Episodes Archives - Cardionerds

Approximately 350,000 adults per year in the US experienced out-of-hospital cardiac arrest (OHCA). Only about 10% of such patients survive their initial hospitalization. The key drivers of successful resuscitation from OHCA are bystander cardiopulmonary resuscitation (CPR) and public use of an automated external defibrillator (AED). Survival rates from OHCA vary dramatically between US regions. For instance, the extracorporeal CPR (eCPR) program at the University of Minnesota has over a 40% survival rate in patients with OHCA and refractory ventricular fibrillation (VF) based on data published in the ARREST trial. In this episode, we are joined by experts from the University of Minnesota, including Dr. Jason Bartos (Interventional and Critical Care Faculty) and Dr. Julie Power (Chief Fellow at University of Minnesota and CardioNerds Academy Fellow), along with Dr. Yoav Karpenshif (Co-Chair Critical Care Series, University of Pennsylvania) and CardioNerds Co-Founders (Amit Goyal and Dan Ambinder) to discuss cardiac arrest, E-CPR, & post-arrest care. This includes targeted temperature management, coronary angiography and revascularization, as well as the growing field of eCPR and VA ECMO.  Episode introduction by CardioNerds Clinical Trialist Dr. Jason Feinman. Audio editing by CardioNerds Academy Intern, Shivani Reddy.

The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif.

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eCPR- extracorporeal cardiopulmonary resuscitation

VA ECMO- veno-arterial extracorporeal membrane oxygenation

VT/VF- ventricular tachycardia/ventricular fibrillation

ACLS- advanced cardiovascular life support

ROSC- return of spontaneous circulation-

OHCA- out-of-hospital cardiac arrest

IHCA- in-hospital cardiac arrest

TTM- targeted temperature management

1. The ARREST trial showed early VA ECMO-facilitated resuscitation for patients with OHCA and refractory VF significantly improved survival to hospital discharge when compared to standard ACLS treatment.
2. Coronary artery disease is common in the setting of cardiac arrest, with up to 96% of patients with STEMI on post resuscitation EKG and up to 85% of refractory out-of-hospital VT/VF arrests.
3. Guidelines recommend emergent coronary angiography for patients with ST-segment elevation on the post-ROSC ECG.
   1. The role of timing of revascularization after ROSC in patients without STEMI or shock is unknown.
   2. The role of coronary angiography in cardiac arrest with nonshockable rhythms is also unclear.
4. The current AHA guidelines recommend initiation of targeted temperature management between 32°C and 36°C for at least 24 hours for all patients who do not follow commands after ROSC in both OHCA and IHCA.

1. What are early post arrest management considerations?

• The key drivers of successful resuscitations from OHCA: CPR and public use of AEDs in the field. After initial stabilization, care of the critically ill post-arrest patient hinges on hemodynamic support, mechanical ventilation, temperature management, attending to adverse sequelae of arrest, and diagnosis and treatment of underlying causes of arrest.
• Coronary artery disease is common in the setting of VT/VF cardiac arrest, with up to 96% of patients with STEMI on post resuscitation EKG and up to 85% of refractory out-of-hospital VT/VF arrests.
• In the early post-arrest state, it is also important to diagnose and treat infections and any neurologic injury. Neurologic compromise is a common cause of mortality in patients who achieve ROSC. Over 50%, and in some cohorts around 75%, of patients with death after resuscitated OHCA die of neurologic injury.

2. What is the current evidence for targeted temperature management (TTM)?

• “[This is] the most hotly debated topic right now in the field of cardiac arrest.” – Dr. Jason Bartos
• Current AHA guidelines recommend initiation of targeted temperature management between 32°C and 36°C for at least 24 hours for all patients who do not follow commands after ROSC in both OHCA and IHCA. TTM is a relatively safe and effective strategy that can improve neurological outcomes in patients who remain comatose after achieving ROSC from cardiac arrest. Current evidence supports a broad range of TTM from 33°C to 36°C and should be maintained for 24 hours. Although TTM should be initiated as early as possible, prehospital initiation of cooling has not been shown to improve survival outcomes.
• The TTM2 trial showed that in patient with coma following OHCA, targeted hypothermia versus normothermia (i.e., fever control) was not associated with improved survival or functional outcomes compared to normothermia. It should be noted that patients on VA ECMO were not included in this trial.

3. What are some possible complications from TTM?

• Arrhythmias: Hypothermia slows cardiac conduction leading to bradycardia and QT prolongation which can exacerbate underlying arrhythmias such as VT/VF. Consideration can be given to actively rewarming the patient in the setting of VT/VF.
• Clotting: Core temperatures below 35°C impede the clotting cascade and platelet function. Because of this, if a patient develops significant non-compressible bleeding while undergoing TTM, consideration should be given to actively rewarm the patient.
• Shivering is a natural response to hypothermia. Suppression of this is crucial for TTM. First line strategies include propofol, fentanyl, or midazolam. Dexmedetomidine is effective, but side effects of bradycardia can limit its use. Buspirone (a 5-HT agonist), when used in conjunction with opiate analgesia or dexmedetomidine, has been shown to lower the shivering threshold. Neuromuscular blocking agents are highly effective at preventing shivering but confound the neurologic examination and may mask seizures. Patients need to be deeply sedated (typically RASS –4 or lower) and be followed with train-of-four assessments.
• Diuresis increases with hypothermia potentially leading to electrolyte loss of potassium, magnesium and phosphorous. Therefore, electrolytes need to be frequently monitored. Interestingly, total body potassium may not actually be low due to cellular shifts; thus, conservative replacement is recommended.
• Insulin resistance can develop as well.

4. How do we select appropriate patients to pursue revascularization and consider the timing of revascularization in patients with recent cardiac arrest?

• Guidelines recommend emergent coronary angiography for patients with ST-segment elevation on the post-ROSC ECG.
• However, the role and timing of revascularization after ROSC in patients without STEMI or shock is unknown.
• The role of coronary angiography in cardiac arrest with non-shockable rhythms is also unknown.

5. What is the physiologic basis for eCPR?

• The biggest predictor of post-arrest outcome is time.
• In the ALPS trial (2016), patients who underwent zero to nine minutes of CPR with ROSC had a survival of 65%. Survival dropped by 17% for every extra 10 minutes of CPR, such that there were no survivors in the amiodarone arm of the trial after 40 minutes.
• The results of this study were replicated at the University of Minnesota: OHCA brought to University of Minnesota Cath lab within 30 minutes of their cardiac arrest had a >90% survival rate. Survival rate drops over elapsed time: for every additional 10 minutes of ACLS, there is 25% additional mortality. If VA ECMO is initiated >90 minutes after arrest, survival is poor (10-15%). The study showed eCPR was associated with improved neurologically favorable survival at all CPR durations <60 minutes, despite severe progressive metabolic derangement. However, CPR duration remains a critical determinate of survival.

6. What is the evidence base for eCPR?

• The ARREST trial (the 1st RCT of eCPR) showed that early VA ECMO-facilitated resuscitation for patients with OHCA and refractory VF significantly improved survival to hospital discharge when compared to standard ACLS treatment.
• The trial comprised of 30 OHCA patients in refractory VT/VF (failed 3 shocks in the field) and ongoing CPR randomized to usual ACLS vs VA ECMO placement in the cath lab with subsequent coronary angiogram.
• The plan was to enroll 77 patients in the trial; however, after the 1st analysis, the trial was stopped early due to reaching pre-specified benefit endpoint. There was a large improvement in the primary outcome of survival to hospital discharge (43% versus 7%). Survival to 3 and 6 months was also better in the VA ECMO CPR group (43% vs 0%, p=0.006).
• The ARREST trial showed that early VA ECMO-facilitated resuscitation for patients with OHCA and refractory VF significantly improved survival to hospital discharge when compared to standard ACLS treatment.
• Based on this evidence, we know the likelihood of ROSC in the field drops significantly after 20-25 minutes. Thus, if the patient receives >3 shocks or >15-20 min of ongoing CPR without recovery of a perfusing rhythm, VA ECMO should be considered.

1. Bartos JA, Grunau B, Carlson C, et al. Improved Survival With Extracorporeal Cardiopulmonary Resuscitation Despite Progressive Metabolic Derangement Associated With Prolonged Resuscitation. Circulation. 2020 Mar 17;141(11):877-886.
2. Garcia S, Drexel T, Bekwelem W, et al.. Early access to the cardiac catheterization laboratory for patients resuscitated from cardiac arrest due to a shockable rhythm: the Minnesota Resuscitation Consortium Twin Cities Unified Protocol.
3. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346(8):549-556. doi:10.1056/NEJMoa012689
4. Inoue A, Hifumi T, Sakamoto T, Kuroda Y. Extracorporeal Cardiopulmonary Resuscitation for Out-of-Hospital Cardiac Arrest in Adult Patients. J Am Heart Assoc. 2020;9(7):e015291.
5. Kudenchuk PJ, Leroux BG, Daya M, et al. Antiarrhythmic Drugs for Nonshockable-Turned-Shockable Out-of-Hospital Cardiac Arrest: The ALPS Study (Amiodarone, Lidocaine, or Placebo). Circulation. 2017 Nov 28;136(22):2119-2131.
6. Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. N Engl J Med. 2019;380(15):1397-1407.
7. Panchal AR, Bartos JA, Cabañas JG, et al. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142(16 2):S366-S468.
8. Sonnier, M, Rittenberger, JC. State-of-the-art considerations in post-arrest care. JACEP Open 2020; 1: 107-116.
9. Yannopoulos D, Bartos J, Raveendran G, et al. Advanced reperfusion strategies for patients with out-of-hospital cardiac arrest and refractory ventricular fibrillation (ARREST): a phase 2, single centre, open-label, randomised controlled trial. Lancet 2020;396(10265):1807-1816.
10. Yannopoulos D, Bartos JA, Aufderheide TP, et al. American Heart Association Emergency Cardiovascular Care Committee. The Evolving Role of the Cardiac Catheterization Laboratory in the Management of Patients With Out-of-Hospital Cardiac Arrest: A Scientific Statement From the American Heart Association.Circulation. 2019; 139:e530–e552.

Dr. Jason Bartos was born and raised in Maple Plain, MN. He completed his undergraduate work in Chemistry and Psychology at St. John’s University and went on to earn his PhD in Pharmacology from the University of Iowa. He then moved to Stanford University School of Medicine where he earned his MD and completed Internal Medicine residency. He moved to the University of Minnesota in 2012 where he completed fellowships in Cardiovascular Medicine, Critical Care Cardiology, and Interventional Cardiology.

Dr. Bartos is board-certified in internal medicine, cardiology, critical care medicine, and interventional cardiology. His clinical interests include cardiac critical care, resuscitation, advanced hemodynamic support, pulmonary embolus, and coronary artery disease and intervention. He is the Medical Director of the Cardiovascular Intensive Care Unit.

Dr. Bartos’s research interests include resuscitation, advanced hemodynamic support, and recovery from cardiac arrest. He has performed research in the field of ischemia and reperfusion injury for 20 years describing the molecular pathways of injury in models of cerebral ischemia and investigating potential therapies to mitigate the effects of reperfusion injury in heart transplantation, myocardial infarction, and refractory cardiac arrest. Dr. Bartos is the Associate Medical Director of the Center for Resuscitation Medicine at the University of Minnesota and the President of the Minnesota Mobile Resuscitation Consortium where he works to improve survival for patients suffering cardiac arrest. This work has resulted in the development of protocols utilizing rapid transport from the field, peripherally placed veno-arterial ECMO, coronary reperfusion, and subsequent cardiac intensive care to improve outcomes for patients with refractory VT/VF cardiac arrest.

Dr. Julie Power @JuliettePower44 is a cheif cardiology fellow at the University of Minnesota. She completed medical school at Drexel University in Philadelphia followed by residency training at Allegheny General Hospital in Pittsburgh where she also served a Chief Resident. In addition to a continued involvement in medical education, Julie plans to pursue additional training in interventional cardiology after her general cardiology fellowship. In her free time, she enjoys spending time with family and friends, including exploring Minnesota with her boyfriend, Steve.

CardioNerd (Amit Goyal), Dr. Zarina Sharalaya (Interventional cardiology fellow at the Cleveland Clinic), Dr. Ashley Mohadjer (Interventional cardiology fellow, Vanderbuilt Heart and Vascular Institute), and Dr. Laurie Mbuntum (Cardiology fellow, UTSW) join Dr. Ki Park (Associate professor of medicine and an interventional cardiologist at the University of Florida and Malcom Randall VA Medical Center in Gainesville, FL.) for a a well-rounded discussion on all things ‘Women-in-Cardiology’ #WIC . Dr. Ki Park discusses how she nurtured her interest in interventional cardiology, and further shares her thoughts and passion for cardio-obsetrics. She shares her advice for trainees thinking about interventional or cardioobetrics and anecdotes from her training as a successful woman in the field. We discuss the need for education on pregnancy outcomes and long-term cardiovascular risk, ideas to lower maternal mortality, how to start a women’s cardiovascular clinic, and her thoughts on how the field may look in the future. Special message by Florida ACC State Chapter Governor, Dr. David Perloff. Episode introduction and audio editing by CardioNerds Academy Intern, Shivani Reddy.

