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Episodes Archives - Cardionerds episodes

April 14, 2023287. Case Report: When Tumors Take Your Breath Away – University of Oklahoma College of Medicine
CardioNerds join Dr. Samid Muhammad Farooqui, Dr. Hiba Hammad, and Dr. Syed Talal Hussain, from the University of Oklahoma Pulmonary and Critical Care Medicine Fellowship Program, in Oklahoma City. The fellows will take us in a fascinating discussion of a case of rapidly progressing dyspnea and pulmonary hypertension in a patient with metastatic breast cancer. They will then reveal an interesting etiology of pulmonary hypertension, where the secret was on the wedge! University of Oklahoma faculty and expert in pulmonary hypertension and right ventricular physiology, Dr. Roberto J. Bernardo provides the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen.
A septuagenarian female, with a past medical history of metastatic breast adenocarcinoma, presented to the hospital with worsening dyspnea over a period of 3 weeks. She was found to be in rapidly progressive hypoxic respiratory failure with unremarkable chest x-ray, CTA chest, and V/Q scan. Transthoracic echocardiogram revealed elevated RVSP and a subsequent right heart catheterization showed pre-capillary pulmonary hypertension with a low cardiac index. She was treated for rapidly progressive RV dysfunction with inotropic support and inhaled pulmonary vasodilators until she decided to pursue comfort measures. Wedge cytology came back positive for malignant cells, confirming a diagnosis of Pulmonary Tumoral Thrombotic Microangiopathy (PTTM).
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).
“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Case Media – When Tumors Take Your Breath Away – University of Oklahoma College of Medicine
Pearls – When Tumors Take Your Breath Away – University of Oklahoma College of Medicine
Pulmonary arterial hypertension (PAH) is a progressive disorder of the pulmonary vasculature, characterized by progressive obliteration and remodeling of the pulmonary circulation, resulting in increased pulmonary vascular resistance and increased right ventricular (RV) wall stress, abnormal right ventricular mechanics, and eventually RV dysfunction and death.
Pulmonary hypertension (PH) is divided into pre-capillary and post-capillary profiles, where pre-capillary PH is hemodynamically characterized by a mean pulmonary artery pressure (mPAP) > 20 mmHg, pulmonary artery wedge pressure (PAWP) ≤ 15 mmHg and a pulmonary vascular resistance (PVR) ≥ 3 Woods Units (WU), and post-capillary PH is defined as mPAP > 20 mmHg, PAWP ≥ 15 mmHg, and PVR can be either < 3 WU (isolated post-capillary PH) or ≥ 3 WU (combined pre- and post-capillary PH). Pulmonary arterial hypertension (PAH) falls under the pre-capillary PH profile.
Dyspnea on exertion is the most common manifestation of PH, and the most common initial complain. Other symptoms and physical findings such as venous congestion, peripheral edema, signs of RV dysfunction or syncope present later in the disease course. As such, PH has to be considered in the differential diagnosis of dyspnea, especially in cases of undifferentiated or unexplained dyspnea.
PAH is a chronic but progressive condition, where symptoms progress over the course of months to years. Subacute or rapidly progressive forms of PH (symptoms rapidly worsening over the course of weeks) should warrant consideration for alternative etiologies (i.e., pulmonary embolism or a different cardiopulmonary disorder as the main driver of symptoms), or unique rapidly progressive phenotypes of PAH such as pulmonary tumor thrombotic microangiopathy (PTTM).
PH in the setting of malignancy warrants special consideration, where the pulmonary vascular disorder could be related to venous thromboembolic disease, external compression of the pulmonary vasculature (if the tumor directly compresses mediastinal structures), related to chemotherapeutic agents (such as tyrosine kinase inhibitors) or thoracic radiotherapy (ie. fibrosing mediastinitis), or related to tumor emboli per se, such as in PTTM. PTTM is a unique manifestation of PH in the setting of malignancy, known to be rapidly progressive, associated with poor RV adaptation, and almost universally fatal. The confirmatory testing of PTTM is by pathology (autopsy), although as in our case, sometimes tumor cells can be identified during cytology of pulmonary artery wedge samples.
Show Notes – When Tumors Take Your Breath Away – University of Oklahoma College of Medicine
1. How do you approach dyspnea?
Dyspnea is a subjective sensation of uncomfortable breathing. It can be caused by pathologies in cardiac, pulmonary, neuromuscular systems as well as in systemic illnesses. Dyspnea is also a manifestation of psychogenic disorders.
Presentation of dyspnea can be divided into acute and chronic forms and the etiology can be identified by a thorough evaluation.
A detailed history and physical exam can help identify the organ system involved. Certain physical signs can be suggestive of the culprit organ system e.g., lower extremity edema in congestive heart failure, increased antero-posterior diameter of the chest in obstructive lung disease, etc. Imaging modalities can be very helpful in determining the cause of dyspnea. Chest radiographs, CT scans of the chest, and echocardiograms can help identify the etiology of dyspnea. Additionally, other testing like pulmonary functions tests can be used too.
2. What are the different Pulmonary Hypertension groups?
Pulmonary Hypertension (PH) is divided into 5 main groups in the WHO classification, as follows:
Group IPulmonary Arterial Hypertension (PAH) Idiopathic, heritable, drugs, congenital heart disease, liver disease, connective tissue disease, toxins, anorexigens among other causesGroup IIPH due to Left Heart DiseaseLeft sided heart failure, valvular pathologyGroup IIIPH due to Lung DiseaseCOPD, Interstitial Lung Disease, Sleep ApneaGroup IVPH due to Chronic Thromboembolic DiseasePulmonary emboliGroup VPH due to Other CausesSarcoidosis, ESRD, Sickle Cell Anemia, Chronic Hemolytic Anemia, Certain Metabolic Disorders
3. How do you approach a patient with Pulmonary Hypertension?
The goal is to discover an identifiable etiology for proper classification of pulmonary hypertension according to the WHO groups, in order to guide prognostication and management.
A thorough history and physical exam is the first step in the diagnosis of pulmonary hypertension. Exertional dyspnea is the most common presenting symptom. Due to the nonspecific symptoms, there is often a delay in the diagnosis. Other symptoms include chest pain, fatigue, edema. In severe cases, patients may have syncopal episodes.
Physical Exam findings concerning for pulmonary hypertension include signs of volume overload (i.e., edema, elevated JVP). Cardiac auscultation may reveal a loud P2 component.
Laboratory workup includes basic assessment of hematology along with testing for HIV and serological markers of connective tissue diseases. Biomarkers of cardiovascular system like BNP are important in identification and prognostication of pulmonary hypertension.
Radiological studies like chest radiographs, CT scans of the chest and ventilation/perfusion scans of the lung are used to identify pulmonary pathologies and the presence of thromboembolic disease respectively.
Echocardiographic assessments are important for diagnosis and assessment of pulmonary hypertension. It allows for the assessment of the left side as well as a detailed analysis of the right side which has diagnostic and prognostic value.
Finally, the gold standard for diagnosis is a right heart catheterization, which allows for accurate measurements of the pressure in the different chambers of the heart and allows for the phenotyping of pulmonary hypertension.
4. What are the considerations for Pulmonary Hypertension etiologies in patient with malignancy? How is Pulmonary Tumoral Thrombotic Microangiopathy diagnosed?
Pulmonary hypertension in a patient with malignancy requires special attention.
Apart from the common reasons for pulmonary hypertension, use of chemotherapeutic agents has been associated with the development of pulmonary arterial hypertension, particularly with Tyrosine Kinase Inhibitors.
Pulmonary Veno-Occlusive Disease (PVOD) can be precipitated by the use of many chemotherapeutic agents especially alkylating agents.
Detrimental effects of chemotherapeutic agents on myocytes can cause Group II pulmonary hypertension.
Chemotherapy and radiation therapy induced lung damage can also cause Group III pulmonary hypertension.
Large tumors may directly compress mediastinal structures causing elevated pulmonary pressures due to external compression.
In patients with adenocarcinoma, tumoral thrombotic microangiopathy can result in sub-acute pulmonary hypertension known as Pulmonary Tumoral Thrombotic Microangiopathy (PTTM).
PTTM results in rapid clinical deterioration and hence requires a high suspicion of index. It is mostly diagnosed postmortem, but can be diagnosed by performing wedge cytology.
5. What is the prognosis of PTTM and how is it treated?
PTTM carries a grave prognosis. It causes accelerated occlusion of pulmonary arteries resulting in acute to subacute pulmonary hypertension and ensuing RV dysfunction and failure.
The mainstay of treatment relies on pulmonary vasodilation and slowing the growth of malignant cells.
Pulmonary vasodilators, especially endothelin receptor antagonists, have been reported to be used.
Imatinib, a tyrosine kinase inhibitor, has been reported to be used with some improvement in survival.
References –
Vonk Noordegraaf A, Chin KM, Haddad F, et al. Pathophysiology of the right ventricle and of the pulmonary circulation in pulmonary hypertension: an update. Eur Respir J. Jan 2019;53(1):1801900. doi:10.1183/13993003.01900-2018. Link:
Bernardo RJ, Haddad F, Couture EJ, et al. Mechanics of right ventricular dysfunction in pulmonary arterial hypertension and heart failure with preserved ejection fraction. Cardiovasc Diagn Ther. Oct 2020;10(5):1580-1603. doi:10.21037/cdt-20-479.
Simonneau G, Montani D, Celermajer DS, et al. Haemodynamic definitions and updated clinical classification of pulmonary hypertension. The European respiratory journal. 2019;53(1):1801913-1801913. doi:10.1183/13993003.01913-2018.
Dumitrescu D, Sitbon O, Weatherald J, Howard LS. Exertional dyspnoea in pulmonary arterial hypertension. Eur Respir Rev. Sep 30 2017;26(145)doi:10.1183/16000617.0039-2017.
Buser M, Felizeter-Kessler M, Lenggenhager D, Maeder MT. Rapidly progressive pulmonary hypertension in a patient with pulmonary tumor thrombotic microangiopathy. Am J Respir Crit Care Med. Mar 15 2015;191(6):711-2. doi:10.1164/rccm.201501-0004IM.
Price LC, Wells AU, Wort SJ. Pulmonary tumour thrombotic microangiopathy. Lippincott Williams and Wilkins; 2016. p. 421-428.
Price LC, Seckl MJ, Dorfmüller P, Wort SJ. Tumoral pulmonary hypertension. European Respiratory Review. 2019;28(151)doi:10.1183/16000617.0065-2018.
Shah AT, Bernardo RJ, Berry GJ, Kudelko K, Wakelee HA. Two Cases of Pulmonary Tumor Thrombotic Microangiopathy Associated with ROS1-Rearranged Non-Small-Cell Lung Cancer. Clin Lung Cancer. Mar 2021;22(2):e153-e156. doi:10.1016/j.cllc.2020.09.020.
Godbole RH, Saggar R, Kamangar N. Pulmonary tumor thrombotic microangiopathy: a systematic review. Pulm Circ. Apr-Jun 2019;9(2):2045894019851000. doi:10.1177/2045894019851000
48 min
April 11, 2023 286. Guidelines: 2021 ESC Cardiovascular Prevention – Question #21 with Dr. Noreen Nazir

