Cardiogenic shock laboratory findings

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

Cardiogenic shock laboratory findings

Overview

Laboratory evaluation in cardiogenic shock supports diagnosis, severity assessment, phenotyping, detection of end-organ injury, and monitoring of therapeutic response. The most clinically useful laboratory markers include lactate, arterial or venous blood gas, renal function, hepatic function, cardiac biomarkers, electrolytes, glucose, complete blood count, coagulation studies, and, when central venous or pulmonary artery access is present, venous oxygen saturation and venous-arterial carbon dioxide gap.[1][2]

Laboratory testing should be repeated serially because cardiogenic shock is dynamic. A single normal or abnormal value may be less informative than the trajectory of lactate, pH, creatinine, transaminases, venous oxygen saturation, and coagulation parameters over the first hours of illness.[3]

The 2025 ACC Expert Consensus Statement recommends supplementing clinical suspicion of cardiogenic shock with readily available laboratory tests, including comprehensive metabolic testing for renal and hepatic injury, arterial or venous blood gas for metabolic acidosis, and venous or arterial lactate greater than 2 mmol/L as evidence of hypoperfusion.[1] The 2017 AHA Scientific Statement recommends complete blood count, electrolytes, creatinine, hepatic function tests, arterial blood gas, lactate, and serial cardiac troponins.[2]

Laboratory category Recommended tests Timing
Metabolic and perfusion markers Arterial or venous lactate; arterial or venous blood gas including pH, pCO2, pO2, bicarbonate, and base deficit At presentation and serially in established shock
Cardiac biomarkers High-sensitivity troponin I or T; BNP or NT-proBNP At presentation; serial troponin when acute coronary syndrome or evolving myocardial injury is suspected
Renal function Serum creatinine, blood urea nitrogen, electrolytes, urine output At presentation and serially
Hepatic function Alanine aminotransferase, aspartate aminotransferase, bilirubin, lactate dehydrogenase, albumin, prothrombin time/INR At presentation and serially
Electrolytes and glucose Sodium, potassium, chloride, bicarbonate, magnesium, phosphate, glucose At presentation and serially
Hematologic Complete blood count with differential and platelet count At presentation and serially
Coagulation Prothrombin time/INR, activated partial thromboplastin time, fibrinogen; D-dimer if disseminated intravascular coagulation or pulmonary embolism is suspected At presentation and as clinically indicated
Venous oxygenation and carbon dioxide gap Central venous oxygen saturation, mixed venous oxygen saturation, venous-arterial carbon dioxide gap When central venous or pulmonary artery catheter access is present

Lactate

Lactate is the central laboratory marker in cardiogenic shock. It is a biochemical marker of systemic hypoperfusion, is incorporated into the SCAI staging system and SHARC definition, and has strong prognostic value across cardiogenic shock populations.[1][4][5]

Lactate elevation in cardiogenic shock reflects multiple mechanisms, including low cardiac output with systemic hypoperfusion, splanchnic ischemia, adrenergic stimulation, post-cardiac arrest physiology, ischemia-reperfusion injury, systemic inflammation, mitochondrial dysfunction, and impaired hepatic or renal clearance.[6] Persistent hyperlactatemia despite improved blood pressure or cardiac index may indicate ongoing microcirculatory dysfunction, impaired clearance, or refractory shock physiology.[3]

Arterial or venous lactate greater than 2 mmol/L is the most widely used threshold for identifying systemic hypoperfusion in cardiogenic shock and is used in contemporary consensus definitions and bedside diagnostic frameworks.[1] Higher thresholds have been used in selected clinical trials, including lactate greater than 2.5 mmol/L in DanGer Shock and greater than 3.0 mmol/L in ECLS-SHOCK.[7]

The Cardiogenic Shock Working Group criteria use lactate thresholds for SCAI staging: stage B may include lactate 2-5 mmol/L, stage D lactate 5-10 mmol/L, and stage E lactate greater than 10 mmol/L.[4] The 2022 SCAI shock stage classification update states that a lactate level greater than 2 mmol/L is consistent with at least SCAI stage C, although some patients may demonstrate other manifestations of end-organ hypoperfusion with a normal lactate level.[8]

