Cardiogenic shock natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: James Nasr[2]
Cardiogenic shock natural history, complications and prognosis
Overview
Cardiogenic shock is a time-sensitive, high-mortality syndrome characterized by impaired cardiac output, systemic hypoperfusion, and progressive end-organ dysfunction. Its clinical course is best understood as a continuum rather than a fixed state, ranging from preshock to classic, deteriorating, and refractory shock. Prognosis is determined by the cause of shock, SCAI shock stage, lactate trajectory, hemodynamic severity, cardiac arrest status, comorbidity burden, and the development of multiorgan failure.[1][2][3]
Major complications include multiorgan failure, acute kidney injury, hepatic injury, neurologic injury after cardiac arrest, bleeding and vascular complications from invasive support, respiratory failure, arrhythmias, secondary infection, and coagulopathy. Although short-term mortality remains high, survivors also face substantial long-term risks, including recurrent heart failure, renal dysfunction, neurocognitive impairment, frailty, rehospitalization, and reduced quality of life.[4][5]
Natural history
Cardiogenic shock is a dynamic clinical syndrome rather than a binary event. The clinical course may progress from preshock to classic shock, deteriorating shock, and refractory shock, corresponding broadly to SCAI shock stages B through E.[1][2]
The typical trajectory begins with impaired stroke volume and reduced cardiac output, followed by systemic tissue hypoperfusion, rising lactate, progressive end-organ dysfunction, and, if uncorrected, multiorgan failure.[3][4] In acute myocardial infarction-related cardiogenic shock, shock may be present at admission or may develop during hospitalization; therefore, patients with early or less severe shock require serial reassessment rather than one-time staging.[6]
Serial SCAI staging has prognostic value. In the Cardiogenic Shock Working Group registry, progression of any SCAI stage from baseline to 24 hours was associated with higher unadjusted in-hospital mortality than improvement, and progression to SCAI stage E at 24 hours was associated with very high mortality.[6] Notably, baseline SCAI stage B patients had higher unadjusted mortality than stage C patients in this registry (28.3% vs. 22.0%; P=0.017), likely reflecting higher rates of stage escalation from stage B; mortality was 33.8% for stage D and 59.6% for stage E.[6]
Complications
| Complication | Clinical significance | Prognostic implication |
|---|---|---|
| Multiorgan failure | Hallmark complication of advanced cardiogenic shock; may involve renal, hepatic, respiratory, neurologic, hematologic, and metabolic systems. | Strongly associated with in-hospital mortality; mortality rises with each additional failing organ system.[7] |
| Acute kidney injury | May result from low renal perfusion, renal venous congestion, inflammation, contrast exposure, and progression to acute tubular necrosis. In the DanGer Shock trial, renal replacement therapy was administered to 41.9% of patients treated with a microaxial flow pump and 26.7% of patients receiving standard care (relative risk, 1.98; 95% CI, 1.27 to 3.09).[8] In the dedicated renal substudy using RIFLE criteria, acute kidney injury occurred in 61% of the microaxial flow pump group and 45% of the control group; all patients alive at 180 days were free of renal replacement therapy.[9] | Need for renal replacement therapy is consistently associated with worse survival. |
| Hepatic injury | Hypoxic hepatitis is commonly defined as aminotransferase elevation greater than 20 times the upper limit of normal and has been reported in approximately 18% of patients with acute myocardial infarction-related cardiogenic shock.[3] Congestive hepatopathy from elevated right-sided filling pressures may coexist. | Marked aminotransferase elevation and worsening synthetic function indicate severe systemic hypoperfusion. |
| Neurologic injury | Most common after preceding cardiac arrest; includes hypoxic-ischemic brain injury and coma. | Major determinant of death and long-term disability, especially after out-of-hospital cardiac arrest.[10] |
| Bleeding and vascular complications | Occur particularly with mechanical circulatory support, large-bore arterial access, anticoagulation, and antiplatelet therapy. In the primary DanGer Shock publication, moderate or severe bleeding by GUSTO criteria occurred in 21.8% of patients treated with a microaxial flow pump and 11.9% of patients receiving standard care; limb ischemia occurred in 5.6% and 1.1%, respectively.[8] | Bleeding, limb ischemia, and vascular injury may limit therapy and increase morbidity. |
| Respiratory failure | May result from pulmonary edema, impaired oxygen delivery, acute respiratory distress syndrome, or need for airway protection after cardiac arrest. | Worsens tissue hypoxia and may increase right ventricular afterload. |
| Arrhythmia | Includes ventricular tachycardia, ventricular fibrillation, bradyarrhythmias, and high-grade atrioventricular block. | May precipitate shock, worsen established shock, or represent a terminal mode of death.[11] |
| Sepsis and secondary infection | May occur during prolonged critical illness, invasive device support, indwelling catheter use, and gut barrier dysfunction. | Adds distributive physiology and may convert isolated cardiogenic shock into mixed shock. |
