Contemporary approach to cardiogenic shock care: a state-of-the-art review

Abstract

Cardiogenic shock (CS) is a time-sensitive and hemodynamically complex syndrome with a broad spectrum of etiologies and clinical presentations. Despite contemporary therapies, CS continues to maintain high morbidity and mortality ranging from 35 to 50%. More recently, burgeoning observational research in this field aimed at enhancing the early recognition and characterization of the shock state through standardized team-based protocols, comprehensive hemodynamic profiling, and tailored and selective utilization of temporary mechanical circulatory support devices has been associated with improved outcomes. In this narrative review, we discuss the pathophysiology of CS, novel phenotypes, evolving definitions and staging systems, currently available pharmacologic and device-based therapies, standardized, team-based management protocols, and regionalized systems-of-care aimed at improving shock outcomes. We also explore opportunities for fertile investigation through randomized and non-randomized studies to address the prevailing knowledge gaps that will be critical to improving long-term outcomes.

Keywords: acute myocardial infarction; cardiogenic shock; heart failure; pulmonary artery catheter; shock team.

Figure 1

Central illustration. Proposed algorithm of cardiogenic shock management within a regionalized shock network by a multidisciplinary shock team. A contemporary systems of care approach for cardiogenic shock (CS) management by a multidisciplinary team in a “hub and spoke” model. This allows for timely diagnosis with early comprehensive invasive hemodynamic assessment. Early, selective, and tailored mechanical circulatory support (MCS) based on CS phenotype and congestive profiles is crucial for CS management in the modern era. This is also predicated on expedited transfer to the level 1 CS centers of excellence for team-based and comprehensive multiorgan system care. AHF, Advance Heart Failure; AMI, Acute Myocardial Infarction; CS, Cardiogenic Shock; IABP, Intra-Aortic Balloon Pump; LV, Left ventricle; LVAD, Left Ventricular Assist Device; MCS, Mechanical Circulatory Support device, SCAI, Society for Cardiovascular Angiography and Interventions; VA-ECMO, Veno-Arterial Extra Corporeal Membrane Oxygenation.

Figure 2

(A,B) schematic representation of the care pathways in the upstream and critical care management of patients with acute myocardial infarction (AMI, 4a) and acute decompensated heart failure (HF, 4b) cardiogenic shock (CS) at the INOVA schar heart and vascular institute. BiV, Biventricular; CPO, Cardiac Power Output = [mean arterial pressure x cardiac output]/451; PAPi, Pulmonary Artery Pulsatility Index = [systolic pulmonary arterial pressure—diastolic pulmonary arterial pressure]/right atrial pressure; PMCS, percutaneous Mechanical Circulatory Support; SBP, Systolic Blood Pressure, other abbreviations as in Figures 1, 2.

Figure 3

Optimizing patient-centric care: mechanical circulatory support considerations for appropriate use of selective and tailored approach to available devices. The figure illustrates the intricate process of achieving optimal patient-centered care in the context of MCS use. The achievement of the right patient, at the right time, with the appropriate MCS device, and in the right clinical setting who should be managed at an appropriate level of CS 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 for Cardiovascular Angiography and Interventions.

Figure 4

Pathophysiology of left ventricular distension during veno-arterial extracorporeal membrane oxygenation. The figure illustrates the pathophysiology of left ventricle (LV) distension which occurs during VA-ECMO as the outflow cannula generates retrograde flow towards the aortic valve, resulting in increased afterload. This results in high LV end-diastolic pressure (LVEDP) and increased LV end-diastolic volume (LVEDV), resulting in subendocardial ischemia, hindering LV recovery. In some cases, mitral valve may act as “pop-off” valve for the LV but leads to pulmonary edema, resulting in increased PCWP, CVP, and subsequently RV distension and RV failure. LV, CVP, Central Venous Pressure; EDP, End-Diastolic Pressure; LV, Left Ventricle; PAP, Pulmonary Artery Pressure; PCWP, Pulmonary Capillary Wedge Pressure, RV, Right Ventricle. Created with BioRender.com.