60. Case Report: Massive Pulmonary Embolus Presenting as STEMI – Cedars-Sinai

CardioNerds (Amit Goyal & Daniel Ambinder) join Cedars-Sinai cardiology fellows (Natasha Cuk, Ronit Zadikany, Neal Yuan) for some drinks at the local pub 3rd Stop after a walk down Hollywood boulevard! They discuss a fascinating case of a massive pulmonary embolus presenting as STEMI. Dr. Babak Azarbal provides the E-CPR and program director Dr. Joshua Goldhaber provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-40s with no known past medical history presented to the ER in PEA arrest with ongoing cardiopulmonary resuscitation (CPR). Prior to his arrest, his coworkers reported that he was complaining of lightheadedness, dizziness and that he was found slumped over at his desk. His EKG in the ambulance showed STE in aVR and V1 - V4 with TWI in III and aVF initially concerning for an anterior STEMI. He was cannulated with VA-ECMO for extracorporeal cardiopulmonary resuscitation (E-CPR) and was taken to the catheterization lab emergently. In the catheterization lab, his coronary angiogram did not show obstructive coronary disease. The interventionalists decided to perform a pulmonary artery (PA) angiogram which revealed a large amount of thrombus bilaterally in the proximal PAs. He underwent surgical embolectomy with removal of almost all his clot burden. The patient was thereafter cooled for neurological protection. Unfortunately, the patient had a very poor neurological exam with lack of brainstem reflexes upon rewarming. There was loss of gray-white differentiation on CT, and EEG and evoked potential testing were consistent with severe anoxic brain injury. After discussions with the patient's family, the patient was transitioned to comfort care and subsequently passed away peacefully. Case Media Click to Enlarge Right Coronary Artery Left Coronary System - 1 Left Coronary System - 2 Left Pulmonary Artery Right Pulmonary Artery Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case The patient presented initially with STE in aVR as well as the septal and anterior leads. What is the differential for an ST elevation in lead aVR? STE in aVR with diffuse ST depression can be a potential finding of LM or LAD stenosis. However, there have been several studies that have shown that the combination of STE and multi-lead STD was not associated with complete occlusion of a culprit vessel. Thus, the differential for STE in aVR more commonly includes significant LM or LAD stenosis, severe three-vessel disease with diffuse sub-endocardial ischemia (e.g., CAD in the setting of sepsis, anemia, shock), as well as pulmonary embolism with right ventricular injury (see below)! Remember that lead aVR is opposite I, aVL, II and V5-6 and thus elevation in aVR may represent reciprocal changes of diffuse sub-endocardial ischemia. Furthermore, aVR doesn't directly overlie myocardium but reflects electrical activity from the RV outflow tract and basal septum. Thus, in the context of an anterior STEMI, STE in aVR (> 1mm) strongly predicts LAD occlusion proximal to the first septal perforator, which supplies the basal septum. The patient was found to have non-obstructed coronaries and was ultimately diagnosed with a PE. Could we have suspected that from the initial EKG? What are the EKG changes that have been noted in patients with a PE? Generally, an EKG does not make the diagnosis of PE, as most findings have low sensitivity and specificity. Rather, an EKG can be helpful in evaluating other causes of a patient's cardiopulmonary symptoms and provide supporting evidence of acute PE. The EKG findings in acute PE can be thought to be secondary to three primary mechanisms: (1) increased adrenergic drive, (2) RV and/or RA dilation, and/or (3) RV myocardial ischemia and injury. The most common EKG fining is sinus tachycardia. Atrial arrhythmia (e.g., atrial fibrillation or flutter) can be seen and is predominantly a result of RA/RV dilation with increased adrenergic drive. Complete or incomplete RBBB may occur as the RBB is vulnerable to stretch, especially early in its course. Due to acute RV dilation with accompanying rotation of the heart in relation to the ECG leads (more commonly in sub-massive or massive PE), we can see right axis deviation, a dominant R-wave in V1, and the R to S transition point in the precordial leads shifting towards V5. As a result of ischemia and/or RV injury, we may see the classic S1Q3T3 pattern, but this is not a sensitive finding and thus its absence should not change decision-making. We can also see an RV strain pattern with T-wave inversions (TWI) in the right precordial leads (V1-V3) as well as the inferior leads. Non-specific ST-T changes are relatively common and along with sinus tachycardia, may be the most frequent finding. ST elevation in aVR with accompanying elevation in V1-V3 may be seen in PE (especially if complicated by obstructive shock). The injury current in the limb leads is directed towards aVR in this circumstance. In the precordial leads the injury current is more variable. A differentiating point between proximal LAD or LM acute MI and acute PE could be the presence of prominent reciprocal STD and the distribution of TWI. This patient presented in cardiac arrest and obstructive shock from a massive PE. What is the treatment for patients with a massive PE and cardiac arrest? In patients with cardiac arrest or circulatory collapse, VA-ECMO in combination with surgical embolectomy or catheter-directed treatment is given a Class IIb recommendation in patients with massive PE per 2019 ESC guidelines. In general, the decision to proceed with active thrombus removal, whether it be with thrombolytic-based, catheter-based, or surgical embolectomy, is driven by first the severity of the PE and secondarily by patient-specific factors for bleeding and co-morbidities. However, if VA-ECMO is pursued, it should not be a stand-alone strategy In patients with massive (AHA) or high risk (ESC) PE – defined as systolic blood pressure 40 mmHg for at least 15 minutes – systemic thrombolytic therapy carries a Class IB recommendation. Trial data has demonstrated earlier hemodynamic improvement with systemic thrombolysis compared to anticoagulation alone, especially if treatment is initiated within 48 hours of symptom onset Catheter directed therapy may have a role in massive PE – whether it be through mechanical, saline or ultrasound lysis – in patients who have persistent hemodynamic instability despite systemic thrombolysis and patients with moderate to high bleeding risk. Embolectomy is indicated in hemodynamically unstable patients with massive PE in whom thrombolytic therapy is contraindicated or patients who fail thrombolytic therapy. Furthermore, it may be considered early in patients with extensive clot burden where there is surgical expertise.Although the patient presented with refractory cardiac arrest, he was able to be stabilized with E-CPR before diagnostic evaluation was performed. What does ECPR stand for? Has it been proven to improve clinical outcomes? As defined by the AHA guidelines, extracorporeal cardiopulmonary resuscitation or ECPR is the use of VA-ECMO during the resuscitation of a patient in cardiac arrest, with the goal of providing end-organ perfusion while reversible causes of arrest are identified and treated. There have been several studies regarding the use of ECPR in out of hospital and in hospital cardiac arrest (OHCA and IHCA), respectively. It remains unclear whether ECPR is of consistent benefit with regards to morbidity and mortality as studies have lacked a uniform definition of EPCR, consisten inclusion criteria for ECPR, and many studies have been single-center introducing the potential for bias. Thus, in the 2019 AHA Focused Updated on ACLS guidelines, ECPR is given a Class 2b indication (with level of evidence C-LD), where it can be considered in select patients as rescue therapy when conventional CPR efforts are failing in clinical settings in which it can be quickly implemented and supported by trained providers. It sounds like the benefits of E-CPR remain to be further elucidated. Are there any specific features that help predict who would benefit from ECPR? While we do not have high quality randomized data, observational data in EPCR has shown that shorter no flow times (i.