| Coagulopathy and disseminated intravascular coagulation | May occur with systemic inflammation, liver dysfunction, shock-induced endothelial injury, or extracorporeal support. | Increases bleeding and thrombotic risk. |
Short-term prognosis
Cardiogenic shock remains a high-mortality syndrome despite contemporary reperfusion, critical care, vasoactive support, and mechanical circulatory support. In acute myocardial infarction-related cardiogenic shock, contemporary 30-day mortality is approximately 30% to 50%, depending on case mix, shock severity, cardiac arrest status, and treatment strategy.[12][4]
Etiology influences early mortality. Among 8,974 patients with cardiogenic shock, in-hospital mortality was 48% in mixed-cause shock, 41% in acute myocardial infarction-related shock, 31% in new heart failure, 31% in secondary causes, and 25% in acute-on-chronic heart failure-related shock.[12][13] A 2026 meta-analysis of 29 studies including 497,368 patients found higher short-term mortality in acute myocardial infarction-related cardiogenic shock than in heart failure-related cardiogenic shock (odds ratio, 1.58; 95% CI, 1.06 to 2.37).[14]
In a single-center registry, heart failure-related cardiogenic shock had lower in-hospital mortality than acute myocardial infarction-related cardiogenic shock (23.9% vs. 39.3%) and lower 1-year mortality (42.6% vs. 52.9%), with similar 30-day readmission rates.[15]
SCAI stage strongly stratifies hospital mortality. In the initial Mayo Clinic validation cohort, the unadjusted odds of hospital mortality increased stepwise from SCAI stage B through stage E compared with stage A.[16] Using Cardiogenic Shock Working Group-defined criteria, in-hospital mortality also rises across SCAI stages B, C, D, and E.[2]
Long-term prognosis
Long-term mortality remains substantial among survivors of cardiogenic shock. In a population-based study of 9,789 consecutive patients with acute myocardial infarction complicated by cardiogenic shock, mortality was 40.9% at 1 year and 58.9% at 5 years, with no clear plateau in mortality up to 10 years after admission.[5]
Among hospital survivors of acute myocardial infarction-related cardiogenic shock who undergo revascularization, long-term survival may be substantially better than early mortality statistics suggest; however, the highest post-discharge risk is concentrated in the early recovery period.[5] In patients aged 65 years or older who survived hospitalization for acute myocardial infarction-related cardiogenic shock, excess post-discharge mortality was concentrated in the first 60 days after discharge; after this period, mortality was similar to patients without cardiogenic shock.[17]
Survivors require structured follow-up for residual ventricular dysfunction, recurrent heart failure, arrhythmia risk, renal dysfunction, frailty, cognitive impairment, and psychosocial sequelae.[18][19]
Predictors of mortality
| Prognostic domain | Adverse predictors | Clinical interpretation |
|---|---|---|
| Shock severity | Higher baseline SCAI stage; maximum SCAI stage during hospitalization; worsening SCAI stage over the first 24 to 72 hours | Serial worsening is more informative than a single baseline assessment.[6] |
| Cardiac arrest status | Out-of-hospital cardiac arrest; in-hospital cardiac arrest; persistent coma or anoxic brain injury | Cardiac arrest increases mortality across SCAI stages and changes the dominant mode of death.[16][10] |
| Hemodynamics | Low mean arterial pressure, low cardiac index, elevated right atrial pressure, low cardiac power output, low cardiac power index, low pulmonary artery pulsatility index, low central venous oxygen saturation | Cardiac power output is a strong hemodynamic marker of mortality. The SHOCK trial registry identified cardiac power output ≤0.53 W as the threshold most accurately predicting in-hospital mortality, with sensitivity and specificity of 0.66 and positive predictive value of 58%.[20] In a post-hoc analysis of two prospective studies, clinically relevant 24-hour hemodynamic thresholds associated with poor outcomes included mean arterial pressure less than 70 mm Hg, cardiac index 1.8 L/min/m² or less, cardiac power index less than 0.27 W/m², and central venous oxygen saturation less than 70%.[21] |
| Lactate and lactate clearance | Elevated baseline lactate, persistently elevated lactate, rising lactate, impaired lactate clearance | Lactate trajectory is more informative than a single value. In IABP-SHOCK II post-hoc analysis, 8-hour lactate was the strongest lactate-based mortality predictor, with an optimal cutoff of 3.1 mmol/L. In the Altshock-2 registry, 24-hour lactate had higher predictive accuracy than baseline lactate; reported optimal cutoffs were 3.2 mmol/L at baseline and 1.7 mmol/L at 24 hours.[22][23] |
| Acid-base and metabolic injury | Systemic pH ≤7.2, severe metabolic acidosis, hyperglycemia | Reflects advanced tissue hypoperfusion and impaired metabolic reserve. |
| End-organ injury | Acute kidney injury, need for dialysis, hepatic injury, respiratory failure, multiorgan failure | Organ failure burden is a major determinant of mortality.[7] |
| Patient factors | Older age, diabetes mellitus, prior myocardial infarction, prior percutaneous coronary intervention, prior coronary artery bypass grafting, frailty | These factors reduce physiologic reserve and increase treatment risk. |
