support, includingECMO) beyond volumeresuscitation to restore perfusion.These patients typically presentwith relative hypotension.
SCAI, society for cardiovascular angiography and intervention; CS, cardiogenic shock; JVP, jugular venous pulse; SBP, systolic blood pressure; CVP, central venous pressure; PA, pulmonary artery; MAP, mean arterial pressure; ECMO, extracorporeal membrane oxygenation; BiPap, Bi‐level positive airway pressure; GFR, glomerular filtration rate; LFT, liver function test; BNP, B‐type natriuretic peptide; BP, blood pressure; PCWP, pulmonary capillary wedge pressure; PAP, pulmonary artery pressure; PAPI, pulmonary artery pressure index; CPR, cardiopulmonary resuscitation; PEA, pulseless electrical activity; VT, ventricular tachycardia; VF, ventricular fibrillation.
Epidemiology
Cardiogenic shock after myocardial infarction (MI) occurs in about 5–6% of cases in the current era of primary PCI, and occurred in about 10% of cases in the era before rapid mechanical reperfusion [6–10]. The incidence of cardiogenic shock may have declined, but mortality after cardiogenic shock remains very high, even in contemporary cohorts, with mortality rates of 40–60% [11, 12].
An early study of 845 patients presenting with acute MI not treated with thrombolysis or mechanical reperfusion investigated risk factors for the occurrence of cardiogenic shock [6]. In this study, cardiogenic shock occurred in 60 patients (7.1%). Predictors of cardiogenic shock included age >65 years, left ventricular ejection fraction at hospital admission <35%, large infarct size (peak creatine kinase‐MB isoenzyme >160 IU/liter), diabetes mellitus, and previous myocardial infarction. Risk factors in the GUSTO (Global utilization of streptokinase and tissue‐plasminogen activator for occluded coronary arteries) trial, conducted in the era of thrombolysis included: age, systolic blood pressure, heart rate, and Killip class upon presentation [13].
In the large (n = 5745) APEX‐AMI (assessment of pexelizumab in acute myocardial infarction) trial, the incidence of shock was only 3.4% (n = 196), most likely due to the fact that this randomized controlled trial enrolled a relatively low‐risk patient population [12]. In APEX‐AMI the following risk factors for developing cardiogenic shock were identified: older age, female sex, hypertension, diabetes mellitus, and being a non‐smoker.
Management of cardiogenic shock
Impact of coronary revascularization
Since the SHOCK trial, early revascularization has been recognized as the primary treatment modality for cardiogenic shock. Current ACC/AHA guidelines state a class I, level of evidence B indication for emergency revascularization with either PCI or CABG in suitable patients with cardiogenic shock due to pump failure after STEMI irrespective of the time delay from MI onset.[14]
The landmark SHOCK trial randomized 302 patients with cardiogenic shock complicating MI in a 1:1 fashion to treatment with emergency revascularization (n = 152) or initial medical stabilization (n = 150). Revascularization incorporated emergency coronary angiography followed by either coronary artery bypass graft surgery (CABG) or PCI. In the SHOCK trial, 30–day mortality rates were numerically lower in the early revascularization arm (46.7% vs. 56.0%, p‐0.11). However, at 6 months mortality rates were significantly lower with early revascularization (50.3% vs. 63.1%, p = 0.027) [1]. Furthermore, emergency revascularization was not only associated with improved survival, but also with improved quality of life, assessed by the multidimensional index of life quality and New York heart association heart failure class (NYHA class) [15].
An important substudy investigated the clinical outcome in patients assigned to emergency revascularization in the SHOCK trial undergoing PCI compared with CABG [16]. Out of 128 patients undergoing emergency revascularization 81 underwent PCI (63.3%), and 47 underwent CABG (36.7%). Patients undergoing CABG were at higher risk at baseline with a greater extent of coronary artery disease and a greater prevalence of diabetes mellitus. In the CABG group, 87.2% of patients were considered completely revascularized whereas only 23.1% of patients in the PCI group were considered completely revascularized. Despite the higher baseline risk profile of patients undergoing CABG one‐year survival was similar in both treatment arms, suggesting a potential benefit of complete revascularization. This hypothesis was tested in the CULPRIT‐SHOCK trial which randomized 706 CS patients with multivessel disease to PCI of the culprit lesion only or immediate multivessel PCI [4]. At 30–days there were higher rates of death or renal‐replacement therapy in the multivessel PCI group compared with the culprit‐lesion‐only PCI group (55.4% vs 45.9%, p = 0.01). At one‐year follow‐up, mortality was similar in both groups (50.0% culprit‐only vs. 56.9% multivessel PCI, p = ns) [17]. This led the European Society of Cardiology to include a Class III recommendation (harm) for routine revascularization of non‐IRA lesions in MI complicated by CS [18].
Left‐ventricular assist devices and the intra‐aortic balloon pump
Mechanical support devices aim to overcome the inability of the heart to pump adequate amounts of blood by supporting the circulation and increasing cardiac output. Moreover, support devices aim to unload the damaged left ventricle by afterload (pressure unloading) or pre‐load reduction (volume unloading). Currently available devices include the intra‐aortic balloon pump (IABP), the Impella axial flow pump, the TandemHeart device, and extra‐corporeal membrane oxygenation (ECMO) [19]. These devices are discussed in further detail in chapter 69 (percutaneous ventricular assist devices).
IABP
IABP In one small study that randomized 40 patients in cardiogenic shock to optimal medical therapy alone or to optimal medical therapy and an IABP, no significant differences were observed in hemodynamic parameters such as cardiac output and systemic vascular resistance between both groups [20]. The 600‐patient IABP SHOCK II trial randomized patients with cardiogenic shock complicating myocardial infarction to treatment with an IABP or no IABP. Early revascularization and optimal medical therapy were provided in both study arms. The use of the IABP did not reduce 30‐day or 1‐year mortality [11, 21]. Moreover, there were no differences in time to hemodynamic stabilization, the length of intensive care unit stay, serum lactate levels, dose and duration of catecholamine administration, and renal function [21]. ESC guidelines therefore recommend against routine use of IABP in patients with CS due to ACS [18].
