Cardiogenic shock other diagnostic studies
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Cardiogenic Shock Microchapters |
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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 other diagnostic studies
Overview
Diagnostic studies beyond the electrocardiogram, chest x ray, echocardiography, and routine laboratory testing may be required to confirm the mechanism of cardiogenic shock, define the hemodynamic phenotype, identify the underlying etiology, guide escalation or de-escalation of support, and distinguish pure cardiogenic shock from mixed or alternative shock states. The principal additional studies are pulmonary artery catheterization with invasive hemodynamic assessment, coronary angiography and left heart catheterization, and selected use of endomyocardial biopsy.[1][2][3]
These studies should be selected according to diagnostic uncertainty, suspected etiology, shock severity, response to initial treatment, and whether temporary or durable mechanical circulatory support is being considered.
Pulmonary artery catheterization and invasive hemodynamic assessment
Guideline position
The 2022 AHA/ACC/HFSA guideline gives pulmonary artery catheterization a class 2b, level B-NR recommendation in patients presenting with cardiogenic shock, stating that placement of a pulmonary artery line may be considered to define hemodynamic subsets and guide management strategies.[4]
The 2025 ACC Expert Consensus Statement supports selective use of invasive hemodynamics to characterize cardiogenic shock phenotype and severity and to inform escalation and weaning of temporary mechanical circulatory support. Observational data cited by the consensus statement associate complete and early hemodynamic profiling with improved outcomes, but definitive randomized evidence is lacking.[1]
Routine pulmonary artery catheter placement in every patient at shock onset is not established. Selective use is most relevant when there is diagnostic uncertainty, suspected mixed shock, right ventricular involvement, inadequate response to initial treatment, need for temporary mechanical circulatory support assessment, or evaluation for durable mechanical circulatory support or heart transplantation.[5][2]
Ongoing randomized evidence
The PACCS trial (NCT05485376) is a multicenter, randomized, parallel-group, adaptive trial evaluating whether early invasive hemodynamic assessment within 6 hours of randomization decreases mortality in 400 patients with heart failure-related cardiogenic shock. Results were not yet available in the supplied evidence base.[5][1]
Observational evidence
A systematic review and meta-analysis of 14 observational studies including 789,553 patients found that pulmonary artery catheter use was associated with lower mortality, with pooled odds ratio 0.70 and time-to-event hazard ratio 0.68. Pulmonary artery catheter use was also associated with greater use of mechanical circulatory support and higher sepsis risk. These findings are observational and should not be interpreted as proof of causal benefit.[6]
In a multicenter Critical Care Cardiology Trials Network analysis, centers with formal shock teams used pulmonary artery catheters more frequently and had lower risk-adjusted cardiac intensive care unit mortality than centers without shock teams.[7]
Key hemodynamic measurements
| Parameter | Measurement | Clinical interpretation |
|---|---|---|
| Right atrial pressure | Directly measured | Elevated RAP suggests right-sided congestion, RV failure, biventricular congestion, or tamponade physiology. Disproportionately elevated RAP relative to PCWP supports RV-dominant shock.[1][8] |
| Pulmonary capillary wedge pressure | Balloon-occlusion pressure | Elevated PCWP supports LV-dominant congestion. Large V waves may suggest severe mitral regurgitation or a left-to-right shunt in the appropriate context.[1] |
