Podcasts about afterload

Download for FREE today -  special Mnemonics Cheatsheet - so you can be SURE that you have that Must Know information down:  bit.ly/nursing-memory   Outline UNLOAD FAST U-sit Upright N-Nitro L-Lasix O-Oxygen A-Aminophylline D-Digoxin F-Fluids – decrease A-Afterload – decrease S-Sodium – decrease T-Tests: dig level, ABG, K+ Description These treatments used in conjunction will help in reducing the symptoms and complications associated with CHF.

The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.  The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Duke University cardiology fellow and CardioNerds FIT Ambassador Dr. Aman Kansal, and then by expert faculty Dr. Javed Butler. Dr. Butler is an advanced heart failure and transplant cardiologist, President of the Baylor Scott and White Research Institute, Senior Vice President for the Baylor Scott and White Health, and Distinguished Professor of Medicine at the University of Mississippi. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #14 Mrs. Hart is a 70-year-old woman hospitalized for a 2-week course of progressive exertional dyspnea, increasing peripheral edema, and mental status changes. She has a history of coronary artery disease, hypertension, and heart failure for which she takes aspirin, furosemide, carvedilol, lisinopril, and spironolactone. On physical exam, the patient is afebrile, BP is 80/60 mmHg, heart rate is 120 bpm, and respiratory rate is 28 breaths/min with O2 saturation of 92% breathing room air. She is sitting upright and is confused. Jugular venous pulsations are elevated. Cardiac exam reveals an S3 gallop. There is ascites and significant flank edema on abdominal exam. Her lower extremities have 2+ pitting edema to her knees and are cool to touch. Her labs are significant for an elevated serum Creatinine of 3.0 from a baseline of 1.0 mg/dL, lactate of 3.0 mmol/L, and liver enzyme elevation in the 300s U/L. Which of the following is the most appropriate initial treatment? A Increase carvedilol B Start dobutamine C Increase lisinopril D Start nitroprusside Answer #14 Explanation The Correct answer is B – start dobutamine. This patient with progressive congestive symptoms, mental status changes, and signs of hypoperfusion and end-organ dysfunction meets the clinical criteria of cardiogenic shock. The Class 1 recommendation is that in patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and maintain end-organ performance (LOE B-NR). Their broad availability, ease of administration, and clinician familiarity favor such agents as first line when signs of hypoperfusion persist. Interestingly, despite their ubiquitous use for management of cardiogenic shock, there is a lack of robust evidence to suggest the clear benefit of one agent over another.  Therefore, the choice of a specific agent is guided by additional factors including vital signs, concurrent arrhythmias, and availability. For this patient, dobutamine is the only inotrope listed. Although she is tachycardic, her lack of arrhythmia makes dobutamine relatively lower risk and does not outweigh the potential benefits. Choice A – Increase carvedilol – is not correct. Beta-blockers should be continued in HF hospitalization whenever possible; however, in a patient with low cardiac output and signs of shock, beta-blockers should be discontinued due to their negative inotropic effects. Choice C – Increase lisinopril – is not correct. Afterload reduction is reasonable to decrease myocardial oxygen demand. However, given the hypotension and renal dysfunction, increasing lisinopril could be potentially dangerous by fur...