The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza.

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1/ Episode #176: @PaChapterACC & @CardioNerds Narratives in Cardiology featured @LMbuntum, @AMohadjer, and @ZarinaSharalaya in discussion with Dr. Park (@cardioPCImom)

Follow this #CardsNarratives🧵on the discussion on #CardioObstetrics pic.twitter.com/xpeHwVwz37

“I like the work life integration as opposed to work life balance. Balance just implies that you always have everything aligned perfectly at all times and that is just not doable.”

Why is screening for OB-GYN history for cardiovascular risk is important, and who should be responsible?

• Pregnancy is nature’s stress test and in some women can unmask someone’s predisposition to cardiac disease
• Yearly screening for diabetes, hypertension, dyslipidemia
• Big interdisciplinary effort in attempt to try to capture all women at risk, as many will not present with manifestation of disease initially

How did you nurture your interest in cardioobsetrics? In interventional cardiology?

• Meetings and societies
• Connect with those who work in the field, social media
• Regarding interventional cardiology – having interest in procedures, do as many cases “hands on” as possible, learning from mistakes

What advise do you have to achieve work and life balance?

• It’s important to understand the various occupational hazards of radiation exposure which include but are not limited to brain tumors, cataracts, thyroid disease, cardiovascular diseases, musculosketal problems and reproductive side effects.

• Have grace, one can’t be 100% at every single thing all the time
• Its more work life integration as opposed to a balance
• Prioritize different things on different days, be honest with children and explain why you do what you do in age appropriate terms

Maternal mortality is high in this country with cardiovascular disease as a leading cause. What are important factors to improve maternal mortality?

• Education
• Improving access to care in the peripartum stage for mothers, particularly since the focus in that period is on baby
• Legislature to improve insurance coverage        

Where do you see cardioobsetrics field going in the next few years?

• Make the knowledge more mainstream
• Education of subspecialty fellows within cardiovascular education
• Collaboration with ACOG and maternal fetal medicine societies
• More registries of patients to continue to learn more about these women

What was involved to create the women’s heart clinic in your institution?

• Start small – there are plenty of women who want to seek specialized care
• Having an MFM and congenital faculty at the same institution was helpful
• Seek advice from those at expert centers          

What advise do you have for trainees looking to pursue a career in interventional cardiology who are worried about work-life integration?

• Understand what you’re getting into, particularly for that year   
• Don’t be afraid to ask for help from friends or family at home to allow for more quality time with significant others, kids, friends, etc — this isn’t a sign of weakness
• You don’t have to be perfect

Physicians have been found to delay childbearing compared to peers in other professions. What are your thoughts on this?

• Progress has been made and overall there is increased awareness and support
• Leave for trainees should be more flexible         
• More societal and institutional support

CardioNerds (Amit Goyal and Daniel Ambinder), ACHD series co-chair Dr. Daniel Clark (Vanderbilt University), and ACHD FIT lead Dr. Danielle Massarella (Toronto University Health Network) join ACHD expert Dr. Yuli Kim (Associated Professor of Medicine & Pediatrics at the University of Pennsylvania), to discuss single ventricular heart disease and Fontan palliation. They cover the varied anatomical conditions that can require 3-step surgical palliation culminating in the Fontan circulation, which is characterized by passive pulmonary blood flow, high venous pressures, and low cardiac output. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship and CardioNerds Academy Fellow). 

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

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1. There are various forms of unpalliated ‘single ventricle’ congenital heart disease. The three main hemodynamic issues that need to be addressed in any form are unbalanced flow, pulmonary over-circulation, and blood mixing. 

1. The Fontan palliation is a series of operations for congenital heart disease patients in whom biventricular repair is not feasible. 

1. In the completed Fontan circulation, systemic venous blood is surgically routed directly to the lungs, effectively bypassing the heart, and creating passive pulmonary blood flow. 

1. The hallmarks of the Fontan circulation (and Fontan failure) are elevated central venous pressure and low cardiac output. 

1. Patients with Fontan circulation may experience significant morbidity in the long term from both cardiac and non-cardiac sequelae, and require lifelong specialist care. 

1. Why do some patients require Fontan palliation? 

• Many different types of anatomies may ultimately require single ventricular palliation via the Fontan procedure due to inadequate biventricular function to support both pulmonary and systemic circulations. Some examples include Tricuspid Atresia (hypoplastic RV), Double Inlet Left Ventricle (DILV; hypoplastic RV), Hypoplastic Left Heart Syndrome (HLHS; hypoplastic LV), and atrioventricular septal defects (AVSD; either RV or LV may be inadequate based on “commitment” of the common AV valve). 
• The Fontan procedure was first described in 1971; at this time, mortality of single ventricular patients exceeded 90% in the first year of life. 

2. What are the stages of Fontan palliation? 

• Effective pulmonary blood flow/balancing flow to the pulmonary and systemic circulations: for many conditions, this involves retrograde pulmonary blood flow from a systemic -> PA shunt (i.e. Blalock-Taussig-Thomas “BTT” shunt in which the subclavian artery is turned down and anastomosed to the pulmonary artery). In infants, the pulmonary vascular resistance (PVR) is high perinatally and gradually lowers over the first 3 months of life to adult levels with exposure to the atmosphere’s natural pulmonary vasodilator: oxygen. Thus, in the first 3 months of life babies have an intrinsic PVR that is too high to directly connect the venous system to the lung arteries and thereby require staged surgeries. 
• Protect the pulmonary vasculature from overcirculation: ultimately, the goal of single ventricular palliation is rerouting systemic venous drainage directly to the pulmonary vasculature passively, without a cardiac pumping chamber. This volume unloads the common ventricle and allows it a better chance to function over the lifespan by pumping only to a single circuit: the systemic vascular bed. Thus, steps 2 and 3 of Fontan palliation are passive head/neck venous connection to the pulmonary arteries (now typically accomplished with the modified bidirectional Glenn operation that anastomoses the SVC to the RPA typically) and finally total cavopulmonary connection by the Fontan conduit connecting the lower body’s venous return from the IVC to the Fontan tunnel and up to the RPA. 

3. What is the ultimate “plumbing” of Fontan circulation?

• Venous blood from the head/neck is connected directly from the SVC to the right pulmonary artery (RPA; typically, via a Glenn operation).
• Venous blood from the legs, abdomen/pelvis and lower body is connected directly to the RPA via the Fontan tunnel.
• In sum, the pulmonary blood flow enters passively, without a pump to send venous blood to the lungs.

4. What are the types of Fontan?

• The classic Fontan operation involved a direct venous connection to the right atrium with an atriopulmonary connection to the RPA.
• Contemporary era Fontan operations typically involve the lateral tunnel (LT) or extracardiac conduit. The LT incorporates pericardium in the creation of the Fontan conduit along the surface of the heart, while the extracardiac conduit is entirely prosthetic material (typically GoreTex).

5. What are the common complications of Fontan circulation?

• Cardiac
  • Arrhythmias: both atrial and ventricular arrhythmias can be common, especially owing to surgical scar lines, residual valvular disease, and hemodynamic sequelae of the Fontan palliation
  • Ventricular dysfunction: this may take the form of both systolic and/or diastolic dysfunction
  • Valvular disease: atrioventricular valvular insufficiency, etc.
  • Thromboembolic complications: venous stasis, endothelial damage, and exposure of von Willebrand factor contribute to a risk of thrombosis and risk of paradoxical emboli into the systemic circulation for patients with residual venous-arterial system connections (such as Fontan fenestration/baffle leak)

• Extracardiac
  • Neurocognitive: mental health disorders (including PTSD, depression, and anxiety) are common, as are executive function limitations that can be identified as early as childhood
  • Fontan-associated liver disease (FALD): including risk of developing hepatocellular carcinoma
  • Renal disease: chronic kidney disease/renal venous hypertension
  • Lymphatic: protein-losing enteropathy (PLE) and plastic bronchitis

6. When is it time to refer a patient with Fontan palliation for heart transplantation evaluation?

• This is a very challenging, multidisciplinary decision that must weigh operative risk, HT candidacy, allosensitization, need for multi-organ transplantation (heart-liver, heart-lung, etc.), and patient-centered discussion about their goals of care.
• The team must way high near-term per-transplantation risk with improved long-term outcomes.

1. Cetta F, Dearani J, O’Leary P and Driscoll D.Tricuspid Valve Disorders: Atresia, Dysplasia and Ebstein Anomaly. In: H. Allen, R. Shaddy, D. Penny, T. Feltes and F. Cetta, eds. Moss and Adams’ Heart Disease in Infants, Children and Adolescents Philadelphia: Wolters Kluwer; 2016.

2. Book WM, Gerardin J, Saraf A, Valente AM, Rodriquez III F. Clinical phenotypes of fontan failure: implications for management. Congenit Heart Dis. 2016;11:296–308. https://pubmed.ncbi.nlm.nih.gov/27226033/

3. Rychlik J, Atz AM, Celermajer DS, Deal BJ, Gatzoulis MA, Gewillig MH et al. American Heart Association Council on Cardiovascular Disease in the Young and Council on Cardiovascular and Stroke Nursing. Evaluation and Management of the Child and Adult With Fontan  Circulation: A Scientific Statement From the American Heart Association. Circulation. 2019 Jul 1. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000696

Adult Congenital Heart Association
Founded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers

CHiP Network

The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information.

Heart University
Heart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease. It is a carefully curated open access library of educational material for all providers of care to children and adults with CHD or children with acquired heart disease, whether a trainee or a practicing provider. The site provides free content to a global audience in two broad domains: 1. A comprehensive curriculum of training modules and associated testing for trainees. 2. A curated library of conference and grand rounds recordings for continuing medical education. Learn more at www.heartuniversity.org/

Yuli Y. Kim, MD, is a board-certified cardiologist in the Cardiac Center and Medical Director of the Philadelphia Adult Congenital Heart Center at Children’s Hospital of Philadelphia. She completed medical school at University of Virginia School of Medicine, Internal Medicine residency at Johns Hopkins Hospital, fellowships in Cardiovascular medicine at the Cleveland Clinic, ACHD/Advanced Congenital Imaging at Children’s Hospital in Boston, and completed a post-doctoral fellowship at the NIH.

Dr. Danielle Massarella received her Hons. BSc. in Biology & Psychology from York University. She excelled and was the recipient of the Dean of Clinical Medicine Award at her graduation.  Her experience in gross anatomy class was particularly inspirational, and led her to pursue a specialty in cardiology. Danielle went on to pursue a 3-year residency in pediatrics and fellowship in pediatric cardiology at Case Western Reserve University and at Rainbow Babies and Children’s Hospital in Cleveland.  From there, Danielle went on to pursue advanced subspecialty training in adult congenital heart disease at Toronto’s University Health Network Adult Congenital Cardiac Clinic

CardioNerds (Amit Goyal), Dr. Natalie Stokes (Cardiology Fellow at UPMC and Co-Chair of the Cardionerds Cardio-Ob series), fellow lead Dr. Victoria Thomas (Cardionerds Ambassador, Vanderbilt University Medical Center), join Dr. Rachel Bond (Women’s Heart Health Systems Director at Dignity Health, Arizona) for a cardio-obstetrics discussion about Black maternal health. Episode introduction by CardioNerds Clinical Trialist Dr. Chistabel Nyange. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen.

This episode was developed in collaboration with the Association of Black Cardiologists. ABC is a 501(c)3 nonprofit organization whose mission is to promote the prevention and treatment of cardiovascular disease, including stroke, in Black persons and other minority populations, and to achieve health equity for all through the elimination of disparities. Learn more at https://abcardio.org/.

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CardioNerds Cardio-Obstetrics Series Page
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1. Why does Black Maternal Health need to be deliberately highlighted episode on CardioNerds?

• Black women are three-four times more likely to die during their pregnancy. The deaths are primarily tied to cardiomyopathy and cardiovascular conditions such as coronary artery disease, pulmonary hypertension, chronic hypertension, preeclampsia, and eclampsia.
• 63-68% of this cardiovascular mortality is preventable depending on one’s racial identity.  As CardioNerds, we must educate ourselves on why this occurs and identifying diseases that may place patients at increased risk.
• Studies have shown the Black maternal mortality crisis exist irrespective of one’s education or socioeconomic status.
• We must recognize and admit that some patients are being treated differently because of their race and ethnicity alone.

