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    Health & Fitness

    Cardionerds: A Cardiology Podcast

    Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge, sharpen your skills, and become a true CardioNerd!

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    Latest Episodes:
    64. Case Report: RV Infarction Treated with RVAD Support – Houston Methodist Oct 02, 2020
    Show notes

    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,...


    63. Case Report: Peripheral Artery Disease (PAD) & Cerebral Hyperperfusion Syndrome – University of Florida Sep 30, 2020
    Show notes

    CardioNerds (Amit Goyal & Daniel Ambinder) join University of Florida cardiology fellows (Ashley Mohadjer, Hussain Khalid, and Morgan Randall) for an authentic Gainesville-style tailgate! They discuss a fascinating case of severe peripheral artery disease (PAD) and cerebral hyperperfusion syndrome. Dr. Khanjan Shah provides the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro 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 woman in her 60s with a past medical history of type 2 diabetes, hypertension, and hypothyroidism presented to the University of Florida with a chief complaint of "Someone told me my neck artery was blocked." Someone call 227-346-6373. What does that spell? CardioNerd! She noted exertional pain in both legs with limited exertion. Has a family history of CAD and MI in her father in his 20s. Her only medications were baby aspirin, atorvastatin 80mg, and thyroid replacement. Her blood pressures were noted to be dropping and so her regimen was being titrated off as a result. Physical exam was notable only for poorly palpable pulses in all extremities. To further work this up, a myocardial perfusion scan, CTA head/neck/abdomen, and ABIs were ordered. ABI on the right was 0.86 and on the left was 0.76 with monophasic doppler waveforms throughout. CT abdomen exhibited an occlusion of the abdominal aorta from just below the renal arteries extending to the common iliac arteries with distal reconstitution. CT head/neck showed occlusion of the right carotid artery, complete occlusion of the right innominate artery, near complete occlusion of the right vertebral artery, and delayed flow in the right posterior cerebral artery. On the left side, she had high-grade subclavian stenosis. Myocardial perfusion imaging exhibited no defects. On subsequent visits her exercise tolerance improved with an exercise regimen, but blood pressures were more and more difficult to obtain. As a result, revascularization was pursued with stenting of the left subclavian artery. She was discharged, but returned a few hours later with severe left sided pulsatile headache and nausea/vomiting. She was admitted for monitoring, but fortunately improved and discharged with close outpatient follow-up. She continued to improve in the outpatient setting. After MRI brain and extensive work-up, she was deemed to have cerebral hyperperfusion syndrome following revascularization. She had no further complications and was monitored thereafter. Final diagnosis: severe peripheral artery disease (PAD) and cerebral hyperperfusion syndrome. Case Media ABCDEFClick to Enlarge A: ECG B: ABIsC: CT Angiogram D: CT Angiogram - head and neck E: Pre and post subclavian stentinng F: CT head and neck - follow up Subclavian via L radial Aortic Root Cine 1 Aortic Root Cine 2 Stent Post Stent Post Stent 2 Post Stent 3 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What are the risk factors and prevalence of PAD? PAD refers to atherosclerotic peripheral artery disease, and is the accumulation of plaque in various peripheral arterial beds akin to CAD involving coronary arteries. 6% of adults over the age of 40 have PAD, and 30% of American adults over the age of 70. This all leads to an annual healthcare expenditure in the US of ~$4 billion! PAD is associated with a 3-4x increased risk of cardiovascular events. Furthermore, mortality overall is 15-20% at 5 years in patients with PAD. Risk factors for PAD include all the risk factors for ASCVD we consider for CAD, including diabetes, hypertension, and hyperlipidemia. What Should We Look for on Physical Exam with PAD? Get a brachial blood pressure (Class Ib AHA/ACC Recommendation), listen for bruits (areas of turbulent flow), and look at the extremities for: skin color changes, temperatures changes, loss of hair, or ulcerations (typically at the tips of digits). In patients with claudication and/or risk factors for PAD, these can all be signs of PAD. In particular, palpate the dorsalis pedis and tibialis pulses. In office maneuvers can also include Buerger's test where the affected limb is elevated from a supine position till pallor is observed. In a normal limb, even elevating to 90 degrees should not elicit pallor; however, in an ischemic limb, especially severe ischemia, elevation to even 20 degrees for 30 to 60 seconds can lead to pallor. Then when returning the limb to resting position, the pink color will return slowly (I.e., >20 seconds) and may demonstrate rubor as there is reactive hyperemia (dilation of the arterioles) in attempt to remove metabolic waste and restore circulation. At the bedside, we should also test for diseases commonly associated with PAD, particularly diabetes. Testing for diabetic neuropathy is critical in patients with PAD, as it is a modifiable risk factor and can make patients prone to developing diabetic foot ulcers. Remember, that there are classic locations for arterial ulcers but often patients have a mixed picture given concomitant venous insufficiency and/or diabetes. These arterial ulcers tend to occur where arteries terminate, including between the digits and tips of the toes. Furthermore, they can occur at areas of increased pressure, including the lateral malleolus. How do we obtain and interpret ABIs in chronic limb ischemia? ABI stands for Ankle-Branchial Index. This means taking the ankle blood pressure and indexing it against the brachial blood pressure. The ABI is an easily done test. To ensure we have an accurate ABI, we typically ask the patient to rest for at least 5-10 minutes prior to measuring ankle pressure. We also want to make sure we have the appropriate cuff size, and thus in the limbs the cuff width should be at least 40% of the limb circumference. We can start by taking the brachial pressure in one arm. After obtaining our initial brachial SBP, we then proceed with taking a blood pressure from either the dorsalis pedis or posterior tibial artery on the same side, with the cuff just above the ankle. We utilize a continuous wave doppler signal to identify the pulse and insufflate the cuff to just above where the Doppler signal disappears. We then slowly release the pressure in the cuff and record where the systolic pressure returns and repeat the process for the artery (e.g., DP or PT) that was not tested and then move onto to the contralateral limb. We then finally obtain the SBP in the brachial on the side opposite from where we started. The ABI for a specific extremity is then the highest pressure in a lower extremity limb (DP or PT) divided by the highest systolic brachial pressure in either limb. As discussed above, we usually calculate the ABI at bedside using a continuous-wave doppler probe, but when blood pressures are low or if there is significant venous congestion leading to pulsatile flow (e.g., congestive heart failure), the venous signal can be difficult to distinguish from the arterial signal. Briefly, a normal ABI is considered 1.0 to 1.4; 0.91 to 0.99 is considered borderline; and 1.4 are considered abnormal. In patients with symptoms of PAD (e.g., claudication), ABI has a sensitivity of ~ 95% and specificity of 100% of diagnosing lesions with >50% stenosis in one or major lower extremity vessels. An ABI > 1.4 suggests the presence of calcified vessels and we need additional vascular studies, such as measurement of the toe brachial index (TBI) or pulse volume recordings (PVR) to assess for significant PAD. The vessels in the toe have been shown to be less prone to medial calcification. Finally, segmental brachial index measurements are also considered abnormal if there is a decrease in 20 mmHg or more between adjacent levels in the lower extremity, a decrease in segmental brachial index of 0.15 or more over time, or a difference in systolic pressure more than 30 mmHg between contralateral limbs. How Do We Treat Symptomatic PAD? Exercise! First and foremost, supervised treadmill exercise training is a Class Ia recommendation from the AHA/ACC guidelines. Multiple studies have shown exercise to be beneficial in improving time and distance to developing claudication symptoms and increasing pain-free walking distance up to 180%. Notably, an exercise trial is recommended prior to any attempted revascularization. As with CAD, lifestyle measures to mitigate ASCVD risk factors are vital, including diet, weight loss, and smoking cessation....