Serial lactate measurement is more informative than a single baseline value. In a post-hoc analysis of IABP-SHOCK II, 8-hour lactate was the strongest predictor of mortality among analyzed variables, with an optimal cutoff of 3.1 mmol/L.[9] In the Altshock-2 registry of 651 patients, baseline and 24-hour lactate were independently associated with in-hospital mortality, but 24-hour lactate had higher predictive accuracy than baseline lactate; optimal cutoffs were 3.2 mmol/L at baseline and 1.7 mmol/L at 24 hours.[5]

Lactate clearance within 24 hours is associated with improved survival. A systematic review and meta-analysis of prognostic factor studies found that lactate clearance was associated with improved survival in cardiogenic shock.[10] 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.[3]

Blood gas and acid-base assessment

Arterial or venous blood gas analysis provides information about oxygenation, ventilation, and metabolic severity. Severe acidemia reflects advanced hypoperfusion and impaired compensation.

Parameter Expected abnormality Clinical interpretation
pH Low in metabolic acidosis; pH ≤7.2 is used as a SCAI stage E criterion Indicates severe metabolic derangement and extremis-level shock physiology.[4]
Base deficit Increased base deficit Reflects severity and duration of hypoperfusion; useful for serial monitoring.
Bicarbonate Decreased Reflects buffering of lactic and other metabolic acids.
pCO2 May be low with respiratory compensation or high with ventilatory failure Rising pCO2 may indicate respiratory fatigue, pulmonary edema, or ventilatory failure.
pO2 and oxygen saturation May be low with pulmonary edema, acute respiratory distress syndrome, or respiratory failure Hypoxemia worsens myocardial ischemia and systemic oxygen delivery.

Venous oxygen saturation and venous-arterial carbon dioxide gap

Mixed venous oxygen saturation is obtained from the distal port of a pulmonary artery catheter and reflects the balance between systemic oxygen delivery and consumption. Central venous oxygen saturation is obtained from a central venous catheter and may be used when a pulmonary artery catheter is not present, but central venous oxygen saturation and mixed venous oxygen saturation may diverge substantially in shock states.[11][12]

Marker Abnormality Clinical interpretation
Mixed venous oxygen saturation Low values, often <65-70% Suggest reduced oxygen delivery, increased oxygen extraction, low cardiac output, or severe systemic hypoperfusion.
Central venous oxygen saturation Low values may suggest impaired oxygen delivery; values may diverge from mixed venous oxygen saturation Useful when central venous access is present, but should not be treated as interchangeable with mixed venous oxygen saturation in shock.
Venous-arterial carbon dioxide gap Gap >6 mm Hg Suggests inadequate microcirculatory flow or insufficient cardiac output; may be useful when venous oxygen saturation is difficult to interpret.[13]

In a post-hoc analysis of the ECMO-CS trial, pCO2 gap greater than 0.8 kPa, approximately 6 mm Hg, identified patients who appeared to benefit from immediate ECMO.[14]

Cardiac biomarkers

High-sensitivity cardiac troponin I or T is used to detect myocardial injury and is particularly important when acute coronary syndrome-related cardiogenic shock is suspected. In non-acute coronary syndrome etiologies, such as myocarditis, stress cardiomyopathy, acute decompensated heart failure, or critical illness, troponin elevation reflects myocardial injury but is not specific for cardiogenic shock.[2]

BNP and NT-proBNP reflect myocardial wall stress and heart failure physiology. BNP is included as a laboratory marker across SCAI stages B through E in the 2022 AHA/ACC/HFSA guideline SCAI table.[15] Natriuretic peptides are prognostically useful in heart failure and shock populations but lack specificity in critical illness because age, renal dysfunction, obesity, sepsis, and pulmonary hypertension can affect levels.[16]

Renal function markers

Acute kidney injury is common in acute myocardial infarction-related cardiogenic shock and reflects low renal perfusion, renal venous congestion, inflammation, contrast exposure, and progression to acute tubular necrosis.[6] Reported rates vary by population and acute kidney injury definition; a national study of acute myocardial infarction-related cardiogenic shock reported acute kidney injury in approximately 35% of admissions, while selected single-center cohorts have reported higher rates.[17][18] Rising serum creatinine, increasing blood urea nitrogen, and decreasing urine output are clinically important markers of renal hypoperfusion and end-organ injury.