The following question refers to Section 4.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Maryam Barkhordarian, answered first by medicine resident Dr. Ahmed Ghoneem, and then by expert faculty Dr. Noreen Nazir.
Dr. Nazir is Assistant Professor of Clinical Medicine at the University of Illinois at Chicago, where she is the director of cardiac MRI and the preventive cardiology program.
The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.

Question #21

Ms. J is a 57-year-old woman with a past medical history of myocardial infarction resulting in ischemic cardiomyopathy, heart failure with reduced ejection fraction, and major depressive disorder who presents today for follow-up. She reports feeling extremely overwhelmed lately due to multiple life stressors. She is on appropriate cardiovascular GDMT agents and is not prescribed any medications for her mood disorder.
True or false: in addition to psychotherapy for stress management, it is appropriate to consider Ms. J for anti-depressant SSRI pharmacotherapy at this time to improve cardiovascular outcomes.
A
True
B
False
Answer #21

Explanation
The correct answer is FALSE.
An ESC class 3 recommendation states that SSRIs, SNRIs, and tricyclic antidepressants are not recommended in patients with heart failure and major depression; this is based on data suggesting potential lack of SSRI efficacy for reducing depression or cardiovascular events, as well as safety data indicating an association between SSRI use and increased risk of CV events and all-cause as well as cardiovascular mortality among HF patients. Mental health disorders are associated with worse outcomes in patients with ASCVD and appropriate treatment effectively reduces stress symptoms and improves quality of life. Nonpharmacologic modalities of treatment (exercise therapy, psychotherapy, collaborative care) should be considered before pharmacotherapy to improve cardiovascular outcomes in patients with heart failure.
Of note, the ESC suggests SSRI treatment be considered for patients with coronary heart disease (without HF) and moderate-to-severe major depression based on data that SSRI treatment is associated with lower rates of CHD readmission (RR 0.63), all-cause mortality (RR 0.56), and the composite endpoint of all-cause mortality/MI/PCI (HR 0.69) vs. no treatment. This is a class 2a recommendation.
ESC also gives a class 2a recommendation to consider referral to psychotherapeutic stress management for individuals with stress and ASCVD to improve CV outcomes and reduce stress symptoms.
The ACC/AHA guidelines do not provide focused recommendations regarding mental health considerations in patients with elevated cardiovascular risk.
Main Takeaway
It is important to consider mental health treatment in patients with ASCVD as mental disorders are associated with increased CVD risk and poor patient prognosis, and data support that mental health interventions can improve overall and CVD outcomes, as well as improve quality of life.
Guideline Loc.
Section 4.4

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8 min
April 11, 2023 285. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #15 with Dr. Ileana Pina

