Triple coronary artery occlusion causing cardiogenic shock and cardiac arrest (early escalation of mechanical circulatory support makes difference)
Presenter
Mohamed Salah Abdelghani, M.D., Hamad Medical Corporation, doha, doha, Qatar
Mohamed Salah Abdelghani, M.D., Hamad Medical Corporation, doha, doha, Qatar, Mohanad Shehadeh, M.D., Hamad Medical Corporation, Doha, Qatar, Shabib Abdullah Al Aasmi, M.D., National Heart Center ,Oman, Muscat, Oman, Ashraf Ahmed Omar, Heart Hospital, Hamad Medical Corporation, Doha, Qatar, Abdulrahman Arabi, M.D., HMC Heart Hospital, Doha, Qatar and Jassim M. Al Suwaidi, MD, Hamad General Hospital, Doha, Qatar
Keywords: Cardiogenic Shock
Title Triple coronary artery occlusion causing cardiogenic shock and cardiac arrest (early escalation of mechanical circulatory support makes difference) Introduction Simultaneous multi-vessel epicardial coronary artery thrombosis is a rare finding in acute ST-segment elevation myocardial infarction (STEMI). It has high likelihood to cause cardiogenic shock and cardiac arrest. We present a case of multi-vessel coronary occlusion leading to cardiac arrest and cardiogenic shock that has been managed with full revascularization, medical, and mechanical circulatory support with an excellent outcome. Emphasizing the importance of getting all the needed information early to manage accordingly, beside having low threshold for escalation whenever it is needed. Clinical Case A-38-Year-old previously healthy gentleman was admitted as a case of STEMI with diffuse ST segment elevation. Upon arrival to the hospital the patient had severe chest pain and sweating his BP was 75/52 mmHg for that he was started on Cath lab the patient had PEA cardiac arrest that required 8 minutes of resuscitation before achieving ROSC. Coronary Angiography showed triple coronary artery thrombosis that was managed with PCI to RCA with DES and POBA to LCX and LAD with final TIMI III flow (Figure 2). The patient was intubated during resuscitation and started on Noradrenaline. Intra-Aortic Balloon pump was inserted, then he was admitted to CICU where he was found to have tachycardia HR 130 bpm, BP 97/69 mmHg with extremely cold extremities as well as bilateral crackles. Lab tests were significant for high sensitive Trop T > 100,000 ng/L (3-15 ng/L), PH 6.97, PO2 71 mmHg on 90 % FIO2, PCO2 60 mmHg, Lactic Acid 12.3 mmol/L that increased in 1 hr to 13.8 mmol/L despite being on IABP and 2 Inotropic support. Bedside Echo showed severely reduced EF 10 %, SV 12 ml, LVOT VTI 5.6 cm and COP 1.5 Liters. Assessment of Cardiogenic shock SCAI stage C was established with high likelihood of deterioration to stage D, so a prompt decision for escalation of mechanical circulatory support to VA-ECMO was made within 60 minutes of admission to CICU. Within 24 hrs perfusion improved significantly with good urine output and normalization of both PH, and ventilation parameters, as well as Lactic acid. Ten days later the patient was decannulated and extubated successfully. Follow up Echocardiography showed improvement in systolic function with EF 41 %. Relook coronary angiography showed patent coronaries (figure 2). The patient had uneventful course in the cardiology ward, before he was discharged home in an excellent functional status. Discussion We would like to highlight the importance of using the available clinical and hemodynamic assessment (invasive or non-invasive) in cardiogenic shock for decision making. Our patient was initially expected to have severely depressed systolic function, so a quick decision for early initiation of inotropic support and IABP while he was in Cath-lab. Repeated and frequent clinical and hemodynamic assessment is crucial as it may predict that the patient is going to deteriorate necessitating escalation of mechanical circulatory support in time, before severe multiorgan hypo-perfusion makes it too late to escalate.