Today, I review, link to, and excerpt from the “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”. [No Abstract] [Full-Text HTML] [Full-Text PDF]. J Am Coll Cardiol. 2025 Apr 29;85(16):1618-1641. doi: 10.1016/j.jacc.2025.02.018. Epub 2025 Mar 17.
All that follows is from the above resource.
Table of Contents
Preface 16191. Introduction 16191.1 Acknowledgments 16202. Assumptions and Definitions 16202.1. General Clinical Assumptions 16202.2. Definitions 16203. Summary Graphic 1621Figure 1. 24 Roadmap in Evaluation and Management of Cardiogenic Shock: SUSPECT CS 16214. Description, Rationale, And Implications 16224.1. Initial Evaluation of CS 1622Figure 2. CS Working Group-SCAI Shock Criteria for Classification of CS Severity 16234.2. Transferring a Patient in CS 1623Figure 3. Proposed Classification of CS Centers of Care Based on Locally Available Resources and Expertise 16244.3. CS Team Activation 1625Figure 4. Factors Influencing the Selection of the Right Therapy for the Right Patient at the Right Place and the Right Time 16264.4. Invasive Hemodynamics 1626Figure 5. Monitoring of the CS Patient in the Intensive Care Unit 16274.5. Pharmacological Management of CS 16274.6. tMCS 1629Figure 6. Common tMCS Devices Used in CS 162Figure 7. AMI-CS Management 1630Figure 8. HF-CS Management 16314.7. Critical Care Management 1632Figure 9. Systems Based Complications in CS 1633Figure 10. Cardiopulmonary Interactions of PEEP (A) and Strategy for Mechanical Ventilation (B) in Patients With CS 1634Figure 11. Weaning tMCS 16354.8. Conclusion 1635Figure 12. Golden Hour of Acute Shock 1636References 1636Appendix 1 1639
Author Relationships With Industry and Other Entities (Relevant) 1639Appendix 2 1640
Peer Reviewer Relationships With Industry and Other Entities (Comprehensive) 1640Appendix 3 1641
Abbreviations 16411 Introduction
Cardiogenic shock (CS) is a complex, heterogenous, multifactorial syndrome in which a cardiac disorder results in insufficient cardiac output culminating in end-organ hypoperfusion.1 CS is one of the most common causes of admission to contemporary cardiac intensive care units and remains a highly morbid and lethal complication given its dynamic and often unpredictable course, with short-term mortality ranging from 30% to 40% and 1-year mortality approaching or exceeding 50%.2-5 Whereas CS due to acute myocardial infarction (AMI-CS) has been the most extensively studied form of CS in randomized controlled trials (RCTs), the incidence and prevalence of CS due to nonacute myocardial infarction (AMI) causes, specifically, heart failure (HF)-related CS (HF-CS), has increased during the past decade in the United States, with notable differences in baseline characteristics, comorbidities, resource utilization, and in-hospital outcomes.5-8 Despite advances in revascularization and increasing use of temporary mechanical circulatory support (tMCS) during the past 2 decades, RCTs have largely failed to identify treatment strategies that reliably improve mortality other than early revascularization for AMI-CS.9 The first trial to demonstrate any benefit with tMCS was the Danish-German Cardiogenic Shock (DanGer Shock) trial, which showed that early use of a microaxial flow pump in select patients with ST-segment elevation myocardial infarction (STEMI)-related shock improved 180-day survival as compared with standard of care.9aRecognizing the urgency of evaluating and managing CS, the American College of Cardiology (ACC) convened a virtual Heart House Roundtable of international experts, including a diverse, multidisciplinary group of stakeholders across multiple specialties, to address important unresolved issues including—but not limited to—early identification and initial evaluation and management of CS; optimal hemodynamic monitoring; pharmacological therapies; tMCS; and critical care management (see Supplemental Appendix for participant list and discussion questions). The objective of this Concise Clinical Guidance is to address pivotal questions around clinical decision making and provide actionable guidance for the interdisciplinary team involved in the evaluation and management of patients with CS.In accordance with ACC’s Relationships With Industry and Other Entities policy, relevant disclosures for the writing committee and comprehensive disclosures for external peer reviewers can be found in Appendices 1 and 2. A list of abbreviations relevant to this Concise Clinical Guidance can be found in Appendix 3. To ensure transparency, a comprehensive table of the writing committee’s relationships with industry, including those not pertinent to this document, has been created. This can be found in the online Supplemental Appendix.2 Assumptions And Definitions
2.1 General Clinical Assumptions