| Cardiac output and cardiac index | Thermodilution or Fick method | Defines low-output physiology and tracks response to therapy. A cardiac index ≤2.2 L/min/m2 is commonly used as a low-output threshold in cardiogenic shock frameworks.[9] |
| Cardiac power output | Commonly calculated as CPO = (CO × MAP) / 451; a pressure-gradient formulation incorporates RAP: CPO = ((MAP − RAP) × CO) / 451 | In the SHOCK trial registry, CPO was the strongest independent hemodynamic correlate of in-hospital mortality, with OR 0.60 per 0.20 W increase. Subsequent cohorts have shown inconsistent performance; the clinical value of CPO is therefore contextual rather than absolute.[10][9] |
| Pulmonary artery pulsatility index | PAPi = (PA systolic pressure − PA diastolic pressure) / RAP | Assesses RV-pulmonary artery interaction and helps identify RV failure. Cutoffs vary by clinical setting and should not be applied as a universal threshold.[8] |
| Mixed venous oxygen saturation | Distal pulmonary artery catheter blood sample | Reflects the balance between oxygen delivery and consumption; low values support inadequate systemic oxygen delivery or increased extraction. |
| Systemic vascular resistance | SVR = ((MAP − RAP) / CO) × 80 | Helps distinguish predominantly cardiogenic shock with vasoconstriction from mixed cardiogenic-distributive shock with low or inappropriately normal SVR. |
| RAP:PCWP ratio | Calculated from directly measured filling pressures | A disproportionately elevated ratio supports RV-dominant congestion and should prompt further evaluation of RV function.[8] |
The 2022 AHA/ACC/HFSA guideline includes suggested hemodynamic criteria relevant to shock phenotyping, including low cardiac power output and RV-shock indices based on PAPi and the CVP:PCWP relationship. These criteria should be interpreted within the full clinical and hemodynamic context rather than as isolated universal cutoffs.[4]
Hemodynamic phenotyping
| Phenotype | Hemodynamic profile | Clinical implication |
|---|---|---|
| LV-dominant shock | Elevated PCWP or LV filling pressure, low cardiac index, relatively lower RAP | Suggests predominant LV pump failure and may support LV-targeted unloading or circulatory support.[1] |
| RV-dominant shock | Elevated RAP, relatively lower PCWP, elevated RAP:PCWP ratio, low PAPi | Suggests RV infarction, pulmonary embolism, pulmonary hypertension, or isolated RV failure and supports RV-specific management.[8] |
| Biventricular shock | Elevated RAP and PCWP with low cardiac index | Indicates combined right- and left-sided failure and may require advanced or biventricular support. |
| Mixed cardiogenic-distributive shock | Cardiac dysfunction with low or inappropriately normal SVR | Suggests vasoplegia, sepsis, systemic inflammation, or post-cardiac arrest physiology superimposed on cardiac dysfunction. |
Limitations
Pulmonary artery catheter-derived cardiac output and cardiac index are difficult to interpret during VA-ECMO because thermodilution and conventional Fick assumptions are altered by extracorporeal flow. ECMO circuit flow represents only the extracorporeal contribution to systemic flow and does not measure total native plus mechanical output. During temporary mechanical circulatory support, invasive measurements should be integrated with clinical examination, laboratory markers, device parameters, and imaging.[8]
Hemodynamic targets
The 2022 AHA Scientific Statement on temporary mechanical circulatory support suggests a goal mean arterial pressure of at least 65 mm Hg for most patients with cardiogenic shock, while acknowledging limited supporting evidence.[8] The 2024 JACC Heart Failure practical guidance suggests targets of RAP 8-12 mm Hg, PCWP ≤15 mm Hg, and cardiac index ≥2.2 L/min/m2.[9] These targets should be individualized according to shock phenotype, end-organ perfusion, ventricular interdependence, mechanical support configuration, and response to therapy. No single blood pressure or filling-pressure target has been definitively established by randomized trial data for all patients with cardiogenic shock.
