Cardionerds: A Cardiology Podcast

CardioNerds (Amit Goyal and Daniel Ambinder), join CardioNerds FIT Ambassador, Dr. Natasha Cuk and her co-fellows, Dr. Lily Stern, and Dr. Paul Marano from the Cedars-Sinai Cardiology Fellowship for some late afternoon smoothies on the beach. They discuss the case of a 46-year-old woman who presented with sudden cardiac arrest and was ultimately found to have a mobile intraluminal aortic thrombus adherent to a penetrating ulcer in the ascending aorta. This mobile thrombus was ultimately thought to be the cause of transient ischemia and the patient’s cardiac arrest. We discuss a differential for sudden cardiac arrest, initial management after resuscitated cardiac arrest, a differential for arterial thrombus, and review an illness script for penetrating atherosclerotic ulcers. Dr. Dominick Megna provides the provides the E-CPR for this episode. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship). This Case Report has been published in JACC Case Reports! Claim free CME just for enjoying this episode!  Disclosures: NoneJump to: Pearls - Notes - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Episode Teaching https://twitter.com/LilySternMD/status/1460811173113184263?s=20 Pearls - Cardiac Arrest due to Aortic Thrombus After cardiac arrest, the initial ECG obtained after the return of spontaneous circulation can provide important information on the etiology of the arrest. The ECG can narrow our structured differential, for which one approach would be the following breakdown: acute ischemic events, structural heart disease, arrhythmogenic syndromes with no structural abnormality, and then non-cardiac causes such as drugs, toxins, trauma, metabolic arrangementsThe risk vs benefit of emergent angiography after sudden cardiac arrest depends on balancing the potential benefit from revascularization in an acute ischemic event vs bleeding risks and potential delays in other aspects of care, particularly given that a large percentage of mortality is related to neurologic injury from the arrest, which would not be impacted by immediate angiography. The available randomized controlled trial evidence has not demonstrated a survival or neurologic outcome benefit to immediate angiography, and the decision depends on weighing the risk/benefit for each patient.Due to high flow, a thrombus in the aorta should prompt an investigation for causes focused on the other two ‘points’ of Virchow’s triad (aside from stasis): endothelial injury and hypercoagulability.A penetrating atherosclerotic ulcer (PAU) is a deep atherosclerotic lesion where there is a focal ulceration of the elastic lamina that extends through the medial layer of the aortic wall. These lesions are most commonly associated with extensive atherosclerosis, but can also occur related to inflammatory, infectious, or traumatic causes.A PAU is a type of acute aortic syndrome and accounts for up to 8% of total acute aortic syndromes. It may present with a spectrum of symptoms, including as an incidental finding on cardiothoracic imaging or a severe chest and back pain, like an aortic dissection. While it is a subtype of aortic syndrome, PAU can also progress to become aortic dissection and rupture. Notes - Cardiac Arrest due to Aortic Thrombus 1. How might a post-ROSC ECG help determine the etiology of a sudden cardiac arrest? During our case, we discussed a systematic approach to the differential diagnosis for sudden cardiac arrest. We broke down the causes into the buckets of: Acute ischemic eventsStructural heart diseaseArrhythmogenic syndromes with no structural heart diseaseNon-cardiac causes such as drugs, toxins, trauma, and metabolic arrangements The post-ROSC ECG can provide immediate information to help narrow our diffe...