1. The guidance in this Concise Clinical Guidance is intended for adult patients noting that pediatric presentations of CS differ and may require a modified Society for Cardiovascular Angiography and Intervention (SCAI) system.102. The principal focus of this document applies to patients hospitalized due to CS secondary to AMI (AMI-CS) or HF (HF-CS).3. The guidance is intended for clinicians across a broad array of disciplines who routinely evaluate and manage patients in CS in diverse clinical settings.4. The writing committee endorses the evidence-based approach to CS diagnosis and management recommended in the 2021 ACC/American Heart Association/SCAI Guideline for Coronary Artery Revascularization11 and in the 2022 American Heart Association/ACC/Heart Failure Society of America Guideline for the Management of Heart Failure.125. Optimal care decisions should reflect evidence-based guidelines that incorporate the individual patient’s preferences, values, and priorities, as well as those of the managing clinician and care team. The writing committee endorses a shared decision-making model framework for care delivery, especially in areas where clinical equipoise exists due to treatment uncertainty.6. This Concise Clinical Guidance is based predominantly on expert consensus integrating the best data available and is not intended to supersede good clinical judgment, as many important clinical questions remain unanswered in CS evaluation and management. Interdisciplinary consultation, communication, and collaboration is strongly encouraged.7. As new data emerge, they will likely inform the considerations and suggestions for clinical practice provided here. Clinicians should thoughtfully incorporate novel discoveries and scientific evidence into their clinical practice.2.2 Definitions
CS: A cardiac disorder that results in both clinical and biochemical evidence of sustained tissue hypoperfusion irrespective of underlying blood pressure.1AMI: Defined as the irreversible necrosis of heart muscle due to myocardial ischemia. A common cause for infarction is deprivation in myocardial oxygen supply because of interruption of blood flow in ≥1 coronary arteries because of plaque rupture, erosion, fissure, or coronary dissection. The data element set for a myocardial infarction event requires both subjective and objective findings, including symptoms, cardiac biomarkers, and electrocardiographic abnormalities. The writing committee endorses data elements that were selected based on published peer-reviewed MI definitions developed by national and international cardiovascular subspecialty societies (American Heart Association, ACC, European Society of Cardiology, and SCAI) and are commonly used by regulatory bodies that oversee the conduct of cardiovascular clinical trials.13AMI-CS: AMI-CS includes patients with CS due to AMI in the presence or absence of ST-segment elevation on 12-lead electrocardiography (ie, STEMI and non-STEMI, respectively).1 Consistent with the Shock Academic Research Consortium standardized definitions, left, right, or biventricular dysfunction may result from ongoing myocardial ischemia, ischemic injury, or mechanical complications of MI as the primary etiology of CS.1 Note that CS resulting from acute bradyarrhythmias, tachyarrhythmias, or advanced heart block, postcardiac arrest, or any other complications in the setting of AMI are also classified as AMI-CS.1HF: Defined as per the universal definition of HF14: symptoms and/or signs of HF caused by structural/functional cardiac abnormalities and ≥1 of the following: 1) elevated natriuretic peptides; or 2) objective evidence of cardiogenic pulmonary or systemic congestion. A HF event, including hospitalization, is defined by the criteria outlined by the 2014 ACC/American Heart Association Key Data Elements and Definitions for Cardiovascular Endpoint Events in Clinical Trials.15HF-CS: HF-CS is due to CS related to primary myocardial dysfunction ascribed to either ischemic or nonischemic etiologies of cardiomyopathy.1 It may be further subcategorized into those with either de novo HF-CS (ie, acute myocardial dysfunction that is known or suspected to be new in onset) vs acute-on-chronic HF-CS (ie, acute decompensation of chronic or progressive HF with dilated cardiomyopathy).1 As with AMI-CS, there may be varying degrees of ventricular involvement, including left, right, or biventricular congestive profiles.1 HF-CS may be further categorized by the specific etiology of the underlying myocardial dysfunction, including—but not limited to—acute myocarditis, takotsubo cardiomyopathy, peripartum cardiomyopathy, tachycardia-related cardiomyopathy, hypertrophic cardiomyopathy, or infiltrative diseases such as cardiac amyloidosis or sarcoidosis, among many others.13 Summary Graphic
The summary graphic (Figure 1) represents key considerations and a proposed road map for the first 24 hours of CS evaluation and management.
