Podcasts about Hypokalemia

Listen as Dr. London Smith (.com) and his producer Cameron discuss Hypokalemia at the Valentine's Day Spectacular! Not so boring! https://www.patreon.com/join/jockdocpodcast Hosts: London Smith, Cameron Clark. Produced by: Dylan Walker Created by: London Smith

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes. When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia. Medical conditions & medications that can cause potassium imbalance. ECG changes seen in hypo and hyperkalemia. Critical lab values that would indicate a need for treatment. Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerd podcast. Check out the pod resources page at passacls.com.Connect with me:Website: https://passacls.com@Pass-ACLS-Podcast on LinkedInGive Back & Help Others: Your support helps cover the monthly cost of software and podcast & website hosting so that others can benefit from these ACLS tips as well. Donations via Buy Me a Coffee at https://buymeacoffee.com/paultaylor are appreciated.Good luck with your ACLS class!

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes.When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia.Medical conditions & medications that can cause potassium imbalance. ECG changes seen in hypo and hyperkalemia. Critical lab values that would indicate a need for treatment. Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerd podcast. Check out the pod resources page at passacls.com.Connect with me:Website: https://passacls.com@Pass-ACLS-Podcast on LinkedInGive Back & Help Others: Your support helps cover the monthly cost of software and podcast & website hosting so that others can benefit from these ACLS tips as well. Donations made via Buy Me a Coffee at https://buymeacoffee.com/paultaylor are appreciated.Make a difference in the fight against breast cancer by donating to my Men Wear Pink fundraiser for the American Cancer Society (ACS) at http://main.acsevents.org/goto/paultaylor Every dollar helps in the battle with breast cancer.Good luck with your ACLS class!

In this episode, we explore why 98% of people in the U.S. aren't getting enough potassium and the health implications of this deficit. Potassium is crucial for nerve function, muscle contractions, fluid balance, blood pressure regulation, and heart rhythm. Despite its importance, many factors, including poor diet, health conditions, and certain medications, contribute to widespread deficiency. We'll discuss symptoms like muscle weakness and high blood pressure, the long-term effects on cardiovascular health, bone density, kidney function, and more. Learn how much potassium you need, top food sources, and tips for increasing your intake to enhance your overall health.

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes.When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively.Two things that may lead us to suspect hypo or hyperkalemia. Medical conditions & medications that can cause potassium imbalance. ECG changes seen in hypo and hyperkalemia. Critical lab values that would indicate a need for treatment.Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerd podcast. Check out the pod resources page at passacls.com.Connect with me:Website: https://passacls.com@Pass-ACLS-Podcast on LinkedInGive Back & Help Others: Your support helps cover the monthly cost of software and podcast & website hosting so that others can benefit from these ACLS tips as well. Donations made via Buy Me a Coffee at https://buymeacoffee.com/paultaylor are appreciated.Make a difference in the fight against breast cancer by donating to my Men Wear Pink fundraiser for the American Cancer Society (ACS) at http://main.acsevents.org/goto/paultaylor Every dollar helps in the battle with breast cancer.Good luck with your ACLS class!

In this new series, Drs. Alice Sheridan and Martina McGrath speak with guest editor Dr. Michael Emmett to discuss his editorial "Cystic Fibrosis and Hypoelectrolytemia With Metabolic Alkalosis" from nephSAP Volume 23, Number 2.

In this new series, Drs. Alice Sheridan and Martina McGrath speak with guest editor Dr. Michael Emmett to discuss his editorial "Cystic Fibrosis and Hypoelectrolytemia With Metabolic Alkalosis" from nephSAP Volume 23, Number 2.

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes. When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia. Medical conditions & medications that can cause potassium imbalance. ECG changes seen in hypo and hyperkalemia.Critical lab values that would indicate a need for treatment.Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerd podcast. 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!

What I Wish I Knew: Potassium-K Lab Value Levels For resources to help you master Potassium and ALL the lab values, we have a FREE Cheatsheet Download at NURSING.com/labvalues.   What do bananas, avocados, and kale all have in common? Potassium! For more resources to help you understand Potassium, Hyperkalemia and Hypokalemia, click here: What role does it play in the body? What's a normal range level for potassium? And what happens when potassium levels are too low or too high? On a shift early in my career, while I was still being oriented to the unit, I held tight to that rule of NEVER pushing IV potassium even when my preceptor was providing instructions that conflicted with that big rule. Here is that story...

What I Wish I Knew: Potassium-K Lab Value Levels For resources to help you master Potassium and ALL the lab values, we have a FREE Cheatsheet Download at NURSING.com/labvalues.   What do bananas, avocados, and kale all have in common? Potassium! For more resources to help you understand Potassium, Hyperkalemia and Hypokalemia, click here: What role does it play in the body? What's a normal range level for potassium? And what happens when potassium levels are too low or too high? On a shift early in my career, while I was still being oriented to the unit, I held tight to that rule of NEVER pushing IV potassium even when my preceptor was providing instructions that conflicted with that big rule. Here is that story...

