Podcasts about Tamponade

CardioNerds cofounders, Dan Ambinder joins Drs. Aishwarya Pastapur, Oyinkansola Osobamiro, and Rafik Issa from the University of Michigan for drinks in Ann Arbor. They discuss the following case of pericardial decompression syndrome. Expert commentary is provided by Dr. Brett Wanamaker. Notes were drafted by Dr. Aishwarya Pastapur and Dr. Rafik Issa. The episode audio was engineered by CardioNerds Intern student Dr. Atefeh Ghorbanzadeh. A woman in her 50s with a past medical history of stage IV lung cancer (with metastatic involvement of the liver, bone, and brain), previous saddle pulmonary emboli, pericardial effusion, and malignant pleural effusions presents with dyspnea. She was found to have a pericardial effusion with tamponade physiology relieved by pericardiocentesis. We discuss the management of cardiac tamponade, indications for pericardiocentesis, how to monitor for post-pericardiocentesis complications, and what to keep on your differential diagnosis for decompensation after pericardiocentesis. We discuss the epidemiology, pathophysiology, diagnosis, and management of pericardial decompression syndrome. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Pericardial Decompression Syndrome Pearls - Pericardial Decompression Syndrome Diminished heart sounds, a low-voltage EKG with electrical alternans, elevated jugular venous pressure/pulsations (JVP), and the presence of pulses paradoxes are important findings that could suggest tamponade. McConnell sign is strongly concerning for right ventricular failure and pulmonary hypertension, potentially due to acute pulmonary embolism. Mechanical thrombectomy for pulmonary embolism is not feasible if the emboli are diffusely scattered without a central lesion to target. For patients who experience decompensation following pericardiocentesis, consider perforation, tamponade re-accumulation, or pericardial decompression syndrome (PDS). When possible, avoid draining more than 1L of pericardial fluid at once to minimize the risk of PDS. Notes - Pericardial Decompression Syndrome What is Pericardial Decompression Syndrome (PDS), and how does it present? Pericardial decompression syndrome is a rare, life-threatening syndrome occurring in about 5-10% of cases with paradoxical worsening of hemodynamics after pericardial drainage. The clinical presentation ranges from pulmonary edema to cardiogenic shock to death, occurring a few hours to days after a successful pericardiocentesis. What is the underlying mechanism for PDS? The pathophysiology behind PDS is debated, but there are three proposed mechanisms: Paradoxical Hemodynamic Derangement: After pericardiocentesis, venous return to the RV rapidly increases, resulting in RV expansion and potentially septal deviation towards the LV. Subsequently, the LV experiences decreased preload while still facing increased afterload as a compensatory response to obstructive shock, leading to decompensation.Myocardial Ischemia: Increased intrapericardial pressure may impair coronary perfusion, leading to myocardial ischemia. Upon pericardiocentesis, there is myocardial stunning with increased demand due to increased venous return and cardiac output Sympathetic Withdrawal: Withdrawal of sympathetic activation after drainage of pericardial fluid can trigger cardiovascular collapse What are the risk factors for developing PDS, and how can we mitigate those risks for prevention? Generally, patients with long-standing pericardial effusion with chronic compression of the heart, such as those with malignant pericardial effusions, are more vulnerable to developing PDS after pericardioc...

When blood, or other fluids, accumulate in the sac around the heart it's called a cardiac tamponade or pericardial tamponade. The effects of tamponade on the electrical system and chambers of the heart. Cardiac tamponade can be acute or chronic and caused by traumatic, iatrogenic, or pathological etiologies. Common traumatic events, medical procedures, and diseases that can result in a pericardial tamponade. Signs & symptoms of cardiac tamponade. Treatment of cardiac tamponade with pericardiocentesis.For additional information on cardiac tamponade, check out the Pod Resources page at PassACLS.com. Connect with me:Website: https://passacls.com@PassACLS on X (formally known as Twitter)@Pass-ACLS-Podcast on LinkedInGive back - buy Paul a bubble tea hereGood luck with your ACLS class!Discover more FOAMed podcasts and earn CE at Conveymed.io

In today's VETgirl online veterinary CE podcast, we review the clinical signs, clinical course and prognosis for dogs diagnosed with pericardial effusion secondary to either left atrial rupture from myxomatous mitral valve disease versus those with neoplastic cardiac tamponade. This is based off a recent study by Sugiura et al entitled “Retrospective evaluation of clinical signs, clinical course, and prognosis between dogs with left atrial rupture secondary to myxomatous mitral valve disease and those with neoplastic cardiac tamponade (2015-2019): 70 cases.”

When blood, or other fluids, accumulate in the sac around the heart it's called a cardiac tamponade or pericardial tamponade. The effects of tamponade on the electrical system and chambers of the heart. Cardiac tamponade can be acute or chronic and caused by traumatic, iatrogenic, or pathological etiologies. Common traumatic events, medical procedures, and diseases that can result in a pericardial tamponade. Signs & symptoms of cardiac tamponade. Treatment of cardiac tamponade with pericardiocentesis. For additional information on cardiac tamponade, check out the Pod Resources page at PassACLS.com. Connect with me:Website: https://passacls.com@PassACLS on X (formally known as Twitter)@Pass-ACLS-Podcast on LinkedInGive back - buy Paul a bubble tea hereGood luck with your ACLS class!

When blood, or other fluids, accumulate in the sac around the heart it's called a cardiac tamponade or pericardial tamponade. The effects of tamponade on the electrical system and chambers of the heart. Cardiac tamponade can be acute or chronic and caused by traumatic, iatrogenic, or pathological etiologies. Common traumatic events, medical procedures, and diseases that can result in a pericardial tamponade. Signs & symptoms of cardiac tamponade. Treatment of cardiac tamponade with pericardiocentesis. For additional information on cardiac tamponade, check out the Pod Resources page at PassACLS.com. Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGive back & support the show:via PayPal Good luck with your ACLS class!

When blood, or other fluids, accumulate in the sac around the heart it's called a cardiac tamponade or pericardial tamponade. Effects of tamponade on the electrical system and chambers of the heart. Cardiac tamponade can be acute or chronic and caused by traumatic, iatrogenic, or pathological etiologies. Common traumatic events, medical procedures, and diseases that can result in a pericardial tamponade. Signs & symptoms of cardiac tamponade. PEA is common because the electrical system of the heart is fine. Treatment of cardiac tamponade with pericardiocentesis. For additional information on cardiac tamponade, check out the Pod Resources page at PassACLS.com. Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGive back & support the show:via PayPal Good luck with your ACLS class!

In this episode, we review the high-yield topic of Cardiac Tamponade ⁠⁠from the Cardiovascular section. Follow ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets

When blood, or other fluids, accumulate in the sac around the heart it's called a cardiac tamponade or pericardial tamponade. Effects of tamponade on the electrical system and chambers of the heart. Cardiac tamponade can be acute or chronic and caused by traumatic, iatrogenic, or pathological etiologies. Common traumatic events, medical procedures, and diseases that can result in a pericardial tamponade. Signs & symptoms of cardiac tamponade. PEA is common because the electrical system of the heart is fine. Treatment of cardiac tamponade with pericardiocentesis. For additional information on cardiac tamponade, check out the Pod Resources page at PassACLS.com. Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGive back & support the show:via PayPal Good luck with your ACLS class!Listen to other medical podcasts and earn CEUs at ConveyMed.io

When blood, or other fluids, accumulate in the sac around the heart it's called a cardiac tamponade or pericardial tamponade. Effects of tamponade on the electrical system and chambers of the heart. Cardiac tamponade can be acute or chronic and caused by traumatic, iatrogenic, or pathological etiologies.Common traumatic events, medical procedures, and diseases that can result in a pericardial tamponade. Signs & symptoms of cardiac tamponade. PEA is common because the electrical system of the heart is fine.Treatment of cardiac tamponade with pericardiocentesis. For additional information on cardiac tamponade, check out the Pod Resources page at PassACLS.com. Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGive back & support the show:via PayPal Good luck with your ACLS class!

In this session I am speaking with Robbie Lendrum on the Myocardial Hypoperfusion & injury in Trauma. We examine the Windkessel concept of pulsatile flow to constant flow, reservoir pressure as an analogue of diastolic pressure, coronary perfusion in diastole. We also explore blood pressure targeted intervention, the disparity between NIBP and IBP, the precision of diagnostics versus intervention, and individually patient centred intervention. We finally fundamentally drill down into the true importance of diastolic blood pressure in trauma care and how this is a succinct shift in mindset and teaching to traditional systolic blood pressure measurements and cut offs. To do this I have Robbie Lendrum with me. Robbie is a consultant in cardiac anaesthesia and critical care. He is also a consultant in Pre-Hospital Care working with London's Air Ambulance. Robbie is an honorary senior lecturer at Queen Mary university London and an Endovascular Resuscitation Researcher within the UK. Within the conversation we also examine: Cardiac hypoperfusion – pathophysiology The Windkessel concept – converting pulsatile flow into constant flow, the generation of pressure. Reservoir pressure equal to diastolic pressure Coronary perfusion in diastole and the fundamental importance of diastole in trauma Arterial injury and respective diastolic hypotension – wide pulse pressures - Effect on coronary perfusion pressure & flow CVD – Cardiovascular Dysfunction with early death/72 hour boundary. Physiological targets (targeted intervention) Why should we move on from blood transfusion and drive faster to hospital. The secondary effects on the heart & essentially outcome. Arterial shock and the proximal thoracic aorta. The two main types of patient and how we approach these (Tamponade and exsanguination) My thanks to Robbie for this interview. This is a fundamental shift in teaching and mindset and is seminal in how we see and approach trauma care in the future. The key pieces of research that Robbie mentions in the interview includes: Importance of the aortic reservoir in determining the shape of the arterial pressure waveform. The forgotten lessons of Frank. https://www.sciencedirect.com/science/article/abs/pii/S187293120700155X The Underlying Cardiovascular Mechanisms of Resuscitation and Injury of REBOA and Partial REBOA https://pubmed.ncbi.nlm.nih.gov/35615678/ Trauma Laparotomy in the UK: A Prospective National Service Evaluation https://pubmed.ncbi.nlm.nih.gov/34015456/ My thanks to Robbie for his insights and reflections.

About Our Guest Dr. Pei-Chun McGregor, MD, FACC (she/her) is currently the Director of Ambulatory Cardiology and Stress Laboratory at the Veterans Affairs Boston Healthcare System, an instructor of medicine at Harvard Medical School, and a Lieutenant Colonel in the US Air Force Reserves. She is a board-certified general cardiologist with a focus on adult echocardiography, nuclear cardiology, and vascular imaging. Dr. McGregor is a graduate of New York University School of Medicine. As a recipient of the Health Professions Scholarship, she went on to complete her internal medicine residency and cardiovascular fellowship at San Antonio Uniformed Services Health Consortium. She served in the United States Air Force for over 11 years and continues her service as a Lieutenant Colonel in the Air Force Reserves to date. Throughout her academic career, Dr. McGregor has demonstrated dedication to medical education as a regular lecturer to trainees and has had a significant contribution to the literature on topics in echocardiography. She has also been featured online by both OncLive and PracticeUpdate. She is an active member of the American College of Cardiology, American Society of Echocardiography, American Registry of Diagnostic Medical Sonography and Society of Vascular Ultrasound. Recently, she was chosen to be part of the first ever I.D.E.A. Group at Inteleos.