Figure 1 24-Hour Roadmap in the Evaluation and Management of Cardiogenic Shock: SUSPECT CSCICU = cardiac intensive care unit; CS = cardiogenic shock; ECG = electrocardiogram; LHC = left heart catheterization; PCI = percutaneous coronary intervention; RHC = right heart catheterization; SCAI = Society for Cardiovascular Angiography and Interventions; SHARC = Shock Academic Research Consortium; tMCS = temporary mechanical circulatory support.4 Description, Rationale, and Implications
4.1 Initial Evaluation of CS
Early diagnosis of CS is of critical importance, as it allows for timely intervention that may ultimately impact outcomes. Traditionally, for purposes of research and enrollment in clinical trials and registries, the criteria used to diagnose CS have included hypotension and end-organ hypoperfusion along with evidence of congestion or decreased cardiac output, (eg, measured using a pulmonary artery catheter)3; however, these criteria dichotomize a dynamic clinical entity across a spectrum of illness severity and they also fail to acknowledge the deleterious consequences of normotensive CS (ie, end-organ hypoperfusion without hypotension), which has been associated with increased mortality.16,17 The diagnosis of CS, however, begins with a suspicion of an underlying state of inadequate cardiac output in patients at risk.16 This suspicion can then be confirmed using readily obtainable clinical, laboratory, and/or imaging data. Regardless of the location of the hospitalized patient (emergency room, medical or cardiac telemetry ward, intensive care unit, etc) and across all hospitals with varying resource infrastructures, clinical symptoms, physical examination, and vital signs form the cornerstone for the initial diagnosis of CS.Presence of hypotension (defined as systolic blood pressure <90 mm Hg, or mean arterial pressure [MAP] <60 mm Hg, or a >30 mm Hg drop from baseline for >30 minutes), a heart rate >100 beats per minute, and a narrow pulse pressure (<25% of systolic blood pressure), in isolation or in combination, should all raise suspicion for CS. Physical exam findings of lethargy, confusion, altered mental status, cold and sweaty extremities, prolonged capillary refill times (>2 s) and reduced urine output (<30 mL/h or <0.5 mL/[kg·h]), even in the absence of hypotension, should similarly raise consideration of CS.1,18-20 A simultaneous assessment of respiratory status may yield additional signs of congestion or volume overload (eg, tachypnea, orthopnea, decreased arterial oxygen saturation, etc). More subtle symptoms of CS may include nausea, vomiting, abdominal pain, early satiety, and decreased appetite, reflecting evidence of gastrointestinal ischemia due to inadequate cardiac output. Clinical suspicion of CS should then be supplemented by readily available laboratory tests, such as a comprehensive metabolic profile assessing for acute kidney and hepatic injury; a venous or arterial blood gas with evidence of metabolic acidosis, and elevated venous or arterial lactate (>2 mmol/L). Additional laboratory data useful in the overall evaluation of patients with CS include serum sodium, and biomarkers including high sensitivity troponin and N-terminal pro brain-type natriuretic peptide.1 A central venous catheter can be helpful to measure central venous pressure and obtain a central venous oxygen saturation.Every patient suspected to be in CS should have a 12-lead electrocardiogram and, where available, a transthoracic echocardiogram or point-of-care cardiac ultrasound1 performed by an experienced clinician. Electrocardiographic evidence of acute ischemia, particularly ST-segment elevation, should lead to early triage to the cardiac catheterization laboratory, either locally or at the nearest capable facility, and revascularization as appropriate to coronary anatomy.21 Sonographic evidence of diminished right ventricular (RV) or left ventricular (LV) systolic function, cardiac tamponade, or acute valvulopathies should prompt a timely consult to a general or interventional cardiologist, cardiac surgeon, or an advanced HF cardiologist, as appropriate.22 To aid clinicians in confirming a suspicion of CS, the writing committee proposes the mnemonic “SUSPECT CS” (Table 1), the components of which include the minimum necessary criteria needed to make an early diagnosis of CS.Table 1 SUSPECT CS: A Mnemonic to Aid in Confirming a Diagnosis of CS