CardioNerd (Daniel Ambinder) and series co-chairs Mark Belkin (AHFT Fellow, University of Chicago) and Karan Desai (Cardiologist, Johns Hopkins), join fellow lead, Dr. Pablo Sanchez (FIT, Stanford) for a discussion with Dr. Ryan Tedford (Professor of Medicine at the Medical University of South Carolina) about Right Ventricular (RV) predominant cardiogenic shock. In this episode we explore risk factors, pathophysiology, hemodynamics, and treatment strategies in this common and complex problem. We dissect three cases that epitomize the range of diagnostic dilemmas and management decisions in RV predominant shock, as Dr. Tedford expertly weaves us through the pathophysiology and decision-making involved in managing the “people's ventricle.” Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds internship program, CardioNerds academy fellow, and IM resident at Brigham and Women's Hospital). The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - RV Predominant Cardiogenic Shock The degree of RV dysfunction and failure are modulated by stretching its capacity to tolerate insults from deranged afterload, preload, and contractility.Afterload insults are MUCH LESS tolerated than other insults and broadly comprise the most common pathophysiologic cause of both acute and chronic RV failure.RV and left ventricular (LV) function are anatomically and physiologically connected.  Progressive derangements in RV function can lead to the deadly “RV spiral,” in which poor RV function causes lower LV preload, leading to hypotension, and thus worsening RV perfusion and function.In RV failure/shock, some basic tenets including treating reversible causes, optimizing preload and afterload, and using inotropes and/or temporary MCS for as limited time as possible.Many acute RV failure patients can recover, but multiorgan injury plays an important role. Therefore, thoughtful and expeditious use of mechanical circulatory support is important. Show notes - RV Predominant Cardiogenic Shock Notes drafted by Dr. Pablo Sanchez. What is the basic difference between RV dysfunction and failure?Dysfunction: Abnormalities in systolic/diastolic function of the RV, but not necessarily to the point of leading to end-organ perfusion defects. RV dysfunction leads to poor outcomes regardless of mechanism.1Failure: Clinical syndrome of inability of RV to maintain adequate output despite adequate preload. 1 How is the RV different from the LV and what impact does it have on pathophysiology and hemodynamics?The LV and RV originate from different embryologic “heart fields.”1,2The RV wall is thinner and more compliant and has only two layers (instead of 3 like the LV).3 Furthermore, unlike the LV which has a significant proportion of endocardial and epicardial transverse myocardial fibers, the RV myocardial fibers are aligned in a longitudinal plane for the most part. Thus, a more significant proportion of RV systolic contraction is longitudinal – base of the ventricle moving towards the apex.The RV is crescent-shaped and has a large surface-to-volume ratio meaning smaller inward motion ejects the same stroke volume. 1Hemodynamically, the RV takes blood from a low-pressure venous system and gives it to a distensible system with low impedance (the normal pulmonary circuit at baseline typically has a resistance one-tenth of the systemic resistance). Therefore, volume loads (preload) are much better handled...

Table at the start

In deze aflevering van Intensief de Podcast bespreek ik samen met Thomas Smits alles omtrent vocht toediening en fluid responsiveness. Thomas is IC-verpleegkundige en verplegingswetenschapper en heeft tijdens zijn studie veel expertise opgedaan over het bepalen van fluid responsiveness en zal deze expertise met ons delen. We bespreken de o.a. volgende onderwerpen:Wat is fluid responsiveness en het Frank-Starling principe?Waarom geven we vocht aan onze IC-patiënten?Waarom moeten we vocht als medicijn gaan zien?Waarom zijn tachycardie, hypotensie, een lage CVD en een hoog lactaat slechte tekenen  voor fluid responsiveness? En wat zijn dynamische en statische parameters?Wat is een fluid challenge en een passive leg raise?Hoe kan je de beademingsmachine gebruiken om fluid responsiveness te bepalen?Waarom moeten we vocht met een drukzak toedienen en niet met een infuuspomp?Wat zijn de nieuwste technieken en hoe ziet de toekomst eruit?Bronnen:CV Physiology | Frank-Starling MechanismFluid responsiveness in acute circulatory failure | Journal of Intensive CareFluid challenges in intensive care: the FENICE studyIV Fluid Overload: Don't Drown your Patients!Ventricular Pressure-Volume Relationship: Preload, Afterload, Stroke Volume, Wall Stress & Frank-Starling's law – ECG & ECHOHypotension: Differential Diagnosis – emupdatesTachycardia DDx • LITFL • CCC Differential DiagnosisWill This Hemodynamically Unstable Patient Respond to a Bolus of Intravenous Fluids? | Acid Base, Electrolytes, Fluids | JAMA | JAMA NetworkNoninterventional follow‐up vs fluid bolus in RESPONSE to oliguria—The RESPONSE trial protocol and statistical analysis plan Fluid Bolus in Resuscitation: Pressure Bag vs. 999ml/hr on the IV PumpPrediction of fluid responsiveness. What's new?Hoeveel zout mag ik eten? | VoedingscentrumBalanced Crystalloids Versus Saline in Critically Ill Adults: A Systematic Review and Meta-analysisEffect of a fluid bolus on cardiovascular collapse among critically ill adults undergoing tracheal intubation (PrePARE): a randomised controlled trial Effect of Fluid Bolus Administration on Cardiovascular Collapse Among Critically Ill Patients Undergoing Tracheal Intubation (PREPAREBedankt voor het luisteren!Volg @intensiefdepodcast op InstagramVragen? intensiefdepodcast@gmail.com

Commentary by Dr. Valentin Fuster

Today's Audio Brick is based on the upcoming Brick 2.0: Contractility, Preload, and Afterload. If you're looking for supplemental information from Bricks 1.0, read up on our Cardiac Muscle Contractility Brick. As a listener of the podcast, you can take 50% off a subscription with code RXPOD. 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.