In the IABP-SHOCK II score, admission creatinine greater than 1.5 mg/dL (>132.6 μmol/L) is one of six prognostic variables.[19] Need for renal replacement therapy is consistently associated with worse survival in cardiogenic shock.[6] The timing of acute kidney injury may also have prognostic significance. In a retrospective study of 369 patients with infarct-related cardiogenic shock, early acute kidney injury within 48 hours was independently associated with higher in-hospital mortality than late acute kidney injury (71.6% vs. 54.8%; adjusted OR 2.12), driven by baseline creatinine and 24-hour lactate.[20]

Novel renal biomarkers such as neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, and cystatin C have not replaced standard clinical assessment with creatinine and urine output in routine cardiogenic shock care.[2] Cystatin C may have value as part of composite biomarker risk scores rather than as a standalone routine test.[21]

Hepatic function markers

Hepatic injury in cardiogenic shock may result from hypoxic hepatitis, congestive hepatopathy, or both. 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 acute myocardial infarction-related cardiogenic shock.[6]

The typical laboratory pattern of hypoxic hepatitis includes marked elevation of AST, ALT, lactate dehydrogenase, bilirubin, and prothrombin time/INR, often peaking within 24 to 72 hours and improving over several days if perfusion is restored.[2] Worsening synthetic function, reflected by rising INR or falling albumin, suggests severe systemic hypoperfusion or advanced hepatic dysfunction.

The Cardiogenic Shock Working Group criteria use ALT as a marker of hypoperfusion: ALT 200-500 U/L may qualify as isolated hypoperfusion in early stages, and ALT greater than 500 U/L is used in stage D criteria.[4]

Glucose

Admission hyperglycemia is associated with mortality in cardiogenic shock, particularly among patients without diabetes. In an IABP-SHOCK II substudy, glucose above the median of 11.5 mmol/L, approximately 207 mg/dL, was associated with higher 30-day and 1-year mortality independent of diabetes status.[22] In the CardShock study, severe hyperglycemia, defined as glucose ≥16 mmol/L, approximately 288 mg/dL, was independently associated with in-hospital mortality.[23] In a Korean cardiogenic shock registry, admission hyperglycemia was associated with in-hospital mortality among patients without diabetes but not among those with diabetes.[24]

Hypoglycemia is uncommon but may indicate critical illness severity, hepatic dysfunction, or treatment-related complications. In the CardShock study, hypoglycemia was associated with high in-hospital mortality.[23]

Admission glucose greater than 191 mg/dL is included in the IABP-SHOCK II prognostic score.[19] The six IABP-SHOCK II score variables are age greater than 73 years (1 point), prior stroke (2 points), admission glucose greater than 191 mg/dL (1 point), admission creatinine greater than 1.5 mg/dL (1 point), admission lactate greater than 5 mmol/L (2 points), and post-PCI TIMI flow grade less than 3 (2 points).[19]

Electrolytes

Electrolyte Clinical relevance in cardiogenic shock
Sodium Hyponatremia may reflect neurohormonal activation, water retention, diuretic therapy, or advanced heart failure physiology. Serum sodium is included among useful laboratory data in the 2025 ACC Expert Consensus Statement.[1]
Potassium Hypokalemia and hyperkalemia increase arrhythmia risk and should be monitored closely in patients receiving vasopressors, inotropes, diuretics, renal replacement therapy, or mechanical circulatory support.
Magnesium Hypomagnesemia may increase risk of ventricular arrhythmias and should be corrected when present.
Phosphate Hypophosphatemia or hyperphosphatemia may occur in critical illness and renal dysfunction; severe abnormalities can impair myocardial and respiratory muscle function.