Symptoms/Signs Altered mental status, confusion, chest pain or pressure, cold and clammy extremities, rapid pulse, low pulse pressure (<25% of SBP), elevated jugular venous pressure, crackles, rales, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema Urine output Oliguria or anuria, <30 mL/h (<0.5 mL/[kg·h]) Sustained hypotension SBP <90 mm Hg, MAP <65 mm Hg for >30 min or a >30-mm Hg decrease from baseline, or the need for pharmacological or mechanical support to maintain SBP >90 mm Hg Perfusion Evaluate markers of end-organ malperfusion, including lactic acid >2 mmol/L, ALT >200 U/L or >3× upper limit of normal, creatinine ≥2× upper limit of normal, pH <7.2, metabolic acidosis without another known cause ECG/Echocardiogram Evaluate acute ischemia, including ECG and sonographic evidence of STEMI (regional wall motion abnormalities); evidence of LV or RV dilation and systolic dysfunction; valvular pathology Congestion Presence or absence of congestion based on physical signs and hemodynamics; elucidation of ventricular involvement (LV vs RV vs BiV) Triage Appropriate triage/shock team activation or possible transfer to a higher level of care ALT = alanine transaminase; BiV = biventricular; CS = cardiogenic shock; ECG = electrocardiogram; LV = left ventricular; MAP = mean arterial pressure; pH = potential of hydrogen; RV = right ventricular; SBP = systolic blood pressure; STEMI = ST-segment elevation myocardial infarction.It is important to highlight that the initial suspicion and diagnosis of CS does not require invasive hemodynamics1; however, invasive hemodynamics are often useful in elucidating the ventricular involvement and congestive profile of the CS patient and may inform therapeutic decision making. Once a diagnosis is made, the severity of CS should be classified using the SCAI stage of CS.2,23 An adaptation of the SCAI stage classification is presented in Figure 2.2,3Figure 2 CS Working Group-SCAI Shock Criteria for Classification of CS SeverityAdapted with permission from Kapur NK, et al.3Source for this figure adaptation: Naidu SS, et al.2BNP = brain natriuretic peptide; CI = cardiac index; CPR = cardiopulmonary resuscitation; Cr = creatinine clearance; CS = cardiogenic shock; CVP = central venous pressure; GFR = glomerular filtration rate; HR = heart rate; JVP = jugular venous pressure; LFT = liver function test; MAP = mean arterial pressure; PA = pulmonary artery; PCWP = pulmonary capillary wedge pressure; pH = potential of hydrogen; SBP = systolic blood pressure; SCAI = Society for Cardiovascular Angiography and Interventions; tMCS = temporary mechanical circulatory support.In addition to etiology, factors such as setting, timing, and other considerations outlined in the Shock Academic Research Consortium’s Standardized Definitions for Cardiogenic Shock Research and Mechanical Circulatory Support Devices may be used to further classify the phenotype of CS, which distinguishes between the following etiologies: AMI-CS; HF-CS; postcardiotomy CS; and secondary CS (due to arrhythmias, valvular disease, pericardial disease, or other etiologies).1 Notably, AMI-CS can be further subcategorized by whether STEMI vs non-STEMI is present; moreover, HF-CS can be subclassified by de novo HF-CS vs acute-on-chronic HF-CS. Once the diagnosis and severity of CS have been established, invasive monitoring or diagnostic procedures such as an arterial line and a pulmonary artery catheter may then be used to continuously monitor hemodynamics to aid in selection of and response to treatment strategies to address congestion and perfusion.24,25 Depending upon the available resources at the hospital where the initial diagnosis of CS is made, transfer to a higher level of care (including a different institution) may be necessary for further management after initial stabilization.4.2 Transferring a Patient in CS
The acuity and complexity of CS patients require an interdisciplinary, collaborative, and standardized team-based approach to management.20,21,26 Whereas most hospitals in the United States can provide acute cardiovascular care, some can serve as CS centers (known as Level 1 CS hospital centers) being equipped with the full gamut of on-site 24/7 medical and surgical expertise, tMCS devices and “high” procedural volumes. In many cases, such CS centers may also provide advanced HF therapies such as durable LV assist device (LVAD) and orthotopic heart transplant. Advanced CS centers are typically concentrated in larger, urban cities, whereas most CS patients present to local, community hospitals (known as Level 2 or Level 3 CS hospital centers) that may not have advanced tMCS, durable LVAD, or transplant capabilities.22 Professional society guidelines recommend (Class 2b) transfer of patients in need of higher acuity care, beyond the scope of capabilities available at the presenting hospital, to Level 