    62. Case Report: RV Failure & Shock After placement of an AV graft – The Johns Hopkins Hospital Sep 27, 2020
    Show notes

    CardioNerds (Amit Goyal & Daniel Ambinder) join Johns Hopkins Hospital cardiology fellows (Rick Vakil, Pranoti Hiremath, and Vasanth Sathiyakumar) for some gelato by the bay in Baltimore, Maryland! They discuss a challenging case of RV failure & shock after placement of an AV graft. Dr. Monica Mukherjee provides the E-CPR and program director Dr. Steven Schulman provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal 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 40s, with a history of type 1 diabetes and prior failed renal and pancreatic transplants currently on iHD, was referred to Johns Hopkins Hospital for dialysis access. A left groin AV loop graft was pursued due to multiple access point failures in the past secondary to severe peripheral artery disease. Pre-op evaluation included risk stratification with RHC which was consistent with WHO Group 2 pulmonary HTN and diffuse atherosclerosis in the RCA on LHC. Intra-op, patient had an episode of significant hypotension after administration of protamine that required phenylephrine and ephedrine. In the PACU, his BPs continued to be low (70s/40s mmHg), requiring admission to the SICU where cardiology was consulted. In the SICU, patient had ongoing hypotension despite pressors and fluids. Exam demonstrated a systolic murmur consistent with TR and elevated JVP. Labs were notable for a mild elevation in liver enzymes, elevated troponin, high NT-proBNP and elevated lactate. TTE demonstrated a moderately dilated and hypokinetic RV, elevated RVSP and evidence of pressure/volume overload. CTA abdomen/pelvis demonstrated extensive mesenteric atherosclerosis and signs of gastric ischemia. Patient was treated for RV failure with norepinephrine, inhaled epoprostenol, and CVVHD for volume removal. He became febrile and was treated empirically with broad spectrum antibiotics. Due to concern for the new loop graft causing high output heart failure vs RV failure, it was temporarily occluded for testing and then permanently ligated by vascular surgery with significant improvement in his BPs and RV function on repeat TTE. Case Media ABCDEClick to Enlarge A. Plato's allegory of the cave by Jan Saenredam, according to Cornelis van Haarlem, 1604, Albertina, ViennaB-C. Anesthesia flow sheets D. CXR: Pulmonary vascular congestion, bibasilar atelectasisE. ECG: Sinus tachycardia to 110, RAD, RBBB, similar to prior TTE: LVEF 60-65%, mild to moderate concentric hypertrophy, trace effusion TTE: Flattened septum in systole and diastole c/f RV pressure and volume overload. RV moderately dilated and hypokinetic. RVSP 63 mmHg. CT Abdomen and Pelvis: Negative for PE, gastric pneumatosis, air within the gastroepiploic veins, and portal venous gas, most concerning for gastric ischemia, extensive atherosclerotic calcifications throughout the mesenteric vessels TTE follow up: Mild/moderate concentric hypertrophy, EF 60%, G2DD TTE follow up: RV mildly dilated and mild global hypokinesis of the RV. TAPSE 1.54. RV S’ was 9.6 cm/s (normal > 9.5) Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. In this case the patient became hypotensive shortly after administration of protamine. What are the risk factors for a protamine reaction and the proposed mechanisms? Protamine is a protein commonly used in cardiovascular procedures to reverse the effects of heparin. Although rare, it can cause severe reactions that have multiple different proposed mechanisms. They include hypotension mediated by histamine release from mast cells and IgE-mediated anaphylaxis. Other proposed mechanisms include acute severe pulmonary hypertension with or without RV failure mediated by complement and thromboxane A2 and fulminant noncardiogenic pulmonary edema likely through a thromboxane-mediated process. Risk factors for protamine reactions have been difficult to rigorously prove, but might include patients with a true fish allergy (Protamine is produced from the sperm of salmon or similar species), men s/p vasectomy (disruption of blood-testes barrier and sensitization against sperm), insulin dependent diabetic patients taking NPH insulin (protamine is used in NPH), and previous exposure to protamine 2. Our patient had signs of RV failure clinically and on TTE following AV graft creation. How common is this, what is the mechanism, and when might one consider avoiding fistula or graft creation in a patient with CHF? AV fistulas (AVF) are the preferred chronic iHD access due to reductions in infections, morbidity, and mortality compared to central venous access. However, this data is based on observational studies. Remember, changes in hemodynamics occur in phases following creation of AV hemodialysis access. Acutely, an AVF or prosthetic graft (AVG) decreases systemic vascular resistance (SVR) through a surgical arterial to venous shunt. This acute decrease in SVR leads to increased stroke volume and a decrease in blood pressure. The decrease in SVR activates the sympathetic nervous system and leads to increased HR and combined with the increased SV, an increase in cardiac output. The increased cardiac output leads to increased right sided venous return and sub-acutely can lead to progressively increasing left and right sided filling pressures. Eventually, there can be worsening RV dilation and systolic dysfunction, elevated pulmonary artery pressures, and myocardial remodeling. Retrospective analyses have shown that creation of an AVF/AVG can increase the prevalence of RV dilation and dysfunction by 2-3 fold in patients with ESRD. The risk of worsening heart failure in patients with pre-existing cardiac disease is generally related to the flow in the AV access. Some small studies have suggested there is increased risk of developing heart failure in patients with an upper-arm AV fistula compared with a forearm fistula Although there are not clear guidelines that dictate when a patient should not receive an AVF/AVG, a permanent dialysis catheter should be considered as an alternative option in patients with pre-existing heart failure or pulmonary hypertension due to increased risk of right heart failure. 3. AV vascular access can lead to high output heart failure. What is high output heart failure and what are the major mechanisms? Most CHF occurs in the setting normal or low CO. However, certain conditions can precipitate high output heart failure (HoHF). The underlying pathophysiologic change in HoHF seems to be disproportionately low SVR +/- increased oxygen consumption. The low SVR leads to decreased afterload, increased LV emptying and thus increased stroke volume and cardiac output. Furthermore, this leads to increased cardiac preload. Increased oxygen demand also requires increased cardiac output. The persistently low SVR causes low renal perfusion pressure (renal hypoperfusion) which leads to RAAS activation and volume expansion. Combined with the increased preload, this can lead to heart failure in susceptible individuals. Obesity (the most common etiology), AV fistulas (congenital or acquired), cirrhosis, and Paget's disease lead to HoHF predominantly due to systemic vasodilation. Lung disease, myeloproliferative disorders, and hyperthyroidism can cause HoHF and have a proportionally larger contribution from increased metabolic demand and therefore increased oxygen consumption. Lower SVR has been associated with higher mortality. 4. How might someone differentiate high output heart failure from low output heart failure or RV failure? RHC is the gold standard to diagnose high output heart failure. Characteristic features include an elevated CO or CI (CI ≥4 L/min/m2) and a low SVR in the setting of clinical signs of heart failure. In a Mayo Clinic study of patients with CI > 4 L/min/m2 with or without signs of heart failure, a CI ≥3.54 L/min/m2 estimated by TTE identified HoHF patients with 62% sensitivity and 96% specificity. Furthermore, patients with HoHF frequently demonstrated doppler-estimated RV systolic pressure ≥ 42 mmHg (92% sensitivity and 100% specificity). 5. After temporary occlusion of his loop graft, our patient had improvement of his blood pressure and a decrease in his HR. What does this indicate and how is it mediated? A rapid rise in BP and decrease in HR after occlusion of an AVF/AVG is called the Nicoladoni-Branham sign and indicates a hemodynamically significant AV fistula that could benefit from