CardioNerds (Amit Goyal and Daniel Ambinder),  ACHD series co-chair Dr. Agnes Koczo (UPMC), and episode FIT lead, Dr. Natasha Wolfe (Washington University) join Dr. Ari Cedars   (Director of the Adult Congenital Heart Disease Program at Johns Hopkins) for a discussion about coarctation of the aorta.   In this episode we discuss the presentation and management of unrepaired and repaired coarctation of the aorta in adults. We discuss the unique underlying congenital anatomy of coarctation and how that impacts physiology, clinical presentation, and diagnostic findings. We discuss the importance of long-term routine follow-up and screening of patients (including those who have been “repaired”) for common complications such as hypertension, re-coarctation, and aneurysm development. We end with a discussion of treatment options for coarctation and its complications. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Coarctation of the aorta can occur as a discrete stenosis or as a long and hypoplastic hypoplastic aortic arch segment. Most commonly it is a discrete stenosis located at the insertion site of the ductus arteriosus just distal to the left subclavian artery.Three quarters of patients with coarctation of the aorta also have a bicuspid aortic valve.Hypertension is the most common long-term complication of coarctation of the aorta, whether repaired or unrepaired. Unrepaired coarctation is a rare cause of secondary hypertension in young adults with a difference in upper extremity and lower extremity BP by ≥ 20 mmHg. Systemic hypertension may not be consistently identifiable at rest in those with repaired coarctation, thus guidelines recommend ambulatory blood pressure monitoring or stress testing to identify hypertension with exertion.Chest and brain imaging via CT or MRI should be done every 5-10 years to screen for other long-term complications including re-coarctation (rate ~11%), aortic aneurysm development (higher risk in those with concurrent bicuspid aortic valve), pseudoaneurysm, aortic dissection, and cerebral aneurysms.Repair of coarctation or re-coarctation is indicated for patients who are hypertensive with a BP gradient ≥ 20 mmHg (Class I recommendation). Catheter-based stenting is the preferred approach when technically feasible. Show notes 1. What is the proposed embryologic origin of coarctation of the aorta? The aortic arch and its branches develop at 6-8 weeks fetal gestation. We all start with six aortic arches that go on to become the great arteries of the head and neck. The 4th arch forms the thoracic aortic arch and isthmus. The 6th arch persists as the proximal pulmonary arteries and ductus arteriosus. Thoracic aortic coarctation is therefore a manifestation of abnormal embryologic development of the 4th and 6th arches.There are two main theories regarding how aortic coarctation occurs.

CardioNerds (Amit Goyal and Daniel Ambinder), Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, and episode FIT lead and UT Southwestern Cardiology Fellow Dr. Laurie Femnou discuss valvular heart disease in pregnancy with cardio-obstetrics expert Dr. Uri Elkayam, Professor of Medicine and OB Gyn at the University of Southern California. In this pearl-packed episode, we discuss the diagnosis, acute management, and long-term considerations of valvular heart disease in pregnancy. Through a series of cases, we review the physiologic changes in pregnancy that make certain valvular lesions well-tolerated, while others are associated with a much higher risk of peripartum complications. We also discuss which patients to consider referring for valvular intervention, the ideal timing, and which valvular interventions are safest in the peripartum period. We promise, you won’t want to miss this clinically high-yield episode with Dr. Elkayam, the father of cardio-obstetrics and an absolute legend in the field! Audio editing by CardioNerds Academy Intern, Adriana Mares. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Most women with severe valvular heart disease can be managed medically throughout pregnancy.Right sided valvular lesions are generally better tolerated than left-sides lesions, and regurgitant lesions are generally better tolerated than stenotic lesions. However, the context and etiology of the valve dysfunction must be taken into consideration. Severe tricuspid valve regurgitation, for example, can be associated with a failing right ventricle and undiagnosed pulmonary hypertension. Changes in BNP, severity of symptoms, and right ventricular systolic pressure (RVSP) assessed by echocardiography can be helpful in differentiating normal pregnancy-related symptoms from symptoms due to hemodynamically significant valvular lesions.Valvular interventions during pregnancy are safe when well-planned and performed by experienced operators, and they can significantly improve morbidity and mortality in women who remain symptomatic despite medical management.A multidisciplinary team-based approach is important when managing patients with valvular heart disease during pregnancy. Quatables “We do not need to perform prophylactic valvular intervention in women prior to pregnancy if they do not meet criteria for intervention otherwise. A patient with regurgitant lesion will tolerate pregnancy well, provided that they are not                candidates for surgery already.” “Valvuloplasty during pregnancy is a great and effective procedure, but restenosis occurs. For women who desire future pregnancies, preconception evaluation is important to determine if valve intervention is indicated prior to conceiving.” Show notes What is the epidemiology of valvular heart disease in pregnancy?Cardiovascular conditions affect up to 4% of pregnancies, with valvular heart disease being the most common cardiac pathology encountered during pregnancy worldwide.In the developing world, rheumatic valve disease is still the most common etiology, with mitral valve most commonly affected, followed by the aortic valve.In the developed world, congenital aortic valve pathology is most common. What are the hemodynamic effects of stenotic vs. regurgitant lesions during pregnancy?In normal pregnancy, there is a significant drop in systemic vascular resistance as early as 5 weeks gestational age. This drop leads to a transient decrease in perfusion to the kidneys, causing an increase in fluid retention and expansion of plasma volume. At the same time, there is an increase in heart rate which becomes more pronounced la...

