In this webinar, the CardioNerds collaborated with the Cardiogenic Shock Working Group (CSWG) to discuss LV unloading and the updated AMI guidelines, which upgraded transvalvular flow pumps to a Class 2A recommendation in AMI shock.

Dr. Rachel Goodman and Dr. Gurleen Kaur from CardioNerds were joined by Dr. Navin Kapur (Tufts Medical Center), Dr. Shashank Sinha (INOVA Fairfax Hospital), and Dr. Rachna Kataria (Brown University) from the CSWG.

Together, they explore a case of an older woman who presented with inferior STEMI and was found to have complete occlusion of an anomalous single coronary artery originating from the right coronary cusp and supplying the entire left ventricle. She was treated with DES to the anomalous RCA. Her course was complicated by AMI shock with re-occlusion of the DES, which was treated with thrombectomy and balloon angioplasty. An IABP was placed. After transfer to a tertiary care center, a pulmonary artery catheter revealed a CI of 0.96. With worsening shock, rising lactate, and end organ dysfunction, the team proceeded with VA-ECMO and Impella CP for LV unloading. Her lactate subsequently normalized.

Produced by CardioNerds in collaboration with the Cardiogenic Shock Working Group.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

CardioNerds Cardiac Critical Care Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

CardioNerds Co-Founder, Dr. Amit Goyal, along with Series Co-Chairs, Dr. Yoav Karpenshif and Dr. Eunice Dugan, and episode Lead, Dr. Sean Dikdan, had the opportunity to expand their knowledge on the topic of ventricular tachycardia and electrical storm from esteemed faculty expert, Dr. Janice Chyou. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian.

Electrical storm (ES) is a life-threatening arrhythmia syndrome. It is characterized by frequently occurring bouts of unstable cardiac arrythmias. It typically occurs in patients with susceptible substrate, either myocardial scar or a genetic predisposition. The adrenergic input of the sympathetic nervous system can perpetuate arrythmia. In the acute setting, identifying reversible triggers, such as ischemia, electrolyte imbalances, and heart failure, is important. Treatment is complex and varies based on previous treatments received and the presence of intra-cardiac devices. Many options are available to treat ES, including medications, intubation and sedation, procedures and surgeries targeting the autonomic nervous system, and catheter ablation to modulate the myocardial substrate. A multidisciplinary team of cardiologists, intensivists, electrophysiologists, surgeons, and more are necessary to manage this complex disease.

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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

CardioNerds Cardiac Critical Care Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

Simple diagram of the classic “triad” of ES (see reference 10).

Treatment algorithm provided by the 2017 AHA/ACC/HRS guidelines (see reference 1).

1. Define electrical storm.

Electrical storm (ES), also called “arrhythmic storm” or “VT storm” refers to a state of cardiac instability associated with 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. Sustained VT refers to 30 seconds of VT or hemodynamically unstable VT requiring termination in < 30 seconds. Incessant VT refers to continued, sustained hemodynamically stable VT that lasts longer than one hour. VT is incessant or recurrent when it recurs promptly despite repeated intervention for termination.1,2

In patients with ICDs for secondary prevention, ES is estimated to occur in 10-28% of patients.3–5 This incidence is much lower in patients who have ICDs implanted for primary prevention in whom the incidence has been estimated as low as 4% at 20 months of follow up.6 ES occurs at similar rates in patients with ischemic or non-ischemic cardiomyopathy.7

ES is associated with a poor prognosis and high cardiovascular mortality. The three-month mortality in patients with an episode of ES has been estimated at up to 18 times higher than in patients without any VT.6 Risk factors for the development of ES include male sex, advanced age, low left ventricular ejection fraction, use of class 1A antiarrhythmic drugs, and the presence of cardiovascular comorbidities.8,9

2. Evaluate the cause of VT storm (e.g., evaluation for ischemia, sarcoidosis , etc)

The classic triad of ES is a trigger, a substrate susceptible to ES, and autonomic input perpetuating the storm.10 Potential triggers are varied and typically include myocardial ischemia, decompensated heart failure, electrolyte abnormalities, hypoxia, drug-related arrhythmogenicity, and thyrotoxicosis.4,11 A clear trigger is often not found (only 13% of the time by some estimates).12 Searching for a trigger should not delay management decisions in the acute setting.

Structural heart disease unrelated to ischemia such as congenital heart disease and infiltrative cardiomyopathies can serve as the substrate for ES. Conditions related to genetic causes such as long QT syndrome or catecholaminergic polymorphic VT may be a rare etiology. These conditions represent an electrophysiologic substrate as opposed to a structural substrate.13

3. Choose an initial management strategy for patients with electrical storm in the CCU.

Treatment of ES is complex. The initial steps in management involve resuscitation, pharmacotherapy, device interrogation and reprogramming, and sedation. ACLS should be used in patients with pulseless VT or VF.

