By Irene Vargas, MD; Edward Richardson, MD; Saraschandra Vallabhajosyula, MD, MSc

Introduction 

Cardiogenic shock (CS) has been most extensively studied in the setting of acute myocardial infarction (AMI); however, a substantial and growing proportion of cases arise from non-AMI etiologies. Common causes of non-AMI-CS include progression of chronic cardiomyopathy, de novo acute heart failure (DNHF), valvular heart disease, and inflammatory or pericardial processes.^1,2 Although these conditions differ in etiology, presentation, and management approach, they often converge on a final pathway of reduced cardiac output, impaired systemic perfusion, and worsening end-organ dysfunction.³ Diagnosis and management of non-AMI-CS require a high index of suspicion and a physiology-driven approach. In this Tip of the Month, we focus on practical strategies for early identification, focused evaluation, and management of non-AMI-CS.

Early Recognition

Early recognition is critical for the management of CS. A high level of suspicion is required in high-risk patients who develop hypotension (defined as systolic blood pressure [SBP] <90 mm Hg, mean arterial pressure [MAP] <60 mm Hg, or a >30 mm Hg drop from baseline for >30 minutes), tachycardia (>100 beats per minute), or a narrow pulse pressure (<25% of SBP).⁴ This should prompt a more thorough evaluation with physical examination, laboratory tests, and imaging. Early physical examination findings in CS include altered mental status, cool or mottled extremities, oliguria, and signs of volume overload such as elevated jugular venous pressure, pulmonary crepitations, or peripheral edema. Laboratory markers showing evidence of end-organ hypoperfusion include elevated lactate >2 mmol/L, marked transaminase elevation, acute kidney injury with creatinine at least twice the upper limit of normal, acidemia with pH less than 7.2, and unexplained metabolic acidosis.⁵ Troponins, N-terminal pro-B-type natriuretic peptide, and inflammatory markers can also be helpful in diagnosing and managing non-AMI-CS.⁶ It should be noted that these laboratory markers suggestive of congestion, hypoperfusion, and end-organ injury may be subtly elevated or normal in early shock stages.²

Diagnostic Evaluation and Structured Shock Staging

Echocardiography is an essential early diagnostic tool providing extensive functional and structural information, as well as hemodynamic insights while being noninvasive and readily available. Techniques in echocardiography allow for estimation of right-sided filling pressures, left-sided filling pressures, and estimation of cardiac output. While these measurements are not gold standard, they can provide early prognostic information to guide disposition and further diagnostic testing. Recent evidence suggests that left ventricular stroke work index measured on echocardiogram can separate patients in low- and high-risk subsets of CS in patients admitted to cardiac intensive care units (ICUs).⁷ Even as noninvasive techniques have evolved, invasive hemodynamic assessment with the pulmonary artery catheter (PAC) remains central in the management of CS, particularly in cases of diagnostic uncertainty or in cases of refractory to treatment. The PAC provides detailed assessments of filling pressures to estimate cardiac output and other advanced hemodynamics. Despite the lack of randomized controlled trials evaluating PAC in CS, observational studies have demonstrated improved outcomes when incorporated into care.^8,9 Together, the parameters provided by these diagnostics facilitate definition of shock phenotype and severity and also guide management, including escalation and de-escalation of therapy. Of note, the use of coronary angiography in non-AMI CS should be selective; in particular, it should be reserved for new or unexplained left ventricular dysfunction or when the coronary anatomy is unknown, rather than performed reflexively, as in AMI-CS.^3,5,10

Structured shock staging provides a framework to guide early management decisions. The SCAI shock classification describes a continuum from at-risk (Stage A) through beginning (Stage B), classic (Stage C), deteriorating (Stage D), and refractory shock (Stage E). Since its initial introduction in 2019, the classification has been refined to emphasize the dynamic nature of CS.¹¹

Initial Medical Stabilization

Initial medical therapy in non-AMI-CS aims to restore organ perfusion while improving congestion and cardiac output. In hypotensive patients, a variety of intravenous vasoactive medications can be used to maintain adequate perfusion, typically targeting an SBP >90 mm Hg or MAP >65 mm Hg, recognizing that optimal targets should be individualized. When vasoactive support is required, norepinephrine is an appropriate first-line agent for hypotensive CS. The lowest effective dose of vasoactive agents should be employed for the shortest possible duration. Inotropes may be used to augment cardiac output when low-flow physiology predominates, with careful monitoring for side effects such as arrhythmias.⁵ Reducing preload with volume removal strategies, including diuretics, helps improve congestion and perfusion, particularly in heart failure-related shock. Assessing volume status and response to diuretics is imperative, as failure to respond to a diuretic challenge should prompt escalation of diuretic strategy or consideration of renal replacement therapy.¹²

Persistent hypoperfusion with worsening organ damage despite appropriate medical therapy should prompt early consideration of invasive diagnostic testing and escalation of therapies, rather than prolonged medical management alone. In particular, early collaboration with a multidisciplinary shock team that can facilitate higher-level care, including transfer to a specialized center if needed, is imperative in patients with rapidly progressive shock or an anticipated need for escalation to mechanical circulatory support (MCS).¹³