    61. Case Report: Cardiac Arrest due to Peripartum Cardiomyopathy – Medical College of Wisconsin Sep 25, 2020
    Show notes

    CardioNerds (Amit Goyal & Daniel Ambinder) join Medical College of Wisconsin cardiology fellows (Katie Cohen, Div Mohananey, and Dave Lewandowski) for some cold brews by Lake Michigan in Cream City aka Milwaukee, WI! They discuss a case of a pregnant woman presenting cardiac arrest due to peripartum cardiomyopathy. Dr. Sarah Thordsen provides the E-CPR and program director, Dr. Nunzio Gaglianello, provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, 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 G2P1 woman in her early 30s with a history palpitations presented after a witnessed out-of-hospital cardiac arrest while at work. She received 6 rounds of CPR and 2 shocks before ROSC was achieved. She was intubated and given fluids but continued to remain hypoxic and hypotensive. Exam demonstrated sinus tachycardia, no murmurs, gravid abdomen and cool extremities. Initial labs demonstrated leukocytosis to 14k, lactic acid at 4.3 mmol/L, troponin-I peak at 0.07 ng/dL and elevated NT-proBNP. CXR demonstrated bilateral effusions and pulmonary congestion, and post-arrest EKG showed a wide complex tachycardia, leading to suspicion of VT arrest. In sinus, there were no ST segment elevations and TTE showed LVEF 10-20%, global hypokinesis and no valvular disease. Given the severity of her shock, she was placed on central VA-ECMO with Impella support as an LV vent. During ECMO cannulation, she underwent emergent cesarean section due to fetal distress. Coronary angiography showed non-obstructive coronaries, but with sluggish flow in the setting of her cardiogenic shock and possible coronary spasm in setting of multiple vasoactive medications. Endomyocardial biopsy was negative for giant cell myocarditis. Within 4-5 days, she was weaned off all vasoactive agents and ECMO was decannulated; repeat echocardiogram showed LV functional recovery. GDMT was slowly titrated and a subcutaneous ICD was eventually placed before discharge. She and her child have done well over the course of a year! Case Media ABClick to Enlarge A: ECG: Initially in sustained wide complex irregular tachycardiaB: CXR: Extensive consolidative changes throughout the lungs TTE: Parasternal Long Axis TTE: Apical 4 Chamber Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. What is the differential for cardiac arrest in pregnant patients? When thinking about a cardiac etiology of arrest, the differential should include pregnancy-induced hypertension, peripartum cardiomyopathy, myocardial infarction from acute coronary syndrome or spontaneous coronary artery dissection, pulmonary embolism, amniotic fluid embolism and aortic dissection. Non-cardiac etiologies include hemorrhagic shock, sepsis, stroke, trauma and anesthetic complications. In addition to these unique considerations, pregnant patients are also susceptible to the usual culprits! As noted in the 2015 AHA Scientific Statement, cardiac arrest in pregnancy is not common, occurring in 1:12,000 admissions for delivery. As of 2016, per the CDC the pregnancy-related mortality rate was ~17 deaths per every 100,000 live births. However, mortality data does not fully capture critical illness in pregnancy, and thus the AHA recommends considering maternal "near-miss" data. Knowledge gaps, provider unfamiliarity, and lack of medical ward or medical/cardiac ICU preparation for cardiac arrest in pregnancy may contribute to morbidity and mortality. Finally, as many of the early warnings signs of impending cardiac arrest may overlap with symptoms of pregnancy (e.g., progressive dyspnea), early interventions may be delayed. Thus, the AHA recommends using a validated obstetric early warning score to risk stratify ill pregnant patients. 