Study (year), [reference] |
Definition of CS |
SHOCK (1999), [53] |
SAP<90 mmHg for >30 min or inotropes to maintain SAP>90 mmHg, end-organ hypoperfusion (urine output<30 mL/h or cold extremities), hemodynamic assessment: CI<2.2 L/min/m2 and PCWP>15 mmHg |
IABP-SHOCK II (2012), [54] |
SAP<90 mmHg for >30 min or catecholamines to maintain SAP>90 mmHg, clinical indications of pulmonary congestion, end-organ hypoperfusion (disorientation, livedo reticularis, urine output<30 mL/h, serum lactates>2 mmol/L, cold extremities) |
ESC-HF Guidelines (2016), [56] |
SAP<90 mmHg after adequate fluid administration, clinical (cold extremities, oliguria, disorientation, pulsus mollis) and laboratory (metabolic acidosis, high serum lactates, high serum creatinine) indications of end-organ damage |
TRIUMPH (2007), [58] |
Patency of infarct-related artery spontaneously or after PCI, refractory CS>1 h after PCI with SAP<100 mmHg despite vasopressors (dopamine≥7 μg/kg/min or epinephrine≥0.15 μg/kg/min), clinical or hemodynamic criteria for elevated LV filling pressure, end-organ hypoperfusion, LVEF<40% |
CULPRIT-SHOCK (2017), [59] |
Planned early revascularization by PCI, multivessel coronary artery disease defined as >70% stenosis in at least two major vessels (≥2 mm diameter) with identifiable culprit lesion, pulmonary congestion, SAP<90 mmHg for >30 min or inotropes to maintain SAP>90 mmHg, indications of end-organ damage (altered mental status, cold/clammy skin and extremities, urine output<30 mL/h, serum lactates>2 mmol/L) |