When blood, or other fluids, accumulate in the sac around the heart it's called a cardiac tamponade or pericardial tamponade. Effects of tamponade on the electrical system and chambers of the heart. Cardiac tamponade can be acute or chronic and caused by traumatic, iatrogenic, or pathological etiologies. Common traumatic events, medical procedures, and diseases that can result in a pericardial tamponade. Signs & symptoms of cardiac tamponade. PEA is common because the electrical system of the heart is fine. Treatment of cardiac tamponade with pericardiocentesis. For additional information on cardiac tamponade, check out the Pod Resources page at PassACLS.com. Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGive back & support the show:via PayPal Good luck with your ACLS class!

In this session we will examine the latest research to emerge from Zane Perkins and Mike Christian around Resuscitative Thoracotomy (RT). The research has been led by Zane and Mike examined over 600 retrospective thoracotomy cases from the LAA database spanning 20 years, looking at the survivors, the pathology (exsanguination versus tamponade), the pre-arrest rhythms, the morbidity and mortality, the time of intervention versus outcome as well as other markers. I wanted to explore the results of this research and the potential implications on practice. Zane Perkins is a consultant Trauma and General Surgeon at the Royal London Hospital, a consultant Physician for London's Air Ambulance, and an Honorary Senior Lecturer at the Centre for Trauma Sciences, Queen Mary's University London. Current thinking on Thoracotomy practice Examine the research in more detail from primary & secondary outcomes Survival rates - Who are the current survivors? What are the main domains of pathology Exsanguination: Results of outcome and pre-arrest rhythms What it shows around intervention and decisions around exsanguination Tamponade: results of outcome and pre-arrest rhythms What it shows around intervention and decisions around tamponade Differentiated decision making and prospective changes to SOP Final thoughts and take-home messages. The study has yet to be published but we will publish the results as they are published. My thanks to Zane for an engaging and insightful interview.

When blood, or other fluids, accumulate in the sac around the heart it's called a cardiac tamponade or pericardial tamponade. Effects of tamponade on the electrical system and chambers of the heart.Cardiac tamponade can be acute or chronic and caused by traumatic, iatrogenic, or pathological etiologies.Common traumatic events, medical procedures, and diseases that can result in a pericardial tamponade.Signs & symptoms of cardiac tamponade.PEA is common because the electrical system of the heart is fine.Treatment of cardiac tamponade with pericardiocentesis.For additional information on cardiac tamponade, check out the Pod Resources page at PassACLS.com. Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

1.31 Cardiac Tamponade   Cardiovascular system review for the USMLE Step 1 exam.

If you are a cardiac nurse, this is your nightmare case!  Cardiac Tamponade is a surgical emergency that requires you know more than ACLS to save this patient.  The signs and symptoms are subtle and takes an astute clinician to figure it out.In this episode we discuss all the classic textbook assessment findings from Beck's Triad to pulsus paradoxus as well as some of the more subtle clues of declining cardiac output. We talk through when you need a pericardiocentesis and when it's time to crack the chest and perform an open arrest.And who better to discuss this case than the person who taught me about cardiac tamponade, my boss and former Cardiac ICU Nurse; Brian McCain.If you want to be prepared for the absolute worst case scenario for your post cardiac surgery patient, than you're gonna want to take notes on this one.

When blood, or other fluids, accumulate in the sac around the heart it's called a cardiac tamponade or pericardial tamponade. Effects of tamponade on the electrical system and chambers of the heart. Cardiac tamponade can be acute or chronic and caused by traumatic, iatrogenic, or pathological etiologies. Common traumatic events, medical procedures, and diseases that can result in a pericardial tamponade. Signs & symptoms of cardiac tamponade. PEA is common because the electrical system of the heart is fine. Treatment of cardiac tamponade is pericardiocentesis by appropriately trained professionals working within their scope of practice. For additional information on cardiac tamponade, check out the Pod Resources page at PassACLS.com. I've placed a link to a Ninja Nerd podcast episode that discusses this topic. **American Cancer Society (ACS) Fundraiser This is the fourth year that I'm participating in Real Men Wear Pink to increase breast cancer awareness and raise money for the American Cancer Society's life-saving mission. I hope you'll consider contributing. Every donation makes a difference in the fight against breast cancer! http://main.acsevents.org/goto/paultaylor (Paul Taylor's ACS Fundraiser) THANK YOU! Connect with me: Website:  https://passacls.com (https://passacls.com) https://twitter.com/PassACLS (@PassACLS) on Twitter https://www.linkedin.com/company/pass-acls-podcast/ (@Pass-ACLS-Podcast) on LinkedIn Good luck with your ACLS class!

In unserer neuen Folge ist die Tamponadeneinlage nach Hämorrhoidektomie Thema. Verhindert sind Nachblutungen und erzeugt sie mehr postoperative Schmerzen? Diesen Fragen geht die NoTamp-Studie nach, die 2022 publiziert wurde. Langenbach, M. R., R. V. Florescu, A. Kohler, J. Barkus, J. P. Ritz, E. Quemalli, R. Siegel, H. Zirngibl, R. Lefering, and L. Bonicke. 2022. 'Tamponade dressing versus no dressing after haemorrhoidectomy: multicentre, randomized clinical trial', BJS Open, 6.

Video for this podcast: https://mehlmanmedical.com/usmle-cardiac-tamponade-vs-pericardial-effusion-in-under-60-seconds Main website: https://mehlmanmedical.com/ Instagram: https://www.instagram.com/mehlman_medical/ Telegram private group: https://mehlmanmedical.com/subscribe/ Telegram public channel: https://t.me/mehlmanmedical Facebook: https://www.facebook.com/mehlmanmedical Podcast: https://anchor.fm/mehlmanmedical Patreon: https://www.patreon.com/mehlmanmedical

Drs. Shriji Patel, Safa Rahmani, and Sarwar Zahid join for a journal club discussion of three recent publications in major ophthalmology journals:Aflibercept or Bevacizumab First for Diabetic Macular Edema (https://www.nejm.org/doi/full/10.1056/NEJMoa2204225)Gas Tamponade for Postoperative Vitreous Hemorrhage Prevention (https://www.ajo.com/article/S0002-9394(22)00251-3/fulltext)Positioning after Macular Hole Surgery (https://ophthalmologyretina.org/article/S2468-6530(22)00322-0/fulltext)Relevant Financial Disclosures: Dr. Sridhar is a consultant for Alcon, DORC, Genentech, and Regeneron. Drs. Patel, Rahmani, and Zahid have no relevant disclosures.You can now claim CME credits via the AAO website. Visit https://www.aao.org/browse-multimedia?filter=Audi

When blood, or other fluids, accumulate in the sac around the heart it's called a pericardial tamponade.  As little as 50 ml of blood, or a little under 1/4 cup, can cause a pericardial tamponade. Pathophysiology of cardiac tamponade. Iatrogenic causes of tamponade. Signs & symptoms that we observe prior to a patient arresting. Differentiating between a cardiac tamponade and a tension pneumothorax; another H&T reversible cause with some shared signs. Emergency treatment of cardiac tamponade with pericardiocentesis. Connect with me: Website:  https://passacls.com (https://passacls.com) https://twitter.com/PassACLS (@PassACLS) on Twitter https://www.linkedin.com/company/pass-acls-podcast/ (@Pass-ACLS-Podcast) on LinkedIn Good luck with your ACLS class!

In this month's EM Quick Hits podcast: Anand Swaminathan on GI balloon tamponade preparation and indications, Jesse McLaren on why troponin is rarely useful in SVT, Christina Shenvi on why we should not use the term "mechanical fall" in older patients, Nour Khatib & Jonathan Wallace on rural vertical vertigo case and Reuben Strayer on VAFEI - Video-Assisted Flexible Endoscopic Intubation for the anatomically challenging airway... The post EM Quick Hits 40 – GI Balloon Tamponade, SVT and Troponin, Falls in Older Patients, Vertical Vertigo, VAFEI Airway appeared first on Emergency Medicine Cases.

Welcome to the 14th episode of 5 Minute Medicine! In this episode, we will be exploring Pericardial Effusion and Cardiac Tamponade. We will discuss a clinical case, definitions, pathophysiology, symptoms, clinical features, diagnosis, supportive tests and treatment! All of the highest yield information is covered, with many easy ways to remember the important features of this pathology such as analysing “Beck's Triad”! We will also delve into understanding why some of the classic features of this condition occur, such as “pulsus paroxidus.” Follow us on Spotify to be notified of our releases. We would really appreciate if you rate us 5 stars and give us a review on Apple Podcasts if you have the time too, as this really helps our discoverability follow our Ig @5.min.medicine for quizzes and notes on the topics!

In this episode, we review the high-yield topic of Cardiac Tamponade from the Cardiovascular section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficialx Twitter: www.twitter.com/medbulletsIn this episode --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

Pericardial tamponade is one of the Ts in our H&T reversible causes of cardiac arrest. Review of physiology/mechanism of tamponade. Some common causes of tamponade and the signs a patient will exhibit prior to arresting. Differentiating Tamponade for Tension pneumothorax. The treatment of cardiac tamponade with pericardiocentesis. Connect with me: Website:  https://passacls.com (https://passacls.com) https://twitter.com/PassACLS (@PassACLS) on Twitter https://www.linkedin.com/company/pass-acls-podcast/ (@Pass-ACLS-Podcast) on LinkedIn Good luck with your ACLS class! Check out the pod resources page at passacls.com for a link to a Ninja Nerd's episode on pericardial tamponade.

Cardiac tamponade typically presents gradually over time, and it can happen multiple times throughout a patient's cancer care journey. Oncology nurses must stay cognizant of the warning signs and management approaches. ONS member Roberta Kaplow, RN, PhD, CCRN, AOCNS®, clinical nurse specialist at Emory University Hospital in Atlanta, GA, and member of the Metro Atlanta ONS Chapter, joins Stephanie Jardine, BSN, RN, oncology clinical specialist at ONS, to discuss the latest nursing management and prevention strategies for cardiac tamponade. This episode is part of a series about oncologic emergencies; the previous ones are linked in the episode notes. Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0 Earn 0.5 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at myoutcomes.ons.org by March 18, 2024. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of NCPD by the American Nurses Credentialing Center's Commission on Accreditation. Episode Notes Check out these resources from today's episode: Complete this evaluation for free NCPD. Previous Oncology Nursing Podcast episodes on oncologic emergencies Clinical Journal of Oncology Nursing article: Cardiac Toxicity Related to Cancer Treatment Oncology Nursing Forum article: Cardiovascular Emergencies: Pericardial Effusion and Cardiac Tamponade ONS book: Cardiac Complications of Cancer Therapy ONS book: Understanding and Managing Oncologic Emergencies: A Resource for Nurses (third edition) ONS course: Essentials in Oncologic Emergencies for the Advanced Practice Provider ONS course: Oncologic Emergencies ONS course: Treatment and Symptom Management—Oncology RN ONS Huddle Cards™ American College of Cardiology information on water bottle heart National Comprehensive Cancer Network guidelines for patients To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org.