Patients with and without cardioverter-defibrillators may be treated differently. Defibrillations from an implanted device accentuate sympathetic tone and may perpetuate further arrhythmia.

Once a patient is stabilized, more advanced therapies involving autonomic modulation or catheter ablation (CA) can be utilized. In the patient with ischemia, emergent revascularization should be pursued. The need for mechanical circulatory support (MCS) should be determined. Inotropes and many vasopressors are sympathetic agonists and may worsen the arrhythmia by accentuating adrenergic tone, and so the benefits of improved hemodynamics need to be weighed against the risk of worsening electrical instability.

Initial pharmacotherapy in ES includes an antiarrhythmic drug and a beta blocker. Typically loading the patient with IV amiodarone and administering a non-selective beta blocker like propranolol is done. This combination has been shown in ES patients to have superior freedom of arrhythmia compared to using metoprolol.14 Propranolol’s superiority may also be due to its ability to cross the blood-brain barrier. Lidocaine has improved efficacy in ischemic VT.15,16 Procainamide has been shown to be useful in patients with hemodynamically stable VT.17

4. Identify predisposing conditions that should be managed to help treat electrical storm such as ischemia and AHF.

Identifying and managing specific triggers is an important initial step in the management of ES. Hypoxia on vital signs or evidence of decompensated HF on exam (with JVD, edema, crackles on auscultation) can implicate volume overload; this can be managed with diuresis.

Ischemic ECG changes on the 12-lead ECG when the patient’s ventricular arrhythmia is broken, can suggest myocardial ischemia. If ischemia is believed to be the trigger, urgent revascularization should be pursued while resuscitation is underway.

Blood work should include screening for electrolyte abnormalities and thyroid disease. Carefully screening the patient’s medication list and checking a digoxin level  (when appropriate) can help detect drug-induced arrhythmia.

Once out of the acute setting, genetic testing may be important in patients without structural disease for determining an etiology. Idiopathic VT, Brugada syndrome, long QT syndrome, short QT syndrome, early repolarization syndrome, catecholaminergic polymorphic VT, arrhythmogenic right ventricular cardiomyopathy, and cardiac sarcoidosis are potential etiologies that may be related to ES.10

5. Recognize when to use general anesthesia to aid in the stabilization of electrical storm and incessant VT.

Intubation and deep sedation are immediate next steps to minimize the sympathetic drive contributing to the arrhythmia. This treatment is very effective at terminating arrythmia and preventing immediate recurrence.18,19 This step is used in the acute setting for ES that persists despite pharmacotherapy. Note that propofol is a negative inotrope with the potential to worsen heart failure in decompensated patients and precipitate shock.

In addition to breaking the sympathetic cycle that drives this pathophysiology, sedation mitigates some of the psychological stress that repeated ICD shocks can cause in patients.20

6. Describe considerations specific to patients with implanted ICDs.

If a patient with an ICD presents with ES, the device should be interrogated. It is important to confirm the shocks are appropriate. Inappropriate shocks can occur in up to 40% of patients with an ICD; causes may include atrial arrythmia, oversensing, and lead fracture.21,22 Inappropriate ICD shocks are associated with a worse outcome.

Overdrive pacing is a possible therapy to prevent ES. If the ES is hemodynamically stable, then the ICD therapies may be disabled manually or with the use of a magnet.

If anti-tachycardia pacing (ATP) treats the ventricular arrythmia effectively, adjusting these settings and increasing the use of ATP can mitigate unnecessary shocks in the future.23

7. Understand the role of catheter ablation in the management of electrical storm.

Research has shown an excellent response of ES to catheter ablation (CA). CA has a class 1 indication in patients with ES due to anti-arrhythmic drug refractory VA in both ischemic and nonischemic cardiomyopathy.2

Treatment of an initial episode of ES with CA has shown a reduction in all-cause mortality compared to other modalities.24 At nearly 1-2 years of follow up, nearly 90% of patients with ES that undergo CA are free from further ES, and roughly two-thirds of these patients are free from any ventricular arrythmia (VA) recurrence.25,26

CA is also relatively safe in this setting, with procedure-related mortality estimated to be less than 1%.27 Rapid transfer to an experienced catheter ablation capable facility is important in all critically ill patients with ES.

8. Consider when it may be appropriate to use mechanical support such as IABP, pVAD and ECMO.

Mechanical circulatory support (MCS) may be necessary to maintain adequate perfusion when the patient is suffering from cardiogenic shock due to unstable arrhythmia.