CardioNerds (Amit Goyal and Daniel Ambinder), join CardioNerds FIT Ambassador, Dr. Pablo Sanchez, and his co-fellows, Dr. Jimmy Tooley and Dr. Maggie Ning from Stanford University for an important case discussion about an An otherwise healthy young adult presented with fatigue and was found to be in complete heart block due to sarcoidosis. Dr. Ronald Witteles, (Stanford University Program Director for the Stanford Internal Medicine residency program and advanced heart failure specialist who's particular expertise focuses in the treatment of amyloidosis, sarcoidosis, and cardio-oncology) provides the E-CPR for this episode.  Claim free CME just for enjoying this episode!  Disclosures: Dr. Witteles reports that he has served as an advisor for Pfizer, Alnylam, Eidos, Regerenon Pharmaceuticals, Janssen, and IonisJump to: Patient summary - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary - Notes - Complete Heart Block due to Sarcoidosis An otherwise healthy young adult presented with fatigue and was found to be in complete heart block. Imaging studies were suspicious for cardiac and pulmonary sarcoidosis. Sarcoidosis was confirmed on biopsy. Given the high risk of future cardiac events our patient underwent a dual chamber ICD implantation. He was started on prednisone and methotrexate for immunosuppression. Case Media - Click to enlarge Episode Teaching - Notes - Complete Heart Block due to Sarcoidosis Pearls - Complete Notes - Complete Heart Block due to Sarcoidosis Cardiac sarcoidosis is a disease characterized by noncaseating granulomas involving the heart that can exist alone or together with other organ system involvementDepending on the sites of cardiac involvement it can present as conduction system disease, ventricular arrhythmia, or heart failureCardiac sarcoidosis should be considered in patients with history of sarcoidosis involving other organ systems who develop left ventricular dysfunction, wall motion abnormalities, or arrhythmiasCardiac sarcoidosis should be considered in patients who present with otherwise unexplained heart block or ventricular tachycardia (VT) It is generally recommended that patients with cardiac sarcoidosis with an indication for pacemaker receive an ICD at time of implantation regardless of history of VT Notes - Complete Heart Block due to Sarcoidosis 1. What is Sarcoidosis? Sarcoidosis is a rare disorder of inflammation characterized by the formation of noncaseating granulomas in affected tissues. It most commonly involves the pulmonary system, but other organ systems can be involved including the heart. Sarcoidosis typically affects young adults, and its etiology is still uncertain. 2. What is Cardiac Sarcoidosis and how is it diagnosed? Cardiac sarcoidosis (CS) can occur alone or with systemic disease and depending on the cardiac sites of involvement, can present as conduction system disease, ventricular arrhythmia, heart failure, or sudden cardiac death. 3. How is Cardiac Sarcoidosis diagnosed? Diagnosis of CS is challenging as the gold standard is endomyocardial biopsy (EMB), though sensitivity of EMB is low given the often-patchy tissue involvement. Societal guidelines on the diagnosis of CS require either a positive EMB or biopsy-confirmed extracardiac sarcoidosis with evidence of secondary criteria to suggest cardiac involvement - unexplained VT, high grade AV block, third degree AV block, LVEF <40%, or characteristic imaging finding on cardiac MRI and cardiac PET. The diagnosis of CS must be considered in all patients with a diagnosis of extra cardiac sarcoidosis who develop symptoms to suggest cardiac involvement. Additionally, screening for CS should be done in all patients <60 years of a...

