The management of shock in patients with pulmonary embolism (PE) is a perennial challenge for intensivists. Patients have traditionally been grouped into low-, intermediate-, and high-risk categories, with reperfusion therapies being reserved for high-risk PE, defined as patients who are hypotensive and in obstructive shock.1–2
Recently, the American Heart Association (AHA), in conjunction with the American College of Cardiology (ACC) and CHEST, released new guidelines, creating risk classes A through E.3 Class D specifically introduces normotensive shock, now a formally recognized concept in PE management, with the goal of helping clinicians identify patients who are normotensive and could benefit from increased monitoring, thrombolytics, or interventional therapies.
How the concept of normotensive shock was developed
Traditionally, hypotension has defined obstructive shock in acute PE. However, a subset of patients in the cardiogenic shock literature began to emerge who, despite a normal BP, demonstrated a depressed cardiac index and worse clinical outcomes.4–7 This was expanded to PE when data from the FLASH registry demonstrated that among patients who were normotensive undergoing mechanical embolectomy, up to 34% had a shock-range cardiac index (< 2.2 L/min per m2).8 Additional studies suggest markers such as acute kidney injury may identify higher-risk patients even in the absence of hypotension.9 Together, these observations have led to incorporation of this concept into contemporary PE risk stratification frameworks.3
How do these guidelines define normotensive shock in PE?
In the 2026 AHA/ACC framework, normotensive shock is currently defined as a state of impaired perfusion despite preserved BP in the setting of right ventricular failure. This concept is incorporated within category D2, where elevated lactate, oliguria, acute kidney injury, altered mental status, mean arterial pressure < 60, or low cardiac index capture these patients despite the absence of sustained hypotension.10–11
However, the definition remains internally inconsistent. While visual summaries label category D2 as normotensive shock, the accompanying text includes elements of transient hypotension, creating ambiguity around what “normotensive” truly represents. Thus, although clinically meaningful with potential implications for management, the concept lacks a standardized, validated definition.10
Pearls and pitfalls of normotensive shock
The identification of normotensive shock represents an important attempt at refinement of PE risk stratification, helping clinicians recognize patients at higher risk of decompensation who may benefit from more rapid intervention or transfer to a higher level of care. In addition to markers of hypoperfusion, elevated troponin, B-type natriuretic peptide, moderate to severe right ventricular dysfunction on transthoracic echo, and tachycardia have all been shown to increase the likelihood of a depressed cardiac index.8 In the same study, 30.5% of patients demonstrated a normalization of cardiac index following mechanical thrombectomy accompanied by greater improvements in dyspnea scores compared with those without normotensive shock, suggesting more aggressive management may be particularly beneficial for these patients. Recent studies have explored the development of validated scoring systems using these clinical characteristics with some success.12 Pairing clinical markers of tissue hypoperfusion with clinical exam findings such as tachycardia and point-of-care ultrasound findings provides an opportunity to identify patients who might be at higher risk for decompensation and may benefit from expedited reperfusion. It may also represent a window of stability where the patient may benefit from transfer to a facility capable of these therapies.
While normotensive shock offers a promising concept in risk assessment of acute PE, is does come with limitations, namely that it remains a derived construct. This concept derives from retrospective observational data in a specific subset of patients who underwent mechanical thrombectomy, not data from prospective randomized controlled trials of all patients with PE.8 Clinicians must also remember that lactate elevation, altered mental status, oliguria, and tachycardia are nonspecific and should not be interpreted in isolation. Moreover, there is no prospective evidence comparing treatment outcomes of those with normotensive shock to those without, so clinicians must use caution before broadly applying this concept. Currently, there are no data to guide clinicians in choosing appropriate therapies for patients with PE and normotensive shock. Several ongoing trials that compare anticoagulation to catheter-based intervention in a randomized, prospective fashion may provide guidance over the next several years.13–15
Serial bedside assessments of patients with acute PE remain foundational. Clinicians should avoid anchoring on BP alone and instead integrate exam findings, imaging, biomarkers, and clinical trajectory, recognizing that normotension does not imply stability and isolated markers of hypoperfusion do not, by themselves, mandate escalation. Ultimately, patients with acute PE require close monitoring, serial reassessment, and early multidisciplinary evaluation, with treatment decisions tailored to each patient.