This episode covers preload and afterload!

Dagáll læknanemans er nýtt hlaðvarp fyrir læknanema og aðra áhugasama um hvaðeina sem viðkemur klíník. Hlaðvarpið fær til sín sérfróða gesti og tekur fyrir ýmis læknisfræðileg vandamál. Stjórnendur Dagáls læknanemans eru Sólveig Bjarnadóttir læknanemi á 6. ári og Teitur Ari Theodórsson læknanemi á 5. ári. Í þessum þætti leiðir Hjálmar Ragnar Agnarsson, sérnámslæknir á Landspítala, hlustendur gegnum bráða hjartabilun frá A til Ö og svarar því hvort hann sé frá Vestamannaeyjum.

In this short episode of Ectopics, we unpack some common cardiac Jargon.  Inotropy, Chronotropy, Stroke Volume, Preload and Afterload. short, sharp, informative and 0.25CPD Check out our HICCs online and other face to face seminars and all our programs.  www.ect4health.com.au   Follow all the Blogs: HERE

In this episode we talk with Michael Perlmutter (@DitchDoc14) who recently released a poster board for an upcoming paper evaluating the safety and efficacy of push-dose nitroglycerin in EMS for patients experiencing sympathetic induced pulmonary edema. In this episode you will hear us refer to this subset as "SCAPE" patients. This term was coined by Scott Weingart in his very first EMCrit podcast and stands for sympathetic crashing acute pulmonary edema (SCAPE). The safety of this method is extremely beneficial for services that do not have access to an IV pump.

Afterload

Afterload and Leplace’s Law --- Support this podcast: https://anchor.fm/kamesa-anota/support