2. Remind us of some important physiologic changes in pregnancy that can affect cardiopulmonary resuscitation Hormonal and physiologic changes during pregnancy make pregnant patients more prone to hypoxia, hypotension, pulmonary edema, and difficult airway intubation. Systemic vascular resistance typically decreases due to the production of endogenous vasodilators, though there are important differences in patients with pre-eclampsia. The enlarging uterus can reduce preload by compressing the IVC and increase afterload by compressing the aorta. In the supine position, which is preferable for resuscitation, this compression can be exacerbated. Furthermore, as the uterus enlarges and limits diaphragmatic movement, functional residual capacity can decrease by 10-25%. At the same time, there is increased oxygen consumption due to metabolic and fetal demands. With limited reserve and increased oxygen demands, hypoventilation or apnea can rapidly precipitate hypoxemia. Cardiac output increases by 30-50% via increased stroke volume, and lesser extent HR, leading to increased circulating volume, making patients prone to pulmonary edema. Finally, pregnancy hormones can lead to airway edema and more friable tissue making intubation more difficult with increased risk of bleeding. For more on pregnancy physiology, enjoy: Ep #48 - Critical Bicuspid Aortic Valve Stenosis Complicating Pregnancy Ep # 57 - Peripartum Cardiomyopathy with Cardiogenic Shock 3. What are some aspects unique to advanced cardiac life support (ACLS) in pregnant patients? Cardiac arrest is inherently different than other cardiac arrest that we typically encounter as there are two patients: mother and the fetus.  Chest compressions, delivery of shocks and medications can continue per standard adult ACLS algorithm. Importantly, while chest compressions are ongoing and patient is in the supine position, there should be continuous manual left uterine displacement (LUD) to relieve aortocaval compression. Furthermore, IVs should be established above the diaphragm so that intravenous infusions and medications are not impeded by caval compression of the uterus. Teams should be prepared for perimortem caesarean delivery (PMCD) and this should occur at the site of arrest. PMCD may facilitate return of spontaneous circulation (ROSC) after the gravid uterus is emptied. PMCD should occur within four minutes due to a rapid decline in fetal survival with longer delays to delivery. 4. What are the considerations for post-arrest care for pregnant patients? Targeted temperature management (TTM) is not contraindicated in pregnancy, and no necessary intervention should be withheld for fear of fetal damage. The primary focus should be maternal outcomes since that best serves fetal outcomes. If TTM is pursued, there should be continuous fetal monitoring. The patient should continue to be in the left lateral decubitus position if it does not compromise other management. Routine cardiac catheterization is certainly not recommended unless post-arrest EKG demonstrates clear signs of ischemia. Remember that embryogenesis is mostly complete by 12 weeks of gestation. Thus, the AHA recommends providing all necessary medications, even teratogenic medications (e.g., corticosteroids, phenytoin) especially if the cardiac arrest occurs after the first trimester. 5. What is the data for extra-corporeal life support (ECLS) during pregnancy and postpartum There are no consensus guidelines, however, ECLS is not contraindicated in pregnancy and should be considered for life-threatening conditions. There is lack of long-term data for maternal and fetal outcomes. Although survival varied depending on indication, one systematic review of ECLS in peripartum patients showed overall 30-day survival of 75% for mother and 64% for fetus. Interestingly, survival in the immediate post-partum group was the highest. Complications includes bleeding, deep vein thrombosis, and vascular complications similar to the non-pregnant population. References Arany Zolt, and Elkayam Uri. “Peripartum Cardiomyopathy.” Circulation 133, no. 14 (April 5, 2016): 1397–1409. Campbell, Tabitha A, and Tracy G Sanson. “Cardiac Arrest and Pregnancy.” Journal of Emergencies, Trauma and Shock2, no. 1 (2009): 34–42. Jeejeebhoy Farida M., Zelop Carolyn M., Lipman Steve, Carvalho Brendan, Joglar Jose, Mhyre Jill M., Katz Vern L., et al. “Cardiac Arrest in Pregnancy.” Circulation 132, no. 18 (November 3, 2015): 1747–73. Gilotra, Nisha A, and Gerin R Stevens. “Temporary Mechanical Circulatory Support: A Review of the Options, Indications, and Outcomes.” Clinical Medicine Insights. Cardiology 8, no. Suppl 1 (February 3,...


    60. Case Report: Massive Pulmonary Embolus Presenting as STEMI – Cedars-Sinai Sep 23, 2020
    Show notes

    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....