Why should pericarditis be considered a diagnosis of exclusion? Which clinical features are most useful in the diagnosis of pericarditis? What are the most common pitfalls in the ECG interpretation? What are the best ways to differentiate the ECG of pericarditis from that of MI and early repolarization? How is uncomplicated viral pericarditis treated differently compared to pericarditis with other etiologies? Why is it so important to include colchicine as part of the treatment of pericarditis? Which patients with pericarditis require admission? and many more... The post Ep 166 Pericarditis and Cardiac Tamponade appeared first on Emergency Medicine Cases.

This week, Rob and Zach will be teaching you everything you need to know about Cardiac Tamponade.We will be discussing:Definition of Cardiac TamponadeCausesPathophysiologyClinical FeaturesPhysical Exam FindingsDiagnosisTreatmentTo follow along with Notes & Illustrations for our podcasts please become a member on our website! https://www.ninjanerd.orgFollow us on:YouTube: https://www.youtube.com/ninjanerdscienceInstagram: https://www.instagram.com/ninjanerdlecturesFacebook: https://www.facebook.com/NinjaNerdLecturesTwitter: https://twitter.com/ninjanerdsciDiscord: https://discord.com/invite/3srTG4dngWTikTok: https://www.tiktok.com/@ninjanerdlecturesSupport the show (https://paypal.me/ninjanerdscience)

Looking for more information on this topic? Check out the Congenital Adrenal Hyperplasia brick. If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/ from our Musculoskeletal, Skin, and Connective Tissue collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology.

In this episode, we cover that terrible T... Tamponade. Sit back, and get your learn on while we go beyond Beck's triad, discussing all things pulses paradox, ultrasound assessment, pitfalls, stabilization, and Josh will even melt your mind with low pressure tamponade.

Episode #21     In this episode, we will discuss cardiac tamponade including:  Etiologic factors, clinical presentation, hemodynamic and diagnostic findings, and patient management strategies.Please check out my website at:  https://www.kayhoppepresents.com  Be sure to subscribe to get my FREE Basic Dysrhythmia Cheat Sheet!You can also contact me via email at::kay@kayhoppepresents.comCome visit me on Facebook for daily [mock] CCRN Questions!  @kayhoppepresentsRemember the Online CCRN Review Course coming to you in January 2022!

This episode covers pericardial effusions.Written notes can be found at https://zerotofinals.com/surgery/cardiothoracic/pericardialeffusion/ or in the cardiothoracic surgery section of the Zero to Finals surgery book.The audio in the episode was expertly edited by Harry Watchman.

In this episode, we review the high-yield topic of Cardiac Tamponade from the Cardiovascular section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets

This episode talks about what Pericardial Effusion is, it's etiology, clinical presentations including Ewart's Sign, Investigations to be done and the line of treatment for the same.It also includes Cardiac tamponade and the various signs associated with it (Kussmaul's Sign etc).

In this weeks podcast, Jacob talks about all things cardiac arrest ultrasound. He tackles 3 different topics starting with ID'ing reversible causes. Not all of the H's and T's are amenable to ultrasound diagnosis, but you can use ultrasound for: Tamponade, Tension PTX, Thromboses, Trauma and Hypovolemia. With procedures, ultrasound-guidance is key, but don't forget that an IO is much faster. Ultrasound-guided pulse checks maybe are a little controversial if you just read abstracts. Remember: ten seconds = ten seconds. The ultrasound does not prolong pulse checks, humans prolong pulse checks. Enjoy! Don't forget to check out Courses.coreultrasound.com for all your CME educational needs! Our new POCUS Question Bank is HERE If you're interested in an online ultrasound fellowship, check out www.ultrasoundleadershipacademy.com!

Dr. Brian Clothier and Cole VanEpps have a discussion about identification of Pericardial Tamponade in the prehospital setting, treatment options and causes of this life threatening emergency.

This episode is a brand-new update 5 Min Sono video for pericardial tamponade (last one was all the way back in 2016!) While the content is similar, there are a few updates.  Check it out!   Check out our CME courses here.  Question bank here Ultrasound Leadership Academy here. 

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Our first in-person interview since the start of the COVID pandemic! Join us for National Stop the Bleed Day as Dr. Kenji Inaba from LAC+USC joins us to discuss management of penetrating cardiac injuries, the Los Angeles County Hospital Emergency Response Team (HERT), and recent updates to the Stop the Bleed campaign. From the utility of FAST to the diagnostic (and potentially therapeutic?!) role of subxyphoid windows, this episode has it all and is not to be missed! Also, remember to check out Season 1 , Episode 11 -  National Stop the Bleed Day & Tourniquet Use in 2020.

Join cardiology fellow Dr. Katye Gayle and faculty discussant Dr. Lisa Mendes as they review the approach to cardiac tamponade!

In this episode, I demonstrate a case of early tamponade in which only right atrial diastolic collapse is visualized (rather than the oft-quoted right ventricular diastolic collapse), as well as review the literature on the sonographic findings.  I also suggest that maybe tamponade should be considered more of a sonographic diagnosis rather than a clinical diagnosis.  Check it out for more info! On a side note, Terren Trott, Ben Smith and I are going to be putting together a new live and online ultrasound course March 15-16th! We're going to spend the first day talking about content creation and the second day talking about how to run an ultrasound division. The content creation course will cover how to create online presentations, how to use microblogging platforms (such as twitter and instagram) and how to give in-person presentations. The ultrasound management course will involve topics that will help you run a successful ultrasound program at your institution. With registration, you will be given access to the recorded lectures for 12 months after the course! Here's the link for more information: https://www.coreultrasound.com/cc_mgmt/ 

Want to experience the greatest in board studying? Check out our interactive question bank podcast- the FIRST of its kind here: emrapidfire.supercast.tech On this episode collaboration with ACEP PEER IX, we cover high yield must-know info for tamponade. We also try to sound smart saying electrical altering multiple times.

Written and Researched By: Caleb Dusdal Peer Review By: Chris Cochrane https://thegenerehlist.ca/ccfp-exam-105-topics-podcast/ Objective One Given a patient with undefined chest pain, take an adequate history to make a specific diagnosis (e.g., determine risk factors, whether the pain is pleuritic or sharp, pressure, etc.). Objective Two Given a clinical scenario suggestive of life-threatening conditions (e.g., pulmonary embolism, tamponade, dissection, pneumothorax), begin timely treatment (before the diagnosis is confirmed, while doing an appropriate work-up). Objective Three In a patient with unexplained chest pain, rule out ischemic heart disease

This episode covers cardiac tamponade!

CardioNerds (Amit Goyal & Daniel Ambinder) join Georgetown University/Washington Hospital Center cardiology fellows (Nitin Malik, AJ Grant, and Tsion Aberra) for some fresh Maryland blue crab cakes at the Georgetown waterfront in Washington, DC. They discuss a rare case of histoplasmosis pericarditis complicated by cardiac tamponade. Dr. Patrick Bering provides the E-CPR and program director Dr. Gaby Weissman provides a message for applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Coming soon Case Media ABCDEClick to Enlarge A. Left: Admission chest x-ray (PA film), which was overall unremarkable. Right: Chest x-ray from hospital day 12 - which revealed pulmonary edema with bilateral perihilar haziness, increased prominence of pulmonary vascularity, and small-moderate bilateral pleural effusions. Note increased size of cardiac silhouette. At the corresponding time, pericardial effusion (without tamponade) had been diagnosed.B. EKG: Sinus tachycardia and low-voltage QRS complexes.C. CT abdomen/pelvis on hospital day 14. Free air noted within the abdomen (left). Moderate pericardial effusion also incidentally appreciated (right).D. Pulse-Wave Doppler of mitral inflow. Flow variation is present, but variation is less than

This episode covers pericardial effusion and cardiac tamponade!

Postpartum hemorrhage is a leading cause of maternal mortality even in the United States. In September 2020, a new device to help treat postpartum hemorrhage was FDA cleared (The Jada System). This is a novel device that uses vacuum pressure for uterine cavity collapse/myometrial compression. In the session, we will review this new data which was published ahead of print September 10, 2020 in Obstetrics Gynecology (Green Journal).

Elizabeth Abu-Haydar, Senior Program Officer in PATH's MDHT program share the story of the Ellavi Uterine balloon tamponadeFind out more about the Ellavi UBT here: https://www.path.org/articles/the-ubt-a-simple-device-to-save-mothers-lives/

Commentary by Drs. Julia Grapsa, Eugene Brailovsky, and Estefania Oliveros Soles

A few months ago I had a wonderful conversation with Scott Weingart regarding the RUSH exam (which he invented) and the sonographic diagnosis of cardiac tamponade. If you'd like to hear Scotts 2019 update on the RUSH exam, click here.  This week I'm cross-posting our interview where he asked me about how to diagnose this at the bedside.  Check it out! If you're interested in an online ultrasound fellowship, check out the Ultrasound Leadership Academy

Ultrasound signs of pericardial tamponade with my buddy, Jacob Avila

On this week’s episode, MS4 Lavinia Turian discusses cardiac tamponade, including signs/symptoms, physiology, and treatment. Although this is a clinical diagnosis, ultrasound can be used to assist in the diagnosis. There are five findings to...

A few weeks ago Lindsay Reardon and Peter Weimersheimer talked to us about a case in which Lindsay uncovered an initially unsuspected tamponade (Click here for part 1 of the podcast). This week, we speak with the cardiologist (Joel Wolkowicz, MD) who took the case after the initial diagnosis. 

This week, Drs. Lindsay Reardon and Peter Weimersheimer talk to us about a case of shortness of breath they had in their community shop that ended up being a life-threatening pathology that was caught early enough to avoid the patient decompensating. Next week, we're publish part 2 of the podcast where we speak with the cardiologist on the case.  Interested in an online ultrasound fellowship?  Check out www.ultrasoundleadshipacademy.com!

Cardiac Tamponade

Cardiac Tamponade

Malignant Pericardial Effusion & Cardiac Tamponade + MCQ from chapter titled Emergencies in Hematology and Oncology in Baliga's Textbook of Internal Medicine available at MasterMedFacts.com authored by Thorvardur Halfdanarson,MD Professor of Oncology Mayo Clinic, Rochester, MN & Eric Engelman, MD Clinical Hematologist/Oncologist Dubuque, Iowa Not Medical Advice or Opinion  

Listen as Dr. London Smith (.com) and his producer Cameron discuss Cardiac Tamponade with special guest The Pilgrim. Not so boring! http://www.londonsmith.com/jockdocpodcast/25-cardiac-tamponade-pilgrims-digress/ Performed by: London Smith, Cameron Clark, Aaron Minton, Dylan Walker. Written by: London Smith, Cameron Clark, Aaron Minton, Dylan Walker. Produced by: London Smith, Cameron Clark, Aaron Minton Dylan Walker. Created by: London Smith

We are at #SMACC in Sydney, Australia, thanks to the Rosh Review, delivering updates from the conference to your earbuds. Advocacy in Emergency Medicine - Esther Choo and Hugh Montgomery Mechanical CPR vs Manual CPR - Ken Milne vs Salim Rezaie Super sick massive GI bleeds and balloon tamponade - Sara Gray Thanks for listening! Jeremy Faust and Lauren Westafer

This episode is all about the fibroelastic sac surrounding your heart- the pericardium! We discuss the continuum of pericarditis, pericardial effusions and cardiac tamponade- including symptoms/signs to look out for and an approach to management. As always, we have an associated infographic as well as relevant resources at www.theinternatwork.com.This episode was written by Dr. David Dorian (Internal Medicine Resident) and reviewed by Dr. Ken Melvin (Cardiologist), Dr. Rupal Shah (General Internist) and Dr. Nadine Abdullah (General Internist).

