https://orcid.org/0000-0002-1777-2045
Abstract
Cardiogenic shock (CS) is a life-threatening condition defined by the heart's inability to adequately pump blood to meet metabolic demands, leading to systemic hypoperfusion and insufficient tissue oxygenation. Despite treatment advancements, CS continues to carry high morbidity and mortality rates, especially when it follows acute myocardial infarction. Various expert groups and scientific societies have proposed recommendations and management pathways, each contributing unique insights yet sometimes overlooking important clinical considerations. This mini-review provides an updated, integrated overview of distinct CS scenarios, including ischaemic, non-ischaemic, and post-cardiotomy categories, and their respective treatment strategies. Additionally, this review explores management approaches that underscore the importance of early detection of inflammatory markers in non-ischaemic CS and targeted therapeutic interventions for each CS subtype. Specifically, the role of pharmacological treatments is examined alongside the relevance and timing of mechanical circulatory support devices. A deeper understanding of the pathophysiology and tailored management pathways for each CS type may enable clinicians to improve interventions and enhance survival and recovery in patients with CS.
Introduction
Cardiogenic shock (CS) is a multifactorial, haemodynamically complex syndrome characterized by profound and refractory circulatory collapse resulting from impaired myocardial contractility, which leads to systemic hypoperfusion, metabolic acidosis, and multiorgan dysfunction.1,2 Despite more than two decades of advancements in interventional techniques, the advent of rapidly deployable temporary mechanical circulatory support (tMCS) devices, organized systems-of-care for managing acute myocardial infarction (AMI), the incidence and mortality associated with CS remains high.2–4 Cardiogenic shock complicates approximately 5–10% of AMI cases with some studies reporting in-hospital mortality rates exceeding 50%.5 These mortality rates vary by aetiology, with ischaemic CS typically associated with poorer prognosis compared with non-ischaemic or post-cardiotomy cases.
This narrative review delves into the pathophysiology of three primary CS phenotypes: ischaemic, non-ischaemic, and post-cardiotomy shock (Figure 1). Understanding each classification and their corresponding diagnostic and management strategies is crucial in optimizing patient outcomes (Figure 2). Here, we will present a review of CS literature focusing on patient phenotypes, management recommendations, and key findings. We suggest algorithms summarizing patient management strategies and highlighting the key differences across CS-related management protocols that are designed as practical tools to support clinical practice and guide future research in the field. By adopting this new classification system, with its three primary CS categories, clinical care may be enhanced through a more structured and individualized approach to diagnosis and management. Differentiating between CS types allows healthcare providers to implement more targeted treatment strategies, which may reduce mortality and improve patient outcomes.
Classification of cardiogenic shock. AMI, acute myocardial infarction; CS, cardiogenic shock; PCCS, post-cardiotomy cardiogenic shock.
Proposed algorithm of cardiogenic shock management within a regionalized shock network by a multidisciplinary shock team. A contemporary system of care approach for cardiogenic shock management by a multidisciplinary team in a ‘hub and spoke’ model. This allows for timely diagnosis with early comprehensive invasive haemodynamic assessment. Early, selective, and tailored mechanical circulatory support based on cardiogenic shock phenotype and congestive profiles is crucial for cardiogenic shock management in the modern era. This is also predicated on expedited transfer to the level 1 cardiogenic shock centers of excellence for team-based and comprehensive multiorgan system care. AMI, acute myocardial infarction; CS, cardiogenic shock; IABP, intra-aortic balloon pump; LV, left ventricular; LVAD, left ventricular assist device; MCS, mechanical circulatory support; SCAI, Society for Cardiovascular Angiography and Interventions; VA-ECMO, veno-arterial extracorporeal membrane oxygenation.
Acute myocardial infarction-related cardiogenic shock
The most common form of CS is ischaemic CS, which typically arises from AMI complicated by mechanical issues like ventricular septal defects, papillary muscle rupture with severe mitral regurgitation, or free wall rupture.6 Diagnosis relies on electrocardiogram (ECG) findings, elevated cardiac biomarkers (e.g. troponins), and imaging such as echocardiography.7–9 Coronary angiography is often performed to determine the location and severity of coronary artery occlusions. The timing of CS onset after AMI varies, but a post-hoc analysis of the SHOCK Trial registry reported a median onset of 6 hours from the start of AMI symptoms.10,11
The cornerstone of ischaemic CS management is rapid revascularization, achieved through percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).12 To maintain haemodynamic stability, pharmacological support with vasopressors and inotropes may also be required.13 In severe cases, tMCS devices, such as intra-aortic balloon pumps (IABP),14 Impella devices, or extracorporeal membrane oxygenation may be employed to augment cardiac output while the patient awaits definitive treatment (Figure 1 and 3).
