To create an experimental animal model of cardiogenic shock for learning and to test new therapeutic strategies.

Adult white pigs (70 kg) received both intravenous anesthesia (acepromazine 0.3 mg/kg, midazolam 0.2 mg/kg, fentanyl 250 μg/kg, thiopental sodium 12.5 mg/kg and pancuronium 0.4 mg/kg) and inhaled anesthesia (halothane 1%), and were intubated and mechanically ventilated. An arterial line was obtained through dissection and puncture of the common femoral artery. A continuous cardiac output catheter (Edwards Lifescience, USA) was introduced through the dissected internal jugular vein and was positioned using the arterial pulmonary pressure curve, allowing monitoring of the right atrial pressure, pulmonary artery pressure, pulmonary wedge pressure (PAop) and SvO₂. Through median sternotomy, the pericardium was opened longitudinally and the heart was exposed. The baseline ECG and hemodynamic data were recorded and after a 6-0 polypropylene suture was passed under the proximal anterior descending coronary artery that was snared for up to 10–15 min. An ECG was then obtained to show typical ischemic alterations, and a regional myocardium color change and regional myocardial hypocontractility were observed. The presence of cardiogenic shock was defined by cardiac output index <1.8 l/min/m², PAop >20 mmHg and mean arterial pressure <50 mmHg. The carotid artery and external jugular vein were cannulated and ECMO support was used (flow 100–150 ml/kg/min) after induced cardiogenic shock.

The model was tested in eight animals. Four animals died immediately after coronary occlusion because of ventricular fibrillation, and cardiogenic shock was reproduced in the other four animals and these animals were kept alive for 4 hours with supportive interventions (inotropic drugs and ECMO).

The experimental animal model created by ischemic myocardial infarction induced cardiogenic shock and can be used to study and test new therapeutic strategies.