory Support (tMCS), Prognostication and Long-term Outcomes - [132]
Grand J, Freund A, Møller JE. “Best of European Heart Journal-Acute Cardiovascular Care (2024-25): cardiogenic shock and mechanical circulatory support.” European heart journal. Acute cardiovascular care (2026). PMID: 41642688 ↗
L5REVIEW_NARRATIVECited in: Temporary Mechanical Circulatory Support (tMCS) - [133]
Thiele H, Hassager C. “Cardiogenic Shock.” The New England journal of medicine (2026). PMID: 41467651 ↗
L5REVIEW_NARRATIVECited in: Temporary Mechanical Circulatory Support (tMCS), Revascularization and Definitive Interventions - [134]
Alarfaj M, Mohamad Alahmad MA, Wallisch WJ et al.. “ELSO-score: A practical pre-ECMO risk model for predicting in-hospital mortality in patients receiving VA-ECMO.” International journal of cardiology (2026). PMID: 42097309 ↗
L2OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [135]
Lewin D, Nersesian G, Rojas SV et al.. “Impact of Partial- to Full-Support Escalation With Microaxial Flow Pumps Prior to Durable Left Ventricular Assist Device Implantation.” European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery (2026). PMID: 42087324 ↗
L3OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [136]
Dahiya G, Bohman JK, Tonna JE et al.. “Acid-Base Status During Venoarterial Extracorporeal Membrane Oxygenator Support in Patients With Cardiogenic Shock.” Journal of the American Heart Association (2026). PMID: 41823232 ↗
L3OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [137]
Lio V, Barbero U, Drago S et al.. “Sheathless Femoral Impella Implantation: A Safer Hemodynamic Support in High-Risk PCI and Cardiogenic Shock.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2026). PMID: 41773429 ↗
L4OTHERCited in: Temporary Mechanical Circulatory Support (tMCS), Revascularization and Definitive Interventions - [138]
Beurton A, Bordier E, Veyret S et al.. “Changes in hemodynamics, cardiac energetics, and cell signaling pathways induced by veno-arterial extracorporeal membrane oxygenation with or without left ventricular active unloading.” The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation (2026). PMID: 41667045 ↗
L4OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [139]
Walther CP, Nair AP. “Management of Dialysis for Patients Receiving Mechanical Circulatory Support.” Journal of the American Society of Nephrology : JASN (2026). PMID: 41563801 ↗
L5OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [140]
Anderson M, Zeeshan A, Katlaps GJ et al.. “Clinical outcomes in acute myocardial infarction cardiogenic shock patients supported with a high-flow, surgically implanted micro-axial flow pump.” The Journal of thoracic and cardiovascular surgery (2026). PMID: 41548842 ↗
L2OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [141]
Baldetti L, Pontillo D, Capoccia M et al.. “Venopulmonary extracorporeal life support: An Extracorporeal Life Support Organization registry analysis.” The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation (2026). PMID: 41506589 ↗
L3OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [142]
Ortuno S, Bachelet D, Varnet O et al.. “Long-Term Functional and Quality-of-Life Outcomes in Survivors of Refractory Cardiogenic Shock Treated With Venoarterial Extracorporeal Membrane Oxygenation.” Critical care explorations (2025). PMID: 41329803 ↗
L3OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [143]
Ahn DJ, White M, Ran G et al.. “Low rates of inotropic support and durable left ventricular assist device placement among status 2 heart transplant candidates with temporary mechanical circulatory support.” The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation (2026). PMID: 41241033 ↗
L3OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [144]
