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