| Comorbidity burden | Higher aggregate comorbidity burden | Comorbidity burden independently modifies mortality risk across SCAI stages and may be most influential in early or preshock states.[24] |
| Treatment course | Prolonged vasopressor requirement, inability to restore perfusion, need for escalation of mechanical circulatory support | Suggests persistent or refractory shock physiology. |
Lactate clearance
Lactate clearance is an important dynamic marker of recovery from cardiogenic shock. Failure of lactate to fall after restoration of macrocirculatory targets suggests persistent tissue hypoperfusion, impaired clearance, or progression to hemometabolic shock.[3]
The SCAI Door-to-Lactate Clearance initiative proposes serial lactate measurement at 2- to 3-hour intervals and lactate clearance within 24 hours as a quality metric and prognostic marker in cardiogenic shock, analogous to door-to-balloon time in ST-elevation myocardial infarction.[25] A secondary analysis of the CardShock registry found that a 50% relative reduction in lactate at 24 hours was predictive of improved survival.[25]
Prognostic scoring systems
Several cardiogenic shock-specific prognostic tools have been externally validated, but no single score should replace serial bedside reassessment, hemodynamic evaluation, and multidisciplinary clinical judgment.
| Score | Population | Components or domains | Main use |
|---|---|---|---|
| CardShock score | Mixed cardiogenic shock populations | Age greater than 75 years, confusion at presentation, prior myocardial infarction or coronary artery bypass grafting, acute coronary syndrome etiology, reduced left ventricular ejection fraction, arterial lactate, and estimated glomerular filtration rate | Early mortality risk stratification |
| Cardiogenic Shock Score | Mixed cardiogenic shock populations | Age, sex, acute myocardial infarction-related cardiogenic shock etiology, systolic blood pressure, heart rate, pH, lactate, glucose, and cardiac arrest | Mortality risk stratification; reported discrimination was higher than IABP-SHOCK II and CardShock in its derivation and validation study.[26] |
| IABP-SHOCK II score | Acute myocardial infarction-related cardiogenic shock | Age greater than 73 years, prior stroke, admission glucose greater than 191 mg/dL, creatinine greater than 1.36 mg/dL, lactate greater than 5.0 mmol/L, and post-PCI TIMI flow less than 3 | Mortality risk stratification after AMI-CS |
| SHOCK trial and registry score | Acute myocardial infarction-related cardiogenic shock | Derived from SHOCK trial-era clinical and hemodynamic predictors | Prognostic assessment in AMI-CS populations |
| ENCOURAGE score | Patients receiving venoarterial extracorporeal membrane oxygenation | Clinical and laboratory variables before or at VA-ECMO initiation | Mortality prediction in VA-ECMO-supported shock |
| SAVE score | Patients receiving extracorporeal life support | Pre-extracorporeal support clinical variables | Survival prediction after extracorporeal support |
A systematic review and meta-analysis of prognostic scores in cardiogenic shock found no statistically significant difference between scores overall, although the CardShock score had the highest pooled discrimination and best calibration among the evaluated tools.[27] No consensus currently mandates use of a specific prognostic score to determine initiation of temporary mechanical circulatory support.[3][12]
Modes of death
In the Critical Care Cardiology Trials Network registry, most in-hospital deaths among patients with cardiogenic shock were cardiovascular, and persistent cardiogenic shock was the dominant specific mode of death.[11] Other modes of death include arrhythmia, anoxic brain injury, respiratory failure, and multiorgan failure.[11][10]
Timing of death varies by mechanism. Primary cardiac death may occur early, whereas death from neurologic injury or multiorgan failure often occurs later during the hospitalization.[10] Patients with preceding cardiac arrest are more likely to die from anoxic brain injury or arrhythmia than patients without cardiac arrest.[11]
Prognosis in older adults
Older age is associated with higher mortality in cardiogenic shock and is associated with increased vulnerability to frailty, bleeding, renal injury, delirium, functional decline, and complications of invasive support.[28] In older adults, prognosis should be assessed using shock severity, reversibility of the underlying cardiac process, neurologic status, comorbidity burden, frailty, pre-illness functional status, and patient goals rather than chronologic age alone.[28]
Survivorship and quality of life
Survivors of cardiogenic shock may experience persistent heart failure, recurrent hospitalization, chronic kidney disease, neurocognitive impairment after cardiac arrest, physical deconditioning, anxiety, depression, and reduced quality of life.[18][19] Post-discharge care should emphasize recovery of ventricular function when possible, optimization of guideline-directed medical therapy, rehabilitation, assessment for implantable cardioverter-defibrillator or cardiac resynchronization therapy when indicated, and evaluation for advanced heart failure therapies in selected patients.[19]
References
- ↑ 1.0 1.1 Baran DA, Grines CL, Bailey S; et al. (2019). "SCAI Clinical Expert Consensus Statement on the Classification of Cardiogenic Shock". Catheterization and Cardiovascular Interventions. 94 (1): 29–37. doi:10.1002/ccd.28329.