Zainab K, Taylor E, Gangasani N et al.. “Aortic Pulsatility Index Predicts Native Recovery in Patients With Cardiogenic Shock Supported by Intra-aortic Balloon Pumps.” Journal of cardiac failure (2025). PMID: 41233015 ↗
L3OTHERCited in: Temporary Mechanical Circulatory Support (tMCS) - [145]
Marquard JM, Beske RP, Hassager C et al.. “Percutaneous Coronary Intervention in Multivessel Disease and Infarct-Related Cardiogenic Shock: A DanGer Shock Substudy.” JACC. Cardiovascular interventions (2025). PMID: 40992803 ↗
L2RCTCited in: Revascularization and Definitive Interventions, Multiorgan Dysfunction and Supportive Care, Prognostication and Long-term Outcomes - [146]
Abumayyaleh M, Thiele H, Rassaf T et al.. “Femoral vs. radial approach for primary percutaneous intervention in cardiogenic shock: a subanalysis from the ECLS-SHOCK trial.” European heart journal. Acute cardiovascular care (2025). PMID: 40042826 ↗
L2RCTCited in: Revascularization and Definitive Interventions - [147]
Kaczorowski DJ, Takeda K, Atluri P et al.. “2025 American Association for Thoracic Surgery (AATS) Expert Consensus Document: Surgical management of acute myocardial infarction and associated complications.” The Journal of thoracic and cardiovascular surgery (2025). PMID: 40320004 ↗
L1GUIDELINECited in: Revascularization and Definitive Interventions, Guidelines and Management Algorithms - [148]
Larik MO, Shaukat A, Khan M et al.. “Impact of Access Site in Percutaneous Coronary Intervention for Patients Complicated With Cardiogenic Shock: A Systematic Review and Meta-Analysis of 33,311 Individuals.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2025). PMID: 40827467 ↗
L2SR_OBSCited in: Revascularization and Definitive Interventions, Prognostication and Long-term Outcomes - [149]
Mondellini GM, van den Enden AJM, Van Mieghem NM. “Perspectives on why DanGer Shock is the first positive trial on mechanical circulatory support in cardiogenic shock.” Heart failure reviews (2025). PMID: 39661305 ↗
L5SR_OBSCited in: Revascularization and Definitive Interventions - [150]
Jung RG, Stotts C, Gupta A et al.. “Prognostic Factors Associated with Mortality in Cardiogenic Shock - A Systematic Review and Meta-Analysis.” NEJM evidence (2024). PMID: 39437131 ↗
L2SR_OBSCited in: Revascularization and Definitive Interventions - [151]
D'Andria Ursoleo J, Baldetti L, Pieri M et al.. “Anti-Platelet Therapy with Cangrelor in Cardiogenic Shock Patients: A Systematic Review and Single-Arm Meta-Analysis.” Medicina (Kaunas, Lithuania) (2024). PMID: 39768971 ↗
L2SR_OBSCited in: Revascularization and Definitive Interventions - [152]
Turner H, Townsend M, Strange J et al.. “Long-Term Survival After Post-Myocardial Infarction Ventricular Septal Defect (VSD) Closure, Multiple Percutaneous Coronary Interventions and Edge-to-Edge Repair.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2025). PMID: 40988354 ↗
L4CASE_REPORTCited in: Revascularization and Definitive Interventions - [153]
Chandra Mohan N, Govier M, Johnson TW et al.. “Advanced Cardiogenic-shock Team versus standard care in cardiogenic SHOCK: a single centre service evaluation project.” Open heart (2026). PMID: 41577369 ↗
L3OTHERCited in: Revascularization and Definitive Interventions - [154]
Vicent L, Salguero-Bodes R, Ynsaurriaga FA et al.. “Cardiogenic Shock; Health Disparities; Equity; Mechanical Circulatory Support; Sex Differences; Multidisciplinary Care; Protocolized Care.” Current heart failure reports (2025). PMID: 41258337 ↗
L5REVIEW_NARRATIVECited in: Revascularization and Definitive Interventions - [155]
An KR, Harik L, Rahouma M et al.. “Trends and Outcomes of Mechanical Circulatory Support in Acute Myocardial Infarction and Cardiogenic Shock Patients Undergoing Coronary Artery Bypass Grafting.” The Annals of thoracic surgery (2026). PMID: 41109582 ↗