Patients with high risk for hemodynamic decompensation during CA can be preemptively supported with MCS. This practice has been shown to improve mortality compared to rescue or no MCS. 28,29 The PAAINESD score may be useful in identifying high risk patients. This score assigns numerical values to the following risk factors: pulmonary disease, age over 60 years, general anesthesia, ischemic cardiomyopathy, NYHA class III or IV, LV EF < 25%, VT storm, and diabetes mellitus. 2,28

An intra-aortic balloon pump may be sufficient but requires the patient to have enough adequate forward flow to generate a pulse. Extracorporeal membrane oxygenation (ECMO) has been studied and shows good long-term outcomes.29 Guidelines have a IIa recommendation for hemodynamic support with ECMO or a temporary LVAD during CA in select patients. 2

9. Discuss other strategies such as sympathectomies (stellate ganglion block vs. surgical), stereotactic radio ablation, and transplant for refractory cases.

There are several therapies available to treat ES that specifically target the autonomic nervous system (ANS).30 While sedation is used for this purpose acutely, other interventions seek to mitigate sympathetic activity in the subacute or chronic setting. These include stellate ganglion blockade (SGB), thoracic epidural anesthesia (TEA), cardiac sympathetic denervation (CSD), and renal artery sympathetic denervation (RSD).

Percutaneous SBG involves an injection of anesthetic directly into the stellate ganglia with or without ultrasound guidance. This is a temporizing measure that can be performed in the acute or subacute setting. It has shown complete suppression of VA in 50% of patients for the subsequent 48 hours.31

TEA involves the percutaneous administration of a local anesthetic directly into the thoracic epidural space. This is also a temporary treatment best used as a bridge to definitive treatment, such as CA or surgical denervation. In ES patients with a failed CA TEA can reduce VA up to 80% in most patients.32

CSD is a surgical measure that offers a more permanent solution. It can be useful in refractory ES that has not responded to multiple treatments. CSD has achieved 80% event-free survival up to 2 years.33 Guidelines recommend CSD in ES when beta-blockade, anti-arrhythmic drugs, and CA are deemed ineffective with a class IIb recommendation.1

RSD functions similarly but has the added benefit of being non-surgical and directly reducing catecholamine secretion.

Cardiac transplantation would be indicated in a patient that has unrelenting ES despite these aggressive measures. Patients with MCS and life-threatening arrhythmias qualify as status 1 for OHT.34 Whereas VT/VF without MCS by itself would qualify a patient as status 2.

The practice of critical care cardiology relies on the use of invasive hemodynamics, mechanical ventilation, mechanical circulatory support, and other advanced techniques to help our patients recover from critical cardiac illnesses. To facilitate these interventions, it is essential to have a broad understanding of how sedation and analgesia keep our patients comfortable and safe throughout their time in the CICU. In this episode, series co-chair, Dr. Yoav Karpenshif, and CardioNerds co-founder, Dr. Daniel Ambinder, are joined by Dr. Natalie Tapaskar, cardiology fellow and CardioNerds FIT Ambassador from Stanford, and faculty expert, Dr. Chris Domenico, to discuss sedation in the cardiac ICU. Notes were drafted by Dr. Natalie Tapaskar. Audio editing by CardioNerds academy intern, Anusha Gandhi.

We discuss the use of analgesics and sedative medications in the cardiac ICU. We dissect three cases of VT storm, heart failure associated cardiogenic shock, and cardiac arrest. We assess the hemodynamic, arrhythmic, and metabolic effects of opioids and sedatives and delve into the altered pharmacokinetics of these drugs during targeted temperature management. Most importantly, we highlight the use of structured pain and sedation scoring systems and discuss the recognition and management of ICU delirium both from a pharmacologic and non-pharmacologic standpoint.

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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

CardioNerds Cardiac Critical Care Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

CardioNerds (Amit and Dan) join Dr. Maria Pabon (cardiology fellow), Dr. Kevin Bersell (cardiology fellow), Dr. Saad Sultan Ghumman (interventional cardiology fellow), and Dr. Rhanderson Cardoso (cardiovascular imaging fellow) from Brigham and Women’s Hospital. Together, they explore a complex case of STEMI that was further complicated by ventricular free wall rupture. Additionally, Dr. Ajar Kochar, Program Director for Interventional Cardiology at Brigham and Women’s Hospital, provides an insightful “ECPR” segment, adding a unique perspective to the case. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah.

This is the case of a patient who presented with STEMI and was found to have a moderate pericardial effusion with echogenic material within the pericardial space concerning for thrombus. Urgent CTA/CT surgery was engaged due to concern for dissection, but no evidence of dissection, rupture or intramural hematoma was found. The patient underwent an urgent pericardiocentesis which yielded 350cc of hemorrhagic fluid, leading to an improvement in hemodynamic status. A coronary angiogram was performed which showed a 100% thrombotic occlusion of OM 1, the culprit lesion for the STEMI. Due to the possibility of a delayed STEMI and high suspicion for mechanical complication of MI, aspirin and IV cangrelor were chosen as the preferred antiplatelet strategy. However, cangrelor was held and cardiac surgery was consulted, as LV free wall rupture was suspected. The patient underwent urgent repair of the LV free wall rupture, with an uneventful post-op recovery and discharge on day 8 to cardiac rehab.

CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

It’s another session of CardioNerds Rounds! In these rounds, Dr. Karan Desai (Formerly FIT at University of Maryland Medical Center and currently faculty at Johns Hopkins School of Medicine) joins Dr. Dan Burkhoff (Director of Heart Failure, Hemodynamics and MCS Research at the Cardiovascular Research Foundation) to discuss mechanical circulatory support options through the lens of pressure-volume loops! Dr. Burkhoff is the author of Harvi, an interactive simulation-based application for teaching and researching many aspects of ventricular hemodynamics. Don’t miss this wonderfully nerdy episode with a world-renowned expert in hemodynamics and MCS! Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. 

CardioNerds Rounds Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

Case Synopsis:

Case Synopsis
We focused on one case during these rounds. A man in his mid-50s presented to his local community hospital with 3 days of chest pain, nausea, and vomiting. He appeared ill in the emergency room with HR in the 150s, BP 90/70s and ECG demonstrating inferior ST elevations. He was taken emergently to the catheterization lab and received overlapping stents to his right coronary artery. Over the next 24 hours, he developed a new harsh systolic murmur heard throughout his precordium and progressed to cardiogenic shock. Echocardiogram demonstrated a large basal inferoseptum ventricular septal rupture. From this point, we discussed the hemodynamics of VSR and MCS options.

Case Takeaways

Enjoy this ACC.org Expert Analysis by Goyal and Menon to learn more about post-myocardial infarction ventricular septal rupture.

Renal replacement therapy (RRT) is routinely utilized in the CICU. Series co-chairs Dr. Eunice Dugan and Dr Karan Desai along with CardioNerds Co-founder Dr. Daniel Ambinder were joined by FIT lead and CardioNerds Ambassador from University of Washington, Dr. Tomio Tran. Our episode expert is world-renowned nephrologist Dr. Joel Topf. Dr. Topf is Medical Director of Research at St. Clair Nephrology, and editor of the Handbook of Critical Care Nephrology. In this episode, we describe a case of cardiogenic shock due to acute myocardial infarction resulting in renal failure, ultimately requiring continuous RRT (CRRT). We discuss the most common causes of AKI within the cardiac ICU, indications for initiating RRT, evidence on the timing of RRT, different modes of RRT, basic management of the RRT circuit, and how to transition patients off of RRT during renal recovery. Episode notes were drafted by Dr. Tomio Tran. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian.

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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

This episode is made possible with support from Glass.Health – The first digital notebook designed for doctors. Follow @GlassHealthHQ for the latest product updates!

Pearls • Notes • References • Production Team

CardioNerds Cardiac Critical Care Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

What are the risk factors and differential for AKI in the CICU?

What is the approach to timing of renal replacement therapy initiation?

For the non-nephrologists, what are options for RRT acutely and how do they work?

What should non-nephrologists understand about daily management of patients on CVVH?

How does the CICU team monitor for native renal recovery and initiate cardiovascular GDMT?

The Cardiorenal Syndrome is commonly encountered, and frequently misunderstood. Join the CardioNerds team as we discuss the complex interplay between the heart and kidneys with Dr. Elliott Miller (Assistant Professor of Medicine at Yale University School of Medicine and Associate Medical Director of the Cardiac Intensive Care Unit of Yale New Haven Hospital), and Dr. Nayan Arora (Clinical Assistant Professor of Medicine and Nephrologist at the University of Washington Medical Center). We are hosted by FIT lead Dr. Matthew Delfiner (Cardiology Fellow at Temple University), Cardiac Critical Care Series Co-Chairs Dr. Mark Belkin (AHFTC faculty at University of Chicago) and Dr. Karan Desai (Cardiologist at Johns Hopkins Hospital), and CardioNerds Co-Found Dr. Dan Ambinder. In this episode we discuss the definition and pathophysiology of the cardiorenal syndrome, explore strategies for initial diuresis and diuretic resistance, and management of the common heart failure medications in this setting. Show notes were developed by Dr. Matthew Delfiner. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig.

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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

CardioNerds Cardiac Critical Care Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

1. Cardiorenal syndrome (CRS) is a collection of signs/symptoms that indicate injury to both the heart and kidneys. Organ dysfunction in one can drive dysfunction in the other. Cardiorenal syndrome can be categorized as:

These categories can be helpful for education, discussion, and research purposes, but they do not usually enter clinical practice on a regular basis since different categories of cardiorenal syndrome are not necessarily treated differently.

2. CRS is caused by either reduced renal perfusion, elevated renal congestion, or a combination of the two. When dealing with CRS, note that:

3. Renal decongestion is achieved primarily through diuresis.

4. It is okay if creatinine rises with diuresis, to a degree.

5. There are multiple ways to manage diuretic resistance.

6. Decisions regarding cessation versus continuation of renin-angiotensin-aldosterone system (RAAS) inhibitors in the setting of CRS should be made on a case-by-case basis.