The following question refers to Section 10.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Boston University cardiology fellow and CardioNerds Ambassador Dr. Alex Pipilas, and then by expert faculty Dr. Ileana Pina.
Dr. Pina is Professor of Medicine and Quality Officer for the Cardiovascular Line at Thomas Jefferson University, Clinical Professor at Central Michigan University, and Adjunct Professor of Biostats and Epidemiology at Case Western University. She serves as Senior Fellow and Medical Officer at the Food and Drug Administration’s Center for Devices and Radiological Health.
The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #15
Mrs. Framingham is a 65-year-old woman who presents to her cardiologist’s office for stable angina and worsening dyspnea on minimal exertion. She has a history of non-insulin dependent type 2 diabetes mellitus and hypertension. She is taking metformin, linagliptin, lisinopril, and amlodipine. Blood pressure is 119/70 mmHg. Labs are notable for a hemoglobin of 14.2 mg/dL, iron of 18 mcg/dL, ferritin 150 ug/L, transferrin saturation 15%, and normal creatine kinase. An echocardiogram shows reduced left ventricular ejection fraction of 25%. Coronary angiography shows obstructive lesions involving the proximal left anterior descending, left circumflex, and right coronary arteries. In addition to optimizing GDMT, which of the following are recommendations for changes in management?
A
Anticoagulation, percutaneous revascularization, and IV iron
B
A change in her diabetic regimen, percutaneous revascularization, and PO iron
C
A change in her diabetic regimen, surgical revascularization, and IV iron
D
A change in her diabetic regimen, medical treatment alone for CAD, and PO iron
E
Anticoagulation and surgical revascularization
Answer #15
Explanation
The correct answer is C – a change in her diabetic regimen, surgical treatment and IV iron.
Multimorbidity is common in patients with heart failure. More than 85% of patients with HF also have at least 2 additional chronic conditions, of which the most common are hypertension, ischemic heart disease, diabetes, anemia, chronic kidney disease, morbid obesity, frailty, and malnutrition. These conditions can markedly impact patients’ tolerance to GDMT and can inform prognosis.
Not only was Mrs. F found with HFrEF (most likely due to ischemic cardiomyopathy), but she also suffers from severe multi-vessel coronary artery disease, hypertension, and non-insulin dependent type 2 diabetes mellitus.
In addition to starting optimized GDMT for HF, specific comorbidities in the heart failure patient warrant specific treatment strategies. Mrs. Framingham would benefit from a change in her diabetic regimen, namely switching from linagliptin to an SGLT2 inhibitor (e.g., empagliflozin, dapagliflozin). In patients with HF and type 2 diabetes, the
use of SGLT2i is recommended for the management of hyperglycemia and to reduce HF related morbidity and mortality (Class 1, LOE A).
Furthermore, as she has diabetes, symptomatic severe multi-vessel CAD, and LVEF≤35%, surgical revascularization with coronary artery bypass grafting is warranted to improve symptoms, cardiovascular hospitalizations, and long-term all-cause mortality (Class 1, LOE B-R). Given the severity of her coronary disease, presence of diabetes mellitus, and coronary anatomy suitable for bypass, percutaneous (i.e., PCI) or medical treatment alone are inappropriate (options B, D).

Although she does not have anemia, she may benefit from IV iron. IV iron supplementation has been shown in the FAIR-HF, IRONOUT HF, and AFFIRM-AHF trials to significantly improve NYHA functional class, 6-minute walk test, quality of life, and decrease hospitalizations for HF, independently of anemia. These effects were not seen with iron given orally (options B, D). Iron deficiency is usually defined as ferritin level <100 μg /L or 100 to 300 μg/L, if the transferrin saturation is <20%. Therefore, in patients with HFrEF and iron deficiency with or without anemia, intravenous iron replacement is reasonable to improve functional status and QOL (Class 2a, LOE B-R).

Although HF is a pro-thrombotic state, anticoagulation is not warranted empirically in Mrs. F, who has no evidence of thrombus or high-risk features suggesting impending thrombus (options A, E).
Main Takeaway
In summary, multimorbidity is frequent in heart failure patients and treatment targeted to specific morbidities is warranted. In patients with heart failure and diabetes, an SGLT2 inhibitor should be part of the medication regimen. Intravenous iron supplementation should be considered in iron-deficient patients independent of anemia. In patients with heart failure with LVEF≤35% and severe coronary artery disease with suitable anatomy, coronary artery bypass grafting is recommended.
Guideline Loc.
Section 10.1, Figure 14