- ↑ 2.0 2.1 2.2 Kapur NK, Kanwar M, Sinha SS; et al. (2022). "Criteria for Defining Stages of Cardiogenic Shock Severity". Journal of the American College of Cardiology. 80 (3): 185–198. doi:10.1016/j.jacc.2022.04.049.
- ↑ 3.0 3.1 3.2 3.3 3.4 Lüsebrink E, Binzenhöfer L, Adamo M; et al. (2024). "Cardiogenic Shock". Lancet. 404 (10466): 2006–2020. doi:10.1016/S0140-6736(24)01818-X.
- ↑ 4.0 4.1 4.2 Samsky MD, Morrow DA, Proudfoot AG; et al. (2021). "Cardiogenic Shock After Acute Myocardial Infarction: A Review". JAMA. 326 (18): 1840–1850. doi:10.1001/jama.2021.18323.
- ↑ 5.0 5.1 5.2 Sterling LH, Fernando SM, Talarico R; et al. (2023). "Long-Term Outcomes of Cardiogenic Shock Complicating Myocardial Infarction". Journal of the American College of Cardiology. 82 (10): 985–995. doi:10.1016/j.jacc.2023.06.026.
- ↑ 6.0 6.1 6.2 6.3 Ton VK, Li S, John K; et al. (2024). "Serial Shock Severity Assessment Within 72 Hours After Diagnosis: A Cardiogenic Shock Working Group Report". Journal of the American College of Cardiology. doi:10.1016/j.jacc.2024.04.069.
- ↑ 7.0 7.1 Vallabhajosyula S, Dunlay SM, Prasad A; et al. (2019). "Acute Noncardiac Organ Failure in Acute Myocardial Infarction With Cardiogenic Shock". Journal of the American College of Cardiology. 73 (14): 1781–1791. doi:10.1016/j.jacc.2019.01.053.
- ↑ 8.0 8.1 Møller JE, Engstrøm T, Jensen LO; et al. (2024). "Microaxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock". The New England Journal of Medicine. 390 (15): 1382–1393. doi:10.1056/NEJMoa2312572.
- ↑ Zweck E, Hassager C, Beske RP; et al. (2024). "Microaxial Flow Pump Use and Renal Outcomes in Infarct-Related Cardiogenic Shock: A Secondary Analysis of the DanGer Shock Trial". Circulation. 150 (25): 1990–2003. doi:10.1161/CIRCULATIONAHA.124.072370.
- ↑ 10.0 10.1 10.2 10.3 Davodian LW, Larsen JKP, Povlsen AL; et al. (2022). "Timing and Causes of Death in Acute Myocardial Infarction Complicated by Cardiogenic Shock (From the RETROSHOCK Cohort)". The American Journal of Cardiology. 171: 15–22. doi:10.1016/j.amjcard.2022.01.050.
- ↑ 11.0 11.1 11.2 11.3 Berg DD, Singal S, Palazzolo M; et al. (2024). "Modes of Death in Patients With Cardiogenic Shock in the Cardiac Intensive Care Unit: A Report From the Critical Care Cardiology Trials Network". Journal of Cardiac Failure. 30 (5): 728–733. doi:10.1016/j.cardfail.2024.01.012.
- ↑ 12.0 12.1 12.2 Thiele H, Hassager C (2026). "Cardiogenic Shock". The New England Journal of Medicine. 394 (1): 62–77. doi:10.1056/NEJMra2312086.