This episode is focused on Palliative Care and Shared Decision-Making in the CICU. In this episode, we learn about how the principles of palliative care and shared decision-making apply to our patients across the spectrum of cardiovascular care, especially in the cardiac intensive care unit. We discuss pivotal trials of specialty palliative care and decision aids in cardiology and how they might inform our practice to enhance patient quality of life and improve goal-concordant care. Finally, we discuss practical tips and communication strategies for how to engage patients about end-of-life decisions and topics that can be utilized from outpatient to inpatient to critical care settings.

“We need to help patients hope for the best and plan for the worst as time goes on.”

Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai, along with CardioNerds Co-founder Amit Goyal are joined by FIT lead, Dr. Sarah Chuzi. Dr. Chuzi is a Chicagoan and completed her internal medicine residency, cardiology fellowship, AHFTC fellowship and is now Assistant Professor at Northwestern University. Our episode expert is a true national leader in shared decision-making and palliative care in heart failure – Dr. Larry Allen, Medical Director of Advanced Heart Failure and the Co-Director of the Colorado Program for Patient-Centered Decisions at the University of Colorado School of Medicine. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen.

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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

CardioNerds Cardiac Critical Care Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

1. “Much of what we do in cardiology is thinking about how to make people feel better (not just improving cardiac function or length of life). So, on a day-to-day basis we are really providing primary palliative care.” – Dr. Larry Allen

2. “Risk models in cardiology can only be so accurate… While risk models can give us some grounding, we also need to embrace the concept of uncertainty, and help patients understand that there are a variety of things that might happen to them, suggest some things they might plan for, and continue to iteratively come back to the patient and reevaluate what their options are.” – Dr. Larry Allen

3. “Our goal is to help people live happy, healthy, full lives. But, everyone dies. So understanding that death is a part of life and understanding how to help them make those transitions is critical” – Dr. Larry Allen

4. “Having good deaths is a part of good healthcare. We can’t ignore that. We can’t fight against it. We should embrace it. And we have the opportunity to do that.” – Dr. Larry Allen

5. We should still keep in mind the concept of medical futility and determining what options are reasonable for patients. Part of shared decision-making includes discussing what interventions would not be feasible or helpful with patients and families

Notes drafted by Dr. Sarah Chuzi.

1. How are the basic principles of palliative care relevant to cardiology, and can you define the key concepts of shared decision-making, primary palliative care, specialty (or secondary) palliative care, and hospice care?

2. What have we learned from existing trials looking at specialty palliative care in heart failure?

3. What are some strategies trainees can use to help elucidate a patient’s goals and values and engage in shared decision-making in high intensity, critical care situations?

4. What is the role of decision aids in the process of deciding whether to pursue LVAD implantation?

5. What are the benefits of hospice for patients with cardiac disease and how does hospice fall short?

Rogers JG, Patel CB, Mentz RJ, et al. The palliative care in heart failure (PAL-HF) randomized, controlled clinical trial. 2017. J Am Coll Cardiol, 70(3): 331-341.

Allen LA, Mcilvennan CK, Thompson JS, et al. Effectiveness of an intervention supporting shared decision making for destination therapy left ventricular assist device: the DECIDE-LVAD randomized clinical trial. 2018. JAMA Intern Med, 178(4): 520-529.

Warraich HJ, Patel CB, Kochar A, Rogers JG, Patel MR. Incorporating shared decision making and palliative care into cardiogenic shock pathways. 2010. J Am Coll Cardiol, 74(4): 501-502.

Chuzi S, Khan SS, Pak ES. Primary palliative care education in advanced heart failure and transplant cardiology fellowships. 2021. J Am Coll Cardiol, 77(4): 501-505.  

In this episode, we discuss the utility of veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) for the temporary management of biventricular failure and cardiogenic shock requiring full cardiopulmonary support. Here, we define the types of ECMO and describe the unique physiology of this mechanical circulatory support platform, as well as review the potential complications and management strategies. Most notably, we highlight indications for and contraindications to the use of VA-ECMO and review the importance of patient selection.  Lastly, we discuss de-escalation and de-cannulation strategies for patients on VA-ECMO as a bridge to recovery.

Join Dr. Amit Goyal (CardioNerds Cofounder and FIT at Cleveland Clinic), Dr. Yoav Karpenshif (Series Co-chair and FIT at University of Pennsylvania), and Dr. Megan Burke (Episode FIT Lead and FIT at University of Pennsylvania) as they learn about how to care for some of our sickest patients from Dr. Ann Gage, interventional and critical care cardiologist at Centennial Heart. At the beginning of the episode, enjoy a message from the very first CardioNerds Scholar, Dr. Katie Vaughan (Chief Resident and soon Cardiology Fellow at BIDMC). Episode notes were developed by Dr. Megan Burke. Audio editing by CardioNerds Academy Intern, Hirsh Elhence.