Episode 112: Does This Patient Have Tamponade?

Does one of you patients have a pericardial effusion and a pesky low blood pressure. Not sure if its the heart or one of their other 47 medical problems lowering the blood pressure. NEWS FLASH: ultrasound can help. But sometimes reality gets in the way and images don’t look like they often do on podcasts and youtube. This account describes a pericardial effusion and tamponade case, with real images. Warning, they’re not pretty. Some of them are even hard to interpret. In this podcast, Mike and Jacob break down a clinical approach to the multiple ultrasound findings in tamponade. Want to learn this stuff live? Check out Castlefest 2019 #FOAMed #FOAMus #FOAMawesome #reallifeUS

Join the crew from EMGuideWire as they review a clinically useful approach to and management of PEA. Dr. Laszlo Littmann will, once again, be our guide on this Cardiology Core Concepts tour.

In today's VETgirl online veterinary continuing education podcast, we discuss whether you detect pericardial effusion and cardiac tamponade on chest radiographs in veterinary medicine.

In today's VETgirl online veterinary continuing education podcast, we discuss whether you detect pericardial effusion and cardiac tamponade on chest radiographs in veterinary medicine.

Dr. Paul Wong:                  Welcome to the monthly podcast, On The Beat, for Circulation: Arrhythmia and Electrophysiology. I'm Dr. Paul Wong, editor in chief, with some of the key highlights from this month's issue. We'll also hear from Dr. Suraj Kapa, reporting on new research from the latest journal articles in the field. In our first article, Ratika Parkash and associates examined whether the outcomes following escalated antiarrhythmic drug therapy, or catheter ablation, depended on whether ventricular tachycardia with amiodarone refractory or sotalol refractory in patients with prior myocardial infarction in the VANISH study. At baseline, 169, or 65%, were amiodarone refractory, while the remaining were sotalol refractory. Amiodarone refractory patients had more renal insufficiency; 23.7% versus 10%. Worse, new ARC Heart Association class, 82.3% versus 65.5% class II or III; and lower ejection fraction, 29% versus 35%. Within the amiodarone refractory group, ablation resulted in a reduction of any ventricular arrhythmias compared to escalated drug therapy, with a hazard ratio of 0.53, P = 0.02. Sotalol refractory patients had trends towards higher mortality in VT storm with ablation, with no effect on ICD shocks. Within the escalated drug arm, amiodarone refractory patients had a higher rate of composite endpoint, with a hazard ratio of 1.94 and a P value of 0.01. In a trend toward higher mortality, hazard ratio 2.4, P = 0.07. While mortality was not different between amiodarone and sotalol refractory patients within the ablation treatment group. In our next study, Junaid Zaman and associates examined 57 cases in which local ablation of persistent atrial fibrillation terminated to sinus rhythm or organized tachycardia. The authors analyze unipolar electrograms collected during atrial fibrillation from multi-polar basket catheters to reconstruct isochronal activation maps for multiple cycles, and computational modeling and phase analysis were used to study mechanisms of map variability. At all signs of atrial fibrillation termination, localized, repetitive activation patterns were observed, 21% with complete rotational activity, 46% with partial rotational circuits, and 33% with focal patterns. In computer simulations incomplete segments of partial rotations coincided with areas of slow conduction, characterized by complex, multi-component electrograms. In our next article, Matthew Kalscheur and associates sought to use a novel machine-learning approach to predict outcomes following resynchronization therapy in the companion trial. The random forest algorithm resulted in the best performing model. In 595 CRTD patients in the companion trial, 105 deaths occurred, with a median follow-up of 15.7 months. The survival difference across subgroups differentiated by bundle branch block morphology and cure restoration did not reach significance, P = 0.08. The random forest model, however, produced quartiles of patients with an eight-fold difference in survival between those with the highest and lowest predictive probability for events, hazard ratio 7.96 with a P value of less than 0.0001. The model also discriminated the risk of composite endpoint of all cause mortality, or heart failure hospitalization, better than subgroups based on bundle branch block morphology and cure restoration. Future studies are needed to validate this model in other populations. In our next paper, Amr Barakat and associates examined the clinical outcomes of trans-venous lead extraction for CIED infection based on renal function. The authors examined 1,420 consecutive patients undergoing trans-venous lead extraction of infected CIEDs over a 14 year period. Groups with normal renal function, Group 1, consisting of 1,159 patients, Group 2, 163 patients with renal dysfunction not requiring dialysis, and Group 3, 98 patients on dialysis. Complete procedural success rates were comparable in the three groups: 94%, 96%, and 94% in Groups 1, 2 and 3, respectively. This was not statistically significant. The mortality rates were significantly higher in dialysis patients at one month. The procedure-related complication was 12.2% in dialysis patients versus 6.5% in Group 1 and 6.1% in Group 2. Other factors associated with mortality were lead material retention, functional New York Heart Association Class, and occurrence of procedural complications. In our next paper, Eric Johnson and associates studied the contribution of the current ITO, two left ventricular re-polarization in the human heart, since the current has been shown to have an important role in animal models. The authors found that using whole-cell voltage clamp recordings from myocytes, isolated from the left ventricle, non-failing human hearts, that there were two, distinct transient currents, ITO fast and ITO slow. The two currents have significantly different rates of recovery from inactivation and pharmacological sensitivities. ITO fast recovers in about 10 milliseconds, 100 times faster than ITO slow, and it's selectively blocked by KV4 channel toxin SNX 482. Using current clamp experiments, they found that regional differences in action potential wave forms, with a notch in phase one in the left ventricular subepicardial myocytes. In failing, left ventricular subepicardial myocytes, ITO fast was reduced, while ITO slow was increased. In addition, the notch and plateau potentials were depolarized, and action potential durations were prolonged, both statistically significantly. Slowing ITO fast inactivation results in a dramatic action potential shortening. The authors concluded that remodeling of ITO fast in failing, human left ventricular subepicardial myocytes, attenuates transmural differences in action potential wave forms. In our next paper, Ravi Vaidyanathan and associates examine the interaction between Caveolin 3 domain in the inward rectifier potassium channels. Although the IK1 current is mainly composed of Kir2.1, there are Kir2.2 and Kir2.3 heterotetromerisoforms that occur and modulate the IK1 current, but these have not been studied. Kir2.x isoforms have unique, subcellular co-localization in human cardiomyoctyes and co-immunoprecipitate with Cav3. Using induced pluripotential stem-cell-derived cardiomyocytes, the LQT9 Cav3 mutation, F97CCav3 resulted in actual potential prolongation. Based on the technique FRET, which is Fluorescent Resonance Energy Transfer, the authors calculated the distance between KR2.2 and cath ray proteins to be 6.61 nanometers. LQT9 is caused by Cav3 mutations. Prior work has shown that F97CCav3 mutation increases the late sodium current, and decreases KR2.1 current density by distinctive mechanisms. This study extends the authors' previous observations on the impact of LQT9 Cav3 mutation on Kir2.1 current, by demonstrating that mutation affects the Kir2.2 current. LQT9 causing Cav3 mutation differentially regulates current density and cell surface expression of Kir2.x homomeric and heteromeric channels. The authors show that the mutation does not affect Kir2.3 current, but the heterotetromer Kir2.2-2.3 demonstrated loss of function. Using the Li-Rudy [inaudible 00:09:45] model and myocyte mathematical model, the authors' data suggest that both loss of IK1 and increased sodium L are required for arrhythmia generation in LQT9. In our next study, Christophe Teuwen and associates use high resolution epicardial mapping electrodes, 128 or 192, with an inter-electrode distance of 2.0mm of the entire atrial surface in 164 patients. These patients were undergoing open-chest cardiac surgery. This study was designed to examine the conduction of atrial extrasystoles. The authors found that a higher degree of aberrancy was associated with a higher instance of conduction disorders. Most conduction disorders were provoked by atrial systoles emerging as epicardial breakthroughs. Atrial extrasystoles cause most conduction disorders in patients with left atrial dilatation or diabetes mellitus. In our next paper, Yuki Komatsu and associates examine 31 patients with idiopathic ventricular arryhthmias, using a two french microcatheter placed in a communicating vein between the great cardiac vein and small cardiac venous system, which passes between the aortic and pulmonary annulae, and is located in close associated with the left ventricular summit. They found that 14 patients had summit ventricular arryhthmias. The remaining 17 patients control group had ventricular arryhthmias originate from the right ventricular outflow track in the aortic cusps.  In patients with summit ventricular arryhthmias, the earliest activation during ventricular arryhthmias in the summit, preceded to cure as onset by 34 milliseconds. The summit ventricular arryhthmias exhibited inferior axes, negative polarity in lead one, deeper Q wave in AVL than AVR, nonspecific bundle branch morphology with an RS ratio in lead V1 of 0.67, distinguishing them from arryhthmias originating from the right ventricular outflow track or right ventricular cusp. Overall, ablation success was achieved in 10, or 71% of patients with summit ventricular arryhthmias, and 88% in the control group, P = 0.24. In our final paper, Deepak Padmanabhan and associates examine differences in mortality in patients with non-MRI conditional CID undergoing brain MRI compared to controls. Patients with CIDs undergoing brain MRI were compared with three control groups matched for age, sex, imaging year, and type of CID. These groups included 1) no CID and brain MRI, 2) CID in brain-computed CT, and 3) no CID in brain CT. They estimated all cause mortality at five years for CID MRI group, was not significantly different from patients who underwent CT, with or without a device. There was a significant increase in the mortality between CIED versus no CID MRI groups, hazard ratio 1.46 with a P value of 0.04. That's it for this month, but keep listening. Saraj Kapa will be surveying all journals for the latest topics of interest in our field. Remember to download the podcasts On the Beat. Take it away Saraj. Saraj Kapa:                          Thank you Paul, and welcome back to On the Beats where this month we'll be focusing on articles that are particularly hard-hitting, published across the literature in December of 2017. It's my pleasure to introduce 20 different articles that seem to have either particular interest or might change the field in the future. First, within the area of atrial fibrillation, we'll focus within the area of anticoagulation and stroke prevention. In the Journal of the American College of Cardiology, Vivek Reddy et al published on the five-year outcomes after left atrial appendage closure, from the Prevail and Protect AF trials. They included a total of 1,114 patients, with a total of 4,343 patient years of follow-up, randomized two to one to closure versus Warfarin. While ischemic stroke and systemic embolism of [inaudible 00:14:32] were numerically higher with closure, this did not reach statistical significance in terms of hemorrhagic stroke, unexplained death, and post-procedure bleeding favor left atrial appendage closure. These findings further support a role for left atrial appendage closure in the specific groups of patients enrolled in the Protect and Prevail Studies. Of course, we always need to understand, that extrapolation to patients who may not have met inclusion criteria will be difficult. In particular, given both trials had their own fundamental limitations in the Prevail study. There was a relatively low rate of [inaudible 00:15:09] in the Warfarin arm. And in turn, there was a relatively high complication rate in Protect AF with left atrial appendage closure. Part of the differences might be due to the fact that, with more experience, complication rates might decrease. Furthermore, a comparison with more novel agents, such as the new oral anticoagulants, remains to be seen. Next, within the realm of cardiac mapping and ablation for atrial fibrillation, we review an article by Vlachos et al published in the Journal of Cardiovascular Electrophysiology entitled Low-Voltage Areas Detected by High-Density Electroanatomical Mapping for Recurrence of Ablation after a Paroxysmal Atrial Fibrillation. They presented the results from a series of 80 patients undergoing ablation for paroxysmal atrial fibrillation, performing high-density voltage mapping to characterize the total area involved by low voltage. They demonstrated, when low voltage areas, defined as less than 0.4 millivolts, were seen in greater than 10% of the left atrial surface area, this served as an independent predictor of atrial fibrillation recurrence. These data support prior research, including that of MRIs, suggesting the characterization of the atrial substrate may correlate with likelihood of ablation success. Identifying methods however, to accurately and reproduce will identify these patients with more atrial substrate prior to ablation, remains to be seen. The importance of this, however, is our ability to better counsel patients on the likelihood of treatment success. Next within the realm of atrial fibrillation, we review elements of risk stratification managements. First, in the December issue of the Journal of American College of Cardiology, Takimoto et al published on how Eplerenone may reduce atrial fibrillation burden without preventing atrial electrical remodeling. In a randomized controlled ovine atrial tachy pacing model of atrial fibrillation. The authors provided daily, oral Eplerenone and compared this with a placebo. They showed that Eplerenone significantly reduced the rate of left atrial dilatation, with less smooth muscle actin protein, atrial fibril [inaudible 00:17:17]. Furthermore, Eplerenone further prolonged the time to persist in atrial fibrillation in 26% of animals. However, interestingly, Eplerenone did not prevent AF-induced electrical remodeling.  