Hematologic and coagulation findings

Complete blood count may show leukocytosis from myocardial infarction, sympathetic activation, systemic inflammation, post-cardiac arrest physiology, or infection. Leukopenia should prompt consideration of sepsis, marrow suppression, or alternative diagnoses. Anemia reduces oxygen-carrying capacity and may worsen tissue hypoxia. Thrombocytopenia may occur from disseminated intravascular coagulation, mechanical circulatory support, heparin-induced thrombocytopenia, sepsis, or consumptive processes.[25]

Coagulation studies should be monitored in patients receiving anticoagulation, antiplatelet therapy, or mechanical circulatory support. Coagulopathy may result from hepatic synthetic dysfunction, disseminated intravascular coagulation, acquired von Willebrand syndrome, heparin-induced thrombocytopenia, or device-related hemolysis and platelet dysfunction.[25]

Disseminated intravascular coagulation may occur in advanced cardiogenic shock, particularly after cardiac arrest, and is characterized by thrombocytopenia, prolonged prothrombin time or activated partial thromboplastin time, elevated D-dimer, reduced fibrinogen, and microangiopathic changes on peripheral smear.[26]

Laboratory markers integrated into SCAI staging

SCAI stage Selected laboratory markers
Stage A: At risk Normal renal function and normal lactate
Stage B: Beginning shock / preshock The original SCAI consensus and the 2022 SCAI update list normal lactate for stage B and lactate ≥2 mmol/L for stage C. The CSWG operational criteria define stage B as including lactate 2-5 mmol/L or ALT 200-500 U/L as isolated hypoperfusion without drug or device therapy. These represent different staging frameworks.[8][4]
Stage C: Classic cardiogenic shock Impaired renal function, increased lactate, elevated BNP, increased liver function tests, and acidosis; the original SCAI framework generally treats lactate ≥2 mmol/L as consistent with at least stage C
Stage D: Deteriorating shock Persistent or worsening stage C laboratory abnormalities; CSWG criteria include lactate 5-10 mmol/L or ALT >500 U/L
Stage E: Extremis Worsening stage C laboratory abnormalities; CSWG criteria include lactate >10 mmol/L or pH ≤7.2

The 2022 AHA/ACC/HFSA guideline includes laboratory abnormalities in SCAI staging, and the Cardiogenic Shock Working Group operational criteria provide specific thresholds for lactate, ALT, and pH.[15][4]

Biomarker-based prognostic scores

The CLIP score is a biomarker-based mortality risk score using cystatin C, lactate, interleukin-6, and NT-proBNP. It was developed in 458 patients from the CULPRIT-SHOCK trial and externally validated in 163 patients from IABP-SHOCK II for 30-day mortality prediction in acute myocardial infarction-related cardiogenic shock. The CLIP score yielded C-statistics of 0.82 in internal validation, 0.82 in temporal internal validation, and 0.73 in external validation, and outperformed SAPS II and the IABP-SHOCK II score in the derivation cohort.[21]

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]

Emerging biomarkers such as dipeptidyl peptidase-3 and adrenomedullin have shown prognostic potential in cardiogenic shock but remain investigational and are not incorporated into routine guideline-based management.[28][16]

Practical laboratory approach

  1. Obtain arterial or venous lactate at presentation in every patient with suspected cardiogenic shock and repeat serially to assess trajectory.
  2. Obtain arterial or venous blood gas to assess pH, base deficit, ventilation, and oxygenation.
  3. Obtain a comprehensive metabolic profile, including creatinine, blood urea nitrogen, electrolytes, glucose, hepatic transaminases, bilirubin, albumin, and bicarbonate.
  4. Obtain high-sensitivity troponin and BNP or NT-proBNP at presentation; repeat troponin when acute coronary syndrome or evolving myocardial injury is suspected.
  5. Obtain complete blood count and coagulation studies, especially when mechanical circulatory support, anticoagulation, antiplatelet therapy, bleeding, or disseminated intravascular coagulation is present or anticipated.
  6. Measure central venous oxygen saturation, mixed venous oxygen saturation, and venous-arterial carbon dioxide gap when central venous or pulmonary artery catheter access is available.
  7. Integrate laboratory results with clinical examination, SCAI stage, imaging, and hemodynamic data rather than interpreting any laboratory marker in isolation.