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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

CardioNerds Cardiac Critical Care Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

Notes drafted by Dr. Megan Burke.

1. What is ECMO and what are the different types?

2. What are the components and “anatomy” of the VA-ECMO circuit?

3. What are the indications for VA-ECMO?

4. What are the pathophysiological consequences of VA-ECMO and how do we monitor and treat them?

5. How is VA-ECMO weaned?

CardioNerd (Daniel Ambinder) and series co-chairs Mark Belkin (AHFT Fellow, University of Chicago) and Karan Desai (Cardiologist, Johns Hopkins), join fellow lead, Dr. Pablo Sanchez (FIT, Stanford) for a discussion with Dr. Ryan Tedford (Professor of Medicine at the Medical University of South Carolina) about Right Ventricular (RV) predominant cardiogenic shock. In this episode we explore risk factors, pathophysiology, hemodynamics, and treatment strategies in this common and complex problem. We dissect three cases that epitomize the range of diagnostic dilemmas and management decisions in RV predominant shock, as Dr. Tedford expertly weaves us through the pathophysiology and decision-making involved in managing the “people’s ventricle.” Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds internship program, CardioNerds academy fellow, and IM resident at Brigham and Women’s Hospital).

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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

CardioNerds Cardiac Critical Care Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll

CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!

1. The degree of RV dysfunction and failure are modulated by stretching its capacity to tolerate insults from deranged afterload, preload, and contractility.
2. Afterload insults are MUCH LESS tolerated than other insults and broadly comprise the most common pathophysiologic cause of both acute and chronic RV failure.
3. RV and left ventricular (LV) function are anatomically and physiologically connected.  Progressive derangements in RV function can lead to the deadly “RV spiral,” in which poor RV function causes lower LV preload, leading to hypotension, and thus worsening RV perfusion and function.
4. In RV failure/shock, some basic tenets including treating reversible causes, optimizing preload and afterload, and using inotropes and/or temporary MCS for as limited time as possible.
5. Many acute RV failure patients can recover, but multiorgan injury plays an important role. Therefore, thoughtful and expeditious use of mechanical circulatory support is important.

Notes drafted by Dr. Pablo Sanchez.

1. What is the basic difference between RV dysfunction and failure?
   • Dysfunction: Abnormalities in systolic/diastolic function of the RV, but not necessarily to the point of leading to end-organ perfusion defects. RV dysfunction leads to poor outcomes regardless of mechanism.1
   • Failure: Clinical syndrome of inability of RV to maintain adequate output despite adequate preload. 1

1. How is the RV different from the LV and what impact does it have on pathophysiology and hemodynamics?
   • The LV and RV originate from different embryologic “heart fields.”1,2
   • The RV wall is thinner and more compliant and has only two layers (instead of 3 like the LV).3 Furthermore, unlike the LV which has a significant proportion of endocardial and epicardial transverse myocardial fibers, the RV myocardial fibers are aligned in a longitudinal plane for the most part. Thus, a more significant proportion of RV systolic contraction is longitudinal – base of the ventricle moving towards the apex.
   • The RV is crescent-shaped and has a large surface-to-volume ratio meaning smaller inward motion ejects the same stroke volume. 1
   • Hemodynamically, the RV takes blood from a low-pressure venous system and gives it to a distensible system with low impedance (the normal pulmonary circuit at baseline typically has a resistance one-tenth of the systemic resistance). Therefore, volume loads (preload) are much better handled than pressure (afterload).1

1. What is RV-PA coupling?
   • As Dr. Tedford noted, RV-PA coupling describes “the interaction of RV contractility and afterload (resistive and pulsatile components). It is the most comprehensive description of RV function and therefore the Gold Standard.” Whether we are referring to the LV or RV, the basic concept of coupling describes the energy transfer between ventricular contractility and arterial afterload.
   • RV-PA coupling has typically been assessed by pressure-volume loops, with ventricular contractility assessed by end-systolic elastance (a load-independent measure of systolic function) and arterial afterload by effective arterial elastance.
   • MODUS OPERANDI: RV dysfunction and eventual failure is modulated by stretching its capacity to tolerate insults from afterload, preload, and contractility.

1. What leads to ACUTE right heart failure?
   • Most commonly results from:1
   • Abrupt increases in afterload (e.g., think PE, hypoxia, and acidemia).
   • Decreased contractility (e.g., think ischemia such as RV infarction, myocarditis, and post-cardiotomy).
   • Volume overload can sometimes lead to acute right heart failure, particularly in the setting of another categorical insult such as septic cardiomyopathy or LVAD support.