Acute myocardial infarction—cardiogenic shock treatment management. Management strategies for cardiogenic shock associated with acute myocardial infarction, emphasizing treatment considerations such as revascularization status, hypoxia, and mechanical complications. Shock severity is stratified using the Society for Cardiovascular Angiography and Interventions staging system, with therapeutic strategies and mechanical circulatory support device recommendations tailored to left ventricular, right ventricular, or biventricular dominant shock profiles. AMI, acute myocardial infarction; CS, cardiogenic shock; SCAI, Society for Cardiovascular Angiography and Interventions; pMCS, percutaneous mechanical circulatory support; VSD, ventricular septal defect; MR, mitral regurgitation; LV, left ventricular; RV, right ventricular; Bi-V, biventricular; SBP, systolic blood pressure; VA-ECMO, veno-arterial extracorporeal membrane oxygenation; ECMELLA, combined use of VA-ECMO and an Impella device.
The care of AMI-CS can be expedited through early acquisition of a 12-lead ECG, administration of vasopressors (preferably norepinephrine and avoiding phenylephrine) to achieve a mean arterial pressure > 65 mm Hg, mechanical ventilation, point-of-care echocardiography to assess for mechanical complications, and immediate transfer to a PCI-capable facility.1,2,9,13
Non-AMI cardiogenic shock
In the past decade, non-AMI-CS has emerged as a distinct aetiology, differing from AMI-CS in terms of pathophysiology, clinical presentation, acute management, and long-term prognosis. Non-AMI-CS can arise from various underlying aetiologies, including organic valvular heart disease (e.g. endocarditis and valvular prosthesis dysfunction), cardiomyopathies (e.g. idiopathic dilated, hypertrophic, hypertensive, peripartum, left ventricular noncompaction, Chagas disease, restrictive, chronic ischaemic, and myocarditis), lung diseases (e.g. pulmonary embolism, pre-existing disease, or arterial pulmonary hypertension), pericardial disease, intracardiac tumours, adult congenital heart disease, and acute aortic syndromes.1,2
The pathophysiology of heart failure (HF)-related CS also varies depending on whether it is de novo or acute onset chronic of HF-CS.2 Chronic HF primarily presents as congestion due to increased systemic vascular resistance and blood redistribution from the splanchnic circulation. These changes, including venoconstriction and elevated central venous pressure, contribute to organ congestion, renal impairment, and hepatic dysfunction. When ventricular function becomes severely impaired, chronic HF progresses to HF-CS, resulting in worsening hypoperfusion and subsequent acute on chronic hepatic and renal injury, lactic acidosis, reduced coronary perfusion, and further activation of baroreceptors and chemoreceptors. This initiates a vicious cycle of deteriorating cardiac function, systemic inflammatory response syndrome, and ultimately, multiorgan failure, and death.2,15 Initial assessment of HF-CS should focus on identifying the underlying cause, determining CS severity, and evaluating haemodynamic congestion and perfusion status to guide targeted management (Figure 4).
Non–acute myocardial infarction cardiogenic shock treatment management. A stepwise approach to managing cardiogenic shock unrelated to acute myocardial infarction, classified by the Society for Cardiovascular Angiography and Intervention stages. Treatment strategies are stratified by shock severity and categorized based on left ventricular, right ventricular, or biventricular dominance, with specific interventions and mechanical circulatory support options according to hypoperfusion markers, haemodynamic instability, and organ dysfunction. AMI, acute myocardial infarction; CS, cardiogenic shock; SCAI, Society for Cardiovascular Angiography and Interventions; BTT, bridge to transplant; BTR, bridge to recovery; pMCS, percutaneous mechanical circulatory support; LV, left ventricular; RV, right ventricular; Bi-V, biventricular; SBP, systolic blood pressure; IABP, intra-aortic balloon pump; VA-ECMO, veno-arterial extracorporeal membrane oxygenation; LVAD, left ventricular assist device; ECMELLA, combined use of VA-ECMO and an Impella device.