2.     When we consider or acknowledge a patient’s race, what should CardioNerds think about?

• Race is an important factor to think about, but we must remember that it is an imperfect variable. We should not focus on biology or genetic make-up. We should think about social determinants of health. 60% of the time social and personal aspects dictate one’s health.
• Unconscious biases and structural racism are likely playing a major role in race-based health inequities.

3.     What are other vulnerable groups that have increased mortality rates related to cardioobstetric care?

• Native American women have similar maternal mortality rates to Black populations.
• Women who are veterans, live in rural communities, and/or are currently incarcerated have increased risk of mortality

4.     What are some of the social determinants of health that should be considered for these patients?

• Food deserts or having poor access to nutrient rich/quality foods make these vulnerable patients have increased risk factors for high cholesterol, high blood pressure, obesity, and diabetes which increase the risk for pregnancy complications and infertility.
• The above vulnerable populations can have less access to higher levels of care for high-risk pregnancies.

5.     What are some of the preventable causes of maternal mortality?

• Clinicians should actively listen to their patients’ concerns. There have been several media stories in the news and on CardioNerds episodes where women’s concerns were not acknowledged or taken seriously.
• Preconception counseling is important to provide to all patients. 50% of women have one risk factor for cardiovascular disease when entering pregnancy. We should have discussions with patients regarding their lifestyles, with an emphasis on exercise and diet.

6.     What are some of the psychosocial or health related differences we see in black mothers when compared to other races?

• The effect of stress is affecting not just black mothers but black women in general by predisposing them to increased cardiovascular disease and cognitive impairment. The stress effects on black women are being called superwoman schema.
• Superwoman schema is a combination/phenomenon of gender and racial oppression’s effect on the allostatic load (cumulative biological stress).  Studies have shown that black women’s chronic stress levels affect their sympathetic nervous system with an inability to fight off or perhaps produce too much inflammatory response. This increases the risk of a variety worsening chronic morbidities in particular worsening cardiovascular health.
• One in eight women will struggle with infertility. Black women are two times more likely to suffer from infertility compared to their White counterparts. This is largely due to increased uterine fibroids. Black women are also less likely to be referred to a reproductive endocrinology specialist.

7.     What pre-counseling assessments or work-up should be considered for women trying to conceive?

• Consider getting a baseline ECG as that would give a nice idea of structurally of what is going on within the heart. If there are several risk factors, there can be consideration for a baseline echocardiogram.
• There should be a specific focus on lifestyle. As cardiologists, we should try to have our patients monitor their weight and follow a well-balanced diet with exercise. They should monitor their   blood pressure.
• Also try to have a birthing plan with OBGYN team as there is data to support that a birthing plan can lead to better outcomes for high-risk pregnancy.

8.     What are some of the tools that have been recently used to help reduce black maternal mortality?

• Patients that are likely to have higher pregnancy complications should be considered to follow not only with a maternal fetal medicine doctor, but there should be consideration for extra help with a doula or a midwife if possible.
• We should promote home blood pressure monitoring during pregnancy and post-partum as there have been trials supporting the fact that blood pressure control was more successful using texting/ambulatory monitoring strategies vs office visits alone.
• Digital platforms such as MAHMEE are closing gaps in care to connect patients in their pregnancy and postpartum care to help with all patients but especially underserved populations.

1.     Bond RM, Gaither K, Nasser SA, et al. Working Agenda for Black Mothers: A Position Paper from the Association of Black Cardiologists on Solutions to Improving Black Maternal Health. Circ Cardiovasc Qual Outcomes. 2021;14(2):e007643. doi:10.1161/CIRCOUTCOMES.120.007643

2.     Havranek EP, Mujahid MS, Barr DA, et al. Social Determinants of Risk and Outcomes for Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2015;132(9):873-898. doi:10.1161/CIR.0000000000000228

3.     Chandra A, Copen CE, Stephen EH. Infertility and impaired fecundity in the United States, 1982-2010: data from the National Survey of Family Growth. Natl Health Stat Report. 2013;(67):1-19.

4.     Woods-Giscombé CL. Superwoman schema: African American women’s views on stress, strength, and health. Qual Health Res. 2010;20(5):668-683. doi:10.1177/1049732310361892

5.     Allen AM, Wang Y, Chae DH, et al. Racial discrimination, the superwoman schema, and allostatic load: exploring an integrative stress-coping model among African American women. Ann N Y Acad Sci. 2019;1457(1):104-127. doi:10.1111/nyas.14188

6.     Ofili EO, Schanberg LE, Hutchinson B, et al. The Association of Black Cardiologists (ABC) Cardiovascular Implementation Study (CVIS): A Research Registry Integrating Social Determinants to Support Care for Underserved Patients. Int J Environ Res Public Health. 2019;16(9):1631. Published 2019 May 10. doi:10.3390/ijerph16091631

7.     Lantz PM, Low LK, Varkey S, Watson RL. Doulas as childbirth paraprofessionals: results from a national survey. Womens Health Issues. 2005;15(3):109-116. doi:10.1016/j.whi.2005.01.002

8.     Pregnancy mortality surveillance system. Centers for Disease Control and Prevention. https://www.cdc.gov/reproductivehealth/maternal-mortality/pregnancy-mortality-surveillance-system.htm. Published November 25, 2020. Accessed December 18, 2021.

9.     Cairns AE, Tucker KL, Leeson P, et al. Self-Management of Postnatal Hypertension: The SNAP-HT Trial. Hypertension. 2018;72(2):425-432. doi:10.1161/HYPERTENSIONAHA.118.10911

10.  Hirshberg A, Sammel MD, Srinivas SK. Text message remote monitoring reduced racial disparities in postpartum blood pressure ascertainment. Am J Obstet Gynecol. 2019;221(3):283-285. doi:10.1016/j.ajog.2019.05.011

11.  Vedam S, Stoll K, MacDorman M, et al. Mapping integration of midwives across the United States: Impact on access, equity, and outcomes. PLoS One. 2018;13(2):e0192523. Published 2018 Feb 21. doi:10.1371/journal.pone.0192523

Rachel M Bond, MD, FACC, Women’s Heart Health & Prevention Specialist is devoted to expert diagnosis and treatment for improved patient outcomes. Her expertise is in cardiovascular disease with special interest in women’s heart health, prevention, lipid disorders, pregnancy-related heart disease, cardio-oncology and autoimmune-related heart disease.Dr. Bond is a board-certified attending cardiologist and the System Director of the Women’s Heart Health Program at Dignity Health in Arizona. She is affiliated with Chandler Regional Medical Center & Mercy Gilbert Medical Center. She is board certificated in cardiovascular disease, internal medicine, echocardiography and nuclear cardiology and is a registered physician in vascular interpretation. Dr. Bond is a well-known spokesperson for the American Heart Association, Go Red for Women Campaign.

Dr. Victoria Thomas @Drvic_thomas is a cardiology fellow at Vanderbilt University. She completed medical school at University of Chicago-Pritzker School of Medicine followed by residency training at Indiana University. Victoria is fervent about medical and patient education along with promoting health equity and decreasing health disparities. She is currently deciding between a Master of Education or Science in Clinical Investigation. Her research interest are curriculum development, cardiac ATTR, and coronary artery disease.

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Jaya Kanduri, Dr. Dan Lu, and Dr. Joe Wang from Weill Cornell Cardiology for Levain cookies in Central Park. The ECPR is provided by Dr. Harsimran Singh (Cardiology Program Director and Interventional Cardiologist with expertise in ACHD). Episode introduction by CardioNerds Clinical Trialist Dr. Jeremy Brooksbank.

We discuss a case of a 24-year-old female with a history of unicuspid aortic valve with associated aortopathy status post mechanical aortic valve replacement and Bentall procedure at age 16 presents with acute onset substernal chest pain and shortness of breath. She was found to have mechanical aortic valve obstruction and severe aortic regurgitation resulting in cardiogenic shock. Unfortunately, the shock quickly progressed to refractory cardiac arrest requiring mechanical support with VA-ECMO before valve debridement was performed in the operating room. The differential for mechanical prosthetic valve stenosis includes pannus, thrombus, or vegetation. She was eventually found to have thrombus obstructing the outflow tract and holding the mechanical leaflets open leading to torrential regurgitation. She underwent successful surgical debridement. We discuss unicuspid aortic valve and associated aortopathy, surgical considerations regarding AVR, diagnosis and management of prosthetic valve dysfunction, approach to cardiogenic shock and considerations around activating and managing VA-ECMO.

With this episode, the CardioNerds family warmly welcomes Weill Cornell Cardiology to the CardioNerds Healy Honor Roll. The CardioNerds Healy Honor Roll programs support and foster the the CardioNerds spirit and mission of democratizing cardiovascular education. Healy Honor Roll programs nominate fellows from their program who are highly motivated and are passionate about medical education. The Weill Cornell fellowship program director, Dr. Harsimran Singh has nominated Dr. Jaya Kanduri for this position.

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• ECG
• CXR
• Echo
• RHC

(1) Unicuspid aortic valves present with aortic stenosis earlier in life. There can be concurrent aortic regurgitation and, like bicuspid aortic valves, unicuspids can be associated with aortopathy as well as other congenital anomalies.

(2) Prosthetic valve stenosis is assessed with different echocardiographic parameters than what we use for native valves. The differential for mechanical valve stenosis includes pannus, thrombus, or vegetation. Patient prosthesis mismatch may also lead to elevated gradients.

(3) VA-ECMO provides robust flow in the setting of cardiogenic shock as well as gas exchange. While this flow may improve end-organ perfusion, it also increases left ventricular afterload, thereby potentially worsening LV ischemia and impeding LV recovery. Elevated afterload may also decrease innate contractility and prevent aortic valve leaflets from opening. Therefore, if a patient with a mechanical valve is on VA-ECMO, ensuring valve opening to prevent valve (or ventricular) thrombosis is paramount.

(4) Venting is sometimes necessary to decrease the left ventricular end diastolic pressure from the high afterload imposed by VA-ECMO. A microaxial temporary LVAD (example – Impella device) directly unloads the left ventricle, but cannot be used in the setting of a mechanical aortic valve. TandemHeart is also a consideration (inflow cannula placed across the interatrial septum in the left atrium) to unload the LV, but does not improve flow across the aortic valve so can lead to thrombus if a mechanical valve is present. Intra-aortic balloon counterpulsation using an IABP can be used to decrease afterload on the native heart and increase coronary perfusion, but does not directly unload the left ventricle.

(5) Acute mechanical valve thrombosis can be managed with emergency surgery or with low dose fibrinolytic therapy. Surgery is preferable when operative risk is low and if there are contraindications to fibrinolytic therapy such as prior intracranial hemorrhage or active bleeding.

(6) VA-ECMO can be weaned by slowly decreasing flow rates and assessing native cardiac function, hemodynamic response, and end-organ perfusion with assessments including echocardiography and pulmonary artery catheterization.

1. What is a unicuspid aortic valve?

• Unicuspid aortic valves (UAVs) are rare with an incidence of only 0.02%.
• There are two types of UAVs. Acommisural UAVs have a single cusp with a stenotic central orifice and rudimentary commissures that do not divide the valve (pin-hole shaped), and are usually complicated by severe stenosis in early childhood. Unicommisural UAVs are composed of a single cusp with a single commissural attachment to the aortic wall and an elongated orifice (slit-like orifice), which has a less aggressive course and is generally discovered in adulthood.
• Aortic stenosis is almost universal among UAVs, present with or without aortic regurgitation in 92% of cases. Some series have shown 14% of cases with concurrent aortopathy.
• UAVs may be associated with congenital abnormalities likes anomalous coronaries, PDA, VSD and coarctation.

2. How do we assess for aortic prosthetic valve stenosis?

• Assessment for mechanical valve stenosis involves different echocardiographic parameters than when evaluating a native valve. Doppler velocity index (DVI) is the dimensionless index with LVOT VTI/AV VTI, with severe stenosis suggested by a ratio of <0.25. Acceleration time (AT) is the time from onset to peak velocity of the continuous wave Doppler jet with severe stenosis suggested by >100msec (it takes longer to gush through a more stenotic valve). Effective orifice area (EOA) <0.8 suggests severe stenosis. A rounded symmetrical contour of the prosthetic valve VTI is more suggestive of severe stenosis, versus a triangular and early peaking jet.
• Acceptable ranges for prosthetic valve gradients are different from native valves due to intrinsically higher gradients, with mechanical being higher than bioprosthetic. In evaluating for prosthetic valve stenosis, we need to compare expected gradients for a given valve against those being measured. Evaluating trends over time is invaluable.