1. What leads to CHRONIC right heart failure?
   • This is different than acute right heart failure. Most commonly chronic right heart failure results from:1
     • Gradual increases in afterload (e.g., think pulmonary arterial hypertension).
     • Chronic volume overload (e.g., longstanding tricuspid regurgitation, atrial septal defect, and other congenital lesions like double outlet RV).
     • Contractility (e.g., including the isolated RV cardiomyopathies like arrhythmogenic right ventricular cardiomyopathy or ischemic cardiomyopathy).
     • Other pathologies certainly affect multiple categories (e.g., Ebstein’s anomaly which is a function of contractility and volume overload or single ventricle physiology like post-Fontan patients – for more on these and other ACHD lesions, enjoy the CardioNerds ACHD Series!)
   • MODUS OPERANDI: The cardiovascular system is wholly connected, and acute decompensation leads to progressive derangements in the above levers (including LV function). This phenomenon is called the RV spiral.

1. How do we manage RV failure?
   • The most important and first step is the treatment of reversible causes. For instance, acute coronary syndrome involving the RV requires percutaneous intervention (PCI) or pulmonary embolism requires anticoagulation and/or thrombolytic/device/surgical therapy.
   • PRELOAD OPTIMIZATION
     • Ensuring that there is adequate preload is a key tenet of diagnosing and treating RV failure. This may require diuresis or judicious volume resuscitation to maintain cardiac output.
     • While guiding fluid management in the setting of RV failure, one should STRONGLY consider invasive hemodynamic monitoring (e.g., over-resuscitation can lead to decreased LV output through septal shift and ventricular interdependence from pericardial constraint).1
     • General target: We could consider a CVP 10-15 mmHg; however, this will be individualized. Another general rule would also be if that a bolus of 500 cc of crystalloid does not result in hemodynamic improvement, further loading should not be continued, especially without invasive hemodynamic guidance.
   • AFTERLOAD OPTIMIZATION 
     • The goal should be to correct reversible causes of elevated pulmonary vascular resistance (e.g., acidosis, hypercapnia, hypoxia, and generally in ventilated patients avoid elevated inspiratory pressures > 30mmHg).1
     • With specialized expert guidance, we can consider selective pulmonary vasodilators (acutely and short-term):
       • One example includes inhaled NO, and in observational studies, short-term use lowered PVR and increased RV ejection.4
       • We also have to remember the consequences of reducing RV afterload. Acutely increasing LV preload in a baseline abnormal LV may lead to distention, lowered cardiac output, and pulmonary edema.1
       • Pulmonary vasodilators can act on specific pathways (e.g., nitric oxide, prostacyclin, endothelin-1, and soluble guanylate cyclase stimulators) and come in various forms (oral, inhaled, and intravenous).
   • CONTRACTILITY AUGMENTATION (INOTROPES)
     • We typically utilize inotropes in concert with the prior two but optimize loading so the time we need inotropes is minimal.1
     • Short-term use can improve hemodynamics. Longer-term use will typically increase myocardial O2 consumption and is associated with increased mortality. 
     • The RV has coronary perfusion in systole and diastole, so peripheral vasopressors are helpful to maintain perfusion, especially if systolic blood pressure is less than RV systolic pressure.1
   • GOAL: Increase contractility without increasing RV afterload.
2. For those failing to respond to these above measures to optimize preload, afterload, and contractility, there may be a role for temporary mechanical circulatory support (see #10 below).

1. How do we decide between dobutamine and milrinone?
   • BOTH inotropes can lead to hypotension, have similar clinical outcomes, hemodynamic efficacy and arrhythmogenic potential1 (despite the adage that attributes more arrhythmias to dobutamine, studies show the risk is typically the same in both5).
   • Milrinone is a more potent vasodilator (systemic and pulmonary) typically leading to greater decreases in end-diastolic pressures in the ventricles.1 It is renally cleared, has a longer half-life, and acts through a separate mechanism pathway compared to beta-blockade, thus patients can be on milrinone and beta blockers at the same time on a case-by-case basis.1
   • Dobutamine has a shorter half-life, with rapid onset/offset and so may be more ideal in unstable/hypotensive patients.1

1. What if the patient is hypotensive?
   • In this circumstance, we would need an ino-constrictor or peripheral vasoconstrictor.
   • Vasopressin has almost no impact on PVR, so unlike catecholamines, it does not directly worsen RV afterload.1