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11 min
April 10, 2023284. Atrial Fibrillation: Mechanical Stroke Prevention in Atrial Fibrillation with Dr. Christopher Ellis
CardioNerds Amit Goyal, Dr. Colin Blumenthal, Dr. Kelly Arps and Dr. Justice Oranefo discuss mechanical stroke prevention in atrial fibrillation with Dr. Christopher Ellis, cardiac electrophysiology lab director and director of the left atrial appendage closure program at Vanderbilt University. There has been a significant increase in the number of patients undergoing left atrial appendage occlusion (LAAO). This trend is expected to continue with current and upcoming clinical data on this topic. In this episode we dive into the rationale behind LAAO and explore several historical facts. We then proceed to the current state of practice including currently available options, appropriate indications, post op care, and potential complications. Notes were drafted by Dr. Justice Oranefo. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah.
This CardioNerds Atrial Fibrillation 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. Kelly Arps and Dr. Colin Blumenthal.
This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds.
We have collaborated with VCU Health to provide CME. Claim free CME here!
Disclosures: Dr. Ellis discloses grant or research support from Boston Scientific, Abbott-St Jude, advisor for Atricure and Medtronic.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls and Quotes – Atrial Fibrillation: Mechanical Stroke Prevention in Atrial fibrillation
Surgical or catheter based left atrial appendage occlusion results in mechanical exclusion of the left atrial appendage, which is the most common source of thrombus leading to embolic events in patients with non-rheumatic atrial fibrillation.
Surgical LAAO should be considered in patients with atrial fibrillation and CHA2DS2VASC score ≥ 2 undergoing cardiac surgery for other indications.
Endocardial LAAO devices such as WATCHMAN FLX and AMULET are approved for stroke prevention in patients with atrial fibrillation with a CHA2DS2VASC score ≥ 2 and have an appropriate reason to seek a non-drug alternative to anticoagulation therapy.
Appropriate patient selection and post-operative anticoagulation and imaging strategy are crucial for prevention and management of complications related to LAAO.
Notes – Atrial Fibrillation: Mechanical Stroke Prevention in Atrial fibrillation
What are the types of LAAO device?
Left atrial appendage occlusion devices can be divided into epicardial closure and endocardial closure.
Epicardial techniques/devices include surgical ligation, Atriclip, and Lariat. These techniques require pericardial access (either by open thoracotomy or thoracoscopic access). The goals are complete exclusion and ischemic necrosis of the LAA.
LARIAT device
Atriclip device
Endocardial techniques include WATCHMAN FLX and AMULET devices. These techniques require the use of nitinol-based devices which are delivered into the LAA via a transeptal approach. These devices become endothelialized over time resulting in occlusion of the LAA.
AMULET device
WATCHMAN FLX
Who is the ideal candidate for surgical LAAO?
Several studies have evaluated the efficacy of surgical LAA occlusion. The most prominent being the LAOS III trial which randomized 4770 patients with atrial fibrillation and CHA2DS2VASC ≥ 2 undergoing cardiac surgery for other reasons to surgical LAAO vs no LAAO (3,4). The primary outcome of ischemic stroke or systemic embolization occurred in 4.8% of patients in the LAAO group vs 7% of patients in control group over an average follow-up of 3.8 years. Though patients were randomized to LAAO, there was no requirement to stop anticoagulation and this difference was seen despite 75% of patients continuing anticoagulation. Additionally, there was no significant difference in operation time and bleeding complications.
Based on these findings, LAAO should be considered in patients with atrial fibrillation undergoing cardiac surgery for other reasons regardless of the anticipated anticoagulation strategy.
This ability to perform surgical LAAO requires safe access to the pericardial space. For this reason, conditions that create pericardial adhesions (e.g., prior cardiac surgery, chest radiation or trauma, multiple prior ablations) can limit the ability to perform surgical LAAO.
Who is the ideal candidate for endocardial LAAO?
Several randomized controlled trials and cohort studies have evaluated the utility of both the AMULET and WATCHMAN devices in stroke prevention with the most notable being the PREVAIL, PROTECT AF, and AMULET IDE trials (5,6,7,8,9,10).
Based on the available data, these devices are indicated for stroke prevention in patients with non-valvular atrial fibrillation, a CHA2DS2VASC score ≥ 2 and an appropriate reason to seek a non-drug alternative to anticoagulation therapy. A classic example is a patient with recurrent GI bleeding despite multiple attempts to tolerate anticoagulation. These devices can also be considered in patients with high-risk professions suck as police officers or fire fighters.
Several individual factors also affect the feasibly of endocardial LAAO. A suitable LAA anatomy is necessary for safe device implant (13). Other important considerations are nickel allergy (consider formal allergy testing in patients with suspected nickel allergy), surgical repair of the atrial septum, and severe kyphoscolisis (making adequate transeptal access difficult).
There is no strong data comparing LAAO to DOAC in patients without high bleeding risk, however this question is being studied in 2 ongoing trials, CHAMPION AF (WATCHMAN FLX) and CATALYST (AMULET).
What are the complications of LAAO?
Surgical LAAO is safe and effective when there is complete occlusion of the LAA, however, historically ~ 20-30% are unsuccessful due to incomplete occlusion. More modern surgical techniques including confirmation with intra-operative transesophageal echocardiogram and the Atriclip have demonstrates a higher rate of success. Though the addition of a LAAO has not been shown to add significant time or risk to an already planned cardiac surgery, this requires a patient to already have an indication for surgery and carries the associated risks of that procedure.
Endocardial LAAO has the advantage of being minimally invasive, but procedural complications such as cardiac tamponade, bleeding, and stroke can occur. More recent data has shown a < 1% procedural risk with the WATCHMAN FLX device. Other post procedural complications of endocardial LAAO devices include peridevice leak (~ 10% incidence; leaks ≥ 3mm are associated with an increased risk of stroke) and device related thrombus (DRT; 2-3% incidence). Device embolism is rare but carries potentially devastating consequences (12).
What is the anticipated post operative care following LAAO?
Post operative care with surgical LAAO is predominently dictated by the primary indication for surgery. Due to the high incidence incomplete exclusion, an intra or post-operative TEE is necessary to document complete LAA occlusion. As for anticoagulation, there is no current randomized control trial data that supports using surgical LAAO as an alternative to AC. As previously discussed, a lower incidence of stroke was seen in the LAOS III trial, but this trial specifically studied using surgical LAAO as an adjunct to OAC, not as a replacement.
With endocardial LAAO, appropriate patient and device selection as well as adequate post-operative care is crucial to maximize safety and efficacy. Patients must be able to tolerate some degree of short-term anticoagulation with the goal to safely transition to single anti-platelet therapy while minimizing the risk of stroke and bleeding. This involves OAC for at least 45 days followed by aspirin monotherapy if no DRT or peridevice leak is seen on post-op imaging. DAPT (aspirin and clopidogrel) can be used instead of OAC in the early phase however there is not strong data for this strategy (11). Post-op imaging (TEE or CTA) is required approximately ~45 days, 6 months, and 1 year after the procedure.
In patients who have undergone LAAO, LAA imaging is recommended prior to cardioversion, however, in the absence of DRT or device leaks anticoagulation is not necessary post cardioversion (14,15).
References
Belcher, J.R. & Somerville, W., 1955. Systemic Embolism and Left Auricular Thrombosis in Relation to Mitral Valvotomy. British Medical Journal, 2(4946), pp.1000–1003.
Blackshear, J.L. & Odell, J.A., 1996. Appendage obliteration to reduce stroke in cardiac surgical patients with atrial fibrillation. The Annals of thoracic surgery, 61(2), pp.755–759.
Friedman, D.J. et al., 2018. Association Between Left Atrial Appendage Occlusion and Readmission for Thromboembolism Among Patients With Atrial Fibrillation Undergoing Concomitant Cardiac Surgery. JAMA : the journal of the American Medical Association, 319(4), pp.365–374.
Whitlock, R.P. et al., 2021. Left Atrial Appendage Occlusion during Cardiac Surgery to Prevent Stroke. The New England journal of medicine, 384(22), pp.2081–2091.
Reddy, V.Y. et al., 2014. Percutaneous Left Atrial Appendage Closure vs Warfarin for Atrial Fibrillation: A Randomized Clinical Trial. JAMA : the journal of the American Medical Association, 312(19), pp.1988–1998.
Belgaid, D.R. et al., 2016. Prospective randomized evaluation of the watchman left atrial appendage closure device in patients with atrial fibrillation versus long-term warfarin therapy: The PREVAIL trial. International journal of cardiology, 219, pp.177–179.
Freeman, J.V. et al., 2020. The NCDR Left Atrial Appendage Occlusion Registry. Journal of the American College of Cardiology, 75(13), pp.1503–1518.
REDDY, V.Y. et al., 2013. Left Atrial Appendage Closure With the Watchman Device in Patients With a Contraindication for Oral Anticoagulation: The ASAP Study (ASA Plavix Feasibility Study With Watchman Left Atrial Appendage Closure Technology). Journal of the American College of Cardiology, 61(25), pp.2551–2556.
Holmes DR Jr, Kar S, Price MJ, et al. Prospective randomized evaluation of the Watchman Left Atrial Appendage Closure device in patients with atrial fibrillation versus long-term warfarin therapy: the PREVAIL trial [published correction appears in J Am Coll Cardiol. 2014 Sep 16;64(11):1186]. J Am Coll Cardiol. 2014;64(1):1-12. doi:10.1016/j.jacc.2014.04.029
Lakkireddy D, Thaler D, Ellis CR, et al. Amplatzer Amulet Left Atrial Appendage Occluder Versus Watchman Device for Stroke Prophylaxis (Amulet IDE): A Randomized, Controlled Trial. Circulation. 2021;144(19):1543-1552. doi:10.1161/CIRCULATIONAHA.121.057063
Magdi M, Renjithal SLM, Mubasher M, et al. The WATCHMAN device and post-implantation anticoagulation management. A review of key studies and the risk of device-related thrombosis. Am J Cardiovasc Dis. 2021;11(6):714-722. Published 2021 Dec 15.
Della Rocca DG, Magnocavallo M, Gianni C, et al. Procedural and short-term follow-up outcomes of Amplatzer Amulet occluder versus Watchman FLX device: A meta-analysis. Heart Rhythm. 2022;19(6):1017-1018. doi:10.1016/j.hrthm.2022.02.007
Maan A, Heist EK. Left Atrial Appendage Anatomy: Implications for Endocardial Catheter-based Device Closure. J Innov Card Rhythm Manag. 2020;11(7):4179-4186. Published 2020 Jul 15. doi:10.19102/icrm.2020.110704
Maarse M, Wintgens LIS, Ponomarenko A, et al. Impact of anticoagulation strategy after left atrial appendage occlusion in patients requiring direct current cardioversion. J Cardiovasc Electrophysiol. 2021;32(3):737-744. doi:10.1111/jce.14889
Sharma SP, Turagam MK, Gopinathannair R, et al. Direct Current Cardioversion of Atrial Fibrillation in Patients With Left Atrial Appendage Occlusion Devices. J Am Coll Cardiol. 2019;74(18):2267-2274. doi:10.1016/j.jacc.2019.08.1045
1 hr 4 min
April 05, 2023283. CardioNerds Rounds: Challenging Cases – Cardio-Obstetrics and Heart Failure with Dr. Mary Norine (Minnow) Walsh
It’s another session of CardioNerds Rounds! In these rounds, Dr. Jenna Skowronski (Chief FIT at University of Pittsburgh) and Dr. Natalie Stokes (Formerly FIT at University of Pittsburgh and now General Cardiology Faculty at University of Pittsburgh) join transformational leader, educator and researcher, Dr. Mary Norine Walsh (Director of Heart Failure and Transplantation at Ascension St. Vincent Heart Center and Program Director of AHFT at St. Vincent) to discuss cardio-obstetrics and heart failure cases. Amongst her many accomplishments, Dr. Walsh is past president of the American College of Cardiology, Deputy Editor of JACC Case Reports, and a preeminent voice and thought leader in women’s cardiovascular health. Audio editing by CardioNerds academy intern, Pace Wetstein.
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.
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Show notes – Cardio-Obstetrics and Heart Failure
Case 1 Synopsis:
A woman in her earlier 30s, G1P1, with a history significant for peripartum cardiomyopathy presents to clinic for pre-conception counseling. Her prior pregnancy was in her late 20s with an uneventful pre-natal course and a spontaneous vaginal delivery at 37w2d. Two weeks after delivery, she experienced symptoms of heart failure and was found to have a new diagnosis of HFrEF. At that time TTE showed LVEF 30-35%, LVIDd 5.1cm (top normal size), diffuse hypokinesis. At that time, she was diuresed and discharged on metoprolol succinate 25mg po daily and furosemide 20mg po daily. She had one follow up visit 6 months postpartum and the furosemide was discontinued. Today in your office, she has NYHA Class I symptoms with no signs of symptoms of congestion. She walks daily and does vigorous exercise 1-2 times per week, while remaining on metoprolol. Repeat TTE with LVEF 45-50% and similar LV size. She would like to have another child and was referred to you for counseling.
Case 1 Rounding Pearls:
Dr. Walsh discussed extensively the importance of full GDMT in this patient who was initially undertreated with only a beta blocker. If patients are breastfeeding, clinicians should consider the addition of ACE-Inhibitor and Spironolactone. Otherwise, if not breastfeeding, they should receive maximally tolerated doses of full GDMT. For more details on medical therapy for Heart Failure during pregnancy and after, refer to this previous CardioNerds Episode with Dr. Julie Damp.
Patients with peripartum cardiomyopathy are at highest risk of worsening LV systolic function when they have persistent LV systolic dysfunction from their initial diagnosis. In this circumstance, shared decision making is paramount. These patients should receive counseling on contraception and risk of pregnancy on worsening LV function, death, & fetal demise. In addition, counseling includes discussing with patients limited options in some states for complete, comprehensive reproductive care, including pregnancy termination.
If patients with prior peripartum cardiomyopathy do become pregnant, a team-based approach including cardiologists, maternal fetal medicine, and obstetrics (amongst other team members) is essential to determine care & delivery timing/method. These patients should also be examined for signs of decompensation throughout the pregnancy, including rales, S3 or a reported history of PND. For more about pregnancy physiology and signs of Heart Failure in pregnancy, refer to this previous episode with Dr. Garima Sharma.
Case 2 Synopsis:
A woman in her early 30s, G4P2022, with a history significant for polysubstance use disorder is transferred to your hospital POD #0 from an emergent C-section at 37w in cardiogenic shock. She presented to the local hospital with cough, dyspnea, and abdominal pain and urine toxicology was positive for methamphetamines. During evaluation she went into an SVT that was treated with metoprolol and was complicated by fetal decelerations. TTE showed LVEF 15%, LV dilation, and RV dysfunction. Given the fetal decelerations she had an emergent C-Section. We discussed her management as she progressed into SCAI Stage E Cardiogenic Shock.
Case 2 Rounding Pearls:
The etiology of cardiomyopathy in this patient could be tachycardia induced, peripartum, toxic, or familial. A full evaluation is essential to determine if anything is reversible. SVT ablation could be considered if this was felt to be a driver.
Approaches to durable mechanical circulatory support (MCS) such as a durable LVAD in patients with polysubstance use disorders are institution specific. Multidisciplinary input should be sought, including cardiology, cardiothoracic surgery, social work, nursing, nutrition, palliative care, and pharmacy.
Consideration of temporary MCS as a bridge to transplant vs durable MCS should be considered again on a case-by-case basis, keeping in mind the current transplant allocation system that has made those patients with durable LVAD less likely to receive a transplant.
We have previously discussed cases on the CardioNerds podcast that reflect this nuance. Consider listening again to these episodes from the CardioNerds team at Medical College Wisconsin and the University of Pennsylvania.
Infographic by CardioNerds Academy Chief of House Jones (2023) Dr. Alaa Diab
References – Cardio-Obstetrics and Heart Failure
Bauersachs J, Arrigo M, Hilfiker-Kleiner D, et al. Current management of patients with severe acute peripartum cardiomyopathy: practical guidance from the Heart Failure Association of the European Society of Cardiology Study Group on peripartum cardiomyopathy. Eur J Heart Fail. 2016;18(9):1096-1105. doi:10.1002/ejhf.586
Bauersachs J, König T, van der Meer P, et al. Pathophysiology, diagnosis and management of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Study Group on peripartum cardiomyopathy. Eur J Heart Fail. 2019;21(7):827-843. doi:10.1002/ejhf.1493
Davis MB, Arany Z, McNamara DM, Goland S, Elkayam U. Peripartum Cardiomyopathy: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(2):207-221. doi:10.1016/j.jacc.2019.11.014
Writing Committee Members; ACC/AHA Joint Committee Members. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. J Card Fail. 2022;28(5):e1-e167. doi:10.1016/j.cardfail.2022.02.010
Production Team
Karan Desai, MD
Natalie Stokes, MD
Amit Goyal, MD
Daniel Ambinder, MD
36 min
April 05, 2023 282. Guidelines: 2021 ESC Cardiovascular Prevention – Question #20 with Dr. Michael Wesley Milks