CardioNerds Dan Ambinder, Dr. Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), and episode lead, Dr. Teodora Donisan (CardioNerds Academy fellow and incoming Chief fellow and Beaumont Health Internal Medicine resident) join Dr. Matthew Budoff (professor of medicine at David Geffen School of Medicine at UCLA and the Endowed Chair of Preventive Cardiology at Harbor-UCLA Medical Center) for a discussion about triglycerides from pathophysiology to clinical outcomes. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Triglyceride (TG) metabolism can produce a by-product called remnant lipoproteins, which can be atherogenic. Most guidelines consider hypertriglyceridemia to start at values ≥ 150 mg/dl. It is the most common dyslipidemia, as it can occur in 30% of the general population. Although fasting levels are usually obtained per the current US protocol, there is evidence that non-fasting TG levels might be a better indicator of cardiovascular (CV) risk as these levels may better reflect the usual levels that the body is exposed to. There are multiple primary (genetic) causes of elevated TG, but these are rarer than lifestyle factors, medical conditions, or medications. Genetic association studies are helping better define the level of CV risk stemming from elevated TG-levels, which will impact how we target lifestyle and treatment interventions in the future. #CardsJC STRENGTH Trial Journal Club Relevant disclosures: Dr. Matthew Budoff has funding from General Electric. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Triglycerides - Pathophysiology to Clinical Outcomes In the process of metabolizing TG, remnant lipoproteins are formed, which have been shown to promote atherogenesis. TG themselves have not been directly linked to this process and have not been studied in large population studies, and so are considered risk enhancing factors, and not risk factors per se. Elevated triglyceride levels measured on our traditional lipid panels act as a proxy for the Apo-B rich lipoproteins, such as VLDL, which directly cause atherogenesis.Hypertriglyceridemia is defined as TG values of ≥150 mg/dl, although there is emerging evidence that even high-normal values (100-140 mg/dl) can still be associated with increased CV risk. You can think of TG in a similar fashion to glucose values (patients with prediabetes are still at higher CV risk than those with normal glycemic level). These are continuous and not binary variables!Fasting lipid levels are not necessarily a better predictor of CV events than non-fasting lipid levels. A non-fasting TG level can potentially provide information on the body’s metabolism similarly to how we interpret glucose tolerance tests, although there isn’t such a standardized approach in the lipid world yet.Before testing for genetic causes, make sure you review secondary causes of elevated TG. Don’t forget to evaluate for lifestyle factors and medical causes (diabetes, alcohol abuse, hypothyroidism, pregnancy) and to review the medication list (pay attention to thiazides, non-selective beta blockers, antipsychotics and others).TG values of ≥ 175 mg/dl are considered a risk enhancing factor and can aid in the decision to be more aggressive with lifestyle changes or starting treatment.Although treatment will be reviewed in depth in future episodes, Dr. Budoff suggests we “back away from using fibrates for CV event protection.” Even though they are efficient at lowering TG levels,

CardioNerds (Amit Goyal and Josh Saef) join ACHD fellow Dr. Prashanth Venkatesh and ACHD program director Dr. Jeannette Lin, both from the University of California, Los Angeles, for a deep dive into the complex disease entity that is Ebstein anomaly. They discuss the anatomic features of the dysplastic tricuspid valve as well as the right ventricle in patients with Ebstein anomaly, and how these structural features affect cardiovascular physiology and clinical presentation. This is followed by an in-depth discussion into associated entities including arrhythmias and atrial-level shunts as well as the appropriate multimodality evaluation. Finally, they tackle the difficult question of when and how to intervene, delving into the various interventional treatments and exploring their outcomes using illustrative case-based examples. Audio editing CardioNerds Academy Intern, Pace Wetstein. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Ebstein anomaly is characterized by an inherent myopathy which is often more clinically consequential than the more obvious tricuspid valvulopathy. This can affect not only the right ventricle due to ‘atrialization’ and severe tricuspid regurgitation (TR) but also the left ventricle that is often small due to chronic preload deprivation from reduced RV outflow (no flow, no grow)!Diagnosing severe TR on echocardiography in patients with Ebstein anomaly is challenging, due to the frequent absence of a clearly defined vena contracta and lack of hepatic vein systolic flow reversal. Be on the lookout for severe low gradient TR, which may manifest as a triangular doppler signal rather than the normal parabolic profile.If an electrocardiogram of a patient with Ebstein anomaly suggests prior inferior myocardial infarction, be very suspicious for a right-sided accessory pathway! These are seen in nearly a third of patients with Ebstein anomaly, and manifest as negative delta waves in the inferior leads, leading to a pseudo-infarct pattern. NOTE: infarction, aberrancy, and ventricular hypertrophy should not be coded in the presence of an accessory pathway (i.e., WPW pattern).Patients with Ebstein anomaly who are planned for tricuspid valve replacement should undergo an electrophysiology study preoperatively, since the cavo-tricuspid isthmus responsible for atrial flutter that plagues a large number (>20%) of these patients will be covered by a tricuspid prosthetic valve ring and be inaccessible for future catheter ablation.Certain patients with Ebstein anomaly with significant baseline RV dysfunction who require tricuspid valve surgery may benefit from a concomitant Glenn shunt, which is a surgical anastomosis of the superior vena cava to the right pulmonary artery. This relieves the dysfunctional RV of a third of its baseline preload, potentially enabling it to recover effectively from the stress of cardiopulmonary bypass. Show notes 1.

CardioNerds, Amit Goyal and Daniel Ambinder, join Duke University CardioNerds Ambassador and Correspondent, Dr. Kelly Arps for the diuretic showdown of a lifetime. Join us for this Cardiology vs. Nephrology discussion and respective approach to volume overload and diuretic strategies with Dr. Michael Felker (Professor of Medicine with tenure in the Division of Cardiology at Duke University School of Medicine), and Dr. Matt Sparks (Founding member of the Nephrology Social Medial Collective and #NephJC and Associate Professor of Medicine and Program Director for the Nephrology Fellowship Program at Duke University School of Medicine). Episode introduction, audio editing and Approach to Diuretic Resistance infographic by Dr. Gurleen Kaur (Director of the CardioNerds Internship). Volume overload is a common indication for hospitalization in patients with heart failure. Loop diuretics are first line therapy for volume overload in heart failure, with assessment for adequate response within 3-6 hours after administration. Elevation in creatinine is common with venous congestion as well as during decongestion. While other causes of renal injury should be considered, an elevated creatinine in this context should not automatically trigger avoidance or cessation of diuresis. Diuretic resistance is an exaggerated form of natural safety mechanisms in the face of diuresis. Strategies for addressing diuretic resistance include optimizing dose and frequency of loop diuretic administration, adding adjunctive medication for sequential nephron blockade (i.e., thiazide diuretic, potassium sparing diuretic, acetazolamide, tolvaptan, SGLT2 inhibitor), and, in refractory cases, hemodialysis with ultrafiltration. In the outpatient setting, transition to a more potent loop diuretic (i.e., torsemide or bumetanide from furosemide), addition of a mineralocorticoid antagonist, or intermittent dosing of thiazide diuretic may augment maintenance diuretic therapy for patients with diminished response to loop diuretics.  Check out the CardioNerds Failure Heart Success Series Page for more heart success episodes and content! Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! The CardioNerds Heart Success Series is developed in collaboration with the Heart Failure Society of America. The Heart Failure Society of America is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org. Pearls - Cardiology vs Nephrology: A Diuretic Showdown Elevation in creatinine is expected in both congested states and during diuresis. Do not avoid or stop diuresis in a patient who is clearly volume overloaded based on an elevated creatinine. There may be a role for right heart catheterization if the fluid and/or hemodynamic status is unclear. Alkalosis in the setting of loop diuretic administration and diuretic resistance may represent a natural response to loop diuretics and not volume depletion. Ensure adequate potassium repletion and try using a mineralocorticoid antagonist to correct this alkalosis. Acetazolamide is rarely necessary but may be of use.Currently available evidence does not support extreme fluid or salt restriction in hospitalized patients with volume overload. Consider permissive restrictions and focus on choosing appropriate diuretic dosing for each individual patient. Diuretic resistance is an exaggerated form of diuretic braking, the kidney’s natural response to prevent dangerous degrees of sodium loss from the NKCC2-blocking effects of loop...