Escalation to MCS

Temporary MCS (tMCS) should be considered when optimized medical therapy fails to improve clinical status. Escalation should be guided by physiologic and hemodynamic assessments prior to development of irreversible multiorgan dysfunction. Support devices for the left ventricle include intra-aortic balloon pump (IABP), Impella (2.5, CP, 5.5), and TandemHeart. Impella RP and Protek Duo offer support for the right ventricle. When biventricular support is needed, options include combinations of devices such as Impella RP plus Impella CP or venoarterial extracorporeal membrane oxygenation (VA-ECMO). Device selection should also account for oxygenation and gas exchange, particularly in patients with pulmonary edema, hypoxemia, or concomitant respiratory failure. Among the aforementioned support modalities, Impella 5.5, TandemHeart, and VA-ECMO offer higher-flow MCS and should be considered for advanced refractory shock. Impella 5.5 offers additional advantages compared to other devices, as it can be used for up to 30 days with endpoints of recovery, placement of a durable ventricular assist device, or transplant. Historically, MCS is more frequently used in AMI-CS than in non-AMI-CS; however, recent studies support more frequent and early utilization of MCS in non-AMI-CS. In a recent analysis of a national sample database, initiation of MCS within 48 hours reduced hospital mortality of all causes.¹⁴ As in AMI-CS, there is little data from randomized control trials for early MCS in non-AMI-CS. We believe such trials are warranted to assess early MCS via a standardized, multidisciplinary approach. Given the risk of complications while on tMCS, frequent reassessment after tMCS initiation is essential. Failure to wean from temporary support should prompt early multidisciplinary discussion regarding recovery potential, transition to durable mechanical support, transplant evaluation, or goals-of-care planning. Timely decision-making is critical to avoid prolonged support without a clear exit strategy.^15,16

Summary

Non-AMI-CS is common and heterogeneous, requiring early recognition, structured shock staging, and physiology-driven management. Focused diagnostic evaluation, time-limited medical stabilization, and timely escalation to tMCS are essential. Early multidisciplinary shock team involvement and clear escalation or exit strategies are critical to improving outcomes.

References

1. Kanwar MK, Billia F, Randhawa V, et al. Heart failure related cardiogenic shock: An ISHLT consensus conference content summary. J Heart Lung Transplantation. 2024 Feb;43(2):189-203.
2. Abraham J, Blumer V, Burkhoff D, et al. Heart Failure-Related Cardiogenic Shock: Pathophysiology, Evaluation and Management Considerations: Review of Heart Failure-Related Cardiogenic Shock. J Card Fail. 2021 Oct;27(10):1126-1140.
3. Barnett CF, Brusca SB, Hanff TC, et al. Management of Cardiogenic Shock Unrelated to Acute Myocardial Infarction. Can J Cardiol. 2023 Apr;39(4):406-419.
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 Am Coll Cardiol. 2022 Mar 8;79(9):933-946.
5. Sinha SS, Morrow DA, Kapur NK, et al. 2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock. A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2025 Apr 29;85(16):1618-1641.
6. van Diepen S, Katz JN, Albert NM, et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association. Circulation. 2017 Oct 17;136(16):e232-e268.
7. Jentzer JC, Burstein B, Ternus B, et al. Noninvasive Hemodynamic Characterization of Shock and Preshock Using Echocardiography in Cardiac Intensive Care Unit Patients. J Am Heart Assoc. 2023 Nov 21;12(22):e031427.
8. Kadosh BS, Berg DD, Bohula EA, et al. Pulmonary Artery Catheter Use and Mortality in the Cardiac Intensive Care Unit. JACC: Heart Fail. 2023 Aug;11(8 Pt 1):903-914.
9. Yoo TK, Miyashita S, Davoudi F, et al. Clinical impact of pulmonary artery catheter in patients with cardiogenic shock: A systematic review and meta-analysis. Cardiovasc Revasc Med. 2023 Oct;55:58-65.
10. Rao SV, O’Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2025 Apr;151(13):e771-e862.
11. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK Stage Classification Expert Consensus Update: A Review and Incorporation of Validation Studies. J Am Coll Cardiol. 2022 Mar 8;79(9):933-946.
12. Mehta C, Shin A, Osorio B, et al. Management of non-Cardiac Organ Failure in cardiogenic shock. Am Heart J Plus. 2025 May 1;55:100549.
13. Godding M, Haji M, Vargas I, et al. Optimizing Patient Selection, Referral Timing, and Advanced Therapies in Cardiogenic Shock. Heart Failure Clin. 2025 Dec;1551-7136.
14. Barssoum K, Patel HP, Abdelmaseih R, et al. Characteristics and Outcomes of Early vs Late Initiation of Mechanical Circulatory Support in Non-Acute Myocardial Infarction related Cardiogenic Shock: An Analysis of the National Inpatient Sample Database. Curr Probl Cardiol. 2023 May;48(5):101584.
15. Mehta A, Vavilin I, Nguyen AH, et al. Contemporary approach to cardiogenic shock care: a state-of-the-art review. Front Cardiovasc Med. 2024 Mar 13;11:1354158.
16. Geller BJ, Sinha SS, Kapur NK, et al. Escalating and De-escalating Temporary Mechanical Circulatory Support in Cardiogenic Shock: A Scientific Statement From the American Heart Association. Circulation. 2022 Aug 9;146(6):e50-e68.