The following question refers to Section 3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Adriana Mares, answered first by Brigham & Women’s medicine intern & Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Michael Wesley Milks.
Dr. Milks is a staff cardiologist and assistant professor of clinical medicine at the Ohio State University Wexner Medical Center where he serves as the Director of Cardiac Rehabilitation and an associate program director of the cardiovascular fellowship. He specializes in preventive cardiology and is a member of the American College of Cardiology’s Cardiovascular Disease Prevention Leadership Council.
The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.

Question #20

Ms. Ruma Toid is a 65-year-old African American woman who presents to your clinic in Ohio for routine follow up. She has a history of rheumatoid arthritis, hypertension, obesity, and sleep apnea. Her medications include methotrexate and atenolol. Her blood pressure in the office is 120/80 mmHg, heart rate 68 bpm, and oxygen saturation 99% on room air. Recent lipid testing revealed total cholesterol 165 mg/dL, HDL 42 mg/dL, and LDL 118 mg/dL. She was recently advised to talk to her doctor about taking a statin due to her risk factors but in the past has heard negative things about those medications and would like your advice on next steps. Her calculated ASCVD risk score based on the Pooled Cohort Equation is 7%. Which of the following choices would be the next step?
A
She is at borderline risk for ASCVD events. A statin is not indicated at this time.
B
Due to her history of rheumatoid arthritis, her calculated ASCVD risk should be multiplied by 1.5, yielding an ASCVD risk of 10.5% placing her in the intermediate risk category. Moderate intensity statin would be indicated.
C
When other risk factors are present, rheumatoid arthritis is no longer an enhancing risk factor.
D
Statins are contraindicated when taking methotrexate.
Answer #20

Explanation
The correct answer is B. Due to her history of rheumatoid arthritis, her calculated ASCVD risk should be multiplied by 1.5, yielding an ASCVD risk of 10.5% placing her in the intermediate risk category. Moderate intensity statin would be indicated.