Common pitfalls

  • Relying on a single lactate value rather than serial lactate trajectory
  • Interpreting lactate elevation as exclusively reflecting tissue hypoxia rather than considering adrenergic drive, impaired clearance, inflammation, and post-cardiac arrest physiology
  • Failing to obtain a blood gas when acidosis or respiratory failure is suspected
  • Using central venous oxygen saturation and mixed venous oxygen saturation interchangeably in shock
  • Overlooking hepatic injury markers, especially ALT and INR
  • Ignoring admission glucose as a prognostic marker
  • Using the IABP-SHOCK II score creatinine threshold incorrectly; the score-specific threshold is creatinine >1.5 mg/dL
  • Failing to monitor coagulation parameters in patients receiving mechanical circulatory support
  • Attributing all laboratory abnormalities to cardiogenic shock without considering mixed shock, sepsis, hypovolemia, pulmonary embolism, bleeding, or drug effects

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Sinha SS, Morrow DA, Kapur NK, Kataria R, Roswell RO (2025). "2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock". Journal of the American College of Cardiology. 85 (16): 1618–1641. doi:10.1016/j.jacc.2025.02.018.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 van Diepen S, Katz JN, Albert NM; et al. (2017). "Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 136 (16): e232–e268. doi:10.1161/CIR.0000000000000525.
  3. ↑ 3.0 3.1 3.2 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.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 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.
  5. ↑ 5.0 5.1 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.
  6. ↑ 6.0 6.1 6.2 6.3 Lüsebrink E, Binzenhöfer L, Adamo M; et al. (2024). "Cardiogenic Shock". Lancet. 404 (10466): 2006–2020. doi:10.1016/S0140-6736(24)01818-X.
  7. ↑ Thiele H, Hassager C (2026). "Cardiogenic Shock". The New England Journal of Medicine. 394 (1): 62–77. doi:10.1056/NEJMra2312086.
  8. ↑ 8.0 8.1 Naidu SS, Baran DA, Jentzer JC; et al. (2022). "SCAI SHOCK Stage Classification Expert Consensus Update: A Review and Incorporation of Validation Studies". Journal of the American College of Cardiology. 79 (9): 933–946. doi:10.1016/j.jacc.2022.01.018.
  9. ↑ Fuernau G, Desch S, de Waha-Thiele S; et al. (2020). "Arterial Lactate in Cardiogenic Shock: Prognostic Value of Clearance Versus Single Values". JACC: Cardiovascular Interventions. 13 (19): 2208–2216. doi:10.1016/j.jcin.2020.06.037.
  10. ↑ Marbach JA, Stone S, Schwartz B; et al. (2021). "Lactate Clearance Is Associated With Improved Survival in Cardiogenic Shock: A Systematic Review and Meta-Analysis of Prognostic Factor Studies". Journal of Cardiac Failure. 27 (10): 1082–1089. doi:10.1016/j.cardfail.2021.08.012.
  11. ↑ Kosyakovsky LB, Earle WB, Wichern C; et al. (2025). "Macrovascular Hemodynamics and Peripheral Perfusion in Cardiogenic Shock: Exploring Current Targets and Future Directions". JACC: Advances. 4 (10 Pt 1): 101964. doi:10.1016/j.jacadv.2025.101964.
  12. ↑ Mathew R, Fernando SM, Hu K; et al. (2022). "Optimal Perfusion Targets in Cardiogenic Shock". JACC: Advances. 1 (2): 100034. doi:10.1016/j.jacadv.2022.100034.
  13. ↑ Al Duhailib Z, Hegazy AF, Lalli R; et al. (2020). "The Use of Central Venous to Arterial Carbon Dioxide Tension Gap for Outcome Prediction in Critically Ill Patients: A Systematic Review and Meta-Analysis". Critical Care Medicine. 48 (12): 1855–1861. doi:10.1097/CCM.0000000000004578.
  14. ↑ Ostadal P, Vondrakova D, Rokyta R; et al. (2025). "Cardiac Index, SvO2 or pCO2 Gap May Determine Benefit From ECMO in Cardiogenic Shock: Post-Hoc Analysis of the Multicenter, Randomized ECMO-CS Trial". Critical Care. 29 (1): 303. doi:10.1186/s13054-025-05513-5.
