Interventional Cardiology. Группа авторов

are similar, but not identical.

      SHOCK trial definition: In the SHOCK trial, cardiogenic shock was defined by a combination of clinical and hemodynamic criteria. [1, 2] Clinical criteria in SHOCK were hypotension (a systolic blood pressure of <90 mm Hg for at least 30 minutes or the need for supportive measures to maintain a systolic blood pressure of ≥90 mm Hg) and end‐organ hypoperfusion (cool extremities or a urine output of <30 ml per hour, and a heart rate of ≥60 beats per minute). The hemodynamic criteria were a cardiac index of no more than 2.2 liters per minute per square meter of body‐surface area and a pulmonary‐capillary wedge pressure of at least 15 mm Hg [1, 2].

      IABP‐SHOCK and CULPRIT‐SHOCK definition: In the IABP‐SHOCK II (intra‐aortic balloon pump in cardiogenic shock) and CULPRIT‐SHOCK (Culprit Lesion Only PCI versus Multivessel PCI in Cardiogenic Shock) trials, the following definition was used: (i) a systolic blood pressure of less than 90 mm Hg for more than 30 minutes or needing infusion of catecholamines to maintain a systolic pressure above 90 mm Hg, (ii) clinical signs of pulmonary congestion, and (iii) impaired end‐organ perfusion. The diagnosis of impaired end‐organ perfusion required at least one of the following: altered mental status; cold, clammy skin and extremities; oliguria with urine output of less than 30 ml per hour; or serum lactate level higher than 2.0 mmol per liter [3, 4].

The Society for Cardiovascular Angiography and Interventions (SCAI) has recently proposed a classification schema for CS which is now endorsed by the major North American cardiovascular societies [5]. This system describes five different stages of CS severity including stage A “at risk for CS”, stage B “beginning CS”, stage C “classic CS”, stage D “deteriorating CS” and stage E “CS in extremis”. A detailed overview of this definition is provided in Table 14.1.

Table 14.1 SCAI Classification of cardiogenic shock.

Stage	Description	Physical exam/bedside findings	Biochemical markers	Hemodynamics
A“At risk”	Patient not currently experiencing signs or symptoms of CS but at risk for its development. E.G. those with large acute myocardial infarction or prior infarction and acute and/or acute on chronic heart failure symptoms	Normal JVPLung sounds clearWarm and well perfusedStrong distal pulsesNormal mentation	Normal labsNormal renal functionNormal lactic acid	Normotensive (SBP≥100 or normal for pt.) If hemodynamics done:cardiac index ≥2.5CVP <10PA sat ≥65%
B“Beginning CS”	A patient who has clinical evidenceof relative hypotension ortachycardia withouthypoperfusion.	Elevated JVPRales in lung fieldsWarm and well perfusedStrong distal pulsesNormal mentation	Normal lactateMinimal renal functionimpairmentElevated BNP	SBP <90 OR MAP <60 OR>30 mmHg drop frombaselinePulse ≥100If hemodynamics donecardiac index ≥2.2PA sat ≥65%
C“Classic CS”	A patient that manifests withhypoperfusion that requiresintervention (inotrope, pressor ormechanical support, includingECMO) beyond volumeresuscitation to restore perfusion.These patients typically presentwith relative hypotension.	May Include Any of:Looks unwellPanickedAshen, mottled, duskyVolume overloadExtensive ralesKillip class 3 or 4BiPap or mechanical ventilationCold, clammyAcute alteration in mental statusUrine output <30 mL/h	May Include Any of:Lactate ≥2Creatinine doublingOR >50% drop in GFRIncreased LFTsElevated BNP	May Include Any of:SBP <90 OR MAP <60 OR>30 mmHg drop frombaseline AND drugs/deviceused to maintain BP abovethese targetsHemodynamicscardiac index <2.2PCWP >15RAP/PCWP ≥0.8PAPI <1.85cardiac power output ≤0.6
D“deteriorating CS”	A patient that is similar to category C but getting worse with failure to respond to initial interventions.	Any of stage C	Any of Stage C AND: Deteriorating	Any of Stage C AND: Requiring multiple pressors OR addition of mechanical circulatory support devices to maintain perfusion
E“CS in extremis”	A patient that is experiencing cardiac arrest with ongoing CPR and/or ECMO, being supported by multiple interventions.	Near Pulselessness Cardiac collapse Mechanical ventilation Defibrillator used	Trying to die CPR (A‐modifier) pH ≤7.2 Lactate ≥5	No SBP without resuscitationPEA or refractory VT/VFHypotension despite maximalsupport

      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