The Management of Cardiogenic Shock From Diagnosis to Devices: A Narrative Review

Abstract

Cardiogenic shock (CS) is a heterogenous syndrome broadly characterized by inadequate cardiac output leading to tissue hypoperfusion and multisystem organ dysfunction that carries an ongoing high mortality burden. The management of CS has advanced rapidly, especially with the incorporation of temporary mechanical circulatory support (tMCS) devices. A thorough understanding of how to approach a patient with CS and to select appropriate monitoring and treatment paradigms is essential in modern ICUs. Timely characterization of CS severity and hemodynamics is necessary to optimize outcomes, and this may be performed best by multidisciplinary shock-focused teams. In this article, we provide a review of CS aimed to inform both the cardiology-trained and non-cardiology-trained intensivist provider. We briefly describe the causes, pathophysiologic features, diagnosis, and severity staging of CS, focusing on gathering key information that is necessary for making management decisions. We go on to provide a more detailed review of CS management principles and practical applications, with a focus on tMCS. Medical management focuses on appropriate medication therapy to optimize perfusion-by enhancing contractility and minimizing afterload-and to facilitate decongestion. For more severe CS, or for patients with decompensating hemodynamic status despite medical therapy, initiation of the appropriate tMCS increasingly is common. We discuss the most common devices currently used for patients with CS-phenotyping patients as having left ventricular failure, right ventricular failure, or biventricular failure-and highlight key available data and particular points of consideration that inform tMCS device selection. Finally, we highlight core components of sedation and respiratory failure management for patients with CS.

Keywords: cardiogenic shock; cardiogenic shock severity classification; mechanical circulatory support.

Figure 1 –

A, B, Diagrams showing SCAI shock classification pyramid (A) and the dynamic evolution of cardiogenic shock and progression or recovery through SCAI shock stages (B). AMI = acute myocardial infarction; CA = cardiac arrest; CS = cardiogenic shock; HF = heart failure; MCS = mechanical circulatory support; SCAI = Society for Cardiovascular Angiography and Interventions; Tx = treatment. (Reproduced with permission from Naidu et al.)

Figure 2 –

Flowchart showing medical management of cardiogenic shock. This management algorithm represents the expert opinions of the authors and is informed by trial data and society guidelines.^,,,,– No singular approach to treating CS exists, and this is meant to serve as a guide, not the only definitive approach. Key components in the management of CS include early recognition, SCAI staging, and phenotyping by PAC. Early treatments for CS prioritize prompt resolution of organ hypoperfusion using vasoactive agents with close monitoring for deterioration. Vasoactive agent use is tailored to an individual patient based on the hemodynamic phenotype. Please see Table 2 for more information on vasoactive agents. BiV = biventricular; CI = cardiac index; CPO = cardiac power output; Cr = creatinine; CS = cardiogenic shock; CVC = central venous catheter; CVP = central venous pressure; CXR = chest radiograph; E/e’ ratio = ratio of early diastolic mitral inflow velocity to early diastolic mitral annulus velocity; IVC = inferior vena cava; JVP = jugular venous pressure; LFT = lung function test; LV = left ventricle; MAP = mean arterial pressure; PAC/PA-C = pulmonary artery catheter; PAH = pulmonary arterial hypertension; PAPi = pulmonary artery pulsatility index; PCW = pulmonary capillary wedge pressure; PH = pulmonary hypertension; POCUS = point-of-care utrasound; PVR = pulmonary vascular resistance; RV = right ventricle; SCAI = Society for Cardiovascular Angiography and Interventions; ScVO₂ = central venous oxygen saturation; SVR = systemic vascular resistance; tMCS = temporary mechanical circulatory support; TTE = transthoracic echocardiography; UOP = urine output; W = watts; WU = Wood unit. ^aPatients who are hypovolemic and have inadequate preload can have low CI and a high SVR mimicking CS. Patients should show adequate filling pressures and be resuscitated as needed before proceeding with CS diagnosis. ^bNitroglycerin provides more venous than arterial vasodilation and often is used in patients with volume overload, acute coronary syndrome, or both. ^cIn CS resulting from acute myocardial infarction, inotropes can increase myocardial oxygen demand and increase or provoke ischemia. These agents should be used with caution and in expert centers. ^dEvidence exists that vasopressin has more impact on SVR than PVR, but norepinephrine often is used also in patients with pulmonary arterial hypertension in shock given the larger titratable range and also a favorable SVR to PVR impact.