Hemodynamic management of cardiogenic shock in the intensive care unit

Abstract

Hemodynamic derangements are defining features of cardiogenic shock. Randomized clinical trials have examined the efficacy of various therapeutic interventions, from percutaneous coronary intervention to inotropes and mechanical circulatory support (MCS). However, hemodynamic management in cardiogenic shock has not been well-studied. This State-of-the-Art review will provide a framework for hemodynamic management in cardiogenic shock, including a description of the 4 therapeutic phases from initial 'Rescue' to 'Optimization', 'Stabilization' and 'de-Escalation or Exit therapy' (R-O-S-E), phenotyping and phenotype-guided tailoring of pharmacological and MCS support, to achieve hemodynamic and therapeutic goals. Finally, the premises that form the basis for clinical management and the hypotheses for randomized controlled trials will be discussed, with a view to the future direction of cardiogenic shock.

Keywords: cardiogenic shock; heart transplantation; hemodynamics; inotropes; left ventricular assist devices; mechanical circulatory support.

Figure 1

The 4 phases of CS – Recognize/Rescue, Optimization, Stabilization and de-Escalation or Exit Therapy (ROSE). During the initial phase of CS (Recognize/Rescue), assessment may be limited to clinical findings, simple hemodynamic parameters (arterial BP and heart rhythm) and point-of-care tests; and hemodynamic management and therapeutic targets are equally limited. However, successful ‘Rescue’ should be followed by a period of ‘Optimization’, a crucial phase that includes the tailoring of pharmaco-MCS therapy based on more granular hemodynamic assessment (from invasive hemodynamic monitoring) and phenotyping, correction of treatment-related complications and extra-cardiac derangements. ‘Stabilization’ is characterized by recovery of organ function, diminishing vasoactive drug requirements (invasive hemodynamic assessment could be minimized) and preparation for ‘de-Escalation and Exit’ therapy. Patients are liberated from pharmaco-MCS therapy in the event of sufficient recovery of cardiovascular function, but alternative ‘Exit’ therapy (e.g.: heart transplantation or durable LVAD) may be considered in the absence of sufficient recovery. Vasoactive drugs may be re-initiated and invasive hemodynamic assessment may need to be re-introduced for close monitoring following liberation from temporary MCS. In selected cases, de-escalating temporary MCS as staged weaning or even re-institution of temporary MCS in the event of hemodynamic deterioration after liberation may be considered. CS, cardiogenic shock; LVAD, left ventricular assist device; MCS, mechanical circulatory support.

Figure 2

State-of-the-art phenotyping of CS patients should include a harmonization of different classification systems considering etiology, hemodynamic profiles, risk scores, SCAI staging, and machine-learning based phenotypes. While RCT-data for the emerging different CS subtypes are lacking, combining these metrics may provide carers with standardized means for risk stratification, treatment decision making and early detection of deterioration. (Design by PresentationGO.com). CS, cardiogenic shock; RCT, randomized controlled trial; SCAI, Society for Cardiovascular Angiography and Interventions.

Figure 3

Phenotyping of CS (incorporating the SCAI staging schema and pathophysiology) should produce actionable insights to guide treatment. The premise is that phenotype-guided intervention results in timely and appropriate pharmaco-MCS therapy (“the right support for the right patient at the right time”). A temporary MCS strategy based on the SCAI staging schema and pathophysiology is presented. Temporary MCS platforms should be selected to restore tissue perfusion with the minimal morbidity and cost. CS, cardiogenic shock; MCS, mechanical circulatory support; SCAI, Society for Cardiovascular Angiography and Interventions.

Figure 4

Improving hemodynamic parameters is a pre-requisite for reversing tissue hypoperfusion in CS. There is no specific treatment that can improve tissue hypoperfusion independent of hemodynamic parameters. Hemodynamic response is defined when hemodynamic targets are achieved. Hemodynamic response is not synonymous with clinical response, which is defined by improvement in markers of hypoperfusion and organ function. Hemodynamic improvement serves as an early marker of response to treatment but is not always accompanied by clinical improvement. In contrast, clinical improvement takes time to manifest (e.g.: lactate clearance is measured over 6–12 hours and improvement liver enzymes may only be evident after hours), but when present is strongly associated with improved survival. Improving survival in CS necessitates hemodynamic and clinical response to treatment and a successful Exit Therapy. CS, cardiogenic shock.

Figure 5

The calculated CI required to achieve a DO₂ of 300 ml/min/m² based on different levels of hemoglobin concentration and oxygen saturation. The color legend indicates the level of CI required. Lowering VO₂ will reduce the DO₂ requirements and the corresponding target CI. This figure does not include the intrinsic variability in cardiac output measurements – the CI target may need to be 12–15% higher to accommodate for the variability in measurements. DO₂, oxygen delivery; VO₂, oxygen consumption.

Figure 6

Hemodynamic-guided optimization of vasoactive medications and temporary MCS in CS. Patients with modest reductions in cardiac output may benefit from inotropic support alone to improve tissue perfusion. Vasopressors or vasodilators may be utilized alone or in conjunction with inotropes (or by selecting inotropes with favorable vasoconstriction or vasodilating effects) depending on the degree of pathophysiologic vasoconstriction or vasodilation present. Patients with severe reductions in both cardiac output and systemic vascular resistance may require escalation to temporary MCS to adequately restore tissue perfusion while maintaining acceptable perfusion pressure. CS, cardiogenic shock; MCS, mechanical circulatory support.