L2OTHERCited in: Revascularization and Definitive Interventions - [156]
Planka RM, Herold L, Glantschnig T et al.. “Applying DanGer Shock Eligibility Criteria to a Real-World Cohort of Cardiogenic Shock Patients.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2025). PMID: 41077835 ↗
L3OTHERCited in: Revascularization and Definitive Interventions - [157]
Ko T, Hosokawa Y, Asai K et al.. “Contribution of First Contact With a Cardiologist to the Door-to-Cardiac Catheterization Laboratory Time in Patients With Acute Myocardial Infarction Complicated by Cardiogenic Shock - Data From K-ACTIVE.” Circulation journal : official journal of the Japanese Circulation Society (2025). PMID: 40976693 ↗
L3OTHERCited in: Revascularization and Definitive Interventions - [158]
Patel R, Ghanem F, Rafique S et al.. “Outcomes of Culprit-Only Versus Multi-Vessel PCI With Impella Support in Acute Myocardial Infarction Complicated by Cardiogenic Shock.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2025). PMID: 40947547 ↗
L2OTHERCited in: Revascularization and Definitive Interventions - [159]
Eastwood GM, Bailey M, Nichol AD et al.. “Impact of mild hypercapnia on renal function after out-of-hospital cardiac arrest.” Resuscitation (2025). PMID: 39742940 ↗
L1RCTCited in: Multiorgan Dysfunction and Supportive Care - [160]
Zweck E, Hassager C, Beske RP et al.. “Microaxial Flow Pump Use and Renal Outcomes in Infarct-Related Cardiogenic Shock: A Secondary Analysis of the DanGer Shock Trial.” Circulation (2024). PMID: 39462276 ↗
L1RCTCited in: Multiorgan Dysfunction and Supportive Care, Landmark Trials and Evidence-Based Evolution - [161]
Ostadal P, Rokyta R, Karasek J et al.. “Extracorporeal membrane oxygenation in the therapy of cardiogenic shock: 1-year outcomes of the multicentre, randomized ECMO-CS trial.” European journal of heart failure (2025). PMID: 39113628 ↗
L1RCTCited in: Multiorgan Dysfunction and Supportive Care - [162]
Ott S, Dresen E, Lee ZY et al.. “The effect of high-dose selenium on mortality and postoperative organ dysfunction in post-cardiotomy cardiogenic shock patients supported with mechanical circulatory support - A post-hoc analysis of the SUSTAIN CSX trial.” Journal of critical care (2024). PMID: 38955117 ↗
L2RCTCited in: Multiorgan Dysfunction and Supportive Care - [163]
Levy B, Girerd N, Amour J et al.. “Effect of Moderate Hypothermia vs Normothermia on 30-Day Mortality in Patients With Cardiogenic Shock Receiving Venoarterial Extracorporeal Membrane Oxygenation: A Randomized Clinical Trial.” JAMA (2022). PMID: 35103766 ↗
L1RCTCited in: Multiorgan Dysfunction and Supportive Care - [164]
Lim O, Anbalakan K, Ruiyang Ling R et al.. “Concurrent Use of Kidney Replacement Therapy and Temporary Left Ventricular Assist Device in Cardiogenic Shock: A Systematic Review and Meta-Analysis.” Blood purification (2025). PMID: 40532684 ↗
L2SR_OBSCited in: Multiorgan Dysfunction and Supportive Care - [165]
Karamat M, Patel B, Khanal R et al.. “Sex-related differences in patients with acute myocardial infarction complicated by cardiogenic shock: A systematic review and meta-analysis.” The American journal of the medical sciences (2025). PMID: 39647638 ↗
L2SR_OBSCited in: Multiorgan Dysfunction and Supportive Care - [166]
Lescroart M, Kemp H, Imauven O et al.. “Cardiogenic shock in patients with active onco-hematological malignancies: A multicenter retrospective study.” Journal of critical care (2025). PMID: 39848115 ↗
L3COHORTCited in: Multiorgan Dysfunction and Supportive Care - [167]
Sitbon A, Coutrot M, Montero S et al.. “Early renal recovery after acute kidney injury in patients on venoarterial extracorporeal membrane oxygenation: A retrospective study.” Journal of critical care (2023). PMID: 37540960 ↗