3. What are the percutaneous mechanical circulatory support options for cardiogenic shock?

• MCS options include counterpulsation using an IABP, microaxial temporary LVAD (like the Impella devie), TandemHeart, and VA-ECMO.
• The IABP improves diastolic coronary perfusion and systolic afterload reduction. However, there is only 0-1 L/min of flow provided, and no direct LV decompression.
• Microaxial temporary LVADs directly unload the LV with the flow pump placed across the aortic valve. These devices can provide 2-5L/min of flow depending on which device is used.
• The TandemHeart directly unloads the LV as well with an inflow cannula placed in the LA and outflow cannula placed in the femoral artery (requiring a transseptal puncture), and provides 2.5-5L/min of flow.
• VA-ECMO can provide up to 3-7L/min of flow.

4. What are unique considerations of mechanical support and VA-ECMO in the setting of a mechanical aortic valve?

• With a mechanical aortic valve, it is important for the valve leaflets open to prevent leaflet thrombosis. High afterload from the VA-ECMO circuit due to retrograde flow can prevent the aortic valve from opening, especially if myocardial contractility is already compromised. Therefore, special consideration needs to be given to the flow rate of the circuit and maintaining native LV output.
• Venting options are limited with a mechanical aortic valve. A device cannot be placed across the valve and so microaxial flow pumps are contraindicated. TandemHeart effectively decompresses the LV by sucking blood from the LA, but does not promote flow across the aortic valve and predisposes to thrombus formation. IABP is the ideal device in the setting of a mechanical aortic valve as flow through the aortic valve is promoted, however there is no direct decompression of the LV and efficacy may be limited.

5. What is the acute management of mechanical valve thrombosis?

• Mechanical valve thrombosis is managed acutely with emergent surgery or use of low dose fibrinolytic therapy.
• Surgery is preferable when surgical expertise is readily available, operative risk is low, and there are contraindications to fibrinolysis.
• Other reasons to prefer surgery include recurrent valve thrombosis, severe heart failure symptoms, large clot size (>0.8cm2), presence of LA thrombus or concomitant CAD in need of revascularization, presence of other valve disease, and presence of possible pannus (which would not respond to fibrinolysis). 

6. What is the approach to weaning VA-ECMO?

• Assessment of echocardiographic features, hemodynamics, and end-organ perfusion is essential for a successful VA-ECMO wean. First a turndown of the circuit is performed where the ECMO flow is decreased in a protocolized fashion. This should reduce afterload and therefore increase LV contractile reserve, as well as increase preload with return of flow through the ventricles. With these changes, successful hemodynamic parameters to look for are stable cardiac index, central venous pressure, pulmonary arterial pressures, and systemic blood pressures. Successful echocardiographic parameters include an increase in LVEF >20-25%, aortic VTI ≥10 cm, lateral mitral annulus peak systolic velocity ≥6 cm/s, and a normal appearing RV with midline septum. Of note the risk of thrombosis increases with lower circuit flows, so particular attention must be given to anticoagulation during weaning.
• As antegrade flow through the native LV increases and retrograde through the VA-ECMO circuit decreases, beware of the north-south syndrome. This is caused by a mixing cloud of oxygenated blood from ECMO and potentially deoxygenated blood from the LV (if pulmonary gas exchange is compromised). As this mixing cloud progressively travels distally from the aortic root, it may predispose to coronary and then neurologic ischemia. We can monitor for this using ABGs obtained from the right arm. Stay tuned for more on this as part of the biventricular shock discussion as part of the CardioNerds Critical Care Cardiology Series.

1. Abbas, A. (n.d.). Echocardiographic Evaluation of Aortic Valve Prosthesis. Retrieved from https://asecho.org/wp-content/uploads/2016/04/4.16-Abbas-Aortic-Valve-Prosthesis.pdf
2. Eckman, P. M., Katz, J. N., El Banayosy, A., Bohula, E. A., Sun, B., & Van Diepen, S. (2019). Veno-Arterial extracorporeal Membrane Oxygenation For cardiogenic shock. Circulation,140(24), 2019-2037. doi:10.1161/circulationaha.119.034512
3. Klein, L., & Dorobanţu, L. (2016). Mechanical circulatory support. Current Approach to Heart Failure,311-333. doi:10.1007/978-3-319-45237-1_15
4. Li, Y., Yan, S., Gao, S., Liu, M., Lou, S., Liu, G., . . . Gao, B. (2018). Effect of an intra-aortic balloon pump with venoarterial extracorporeal membrane oxygenation on mortality of patients with cardiogenic shock: A systematic review and meta-analysis†. European Journal of Cardio-Thoracic Surgery,55(3), 395-404. doi:10.1093/ejcts/ezy304
5. Malekan, R., Spielvogel, D., Saunders, P. C., Lansman, S. L., & Griepp, R. B. (2011). The completion bentall procedure. The Annals of Thoracic Surgery,92(1), 362-363. doi:10.1016/j.athoracsur.2011.02.078
6. Otto, C. M., Nishimura, R. A., Bonow, R. O., Carabello, B. A., Erwin, J. P., Gentile, F., . . . Toly, C. (2021). 2020 ACC/AHA guideline for the management of patients with Valvular heart disease: A report of the American College OF CARDIOLOGY/AMERICAN Heart ASSOCIATION Joint Committee on clinical practice guidelines. Circulation,143(5). doi:10.1161/cir.0000000000000923
7. Patel, S. M., Lipinski, J., Al-Kindi, S. G., Patel, T., Saric, P., Li, J., . . . Bezerra, H. G. (2019). Simultaneous Venoarterial extracorporeal Membrane oxygenation AND Percutaneous left Ventricular Decompression therapy WITH IMPELLA is associated with improved outcomes in REFRACTORY cardiogenic shock. ASAIO Journal,65(1), 21-28. doi:10.1097/mat.0000000000000767
8. Rao, P., Khalpey, Z., Smith, R., Burkhoff, D., & Kociol, R. D. (2018). Venoarterial extracorporeal Membrane Oxygenation For cardiogenic shock and cardiac arrest. Circulation: Heart Failure,11(9). doi:10.1161/circheartfailure.118.004905
9. Salazar, M. (n.d.). Echocardiographic Evaluation of Prosthetic Valves. Retrieved from https://www.asefoundation.org/wp-content/uploads/2016/10/Evaluation-of-Prosthetic-Valves-Supe.pdf
10. Thota, V., & Mookadam, F. (2011). Unicuspid aortic valve. Aortic Valve. doi:10.5772/24280

• Karan Desai, MD
• Amit Goyal, MD
• Daniel Ambinder, MD

The hemodynamic evaluation of cardiogenic shock obtained via a Swan-Ganz catheter plays an essential role in the characterization of cardiogenic shock patients. Join Dr. Nosheen Reza, (Assistant Professor of Medicine and Advanced Heart Failure and Transplant cardiologist at the Hospital of the University of Pennsylvania), episode fellow lead Dr. Brian McCauley (Interventional and Critical Care Fellow at the Hospital of the University of Pennsylvania), Dr. Mark Belkin (Cardiac Critical Care Series Co-Chair and AHFT fellow at University of Chicago), and CardioNerds Co-Founders, Amit Goyal and Dan Ambinder, for this tour through the heart aboard the Swan-Ganz catheter. In this episode, we evaluate three separate admissions for a single patient to highlight pearls regarding waveform assessment, evaluating cardiac output, phenotyping hemodynamic profiles, targeted therapies based on hemodynamics and so much more. Episode introduction and audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship).

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1. Swan-Ganz catheters are not dead #ReviveTheSwan!  They remain a useful tool to characterize cardiac patients & to help direct therapy, especially in Cardiogenic Shock.
2. When looking at Swan-Ganz catheter data, it is important to always interpret your own tracings, to know what values are acquired directly, and which values are derived.
3. It is important to understand the strengths and weakness of hemodynamic characterization by Swan-Ganz catheters
4. Advanced metrics such as cardiac power output, pulmonary artery pulsatility index, and aortic pulsatility index are extremely useful in further phenotyping patients as well as guiding mechanical support platforms
5. “The data will be wrong if the preparation is not right”

1. Swan-Ganz catheters are a useful tool to characterize cardiac patients and to direct therapy. 

• With the ESCAPE trial in 2004, Swan-Ganz catheter utilization dropped drastically outside transplant centers across the United States (2). 
• While the ESCAPE trial did demonstrate the possibility of harm when using a Swan-Ganz catheter, many of the truly ill cardiac patients we care for would have been excluded from the trial. For instance, patients on dobutamine at doses above 3 µg/kg/min or any dose of milrinone during the hospitalization were excluded from the trial.
• This is a classic example of “throwing the baby out with the bath water.”
• In a recent large, multicenter cardiogenic shock registry, complete hemodynamic assessment using pulmonary artery catheters prior to MCS is associated with lower in-hospital mortality compared with incomplete or no assessment (3).

2. When looking at Swan-Ganz catheter data, it is important to always interpret your own tracings, to know what values are acquired directly, and which values are derived.

• Incomplete or incorrect data can lead to mischaracterization of our patients. 
• Therefore, it is essential to review all of the tracings, calculations, and data acquired for each individual patient before any clinical adjustments are made (1). 
• An incomplete pulmonary capillary wedge tracing is an example from clinical practice (causing the PCWP, and therefore the left-sided filling pressures to be overestimated).  It is equally important to know the limitations of cardiac output equations, and that no one measurement is perfect.
• Foibles of the Fick equation include assumed rather than measured oxygen consumption and variations in hemoglobin concentration. 
• Traditionally, thermodilution has been thought to be likely less accurate in presence of tricuspid regurgitation, which could lead to blending of the cold dilutant, but recent data suggests even in these circumstances it remains the preferred method for estimating cardiac output over indirect Fick.

3. What are some tips of measuring a PCWP correctly?

• To ensure that we get the wedge pressure correctly, we must first make sure we understand the wedge pressure in relation to the respiratory cycle. For the majority of patients, the end expiratory intrathoracic pressure will be close to 0, and it will have the least influence on our readings. Thus, for most patients, that is why we measure the wedge pressure at end expiration.
• However, in patients with severe lung disease or significant obesity, the intrathoracic pressure may not be close to 0 at end expiration or there may be wide swings in intrathoracic pressure. For these patients, it is a reminder to look at the tracings yourself, and we may need to average the PCWP over the respiratory cycle.
• When we are measuring the PCWP, we have to remember that we are using it as a surrogate of the LV end-diastolic pressure. The point of the cardiac cycle when the pressure in the pulmonary veins, left atrium and LV are closest to equal is end-diastole. Thus, we typically want to measure the PCWP in end-diastole, which would specifically be measuring the mean of the A-wave.
• Now, for patients with severe mitral regurgitation and/or significant atrial myopathy leading to large V-waves, the wedge pressure estimated at end-diastole will not necessarily reflect the mean wedge (averaged throughout the cardiac cycle) that the pulmonary circulation “sees” throughout the cardiac cycle. As has been a theme in this episode, we have to make sure our inputs are accurate to appropriately help our patients. In this circumstance of large V-waves, if we were calculating the pulmonary vascular resistance (Mean PA Pressure – PCWP / CO), but used the end-diastolic PCWP instead of the PCWP averaged through the cardiac cycle we may end up with an inaccurate estimation of PVR.

4.Advanced metrics such as cardiac power output, pulmonary artery pulsatility index, and aortic pulsatility index are extremely useful in further characterizing hemodynamics.

• Over the past several years individual indices of ventricular performance have been developed and studied, these include CPO, PAPi, API, and LVSWI (4,5,10-12). These values can further flesh out our hemodynamic profiles, and help guide decision-making for choosing the proper mechanical circulatory support platform (7,8,9).
• See the infographic developed by CardioNerds Academy Fellow Ahmed Ghoneem for more information on different thresholds for these parameters.
• The API is a novel hemodynamic parameter that was recently applied to ESCAPE trial patients by series Co-Chair, Mark Belkin.

5. “The data will be wrong if the preparation is not right.”

• Dr. Reza’s point on the episode is apt and high-yield.
• Incorrect data acquisition and/or interpretation will not benefit our patients. We need to know what values are measured directly (chamber pressures, SvO2) and which are derived (cardiac output/index, SVR/PVR, CPO/PAPi/API, and so forth). 
• As cardiologists and intensivists, we need to be critical of the tracings themselves, avoid anchoring to a single value, and be observant of the overall hemodynamic trajectory our patient is taking. 
• Only through thoughtful intervention in coordination with careful and consistent monitoring will we bring to bear the benefits bestowed by Swan-Ganz catheter supplemented-care (1).