These data suggest that Eplerenone, or other medications that can be used to prevent or reverse structural remodeling, may offer an upstream therapy to reduce atrial fibrillation burden, and decrease likely the persistent atrial fibrillation. Giving the ever-growing population of patients suffering from atrial fibrillation, identifying upstream approaches to prevent it will be critical. Of course, these need to be taken with due consideration, however. Specifically, the model used here, namely that of an atrial tachy pacing model, might not be applicable to all human atrial fibrillation. Thus, whether or not such therapies actually offer benefit in clinical models, is as of yet unclear. Finally, from the realm of atrial fibrillation, we review the article by Rowin et al published in circulation entitled Clinical Profile of Consequences of Atrial Fibrillation Hypertrophic Cardiomyopathy. In patients presenting with hypertrophic cardiomyopathy, atrial fibrillation is known to be a significant co-morbidity. However, the implications of atrial fibrillation in terms of worsening of heart failure status, or long-term morbidity mortality are less clear. Rowin et al reviewed the natural history of atrial fibrillation amongst 1,558 patients, prospectively followed at a single center. Nearly 20% of the population developed atrial fibrillation with the majority having symptomatic paroxysmal atrial fibrillation. However, atrial fibrillation was not associated with any increase in cardiovascular mortality or worsening of heart failure status. Furthermore, mortality that was directly related to atrial fibrillation was nearly exclusively related to thrombolic stroke. Anticoagulation [inaudible 00:19:13] reduced this risk. The traditional scoring systems fared poorly in assessing the stroke risk of this population. About 121 patients underwent invasive rhythm control approaches, including 72 patients undergoing maze and 49 catheter ablation. The success rate of maze was significantly greater at around 75%. These data are important when counseling hypertrophic cardiomyopathy patients presenting with new-onset atrial fibrillation. While it is clear that paroxysmal atrial fibrillation has a significant impact on symptoms and quality of life, it does not cause worsened, overall, long-term outcomes. However, it does highlight the importance of anticoagulation in this population, nearly irrespective of the underlying risk score. In terms of rhythm control options, it appears that rhythm control options can be successful in these patients. Finding that catheter ablation is associated with a 40 to 50% success rate is in keeping with prior published data. Thus, consideration of when a patient needs to be referred to maze, needs to be considered in the clinical inpatient context. Changing gears, we will next review articles within the realm of ICDs, pacemakers, and CRT. In the New England Journal of Medicine this past month, Nazarian et al published on their experience regarding the safety of magnetic resonance imaging in patients with cardiac devices. They performed a prospective non-randomized study of the safety of, specifically, 1.5 tesla-strength MRI scans on legacy. In other words, not MRI conditionally-safe pacemakers and defibrillators. A total of 2,103 scans were done among 1,580 patients. They demonstrated no long term clinically significant adverse events. Nine patients did experience a reset to a backup mode, though eight of which were transients. The most common change seen acutely was a decrease in PVA amplitude in one percent of patients, and in a long term follow-up, 4% of patients experiencing a decrease in PVA amplitude, increase in atrial catheter sheer threshold, or increase in right or left ventricular capture threshold. However, none of these events were considered clinically significant. Furthermore, there was not a good [inaudible 00:21:23] group to know if this long term change in amplitudes or thresholds might have been seen in patients who had devices that were not exposed to MRI. These findings are complimentary to multiple, prior, published reports, indicating the safety of performing MRIs under clinical protocol in legacy pacemakers and defibrillators. It calls into question whether MRI conditional devices truly offer an additional safety factor furthermore, over legacy devices. Next we review an article by Lakkireddy et al published in Heart Rhythm entitled A Worldwide Experience, the Management of Battery Failures and Chronic Device Retrieval of the Nanostim Leadless Pacemaker. Lakkireddy et al reported their large multi-center experience on the overall risk of battery failure. Amongst 1,423 implanted devices there were 34 battery failures occurring, on the average, three years after implants. Furthermore, about 73 patients underwent attempted device retrieval, and this was successful in 90%, with the seven failures of retrieval being due to either inaccessibility of the docking button, or dislodgement of the docking button in one patient, in whom it embolized to the pulmonary artery. An additional 115 patients interestingly received an additional pacemaker after release of the device advisory. These data suggest that there may be as high as an overall 2% risk of battery failure with the Nanostim device, even late after implants. This highlights the need for close follow-up, even if the battery appears relatively stable up to two year after implants. Furthermore, almost 10% of devices cannot be successfully retrieved. However, in those patients, even with re-implantation of a separate device, there was no device-device interaction seen. Further innovation will be needed to optimize device longevity, and close follow-up of all patients undergoing implantation will be critical to understand the overall long term efficacy and safety when compared to other traditional devices. Finally, within the realm of device care, we focus on an article by Kiehl et al, again published in Heart Rhythm this past month entitled Incidence and Predictors of Late Atrial Ventricular Conduction Recovery Among Patients Requiring Permanent Pacemaker for complete heart block after cardiac surgery. They reviewed the likelihood of recovery of conduction in their retrospective cohort of 301 patients. Interestingly, 12% of patients had recovery of AV conduction on average six months after surgery. Those who did not recover tended to more likely have preoperative conduction abnormalities. Saraj Kapa:                          Findings that suggested a higher likelihood of long term conduction recovery included female sex and the existence of transient periods of AV conduction postoperatively. These data highlight that recovery of AV conduction is possible in a significant number of patients undergoing cardiac surgery. However, being able to predict long term recovery may assist in device selection, to avoid more costly device implantations that may not be needed over chronic follow-up. Prospective studies amongst larger numbers of patients are needed to better understand mechanisms of block, mechanisms of recovery, an optimal device in patient selection. Changing focus, we will next review two articles within the realm of supraventricular tachycardias. First we read an article by Han et al published in JACC Clinical Electrophysiology, entitled Clinical Features in Sites of Ablation for Patients With Incessant Supraventricular Tachycardia From Concealed Nodofascicular and Nodoventricular Tachycardias. Han and group describe three cases of concealed nodovascicular, nodoventricular re-entrant tachycardias, and focus on the different mechanisms of proving their participation in tachycardia. In all cases, atrial ventricular re-entering tachycardia was excluded. Successful ablation for these tachycardias occurred either at the slow pathway region, the right bundle branch, or the proximal coronary sinus. This is the first described case of incessant, concealed tachycardias related to these pathways. The importance of this article highlights an understanding the mechanisms proving the contribution to tachycardia, and the importance of recognition when performing electrophysiology studies, and being unable to reveal traditional mechanisms, which exist in most patients, such as atrial tachycardia, AVNRT or AVRT. Next we review an article by Guo et al published in Europace entitled Mapping and Ablation of Anteroseptal Atrial Tachycardia in Patients With Congenitally Corrected Transposition of the Great Arteries: Implications of Pulmonary Sinus Cusps. They reviewed three separate cases of anteroseptal atrial tachycardias in the setting of congenitally corrected transposition. They demonstrated that in these cases, there was successful ablation performed with the pulmonary sinus cusps. The result is successful and durable suppression. The reason this article is important lies in the fact that it's critical to understand both cardiac anatomy and cardiac nomenclature. The pulmonary valve in CCTJ is affectively the systemic ventricular arterial valve, given that the right ventricle is the systemic ventricle. Thus, mapping in this region of CCTJ abides the same principles as mapping the aortic valve in structurally normal hearts for similar tachycardias. However, understanding the nomenclature and that despite the variant anatomy, the utility of similar approaches to mapping of the systemic outflow are important when matching these complex, congenital anatomy or arrhythmia patients. Changing gears yet again, we review an article within the realm of sudden death and cardiac arrest. Baudhuin et al published in Circulation and Genetics entitled Technical Advances for the Clinical Genomic Evaluation of Sudden Cardiac Death. Baudhuin et al reviewed the utility of formal and fixed paraffin-embedded tissue, which is routinely obtained in an autopsy, to perform post-mortem, genetic testing. One of the main limitations to advising family members who have had prior family history of sudden death in closely related relatives, is that blood is often not available to perform DNA screening late after death. DNA however is often degraded in the tissues that are commonly available at autopsy, namely the formal and fixed paraffin-embedded tissues. The authors sought to evaluate if your next generation techniques could make these types of tissue adequate for diagnosis. They demonstrated amongst 19 samples, that performance characteristics were similar between whole blood and these tissue samples, which could be as old as 15 years. It can be critical to identify disease-causing mutations in family members, as individuals who might not yet be affected, but at risk, need to know about that overall risk. Given that decision to sequence might also not be universally applied at all centers, or in all situations, oftentimes these paraffin-embedded tissues might be the only available option, sometimes over a decade after death. This represents the first report of using next-generation sequencing approaches to successfully and accurately sequence for specific mutations using paraffin-embedded tissue. This may offer additional options to help family members achieve diagnoses for sudden death-inducing conditions. Within the realm of cellular electrophysiology, we review an article by Lang et al published in Circulation Research entitled Calcium-Dependent Arrhythmogenic Foci Created by Weakly Coupled Myocytes in the Failing Heart. Lang et al reviewed the effect of cell-cell coupling on the likelihood of triggered arryhthmias. In a [inaudible 00:28:45] model, they demonstrated the myocytes that are poorly synchronized with adjacent myocytes were more prone to triggered activity due to abnormal calcium handling when compared to myocytes with normal connection to adjacent cells. Thus, adequate coupling leads to voltage clamping during calcium waves, thus preventing triggering arrhythmias. While poorly coupled myocytes aren't able to to this due to a weakened currency, making them more prone arrhythmogenesis. These data highlight another critical cellular basis for arrhythmogenesis. In heart failure, while the focus for clinical management is typically areas of scar, there's clearly a role at the cellular level where cell-cell coupling abnormalities can lead to dynamic changes that can increase tendencies to arrhythmogenesis. The role in understanding the varying, arrhythmogenic risk based on varying factors, is important, and might have importance in the future advances in mapping technologies. Changing gears, we review an article published in the Journal of the American College of Cardiology by Mazzanti et al within the realm of genetic channelopathies entitled Hydroxyquinoline Prevents Life-Threatening Arrhythmic Events in Patients With Short QT Syndrome. They reviewed a cohort of 17 patients and demonstrated that hydroxyquinoline resulted in a reduction of arrhythmic events from 40% to 0% of patients. QTc prolongation was seen in all patients. These data clearly demonstrate that hydroxyquinoline plays a role in lowering the incidence of arrhythmic events in patients suffering from short QT syndrome. However, it's important to note that in many markets, quinoline has been difficult to access. In the specific case of QT syndrome thus, there's clearly a role for hydroxyquinoline. However, it also must be noted, the comparative efficacy with more commonly available drugs still needs to be evaluated. This past month has been of particular interest in the realm of ventricular arrhythmias, with multiple, potentially ground-breaking articles. One of the well-recited articles published this past month already is by Cuculich et al entitled Noninvasive Cardiac Radiation for Ablation of Ventricular Tachycardia published in the New England Journal of Medicine. Cuculich et al reported the first in-human data on the use of stereotactic body radiation therapy to perform noninvasive ablation of ventricular arryhthmias. Using a combination of noninvasive electrocardiographic imaging curing ventricular tachycardia, and stereotactic radiation, patients were treated with a single fraction of 25 [inaudible 00:31:15] while awake. A total of five patients were included with a mean ablation time of only 14 minutes. During the three months prior to treatment, there was a total of 6,577 VT episodes seen, and during a six week post-ablation period, considered a blanking period, there were 680 episodes. After this blanking episodes, there were only four episodes of VT seen over the ensuing 46 patient months. This study is important because it reflects the first in-human proof of concept that noninvasive ablation using radiation therapy traditionally as for treatment of solid tumors, may be affective in targeting cardiac tissue. Furthermore, modern techniques such as noninvasive electrocardiographic imaging might allow for a fully noninvasive experience for the patients. This is a vast advance seen within the realm of cardiac electrophysiology. In the early days, all we could do was map invasively and then have to go to much more invasive, open-heart surgery to treat arryhthmogenic substrates. Since the advent of catheter and radiofrequency ablation, surgical ablation is relatively fallen by the wayside, to a less invasive approaches. A completely noninvasive approach to successfully targeting tissue is potentially ground-breaking. However, there are several limitations in this study that can