1 CS hospital centers12; however, at present, there is no consensus around classification of hospital centers into levels or tiers of CS care akin to trauma systems of care. Professional cardiology societies have proposed a few different approaches based on available expertise and resource infrastructure19,20,22,27-29 but these frameworks are largely based on expert consensus (Figure 3). Data pertaining to the outcomes of transferred patients are scarce, pointing to an evidence gap in CS care.30,31Figure 3 Proposed Classification of CS Centers of Care Based on Locally Available Resources and ExpertiseAHFTC = advanced heart failure and transplant cardiology; CCC = critical care cardiology; CCL = cardiac catheterization laboratory; CICU = cardiac intensive care unit; CTS = cardiothoracic surgery; IABP = intra-aortic balloon pump; IC = interventional cardiology; LVAD = left ventricular assist device; PAC = pulmonary artery catheter; PCI = percutaneous coronary intervention; pLVAD = percutaneous left ventricular assist device; pRVAD = percutaneous right ventricular assist device; STEMI = ST-segment elevation myocardial infarction; tMCS = temporary mechanical circulatory support.Observational studies of patients transferred to dedicated CS centers have shown mixed results with respect to associated mortality for the transferred cohort. A multicenter, retrospective observational analysis showed higher associated mortality among transferred patients that was driven by HF-related CS.31 In a separate study comparing AMI-CS and HF-CS patients presenting initially to Level 2 or 3 CS hospital centers or a Level 1 CS hospital center in a dedicated, regionalized network across multiple hospital systems encompassing 3 states, the authors found comparable short-term outcomes (including in-hospital and 30-day mortality) and similar rates of bleeding, vascular, and stroke complications.30 The predictors of outcomes among patients transferred for management of CS vary based on etiology of CS. Among HF-CS patients, older age, mechanical ventilation, renal replacement therapy, and multiple vasoactive drugs were associated with worse outcomes while use of a pulmonary artery catheter was associated with favorable outcomes. On the other hand, among AMI-CS patients, overweight size (body mass index >28 kg/m2), worsening renal failure, lactate >3 mg/dL, and increasing number of vasoactive agents were associated with higher mortality rates, while use of any tMCS device was associated with beneficial outcomes.31 It is important to recognize the limitations inherent with these observational data and the merits and challenges of rigorously studying regionalized networks and systems of care in CS as an area of fertile investigation.32The writing committee recommends that Level 2 and 3 CS hospital centers identify: 1) locally available resources; and 2) a dedicated CS regional center that would accept appropriately selected CS patients for further evaluation and treatment as well as might provide remote consultation for patients who may not be appropriate for transfer and/or need further stabilization before a transfer can be initiated. Conversely, Level 1 CS hospital centers should welcome consultations from their regional referring hospitals and accept appropriately selected CS patients for transfer and may provide remote consultation on CS patients who may have been deemed unstable or inappropriate for transfer. Additionally, referring hospitals are encouraged to identify on-site “CS champions” who could help facilitate CS care both locally and in concert with the CS center. Patients with AMI-CS who are triaged to a local cardiac catheterization laboratory and remain in refractory CS postrevascularization should almost always be transferred to a Level 1 CS hospital center.22 Patients who have experienced a cardiac arrest with tenuous neurological status, or patients who have been initiated on ≥1 vasoactive medication, or those in whom a tMCS device is being considered, should also prompt communication with the CS regional center to determine whether, and when, transfer should be pursued. Once the initial suspicion of CS has been confirmed, the writing committee believes it is never too early to contact the CS regional center to discuss potential transfer vs continued management at the initial institution.334.3 CS Team Activation
