Cardiogenic shock vs pulmonary oedema

Acute pulmonary oedema (ESC 2021): rapid onset over hours, driven by increased afterload and/or predominant LV diastolic dysfunction or valve disease; wet and warm; treated with diuretics and vasodilators — IV vasodilators may be considered when SBP is over 110 mmHg.^[1] Cardiogenic shock (ESC 2021): diagnosis requires hypoperfusion — cold sweated extremities, oliguria, mental confusion, dizziness, narrow pulse pressure — with raised creatinine, metabolic acidosis and lactate; wet and cold; treated with inotropes/vasopressors, short-term MCS and RRT. Inotropes are reserved for LV systolic dysfunction, low output and low SBP (for example under 90 mmHg) with poor perfusion. SCAI stages run A to E, with hypoperfusion separating B from C.^[1][4] The bedside discriminator is the Nohria profile — congestion and perfusion. In 452 admissions, wet-cold was 91 and wet-warm 222; congested profiles predicted death or urgent transplantation.^[2] Vasopressor: noradrenaline over dopamine (SOAP II: more arrhythmia and more cardiogenic-shock deaths with dopamine) and over adrenaline (OptimaCC: more refractory shock with adrenaline, 37 vs 7 percent).^[3][8] Mechanical support: IABP-SHOCK II and ECLS-SHOCK showed no 30-day mortality benefit; DanGer Shock found a microaxial flow pump lowered 180-day death in STEMI shock with more adverse events. ESC 2021: unselected MCS use is not supported.^[5][6][7][1]