Guiding Cardiogenic Shock Management: Filling in the (Wide) Data Gaps

Last Updated: July 21, 2022

Disclosure: ARG is a consultant for NupulseCV, a member of the scientific advisory board for Abiomed, and has received research support from Verantos and Abbott. DB reports an unrestricted, educational grant from Abiomed.
Pub Date: Thursday, Jul 07, 2022
Author: A. Reshad Garan, MD, MS(1), Daniel Burkhoff MD, PhD(2)
Affiliation: (1)Beth Israel Deaconess Medical Center, Boston, MA, USA, (2)Cardiovascular Research Foundation, New York, NY, USA

Since the seminal publication of the SHOCK trial1 more than 20 years ago, the cardiovascular community has struggled to make further inroads into completing randomized trials to guide the management of patients with cardiogenic shock (CS). With their broad-reaching Scientific Statement on the use of temporary mechanical circulatory support devices (tMCS) Geller et al. provide a framework for thinking about the initiation, intensification (or escalation) and subsequent de-escalation of therapy aimed at treating shock2. Many randomized trials in CS have either been underpowered or have failed to meet their enrollment targets3. As such, much of what the clinician is taught must rely on expert opinion.

We should not be satisfied with expert opinion; however, until we have high quality randomized data, expert opinion must provide the framework for management of this complex condition while real world data derived from registries such as the Cardiogenic Shock Working Group, the National Cardiogenic Shock Initiative and the Critical Care Cardiology Trial Network provide important insights4-6. Furthermore, it is likely that we will never generate high quality RCT-derived data to inform many of the decisions that the bedside clinicians must make regarding CS management. Therefore, statements such as this one which draw on the collective opinions of selected experts to outline a practical approach to CS patient management are necessary to guide future generations of clinicians.

At the highest level, the authors advocate for a multi-disciplinary team of clinicians to be available for emergent consultation regarding intensification of CS treatment. Importantly, they do not advocate for routine tMCS use for every CS patient; instead, they call for a tailored approach with inputs from each member of this multi-disciplinary team to guide decision-making. Similarly, and consistent with prior recommendations, they provide criteria for the judicious use of the pulmonary artery catheter (PAC) to guide therapy, especially when tMCS devices are deployed or when an unfavorable clinical trajectory is evident.

A handful of on-going trials in Europe will shed light on different devices for patients with acute myocardial infarction-CS (AMI-CS) though these, too, have required long periods of time to meet their enrollment targets and have recognized limitations (e.g. DanGer trial which has been enrolling for > 6 years)3. Furthermore, current studies focus on the efficacy of a particular device (e.g., Impella or extra-corporeal membrane oxygenation [ECMO]) versus “standard of care”. Accordingly, direct head-to-head comparisons of different devices and/or specific algorithms of care are not being studied, which will undoubtedly leave many questions unanswered. Also, importantly, few trials focus exclusively on the heart failure-CS (HF-CS) patient population which is increasingly recognized as a distinct disease state from AMI-CS8. As a consequence of such difficulties in their design and execution, the results of clinical trials have not always impacted clinical practice uniformly throughout the entire cardiology community. For example, the original SHOCK trial did not meet its primary endpoint, and the primary means of revascularization was coronary artery bypass surgery1. Yet, urgent percutaneous revascularization is the standard of care in AMI-CS. On the other hand, the IABP SHOCK-II study showed that intra-aortic balloon pumping (IABP) did not influence mortality in AMI-CS9. Yet, IABPs remain the most commonly used circulatory support device in the United States. Thus, clinical practice appears to be guided, to some extent, by factors other than clinical trial results.

One critical aspect of CS management highlighted by the authors is the impact of time on outcomes. Time spent under-supported (i.e. in a state of hypoperfusion) significantly increases the risk of end-organ injury, which dramatically reduces the patient’s chance of survival. This occurs, in part, because it may limit the opportunity to bridge to either left ventricular assist device (LVAD) or transplant if the patient has not experienced ventricular recovery. As noted above, the PAC provides an important means of real-time assessment of the hemodynamic status. The authors suggest use of this monitoring tool to make the initial choice of therapy but perhaps even more importantly, as a means to rapidly evaluate when the initial therapy has not sufficiently augmented hemodynamics to reverse end-organ dysfunction. Without this, clinicians must wait for markers of end-organ perfusion to improve (or not) and this may lead to unnecessary delays in further treatment intensification. Once a device strategy has been implemented, an inadequate hemodynamic improvement should trigger a consideration of escalation of the degree of support. This may take the form of transition from one device to another capable of providing a higher degree of circulatory support. In many instances the first device may remain in place to provide on-going hemodynamic support (e.g. addition of veno-arterial ECMO to either IABP or Impella CP or addition of a percutaneous right ventricular assist device to a pre-existing percutaneous LVAD when right ventricular [RV] failure is recognized). One important role of the PAC is the early recognition of concomitant RV failure which may be exacerbated by percutaneous LVAD support10.