A standardized, interdisciplinary, team-based approach to CS management has been associated with improved clinical outcomes. Several single-center protocols initially established the proof of concept with associated lower in-hospital mortality.34,35 A multicenter observational analysis among 10 of 24 centers with shock teams showed that shock team centers were more likely to obtain invasive hemodynamics, use advanced types of tMCS (ie, beyond an intra-aortic balloon pump), and have lower risk-adjusted cardiac intensive care unit mortality.36 While the exact composition of CS teams has varied across institutions, key stakeholders from the following specialties have typically been included: critical care cardiology (whenever available) or general critical care in collaboration with a cardiac intensive care unit cardiologist (when it is not); advanced HF and transplant cardiology; interventional cardiology; and cardiac surgery. Extracorporeal membrane oxygenation intensivists or perfusionist and/or palliative care specialists may be included in some centers.33 For Level 2 and 3 CS hospital centers that may not have on-site expertise or an established CS team, the writing committee strongly recommends early contact with the regional Level 1 CS hospital center after confirming the initial diagnosis of CS. The following key considerations may be helpful for triage, potential transfer, appropriate risk stratification, and treatment of CS patients: 1) What is the SCAI Stage and Shock Academic Research Consortium classification? 2) Does the patient need or require escalation of tMCS support at this time? 3) Are there any absolute contraindications to escalation of treatment (eg, do not resuscitate order, or terminal illness, etc)? 4) Does the institution have the resources to support this patient’s anticipated needs (eg, intensive care unit bed availability, clinical expertise, and tMCS resources and availability)? 5) Is the patient hemodynamically stable for transfer?Common elements across shock team models at Level 1 CS hospital centers include early interdisciplinary engagement and consultation to deliver necessary multifaceted care, a coordinating physician (eg, a cardiac intensive care unit cardiologist, advanced HF and transplant cardiologist, or interventional cardiologist, depending on clinical setting) for efficient patient triage, a rapid system for concurrent team activation, efficient virtual and/or bedside communication, and use of invasive hemodynamics to guide therapy selection (Figure 4).21,26Figure 4 Factors Influencing the Selection of the Right Therapy for the Right Patient at the Right Place and the Right TimeAdapted with permission from Mehta A, et al.26CICU = cardiac intensive care unit; LVAD = left ventricular assist device; SCAI = Society for Cardiovascular Angiography and Interventions; SHARC = Shock Academic Research Consortium.4.4 Invasive Hemodynamics
Observational data suggest there is utility in applying invasive hemodynamics to characterize the phenotype of CS, assess the severity of shock, and to guide tMCS-related escalation and weaning decisions in the cardiac intensive care unit.38,39 While there are no definitive randomized data to support the use of pulmonary artery catheters in the setting of CS, the results of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial, studied in severe symptomatic and recurrent HF patients without CS, do not apply to the contemporary CS patient population. Both retrospective claims-based and multicenter, registry-based data suggest that the use of pulmonary artery catheters is associated with improved outcomes.24,25,40-43 In fact, complete hemodynamic profiling as compared with incomplete or no hemodynamic assessment has been associated with lower in-hospital mortality and early hemodynamic assessment within the first 12 hours has been associated with improved clinical outcomes.24,25 This scientific hypothesis that early invasive hemodynamic assessment (within 6 hours of randomization) decreases mortality is currently being tested in a multicenter, randomized, parallel group, adaptive trial, the Pulmonary Artery Catheter in Cardiogenic Shock (PACCS) trial, in HF-CS patients.44Hemodynamics enable the bedside clinician to elucidate the congestion profile (LV dominant, RV dominant, or biventricular shock), which have been associated with adverse outcomes in both AMI-CS and HF-CS. LV dominant congestion in CS is often characterized by an elevated pulmonary capillary wedge pressure or LV end-diastolic pressure >15 mm Hg. In contrast, RV dominant congestion in CS is accompanied by a relatively normal pulmonary capillary wedge pressure in the setting of an elevated right atrial pressure (right atrial or central venous pressure >15 mm Hg). Biventricular congestive profiles suggest elevation in both right atrial and pulmonary capillary wedge pressures. Both biventricular and RV congestion