Due to her history of rheumatoid arthritis, her calculated ASCVD risk should be multiplied by 1.5, yielding an ASCVD risk of 10.5% placing her in the intermediate risk category. Moderate intensity statin would be indicated. The ESC gives a Class IIa (LOE B) indication to multiply the calculated total CVD risk by a factor of 1.5 in adults with rheumatoid arthritis due to the observed 50% increased CVD risk in patients with rheumatoid arthritis.

This 50% increase in CVD risk attributed to RA is present beyond traditional risk factors, making answer choice C wrong.

Answer A is incorrect because when borderline risk is calculated, one should still look for risk enhancers that could potentially increase ASCVD risk before final determination of statin indication.

Answer choice D is false as there is no contraindication to take both methotrexate and statins together.

Note that it is appropriate to use the pool cohort equations and American risk thresholds for this patient since she is in America where the PCE was validated (versus using SCORE2 risk model which would be more appropriate for European populations).
Main Takeaway
Inflammatory conditions including rheumatoid arthritis and inflammatory bowel disease increase a person’s risk for ASCVD events. Specifically for rheumatoid arthritis, there is a Class IIa indication to multiply the calculated risk score by 1.5 to account for rheumatoid arthritis as a risk enhancer.
Guideline Loc.
Section 3.4.6

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14 min
April 04, 2023 281. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #14 with Dr. Javed Butler

The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Duke University cardiology fellow and CardioNerds FIT Ambassador Dr. Aman Kansal, and then by expert faculty Dr. Javed Butler.
Dr. Butler is an advanced heart failure and transplant cardiologist, President of the Baylor Scott and White Research Institute, Senior Vice President for the Baylor Scott and White Health, and Distinguished Professor of Medicine at the University of Mississippi.
The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #14
Mrs. Hart is a 70-year-old woman hospitalized for a 2-week course of progressive exertional dyspnea, increasing peripheral edema, and mental status changes. She has a history of coronary artery disease, hypertension, and heart failure for which she takes aspirin, furosemide, carvedilol, lisinopril, and spironolactone. On physical exam, the patient is afebrile, BP is 80/60 mmHg, heart rate is 120 bpm, and respiratory rate is 28 breaths/min with O2 saturation of 92% breathing room air. She is sitting upright and is confused. Jugular venous pulsations are elevated. Cardiac exam reveals an S3 gallop. There is ascites and significant flank edema on abdominal exam. Her lower extremities have 2+ pitting edema to her knees and are cool to touch. Her labs are significant for an elevated serum Creatinine of 3.0 from a baseline of 1.0 mg/dL, lactate of 3.0 mmol/L, and liver enzyme elevation in the 300s U/L.

Which of the following is the most appropriate initial treatment?
A
Increase carvedilol
B
Start dobutamine
C
Increase lisinopril
D
Start nitroprusside
Answer #14
Explanation
The Correct answer is B – start dobutamine.
This patient with progressive congestive symptoms, mental status changes, and signs of hypoperfusion and end-organ dysfunction meets the clinical criteria of cardiogenic shock. The Class 1 recommendation is that in patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and maintain end-organ performance (LOE B-NR). Their broad availability, ease of administration, and clinician familiarity favor such agents as first line when signs of hypoperfusion persist. Interestingly, despite their ubiquitous use for management of cardiogenic shock, there is a lack of robust evidence to suggest the clear benefit of one agent over another. Therefore, the choice of a specific agent is guided by additional factors including vital signs, concurrent arrhythmias, and availability. For this patient, dobutamine is the only inotrope listed. Although she is tachycardic, her lack of arrhythmia makes dobutamine relatively lower risk and does not outweigh the potential benefits.
Choice A – Increase carvedilol – is not correct. Beta-blockers should be continued in HF hospitalization whenever possible; however, in a patient with low cardiac output and signs of shock, beta-blockers should be discontinued due to their negative inotropic effects.
Choice C – Increase lisinopril – is not correct. Afterload reduction is reasonable to decrease myocardial oxygen demand. However, given the hypotension and renal dysfunction, increasing lisinopril could be potentially dangerous by further exacerbating hypotension and renal dysfunction. Furthermore, given her tenuous hemodynamic status, it would be more beneficial to start an IV medication that is easier to monitor and rapidly titrate.
Choice D – Start nitroprusside – is not correct. Intravenous Vasodilators are helpful for improving cardiac output in high SVR states when the patient is normotensive or even hypertensive. However, this patient is HYPOtensive and so vasodilators should be held.
Main Takeaway
In patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ performance.
Guideline Loc.
Section 9.5