- ↑ Zweck E, Kanwar M, Li S; et al. (2023). "Clinical Course of Patients in Cardiogenic Shock Stratified by Phenotype". JACC: Heart Failure. 11 (10): 1304–1315. doi:10.1016/j.jchf.2023.05.007.
- ↑ Yilmaz MB, Kilic ME, Biegus J; et al. (2026). "Acute Myocardial Infarction Versus Acute Decompensated Heart Failure in Cardiogenic Shock: A Systematic Review and Meta-Analysis of Clinical Phenotypes and Mortality". European Journal of Heart Failure. doi:10.1093/ejhf/xuag186.
- ↑ Sinha SS, Rosner CM, Tehrani BN; et al. (2022). "Cardiogenic Shock From Heart Failure Versus Acute Myocardial Infarction: Clinical Characteristics, Hospital Course, and 1-Year Outcomes". Circulation: Heart Failure. 15 (6): e009279. doi:10.1161/CIRCHEARTFAILURE.121.009279.
- ↑ 16.0 16.1 Jentzer JC, van Diepen S, Barsness GW; et al. (2019). "Cardiogenic Shock Classification to Predict Mortality in the Cardiac Intensive Care Unit". Journal of the American College of Cardiology. 74 (17): 2117–2128. doi:10.1016/j.jacc.2019.07.077.
- ↑ Shah RU, de Lemos JA, Wang TY; et al. (2016). "Post-Hospital Outcomes of Patients With Acute Myocardial Infarction With Cardiogenic Shock: Findings From the NCDR". Journal of the American College of Cardiology.
- ↑ 18.0 18.1 Hall EJ, Agarwal S, Cullum CM; et al. (2025). "Survivorship After Cardiogenic Shock". Circulation. 151 (3): 257–271. doi:10.1161/CIRCULATIONAHA.124.068203.
- ↑ 19.0 19.1 19.2 Blumer V, Sinha SS, Carnicelli AP; et al. (2026). "Cardiogenic Shock Survivorship: A Multidisciplinary Approach Across the Continuum of Care". Journal of the American College of Cardiology. doi:10.1016/j.jacc.2026.02.5080.
- ↑ Fincke R, Hochman JS, Lowe AM; et al. (2004). "Cardiac Power Is the Strongest Hemodynamic Correlate of Mortality in Cardiogenic Shock: A Report From the SHOCK Trial Registry". Journal of the American College of Cardiology. 44 (2): 340–348. doi:10.1016/j.jacc.2004.03.060.
- ↑ Levy B, Curtiaud A, Duarte K; et al. (2025). "Association Between Mean Hemodynamic Variables During the First 24 h and Outcomes in Cardiogenic Shock: Identification of Clinically Relevant Thresholds". Critical Care. 29 (1): 137. doi:10.1186/s13054-025-05356-0.
- ↑ IABP-SHOCK II post-hoc lactate analysis. Eight-hour lactate and mortality prediction in acute myocardial infarction-related cardiogenic shock.
- ↑ Pagnesi M, Riccardi M, Sacco A; et al. (2025). "Lactate Values and Mortality in Patients With Cardiogenic Shock: Insights From the Altshock-2 Registry". Critical Care Medicine. doi:10.1097/CCM.0000000000006738.
- ↑ Sundermeyer et al. Comorbidity burden and mortality modification across SCAI shock stages. Journal of the American College of Cardiology. 2025.
- ↑ 25.0 25.1 Naidu SS, Nathan S, Basir MB; et al. (2025). "SCAI Door to Lactate Clearance (SCAI DLC) Cardiogenic Shock Initiative: Definition, Hypothesis, and Call to Action". Journal of the Society for Cardiovascular Angiography & Interventions. 4 (11): 103996. doi:10.1016/j.jscai.2025.103996.
- ↑ Beer BN, Jentzer JC, Weimann J; et al. (2022). "Early Risk Stratification in Patients With Cardiogenic Shock Irrespective of the Underlying Cause - the Cardiogenic Shock Score". European Journal of Heart Failure. 24 (4): 657–667. doi:10.1002/ejhf.2449.
- ↑ Ng et al. Prognostic scores in cardiogenic shock: systematic review and meta-analysis. Critical Care Medicine. 2025.
- ↑ 28.0 28.1 Blumer V, Kanwar MK, Barnett CF; et al. (2024). "Cardiogenic Shock in Older Adults: A Focus on Age-Associated Risks and Approach to Management: A Scientific Statement From the American Heart Association". Circulation. 149 (14): e1051–e1065. doi:10.1161/CIR.0000000000001214.