    59. Case Report: Constrictive Pericarditis & Severe Mitral Regurgitation – Mayo Clinic Sep 21, 2020
    Show notes

    CardioNerds (Amit Goyal & Daniel Ambinder) join join Mayo Clinic cardiology fellows (Mays Ali, Charlie Jain, Korosh Sharain) for a scenic walk through gorgeous Rochester, Minnesota! They discuss a fascinating case of constrictive pericarditis and severe mitral regurgitation. Dr. Rick Nishimura provides the E-CPR and program director Dr. Frank Brozovich 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 Constrictive Pericarditis & Severe Mitral Regurgitation - Patient Summary A woman in her late 40s with a history of lupus and hypertension presented with worsening dyspnea on exertion and orthopnea over a year. She reported intermittent pleuritic chest discomfort that had persisted since an episode of acute pericarditis years prior. A TTE suggested severe mitral regurgitation, and she was referred to the Mayo Clinic for mitral valve intervention. The official TTE report from the OSH suggested non-dilated LV, EF 55-60%, normal RV function, severe MR with thickened leaflets and sub-valvular apparatus, moderate to severe TR and a dilated IVC. Furthermore, the CXR showed pericardial calcifications. Upon evaluation by the Mayo Clinic fellows, the JVP was elevated to about 10-12 cm with rapid x and y descents, a positive Kussmaul’s sign, and the murmurs of MR and TR. Her lungs were clear to auscultation and extremities did not demonstrate edema. Re-review of the TTE images revealed posterior pericardial thickening, no septal shift on respiration, but suggestion of annulus reversus where medial mitral annulus tissue doppler (9 cm/s) was greater than lateral (8 cm/s). Further, there was evidence of expiratory hepatic vein diastolic flow reversal. For the team, there was discordance between the apparent severity of her MR reported by echocardiogram and her clinical symptoms. In addition, the echocardiogram was suggestive of specific signs of constrictive pericarditis. Thus, simultaneous RHC/LHC was obtained. There was equalization of RV/LV pressures during diastole, demonstration of a “square root sign” and importantly discordance between LV and RV pressures with respiration. Thus, discordant clinical findings led to a suspicion for constrictive pericarditis and was corroborated by discordance on invasive hemodynamics! Further, the V-waves were not prominent on wedge pressure tracing and to investigate the mitral regurgitation further, an LV ventriculogram was done. This demonstrated 3+ to 4+ MR. Based on all the findings, the patient was diagnosed with constrictive pericarditis, severe MR and moderate to severe TR. She underwent pericardiectomy, mitral valve replacement (given that repair was not feasible due to the sub-valvular thickening) and given that TR has been shown to worsen after pericardiectomy and is a poor prognostic factor, she additionally underwent tricuspid valve repair. Her symptoms improved markedly following intervention. Case Media ABCDEFGHClick to Enlarge A. CXR: Heart size was borderline enlarged with biatrial enlargement. LV does not appear very enlarged. B. Mitral Regurgitation by CW Doppler C. Tricuspid regurgitation by CW Doppler. TR Max 2.43D. Tissue Doppler of the mitral valve annulus: Medial e' = 9 cm/s, Lateral e' 8 cm/sE. Hepatic Vein PW Doppler F. Right atrial pressure tracingG. RV and LV simultaneous pressure tracings H. Wedge pressure and LV simultaneous pressure tracings Neck Vein Exam TTE TTE: Color Doppler across mitral valve TTE: Short Axis TTE: Short Axis, TV TTE: Hepatic Vein Doppler Left ventriculogram with severe mitral regurgitation Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case- Constrictive Pericarditis & Severe Mitral Regurgitation One of the early clues to the etiology of this patient’s dyspnea was a positive Kussmaul's sign. What is the mechanism and differential of Kussmaul’s Sign? Typically the JVP decreases with inspiration as the negative intrathoracic pressure "sucks in" blood from the vena cavae. When there is a lack of decrease or an increase in JVP with inspiration, this finding is called Kussmaul’s sign. Kussmaul’s sign reflects conditions where there is right ventricular dysfunction, impaired RV filling and elevated right atrial pressure Kussmaul’s sign is classically associated with constrictive pericarditis. Remember, during normal inspiration, the diaphragm contracts and increases abdominal pressure with variable effect on venous return. However, in constriction, the rise in abdominal pressure increases venous return from the congested hepato-splanchnic vasculature. And since RV filling is constrained by a non-compliant pericardium, there is a rise in JVP during inspiration. Other conditions where we may see a positive Kussmaul’s sign include restrictive cardiomyopathy, RV predominant infarction, massive pulmonary embolism, tricuspid stenosis, and severe tricuspid regurgitation. 2. A decision was made to pursue invasive hemodynamic evaluation to differentiate between restrictive and constrictive physiology. How do we differentiate between the two on echocardiogram? Differentiating between the two diagnoses requires an understanding of the pathophysiologic differences between constriction and restriction. Enjoy Ep #58 and CN5 for understanding constrictive physiology and echocardiographic findings! In restriction we do not have intrathoracic-intracardiac disassociation as intrathoracic pressures are transmitted normally to the cardiac chambers during respiration. Further, there is no exaggerated interventricular dependence. We may see increased myocardial thickness in restriction (secondary to infiltrative or storage disorders - enjoy Ep #50 - restrictive cardiomyopathy) and increased pericardial thickness/calcification in constriction. Unlike constrictive pericarditis, restrictive cardiomyopathies should not demonstrate respirophasic septal shift or variation across the atrioventricular valves. Both conditions will demonstrate hepatic vein diastolic flow reversal. However, in constriction, the exaggerated ventricular interdependence and greater LV filling during expiration causes septal bowing into the RV and results in greater hepatic vein diastolic flow reversal during expiration. In restriction, hepatic vein flow reversal is more prominent in inspiration as the stiff myocardium is unable to tolerate the increased RV preload that occurs during inspiration. The estimated pulmonary artery systolic pressures tend to be elevated (>55-60 mmHg) in restrictive cardiomyopathy and are often normal in constriction. In constriction, the annular tissue velocity is preserved except at the lateral annulus, where tethering of the lateral wall results in decreased velocities and annulus reversus (See Ep#58 and CN5). Meanwhile, annular tissue velocity (e’) is significantly reduced in restrictive cardiomyopathy. Enjoy Ep #58 and CN5 for differences on invasive hemodynamics! 3. Given that the patient had subvavlular thickening, the patient was not a candidate for mitral valve repair and the patient underwent mitral valve replacement. What are the indications for mitral valve surgery in patients with severe chronic MR? Why is mitral valve repair preferred for primary MR? Class I indications for mitral valve surgery include (1) symptomatic patients in the absence of severe LV dysfunction (defined as EF 60% and LVESD 95% and expected mortality is 50 mmHg) and preserved LVEF. For primary mitral regurgitation involving an abnormality of the valve apparatus (e.g., leaflets, chordae, annulus, papillary muscles) – MV repair is preferred over MV replacement in most patients as it is associated with lower operative mortality and improved long term survival. Feasibility of valve repair will generally depend on valve anatomy and surgical experience....