only be ascertained by reading the actual article. When we actually review the patients included, the long term follow-up was limited to only four patients, as one patient actually died within the blanking period, and in fact, this patient suffered from the largest burden overall of VT. Furthermore, amongst the remaining four patients, one required a redo ablation within the blanking period, and one had to be restarted on amioderone after the blanking period was over. Thus further data is really needed to clarify efficacy, given the overall success rate appears to be less than 50% on a per patient basis. Though on an overall episode basis, there was significant reduction. The exact type of radiation to be used also needs to be considered, within the realm of solid oncology. Stereotactic radiation is considered an older modality, with proton beam, and more recently, carbon beams offer more directed therapy. Thus, a lot more data is required to identify the promise of radiation therapy. Though again, this is a significant advance. Next, within the realm of invasive electrophysiology, we review an article by Turagam et al published in the JACC Clinical Electrophysiology entitled Hemodynamic Support in Ventricular Tachycardia Ablation: An International VT Ablation Center Collaborative Group Study. The utility of hemodynamic support during VT ablation is relatively unclear. Studies have been variable and limited. This group included 1,655 patients who underwent 105 VT ablations using hemodynamic support with a percutaneous ventricular assist device. Those undergoing support overall tend to be sicker, including lower ejection fractions and [inaudible 00:34:07] classes, and more VT events, including ICD shocks and VT storm. Hemodynamic support use interestingly, was an independent predictor of mortality with a hazard ratio of 5, though there was no significant difference in VT recurrence rates irrespective of the subgroup considered. These data indicate that, while patients are receiving hemodynamic support were overall sicker, there was no clear incremental benefit in use of hemodynamic support in terms of long term outcomes. In the area of substrate ablation, whether use of hemodynamic support to facilitate mapping during VT, actually alters outcomes remains to be seen. This study highlights the potential importance of randomized clinical approaches to better evaluate whether hemodynamic support truly alters the long term outcomes of the VT ablation. Next, we review an article by Munoz et al that focuses more on prediction of those patients who might be at risk for ventricular arrhythmias, again published in the last edition of JACC Clinical Electrophysiology and entitled Prolonged Ventricular Conduction and Repolarization During Right Ventricular Stimulation Predicts Ventricular Arrhythmias and Death in Patients With Cardiomyopathy. Munoz et al reviewed the relationship between paced QRS and pace Qtc and long term risk. A total of 501 patients with mean ejection fractions of 33% were included. Longer paced ventricular QRS and Qtc was associated with a higher risk of ventricular arrhythmia, and all caused death or arrhythmia, irrespective or ejection fraction. A paced QRS duration of 190 milliseconds was associated with 3.6 fault higher risk of arrhythmia, and a 2.1 fault higher risk of death or arrhythmia. These data suggest that findings during [inaudible 00:35:47] pacing and otherwise normal rhythm, including paced QRS and QTc may independently result in elevation of overall risk of ventricular arrhythmia and death. Physiologically these data make sense. In light of the fact that longer cure restorations are probably related to a greater degree of myopathy. While these data offer a prognostic indication, whether they alter outcomes or decision making regarding ICM implantation, remains to be seen. Next, also published in JACC Clinical Electrophysiology, Vandersickel et al reviewed a more cellular basis for toursades in an article entitled Short-Lasting Episodes of Toursades de Pointes in the Chronic Atrial Ventricular Model Have Focal Mechanism While Longer-Lasting Episodes are Maintained by Reentry. Vandersickel et al reviewed the mechanisms underlying toursades, and demonstrated that both focal and reentry mechanisms may exist. In five canines they used broadly distributed neuro electrodes to simultaneously map across the heart. They demonstrated that initiation and termination was always focal, but longer and non-terminal episodes always had reentry mechanisms. These data suggest that the mechanisms underlying toursades actually reflect a spectrum of potentially dynamic, electrophysiologic phenomenon the heart, including both focal and reentry activity. Understanding these mechanisms, and the fact that focal mechanisms almost universally underlie initiation may bring into consideration the optimal treatments whether in the form of pacing and defibrillation techniques or medication techniques for toursades. Finally, in the realm of ventricular arrhythmia, we review an article published in the last month's edition of Heart Rhythm by Penela et al entitled Clinical Recognition of Pure Premature Ventricular Complex-Induced Cardiomyopathy at Presentation. As we know, it's sometimes difficult to recognize patients when they present with frequent PVCs and a depressed injection fraction in terms of, whose injection fractions are purely caused by the presence of PVCs, and whose PVCs are only exacerbated by the presence of an underlying myopathy. The group included 155 patients and excluded all patients who did not normalize their elevated ejection fraction, or who had previously diagnosed structural heart disease, leaving a total cohort under consideration, of 81 patients. About 50% were diagnosed as having a PVC-induced cardiomyopathy on the basis of normalization of elevated function after PVC suppression. While the remainder was considered to have PVC exacerbated cardiomyopathy on the basis that things did not entirely resolve, and thus had an independent mechanism for nonischemic myopathy. Characteristics that suggested patients with a lower likelihood of EF normalization included those with longer intrinsic QRSs, above 130 milliseconds, a lower PVC burden of baseline, considered less than 17%, and larger [inaudible 00:38:33] greater than 6.3 cm. PVCs as a cause of [inaudible 00:38:35] are obviously a well-recognized treatable cause of myopathy, however again, it might be difficult to differentiate. Those patients whose PVCs are a result of the underlying myopathy versus those whose PVCs are the cause, and for whom ablation or suppression may reverse the myopathic process. The work of Penela et at offers an initial attempt at helping differentiate these processes, however validation of larger cohort is necessary. Next we review an article within the realm of syncopy entitled Prohormones in the Early Diagnosis of Cardiac Syncopy by Badertscher et al published in the Journal of the American Heart Association this month. They review the utility of circulating prohormones [inaudible 00:39:14] autonomic dysfunction or neurohormonal abnormalities, to differentiate cardiac from non-cardiac causes of syncopy in the emergency departments. They measured four novel prohormones in a multi-center study. In the emergency departments there is a specific protocol used to determine the perceived likelihood of the cause of syncopy to be cardiac versus non-cardiac. In addition to this, the prohormones are drawn. After this, everyone's final diagnosis was reached. Two independent cardiologists reviewed the cases to determine if it was a truly cardiac or non-cardiac cause of syncopy. Among 689 patients included, 125 overall were adjudicated as cardiac syncopy. Measure of the specific marker MR-proANP in combination with emergency department suspicion of syncopy, performed better than suspicion alone, to differentiate cardiac causes of syncopy. A combination of a circulating MR-proANP, less than 77, picomoles per liter, an [inaudible 00:40:17] probability of cardiac syncopy could be less than 20%, had a very high sensitivity negative predictive value of 99%. The significant resources are often used to manage patients with syncopy presenting to the emergency departments, and it's often extremely difficult at this stage to differentiate cardiac from non-cardiac causes of syncopy. And the amount of evaluation that can be done in the emergency department is often limited. Cardiac caused of syncopy are not good to miss, however, since these can include ventricular arrhythmias, and transient AV block, that might result in death as well. As is well-recognized, emergency department evaluation in clinical [inaudible 00:40:49] are limited in terms of their utility. This raises the utility of objective measures to help differentiates. These data suggest that circulating prohormones [inaudible 00:40:59] your hormonal function drawn during your emergency department evaluation, may be a useful adjunct to differentiate cardiac from non-cardiac syncopy. Whether they can be used to prospectively differentiate those patients requiring inpatient admission or now, however, remains to be seen. The last two articles we'll choose to focus on will fall under the realm of broader, other EP concepts. The first article we will review is by Varghese et al published in Cardiovascular Research entitled Low-Energy Defibrillation With Nanosecond Electric Shocks. Varghese et al reviewed the potential of low-energy nanosecond duration shocks for defibrillation in rapid hearts. In induced fibrillation examples, the repeated defibrillated nanosecond impulses as low as three kilovolts demonstrated effective defibrillation. The energy required is significantly lower than from monophasic shocks and longer pulse durations. Furthermore, there was no detectable evidence of electroporation, namely cardiac or so injury after defibrillation. Using nanosecond impulses, it may be feasible to defibrillate the heart with significantly lower energies. The implications for patients experiencing defibrillation, for example pain, is unclear without in-human studies. However, the ability to use lower energies could have implications in battery life. Further [inaudible 00:42:11] studies will be critical to study ambulatory efficacy as this research is performed in [inaudible 00:42:19] hearts. Finally, we review an article published in Circulation entitled Mortality in Supravascular Events After Heart Rhythm Disorder Management Procedures by Lee et al. Amongst three centers, a retrospective cohort study regarding the mortality and risk of supravascular events, was performed. They included a variety of heart rhythm [inaudible 00:42:40] procedures, including defibrillation threshold testing, lead extraction, device implant, and invasive electrophysiology studies and ablation procedures. Amongst 48,913 patients, 62,065 procedures were performed and an overall mortality of .36% was seen. Supravascular [inaudible 00:42:58] was lower at .12%. Interestingly, and expectedly, the highest risk was seen with lead extraction patients, with an overall mortality risk of 1.9%. Less than half of the deaths seen, however, were directly attributable to the procedure itself. The most common cause of procedural death was cardiac tamponade, largely seen amongst device implant patients. This is critical, as the number of ablation and other invasive electrophysiology procedures performed, is increasing. These data provide a large, contemporary experience regarding the overall risk attributable to a variety of heart rhythm disorder procedures. Interestingly, half of the procedure related deaths were associated with device implantation procedures. With the predominant cause being tamponade, highlighting the importance of early recognition of this treatable complication. Tamponade may not always be considered as a major issue after device implantation, however these data clearly suggest that it is. In addition, extraction, as expected, carried the highest incident of both supravascular events and mortality. Though, this is likely related to the higher rate of core morbidity in this population, including active infection. In summary, this month, we have reviewed 20 articles in various areas of electrophysiology published across the literature. Particularly high impact articles range from those reviewing experience regarding left atrial appendage closure and the efficacy of this, to the utility of using atrial fibrillation to predict risk and long term morbidity and mortality in hypertrophic cardiomyopathy, to further evidence regarding the safety of magnetic resonance imaging in legacy pacemakers and defibrillators, and novel considerations regarding supraventricular tachycardias and there diagnosis and management, especially invasively. Other potential groundbreaking articles included evidence that we can successfully use formal and fixed paraffin-embedded tissue that can be as old as 15 years, to successfully identify genetic mutations that might be responsible for sudden death. And evidence that using novel techniques, we might be able to perform completely noninvasive therapies for arrhythmias by using radiation therapies. However questions were also raised such as regarding the role of hemodynamic support for VT ablation. How to better differentiate those patients who will have recovery of AV conduction from those who won't, as they meet class I indications post cardiac surgery? And whether other factors such as right ventricular pacing during [inaudible 00:45:28] study might further differentiate patients at risk for ventricular arrhythmias in spite of a low ejection fractions. Many of the papers had to deal with tranlational work that still remains to be proven in terms of value at a clinical level, such as demonstrating mechanisms underlying trousades de pointes. Or the potential value of low-energy defibrillation with nanosecond electric shocks. Clinical protocols involving the use of prohormones in the early diagnosis of cardiac syncopy. How to differentiate PVC induced from other causes of myopathy, and how to manage, in the long term, these devices. Also, likely requires further study. Finally, covering all areas of electrophysiology, we reviewed one large article focusing on mortality in supravascular events after heart rhythm management disorder procedures at large. This article highlights the importance of considering institutional experience and reporting it to use as a benchmark to help better optimize our counseling of patients, as well as our procedures and protocols. I appreciate everyone's attention to these key and hard-hitting articles that we just focused on from this past month of cardiac electrophysiology across the literature. Thanks for listening. Now, back to Paul. Dr. Paul Wong:                  Thanks Seraj. You did a terrific job surveying all journals for the latest articles on topics of interest in our field. There's not an easier way to stay in touch with the latest advance. These summaries, and a list of all major articles in our field each month, can be downloaded from the Circulation Arrhythmia and Electrophysiology website. We hope you'll find the journal to be the go-to place for everyone interested in the field. See you next month.  