Coronary angiography and left heart catheterization
Diagnostic role
The 2025 ACC/AHA/ACEP/NAEMSP/SCAI acute coronary syndromes guideline gives emergency culprit-vessel revascularization by PCI or CABG a class 1, level B-R recommendation in patients with acute coronary syndrome and cardiogenic shock or hemodynamic instability, irrespective of time from symptom onset.[11]
Coronary angiography serves diagnostic and therapeutic functions:
- Identifies the culprit lesion
- Defines the burden and distribution of coronary artery disease
- Determines technical feasibility of PCI or CABG
- Supports planning for vascular access when large-bore temporary mechanical circulatory support may be required
- Allows measurement of LV end-diastolic pressure when clinically useful
The 2021 AHA Scientific Statement on invasive management of acute myocardial infarction-related cardiogenic shock recommends consideration of LV end-diastolic pressure measurement before contrast administration and suggests avoiding unnecessary contrast ventriculography when diagnostic echocardiography is available, particularly with severe elevation in LV filling pressure or renal dysfunction.[12]
Multivessel disease: diagnostic-to-treatment implications
In the CULPRIT-SHOCK trial, culprit-lesion-only PCI with the option for staged revascularization reduced the 30-day composite of death or renal replacement therapy compared with immediate multivessel PCI in patients with acute myocardial infarction-related cardiogenic shock and multivessel disease. The composite primary endpoint occurred in 45.9% of the culprit-lesion-only group and 55.4% of the immediate multivessel PCI group (RR 0.83; 95% CI 0.71-0.96; P=0.01); the relative risk of death alone was 0.84 (95% CI 0.72-0.98; P=0.03).[13]
At 1 year, mortality was 50.0% with culprit-lesion-only PCI and 56.9% with immediate multivessel PCI (RR 0.88; 95% CI 0.76-1.01), while repeat revascularization and rehospitalization for heart failure were more frequent in the culprit-lesion-only group.[14]
The 2025 acute coronary syndromes guideline gives routine PCI of a non-infarct-related artery during the index primary PCI a class 3: Harm, level B-R recommendation in cardiogenic shock.[11] Detailed procedural management belongs in the revascularization or procedural therapy microchapter.
Endomyocardial biopsy
Endomyocardial biopsy is not routine in cardiogenic shock. It is reserved for selected patients in whom histologic diagnosis is likely to alter management.
The 2024 ACC Expert Consensus Decision Pathway on myocarditis supports endomyocardial biopsy when the expected diagnostic and prognostic value outweighs procedural risk. In the supplied evidence base, early biopsy within 2 days of ICU admission was associated with improved survival free from heart transplantation or LVAD implantation in a propensity-matched observational cohort.[15]
The 2020 AHA Scientific Statement on fulminant myocarditis and the 2021 HFA/HFSA/JHFS position statement support consideration of biopsy in fulminant or acute myocarditis with cardiogenic shock, severe ventricular dysfunction, malignant ventricular arrhythmias, or conduction disease when the result may change therapy.[16][17]
Clinical scenarios favoring biopsy
- Suspected giant cell myocarditis with rapidly progressive heart failure, ventricular arrhythmias, or high-grade atrioventricular block
- Suspected eosinophilic myocarditis
- Suspected cardiac sarcoidosis when tissue diagnosis is needed
- Suspected immune checkpoint inhibitor-related myocarditis
- Unexplained new-onset cardiomyopathy with hemodynamic compromise
- Persistent myocardial injury with suspected inflammatory or autoimmune etiology when histologic diagnosis would alter treatment
In clinically suspected myocarditis complicated by cardiogenic shock, the supplied evidence reports histologic myocarditis in up to 74% of biopsied patients. In a large cohort of unexplained acute heart failure with hemodynamic compromise, biopsy provided a diagnosis in 39% and altered therapy in nearly one-third of patients.[18][17]
Earlier biopsy and adequate tissue sampling improve diagnostic yield. Sampling strategy should be determined by operator experience, suspected pathology, and the need for histology, immunohistochemistry, molecular testing, or electroanatomic guidance.[15]
Computed tomography and cardiac magnetic resonance imaging
CT and cardiac MRI are addressed in their respective microchapters. In the context of other diagnostic studies, CT pulmonary angiography may be relevant when massive pulmonary embolism is suspected as a cause of or contributor to shock, and CT aortography when acute aortic syndrome is suspected. Cardiac MRI is generally not performed during acute hemodynamic instability but may be considered after stabilization when tissue characterization is likely to clarify etiology and change management, particularly in suspected myocarditis, stress cardiomyopathy, or infiltrative cardiomyopathy.[3][15]