CardioNerds (Amit Goyal and Daniel Ambinder), join Dr. Anjali Wagle (Internal medicine resident, Johns Hopkins Hospital) and Dr. Nick Smith (Cardiology fellow, Johns Hopkins Hospital) for an important discussion involving a patient with non-ischemic dilated cardiomyopathy and biventricular heart failure who had developed diuretic resistance. They discuss the role for invasive hemodynamic assessment of volume overload, initial strategies in managing a patient with volume overload, the role of guideline directed therapy in the management of patients with recurrent volume overload, and advanced strategies for diuretic resistance. Dr. Nisha Gilotra (Director of the Cardiac Sarcoidosis Program and assistant professor of medicine, Johns Hopkins Hospital) provides the E-CPR for this episode. Audio editing and Approach to Diuretic Resistance infographic by Dr. Gurleen Kaur (Director of the CardioNerds Internship). This episode is made possible with support from Panacea Financial. Panacea Financial is a national digital bank built for doctors by doctors. Visit panaceafinancial.com today to open your free account and join the growing community of physicians nationwide who expect more from their bank. Panacea Financial is a division of Primis, member FDIC. Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Patient summary - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary - Diuretic Resistance A young woman in her 20s with non-ischemic dilated cardiomyopathy and NYHA class IV ACC stage D biventricular heart failure with an LV ejection fraction of 30-35% on palliative inotropic therapy complicated by cardiogenic cirrhosis and stage IIIb chronic kidney disease presented with acute decompensated heart failure with volume overload. During her hospitalization she exhibited profound signs of diuretic resistance with minimal improvement after increasing inotropes, increasing IV loop diuretics, adding IV thiazides, and trialing continuous IV furosemide. She was given high dose mineralocorticoids, IV acetazolamide, and hypertonic saline paired with IV furosemide and had a durable treatment response. Episode Teaching - Diuretic Resistance Pearls - Diuretic Resistance Diuretic resistance is a complex clinical problem defined as inadequate natriuresis despite an adequate diuretic regimen. However, the practitioner cannot overlook low output heart failure and/or insufficient renal perfusion as the causes for inadequate diuretic response. In cases of inadequate urine output due to low cardiac output, increased inotropic or mechanical support would be the first objective.Confirming adequate cardiac output to support renal perfusion and/or confirming high filling pressures may require invasive hemodynamic assessment.Sodium avidity is most effectively blunted by treating the patient with maximally tolerated guideline directed therapy. This includes but is not limited to a backbone of ARNI (or ACE or ARB), mineralocorticoid receptor antagonists, beta-blockers, and SGLT-2 inhibitors.In cases of advanced diuretic resistance, hypertonic saline paired with high dose IV furosemide can be an effective strategy.In cases of diuretic resistance combined with cirrhosis and heart failure there is a synergistic hyperaldosteronism that can be targeted with higher doses of mineralocorticoid receptors as is seen in the treatment of cirrhosis with ascites. Notes - Diuretic Resistance 1. What is the role for invasive hemodynamic assessment in acute decompensated heart failure? Cases where intracardiac filling pressures are in question: right heart catheterization (RHC) can give insight into the presence and degree of right versus left sided filling pressures.