1. What are some important invasive hemodynamic parameters to be aware of?
   • RAP/PCWP ratio: Disproportionate RV dysfunction can be portrayed by an RAP/PCWP ratio > 0.5-0.8 (depending on the clinical situation). In other words, the closer that RAP and PCWP are, the more likely you have disproportionate RV dysfunction.
     • The predictive power of this ratio is different depending on the situation. Pre-operatively, a ratio > 0.63 is associated with RHF post-LVAD.6 In acute inferior MI, a ratio of > 0.86 is associated with RHF.7
   • PAPi: The PA pulse pressure gives us an idea of the ability of the RV to generate SV. Dividing this by the RAP, gives us an index that takes into account right-sided filling pressures.
     • As above, the context is important. In acute inferior MI a PAPi of < 1.0 is predictive of mortality or MCS need,8 while a pre-operative PAPi < 1.8 was predictive of RHF after LVAD.9
     • Caveats: As Dr. Tedford mentioned, the PAPi is related to RV function, but not a direct measure of it. Manipulation of each component (e.g., pulse pressure or RA pressure) can ultimately lead to a similar absolute value of PAPi under very different loading conditions.
     • PA pulse pressure is a function not only of SV but also of PA capacitance. In other words, a narrow pulse pressure can be due to a failing RV or a low pulmonary capacitance (from fluid overload for example). This isn’t clearly gleaned from the PAPi alone and requires us to keep in mind the context of the equation.
   • Note: The gold standard assessments of RV contractility are derived from Pressure-Volume loops which require both simultaneous assessment of pressure and volume as well as alteration of preload over multiple beats. This limits applicability because it is technically challenging to do.10 

1. What are important concepts to remember for Mechanical Support of the RV?
   • One of the first things to consider is the end-game: are we using MCS as a bridge to recovery, bridge to decision, bridge to transplant, or bridge to durable MCS?
   • Many acute RHF patients can recover with adequate support and a significant prognostic factor is preventing multiorgan failure.11,12 If MCS is needed, early use is better than later.
   • Another important question is if we need oxygenation? Many of the MCS options, except the Impella RP, can have an oxygenator spliced into the system.11
   • A key question will be if we need RV-only support or biventricular support?11
     • RV-targeted support will increase LV preload, and the LV has to be able to accommodate the increased volume.
     • If the LV is unable to tolerate the increased return, systemic cardiac output can become inadequate, LV filling pressures will rise, which can lead to pulmonary edema and increase mean PA pressures further (which can also lead to acute lung injury and worse outcomes). In these circumstances, biventricular support with either VA-ECMO or permutations of isolated RV + LV support may be needed.
   • We also have to ask ourselves, if pulmonary arterial HTN primarily responsible for RV shock?11
     • If so, then VA-ECMO may be the most appropriate option.
     • Increased flow from an RVAD, combined with a pre-existing elevated PVR can lead to elevated pulmonary artery pressures, which can precipitate pulmonary hemorrhage.1

Konstam MA, Kiernan MS, Bernstein D, et al. Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation. 2018;137(20). doi:10.1161/CIR.0000000000000560

Haddad F, Hunt SA, Rosenthal DN, Murphy DJ. Right ventricular function in cardiovascular disease, part I: Anatomy, physiology, aging, and functional assessment of the right ventricle. Circulation. 2008;117(11). doi:10.1161/CIRCULATIONAHA.107.653576

Sheehan F, Redington A. The right ventricle: Anatomy, physiology and clinical imaging. Heart. 2008;94(11). doi:10.1136/hrt.2007.132779

Wasson S, Govindarajan G, Reddy HK, Flaker G. The Role of Nitric Oxide and Vasopressin in Refractory Right Heart Failure. J Cardiovasc Pharmacol Ther. 2004;9(1). doi:10.1177/107424840400900i102

Mathew R, Di Santo P, Jung RG, et al. Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock. N Engl J Med. 2021;385(6). doi:10.1056/nejmoa2026845

Kormos RL, Teuteberg JJ, Pagani FD, et al. Right ventricular failure in patients with the HeartMate II continuous-flow left ventricular assist device: Incidence, risk factors, and effect on outcomes. J Thorac Cardiovasc Surg. 2010;139(5). doi:10.1016/j.jt

Lopez-Sendon J, Coma-Canella I, Gamallo C. Sensitivity and specificity of hemodynamic criteria in the diagnosis of acute right ventricular infarction. Circulation. 1981;64(3 I). doi:10.1161/01.CIR.64.3.515

Korabathina R, Heffernan KS, Paruchuri V, et al. The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv. 2012;80(4). doi:10.1002/ccd.23309

Morine KJ, Kiernan MS, Pham DT, Paruchuri V, Denofrio D, Kapur NK. Pulmonary Artery Pulsatility Index is Associated with Right Ventricular Failure after Left Ventricular Assist Device Surgery. J Card Fail. 2016;22(2). doi:10.1016/j.cardfail.2015.10.019

El Hajj MC, Viray MC, Tedford RJ. Right Heart Failure: A Hemodynamic Review. Cardiol Clin. 2020;38(2). doi:10.1016/j.ccl.2020.01.001

Esposito ML, Bader Y, Morine KJ, Kiernan MS, Pham DT, Burkhoff D. Navin K. Kapur, MD Mechanical Circulatory Support Devices for Acute Right Ventricular Failure. Circulation. 2017;136.

Cheung AW, White CW, Davis MK, Freed DH. Short-term mechanical circulatory support for recovery from acute right ventricular failure: Clinical outcomes. J Hear Lung Transplant. 2014;33(8). doi:10.1016/j.healun.2014.02.028