L3COHORTCited in: Multiorgan Dysfunction and Supportive Care - [168]
De Oliveira-Gomes D, Guilliod C, Vavilin I et al.. “Renal Dysfunction Across the Spectrum of Cardiogenic Shock: Mechanisms, Clinical Implications, and Therapeutic Strategies.” Current heart failure reports (2025). PMID: 40560292 ↗
L5REVIEW_NARRATIVECited in: Multiorgan Dysfunction and Supportive Care - [169]
Sarma D, Jentzer JC. “Cardiogenic Shock: Pathogenesis, Classification, and Management.” Critical care clinics (2024). PMID: 37973356 ↗
L5REVIEW_NARRATIVECited in: Multiorgan Dysfunction and Supportive Care - [170]
Tavazzi G. “Mechanical ventilation in cardiogenic shock.” Current opinion in critical care (2021). PMID: 33929345 ↗
L5REVIEW_NARRATIVECited in: Multiorgan Dysfunction and Supportive Care - [171]
Rubini Gimenez M, Zeymer U, Desch S et al.. “Sex-Specific Management in Patients With Acute Myocardial Infarction and Cardiogenic Shock: A Substudy of the CULPRIT-SHOCK Trial.” Circulation. Cardiovascular interventions (2020). PMID: 32151161 ↗
L1RCTCited in: Landmark Trials and Evidence-Based Evolution - [172]
Henry TD, Tomey MI, Tamis-Holland JE et al.. “Invasive Management of Acute Myocardial Infarction Complicated by Cardiogenic Shock: A Scientific Statement From the American Heart Association.” Circulation (2021). PMID: 33657830 ↗
L1REVIEW_NARRATIVECited in: Landmark Trials and Evidence-Based Evolution - [173]
Lüsebrink E, Binzenhöfer L, Hering D et al.. “Scrutinizing the Role of Venoarterial Extracorporeal Membrane Oxygenation: Has Clinical Practice Outpaced the Evidence?” Circulation (2024). PMID: 38527130 ↗
L5REVIEW_NARRATIVECited in: Landmark Trials and Evidence-Based Evolution - [174]
Schrage B, Ibrahim K, Loehn T et al.. “Impella Support for Acute Myocardial Infarction Complicated by Cardiogenic Shock.” Circulation (2019). PMID: 30586755 ↗
L3OTHERCited in: Landmark Trials and Evidence-Based Evolution - [175]
Basir MB, Kapur NK, Patel K et al.. “Improved Outcomes Associated with the use of Shock Protocols: Updates from the National Cardiogenic Shock Initiative.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2019). PMID: 31025538 ↗
L2OTHERCited in: Landmark Trials and Evidence-Based Evolution - [176]
Dimitriadis K, Pyrpyris N, Aznaouridis K et al.. “Direct Comparison of Urgent Transcatheter Aortic Valve Implantation and Balloon Aortic Valvuloplasty: A Systematic Review and Meta-Analysis.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2025). PMID: 40988363 ↗
L2SR_OBSCited in: Prognostication and Long-term Outcomes - [177]
Soh BWT, Gracias CS, Dean A et al.. “A Systematic Review and Meta-Analysis of the Efficacy and Safety of Combined Mechanical Circulatory Support in Acute Myocardial Infarction Related Cardiogenic Shock.” Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (2025). PMID: 39718168 ↗
L2SR_OBSCited in: Prognostication and Long-term Outcomes - [178]
Schupp T, Thiele H, Rassaf T et al.. “Prognostic Impact of Admission Time in Infarct-Related Cardiogenic Shock: An ECLS-SHOCK Substudy.” JACC. Cardiovascular interventions (2024). PMID: 39415381 ↗
L2RCTCited in: Prognostication and Long-term Outcomes - [179]
Ahmed A, Contreras R, Gurram A et al.. “Clinical outcomes of transcatheter edge-to-edge repair in patients with acute mitral regurgitation complicated by cardiogenic shock: a systematic review and meta-analysis.” BMC cardiovascular disorders (2025). PMID: 40389818 ↗
L2SR_OBSCited in: Prognostication and Long-term Outcomes - [180]
Zordok M, Buda KG, Etiwy M et al.. “Comparative analysis of the DanGer Shock trial to randomized cardiogenic shock trials and real-world registries.” Cardiovascular revascularization medicine : including molecular interventions (2025). PMID: 39890500 ↗
