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240: CARDIOGENIC SHOCK AFTER VENTRICULAR SEPTAL DEFECT REPAIR

Introduction: Central venous oxygen saturation is useful in detecting acute changes in perfusion. Though its use has become less common with the integration of noninvasive monitoring techniques, it remains a valuable tool to guide therapy. We present a case involving the diagnostic workup and treatment of a patient in cardiogenic shock after surgical repair of a post myocardial infarction (MI) ventricular septal defect (VSD). Description: A 66-year-old man with known post MI VSD presented to the ER with dyspnea and chest pain several weeks after STEMI and subsequent PCI. Following repair of the VSD, he was admitted to the ICU, extubated on POD0 and was being weaned off vasoconstrictors. Low-dose epinephrine was continued. On POD2 he developed oliguria, elevated lactate, and elevated LFTs. Bedside and formal TTE showed the VSD repair was intact. Additionally, there were no major changes to ventricular function (LVEF 20%) compared to the preoperative or immediate postoperative echocardiogram that would explain the rapidly changing clinical picture. The only difference was an acute drop in central venous O2 saturation (ScvO2) from 49% to 25% and morphologic changes in the CVP waveform showing a pronounced a wave and steep y descent, indicating increased right-sided filling pressure and decreased compliance. Low-dose epi was changed to dobutamine and milrinone and aggressive diuresis was started. Within 2.5 hours, the following changes were recorded: ScvO2 25% to 64%, lactate 3.6 to 1.8 mMol/L, CVP 13 to 8 mmHg with normalization of the waveform, HR and BP (95,123/71) to (96,125/58). After 72 hours the patient was net negative by 9.2 L and weaned off inotropes. His liver and kidney function returned to normal. Repeat TTE at discharge remained unchanged. Discussion: The use of ScvO2 and CVP waveform can contribute to the timely and accurate diagnosis and treatment of cardiogenic shock, as derangements in ScvO2 may appear prior to other indicators of poor perfusion. Further, noninvasive methods alone, such as TTE, may fail to reveal the complete clinical picture. Ultimately, this case demonstrates the utility of a multimodal diagnostic approach, including careful interpretation of CVP waveform and ScvO2, which help detect subtle but critical hemodynamic changes associated with states of hypoperfusion.