Multidisciplinary shock team assessment
The 2022 AHA/ACC/HFSA guideline gives management by a multidisciplinary team experienced in shock a class 2a, level B-NR recommendation.[4] The 2025 ACC Expert Consensus Statement supports standardized interdisciplinary management involving clinicians with expertise in critical care cardiology, advanced heart failure, interventional cardiology, cardiac surgery, and, when relevant, ECMO and perfusion support.[1]
In the Critical Care Cardiology Trials Network analysis of 1,242 cardiogenic shock admissions across 24 cardiac intensive care units, centers with shock teams used pulmonary artery catheters more frequently and had lower risk-adjusted cardiac intensive care unit mortality than centers without shock teams.[7]
Shock teams may improve diagnostic coordination by:
- Facilitating rapid multidisciplinary assessment
- Ensuring early echocardiographic and invasive hemodynamic phenotyping when indicated
- Expediting emergent coronary angiography
- Integrating hemodynamics with mechanical circulatory support selection
- Identifying patients requiring transfer to advanced shock, transplant, or durable mechanical support centers
Practical diagnostic approach
- Use pulmonary artery catheterization selectively when the diagnosis or hemodynamic phenotype is uncertain, shock is persistent or worsening despite initial therapy, RV failure or mixed shock is suspected, temporary mechanical circulatory support is being considered or managed, or durable support/transplant candidacy is under evaluation.
- When a pulmonary artery catheter is placed, obtain a complete profile including RAP, pulmonary artery pressures, PCWP, cardiac output, cardiac index, mixed venous oxygen saturation, SVR, CPO, PAPi, and RAP:PCWP relationship when clinically relevant.
- Repeat invasive measurements serially rather than relying on a single profile.
- Individualize hemodynamic goals; commonly suggested targets include MAP ≥65 mm Hg, RAP 8-12 mm Hg, PCWP ≤15 mm Hg, and cardiac index ≥2.2 L/min/m2.
- Perform emergent coronary angiography when acute coronary syndrome-related shock is suspected and revascularization is indicated.
- Avoid routine immediate multivessel PCI during primary PCI for acute myocardial infarction-related cardiogenic shock.
- Consider endomyocardial biopsy in unexplained acute cardiomyopathy with hemodynamic compromise when myocarditis or another specific inflammatory or infiltrative diagnosis is suspected and histology could alter management.
- Use CT angiography selectively when pulmonary embolism or acute aortic syndrome is suspected; defer detailed CT assessment to the relevant imaging microchapter.
- Use cardiac MRI after stabilization when tissue characterization is likely to clarify etiology and change management; defer detailed MRI interpretation to the relevant imaging microchapter.
- Activate a multidisciplinary shock team early in severe, persistent, phenotypically unclear, or mechanically supported cardiogenic shock.
Common pitfalls
- Treating pulmonary artery catheterization and echocardiography as competing rather than complementary modalities
- Using incomplete invasive hemodynamic data without measuring both right- and left-sided filling pressures and forward flow
- Applying a single PAPi or RAP:PCWP cutoff universally across different cardiogenic shock etiologies
- Treating CPO as a universally reliable mortality predictor despite variable performance across cohorts
- Using only the simplified CPO formula without recognizing that a pressure-gradient formulation may incorporate RAP
- Assuming observational associations between pulmonary artery catheter use and survival prove causal benefit
- Using thermodilution or conventional Fick cardiac output uncritically during VA-ECMO
- Delaying emergent coronary angiography for nonessential additional testing in acute coronary syndrome-related shock
- Performing routine immediate multivessel PCI during primary PCI in acute myocardial infarction-related cardiogenic shock
- Performing endomyocardial biopsy without a clear clinical question or expectation that histology may alter management
- Sending an unstable patient for CT or cardiac MRI when bedside or invasive alternatives are more appropriate
- Failing to reassess the diagnosis when shock physiology does not match the presumed etiology
- Delaying shock team activation until refractory multiorgan failure has developed
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 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.
- ↑ 2.0 2.1 Thiele H, Hassager C (2026). "Cardiogenic Shock". The New England Journal of Medicine. 394 (1): 62–77. doi:10.1056/NEJMra2312086.