References
1. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Heart J. 2020;41(4):543-603. doi:10.1093/eurheartj/ehz405
2. Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370(15):1402-1411. doi:10.1056/NEJMoa1302097
3. Writing Committee Members; Creager MA, Barnes GD, Giri J, et al. 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2026;153(12):e977-e1051. doi:10.1161/CIR.0000000000001415
4. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK Stage Classification Expert Consensus Update: A Review and Incorporation of Validation Studies: This statement was endorsed by the American College of Cardiology (ACC), American College of Emergency Physicians (ACEP), American Heart Association (AHA), European Society of Cardiology (ESC) Association for Acute Cardiovascular Care (ACVC), International Society for Heart and Lung Transplantation (ISHLT), Society of Critical Care Medicine (SCCM), and Society of Thoracic Surgeons (STS) in December 2021. J Soc Cardiovasc Angiogr Interv. 2022;1(1). doi:10.1016/j.jscai.2021.100008
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6. Patel SM, Berg DD, Bohula EA, et al. Continuum of preshock to classic cardiogenic shock in the Critical Care Cardiology Trials Network registry. JACC Heart Fail. 2024;12(9):1625-1635. doi:10.1016/j.jchf.2024.06.009
7. Jentzer JC, Burstein B, Van Diepen S, et al. Defining shock and preshock for mortality risk stratification in cardiac intensive care unit patients. Circ Heart Fail. 2021;14(1):e007678. doi:10.1161/circheartfailure.120.007678
8. Bangalore S, Horowitz JM, Beam D, et al. Prevalence and predictors of cardiogenic shock in intermediate-risk pulmonary embolism: insights from the FLASH registry. JACC Cardiovasc Interv. 2023;16(8):958-972. doi:10.1016/j.jcin.2023.02.004
9. Murgier M, Bertoletti L, Bikdeli B, et al. Prognostic impact of acute kidney injury in patients with acute pulmonary embolism data from the RIETE registry. J Thromb Thrombolysis. 2022;54(1):58-66. doi:10.1007/s11239-022-02633-5
10. Yuriditsky E, Zhang RS, Zhang P, et al. Right ventricular-pulmonary arterial uncoupling as a predictor of invasive hemodynamics and normotensive shock in acute pulmonary embolism. Am J Cardiol. 2025;236:1-7. doi:10.1016/j.amjcard.2024.10.036
11. Najarro M, Briceño W, Rodríguez C, et al. Shock score for prediction of clinical outcomes among stable patients with acute symptomatic pulmonary embolism. Thromb Res. 2024;233:18-24. doi:10.1016/j.thromres.2023.11.011
12. Zhang RS, Alam U, Sharp ASP, et al. Validating the Composite Pulmonary Embolism Shock score for predicting normotensive shock in intermediate-risk pulmonary embolism. Circ Cardiovasc Interv. 2024;17(2):e013399. doi:10.1161/CIRCINTERVENTIONS.123.013399
13. Rosenfield K, Klok FA, Piazza G, et al. Ultrasound-facilitated, catheter-directed fibrinolysis for acute pulmonary embolism. N Engl J Med. Preprint. Posted online March 28, 2026. doi:10.1056/NEJMoa2516567
14. Lookstein RA, Konstantinides SV, Weinberg I, et al. Randomized controlled trial of mechanical thrombectomy with anticoagulation versus anticoagulation alone for acute intermediate-high risk pulmonary embolism: primary outcomes from the STORM-PE trial. Circulation. 2026;153(1):21-34. doi:10.1161/CIRCULATIONAHA.125.077232
15. Sista AK, Troxel AB, Tarpey T, et al. Rationale and design of the PE-TRACT trial: a multicenter randomized trial to evaluate catheter-directed therapy for the treatment of intermediate-risk pulmonary embolism. Am Heart J. 2025;281:112-122. doi:10.1016/j.ahj.2024.11.016