    58. Case Report: Constrictive Pericarditis – University of Tennessee Sep 18, 2020
    Show notes

    CardioNerds (Amit Goyal & Daniel Ambinder) join join University of Tennessee cardiology fellows (Rachel Goodwin, Emmanuel Isang, and William Black) for some chocolate cake and hikes in the Smoky Mountains! They discuss a fascinating case of constrictive pericarditis. Dr. Tjuan Overly provides the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song 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 late 40s with a history of renal failure secondary to IgA nephropathy and now status post a kidney transplant 10-15 years ago was referred by hepatology for evaluation of recurrent ascites and LE edema. He appeared grossly volume overloaded on exam with JVP elevated past the mandible, RV heave, and 2+ pitting edema. TTE demonstrated LVEF of 55-60%, RVSP 40mmHg, abnormal septal motion with respiration, and respirophasic variation in mitral inflow across the mitral valve raising the suspicion for constrictive pericarditis. RHC pressures demonstrated a mean RA pressure of 20mmHg, RV 40/25mmHg, PA 38/30mmHg (mean 32 mmHg) and PCWP mean of 26 with V-waves at 28 mmHg. Simultaneous LV and RV pressure tracings showed ventricular discordance with respirophasic variation, consistent with constrictive physiology. Patient underwent pericardiectomy with markedly improved heart failure symptoms. Repeat TTE showed no evidence of constriction. Case Media ABCClick to Enlarge! A. ECGB. Pulsed-wave Doppler spectrum of tricuspid inflow velocities demonstrates a marked respiratory variation (In irregular rhythms, such as the atrial fibrillation seen here, respirophasic changes may still be seen but are confounded by the varying R-R interval)C. Simultaneous LV and RV pressure tracings showing discordance with respirophasic variation Apical 4-chamber view demonstrating abnormal septal motion due to interventricular dependence – dissociation of thoracic and cardiac chamber pressures leads to increased RV filling during inspiration Short axis view of the LV demonstrating a D-shaped interventricular septum during inspiration. Note the presence of a pericardial effusion as well. Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case The initial presentation clinically seemed to be right greater than left heart failure. What are the signs and common causes of right heart failure? The signs and symptoms of RHF are often similar to left-sided CHF, but may describe more severe dyspnea on exertion, significant abdominal distension, and early satiety due to ascites or gut edema. Symptoms of pulmonary edema from elevated left-sided filling pressures (orthopnea, paroxysmal nocturnal dyspnea) may be absent. On examination, there will be elevated JVP with likely prominent v-waves, possibly Kussmaul’s sign (inspiratory rise in JVP rather than fall) depending on the pathology, abdominal ascites, pulsatile hepatomegaly, and lower extremity edema. An RV heave may be discernible along with a loud P2 component and murmur of TR. Broadly, RV failure may be caused by pressure overload (ex: pulmonary hypertension, pulmonic stenosis), volume overload (ex: intracardiac shunt, tricuspid regurgitation), or myocardial disease (ex: cardiomyopathies, ischemia/infarct). The most common cause of chronic right heart failure is LV failure (causing post-capillary pulmonary hypertension). Other causes of RV failure include pre-capillary pulmonary hypertension, congenital heart disease (e.g., ASD, residual RVOT obstruction in Tetralogy of Fallot patients), ARVC, RV ischemia, myocarditis, right sided valvular disease, constrictive pericarditis, and restrictive cardiomyopathy. The patient in this case was diagnosed with constrictive pericarditis (CP). What are the causes of CP? Remember that the etiology of CP can vary considerably depending on the patient’s demographics. In developed countries, the majority of cases are idiopathic or viral, post-operative, or post-radiation therapy. In developing countries, infectious etiologies are more common, with tuberculosis the most common cause. Amongst the causes, remember that acute bacterial and tuberculosis pericarditis have the highest chances of progressing into constriction. With post-radiation constrictive pericarditis, remember there can be significant delay (even up to 20 years) between radiation therapy and development of constriction and often accompanies concomitant myocardial fibrosis with restrictive physiology as well. Other etiologies include immunologic disorders (e.g., rheumatoid arthritis, lupus, sarcoidosis), malignancy (e.g., breast and lung cancers, lymphoma, mesothelioma), and myocardial infarction. 3. What are the TTE findings suggestive of constrictive pericarditis? To understand the basic TTE findings, we need a basic understanding of the pathophysiology. Constriction leads to a noncompliant pericardium that encases the heart. Heart failure occurs because there is impaired diastolic ventricular filling. The ventricles fill almost entirely in early diastole, because once they can no longer expand because of the non-distensible pericardium, diastolic filling abruptly stops. This pathophysiology reflects one of the key findings in CP: equalization of the end-diastolic pressures. At the same time, the thickened/fibrotic/calcified pericardium prevents the normal transmission of intrathoracic pressures to the cardiac chambers. However, structures “outside” the pericardium – such as the pulmonary vasculature – still “see” the normal changes in intrathoracic pressure. Normally, when we take a breath in: the intrathoracic pressure falls and this is transmitted equally to the pulmonary capillaries (e.g., the wedge pressure) and the cardiac chambers. The gradient for mitral valve inflow reflects the difference in wedge pressure and intra-cardiac chamber (LV) pressure. In CP, the drop in intrathoracic pressure with inspiration is transmitted to the pulmonary capillaries but not the cardiac chambers. Thus, there is now a decreased gradient for mitral valve inflow during inspiration. This is called intrathoracic-intracardiac pressure disassociation. At the same time, with inspiration right heart preload increases and to accommodate this volume the RV expands. However, RV expansion is limited by the encasing noncompliant pericardium, and thus to accommodate the volume the interventricular septum shifts to the left. This, further decreases the gradient for mitral valve inflow and the physiology is termed enhanced ventricular interdependence. The opposite occurs on expiration. Thus, on echocardiogram we may see abnormal respirophasic septal shift, reflecting enhanced ventricular interdependence. The septum moves to the left in early diastole with inspiration and then back to the right on expiration. This is one of the most sensitive echocardiographic findings for CP. Reflecting compromised diastolic filling, markedly elevated filling pressures, and equalization of end-diastolic pressures, there will be a high E-wave velocity with a decreased A-wave velocity (E/A > 1) across the mitral valve. Due to pericardial restraint, this early rapid diastolic filling (high velocity with a tall E wave) stops abruptly and so the E wave has a short deceleration time. The latter is analogous to the pericardial knock heard on physical exam and the ventricular early diastolic "square root" sign (dip and plateau) on the RHC. Reflecting intrathoracic-intracardiac pressure disassociation and enhanced ventricular interdependence, there will be increased respirophasic variation in mitral and tricuspid valve inflow. This typically is best demonstrated with the first few beats of inspiration and expiration. Specific cut-offs include a decrease in peak mitral E-wave velocity > 25% and increase in peak tricuspid E-wave velocity > 40% during inspiration (opposite during expiration). In other words, as you inspire there is increased filling of the RV with decreased filling of the LV. Expiratory hepatic vein diastolic flow reversal is one of the most specific findings of CP. Reflecting intrathoracic-intracardiac pressure disassociation and enhanced ventricular interdependence, during expiration RV filling is compromised (as the LV is filling with septal shift to the right) and thus there is “back-flow” from the right heart and we see more prominent flow reversal in the hepatic veins during expiration. In contrast, hepatic vein diastolic flow reversal occurs predominantly durin