- ↑ 3.0 3.1 van Diepen S, Katz JN, Albert NM; et al. (2017). "Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 136 (16): e232–e268. doi:10.1161/CIR.0000000000000525.
- ↑ 4.0 4.1 4.2 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.
- ↑ 5.0 5.1 Lüsebrink E, Binzenhöfer L, Adamo M; et al. (2024). "Cardiogenic Shock". Lancet. 404 (10466): 2006–2020. doi:10.1016/S0140-6736(24)01818-X.
- ↑ Ortega-Hernández JA, Chacon-Lozsan FJ, Baldetti L; et al. (2026). "Pulmonary Artery Catheter Monitoring in Cardiogenic Shock: A Systematic Review and Meta-Analysis". Shock. 65 (4): 648–659. doi:10.1097/SHK.0000000000002784.
- ↑ 7.0 7.1 Papolos AI, Kenigsberg BB, Berg DD; et al. (2021). "Management and Outcomes of Cardiogenic Shock in Cardiac ICUs With Versus Without Shock Teams". Journal of the American College of Cardiology. 78 (13): 1309–1317. doi:10.1016/j.jacc.2021.07.044.
- ↑ 8.0 8.1 8.2 8.3 8.4 8.5 Geller BJ, Sinha SS, Kapur NK; et al. (2022). "Escalating and De-Escalating Temporary Mechanical Circulatory Support in Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 146 (6): e50–e68. doi:10.1161/CIR.0000000000001076.
- ↑ 9.0 9.1 9.2 Rajagopalan N, Borlaug BA, Bailey AL; et al. (2024). "Practical Guidance for Hemodynamic Assessment by Right Heart Catheterization in Management of Heart Failure". JACC: Heart Failure. 12 (7): 1141–1156. doi:10.1016/j.jchf.2024.03.020.
- ↑ 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.
- ↑ 11.0 11.1 Rao SV, O'Donoghue ML, Ruel M; et al. (2025). "2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes". Journal of the American College of Cardiology. 85 (22): 2135–2237. doi:10.1016/j.jacc.2024.11.009.
- ↑ Henry TD, Tomey MI, Tamis-Holland JE; et al. (2021). "Invasive Management of Acute Myocardial Infarction Complicated by Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 143 (15): e815–e829. doi:10.1161/CIR.0000000000000959.
- ↑ Thiele H, Akin I, Sandri M; et al. (2017). "PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock". The New England Journal of Medicine. 377 (25): 2419–2432. doi:10.1056/NEJMoa1710261.
- ↑ Thiele H, Akin I, Sandri M; et al. (2018). "One-Year Outcomes after PCI Strategies in Cardiogenic Shock". The New England Journal of Medicine. 379 (18): 1699–1710. doi:10.1056/NEJMoa1808788.
- ↑ 15.0 15.1 15.2 Drazner MH, Bozkurt B, Cooper LT; et al. (2025). "2024 ACC Expert Consensus Decision Pathway on Strategies and Criteria for the Diagnosis and Management of Myocarditis". Journal of the American College of Cardiology. 85 (4): 391–431. doi:10.1016/j.jacc.2024.10.080.
- ↑ Kociol RD, Cooper LT, Fang JC; et al. (2020). "Recognition and Initial Management of Fulminant Myocarditis: A Scientific Statement From the American Heart Association". Circulation. 141 (6): e69–e92. doi:10.1161/CIR.0000000000000745.
- ↑ 17.0 17.1 Seferović PM, Tsutsui H, Mcnamara DM; et al. (2021). "Heart Failure Association, Heart Failure Society of America, and Japanese Heart Failure Society Position Statement on Endomyocardial Biopsy". Journal of Cardiac Failure. 27 (7): 727–743. doi:10.1016/j.cardfail.2021.04.010.
- ↑ Ammirati E, Moslehi JJ (2023). "Diagnosis and Treatment of Acute Myocarditis: A Review". JAMA. 329 (13): 1098–1113. doi:10.1001/jama.2023.3371.