Amanda Curry, MD
A 72 y/o male with PMH type 2 diabetes, CAD, HFrEF, HTN, and HLD is admitted to the MICU for frequent neurologic monitoring after an endovascular thrombectomy for an acute ischemic stroke caused by thrombosis of the M2 branch of the left MCA. While reviewing his chart, you notice that the patient was recently admitted for 1 week about 10 days ago for dyspnea secondary to acute decompensated heart failure. You also note on his admission labs that he is newly thrombocytopenic, with a platelet count of 80,000. His last platelet count on discharge was 250,000, and he has never been thrombocytopenic before. What is causing his thrombocytopenia?
As we learn more about the pathophysiology of COVID-19, alternative treatments are being explored for the severe sequelae of this disease. SARS-CoV-2 enters human cells via the ACE2 receptor, located in many organs, including the heart, vascular endothelium, and alveolar epithelium causing an inflammatory cascade that can lead to ARDS, vasodilatory shock, myocarditis, acute kidney injury and capillary leak. Given the relationship between SARS-CoV-2 and the RAAS, is there a role for angiotensin II in vasodilatory shock caused by COVID-19?
Bradycardia is defined as a heart rate of less than 60 BPM. In the ED, we may not always have the time to stop to consider the etiology of bradycardia after we have stabilized our patient (and after we likely already consulted cardiology!) Having a thoughtful approach to the differential diagnosis for bradycardia can be extremely helpful in treating the underlying cause. The next time a bradycardic patient presents to your ED, think to yourself, “The Brady Bunch is on a DIET.”