profiles are common in CS patients and have been associated with adverse outcomes, including death, and the need for durable LVAD and heart transplant in multicenter, observational registries.7,42,45Hemodynamic parameters associated with adverse mortality in CS include low MAP, elevated right atrial pressure, an elevated right atrial pressure to pulmonary capillary wedge pressure ratio (>0.6 mm Hg), and a reduced pulmonary artery pulsatility index (the ratio of the difference between the pulmonary artery systolic pressure and diastolic pressure divided by the central venous pressure).42,45,46 The PAPi is a derived value that reflects an amalgam of factors, including RV contractility, RV pulsatile load, and RV congestion, and is most useful in the setting of an elevated right atrial pressure >10 mm Hg and in the absence of moderate or severe pulmonary hypertension (pulmonary artery systolic pressure >50 mm Hg). Criteria for low PAPi values differ between AMI-CS (<0.9 mm Hg) and HF patients undergoing LVAD implantation (<1.85 mm Hg).47-49 The writing committee suggests integrating invasive hemodynamic assessment with noninvasive cardiac imaging (ie, echocardiography or point-of-care ultrasound whenever available) to more precisely characterize the phenotype of CS patients (Figure 5).27,50Figure 5 Monitoring of the CS Patient in the Intensive Care UnitALT = alanine aminotransferase; AST = aspartate aminotransferase; BUN = blood urea nitrogen; CI = cardiac index; CPO = cardiac power output [mean arterial pressure x cardiac output]/451; Cr = creatinine; CS = cardiogenic shock; ECG = electrocardiography; ECMO = extracorporeal membrane oxygenation; FiO2 = fraction of inspired oxygen; HJR = hepatojugular reflux; HR = heart rate; JVP = jugular venous pressure; LV = left ventricular; MAP = mean atrial pressure; PaO2 = partial pressure of oxygen; PAPi = pulmonary artery pulsatility index [systolic pulmonary arterial pressure—diastolic pulmonary arterial pressure]/right atrial pressure; PCWP = pulmonary capillary wedge pressure; PEEP = positive end-expiratory pressure; pH = potential of hydrogen; PVC = premature ventricular contraction; RAP = right atrial pressure; RV = right ventricular; SBP = systolic blood pressure; ScvO2 = central venous oxygen saturation; SpO2 = oxygen saturation; SvO2 = mixed venous oxygen saturation; tMCS = temporary mechanical circulatory support.4.5 Pharmacological Management of CS
In CS, the goal of pharmacological therapies is to mitigate congestion (whenever present), optimize cardiac output, and enhance perfusion to vital organs.51,52 Whenever a congestive phenotype exists, it should be addressed through intravenous loop diuretics, augmentation with thiazide diuretics, and renal replacement therapy for ultrafiltration if congestion is refractory to medical management. Failure to address congestion may lead to microcirculatory ischemia and damage to multiple organs, including the kidneys, liver, and gastrointestinal tract. In this regard, the transrenal perfusion pressure may serve as a useful conceptual model that represents the difference between the MAP and the central venous pressure. Hypoperfusion can be addressed by starting intravenous vasoactive medications, including inotropes, chronotropes, inopressors, inodilators, vasodilators, and vasopressors (Table 2).Table 2 Vasoactive Agents Used in CS
Category Agent(s) Mechanism of Action/Receptor Binding Dosing Hemodynamic Effects SVR BP CO HR Inopressor Norepinephrine α1 (+++), β1 (++), β2 (+) 0.05-1 μg/kg/min ↑↑ ↑↑ ↑ ↑ Epinephrine β1 (+++), α1 (++), β2 (++) 0.01-0.5 μg/kg/min ↑↑ ↑↑ ↑↑ ↑↑ Dopamine D1 (+++), β1 (++), α1 (+) Low: 2-5 μg/kg/min
Intermediate: 5-10 μg/kg/min
High: 10-20 μg/kg/min↑↑ ↑↑ ↑ ↑↑ Inodilator Dobutamine β1 (+++), β2 (++) 2-10 μg/kg/min ↓↔ ↓↔ ↑↑ ↑ Milrinone PDE-3 inhibitor 0.125-0.5 μg/kg/min ↓↓ ↓↓ ↑↑ ↔↑ Vasopressor Phenylephrine α1 (+++) 0.1-10 μg/kg/min ↑ ↑↑ ↔↓ ↔↓ Vasopressin Vasopressin receptor 0.01-0.04 U/min ↑↑ ↑↑ ↔↓ ↔↓ Vasodilator Nitroprusside NO production 0.3-10 μg/kg/min ↓ ↓ ↑↔ ↑↔ Nitroglycerin Converts to NO 25-200 μg/min ↓ ↓ ↑↔ ↑↔ Chronotrope Isoproterenol β1 (+++), β2 (+++) 2-20 μg/min ↓ ↔ ↑ ↑↑ Dopamine See above Inotrope Levosimendan∗ Binds to troponin C, making it more sensitive to calcium thereby improving interaction between troponin C and I 0.05-0.2 μg/kg/min ↓ ↓ ↑ ↔ ↑ = increased effects; ↓ = decreased effects; ↔ = neutral effects; (+++) = strong binding; (++) = moderate binding; (+) = weak binding; α1 = α-1 receptor; β1 = β-1 receptor; β2 = β-2 receptor; BP = blood pressure; CO = cardiac output; CS = cardiogenic shock; D1 = D1 receptor; FDA = U.S. Food and Drug Administration; HR = heart rate; NO = nitric oxide; PDE-3 = phosphodiesterase 3; SVR = systemic vascular resistance.