What I Wish I Knew: Potassium-K Lab Value Levels For resources to help you master Potassium and ALL the lab values, we have a FREE Cheatsheet Download at NURSING.com/labvalues.   What do bananas, avocados, and kale all have in common? Potassium! For more resources to help you understand Potassium, Hyperkalemia and Hypokalemia, click here: What role does it play in the body? What's a normal range level for potassium? And what happens when potassium levels are too low or too high? On a shift early in my career, while I was still being oriented to the unit, I held tight to that rule of NEVER pushing IV potassium even when my preceptor was providing instructions that conflicted with that big rule. Here is that story...

What I Wish I Knew: Potassium-K Lab Value Levels For resources to help you master Potassium and ALL the lab values, we have a FREE Cheatsheet Download at NURSING.com/labvalues.   What do bananas, avocados, and kale all have in common? Potassium! For more resources to help you understand Potassium, Hyperkalemia and Hypokalemia, click here: What role does it play in the body? What's a normal range level for potassium? And what happens when potassium levels are too low or too high? On a shift early in my career, while I was still being oriented to the unit, I held tight to that rule of NEVER pushing IV potassium even when my preceptor was providing instructions that conflicted with that big rule. Here is that story...

What I Wish I Knew: Potassium-K Lab Value Levels For resources to help you master Potassium and ALL the lab values, we have a FREE Cheatsheet Download at NURSING.com/labvalues.   What do bananas, avocados, and kale all have in common? Potassium! For more resources to help you understand Potassium, Hyperkalemia and Hypokalemia, click here: What role does it play in the body? What's a normal range level for potassium? And what happens when potassium levels are too low or too high? On a shift early in my career, while I was still being oriented to the unit, I held tight to that rule of NEVER pushing IV potassium even when my preceptor was providing instructions that conflicted with that big rule. Here is that story...

What I Wish I Knew: Potassium-K Lab Value Levels For resources to help you master Potassium and ALL the lab values, we have a FREE Cheatsheet Download at NURSING.com/labvalues.   What do bananas, avocados, and kale all have in common? Potassium! For more resources to help you understand Potassium, Hyperkalemia and Hypokalemia, click here: What role does it play in the body? What's a normal range level for potassium? And what happens when potassium levels are too low or too high? On a shift early in my career, while I was still being oriented to the unit, I held tight to that rule of NEVER pushing IV potassium even when my preceptor was providing instructions that conflicted with that big rule. Here is that story...

What I Wish I Knew: Potassium-K Lab Value Levels For resources to help you master Potassium and ALL the lab values, we have a FREE Cheatsheet Download at NURSING.com/labvalues.   What do bananas, avocados, and kale all have in common? Potassium! For more resources to help you understand Potassium, Hyperkalemia and Hypokalemia, click here: What role does it play in the body? What's a normal range level for potassium? And what happens when potassium levels are too low or too high? On a shift early in my career, while I was still being oriented to the unit, I held tight to that rule of NEVER pushing IV potassium even when my preceptor was providing instructions that conflicted with that big rule. Here is that story...

HOST: Andy Herber, P.A.-C. GUEST: Mira T. Keddis, M.D. Join our host, Andy J. Herber, P.A.-C., as he explores potassium disorders that are commonly encountered by Primary Care Providers. High and Low potassium if not appropriately managed can lead to lethal complications. This episode provides a discussion about the workup and management of Hyperkalemia and Hypokalemia with Mira T. Keddis, M.D. Mayo Clinic Talks: Lab Medicine Edition | Mayo Clinic School of Continuous Professional Development Connect with the Mayo Clinic's School of Continuous Professional Development online at https://ce.mayo.edu/ or on Twitter @MayoMedEd. 

In deze aflevering bespreken we alles over hypokaliëmie. We behandelen de volgende onderwerpen:Waarom is kalium belangrijk?Wat is hypokaliëmie en wat zijn de symptomen?Is het gevaarlijk?Wanneer moeten we het behandelen, en hoe?Waarom moeten we altijd eerst magnesium geven?Welke richtwaarden moeten we aanhouden?Bronnen:Electrophysiology of Hypokalemia and Hyperkalemia - American Heart Association Deranged Physiology - Hypokalemia Het Acute Boekje - Hypokaliëmie EMCrit - HypokalemiaMechanism of Hypokalemia in Magnesium Deficiency : Journal of the American Society of Nephrology (lww.com)Association between potassium concentrations, variability and supplementation, and in-hospital mortality in ICU patients: a retrospective analysis | Annals of Intensive Care | Full Text (springeropen.com)Association of Intravenous Potassium and Magnesium Administration With Spontaneous Conversion of Atrial Fibrillation and Atrial Flutter in the Emergency Department | Cardiology | JAMA Network Open | JAMA NetworkExamining the "Repletion Reflex": The Association between Serum Potassium and Outcomes in Hospitalized Patients with Heart FailureAssociation of serum potassium concentration with mortality and ventricular arrhythmias in patients with acute myocardial infarction: A systematic review and meta-analysis - PubMed (nih.gov)Association between hyperkalemia at critical care initiation and mortality - PubMed (nih.gov)Bedankt voor het luisteren!Volg @intensiefdepodcast op InstagramVragen? intensiefdepodcast@gmail.com