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14 min
April 02, 2023280. CCC: Sedation in the Cardiac ICU with Dr. Christopher Domenico
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
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Pearls and Quotes – Sedation in the Cardiac ICU with Dr. Christopher Domenico
Think about analgesia and sedation as separate entities with management of analgesia first and sedation second. Frequent re-assessment of needs should be performed to reduce ICU delirium and improve long-term outcomes.
Fentanyl is generally a good starting point for analgesia in the ICU since it is fast on/fast off, but can stick around for a long time the longer it is used. The choice of bolus or continuous infusion opioids depends on the clinical scenario and personal/institutional preference. Remember to administer bolus doses that are 50-100% of the hourly continuous infusion dose to reach steady state faster.
When managing refractory VT storm with sedative agents (propofol, benzodiazepines and/or dexmedetomidine), you should target the deepest level of sedation necessary to suppress sympathetic drive.
For cardiogenic shock patients, the choice of sedative agent is a nuanced decision. Think about etomidate first for intubation as it has the least cardiovascular and hemodynamic impact. And remember the propofol trifecta: negative inotropy, direct vasodilation, and bradycardia!
Pharmacokinetics are disrupted during targeted temperature management, thus be weary of overly sedating patients due to reduced drug clearance.
Show notes – Sedation in the Cardiac ICU with Dr. Christopher Domenico
How do we initiate analgesics and sedatives?
Analgesia first and sedation second!
Analgesia: think about how to reduce a patient’s pain
Everyone has a different pain tolerance and critically ill patients can have moderate to severe pain at baseline.
Metrics to assess pain include self-reported scales, behavioral scales, facial expressions, extremity movement, compliance with the ventilator, tachycardia, tachypnea, and hypertension.
Sedation: think about how to reduce a patient’s agitation or anxiety
The target depth of sedation depends on the clinical scenario.
For example, a patient with a femoral balloon pump may need more sedation if agitation is causing excessive lower extremity movement and thus a higher risk of device dislodgement.
Use the Richmond Agitation and Sedation Scale (RASS) for titrating sedation leve.
-5 – Unarousable. No response to voice or physical stimuli
-4 – Deep sedation. No response to voice, but movement or eye opening to physical stimulation
-3 – Moderate sedation. Movement or eye-opening to voice
-2 – Light sedation. Briefly awakens to voice
-1 – Drowsy. Not fully alert, but has sustained awakening to voice
0 – Alert and calm
+1 – Restless. Anxious, apprehensive, but not aggressive
+2 – Agitated. Frequent non-purposeful movement, fights vent
+3 – Very agitated. Pulls or removes tubes/catheters
+4 – Combative. Violent, immediate danger to staff
What are the different opioid options and when should we use them?
Break down opioids into 3 groups (as per Dr. Domenico):
Group 1 (morphine, hydromorphone, fentanyl) for pain management in the ICU.
Onset of action: Fentanyl is the quickest on/off (30 seconds-2 minutes), but is highly lipophilic, redistributing in fatty tissues after ~30 minutes. The longer you use fentanyl, the longer it will stick around – i.e. “context-sensitive half-time.” Morphine and Hydromorphone have an onset from 5-15 minutes.
Half-life: All 3 are similar at 2-4 hours. (Fentanyl can be even higher the longer it is used).
Metabolism: Morphine is metabolized by the liver, but has active metabolites that are renally cleared; thus, be cautious with high doses in renal impairment. Fentanyl is metabolized by the CYP system thus it accumulates in hepatic dysfunction.
Group 2 (remifentanil and sufentanil) generally for use in the operating room.
Onset of action: Both are very quick on/off ranging from 1-3 minutes.
Half-life: Remifentanil’s is 3-10 minutes, whereas sufentanil’s is 2-3 hours.
Metabolism: Remifentanil demonstrates no accumulation in hepatic or renal impairment, thus is a good choice in these scenarios. Beware of the rare possibility of serotonin syndrome with both these agents.
Group 3 (methadone) as a bridge to wean off from long term infusions of other opioids.
Onset of action: 1-20 minutes when given intravenously, but 3-5 days when given orally.
Half-life: Ranges from 8-60 hours.
Metabolism: Hepatic, exercise caution with dysfunction. Also monitor for QT prolongation.
Should we administer opioids as boluses or continuous infusions?
There is no strong data to guide bolus versus continuous infusion dosing of opioids and the choice is often left up to personal/institutional preference. Small studies in emergency department patients suggest there is less ICU delirium post-intubation with bolus dosing over continuous infusions of opioids.
Generally, think about starting with bolus dosing to assess a patient’s true needs, but patients may require continuous infusions if they are receiving frequent boluses.
When increasing the rate of a continuous infusion, one can reach steady state faster by administering bolus doses at 50-100% of the hourly dose of the infusion.
How should we use analgesics and sedatives for management of arrhythmias, specifically VT storm?
The main goal in refractory VT storm is to sedate the patient as deeply as necessary to suppress their sympathetic drive. Generally, the choice of sedative agent is less important than the level of sedation achieved.
Propofol, benzodiazepines, and dexmedetomidine can all decrease sympathetic drive.
Propofol has some anti-arrhythmic effects via autonomic nervous system modulation.
Dexmedetomidine may increase the arrhythmogenic threshold.
Benzodiazepines have no direct effect on the conduction system.
Opioids have GABA agonist properties and thus have some anti-arrhythmic properties. However, opioids alone are rarely effective in managing malignant arrhythmias unless pain is the main trigger for the arrhythmia.
In some animal studies, fentanyl and morphine are thought to increase the ventricular fibrillation threshold, but this is not validated with hard outcomes in clinical trials.
What sedatives are safe to use for intubation in cardiogenic shock?
Induction: Etomidate, ketamine, and propofol are common agents used for induction of sedation peri-intubation.
Etomidate – has minimal cardiovascular/hemodynamic effects and should be considered first for induction in cardiogenic shock. Can lead to adrenal insufficiency.
Ketamine – is a direct vasoconstrictor (including coronary arteries) and results in hypertension and tachycardia. It should be avoided in patients with ACS. It may have a direct myocardial depressant effect, so its use is avoided in prolonged shock states.
Propofol – has a plethora of properties-sedative, hypnotic, amnestic, antiemetic, and anticonvulsant, but importantly has NO ANALGESIC properties. Remember its hemodynamic trifecta: negative inotropy, direct vasodilation, and bradycardia. It is also highly lipophilic, with a long half-life with extended infusions- i.e. “context-sensitive half-time”. Don’t forget to check triglyceride levels at baseline and at regular intervals while on a continuous infusion.
Maintenance: Propofol, benzodiazepines, and dexmedetomidine can be used for maintenance of sedation post-intubation.
Benzodiazepines
Also have a plethora of properties- sedative, amnestic, anticonvulsant, anxiolytic, and hypnotic but NO ANALGESIC properties.
Midazolam is quicker on/off (2-5 minutes) compared to lorazepam. Midazolam can accumulate in renal dysfunction. Think about polyethylene toxicity when patients on lorazepam at high doses for extended periods of time develop metabolic acidosis.
In general, benzodiazepines use is associated with increased ventilator time, ICU delirium, and ICU length of stay.
Dexmedetomidine
Is an alpha 2 agonist and thus monitor for hypotension and bradycardia with ongoing use. It does not cause respiratory depression. It generally does not result in deep sedation (less than -2) and is not very effective for acute management of agitation. Consider its use for patients that require mild sedation during extubation.
What are general principles of analgesia and sedation during targeted temperature management?
Always assess baseline pain and RASS prior to medication initiation. Once the need for analgesia and sedation is established, these medications should be started prior to initiating cooling protocols.
Consider using the lowest effective doses of medications to increase the ability to perform accurate neuro-prognostication.
Pharmacokinetics are disrupted during TTM, including absorption, distribution, metabolism, and excretion. These properties may vary among drugs of the same class.
In hypothermia, there is a general decrease in global drug perfusion as there is shunting of blood away from non-vital organs and intra-vascular volume of distribution is reduced. Drug clearance may be reduced, thus be cautious of over-sedation.
Serum creatinine may not be a reliable indicator of renal function during TTM as there is a decrease in creatinine synthesis and secretion.
Remember that hypothermia can cause hypomagnesemia, check and replete often!
How should we manage shivering?
Shivering increases baseline metabolic activity and is associated with decreased brain tissue oxygenation and can lead to worsening hypoxic brain injury.
Assess shivering using the bedside shivering assessment scale (BSAS).
Use the Columbia anti-shivering protocol to achieve shiver control with the least sedating regimen.
There is limited data on opioids versus neuromuscular blockade for shivering, both strategies may be effective. Generally, neuromuscular blockade is considered after other strategies have failed.
How do we assess and treat ICU delirium?
Delirium should be assessed frequently using metrics such as the Confusion Assessment Method (CAM-ICU) or the Intensive Care Delirium Screening checklist (ICDSC).
CAM-ICU assesses for acute changes or fluctuation in mental status, inattention, altered level of consciousness, and disorganized thinking.
There is not a lot of data on the use of antipsychotics to treat ICU delirium.
Haloperidol is most often used even though data is limited.
Quetiapine has some positive data in small studies. Try to start with 15 mg q12 hours and titrate up to reach a target dose of 200 mg q12 hours as needed. Be cautious of hypertension and QT prolongation.
Very few patients will require antipsychotics once they leave the hospital, unless they have a pre-existing indication.
Non-pharmacologic methods should always be used such as sleep hygiene, freedom from lines/catheters, early mobilization, avoidance of constipation, and providing glasses/hearing aids as needed.
What strategies can be used to limit analgesia and sedation and why is that important?
Constant re-evaluation of the need for analgesia and sedation is paramount to reducing ventilator time, ICU delirium, and ICU and hospital length of stay.
Ask yourself if the RASS goal is the same today as it was yesterday. Re-evaluate often.
Take sedation vacations! Spontaneous breathing and spontaneous awakening trials should be performed at least daily if it is safe for the patient.
Consider re-introduction of home medications when appropriate, such as gabapentin for neuropathic pain or prior psychiatric medications.
References
Riker RR, Gagnon DJ, May T, Seder DB, Fraser GL. Analgesia, sedation, and neuromuscular blockade during targeted temperature management after cardiac arrest. Best Practice & Research Clinical Anaesthesiology. 2015;29(4):435-450. doi:10.1016/j.bpa.2015.09.006
Zakaria S, Kwong HJ, Sevransky JE, Williams MS, Chandra-Strobos N. Editor’s Choice-The cardiovascular implications of sedatives in the cardiac intensive care unit. European Heart Journal: Acute Cardiovascular Care. 2018;7(7):671-683. doi:10.1177/2048872617695231
Schenone A, Chen K, Andress K, Militello M, Cho L. Editor’s Choice- Sedation in the coronary intensive care unit: An adapted algorithm for critically ill cardiovascular patient. European Heart Journal: Acute Cardiovascular Care. 2019;8(2):167-175. doi:10.1177/2048872617753797
Van Diepen S, Katz JN, Albert NM, et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement from the American Heart Association. Circulation. 2017;136(16):e232-e268. doi:10.1161/CIR.0000000000000525
55 min
March 29, 2023279. Guidelines: 2021 ESC Cardiovascular Prevention – Question #19 with Dr. Eugene Yang
The following question refers to Section 3.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern, student Dr. Hirsh Elhence, answered first by Ohio State University Cardiology Fellow Dr. Alli Bigeh, and then by expert faculty Dr. Eugene Yang.
Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and current chair of the ACC Prevention of CVD Section.
The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.