    57. Case Report: Peripartum Cardiomyopathy with Cardiogenic Shock – University of Pennsylvania Sep 16, 2020
    Show notes

    CardioNerds (Amit Goyal & Daniel Ambinder) join Penn cardiology fellows (Brian McCauley, Norrisa Haynes, and Mahesh Vidula) for a rooftop picnic in sunny Philadelphia! They discuss an informative case of peripartum cardiomyopathy with cardiogenic shock. Program director Dr. Frank Silvestry provides the E-CPR segment and a message to applicants. Johns Hopkins internal medicine resident Colin Blumenthal 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 Two weeks postpartum, a woman in her mid 20s, G1P1, with no past medical history presented following a tonic-clonic seizure. Prior to this, she had been experiencing 1 week of worsening dyspnea and lower extremity edema. Initial work-up revealed a left MCA stroke and she underwent thrombectomy. Limited TTE found LVEF R-side filling pressures with low cardiac index despite inotropes. Cardiac power output (CPO) was severely decreased with borderline pulmonary artery pulsatility index (PAPI), corroborating left > right heart failure. Patient ultimately required a durable left ventricular assist device (LVAD). Over the course of 9 months her guideline directed medical therapy (GDMT) was titrated and her intrinsic cardiac function and symptoms improved. Her EF improved to 35-40% and she tolerated an LVAD weaning protocol, so her LVAD was ultimately explanted! She is currently doing well on GDMT alone! Case Media CXR: Mild interstitial edema, +ET tubeST (131), LAD, nonspec T wave flattening, nl intervalsClick to Enlarge TTE 1 TTE 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. How do we define Peripartum Cardiomyopathy? Diagnosis is made by the development of heart failure towards the end of pregnancy or in the months following delivery (~5 months postpartum), no other identifiable cause of HF, and demonstration of LV systolic dysfunction with LVEF typically less than 45% with or without dilation. Risk factors include history of pre-eclampsia, hypertension, cocaine use, multifetal pregnancies, older maternal age, and African descent. Keep a broad differential diagnosis for new onset heart failure in the peripartum period. The differential includes pre-existing cardiomyopathy, valvular disease or congenital cardiomyopathy unmasked by the hemodynamic changes of pregnancy (see CNCR episode 48 for more on the hemodynamic changes of pregnancy!). Other differentials should include ischemia/spontaneous coronary artery dissection (SCAD), stress-induced cardiomyopathy, CM due to systemic disease (e.g. sepsis, rheumatologic disease), myocarditis and tachycardia-induced CM. 2. The team used invasive hemodynamics to guide shock management. Why is a PAC helpful? Despite data from the ESCAPE trial, a pulmonary artery catheter (PAC) can be very useful in the diagnosis and management of cardiogenic shock. Remember, the ESCAPE trial included chronic HF patients in whom there was clinical uncertainty on whether a PAC may be useful. Further, any patient on milrinone was excluded. Cardiac power output (CPO) and pulmonary artery pulsatility index (PAPi) are some of the parameters obtained from a PAC that can guide cardiogenic shock therapy and need for mechanical circulatory support (MCS). Resting CPO = CO x MAP / 451. CPO measures the "pumping power" of the LV and correlates with end-organ perfusion. In the SHOCK registry, CPO 50%) as they are at higher risk of future recurrence. The 2018 ESC guidelines advise against pregnancy if EF has not recovered to >50-55%. Contraception counseling should be done early: before discharge or at the time of diagnosis. Patients should avoid estrogen-containing methods especially in the early postpartum period as thromboembolism risk is high. If a patient plans on another pregnancy, teratogenic HF medications, like ACE/ARB/ARNI and spironolactone, must be stopped prior to stopping contraception. Following cessation of these GDMT medication, follow-up echocardiography to ensure LV functional stability should be performed after at least 3 months off therapy. The patient should be monitored very closely during a subsequent pregnancy for changes in symptoms and followed with serial echocardiograms and NT-proBNP levels duri