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes. When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia. Medical conditions & medications that can cause potassium imbalance. ECG changes seen in hypo and hyperkalemia. Critical lab values that would indicate a need for treatment.Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerd podcast. 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!

Show notes at pharmacyjoe.com/episode894. In this episode, I’ll discuss how correction of hypokalemia in a hyponatremic patient makes inadvertent overcorrection of hyponatremia more likely. The post 894: Correction of hypokalemia in a hyponatremic patient makes inadvertent overcorrection of hyponatremia more likely appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode894. In this episode, I’ll discuss how correction of hypokalemia in a hyponatremic patient makes inadvertent overcorrection of hyponatremia more likely. The post 894: Correction of hypokalemia in a hyponatremic patient makes inadvertent overcorrection of hyponatremia more likely appeared first on Pharmacy Joe.

Hypokalemia gets a lot of attention in the literature, but Dr. Pregerson said he has never had a patient with hyperkalemic cardiac arrest. Listen in as he discusses the ECG changes seen with hypokalemia and how to treat hypokalemic arrest if you see it. Read more in the Show Notes.

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes. When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia. Medical conditions & medications that can cause potassium imbalance. ECG changes seen in hypo and hyperkalemia. Critical lab values that would indicate a need for treatment. Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerd podcast. 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!

Contributor: Dylan Luyten MD Educational Pearls: What is a Bradyarrhythmia? Also known as a bradyarrhythmia, it is an irregular heart rate that is also slow (below 60 beats per minute). What can cause it? Complete heart block AKA third-degree AV block; identified on ECG by a wide QRS, and complete dissociation between the atrial and ventricular rhythms with the ventricular being much slower. Treat with a pacemaker. Medication overdose, especially beta blockers. Many other drugs can slow the heart as well including: opioids, clonidine, digitalis, amiodarone, diltiazem, and verapamil to name a few. Electrolyte abnormalities, specifically hyperkalemia. Hypokalemia, hypocalcemia, and hypomagnesemia can also cause bradyarrhythmias. Myocardial infarction. Either by damaging the AV node or the conduction system itself or by triggering a process called Reperfusion Bradycardia. Hypothermia. Bradycardia is generally a sign of severe or advanced hypothermia. References Jurkovicová O, Cagán S. Reperfúzne arytmie [Reperfusion arrhythmias]. Bratisl Lek Listy. 1998 Mar-Apr;99(3-4):162-71. Slovak. PMID: 9919746. Simmons T, Blazar E. Synergistic Bradycardia from Beta Blockers, Hyperkalemia, and Renal Failure. J Emerg Med. 2019 Aug;57(2):e41-e44. doi: 10.1016/j.jemermed.2019.03.039. Epub 2019 May 30. PMID: 31155316. Wung SF. Bradyarrhythmias: Clinical Presentation, Diagnosis, and Management. Crit Care Nurs Clin North Am. 2016 Sep;28(3):297-308. doi: 10.1016/j.cnc.2016.04.003. Epub 2016 Jun 22. PMID: 27484658. Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII  

Show notes at pharmacyjoe.com/episode862. In this episode, I’ll discuss why hypokalemia can result from digoxin immune fab fragment administration. The post 862: Why hypokalemia can result from digoxin immune fab fragment administration appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode862. In this episode, I’ll discuss why hypokalemia can result from digoxin immune fab fragment administration. The post 862: Why hypokalemia can result from digoxin immune fab fragment administration appeared first on Pharmacy Joe.