1.Ragosta M. Textbook of Clinical Hemodynamics. Elsevier; 2017.

2.Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA. 2005;294(13):1625-33. https://jamanetwork.com/journals/jama/fullarticle/201634

3. Garan AR, Kanwar M, Thayer KL, et al. Complete hemodynamic profiling with pulmonary artery catheters in cardiogenic shock is associated with lower in-hospital mortality. JACC Heart Fail. 2020;8(11):903-913.  https://pubmed.ncbi.nlm.nih.gov/33121702/

4.Korabathina R., Heffernan K.S., Paruchuri V., Patel A.R., Mudd J.O., Prutkin J.M., et al: The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv 2012; 80: pp. 593-600.  https://pubmed.ncbi.nlm.nih.gov/21954053/

5.Fincke R, Hochman JS, Lowe AM, et al. Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. J Am Coll Cardiol. 2004;44(2):340-8.  https://pubmed.ncbi.nlm.nih.gov/15261929/

6.Kochav SM, Flores RJ, Truby LK, Topkara VK. Prognostic impact of pulmonary artery pulsatility index (Papi) in patients with advanced heart failure: insights from the escape trial. J Card Fail. 2018;24(7):453-459. https://pubmed.ncbi.nlm.nih.gov/29597051/

7.Feldman D, Naidu SS.  Percutaneous Mechanical Circulatory Support Devices. Cardiac Interventions Today. 2016; 10 (1): 26-33.  https://citoday.com/articles/2016-jan-feb/cover-stories

8.Briceno N, Kapur NK, Perera D. Percutaneous mechanical circulatory support: current concepts and future directions. Heart. 2016;102(18):1494-507.  https://pubmed.ncbi.nlm.nih.gov/27503999/

9.Baran DA, Grines CL, Bailey S, et al. Scai clinical expert consensus statement on the classification of cardiogenic shock: this document was endorsed by the american college of cardiology (Acc), the american heart association (Aha), the society of critical care medicine (Sccm), and the society of thoracic surgeons (Sts) in april 2019. Catheter Cardiovasc Interv. Published online May 19, 2019:ccd.28329.  https://pubmed.ncbi.nlm.nih.gov/31104355/

10.Drazner MH, Velez-Martinez M, Ayers CR, et al. Relationship of right- to left-sided ventricular filling pressures in advanced heart failure: insights from the ESCAPE trial. Circ Heart Fail. 2013;6(2):264-270.  https://pubmed.ncbi.nlm.nih.gov/23392790/

11.Belkin MN, Alenghat FJ, Besser SA, et al. Aortic pulsatility index predicts clinical outcomes in heart failure: a sub-analysis of the ESCAPE trial. ESC Heart Fail. 2021;8(2):1522-1530.  https://pubmed.ncbi.nlm.nih.gov/33595923/

12. Belkin MN, Kalantari SA, Kanelidis AJ, et al. Aortic Pulsatility Index: A Novel Hemodynamic Variable for Evaluation of Decompensated Heart Failure. J Card Fail. 2021;27(10):1045-1052. https://pubmed.ncbi.nlm.nih.gov/34048919/

13. Araj FG, Mammen PPA. Alternans of the Pulse Is Rarely an Alternans of Prognosis. J Card Fail. 2021 Nov;27(11):1302-1303. doi: 10.1016/j.cardfail.2021.06.023. Epub 2021 Jul 26. PMID: 34324926.

Dr. Nosheen Reza is a cardiologist and translational researcher at the University of Pennsylvania focusing on advanced heart failure and transplant cardiology and cardiovascular genetics, genomics, and phenomics. She obtained her medical degree from the University of Virginia School of Medicine in 2012 and completed her internal medicine residency training at the Massachusetts General Hospital in 2015. She then completed her Cardiovascular Disease fellowship at the University of Pennsylvania in 2018 and served as 2017-2018 Chief Fellow. At Penn, Dr. Reza pursued additional scholarship in genomic medicine as an NIH T32-funded postdoctoral fellow and in healthcare quality as a Penn Benjamin & Mary Siddons Measey Fellow in Quality Improvement and Patient Safety. She completed her final year of clinical training at Penn in Advanced Heart Failure and Transplant Cardiology and joined the faculty at the University of Pennsylvania in July 2020. Dr. Reza is passionate about medical education and has won many distinctions in the field throughout her training. She serves as an editorial board member for JACC: Case Reports, JACC: CardioOncology, and Current Cardiovascular Risk Reports. Dr. Reza is an active leader in the Heart Failure Society of America, American Heart Association, and American College of Cardiology at the local and national levels and volunteers on multiple leadership councils and steering committees within these organizations.

Dr. Brian McCauley is an interventional cardiology fellow at the University of Pennsylvania where he also completed his general cardiology fellowship. Received his medical degree from Cooper Medical School of Rowan University, and internal medicine residency at Brown University.

• Karan Desai, MD
• Dr. Mark Belkin
• Amit Goyal, MD
• Daniel Ambinder, MD

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Zarina Sharalaya (Interventional Cardiology Fellow at the Cleveland Clinic), and Dr. Simrat Kaur (General Cardiology Fellow at the Cleveland Clinic) join Dr. Samir Kapadia, the Chair of the Robert and Suzanne Tomsich Department of Cardiovascular Medicine, Sydell and Arnold Miller Family Heart, Vascular & Thoracic Institute at Cleveland Clinic. They discuss future advancements in the field of structural interventional cardiology. Dr. Kapadia sheds light on his journey starting as an international medical graduate from India and speaks about his mentors that helped shape his career and his life. We later delve into several advancements in the field of structural and interventional cardiology, along with the amalgamation of different sub-specialities with intervention such as heart failure and critical care cardiology. We also discuss the measures being taken to reduce the occupational hazards associated with interventional cardiology and how to make this field more appealing to women in cardiology. Special message by Ohio ACC State Chapter Governor, Dr. Kanny Grewal.

The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza.

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1/ In the latest @PaChapterACC & @CardioNerds Narratives in Cardiology episode, @AmitGoyalMD, @Dr_DanMD, @ZSharalayaMD, & @SimratKaurMD talk with @tavrkapadia

Follow this #CardsNarratives🧵on the discussion about IMGs & Innovation, Excellence, Leadership in IC pic.twitter.com/hkCuMF4UPB

“A very important thing for all international medical graduates and for everybody, for that matter – it is important to recognize that the opportunities are what you perceive and not what others perceive.”

How do international medical graduates contribute to the work force in medicine across the United States of America?

• International medical graduates account for 25% of the physician work force, with over 85% being involved in direct patient care.
• IMGs are usually accomplished, consummate and highly motivated physicians who often have to overcome challenges such as language proficiency, acculturation and difficulties with obtaining a visa status in the United States.
• IMGs also help fill gaps in health care by working in geographical areas that are otherwise not desirable by US or Canadian medical graduates.
• IMGs contribute to diversity of the field which provides a richer training environment, improved access to health care for underrepresented minorities, as well as better patient outcomes.

What are key qualities of a good mentor?

• A good mentor is responsible for enhancing the education of his or her mentees along with motivating them to challenge their limits.
• Qualities of a good mentor extend beyond mere mentorship to sponsorship, where the mentor opens up his or her network for the mentee allowing them to pursue a path of success.
• A mentor serves as an advisor and a counselor, helping his or her mentees navigate difficult paths teaching them to become resilient physicians.
• A mentor also serves as a confidante for the trainee with whom mentees can share their dreams, aspirations and vulnerabilities knowing not only will this be kept in confidence but will also provide a catalyst for their growth.

What are the recent advancements in minimizing radiation exposures for structural cardiologists?

• It’s important to understand the various occupational hazards of radiation exposure which include but are not limited to brain tumors, cataracts, thyroid disease, cardiovascular diseases, musculosketal problems and reproductive side effects.
• When dealing with possible occupational radiation exposure, we should strive for the ALARA (as low as reasonably achievable) principle of radioprotection.
• The RADPAD (RADPAD 5100A-O; Worldwide Innovations & Technologies, Inc, Lenexa, KS) is a new development that is a lead field shield that is placed between the patient and the operator to reduce scatter radiation and significantly reduce operator radiation exposure.
• The use of Zero gravity lead is a novel suspension shield which has also been shown to significantly reduce the operator radiation exposure and potentially decrease orthopedic injuries particularly spinal injuries secondary to the protective lead garments.

What are the future directions for structural interventions and how is the field of structural cardiology going to evolve in the next few years?

• The future of structural cardiology provides great promise. After the success of transcatheter aortic valve replacement (TAVR) and transcatheter mitral valve edge to edge repair (TEER), there has been increasing development in tricuspid interventions as well as interventions for severe mitral stenosis due to mitral annular calcification.
• The amalgamation of structural interventional cardiology and heart failure as well as with critical care are also exciting fields that is still developing. Advancements in left ventricular restoration devices such as the Revivant TC system may help several patients with end stage congestive heart failure due to ischemic heart disease.

1. Steward DE. The internal medicine workforce, international medical graduates, and medical school  departments of medicine. Am J Med 2003;115(1):80–4. Doi: 10.1016/s0002-9343(03)00307-3.
2. Kostis JB., Ahmad B. International medical graduates and the cardiology workforce. J Am Coll Cardiol 2004;44(6):1172–4. Doi: 10.1016/j.jacc.2004.05.081.
3. Al Hussein Al Awamlh B. Alien J-1 Physicians in a Pandemic. JAMA Intern Med 2021;181(6):743–4. Doi: 10.1001/jamainternmed.2021.0730.
4. David YN., Issaka RB. Advancing diversity: the role of international medical graduates. Lancet Gastroenterol Hepatol 2021;6(12):980–1. Doi: 10.1016/S2468-1253(21)00376-9.
5. Shikhar A. Mentorship During Fellowship. J Am Coll Cardiol 2014;64(15):1637–8. Doi: 10.1016/j.jacc.2014.08.017.
6. Tobin MJ. Mentoring: seven roles and some specifics. Am J Respir Crit Care Med 2004;170(2):114–7. Doi: 10.1164/rccm.2405004.
7. Picano E., Vano E. The Radiation Issue in Cardiology: the time for action is now. Cardiovasc Ultrasound 2011;9(1):35. Doi: 10.1186/1476-7120-9-35.
8. Vlastra W., Delewi R., Sjauw KD., et al. Efficacy of the RADPAD Protection Drape in Reducing Operators’ Radiation Exposure in  the Catheterization Laboratory: A Sham-Controlled Randomized Trial. Circ Cardiovasc Interv 2017;10(11). Doi: 10.1161/CIRCINTERVENTIONS.117.006058.
9. Zanca F., Dabin J., Collard C., et al. Evaluation of a suspended radiation protection system to reduce operator exposure in  cardiology interventional procedures. Catheter Cardiovasc Interv  Off J Soc  Card Angiogr Interv 2021;98(5):E687–94. Doi: 10.1002/ccd.29894.
10. GP., Y.S. C. Continuing Advances and Challenges of Structural Heart Imaging. JACC Cardiovasc Imaging 2021;14(1):128–30. Doi: 10.1016/j.jcmg.2020.12.002.
11. Klein P., Anker SD., Wechsler A., et al. Less invasive ventricular reconstruction for ischaemic heart failure. Eur J Heart Fail 2019;21(12):1638–50. Doi: 10.1002/ejhf.1669.

In this episode, CardioNerds (Amit Goyal), ACHD series co-chair,  Dr. Josh Saef (ACHD fellow at University of Pennsylvania) and episode lead fellow, Dr. Brynn Connor (Pediatric Cardiology fellow at Lucile Packard Children’s Hospital at Stanford) are joined by Dr. Maan Jokhadar (Advanced heart failure and adult congenital heart disease specialist at Emory University) to discuss transposition of the great arteries. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian.

For a brief review of the basic anatomy and physiology of D-TGA, check-out this great video by Dr. Maan Jokhadar!

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

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(1) In D-TGA following an atrial switch operation, the right ventricle IS the systemic ventricle!

(2) Evaluation of systemic right ventricular function often requires use of both transthoracic echocardiography and cardiac MRI.

(3) Use of medical heart failure therapies should be individualized, without any proven long-term mortality benefit and potential unique complications in this patient population (i.e. SA node dysfunction). 

D-transposition of the great arteries (D-TGA) is one of the most common forms of cyanotic congenital heart disease presenting in the newborn period. Anatomically, d-transposition of the great arteries is characterized by atrioventricular concordance and ventriculoarterial discordance, such that the aorta arises from the morphologic right ventricle and pulmonary artery arises from the morphologic left ventricle. The resultant physiology is that of a parallel circulation, with deoxygenated blood recirculating in the systemic circulation (via the RA-RV) and oxygenated blood recirculating in the pulmonary circulation (via the LA-LV). At birth, this invariably results in cyanosis, with survival dependent upon adequate mixing of the two circulations via an atrial or ventricular level defect.