Causes (Four T’s): Tone: Atony Pitocin Misoprostol: CI-allergy, SI-transient hyperthermia Methergine: CI-HTN, SE-HTN Hemabate: CI-asthma. SE-diarrhea Tamponade: bakri/utah balloons Trauma: Lacerations Tissue: Retained POC (placenta or membranes) Thrombin: Coagulopathy   Other: Involution

Learn how to finally figure out the Duke criteria. The post S2 E018 Endocarditis, Pericarditis and Tamponade appeared first on Physician Assistant Exam Review.

Using point of care ultrasound for E-point septal separation and estimation of ejection fraction, tricuspid annual plane of systolic excursion for right ventricular dysfunction and inflow velocities for sonographic tamponade

Cardiac surgery can vary from being routine elective surgery to time-critical emergency surgery. The term encompasses a broad range of procedures carried out on patients from neonates to nonagenarians. In the 63 years since the first open heart surgery was performed using cardiopulmonary bypass enormous advances have been made in the field such that an average person presenting for coronary bypass grafting in 2016 can expect a very low chance of peri-operative morbidity or mortality. When things go wrong however they can go badly wrong and at the worst possible moment (see Murphy’s Law). This talk focuses on describing common complications encountered in the postoperative period, with a focus on anticipation, prevention and planning for rapid recognition and successful management of potentially life threatening complications.

30 minute practical discussion on how to assess patients for LV dysfunction, RV dysfunction and Tamponade using ultrasound