Reading First Aid: afterload

  Session 06 Today, we start our board content. We thought that there is no better way to start than with the heart. As always, I'm joined by Dr. Andrea Paul from Board Vitals, a company that helps you with your board prep. They feature an amazing QBank and software platform to help you maximize your score. Save 15% off any of their QBank packages by using the promo code BOARDROUNDS at checkout. [03:11] Scenario of a Heart Murmur in a 60-Year-Old Male Case: A 60-year-old male is undergoing evaluation for a heart murmur. He's asymptomatic and his physician discovers a holosystolic murmur at the cardiac apex. The frequency of that murmur is increased when he expires and an echo confirms that there's a diagnosis to be found. Question: Compared to a normal patient, which of the following hemodynamic changes would be most likely present? Note: This involves multi-steps where you have to figure out from the murmur and it's confirming there is something so you could look at the murmur and decide what you think the diagnosis is. From there, you go one step further and say what physiologic effect that would have. [04:10] Knowing the Types of Murmur First, you have to know the types of murmurs out there. Holosystolic means that the murmur is present during the entire systole phase. There are some that fade off before the end or would just be a click sound at the beginning of systole. Holocystolic refers to the sound that is present the entire time. It can be one consistent sound for all systole or maybe it's something that starts at an increased volume or decreases. So you're left with different options. In this case, it says it's in the cardiac apex. You have to look at other components like the student's age to determine what exactly is causing the murmur. But here we're lucky since they're telling us here that it's right in the apex. [06:35] Mitral Valve Regurgitation When you're hearing this whole systolic murmur at the cardiac apex, you immediately start to think of mitral valve. When you look at the diagram, you will find different areas where you can picture where the apex of the heart is and what would be causing a sound in that direction. If you're visual, you can picture the mitral valve in the direction of the flow. If it weren't functioning properly, it would be right to the apex of the heart. So this would lead you to suspect mitral valve regurgitation. Another thing you can think of is mitral stenosis, however, that's diastolic so it would be heard in a similar area at a different time. Other things to think of when you have mitral valve regurgitation is that it kind of fits with the patient. If the question had said something about an irregular pulse or displaced apex, that would be the first thing that would fit with mitral valve regurgitation as well. Although the patient here is asymptomatic, common symptoms would be rhematic fever, palpitation, fatigue, shortness of breath, and it can go as far as having signs of heart failure. So any of those components in any combination could be present in the question that would lead to the same answer in the end. [09:25] Answer Choices A Increased after load B Decreased pre-load C Increased ejection fraction D Decreased ejection fraction E Decreased contractility Now, you have to understand what all of those components mean. In most cases, mitral valve regurgitation would be easily heard during expiration. This specific murmur isn't one that is always so strongly correlated. But this is something to keep in mind that expiration is more positive pressure down on the heart, more pressure on the ventricle and potentially easier to have a bit more of regurgitation. [11:11] Understanding the Terms: Afterload Afterload is the pressure against which the heart is working to eject the blood during systole. It's a systolic murmur so this is the one we're hearing here. And it's the component where the answer option is asking whether there would be increased afterload. In this case, that would not be correct since we're having regurgitation. Afterload does have an effect on the stress volume because the maximum pressure of the heart that can develop becomes smaller when there's volume inside the ventricle. During the systolic phase of the heart, this afterload is the pressure that's coming on the blood way out of the heart. As you're contracting, that mitral valve cannot hold itself shut. And you're having that regurgitation coming back in the opposite direction. [13:04] Understanding the Terms: Afterload and Ejection Fraction The preload is the filling pressure of the heart at the end of diastole. Once it's filled, the left atrial pressure at the end of diastole. We imagine Starling's Law which states that the heart is going to eject to a greater volume if it's filled to a greater volume at the end of diastole. That relationship can be modified by contractility in the afterload that would affect what ends up resulting. Ejection fraction is just the percentage of the blood left in the ventricle after a contraction. So if you have systole, the ventricles contract. 50% remains and that's the ejection fraction. [14:30] Causing Ejection Fraction After you've determined that it's mitral valve regurgitation, you can look at the electrocardiogram. We have shown that since the patient has no symptoms, probably compensating for this is a chronic disease that's why he's not coming in with any specific symptoms other than the murmur heard. Most likely, he has dilated his left atrium or left ventricle to compensate. Most patients with chronic mitral valve regurgitation have that. Then you have this retrograde flow happening over that mitral valve. So you would probably see a slight decrease in his afterload because of the resistance across that valve. The most likely though is you would see increased ejection fraction. [16:20] Starling's Law Think of the volume of the heart at the end of the diastole phase. That's going to give you a filling pressure, which is the preload. You would see that if you have that increased volume and pressure of blood in there to start with, that's going to lead to increased volume in systole and it affects contractility and afterload. But it's just sort of a volume and pressure play and less to do with the actual muscle fibers. If you look overall the spectrum of clinical cases, you can see mostly that it all comes down to volume and pressure. [17:45] More Options to Think Through This question is great because it brings up not just all the different types of murmurs that you have to run through but it also gives you all those different scenarios to think through for all the different murmurs. So you would have to go through all these options and assess each. If you just think through where is blood flowing during what phase of the cardiac cycle, you can almost figure out which answer you can immediately eliminate. This is the nice thing about cardiac physiology is that once you can think through oeach of the different causes of the murmur and think about afterload and preload and each one, it's something you probably won't forget because you've made sense of it, and not just memorized it. [19:55] Some Tips to Help You Study Effectively There are mnemonics you can use for the different types of murmurs so it's easier for you, like to know which sound and during which phase can lead to whether mitral stenosis or mitral valve regurgitation or aortic regurgitation. So if you're someone who can easily figure out how to memorize this then this is something you can jot down for sure. Moreover, rheumatic fever can also be something to consider that can cause aortic stenosis as well. If you know the basics and you know how to recognize mitral regurgitation and understand the physiology behind it, then you'll be able to lead yourself to any of those types of questions. Again, understand the causes of any of these murmurs. Know the signs. For instance, in aortic stenosis, that slow rising pulse is going to be in the question almost definitely, since that's one of those really unique cardinal signs of aortic stenosis, or the opposite is the collapsing pulse in aortic regurgitation. Knowing some of those clinical signs is super helpful in these types of questions. Links: Board Vitals (Save 15% off any of their QBank packages by using the promo code BOARDROUNDS at checkout.)

UNLOAD FAST   U sit Upright Nitro Lasix Oxygen Aminophylline Digoxin   Fluids – decrease Afterload – decrease Sodium – decrease Tests: dig level, ABG, K+   The post Ep36 CHF (UNLOAD FAST) appeared first on NURSING.com.

What is Preload? The best way to think of preload is as a volume. Essentially, preload is the VOLUME of blood in the ventricles at the end of diastole.  This is termed End Diastolic Volume (EDV), thus at the very end… The post Preload vs Afterload |Hemodynamics | Blood Pressure appeared first on NURSING.com.