64. Case Report: RV Infarction Treated with RVAD Support – Houston Methodist

CardioNerds (Amit Goyal & Daniel Ambinder) join Houston Methodist cardiology fellows (Isaac Tea, Stephanie Fuentes, Peter Rothstein) for a trip to Hermann Park! They discuss a challenging case of right ventricular (RV) infarction leading to acute RV failure treated with right ventricular assist device (RVAD) support. Dr. Mahwash Kassi provides the E-CPR and program director Dr. Stephen Little provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References 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 early 70s with ASCVD risk factors and known CAD (PCI to proximal LAD 4 years prior) presented with typical angina refractory to maximal medical therapy. A nuclear stress test showed a reversible perfusion defect in the RCA territory, and he was referred for PCI. Coronary angiogram showed severe stenosis of the proximal RCA and a DES was successfully deployed with TIMI 3 flow, though several large acute marginal branches were jailed. The night following PCI, the patient developed bradycardia, hypotension, and tachypnea. Physical exam showed newly elevated JVP, lower extremity edema, and bibasilar crackles without a new cardiac murmur. ECG showed ST elevation in V1-V4, and bedside echocardiogram showed a severely dilated RV with decreased systolic function. With concern for acute RV failure, the patient was fluid resuscitated, started on dopamine for chronotropy, and was admitted to the CCU. A Swan-Ganz catheter was placed, showing a CVP 12, RV 41/15, PA 36/20 (25), PCWP 18, CI 1.6 (by Fick method). The calculated PAPi was 0.84. The patient was transitioned to dobutamine to improve RV inotropy, epinephrine in the setting of hypotension, and inhaled nitric oxide in an attempt to decrease RV afterload. Despite these interventions, the patient had worsening shock, anuric renal failure requiring CVVH, and respiratory failure requiring intubation. A centrifugal RA to PA pump was placed (Protek Duo) for right-sided mechanical circulatory support, with improvement in RV hemodynamics and cardiogenic shock. Notably, a repeat angiogram was done, which showed a patent left coronary circulation as well as a right coronary artery without flow in the acute marginal branches. After 6 days of mechanical circulatory support, the patient was ultimately able to be weaned from vasoactive agents, and the Protek Duo was removed. He continued to have junctional bradycardia, and a permanent pacemaker was placed. After a nearly month-long admission, the patient was discharged to rehab; at 4 months follow-up, the patient's RV function had improved on TTE, and he was not limited from heart failure symptoms. Case Media ABCDEFGClick to Enlarge A: ECG, initialB: ECG: 8 hours post PCI he was noted to have junctional bradycardia with ST-segment elevations in V1-V4.C: Pre and post RCA PCI D: TTE: EF 50-55%, Severely enlarged RV with severely reduced systolic function, TAPSE 1.4 cm, Myocardial systolic excursion velocity (S’): 5.9E: CXR- shock F: Swan, Protek Duo Cannula, Temporary pacer G: CXR and TTE images demonstrating Protek Duo cannula placement Left Coronary System -1 Left Coronary System - 2 Severe eccentric serial stenoses in the proximal to mid RCA - 1 RCA - 2 RCA PCI - 1 RCA PCI - 2 RCA PCI - 3 RCA PCI - 4 RCA - Final TTE -1 TTE -2 Repeat angiogram: Patent stents, sluggish flow Protek Duo Placement Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) Don’t forget about the RV, because it sure won't forget about you! Cardionerds, how do you break down the pathophysiology of acute RV failure? Understanding the pathophysiology of RV failure requires a basic understanding of RV physiology. Normal RV function depends on systemic venous return, RV afterload, pericardial compliance/constraint, and native RV contractility. Remember, the thin-walled RV requires much less energy to generate output compared to the LV as the RV is pumping into the highly compliant, low-resistance pulmonary circulation. Overall, the RV is highly sensitive to changes in RV afterload. Thus, when we think of acute RV failure, our primary considerations are factors that rapidly increase RV afterload (e.g., pulmonary embolus), as well as conditions with decreased RV contractility (e.g., RV ischemia). The RV is more adept to tolerating changes in volume rather than pressure (since it is coupled to the low-resistance, high compliance pulmonary circulation). Contrast this with the LV, which tolerates changes in pressure more than volume. An acute increase in RV afterload can abruptly precipitate a fall in RV cardiac output! With an acute decreased in RV contractility (e.g., RV infarct), the RV can dilate leading to functional TR; this can further exacerbate RV dilation, leading to impaired LV filling due to ventricular interdependence. As the septum shifts leftward, this can impair LV filling by increasing LVEDP and lead to hypotension. Direct RV injury can promote more RV injury/ischemia, as elevated right heart pressures can cause coronary sinus congestion reducing coronary blood flow and leading to more RV ischemia. For more detailed explanation of Right-Sided Heart Failure, see this fantastic Scientific Statement from the AHA! 2) Lets focus on ischemic RV disease: what is the coronary supply to the RV, and how does coronary blood flow to the RV differ than that of the LV? Compared to the LV, the RV is more resistant to irreversible ischemia. Coronary blood flow to the RV occurs both in systole and diastole, RV myocardial oxygen demand at rest is lower than that of the LV with smaller muscle mass, and there is often extensive collateral circulation from the left coronary system. However, RV coronary perfusion pressure can decrease rapidly in the setting of systemic hypotension and increased RV intracavitary pressure. In most patients, the RV is supplied by the RCA via RV acute marginal branches largely supplying the anterior RV free wall. Significant RV involvement in an RCA culprit acute myocardial infarction tends to only occur if the occlusion is proximal to the acute marginal branch. Furthermore, the extent of RV involvement may be attenuated by the amount of left to right collateralization. Note, the LAD supplies the RV apex, as well as a portion of the RV anterior wall that is contiguous with the anterior septum. Notably, in patients with a left dominant coronary system or in patients with a chronically occluded RCA with extensive left to right collateral flow, more than half of the RV free wall may be supplied by the left system. 3) Now that we know what causes acute RV failure, what can we do to assess for acute RV failure, both at the bedside and with advanced diagnostics? Physical exam: In acute RV failure, we will likely see elevated neck veins +/- Kussmaul's sign, hypotension, possibly clear lungs depending on etiology, and tricuspid regurgitation murmur. Enjoy Ep #58 - Constrictive Pericarditis CN5 for more details on right-sided exam findings! ECG: Unfortunately, the standard 12-lead ECG provides limited definitive information on RV failure. However, we should evaluate for acute occlusive myocardial infarction (MI) involving the RV, including ST elevation in the inferior leads (classically with III > II), V1 > V2, and/or V1 +/- ST depression in V2. Right-sided leads can further confirm acute occlusive MI, with STE > 1mm in lead V4R sensitive and specific for RV infarct. With a large RV infarct, we may see brady-arrhythmias. Other signs of acute RV failure may include RV strain pattern (e.g., ST depression and T wave inversions in V1-V3). Enjoy Ep #60 - Massive PE for more on ECG changes in acute PE and RV failure! CT: While usually not obtained in the setting of acute RV failure unless evaluating for acute PE or parenchymal lung disease, RV:LV ratio >1.0, pulmonary trunk enlargement, and contrast reflux into the inferior vena cava and hepatic veins suggest right heart failure. A gated cardiac contrast-enhanced CT can provide more information about chamber size/function and valvular pathology. TTE: Echo is crucial in the diagnosis of RV failure! One of the first things to pay attention to is RV size, with RV dilation being a poor prognostic sign; RV:LV ratio > 1 is associated with increased in-hospital mortality in some studies of acute PE patients. Evaluate the position of the interventricular septum,