L1SR_OBSCited in: Prognostication and Long-term Outcomes - [181]
Xie L, Luo S. “Prognostic value of glycaemic variability for mortality in cardiogenic shock patients: a retrospective cohort study.” Cardiovascular diabetology (2025). PMID: 41074054 ↗
L3COHORTCited in: Prognostication and Long-term Outcomes - [182]
Mudrovcic N, Tegnesjö E, Green RW et al.. “Clinical Features of Myocardial Infarction in Women With a History of Preeclampsia: A Population-Based Cohort Study.” Circulation. Cardiovascular quality and outcomes (2025). PMID: 40151932 ↗
L2COHORTCited in: Prognostication and Long-term Outcomes - [183]
Shen C, Wang S, Huo R et al.. “Comparison of machine learning and nomogram to predict 30-day in-hospital mortality in patients with acute myocardial infarction combined with cardiogenic shock: a retrospective study based on the eICU-CRD and MIMIC-IV databases.” BMC cardiovascular disorders (2025). PMID: 40108540 ↗
L3COHORTCited in: Prognostication and Long-term Outcomes - [184]
Mumbulu ET, Nkodila AN, Saint-Joy V et al.. “Survival and predictors of mortality in patients with heart failure in the cardiology department of the Center Hospitalier Basse Terre in Guadeloupe: historical cohort study.” BMC cardiovascular disorders (2024). PMID: 39468485 ↗
L3COHORTCited in: Prognostication and Long-term Outcomes - [185]
Baron SJ, Chou JC, Shah T et al.. “SCAI/EAPCI/ACVC Expert Consensus Statement on Cardiogenic Shock in Women.” EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology (2025). PMID: 40387531 ↗
L5GUIDELINECited in: Guidelines and Management Algorithms - [186]
Grant MC, Kanwar MK, Spelde AE et al.. “Temporary Mechanical Circulatory Support in Cardiogenic Shock: Executive Summary of the Joint Consensus Reports of the PeriOperative Quality Initiative and the Enhanced Recovery After Surgery Cardiac Society.” The Annals of thoracic surgery (2025). PMID: 40185355 ↗
L1GUIDELINECited in: Guidelines and Management Algorithms - [187]
Spelde AE, Barron LM, Cangut B et al.. “Escalation and De-escalation of Temporary Mechanical Circulatory Support: Joint Consensus Report of the PeriOperative Quality Initiative and the Enhanced Recovery After Surgery Cardiac Society.” The Annals of thoracic surgery (2025). PMID: 40187586 ↗
L1GUIDELINECited in: Guidelines and Management Algorithms - [188]
Kalla K, Christ G, Karnik R et al.. “Implementation of guidelines improves the standard of care: the Viennese registry on reperfusion strategies in ST-elevation myocardial infarction (Vienna STEMI registry).” Circulation (2006). PMID: 16702474 ↗
L2GUIDELINECited in: Guidelines and Management Algorithms - [189]
Pilarczyk K, Werdan K, Russ M et al.. “The German-Austrian S3 Guideline "Cardiogenic Shock Due to Myocardial Infarction: Diagnosis, Monitoring, and Treatment".” The Thoracic and cardiovascular surgeon (2021). PMID: 33368106 ↗
L1GUIDELINECited in: Guidelines and Management Algorithms - [190]
Hermes C, Ochmann T, Keienburg C et al.. “[Intensive care of patients with [infarct-related] cardiogenic shock : Abridged version of the S1 guideline].” Medizinische Klinik, Intensivmedizin und Notfallmedizin (2022). PMID: 36040499 ↗
L5GUIDELINECited in: Guidelines and Management Algorithms - [191]
Bonello L, Delmas C, Schurtz G et al.. “Mechanical circulatory support in patients with cardiogenic shock in intensive care units: A position paper of the "Unité de Soins Intensifs de Cardiologie" group of the French Society of Cardiology, endorsed by the "Groupe Athérome et Cardiologie Interventionnelle" of the French Society of Cardiology.” Archives of cardiovascular diseases (2018). PMID: 29903693 ↗
L5GUIDELINECited in: Guidelines and Management Algorithms