As an aside, we would point out that in contrast to what was written, the Fick principle with a PAC-acquired pulmonary artery blood gas sample can be used to estimate cardiac output even in the presence of veno-arterial ECMO as long as the equation is based on oxygen content (which depends on partial pressure of oxygen and mixed venous oxygen saturation) instead of oxygen saturation alone.

The authors also highlight the importance of recognizing that every device carries a risk of several types of complication, some of which can be potentially life-threatening. As such, unnecessary delay in tMCS removal exposes the patient to life-threatening risk. Decisions around the timing of device removal must incorporate the progress towards reversal of the underlying pathologic insult that resulted in CS, the ultimate destination (i.e. ventricular recovery, bridge to LVAD, bridge to transplant, or palliation), and the risk of on-going device support. At the earliest signs of reversal of the shock state, an assessment of ‘readiness to wean’ from device support should be made. Importantly, the authors recommend early transfer to a center capable of providing access to LVAD and/or transplant for patients in whom weaning from tMCS devices is unsuccessful and in whom recovery is unlikely.

As noted above, another key point highlighted in this statement is the differentiation between the two most commonly encountered types of CS: AMI-CS and HF-CS. Only recently have these two entities been recognized as distinct disease states, similar only in the general sense that embarrassment of cardiac function leads to end-organ hypoperfusion8. The differences in pathophysiologies and trajectories necessitate disease-specific approaches as the authors have highlighted in the form of two separate algorithms which take into account these important differences. As we strive to produce high quality data to inform management decisions in CS we must also avoid the tendency to view different disease states through the same lens and blindly apply data learned from one subset of CS patients to other subsets.

Overall, the authors have provided an important framework for the management of CS patients with a focus on tMCS use. Such statements are critical to the dissemination of clinical expertise while the cardiovascular community awaits high-quality data but also recognizes that such data will undoubtedly leave wide gaps. It is evident that real-world data and expert opinion will be important in the management of patients with CS for the foreseeable future. Accordingly, the Scientific Statement prepared by Geller and colleagues provides timely and much needed guidance for the care of patients with CS.


Geller BJ, Sinha SS, Kapur NK, Bakitas M, Balsam LB, Chikwe J, Klein DG, Kochar A, Masri SC, Sims DB, Wong GC, Katz JN, van Diepen S; on behalf of the American Heart Association Acute Cardiac Care and General Cardiology Committee of the Council on Clinical Cardiology; Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular and Stroke Nursing; Council on Peripheral Vascular Disease; and Council on Cardiovascular Surgery and Anesthesia. Escalating and de-escalating temporary mechanical circulatory support in cardiogenic shock: a scientific statement from the American Heart Association [published online ahead of print July 7, 2022]. Circulation. doi: 10.1161/CIR.0000000000001076


  1. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med. 1999 Aug 26;341(9):625-34.
  2. 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.
  3. Thiele H, Ohman EM, de Waha-Thiele S, Zeymer U, Desch S. Management of cardiogenic shock complicating myocardial infarction: an update 2019. Eur Heart J. 2019 Aug 21;40(32):2671-2683.
  4. Thayer KL, Zweck E, Ayouty M, et al. Invasive Hemodynamic Assessment and Classification of In-Hospital Mortality Risk Among Patients With Cardiogenic Shock. Circ Heart Fail. 2020 Sep;13(9):e007099.
  5. Basir MB, Kapur NK, Patel K, et al. Improved Outcomes Associated with the use of Shock Protocols: Updates from the National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019 Jun 1;93(7):1173-1183.
  6. Bohula EA, Katz JN, van Diepen S, et al. Demographics, Care Patterns, and Outcomes of Patients Admitted to Cardiac Intensive Care Units: The Critical Care Cardiology Trials Network Prospective North American Multicenter Registry of Cardiac Critical Illness. JAMA Cardiol. 2019 Sep 1;4(9):928-935.
  7. Saxena A, Garan AR, Kapur NK, et al. Value of Hemodynamic Monitoring in Patients With Cardiogenic Shock Undergoing Mechanical Circulatory Support. Circulation. 2020 Apr 7;141(14):1184-1197.
  8. 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.
  9. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012 Oct 4;367(14):1287-96.
  10. Jain P, Thayer KL, Abraham J, et al. Right Ventricular Dysfunction Is Common and Identifies Patients at Risk of Dying in Cardiogenic Shock. J Card Fail. 2021 Oct;27(10):1061-1072.

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-- The opinions expressed in this commentary are not necessarily those of the editors or of the American Heart Association --