CardioNerds (Amit Goyal and Daniel Ambinder), Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, episode lead fellow, Dr. Kaitlyn Ibrahim (Temple University now practicing with Lankenau Heart Group), join Dr. Afshan Hameed (Maternal-Fetal Medicine, Obstetrics & Gynecology, UC Irvine), Dr. Paul Forfia (Co-Director, Pulmonary Hypertension, Right Heart Failure & CTEPH Program, Temple University Hospital), and Dr. Marie-Louise Meng (Obstetric and Cardiothoracic Anesthesiology, Duke University) to discuss pregnancy and multidisciplinary critical care. Three experts from varied subspecialties including Cardiology, Pulmonary Hypertension, Maternal Fetal Medicine, Cardiac Anesthesia and Obstetrical Anesthesia guide listeners through a case of a patient with a congenital conotruncal ventricular septal defect, Eisenmenger physiology, and pulmonary hypertension who becomes pregnant. The discussion touches on pre-conception risk assessment, pulmonary hypertension medical therapy in pregnancy, maternal monitoring during pregnancy, development of detailed multidisciplinary delivery plans and accessibility of such plans, and peri- and post-partum multidisciplinary management of high-risk patients. Audio editing and episode introduction by CardioNerds Academy Intern, Christian Faaborg-Andersen. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Cyanotic congenital heart disease presents multiple risks to the fetus, the most significant being intrauterine growth restriction. In a patient with Eisenmenger physiology, maternal oxygenation should be monitored closely throughout pregnancy, as hypoxia is often a marker of increased right to left shunting in these patients.In patients with pulmonary hypertension, the RV-PA coupling relationship is the best indicator of maternal cardiovascular reserve through the pregnancy and post-partum period. The goal of therapy is to get the pulmonary vascular resistance down to a point where the right heart can adapt to that load and function either at a normal or a near-normal level.When a high-risk patient meets with Anesthesia, it is important to consider the A’s: 1. Airway (anticipating any potential difficulties); 2. Access (whether this may present a challenge at the time of delivery); 3. Anxiety (specifically differentiating true hemodynamic changes in high-risk patients versus physiologic changes from anxiety); 4. Anticoagulation (knowledge of what agent the patient is on to determine safety of neuraxial anesthesia); 5. Availability (determining who else needs to be in the room, i.e. CT surgery, cardiothoracic anesthesia, ECMO team); 6. Arena (where is the safest place for this patient to deliver).In patients with a shunt who undergo a Cesarean section, the uterus should not be exteriorized due to risk of venous micro air emboli.As Dr. Forfia says, “panic is more dangerous sometimes than pulmonary hypertension!” Meaning, it is important to meet as a multidisciplinary team to develop a clear, easily accessible delivery plan for the patient. It is also prudent to have “everyone functioning in the environment they function best” like delivering the baby on the labor and delivery floor where all the necessary equipment and team members are available and bringing in other experts if needed rather than a cardiac operating room. For a deep dive into Pregnancy & Pulmonary Hypertension, enjoy: Episode #124 with Dr. Candice Silversides.Episode #144 – Case Report: A Mother with Shortness of Breath Show notes 1. How does a multidisciplinary team play a role in the care for a high risk cardio-obstetrics patient, particularly one with congenital heart disease and pulmonary...

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 6 Dr. Packer reflects on a conversation he had with Dr. Eugene Braunwald about mentorship and its role in immortality. This episode is particularly meaningful to the CardioNerds team as mentorship and sponsorship is such an important part of the CardioNerds mission. Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.