∗Not FDA approved for clinical use in the United States.These drugs are commonly used in clinical practice for the management of CS but some have been associated with increased adverse effects, including arrhythmias, and increased myocardial oxygen consumption.51 Therefore, the writing committee advises that vasoactive medications be used in CS at the lowest possible dose to support adequate perfusion and for the shortest possible duration.Inotropes enhance cardiac function by increasing the load-independent contractility of the myocardium. More specifically, cardiac calcitropes, including catecholamines and phosphodiesterase 3 inhibitors, increase the concentration of intracellular calcium to augment contractility. Notably, these agents exert their myocardial forces through direct action as opposed to secondary effects on chronotropy and vascular tone. Chronotropes, on the other hand, increase cardiac output by predominantly increasing the heart rate. Inopressors (eg, dopamine, norepinephrine, and epinephrine) increase cardiac output while increasing systemic vascular resistance, whereas inodilators (eg, milrinone or dobutamine) increase cardiac output and reduce afterload through systemic vasodilation. Vasodilators decrease preload and/or LV afterload through reduction in systemic vascular resistance, thereby potentially augmenting cardiac output. Pure vasopressors increase MAP by increasing systemic vascular resistance. The balance between alpha- and beta-adrenergic receptor activity determines the predominant effects of catecholamines, which run the gamut from pure inotropes to pure vasopressors (Table 2).A Cochrane analysis found insufficient evidence to support the superiority of a particular inotrope or vasodilating agent in CS, especially with respect to a mortality benefit.53 The Dobutamine Compared with Milrinone (DOREMI) trial evaluated dobutamine vs milrinone in 192 CS patients in a single quaternary care academic center, ranging from SCAI B through E and excluding patients with cardiac arrest, and found no difference with respect to the primary composite endpoint of in-hospital death from any cause, resuscitated cardiac arrest, receipt of a cardiac transplant or mechanical circulatory support, nonfatal myocardial infarction, transient ischemic attack or stroke diagnosed by a neurologist, or initiation of renal replacement therapy.54 Given the heterogenous nature of CS and the various physiological derangements, several vasoactive medications may be attempted to normalize a CS patient’s hemodynamic and/or metabolic profile. Inodilators or vasodilators may be considered in normotensive CS, especially in patients with increased systemic vascular resistance. Intravenous milrinone, given its relatively long half-life and renal excretion, should be judiciously used in patients with worsening renal function. Chronotropes might be trialed in bradycardia-induced CS. Since pure vasopressors (ie, phenylephrine) can cause reflex bradycardia and reduce cardiac output in CS, their use as a single first-line continuous intravenous medication is strongly discouraged. Although there is no clear consensus regarding the choice of first-line vasoactive agent, the writing committee agrees that norepinephrine is a reasonable first choice for most patients with CS who are hypotensive. Level 2 and 3 CS hospital centers should pursue consultation and consider potential transfer to a Level 1 CS hospital center when patients are refractory to the initial pharmacological therapy for consideration of tMCS support and/or advanced therapies.4.6 tMCS
RCTs examining tMCS in CS have primarily been focused on STEMI-CS and have been limited by sample size, study design, patient selection, timing, and other key limitations. Few head-to-head randomized comparisons exist between various tMCS devices, and the potential therapeutic benefits must be weighed against bleeding, vascular, neurological, infectious, and other complications (Figure 6).21Figure 6 Common tMCS Devices Used in CSAdapted with permission from Tehrani BN, et al.21AO = aorta; CP = cardiac power; CS = cardiogenic shock; F = French; IABP = intra-aortic balloon pump; LV = left ventricular; NA = not applicable; PA = pulmonary artery; pVAD = percutaneous ventricular assist device; RA = right atrium; RA-PA = right atrium to pulmonary artery; RP = right percutaneous; rpm = revolutions per minute; RV = right ventricular; tMCS = temporary mechanical circulatory support; VA-ECMO = venoarterial extracorporeal membrane oxygenation.