  15. ↑ 15.0 15.1 Heidenreich PA, Bozkurt B, Aguilar D; et al. (2022). "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure". Journal of the American College of Cardiology. 79 (17): e263–e421. doi:10.1016/j.jacc.2021.12.012.
  16. ↑ 16.0 16.1 Jozwiak M, Lim SY, Si X, Monnet X (2024). "Biomarkers in Cardiogenic Shock: Old Pals, New Friends". Annals of Intensive Care. 14 (1): 157. doi:10.1186/s13613-024-01388-x.
  17. ↑ Vallabhajosyula S, Dunlay SM, Barsness GW; et al. (2019). "Temporal Trends, Predictors, and Outcomes of Acute Kidney Injury and Hemodialysis Use in Acute Myocardial Infarction-Related Cardiogenic Shock". PLOS ONE. 14 (9): e0222894. doi:10.1371/journal.pone.0222894.
  18. ↑ Marenzi G, Assanelli E, Campodonico J; et al. (2010). "Acute Kidney Injury in ST-segment Elevation Acute Myocardial Infarction Complicated by Cardiogenic Shock at Admission". Critical Care Medicine. 38 (2): 438–444. doi:10.1097/CCM.0b013e3181b9eb3b.
  19. ↑ 19.0 19.1 19.2 Pöss J, Köster J, Fuernau G; et al. (2017). "Risk Stratification for Patients in Cardiogenic Shock After Acute Myocardial Infarction". Journal of the American College of Cardiology. 69 (15): 1913–1920. doi:10.1016/j.jacc.2017.02.027.
  20. ↑ Boettger P, Preusse-Sondermann H, Sedighi J; et al. (2026). "Timing of Acute Kidney Injury in Infarction-Related Cardiogenic Shock: Early Onset Signals a High-Risk Phenotype - A Retrospective Observational Study". BMC Nephrology. doi:10.1186/s12882-025-04730-y.
  21. ↑ 21.0 21.1 Ceglarek U, Schellong P, Rosolowski M; et al. (2021). "The Novel Cystatin C, Lactate, Interleukin-6, and N-Terminal Pro-B-Type Natriuretic Peptide (CLIP)-based Mortality Risk Score in Cardiogenic Shock After Acute Myocardial Infarction". European Heart Journal. 42 (24): 2344–2352. doi:10.1093/eurheartj/ehab110.
  22. ↑ Abdin A, Pöss J, Fuernau G; et al. (2018). "Prognostic Impact of Baseline Glucose Levels in Acute Myocardial Infarction Complicated by Cardiogenic Shock-a Substudy of the IABP-SHOCK II Trial". Clinical Research in Cardiology. 107 (6): 517–523. doi:10.1007/s00392-018-1213-7.
  23. ↑ 23.0 23.1 Kataja A, Tarvasmäki T, Lassus J; et al. (2017). "The Association of Admission Blood Glucose Level With the Clinical Picture and Prognosis in Cardiogenic Shock - Results From the CardShock Study". International Journal of Cardiology. 226: 48–52. doi:10.1016/j.ijcard.2016.10.033.
  24. ↑ Choi SH, Yoon GS, Lee MJ; et al. (2022). "Prognostic Impact of Plasma Glucose on Patients With Cardiogenic Shock With or Without Diabetes Mellitus From the SMART RESCUE Trial". The American Journal of Cardiology. 175: 145–151. doi:10.1016/j.amjcard.2022.04.008.
  25. ↑ 25.0 25.1 Van Edom CJ, Tavazzi G, Vandenbriele C (2023). "Haematological Challenges in Cardiogenic Shock". Current Opinion in Critical Care. 29 (4): 392–396. doi:10.1097/MCC.0000000000001064.
  26. ↑ Gando S, Wada T (2019). "Disseminated Intravascular Coagulation in Cardiac Arrest and Resuscitation". Journal of Thrombosis and Haemostasis. 17 (8): 1205–1216. doi:10.1111/jth.14480.
  27. ↑ Ng GWY, Low CJW, Ng KJ; et al. (2025). "Predictive Models for Mortality in Cardiogenic Shock: A Systematic Review and Meta-Analysis". Critical Care Medicine. doi:10.1097/CCM.0000000000006937.
  28. ↑ Wenzl FA, Bruno F, Kraler S; et al. (2023). "Dipeptidyl Peptidase 3 Plasma Levels Predict Cardiogenic Shock and Mortality in Acute Coronary Syndromes". European Heart Journal. 44 (38): 3859–3871. doi:10.1093/eurheartj/ehad545.
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