Question #19

True or False: A 70-year-old male has an estimated 10-year ASCVD risk (using SCORE2-OP) of 7.5% which confers a very high CVD risk and necessitates treatment with a statin.
TRUE
FALSE
Answer #19
Explanation
FALSE – CVD risk thresholds for risk factor treatment are higher in apparently healthy people 70 years and older in order to prevent overtreatment in the elderly. A 10-year CVD risk ≥15% is considered “very high risk” for individuals ≥70 years of age (compared to a ≥7.5% cut-off for “very high risk” in younger patients <50 years old). For these patients, treatment of ASCVD risk factors, including lipid-lowering medications, is recommended (class IIb). Lifetime benefit of treatment in terms of time gained free of CVD is lower in older people. The SCORE2-OP algorithm estimates 5-year and 10-year fatal and non-fatal CVD events adjusted for competing risks of non-CVD mortality. Treatment and risk stratification should (as with all patients) be individualized.
For patient >70 years of age, a 10-year CVD risk of 7.5 to <15% is considered “high risk”, and treatment of risk factors should be considered taking CVD risk modifiers, frailty, lifetime treatment benefit, comorbidities, polypharmacy, and patient preference into account.
For patient >70 years of age, a 10-year CVD risk of <7.5 is considered “low-to-moderate risk” and would generally not qualify for risk factor treatment unless one or several risk modifiers are present.
Smoking cessation, lifestyle recommendations and a SBP <160 mmHg are recommended for all.
Main Takeaway
CVD risk assessment for patients 70-years and older is estimated using the SCORE2-OP algorithm. A predicted 10-year CVD risk score of ≥15% confers a very high CVD risk, however, this it is a class IIb indication to initiate/intensify lipid lowering therapies in these patients. Decision should be individualized and based on benefits vs risk assessment.
Guideline Loc.
3.2.3.5
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March 29, 2023 278. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #13 with Dr. Anu Lala

The following question refers to Section 9.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Duke University cardiology fellow and CardioNerds FIT Ambassador Dr. Aman Kansal, and then by expert faculty Dr. Anu Lala.
Dr. Lala is an advanced heart failure and transplant cardiologist, associate professor of medicine and population health science and policy, Director of Heart Failure Research, and Program Director for the Advanced Heart Failure and Transplant fellowship training program at Mount Sinai. Dr. Lala is deputy editor for the Journal of Cardiac Failure. Dr. Lala has been a champion and role model for CardioNerds. She has been a PI mentor for the CardioNerds Clinical Trials Network and continues to serve in the program’s leadership. She is also a faculty mentor for this very 2022 heart failure decipher the guidelines series.
The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #13
Mrs. Hart is a 63-year-old woman with a history of non-ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 20-25%) presenting with 5 days of worsening dyspnea and orthopnea. She takes carvedilol 12.5mg BID, sacubitril-valsartan 24-46mg BID, empagliflozin 10mg daily, and furosemide 40mg daily and reports that she has been able to take all her medications. What is the initial management for Mrs. H?

A
Assess her degree of congestion and hypoperfusion
B
Search for precipitating factors
C
Evaluate her overall trajectory
D
All of the above
E
None of the above
Answer #13
Explanation
The correct answer is D – all of the above.

Choice A is correct because in patients hospitalized with heart failure, the severity of congestion and adequacy of perfusion should be assessed to guide triage and initial therapy (Class 1, LOE C-LD). Congestion can be assessed by using the clinical exam to gauge right and left-sided filling pressures (e.g., elevated JVP, S3, edema) which are usually proportional in decompensation of chronic HF with low EF; however, up to 1 in 4 patients have a mismatch between right- and left-sided filling pressures. Hypoperfusion can be suspected from narrow pulse pressure and cool extremities, intolerance to neurohormonal antagonists, worsening renal function, altered mental status, and/or an elevated serum lactate. For more on the bedside evaluation of heart failure, enjoy Episode #142 – The Role of the Clinical Examination in Patients With Heart Failure – with Dr. Mark Drazner.

Choice B, searching for precipitating factors is also correct. In patients hospitalized with HF, the common precipitating factors and the overall patient trajectory should be assessed to guide appropriate therapy (Class 1, LOE C-LD). Common precipitating factors include ischemic and nonischemic causes, such as acute coronary syndromes, atrial fibrillation and other arrhythmias, uncontrolled HTN, other cardiac disease (e.g., endocarditis), acute infections, anemia, thyroid dysfunction, non-adherence to medications or new medications. When initial clinical assessment does not suggest congestion or hypoperfusion, symptoms of HF may be a result of transient ischemia, arrhythmias, or noncardiac disease such as chronic pulmonary disease or pneumonia, and more focused assessments may be warranted.

Lastly, Choice C, evaluation of a patient’s trajectory is correct as hospitalization for HF is a sentinel event that signals worse prognosis and provides key opportunities to redirect the disease trajectory – including establishment of optimal volume status before and after discharge. During the HF hospitalization, the approach to management should include and address precipitating factors, comorbidities, and previous limitations to ongoing disease management related to social determinants of health. The disease trajectory for patients hospitalized with reduced EF is markedly improved by optimization of recommended medical therapies, which should be initiated or increased toward target doses once the efficacy of diuresis has been shown.
Main Takeaway
In summary, when a patient is admitted for acute decompensated heart failure, initial management involves assessing the patient’s degree of congestion and hypoperfusion, identifying and addressing precipitating factors, and evaluating overall patient trajectory to guide appropriate triage and therapy.
Guideline Loc.
Section 9.1, Table 21

Decipher the Guidelines: 2022 Heart Failure Guidelines Page
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