Prior to surgical advances in the late 1950s, this lesion was uniformly fatal, with most infants dying before their first birthday. The subsequent development of the Senning and Mustard atrial-level repairs led to good immediate outcomes and improved long-term survival. However, following these “physiologic” types of repair, patients are far from cured, with several long-term established complications, including (1) dysfunction of the systemic right ventricle, (2) tricuspid regurgitation (the systemic atrioventricular valve), (3) atrial and ventricular arrhythmias, and (4) systemic and pulmonary venous baffles leaks and obstruction. These complications ultimately lead to substantial morbidity and premature mortality, with ACHD providers facing unique challenges in the medical and surgical management of this heterogenous patient population.

1. What are the basic anatomic features of d-transposition of the great arteries (d-TGA)?

• D-transposition of the great arteries is defined by the origin of the arterial trunks from the morphologically inappropriate ventricle, specifically with the aorta arising from the morphologic right ventricle (now the systemic ventricle) and the pulmonary trunk arising from the morphologic left ventricle.
• This is termed “ventriculoarterial discordance”, and importantly, does not define the spatial relationship of the great arteries. Rather, the “d” terminology refers to the looping of the ventricles and distinguishes d-TGA from l-TGA (or congenitally corrected transposition), where there is additional atrioventricular discordance. 
• The resultant physiology is that of a parallel circulation, with deoxygenated blood recirculating in the systemic circulation and oxygenated blood recirculating in the pulmonary circulation. At birth, this invariably results in cyanosis, with survival dependent upon adequate mixing of the two circulations via an atrial or ventricular level defect.
• There are three major anatomic variations in dTGA, including dTGA with an intact ventricular septum (most common), dTGA with a ventricular septal defect, and dTGA with LVOT obstruction. These anatomic subtypes can lead to variable presentations in the neonatal period, as well as pose unique challenges to surgical repair, and are therefore important diagnostic considerations.
• The arrangement of the coronary arteries and their spatial course can additionally be highly variable, posing added complications when performing the arterial switch operation (which requires reimplantation of the coronary arteries into the neo-aortic root). The most common, “usual,” arrangement is the left coronary artery originating off the anterior facing sinus, and the right coronary artery originating off the posterior facing sinus.

2. What surgical approaches have been utilized in the management of D-TGA?What are the key features of aortic coarctation anatomy?

• Prior to surgical advances in the late 1950s, this lesion was uniformly fatal, with most infants dying before the age of 1 year.
• Infants were initially palliated with an atrial septostomy, which allowed for mixing at the atrial level and improved survival in the immediate newborn period. However, these infants were still left with profound cyanosis, with inevitable mortality in the first year of life.
• In the mid-1950s, the Senning (1958) and Mustard (1964) atrial-level repairs were first performed, with good short-term outcomes and improved long-term survival.
  • In the Senning procedure, a baffle is created within the atria that redirects the deoxygenated caval blood to the mitral valve and the oxygenated pulmonary venous blood to the tricuspid valve with use of native atrial tissue.
  • Mustard subsequently described a simpler technique with creation of an atrial baffle using synthetic patch material.

• By the late 1980s, late complications of these repairs became well recognized, with the ultimate adoption of the neonatal arterial switch operation, which remains the gold standard for surgical management of transposition.

3. What are the long-term complications of the Mustard and Senning procedures?

• Systemic Right Ventricular Dysfunction:
  • Clinical Features – Systemic RV dysfunction is an evitable consequence of the atrial switch operation, with 50% of patients developing right ventricular systolic dysfunction by 30 years of age.
  • While right ventricular dysfunction is often mild and clinically asymptomatic for several years, patients ultimately develop related symptomatology over the subsequent 10-20 years.
  • Most commonly, patients present to care with diminished exercise tolerance, with symptomatic arrhythmias being an additional common reason for patients to seek care.

• Diagnosis
  • Accurate assessment of RV size and function in this population is critical for adequate surveillance and management planning. However, quantitative right ventricular assessment remains challenging, with no model for comparison and no clear criteria for abnormalities.
  • Volumetric assessments are the gold standard, although made difficult by the complex geometry of the right ventricle.
  • Cardiac MRI is most commonly utilized to assess RV size and systolic function, and additionally permits simultaneous evaluation of the systemic and pulmonary venous baffles and quantitative assessment of the degree of tricuspid regurgitation (the systemic AV valve).
  • Transthoracic echocardiography is still routinely employed for serial evaluation of systemic right ventricular function. However, providers should have a low threshold to obtain further advanced imaging with any significant change in symptomatology or qualitative decrement in right ventricular systolic function on serial echocardiographic assessment.
  • Management
    • Medical Therapy: In contrast to ischemic cardiomyopathy, there are no long-term, randomized, placebo-controlled drug trials evaluating the efficacy of ACEI/ARB/ARNI or beta-blockers on systemic RV function. Small studies performed to date have not shown any appreciable benefit of ACEI/ARB on improving right ventricular ejection fraction or exercise capacity, which may reflect minimal baseline activation of the renin-angiotensin-aldosterone system in this form of heart failure. Use of beta-blocker therapy pathophysiologically makes sense, specifically reducing myocardial oxygen demand and allowing for improved ventricular filling; however, prior studies have produced mixed results, with evidence of improved right ventricular remodelingalthough no appreciable improvement in right ventricular ejection fraction, functional class, or long-term survival. Use of beta-blockers should also be cautioned in patients with established SA node dysfunction.
    • Left Ventricular Re-Training: Conversion to an arterial switch operation often requires a staged approach to ensure that the left ventricle is adequately “trained” to handle systemic pressures. The left ventricle becomes rapidly deconditioned with time when continually exposed to the low-resistant pulmonary circuit, losing its ability to generate systemic pressure. Therefore, initial pulmonary artery banding is often required for left ventricle re-training, although this strategy has had variable success rates. Historically, age has been deemed an important factor in predicting the success of pulmonary artery banding, although this has not been consistently shown. The criteria for successful conversion post-banding are often extrapolated from l-TGA literature, and include generation of near systemic or systemic left ventricular pressures, presence of normal left ventricular systolic function, absent left ventricular diastolic dysfunction (LVEDP <12), an adequate LV mass (65 g/m2), and absent significant AV valve regurgitation.
    • Cardiac transplantation has been successfully performed in this patient population, and should remain a consideration in medically refractory heart failure.
• Arrhythmias & Sudden Cardiac Death
  • Arrhythmias are the most frequently observed adverse event following the atrial switch operation, with normal sinus rhythm being maintained in only 40-50% of patients at 15-20 years. In the initial post-operative period (first ~15 years), bradyarrhythmias predominate, with development of SA node dysfunction attributable to ischemic injury incurred at the time of surgery or fibrosis related to surgical suture/scar lines. Resultant chronotropic incompetence is commonly observed, with up to 20% of patients requiring pacemaker placement.
  • Atrial arrhythmias are initially observed in the immediate post-operative period and have been shown to progress across the lifespan (affecting up to 50% of patients). These are typically re-entrant in nature, with IART and atrial flutter/fibrillation frequently observed. The underlying risk factors for their development are likely multifactorial, including atrial enlargement related to tricuspid regurgitation, suture line related fibrosis, and chronic hemodynamic stress from systemic RV failure.
  • Given challenges imposed with use of anti-arrhythmic therapies (specifically with the high prevalence of SA and AV node dysfunction in this patient population), catheter ablation is typically employed for management of atrial arrhythmias (with a success rate upwards of 80%).
  • Sudden cardiac death is known to occur in 2-15% of patients following the atrial switch operation and is predominantly felt to be arrhythmic in nature. Unlike in other forms of congenital heart disease (i.e. tetralogy of Fallot) and ischemic heart disease, there are no well-established risk factors for sudden cardiac death. Prior studies have found an association with surgical risk factors (initial surgery performed at an early age, earlier era of surgical repair, presence of VSD), and prior documented atrial arrhythmias, although there does not appear to be any consistent correlation with other traditional risk variables, including the presence of right ventricular systolic dysfunction, a prolonged QRS duration, history of ventricular arrhythmias on event monitor, or inducible ventricular arrhythmias on EP study.
  • As a result, indications for ICD implantation are not well established and should be individualized, especially given the potential risks for development of baffle obstruction and “inappropriate” shocks in this patient population. Historic indications for ICD implantation have included a prior history of syncope with documented ventricular arrhythmias.
• Systemic/Pulmonary Venous Baffle Obstruction: Occurs in up to 30% of patients, with the systemic venous baffle most commonly involved.
  • Diagnosis can often be made on cardiac MRI or with cardiac catheterization.
  • Management typically involves systemic anticoagulation and transcatheter stenting and/or balloon dilation.

4. What are the long-term outcomes of d-TGA following an atrial switch operation?

• When compared with prior largely palliative procedures, the atrial switch operation substantially improved long-term survival in d-TGA, with an 80% survival rate at 25 years and 70% survival at 40 years post-repair.
• Early mortality is typically incurred in the setting of post-operative arrhythmias, with late mortality being predominantly related to systemic right ventricular dysfunction and fatal arrhythmias.
• As highlighted above, substantial morbidity is still incurred, with only a 19% event free survival at 40 years.
• Reintervention is predominantly required for (1) baffle related complications (stenosis and/or obstruction), (2) arrhythmias (requiring pacemaker and/or ICD implantation), and tricuspid regurgitation

For a great discussion on dTGA following the atrial switch operation, check-out this great ACHA webinar by Dr. Lui:

https://www.achaheart.org/your-heart/webinars/archive/living-life-fully-post-mustard-or-senning-in-the-adult-tga-patient/

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8. Fricke TA, Konstantinov IE. Arterial Switch Operation: Operative Approach and Outcomes. Ann Thorac Surg. 2019 Jan;107(1):302-310. doi: 10.1016/j.athoracsur.2018.06.002. PMID: 30009809.
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11. Jimenez-Juan L, Joshi SB, Wintersperger BJ, Yan AT, Ley S, Crean AM, Nguyen ET, Deva DP, Paul NS, Wald RM. Assessment of right ventricular volumes and function using cardiovascular magnetic resonance cine imaging after atrial redirection surgery for complete transposition of the great arteries. Int J Cardiovasc Imaging. 2013 Feb;29(2):335-42. doi: 10.1007/s10554-012-0083-8. Epub 2012 Jul 12. PMID: 22790330.
12. Kammeraad JA, van Deurzen CH, Sreeram N, Bink-Boelkens MT, Ottenkamp J, Helbing WA, Lam J, Sobotka-Plojhar MA, Daniels O, Balaji S. Predictors of sudden cardiac death after Mustard or Senning repair for transposition of the great arteries. J Am Coll Cardiol. 2004 Sep 1;44(5):1095-102. doi: 10.1016/j.jacc.2004.05.073. PMID: 15337224.
13. Khairy P. Sudden cardiac death in transposition of the great arteries with a Mustard or Senning baffle: the myocardial ischemia hypothesis. Curr Opin Cardiol. 2017 Jan;32(1):101-107. doi: 10.1097/HCO.0000000000000353. PMID: 27801691.
14. Khairy P, Clair M, Fernandes SM, Blume ED, Powell AJ, Newburger JW, Landzberg MJ, Mayer JE Jr. Cardiovascular outcomes after the arterial switch operation for D-transposition of the great arteries. Circulation. 2013 Jan 22;127(3):331-9. doi: 10.1161/CIRCULATIONAHA.112.135046. Epub 2012 Dec 12. PMID: 23239839.
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Adult Congenital Heart Association
Founded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers

CHiP Network

The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information.

Heart University
Heart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease. It is a carefully curated open access library of educational material for all providers of care to children and adults with CHD or children with acquired heart disease, whether a trainee or a practicing provider. The site provides free content to a global audience in two broad domains: 1. A comprehensive curriculum of training modules and associated testing for trainees. 2. A curated library of conference and grand rounds recordings for continuing medical education. Learn more at www.heartuniversity.org/

Dr. Maan Jokhadar is associate professor of medicine with specialization in heart failure/transplant and in adult congenital heart disease at Emory University in Atlanta. He is the fellowship director for the Emory Adult Congenital Heart Disease training program and is board certified in internal medicine, cardiovascular disease, advanced heart failure/transplantation, adult congenital heart disease, and echocardiography. Dr. Jokhadar graduated from the University of Damascus School of Medicine in Syria and then went to Mayo Clinic in Rochester, Minnesota for internal medicine residency. He then completed cardiology and subspecialty training at Emory University, where he is currently on faculty. Dr. Jokhadar is the recipient of numerous teaching awards.

