Mixed Cardiogenic-Vasodilatory Shock: Current Insights and Future Directions

Abstract

This state-of-the-art review describes the potential etiologies, pathophysiology, and management of mixed shock in the context of a proposed novel classification system. Cardiogenic-vasodilatory shock occurs when cardiogenic shock is complicated by inappropriate vasodilation, impairing compensatory mechanisms, and contributing to worsening shock. Vasodilatory-cardiogenic shock occurs when vasodilatory shock is complicated by myocardial dysfunction, resulting in low cardiac output. Primary mixed shock occurs when a systemic insult triggers both myocardial dysfunction and vasoplegia. Regardless of the etiology of mixed shock, the hemodynamic profile can be similar, and outcomes tend to be poor. Identification and treatment of both the initial and complicating disease processes is essential along with invasive hemodynamic monitoring given the evolving nature of mixed shock states. Hemodynamic support typically involves a combination of inotropes and vasopressors, with few data available to guide the use of mechanical circulatory support. Consensus definitions and novel treatment strategies are needed for this dangerous condition.

Keywords: cardiac arrest; cardiac intensive care unit; cardiogenic shock; myocardial infarction; sepsis; shock.

Graphical abstract

Figure 1

Proposed Classification of Mixed Shock Patients are classified based on the primary (inciting) shock phenotype and the secondary (complicating) process in a “two-hit” model. This model is conceptual, recognizing that there may be overlap between groups and it may not be possible to clinically classify patients who present late during mixed shock. HF = heart failure; MCS = mechanical circulatory support; SIRS = systemic inflammatory response syndrome.

Central Illustration

Conceptual Model of Mixed Shock Etiology and Pathogenesis Abbreviation as in Figure 2.

Figure 2

Pathophysiological Pathways in Mixed Cardiogenic-Vasodilatory Shock, Including Classical Mechanisms of Typical Cardiogenic Shock and Established Mechanisms of Mixed Shock Mixed shock commonly arises when tissue injury triggers a systemic inflammatory response, resulting in maladaptive vasodilation, microcirculatory dysfunction, and worsening myocardial dysfunction. ABG = arterial blood gas; CRP = C-reactive protein; LFT = liver function test; LV = left ventricular; LVEDP = left ventricular end-diastolic pressure; ROS = reactive oxygen species; SVR = systemic vascular resistance; TNF = tumor necrosis factor; other abbreviations as in Figure 1.

Figure 3

Overview of Hemodynamic Support in Mixed Shock Vasopressors (drugs that cause vasoconstriction and increase systemic vascular resistance) and adjunct drugs that inhibit vasodilation are titrated to restore mean arterial pressure, while inotropes (drugs that stimulate myocardial contractility) and mechanical circulatory support are titrated to restore cardiac output VA. ECMO = venoarterial extracorporeal membrane oxygenator.

Figure 4

Integration of Central Hemodynamics and Perfusion in Selection of Support Therapies in Mixed Shock The vascular effects of vasoactive drugs must be considered when selecting inotropes and vasopressors in patients with mixed shock, as these drugs can potentially improve or worsen vasodilation or low cardiac output. PAC = pulmonary artery catheter; SVO₂ = venous oxygen saturation; other abbreviation as in Figure 3.