    56. Case Report: Arrhythmogenic Desmoplakin Cardiomyopathy – Northwestern University Feinberg School of Medicine Sep 14, 2020
    Show notes

    CardioNerds (Amit Goyal & Daniel Ambinder) join Northwestern University cardiology fellows (Sarah Hale, Sarah Chuzi, and Graham Lohrmann) for burgers and a great case by the Chicago River! They discuss a fascinating case of arrhythmogenic desmoplakin cardiomyopathy. Dr. Lisa Wilsbacher provides the E-CPR and program director Dr. Benjamin Freed provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro 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 male in his early 40s presented for second opinion regarding multiple ICD shocks. 10 years prior he was diagnosed with a "weak heart," thought secondary to a viral illness and a dual-chamber ICD was placed at that time. He noted shocks occurring for the first time 5 years prior, at which time amiodarone was started. They recurred two years prior, when he was diagnosed with paroxysmal atrial fibrillation. Finally, he was hospitalized one month before presentation with multiple ICD shocks and was found to have high defibrillation thresholds (DFTs) and amiodarone was stopped. He then presented for a second opinion from the Northwestern CardioNerds! The patient had been doing well on GDMT and had NYHA Class I symptoms (Enjoy Ep #13 - Approach to GDMT). He did note a family history of a cousin with "cardiac issues" and did not know his father's family history. Physical exam demonstrated bradycardia and ECG demonstrated an a-paced, v-sensed rhythm at 50 bpm. TTE demonstrated a moderately dilated LV with LVEF 30%, globally reduced LV function and multiple wall motion abnormalities without a vascular distribution. PET-CT was performed which showed diffuse uptake and high-intensity signal at the inferolateral and basal anterior walls. Cardiac MRI showed diffuse circumferential epicardial delayed enhancement with associated diffuse, enhancing thickening of the pericardium favoring inflammatory versus fibrotic process. Patient was initially diagnosed with cardiac sarcoid and started on prednisone and weekly methotrexate. On return of genetic testing, patient found to have a pathogenic variant for desmoplakin gene, and it was felt his cardiomyopathy was secondary to desmoplakin Left Dominant Arrhythmogenic Cardiomyopathy (LDAC, or left-dominant ARVC) presenting with inflammatory myocardial injury. On follow up the patient remained listed for transplant, and DFTs improved off amiodarone. Case Media CXRECGCardiac MRIPET CT (Cardiac Sarcoid Protocol)Click to Enlarge Episode Schematics & Teaching Created by Dr. Karan DesaiClick to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case We started the case talking about DFTs. What are DFTs?! Defibrillation Thresholds (DFTs) are the minimal amount of energy required to return a patient to sinus rhythm that is in a cardiac dysrhythmia. Most modern ICD leads have thresholds less than 15 joules and typically less than 10 joules with biphasic shocks. High DFT thresholds tend to be defined as >25J or a safety margin of


    55. Case Report: Suicide LV post-TAVR – The University of Texas at Austin, Dell Medical School Sep 11, 2020
    Show notes

    CardioNerds (Amit Goyal & Daniel Ambinder) join UT-Austin cardiology fellows (Priya Kothapali, Sergio Montano, Travis Benzing, and Michael Grzeskowiak) for a speedboat adventure on Lake Travis! They discuss a fascinating case of Suicide LV post-TAVR. Dr. Mark Pirwitz provides the E-CPR and program director Dr. Clay Cauthen provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song 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 woman in her early 70s, with a history of CAD s/p PCI to LAD & RCA with DES six months prior, to presentation, paroxysmal atrial fibrillation s/p ablation, type 2 diabetes mellitus, hypertension, prior TIA, and severe symptomatic AS was admitted for elective TAVR. She underwent successful implantation of a 29mm Medtronic Evolut Pro valve via left common femoral artery access. Post-valve deployment and following protamine administration for heparin reversal, course was complicated by hypotension with PEA arrest requiring CPR for 4 minutes. Intra-op TEE and angiogram showed a well-seated prosthetic valve with trace paravalvular leak and no evidence of acute aortic regurgitation, significant paravalvular leak, pericardial effusion, coronary obstruction, aortic dissection, or access site complications. She was treated for suspected Protamine reaction with high dose steroids & epinephrine. However, she remained hypotensive with MAP in the 50s on high dose Epinephrine, Norepinephrine, and Vasopressin. Hemodynamics by pulmonary artery catheter demonstrated CVP 7, mPA 26, PCWP 18 mmHg and CO/CI 2.8 L/min and 1.3 L/min/m2. Her lactate was elevated at 5.92 mmol/L and EKG demonstrated normal sinus rhythm. Bedside TTE in the ICU showed hyperdynamic LV function with LVEF 70% and near-complete mid to distal cavity obliteration with significant intracavitary gradient. She was diagnosed with post-TAVR suicide LV and managed with aggressive volume resuscitation and rapid wean of Epinephrine/Norepinephrine with improvement in her hemodynamics. She was eventually extubated and discharged on beta-blocker therapy. Case Media A. ECGB. CXRClick to Enlarge A. ECG: Normal sinus rhythm, no evidence of AV block, no ST segment elevation or depression.B. CXR: Pulmonary vascular congestion, no pneumothorax, ETT at level of carina, PAC in appropriate position Pre-Aortogram Implantation Post-Dilation Post-Aortogram TEE: Mid-Esophageal Three-Chamber View TEE: Mid-Esophageal Short Axis View Abdominal aortography showed no evidence of vascular access site complication or contrast extravasation. Aortic root angiography showed no evidence of AI, coronary obstruction, or dissection. TTE: PLAX and A4C Episode Schematics & Teaching Created by Dr. Karan DesaiGraphic by Dr. Carine HamoClick to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Remind all CardioNerds – how do we define Severe Aortic Stenosis? By TTE, severe AS is defined as a mean gradient >40 mmHg, a peak velocity >4 m/s, an aortic valve area


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