Dr. Brynn Connor is currently a Pediatric Cardiology fellow at Lucile Packard Children’s Hospital at Stanford. She completed her combined Internal Medicine and Pediatrics Residency at George University Hospital, and will ultimately be pursuing a career in Adult Congenital Heart Disease.

• Amit Goyal, MD
• Daniel Ambinder, MD

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Patrick Azcarate and Dr. Antoinette Birs from the University of California San Diego along with a guest host Dr. Christine Shen from Scripps Health for a hike along Torrey Pines. They discuss a case of a 30-year-old man with a history of malignant thymoma status post two partial lung resections and radiation for pleural/pulmonary metastasis, as well as a history of myasthenia gravis on rituximab, and Ig deficiency on IVIG presents with progressive exertional chest pain. We focus on the differential diagnosis of patients with a history of chest radiation exposure and dive into the complex management and surveillance for patients with radiation associated cardiac disease (RACD). The E-CPR is provided by Dr. Milind Desai (multimodality cardiovascular imaging expert, Director of Clinical Operations, Director of Center for HCM, Medical Director for Center for Aortic Diseases, and Medical Director for Center for Radiation Heart Disease at the Cleveland Clinic).

Claim free CME just for enjoying this episode! 

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1. Radiation-associated cardiac disease (RACD) is a heterogeneous disease that can manifest several years, or decades following radiation exposure to the chest and is associated with high morbidity and mortality. Given the non-specific or vague symptoms, one of the greatest challenges for this patient population may be diagnosing RACD which requires high clinical suspicion. 
2. In patients with a history of chest radiation, we should remember to ask three important questions: 1. What was the total dose of radiation given? 2. How long ago was radiation therapy administered? 3. Was the heart exposed?
3. A cumulative dose of >30 Gray (Gy) chest radiation significantly increases the risk of RACD long-term, but cardiac damage can occur at even lower doses. 
4. Effects from chest radiation can take years to become clinically detectable. Screening for radiation induced coronary artery disease with stress testing should start 5 years following XRT and in low-risk patients (without risk factors for typical coronary artery disease) and continue at 5-year intervals, and 2-year intervals in high-risk patients. Valvular heart disease surveillance should begin 10 years post XRT and can be accomplished with echocardiogram. 
5. Regarding revascularization planning, a Heart Team approach is recommended. However, percutaneous intervention is preferred over bypass surgery in most cases.

1. What is Radiation-Associated Cardiac disease (RACD)?

A spectrum of disease that can affect any part of the heart and typically develops anywhere from 5 to 20 years after radiation. It may present with non-specific or vague symptoms. Manifestations include myocarditis, pericarditis (typically early in the course) and well as long term sequela such as myocardial fibrosis, valvular heart disease (regurgitation or stenosis), pericardial disease, vasculopathy (CAD), conduction system disease. Radiation may impact any tissue of the heart:

• Vascular: microvascular, coronary artery disease, macrovascular (ascending aorta)

• Valvular: has a longer latency ~10-20 years with the left sided valves being more commonly affected; Aorto-mitral curtain thickening/calcification is a hallmark of previous heart radiation and associated with higher mortality 

• Conduction: Sick sinus syndrome, AV nodal block, atrial fibrillaiton; infra-nodal conduction disease and RBBB are common.

• Myocardial: fibrosis in the myocardium leading to HFpEF, or HFrEF; XRT + anthracycline is thought to be synergistic.

• Pericardial: chronic pericardial inflammation, scarring, calcification, restrictive physiology. Constrictive pericarditis from radiation has a particularly poor prognosis given often concurrent myocardial involvement.

2. What is the Pathophysiology of RACD?

The severity of disease is related to total radiation dose, fraction size and volume of the heart in the radiotherapy field. The resulting cell damage leads to activation of the acute inflammatory cascade and pro-fibrotic milieu.

3. What are the additional risk factors for RACD?

• Therapy-related risk factors:
  • Net dosage (dependent on cancer type and tumor site) > 30Gy received by the heart.
  • Proximity to heart to the radiation field.
  • Concomitant chemotherapy – anthracyclines may particularly have a radiation sensitizing effect, thereby increasing the risk of RACD.
• Patient-related risk factors:
  • Life expectancy – younger age at the time of radiation and a good cancer prognosis, as these patients may have more time to manifest the longer-term sequelae of RACD.
  • Presence of traditional cardiovascular risk factors

4. How common is RACD? 

• RACD is most often seen in those receiving chest radiation for breast cancer (particularly left sided), Hodgkin Lymphoma, lung cancer and esophageal cancers.
• There is a distinct population presenting with latent symptoms from treatment with wide-field radiation of Hodgkin lymphoma that was more commonly practiced 20-40 years ago.
• Prevalence of radiation associated cardiomyopathy is ~10% based on population studies although difficult to determine given the heterogeneity of presentation and under-recognition. 
  • Valvular abnormalities in 7-39% at 10 years, 12-60% at 20 years 
    • Mitral and aortic valves are most affected; symptoms arise 1-2 decades after radiation and later than CAD; AR in 60% vs 4% at 20 years vs 10 years post treatment. 
    • Aorto-mitral curtain thickening/calcification is a hallmark of previous heart irradiation, and its extent is strongly associated with mortality in subjects undergoing cardiac surgery. 
  • Radiation induced coronary vasculopathy has a prevalence of 85%. 

5. What is Radiation induced coronary artery disease (RICAD)?  

• Pathophysiology: inflammatory plaque, with accumulation of myofibroblasts, resulting in intimal proliferation with aggregation of lipid-rich macrophages; high collagen and fibrin content like accelerated atherosclerosis; doses of > 0.50 Gy can initiate atherosclerosis and affects micro and macro vasculature.
• Angiographically: Ostial or proximal epicardial coronary lesions of the anterior and central vessels are most common (left main trunk, proximal LAD, mid diagonal, or RCA) given the location of the heart in the chest.
• Lesions are often severe, proximal, and diffuse. They are typically long, smooth, concentric, and tubular and may require intravascular ultrasound (IVUS) for diagnosis as they can appear normal on coronary angiography (lumenography).

6. What are different types of radiation?  

• 3D vs Intensity modulated radiation therapy (IMRT): both are x-ray-based radiation
• Proton therapy: Unlike x-rays which go all the way through the body, protons are charged and can go to a specified depth causing less scatter radiation

7. What techniques may be used to reduce cardiac exposure to the radiotherapy field?

• ABC device, breathing techniques such as deep inspiratory breath hold (DIBH) which pulls the heart more inferiorly in the chest and allows treatment of the upper mediastinum with less cardiac exposure, shielding 

8. What are the surveillance recommendations? 

• The risk of RACD is 7.5% per Grey Unit (Gy) and is constant, beginning several years after exposure and persists for at least 2-3 decades (>50% of excess ischemic events occurring >10 years after RT). Those who will receive >30 Gy may warrant cardiology consultation prior to treatment
  • Screening for CAD: 5 years after radiation exposure
  • Screening for valvular disease: 10 years after exposure with 5-year surveillance intervals 

9. What is the recommended approach for revascularization for RICAD?

• PCI is generally preferred if feasible over bypass given chest radiation as this patient group has increased risk of complications from bypass surgery related to severely calcified aorta, possible radiation injury to the IMAs, restrictive lung disease, difficulty weaning patient from a ventilator, and lack of intra-thoracic lymphatics 

1. Desai MY, Jellis CL, Kotecha R, Johnston DR, Griffin BP. Radiation-Associated Cardiac Disease: A Practical Approach to Diagnosis and Management. JACC Cardiovasc Imaging. 2018 Aug;11(8):1132-1149. doi: 10.1016/j.jcmg.2018.04.028. PMID: 30092970. https://www.jacc.org/doi/abs/10.1016/j.jcmg.2018.04.028

• Desai MY, Windecker S, Lancellotti P, Bax JJ, Griffin BP, Cahlon O, Johnston DR. Prevention, Diagnosis, and Management of Radiation-Associated Cardiac Disease: JACC Scientific Expert Panel. J Am Coll Cardiol. 2019 Aug 20;74(7):905-927. doi: 10.1016/j.jacc.2019.07.006. https://www.jacc.org/doi/full/10.1016/j.jacc.2019.07.006

• Cuomo JR, Javaheri SP, Sharma GK, Kapoor D, Berman AE, Weintraub NL. How to prevent and manage radiation-induced coronary artery disease. Heart. 2018 Oct;104(20):1647-1653. doi: 10.1136/heartjnl-2017-312123. Epub 2018 May 15. PMID: 29764968; PMCID: PMC6381836. https://heart.bmj.com/content/104/20/1647.long

• Wu W., Masri A., Popovic Z.B.et al. : “Long-term survival of patients with radiation heart disease undergoing cardiac surgery: a cohort study”. Circulation 2013; 127: 1476. https://www.ahajournals.org/doi/epub/10.1161/CIRCULATIONAHA.113.001435

• Karan Desai, MD
• Amit Goyal, MD
• Daniel Ambinder, MD

Cardiogenic shock is a state of cardiac dysfunction leading to hemodynamic instability and end-organ hypoperfusion. At the bedside, clinicians take various data points – from history to physical exam to labs/imaging and invasive hemodynamics – to make an assessment of the etiology, severity and management of cardiogenic shock. Health systems have developed “Shock Teams” to collectively interpret this data to deliver the optimal care for each patient. In this episode, Dr. Mark Dela Cruz (Advanced Heart Failure and Transplant Fellow at University of Chicago), CardioNerds Critical Care Series Co-Chairs Dr. Mark Belkin (Advanced Heart Failure and Transplant Fellow at University of Chicago) and Dr. Karan Desai (General Cardiology Fellow at University of Maryland), and CardioNerds Co-Founder Dr. Daniel Ambinder (Structural Fellow at Johns Hopkins Hospital) join Dr. Anu Lala (Director of the AHFT Fellowship, Associate Professor of Medicine and Cardiology at Mount Sinai Hospital and Deputy Editor of the Journal of Cardiac Failure) on a Shock Team Call! Dr. Lala leads us in a discussion of the systematic bedside evaluation of cardiogenic shock, from understanding a patient’s physiology and their humanity, to manage their illness and make a rapid but thorough evaluation when on the Shock Call. Audio editing and episode introduction by CardioNerds Academy Intern, Hirsh Elhence.

Claim free CME for enjoying this episode! Disclosures: None

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1. The classic definition of cardiogenic shock was derived from studies of left ventricular dysfunction in the setting of acute myocardial infarction. With the advent of early primary percutaneous coronary intervention (PCI) and trends in cardiovascular disease risk factors, the prevalence of non-ischemic etiologies of cardiogenic shock (e.g., progression/exacerbation of chronic heart failure) has increased significantly. 

• The diagnosis of cardiogenic shock should be made by integrating key clinical features such as physical exam findings and objective laboratory and imaging data in an iterative fashion. Focused transthoracic echocardiography and invasive hemodynamics are helpful in further characterizing the type of shock and the etiology of cardiogenic shock.

• Early evaluation of right ventricular function is an important aspect of cardiogenic shock evaluation. Significant RV dysfunction portends poor prognosis, can necessitate more aggressive interventions, and defines the types of mechanical circulatory support necessary.

•  Classification systems for cardiogenic shock help to further characterize a patient’s illness severity. The INTERMACS and SCAI classification systems are particularly designed to allow for early identification of patients who would most benefit from more advanced interventions such as vasoactive medications or mechanical circulatory support. 

• Shock Team Calls improve mortality for patients in cardiogenic shock. By rapidly bringing together heart failure specialists, interventional cardiologists, cardiothoracic surgeons, and critical care physicians, appropriate interventions and contingencies can be discussed and quickly implemented without adding delays to patient care. Importantly, these calls should attempt to integrate patient goals of care in order to best serve our patients. 

1. What is the classic definition of cardiogenic shock?

• The classic definition of cardiogenic shock was initially derived from the Shock Trial published in 1999 (1). In this trial, cardiogenic shock was defined as shock due to left ventricular dysfunction occurring in the setting of acute myocardial infarction in the setting of acute MI as confirmed by specific criteria:
  • Clinical criteria: 
    • SBP<90mmHg for at least 30 minutes
    • Need for supportive measures to maintain SBP > 90mmHg
    • End-organ hypoperfusion as defined by cool extremities, UOP <30ml/hr, HR > 60bpm
  • Hemodynamic criteria: 
    • CI ≤ 2.2 L/min/m2 BSA
    • PCWP ≥ 15mmHg
• With the advent of primary percutaneous coronary intervention, non-ischemic etiologies have become more prevalent as the etiology of cardiogenic shock such as decompensation of chronic heart failure, valvular heart disease, etc.
• As discussed on the episode, cardiogenic shock occurs on a spectrum from a “pre-shock” state to “extremis.” To facilitate early recognition of cardiogenic shock, appropriate phenotyping (e.g., LV-predominant, RV-predominant, biventricular, pericardial, valvular, pulmonary vascular, etc), timely interventions, and allocation of advanced therapies (e.g., mechanical circulatory support), a more granular approach to the classification is needed (see below regarding SCAI classification).