Post-cardiotomy cardiogenic shock
Post-cardiotomy CS (PCCS) refers to a sustained low cardiac output syndrome (LCOS) that can complicate the weaning process from cardiopulmonary bypass (CPB) or occur shortly after surgery despite optimal medical treatment.16,17 Clinical presentation may involve left, right, or biventricular heart dysfunction, with or without pulmonary congestion, accompanied by significant haemodynamic compromise and end-organ hypoperfusion (Figure 5). PCCS may stem from pre-existing HF exacerbated by surgical trauma or may develop acutely from intraoperative factors, such as inadequate myocardial protection or iatrogenic myocardial ischaemia.18 Notable risk factors for developing post-cardiotomy HF include older age, high body mass index, preoperative ventricular dysfunction, recent myocardial infarction, kidney dysfunction, emergency or repeat surgeries, exposure to myocardial toxic pharmacologic agents, mediastinal radiation, chronic pericardial disease, and extended durations of bypass or aortic cross-clamping. Furthermore, PCCS has a significant impact on patient outcomes, leading to increased morbidity rates, short- and long-term mortality, and greater healthcare resource utilization.19,20 Its incidence ranges from 2 to 20%, depending on the underlying condition and surgical procedure. Although persistent LCOS is associated with extremely poor survival rates, the application of temporary MCS can raise survival rates 20–42%.
Post-cardiotomy cardiogenic shock treatment management. Treatment considerations and strategies for managing post-cardiotomy cardiogenic shock, where shock profiles are categorized into pre-operative, intraoperative, and postoperative phases. Highlighted here are risk factors, haemodynamic indicators, and appropriate interventions, including mechanical circulatory support tailored for left ventricular, right ventricular, and biventricular dysfunction. PCCS, post-cardiotomy cardiogenic shock; LV, left ventricular; RV, right ventricular; Bi-V, biventricular; PCS, post-cardiotomy shock; LVEF, left ventricular ejection fraction; MI, myocardial infarction; CAD, coronary artery disease; CPB, cardiopulmonary bypass; SBP, systolic blood pressure; VIS, vasoactive inotropic score; CI, cardiac index; PCWP, pulmonary capillary wedge pressure; CVP, central venous pressure; EF, ejection fraction; SVO2, mixed venous oxygen saturation; ScVO2, central venous oxygen saturation; WMA, wall motion abnormality; MCS, mechanical circulatory support; IABP, intra-aortic balloon pump; VA-ECMO, veno-arterial extracorporeal membrane oxygenation; V-PA, veno-pulmonary artery extracorporeal membrane oxygenation; PAPi, pulmonary artery pulsatility index; CVP, central venous pressure; TAPSE, tricuspid annular plane systolic excursion; ECMELLA, combined use of VA-ECMO and an Impella device.
In post-cardiotomy HF, two primary clinical scenarios may be encountered. First, the failure to wean from CPB, or second, refractory LCOS following CPB removal. The main challenge is identifying patients whose cardiac function is unlikely to recover quickly and who may therefore benefit from immediate transition to temporary MCS. Early identification and intervention are critical for improving patient outcomes in this high-risk population.
Role for early identification and dynamic assessment
Cardiogenic shock is a multifaceted syndrome with complex clinical manifestations, making rapid, early identification, and risk stratification essential. Implementing a ‘cardiogenic shock alert’ system, which integrates SCAI stages, clinical history, demographic information, and haemo-metabolic markers of organ perfusion (e.g. lactate, renal function, transaminases, systolic blood pressure, and/or mean arterial pressure), may expedite timely diagnosis, facilitate appropriate intervention, and streamline transfer to higher levels of care when necessary.11
Role for risk prediction in cardiogenic shock
Although multiple risk prediction scores for CS exist, none have been widely adopted in contemporary clinical practice. While the IABP-SHOCK II score is specific to AMI-CS patients, the CardShock risk score and the SCAI staging system have broader applicability across different CS types (Table 1). Despite the availability of these tools, the development of a comprehensive, unified scoring system that supports early prognostication, informs therapeutic decisions, and encompasses risk prediction at multiple time points across various CS subtypes remains a challenge. Ideally, risk scores for CS should be contemporary, tailored to specific aetiologies and phenotypes, and adaptable to the evolving nature of the disease.