Do we recognize shock early enough? How do we prioritize our interventions? How can we tell whether we’re making our patient better or worse?   World wide, shock is a leading cause of morbidity and mortality in children, mostly for failure to recognize or to treat adequately. So, what is shock? Simply put, shock is the inadequate delivery of oxygen to your tissues.  That’s it.  Our main focus is on improving our patient’s perfusion. Oxygen delivery to the tissues depends on cardiac output, hemoglobin concentration, the oxygen saturation of the hemoglobin you have, and the environmental partial pressure of oxygen. At the bedside, we can measure some of these things, directly or indirectly.  But did you notice that blood pressure is not part of the equation?  The reason for that is that blood pressure is really an indirect proxy for perfusion – it’s not necessary the ultimate goal. The equation here is a formality: DO2 = (cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] + (PaO2  x 0.003)     Shock CAN be associated with a low blood pressure, but shock is not DEFINED by a low blood pressure.     Compensated Shock: tachycardia with poor perfusion.  A child compensates for low cardiac output with tachycardia and a increase in systemic vascular resistance.     Decompensated Shock: frank hypotension, an ominous, pre-arrest phenomenon.   Shock is multifactorial, but we need to identify a primary cause to prioritize interventions.     How they "COHDe": Cardiogenic, Obstructive, Hypovolemic, and Distributive.   Cardiogenic Shock All will present with tachycardia out of proportion to exam, and sometimes with unexplained belly pain, usually due to hepatic congestion.  The typical scenario in myocarditis is a precipitous decline after what seemed like a run-of-the-mill URI. Cardiogenic shock in children can be from congenital heart disease or from acquired etiologies, such as myocarditis.  Children, like adults, present in cardiogenic shock in any four of the following combinations: warm, cold, wet, or dry. "Warm and Dry" A child with heart failure is “warm and dry” when he has heart failure signs (weight gain, mild hepatomegaly), but has enough forward flow that he has not developed pulmonary venous congestion.  A warm and dry presentation is typically early in the course, and presents with tachycardia only. "Warm and Wet" If he worsens, he becomes “warm and wet” with pulmonary congestion – you’ll hear crackles and see some respiratory distress.  Infants with a “warm and wet” cardiac presentation sometimes show sacral edema – it is their dependent region, equivalent to peripheral edema as we see in adults with right-sided failure. “Warm” patients – both warm and dry and warm and wet -- typically have had a slower onset of their symptoms, and time to compensate partially. Cool patients are much sicker. "Cold and Dry” A patient with poor cardiac output; he is doing everything he can to compensate with increased peripheral vascular resistance, which will only worsen forward flow.  Children who have a “cold and dry” cardiac presentation may have oliguria, and are often very ill appearing, with altered mental status. "Cold and Wet" The sickest of the group, this patient is so clamped down peripherally that it is now hindering forward flow, causing acute congestion, and pulmonary venous back-up.  You will see cool, mottled extremities. Cardiogenic Shock: Act Use point-of-care cardiac ultrasound: Good Squeeze? M-mode to measure fractional shortening of the myocardium or anterior mitral leaflet excursion. Pericardial Effusion? Get ready to aspirate. Ventricle Size? Collapsed, Dilated, Careful with fluids -- patients in cardiogenic shock may need small aliquots, but go quickly to a pressor to support perfusion Pressor of choice: epinephrine, continuous IV infusion: 0.1 to 1 mcg/kg/minute.  Usual adult starting range will end up being 1 to 10 mcg/min. Avoid norepinephrine, as it increases systemic vascular resistance, may affect afterload Just say no to dopamine: increased mortality when compared to epinephrine   Obstructive Shock Mostly one of two entities: pulmonary embolism or cardiac tamponade. Pulmonary embolism in children is uncommon – when children have PE, there is almost always a reason for it – it just does not happen in normal, healthy children without risk factors. Children with PE will either have a major thrombophilic comorbidity, or they are generously sized teenage girls on estrogen therapy. Tamponade -- can be infectious, rheumotologic, oncologic, or traumatic.  It’s seen easily enough on point of care ultrasound.  If there is non-traumatic tamponade physiology, get that spinal needle and get to aspirating. Obstructive Shock: Act Pulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial.  PE with symptoms: heparin. Tamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided.   Hypovolemic Shock The most common presentation of pediatric shock; look for decreased activity, decreased urine output, absence of tears, dry mucous membranes, sunken fontanelle.  May be due to obvious GI losses or simply poor intake. Rapid reversal of hypovolemic shock: may need multiple sequential boluses of isotonic solutions. Use 10 mL/kg in neonates and young infants, and 20 mL/kg thereafter. Hypovolemic Shock: Act Tip: in infants, use pre-filled sterile flushes to push fluids quickly.  In older children, use a 3-way stop cock in line with your fluids and a 30 mL syringe to "pull" fluids, turn the stop cock, and "push them into the patient. Titrate to signs of perfusion, such as an improvement in mental status, heart rate, capillary refill, and urine output. When concerned about balancing between osmolality, acid-base status, and volume status, volume always wins.  Our kidneys are smarter than we are, but they need to be perfused first.   Distributive Shock The most common cause of distributive shock is sepsis, followed by anaphylactic, toxicologic, adrenal, and neurogenic causes.  Septic shock is multifactorial, with hypovolemic, cardiogenic, and distributive components. Children with sepsis come in two varieties: warm shock and cold shock. Distributive Shock: Act Warm shock is due to peripheral vascular dilation, and is best treated with norepinephrine. Cold shock is due to a child’s extreme vasoconstriction in an attempt to compensate.  Cold shock is the most common presentation in pediatric septic shock, and is treated with epinephrine. Early antibiotics are crucial, and culture everything that seems appropriate.   Shock: A Practical Approach   "How FAST you FILL the PUMP and SQUEEZE" Sometimes things are not so cut-and-dried.  We'll use a practical approach to diagnose and intervene simultaneously. Look at 4 key players in shock: heart rate, volume status, contractility, and systemic vascular resistance. How FAST you FILL the PUMP and SQUEEZE First, we look at heart rate -- how FAST? Look at the heart rate – is it sinus?  Could this be a supraventricular tachycardia that does not allow for enough diastolic filling, leading to poor cardiac output?  If so, use 1 J/kg to synchronize cardiovert.  Conversely, is the heart rate too slow – even if the stroke volume is sufficient, if there is severe bradycardia, then cardiac output  -- which is in liters/min – is decreased.  Chemically pace with atropine, 0.01 mg/kg up to 0.5 mg, or use transcutaneous pacing. If the heart rate is what is causing the shock, address that first. Next, we look at volume status. How FAST you FILL the PUMP and SQUEEZE Look to FILL the tank if necessary.  Does the patient appear volume depleted?  Try a standard bolus – if this improves his status, you are on the right track. Now, we look at contractility. How FAST you FILL the PUMP and SQUEEZE Is there a problem with the PUMP?  That is, with contractility?  Is this in an infarction, an infection, a poisoning?  Look for signs of cardiac congestion on physical exam.  Put the probe on the patient’s chest, and look for effusion.  Look to see if there is mild, moderate, or severe decrease in cardiac contractility.  If this is cardiogenic shock – a problem with the pump itself -- begin pressors. And finally, we look to the peripheral vascular resistance. How FAST you FILL the PUMP and SQUEEZE Is there a problem with systemic vascular resistance – the SQUEEZE? Look for signs of changes in temperature – is the patient flushed?  Is this an infectious etiology?  Are there neurogenic or anaphylactic concerns?  After assessing the heart rate, optimizing volume status, evaluating contractility, is the cause of the shock peripheral vasodilation?  If so, treat the cause – perhaps this is a distributive problem due to anaphylaxis.  Treat with epinephrine. The diagnosis of exclusion in trauma is neurogenic shock.  Perhaps this is warm shock, both are supported with norepinephrine.  All of these affect systemic vascular resistance – and the shock won’t be reversed until you optimize the peripheral squeeze.   Summary The four take-home points in the approach to shock in children To prioritize your innterventions, remember how patients COHDe: Cardiogenic, Obstructive, Hypovolemic, and Distributive. Your patient's shock may be multifactorial, but mentally prioritize what you think is the MAIN case of the shock, and deal with that first. To treat shock, remember: How FAST You FILL The PUMP and SQUEEZE: Look at the heart rate – how FAST.  Look at the volume status – the FILL.  Assess cardiac contractility – the PUMP, and evaluate the peripheral vascular tone – the SQUEEZE. In pediatric sepsis, the most common type is cold shock – use epinephrine (adrenaline) to get that heart to increase the cardiac output. In adolescents and adults, they more often present in warm shock, use norepinephrine (noradrenaline) for its peripheral squeeze to counteract this distributive type of shock. Rapid-fire word association: Epinephrine for cardiogenic shock Intervention for obstructive shock Fluids for hypovolemic shock Norepinephrine for distributive shock References Agha BS, Sturm JJ, Simon HK, Hirsh DA. Pulmonary embolism in the pediatric emergency department. Pediatrics. 2013 Oct;132(4):663-7. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013; 41:580-637. Jaff MR et al. for the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011; Apr 26;123(16):1788-830. Levy B et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med. 2011; 39:450. Micek ST, McEvoy C, McKenzie M, Hampton N, Doherty JA, Kollef MH. Fluid balance and cardiac function in septic shock as predictors of hospital mortality. Crit Care. 2013; 17:R246. Osman D, Ridel C, Ray P, et al. Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge. Crit Care Med. 2007; 35:64-8. Ventura AM, Shieh HH, Bousso A, Góes PF, de Cássia F O Fernandes I, de Souza DC, Paulo RL, Chagas F, Gilio AE. Double-Blind Prospective Randomized Controlled Trial of Dopamine Versus Epinephrine as First-Line Vasoactive Drugs in Pediatric Septic Shock. Crit Care Med. 2015;43(11):2292-302. This post and podcast are dedicated to Natalie May, MBChB, MPHe, MCEM, FCEM for her collaborative spirit, expertise, and her super-charged support of #FOAMed.  You make a difference.  Thank you. Undifferentiated Shock Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Dr. Lorrel Brown returns to discuss tamponade cardiac physiology (including demystifying pulsus pardoxus). She continues to cover the differentiation of constrictive and restrictive cardiomyopathies. This action-packed lecture concludes with stress cardiomyopathy and HFpEF (heart failure with preserved ejection fraction).

Haney Mallemat discusses the crashing patient with pericardial tamponade. Download Episode

"Rescue Cardiac Windows" is meant to describe 3 main windows of the heart one would obtain to rule out poor contractility, empty LV, RV strain, and Tamponade.

Stan Yastrebov is an echo guru and an ICU professor of echo at St George hospital in Sydney. In this talk that he gave at an ICN NSW meeting last month he goes through the nuts and bolts of haemodynamic assessment with echo. Whether you're a novice or a regular echo user in crit care, this talk has something for you. Echo talks can be a bit boring but Stan's energy and enthusiasm really come across and his accent was one reason trainees came from all over Sydney to hear this talk.

Nicola Stanley describes how ultrasound has changed the way we do critical care procedures and in the video, shows you a few new tricks.

  Li Tan is an Intensivist and Echo Fellow at St George hospital in Sydney. She has a particular interest in critical care echocardiography and in this talk describes how useful it can be when investigating obstructive shock.

  Cartan Costello is an Intensivist from St George hospital in Sydney. He has a particular interest in critical care echocardiography and in this talk describes how useful it can be for trauma patients. Go to www.intensivecarenetwork.com for the slides and video.

Mark Rosen, MD

Joan Stephenson, PhD, discusses Cardiac Tamponade with Dr Niteesh K. Choudhry.

Funktionelle endoskopische Nasennebenhöhlenchirurgie ist mittlerweile als Therapiestandard für konservativ therapierefraktäre chronische Rhinosinusitis (CRS) und Polyposis nasi anzu-sehen. Regelmäßig wird diese Operation mit einer Nasentamponade abgeschlossen, um Schleimhautnachblutungen zu minimieren und die Wundheilung zu unterstützen. Sowohl das Tragen der Tamponade als auch die Detamponade sind für den Patienten oft wenig komforta-bel und in einigen Fällen äußerst schmerzhaft. Ziel der vorliegenden Arbeit war es, eine moderne Nasentamponade aus Carboxymethylcellu-lose, das RapidRhino® Sinu-knit™, hinsichtlich ihrer Eigenschaften in Bezug auf die Blu-tungskontrolle, Beeinflussung der Wundheilung, Nebenwirkungen und den Tragekomfort für die Patienten zu untersuchen. In einer teilweise doppelblinden, randomisierten, kontrollierten prospektiven klinischen Un-tersuchung wurden n=21 Patienten einer beidseitigen funktionellen endoskopischen Nasenne-benhöhlenoperation unterzogen. Die Operation fand in Übereinstimmung mit den Regeln der Grazer Schule statt. Nach Aufklärung und mit dem Einverständnis der Patienten erfolgte prä-operativ die Zulosung der Seite der CMC-Tamponade. Zum Abschluss der Operation wurde das Carboxymethylcellulose-Netz auf die Operationswunde aufgebracht und mit 6 ml sterilem Aqua hydrolysiert. Die entsprechend andere Seite verblieb ohne Tamponade. Am ersten postoperativen Tag wurden die Patienten von einem an der Operation unbeteiligten Stationsarzt unter Zuhilfenahme einer visuellen Analogskala (0-10) nach jeweils seitenspezi-fischer Nasenatmungsbehinderung, Sekretion, lokalen Schmerzen, Kopfschmerzen sowie Schlafstörung und Gesamtbefinden befragt, ohne die tamponierte Seite zu kennen. Darüber hinaus erfolgte jeweils zwei Wochen, vier Wochen und drei Monate post-OP eine Nachsorge-untersuchung durch den Operateur, bei der die Merkmale endoskopisch sichtbare Tamponade, Nachblutung, Krustenbildung, Schleimhautstatus, Verwachsungen, Bildung von Granulati-onsgewebe und Infektion untersucht und dokumentiert wurden. Das mittlere Patientenalter betrug 49 Jahre, 33% der Patienten waren weiblich. Die Operati-onsindikation stellte bei 15 Patienten eine Polyposis nasi, bei 5 Patienten eine chronische Rhinosinusitis und bei einem Patienten eine akute Rhinosinusitis dar. Bei 86% der Patienten war das operative Vorgehen seitenidentisch. 11mal wurde die rechte OP-Seite tamponiert, 10mal die linke. Eine Beeinflussung der postoperativen Blutungen durch die Carboxymethylcellulose war nicht nachzuweisen; es fanden sich hierbei sowohl kurz- als auch mittelfristig keine Seitenun-terschiede. Bei der Interpretation dieser Ergebnisse ist kritisch zu hinterfragen, in wieweit bei insgesamt sehr geringer Nachblutung eine Tamponade nach funktioneller endoskopischer Nasennebenhöhlenchirurgie zur Blutungskontrolle überhaupt notwendig ist. Sichere Aussagen über hämostatische Effekte von CMC lassen sich anhand der hier gewonnen Erkenntnisse nicht treffen. Nebenwirkungen oder Komplikationen bei der Verwendung von CMC als mo-derne Nasentamponade traten nicht auf. Die mit CMC tamponierte Seite zeigte im Vergleich zur Gegenseite in keinem der untersuchten Parameter Unterschiede hinsichtlich der Wundhei-lung oder Krustenbildung, womit weder eine positive noch eine negative Beeinflussung zu zeigen war. Der Einsatz von CMC besitzt hinsichtlich des Tragekomforts die gleichen Eigen-schaften wie "keine Nasentamponade". Damit ist der Patientenkomfort - besonders auch im Vergleich zu anderen Tamponaden - als ausgezeichnet einzustufen. Zur abschließenden Beurteilung der Anwendung von CMC als moderne Nasentamponade sind weitere Untersuchungen notwendig. Eine interessante Option könnte der Einsatz von CMC in ihrer Gelform als Trägersubstanz für diverse Pharmaka darstellen.

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