2. What are some of the clinical features of cardiogenic shock?

• Physical Exam Findings – A careful head-to-toe assessment should be conducted during the initial patient encounter. Important markers include (but are not limited to):
  • Signs of hypervolemia
    • Patient positioning as a sign of orthopnea
    • Elevated JVP
    • Tachypnea
    • Presence of pulmonary rales
    • Lower extremity edema
    • Hepatomegaly
    • Ascites
  • Signs of poor organ perfusion
    • Cool extremities
    • Poor hourly urine output.
    • Confusion or Altered Mental Status
  • Signs of poor cardiac output
    • Pulse quality – is it fast, slow, thready?
    • Pulsus alternans – alternation between strong and weak beats in sinus rhythm without change in cadence or cycle length (a marker of low output and ejection from the LV) (2).
    • Narrow pulse pressure
  • Clues to help determine the etiology of the shock
    • Point of maximal impulse displacement
    • Right ventricular heave
    • Auscultation of murmurs may indicate a valvular and/or congenital anomalies
    • An accentuated P2 may indicate pulmonary hypertension
    • Gallops may indicate filling pressures and/or underlying cardiomyopathy
    • A pericardial knock may indicate constrictive pericarditis
    • An irregular pulse may indicate an arrhythmia causing or contributing to shock
• Laboratory studies
  • Laboratory markers of end organ hypoperfusion include markers of renal function such as creatinine and of hepatic injury (AST, ALT) and function (INR).
  • Lactate has also been shown to display prognostic significance though clear correlations between objective thresholds to clinical outcomes have yet to be fully established.
  • More important than individual values themselves are their temporal trends and the integration of multiple data points across numerous variables. 
• Early Imaging studies
  • EKG should be obtained and reviewed early after presentation to evaluate for acute coronary syndrome and need for urgent coronary angiography.
  • Chest x-ray findings of pulmonary edema or effusions, assessment of heart size, and presence of cardiovascular hardware (sternal wires, implantable electrical devices, valvular interventions, etc). 
  • Focused transthoracic echocardiography, if available in the acute setting, can be helpful.
    • Focused TTE should assess left and right ventricular morphology and function, the presence of a left ventricular thrombus, stenotic or regurgitant valvular lesions, or dynamic outflow tract obstructions.
    • Echo surrogates of filling pressures may be supportive though may be limited by technique and image quality. 
• Evaluation of RV function and illness severity
  • Significant RV dysfunction is a marker of illness severity and leads to worse clinical outcomes.
  • RV dysfunction limits total cardiac output, worsens systemic venous congestion, and worsens end organ dysfunction.
  • RV assessment is critical when evaluating for the need for mechanical circulatory support, and severe RV dysfunction may increase the likelihood that MCS will be necessary.
  • Severe RV dysfunction may necessitate the use of specific MCS devices (e.g., RV assist devices). It may also impact decision-making regarding what types of temporary or, even more importantly, durable MCS devices the patient may qualify for. 
  • Enjoy the upcoming RV-Predominant Shock Episode with Dr. Ryan Tedford for a more in-depth discussion!
• Invasive hemodynamic assessment
  • Invasive hemodynamic evaluation with a pulmonary arterial catheter (PAC) is particularly useful for confirming and profiling cardiogenic shock as well as tailoring initial and subsequent management.
  • An accurate assessment of filling pressures, cardiac output (by Thermodilution or Indirect Fick), right ventricular function, systemic vascular resistance, and specific calculated indices (e.g., CPO, PAPi, RA/PCWP) provide a more nuanced evaluation of a patient’s shock.
  • Specifically, a PAC can assist in early identification of an under-recognized form of cardiogenic shock, under the classic Stevenson paradigm, a “wet and warm” picture. These patients have a systemic inflammatory response in addition to or as a result of their cardiac pathology, with a reduced cardiac index, low to normal SVR, and elevated pulmonary capillary pressures.
  • Enjoy the upcoming Invasive Hemodynamics episode with Dr. Nosheen Reza and the following infographic from CardioNerds Academy Fellow, Dr. Ahmed Ghoneem, for more details!

3. How is cardiogenic shock classified and how are these classifications useful in the management of cardiogenic shock?

• Differentiating cardiogenic shock from other types of shock and the severity of shock can often be challenging. Constructs such as Dr. Lynne Warner Stevenson’s physical exam-based shock classifications are helpful in broadly phenotyping cardiogenic shock at the bedside (3). However, these classification systems may have their limitations. Determining the underlying etiology relies heavily on integrating various pieces of clinical information ranging from the physical exam as well as laboratory and imaging information. In clinical practice, the following classification systems and schemas are most used – Cardiogenic Shock Classification Systems:
  • Killip Classification (4) – limited to acute myocardial infarction etiologies of cardiogenic shock:
    • Class I – No evidence of heart failure
    • Class II – Findings consistent with mild to moderate heart failure (e.g., S3 gallop, pulmonary rales less than one-half way up the posterior lung fields, or jugular venous distension)
    • Class III – Overt pulmonary edema
    • Class IV – Cardiogenic shock
  • INTERMACS (5) – Provides more granularity to the illness severity by dividing NYHA Class III to IV heart failure patients into 7 distinct profiles:
    • 1 – “Crash and Burn”: life-threatening hypotension refractory to intravenous inotropes, developed to understand patients who will require mechanical circulatory support (i.e., critical cardiogenic shock).
    • 2 – “Sliding on inotropes”: worsening end-organ dysfunction despite use of intravenous inotropic medications.
    • 3 – “Dependent stability”: stable hemodynamics and end-organ dysfunction but failure to wean from intravenous inotropes (i.e., inotrope-dependent)
    • 4 – Resting symptoms, ambulatory NYHA IV: at home on oral therapy but with frequent symptoms of congestion at rest or with any activities of daily living
    • 5 – Exertion intolerant: comfortable at rest but unable to engage in any activity, living predominantly within the house or housebound, but without overt congestion
    • 6 – Exertion limited: comfortable at rest without evidence of fluid overload and able to do some mild activities of daily living, but gets fatigued within a few minutes of any meaningful exertion
    • 7 – Advanced NYHA Class III: clinically stable with a reasonable level of comfortable activity, despite history of previous decompensation that is not recent
  • SCAI Classification System (6 – see Figure) – specifically geared towards the classification of cardiogenic shock, defining disease severity, and following patients through their hospital stay
    • A – At risk for cardiogenic shock 
    • B – Beginning of Cardiogenic Shock
    • C – Classic Cardiogenic Shock
    • D – Deteriorating
    • E – Extremis
• Acute Ischemic Cardiogenic Shock vs Heart-Failure Cardiogenic Shock
  • Understanding the underlying etiology of cardiogenic shock (e.g., acute ischemic vs. worsening chronic heart failure cardiogenic shock vs. acute heart failure cardiogenic shock) is very important in terms of management.
  • The clinical trajectory (and often the hemodynamics) of acute MI shock is different from the trajectory of chronic heart failure derived cardiogenic shock. At the basic level, acute-MI shock is an abrupt event often affecting an otherwise potentially stable or ambulatory patient, and thus warrants consideration for revascularization. On the other hand, decompensation of chronic heart failure may necessitate consideration of advanced therapies such as temporary or durable mechanical circulatory support or heart transplantation.

4. What is a Shock Team and how do we prepare for a shock team call?

• Shock Team
  • A shock team is designed to expeditiously bring together key members of the care team to determine patient management for a patient suspected to be in cardiogenic shock (7).
  • These members often include the referring physician, advanced heart failure cardiologist, interventional cardiologist, and cardiothoracic surgeon. Cardiac intensivists, electrophysiologists, or cardiac anesthesiologists may also be included when appropriate.  Each institution has their own policies regarding activation and composition of their teams.
  • The Shock Team call allows for expedited discussions to 1) confirm the diagnosis and severity of cardiogenic shock and 2) determine next therapeutic steps along with contingencies.
  • These discussions can include discussion of survival benefit, availability and type of interventions that can be offered, candidacy for advanced options, and patient values and preferences. Multiple studies have shown that these calls do not delay critical decision-making but in fact ensure appropriate level of support and allows for planning for care escalation. Shock teams have been shown to improve clinical outcomes for patients in cardiogenic shock (8). 
• Preparing for a Shock Team Call
  • The referring or presenting provider should include key clinical exam findings and objective laboratory or imaging data as outlined above.
  • In addition to this, providers should strive to include information regarding who the patient is outside of the hospital. This can include their history within healthcare, the patient’s support system, and goals of care. Obtaining these details to whatever extent possible allows us to best serve our patients. 
  • Importantly, this information, along with consideration of the overall trajectory of the patient can be factored into decisions regarding appropriate interventions.
  • The presenting provider may expect decisions that can range from initial stabilization on vasoactive medications to additional information needed from the cardiac catheterization laboratory to immediate plans for escalation to temporary or durable mechanical circulatory support.

Supplemental Images

1. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med. Aug 26 1999;341(9):625-34. doi:10.1056/NEJM199908263410901 

1. Araj FG, Mammen PPA. Alternans of the Pulse Is Rarely an Alternans of Prognosis. J Card Fail. 2021 Nov;27(11):1302-1303. doi: 10.1016/j.cardfail.2021.06.023. Epub 2021 Jul 26. PMID: 34324926. 

1. Stevenson LW. Tailored therapy to hemodynamic goals for advanced heart failure. Eur J Heart Fail. Aug 1999;1(3):251-7. doi:10.1016/s1388-9842(99)00015-x 

1. Killip T, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol. Oct 1967;20(4):457-64. doi:10.1016/0002-9149(67)90023-9 

1. Stevenson LW, Pagani FD, Young JB, et al. INTERMACS profiles of advanced heart failure: the current picture. J Heart Lung Transplant. Jun 2009;28(6):535-41. doi:10.1016/j.healun.2009.02.015 

1. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019. Catheter Cardiovasc Interv. Jul 01 2019;94(1):29-37. doi:10.1002/ccd.28329 

1. Taleb I, Koliopoulou AG, Tandar A, et al. Shock Team Approach in Refractory Cardiogenic Shock Requiring Short-Term Mechanical Circulatory Support: A Proof of Concept. Circulation. 07 02 2019;140(1):98-100. doi:10.1161/CIRCULATIONAHA.119.040654 

1. Papolos AI, Kenigsberg BB, Berg DD, et al. Management and outcomes of cardiogenic shock in cardiac ICUs with versus without shock teams. J Am Coll Cardiol. 2021;78:1309-1317. 

Dr. Anu Lala-Trindade is an advanced heart failure and transplant specialist at Mount Sinai Hospital in New York City. She serves as the Director of Heart Failure Research and as Data Coordinating Center leadership for the NHLBI Cardiothoracic Surgery Network. A prolific educator, Dr. Lala has won numerous teaching awards and leads the fellowship program in Advanced Heart Failure and Transplant. A physician-scientist par excellence, she has authored numerous peer reviewed scientific publications and is the principal investigator for a number of clinical trials in heart failure. She serves as the deputy editor of the Journal of Cardiac Failure and also serves on local and national committees in the American Heart Association, American College of Cardiology, Heart Failure Society of America among others, devoted to advanced heart disease.

Dr. Mark Dela Cruz is currently an Advanced Heart Failure Fellow at the University of Chicago. Before then, he obtained his Bachelor of Arts degree at the University of Pennsylvania, where he graduated Summa Cum Laude with a double major in French Studies and with Distinction in Biological Basis of Behavior. He went on to obtain his medical degree and completed his internal medicine residency at the University of California, San Francisco where he participated in the clinical research pathway, Program in Residency Investigation Methods and Epidemiology. He served as a heart failure hospitalist before coming to the University of Chicago for Cardiology Fellowship. He has conducted research on vascular endothelium, and the interaction between HIV and Cardiology. Now, he focuses on translational research on the impact of the gut microbiome in heart transplantation. Born in Manila, Philippines, Dr Dela Cruz also maintains an interest in Filipino cardiovascular health and is an avid traveler.

• Karan Desai, MD
• Dr. Mark Belkin
• Amit Goyal, MD
• Daniel Ambinder, MD