Cardiogenic shock risk prediction tools
| Risk prediction tool | Year | Variables | |
|---|---|---|---|
| CardShock21 | 2015 |
|
|
| IABP SHOCK II14 | 2017 |
|
|
| IHVI22 | 2019 |
|
|
| CLIP23 | 2021 |
|
|
| SCAI24 | 2022 | Multiple clinical and laboratory parameters that risk stratify into 5 stages A to E, with cardiac arrest and arrhythmia modifier | |
| Risk prediction tool | Year | Variables | |
|---|---|---|---|
| CardShock21 | 2015 |
|
|
| IABP SHOCK II14 | 2017 |
|
|
| IHVI22 | 2019 |
|
|
| CLIP23 | 2021 |
|
|
| SCAI24 | 2022 | Multiple clinical and laboratory parameters that risk stratify into 5 stages A to E, with cardiac arrest and arrhythmia modifier | |
ACS, acute coronary syndrome; CABG, coronary artery bypass grafting; CPO, cardiac power output; LVEF, left ventricular ejection fraction; MI, myocardial infarction; PAPi, pulmonary artery pulsatility index; TIMI, thrombolysis in myocardial infarction score.
Cardiogenic shock risk prediction tools
| Risk prediction tool | Year | Variables | |
|---|---|---|---|
| CardShock21 | 2015 |
|
|
| IABP SHOCK II14 | 2017 |
|
|
| IHVI22 | 2019 |
|
|
| CLIP23 | 2021 |
|
|
| SCAI24 | 2022 | Multiple clinical and laboratory parameters that risk stratify into 5 stages A to E, with cardiac arrest and arrhythmia modifier | |
| Risk prediction tool | Year | Variables | |
|---|---|---|---|
| CardShock21 | 2015 |
|
|
| IABP SHOCK II14 | 2017 |
|
|
| IHVI22 | 2019 |
|
|
| CLIP23 | 2021 |
|
|
| SCAI24 | 2022 | Multiple clinical and laboratory parameters that risk stratify into 5 stages A to E, with cardiac arrest and arrhythmia modifier | |
ACS, acute coronary syndrome; CABG, coronary artery bypass grafting; CPO, cardiac power output; LVEF, left ventricular ejection fraction; MI, myocardial infarction; PAPi, pulmonary artery pulsatility index; TIMI, thrombolysis in myocardial infarction score.
Conclusion
Cardiogenic shock is a complex, multifactorial, haemo-metabolic syndrome with rising prevalence in the modern cardiac intensive care unit. Despite significant advances in medical and device-based therapies, CS remains associated with high morbidity and mortality, especially with the increasing incidence of HF-CS. The classification of CS into ischaemic, non-ischaemic, and post-cardiotomy subtypes highlights the importance of understanding the diverse aetiologies and distinct pathophysiologies within these categories. Diagnosis relies on a combination of clinical evaluation, imaging, and laboratory testing, while effective management demands a tailored approach based on the underlying cause (Figure 6). Early interventions, including pharmacologic support and timely use of MCS devices, are essential for improving survival rates in patients diagnosed with CS. Furthermore, managing these critically ill patients requires a standardized, multidisciplinary, team-based approach within a regionalized system of care.
Optimizing patient-centric care. Mechanical circulatory support considerations for appropriate use of selective and tailored approaches to available devices. Illustrated here is the intricate process of achieving optimal patient-oriented care in the context of mechanical circulatory support use. The achievement of the right patient, at the right time, with the appropriate mechanical circulatory support device, and in the right clinical setting who should be managed at an appropriate level of cardiogenic shock center in a regionalized shock network, is a complex endeavor influenced by a multitude of factors. AMI, acute myocardial infarction; CICU, cardiac intensive care unit; CS, cardiogenic shock; HF, heart failure; LVAD, left ventricular assist device; SCAI, Society of Cardiovascular Angiography and Interventions.
Acknowledgements
This manuscript is one of nine manuscripts published as a Supplement to address Mechanical Circulatory Support in Special Settings and the importance of the Heart Team Approach. JetPub Scientific Communications, LLC, provided editorial assistance to the authors during preparation of this manuscript.
Funding
This paper was published as part of a supplement financially supported by Abiomed Europe GmbH.
Data availability
No new data were generated or analysed in support of this research.
References
Author notes
Conflict of interest: R.L. has received research grant, consulting fees paid to the university, and receipt of material for animal experiments from Medtronic and Livanova; Speaker fees from Abiomed and support for attending meetings and/or travel as a part of the consulting contract from Medtronic; Participation on a Data Safety Monitoring Board or Advisory Board (paid to the institution) from Eurosets and Xenios; A.M. and G.B. have nothing to disclose.