Welcome to the Instant Trivia podcast episode 947, where we ask the best trivia on the Internet. Round 1. Category: i made it through the reign 1: For 164 years, 1610 to 1774, France was ruled by just 3 kings, all of this name. Louis. 2: Franz Joseph got plenty of new clothes when he ruled Austria for 68 years with this loftier title than king. emperor. 3: Fath Ali Shah ruled this country from 1797 to 1834 and led it in disastrous wars against Russia. Iran. 4: Averaging 23 years per reign, the last 5 Russian czars were named either Nicholas or this. Alexander. 5: Otto, who ruled Greece from 1832 to 1862, was the son of King Ludwig of this German state. Bavaria. Round 2. Category: behold the power of cheese 1: "On top of spaghetti, all covered with cheese, I lost my poor meatball, when" this happened. somebody sneezed. 2: Things concocted in 1915 include Corning's Pyrex and this company's processed cheese. Kraft. 3: Bearing the name of a Belgian province, it's a cheese with a really strong aroma. Limburger. 4: It's wonderful to do this to cheese, reducing it to fragments by rubbing it against an abrasive surface. grating. 5: Salata is the dense processed form of this "recooked" Italian cheese. ricotta. Round 3. Category: familial phrases 1: Here's this figure personified. Father Time. 2: Enacting this 2-word phrase of concession can sometimes stop a tickle attack. saying uncle. 3: The stars of this reality series on TLC marched on the Utah capitol to protest a ban on polygamy. Sister Wives. 4: All of a computer's components and peripherals connect to this; ATX is the main design today. a motherboard. 5: Term for a ready target of criticism, or the female relative who wants to adopt Huck Finn. Aunt Sally. Round 4. Category: "tas"-mania 1: Another word for disaster; in drama, it's a synonym for denouement. catastrophe. 2: Hypokalemia is a deficiency of this mineral. potassium. 3: It's the group of threadlike strings on the top of a stalk of corn. tassel. 4: This Mexican dish whose name means "little meats" is shredded pork. carnitas. 5: This lake is considered the main source of the Mississippi River. Itasca. Round 5. Category: geographical words and phrases 1: A shade of grayish blue is named for this Danish capital. Copenhagen. 2: This nationality precedes onyx, hairless, and jumping bean. Mexican. 3: This nationality precedes uncle, treat, and elm disease. Dutch. 4: This tuber with a city in its name is also called a sunchoke. Jerusalem Artichoke. 5: This high quality black tea is named for a district in West Bengal. Darjeeling. Thanks for listening! Come back tomorrow for more exciting trivia! Special thanks to https://blog.feedspot.com/trivia_podcasts/

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes.When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia.Medical conditions & medications that can cause potassium imbalance.ECG changes seen in hypo and hyperkalemia. Critical lab values that would indicate a need for treatment. Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerd podcast. 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!

The following episode covers the basics of hypokalemia. The episode discusses the three primary causes of hypokalemia, the clinical manifestations, and general resuscitation guidance.    For further reading: https://emcrit.org/ibcc/hypokalemia/  

Specific considerations of hypokalemia in the CVICU/CICU. 

Visit: https://nursing.com/140meds to request your free copy of "140 Must Know Meds" Generic Name Furosemide Trade Name Lasix Indication Edema, hypertension Action Prevents reabsorption of sodium and chloride in the kidneys, increase excretion of water, sodium, chloride, magnesium, potassium Therapeutic Class Diuretics Pharmacologic Class Loop diuretics Nursing Considerations • Use caution with liver disease • May cause hypotension, dry mouth, excessive urination, dehydration, electrolyte abnormalities, metabolic alkalosis • Hypokalemia may lead to increase risk of digoxin toxicity • Monitor renal panel • Use caution with other antihypertensives • Causes arthritic symptoms/do not administer with aminoglycosides due to ototoxicity

Question-based review on differential diagnosis and algorithmic approach to workup & management of hypokalemia followed by a discussion of magnesium abnormalities.

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes. When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia. Medical conditions & medications that can cause potassium imbalance. ECG changes seen in hypo and hyperkalemia. Critical lab values that would indicate a need for treatment. Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerdpodcast. 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!

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 6 L's L-Lethargy L-Leg cramps L-Limp muscles L-Low, shallow respirations L-Lethal cardiac dysrythmias L-Lots of urine (polyuria) Description Hypokalemia is LOW potassium, which starts with L. So the 6 L's can help you recognize the signs and symptoms of LOW potassium or hypokalemia

Visit: https://nursing.com/140meds to request your free copy of "140 Must Know Meds" Generic Name Digoxin Trade Name Lanoxin Indication CHF, AFib, A-flutter Action Positive inotropic effect (increases force of myocardial contraction), prolongs refractory period, ↓ conduction through SA and AV nodes. Essentially digoxin is given to increase cardiac output and slow the rate. Therapeutic Class Antiarrhythmic, inotropics Pharmacologic Class Digitalis glycosides Nursing Considerations • Excreted by kidneys • Assess patient for hypersensitivity • Contraindicated with uncontrolled ventricular arrhythmias • Hypokalemia increase risk for toxicity • Hypercalcemia ↑ risk for toxicity • Use caution with diuretic use as they may cause electrolyte abnormalities that can lead to toxicity • Assess patient for cardiac arrhythmias including bradycardia • Signs of toxicity include vision changes (blurred vision, yellow, green vision disturbances) • Monitor pulse rate for 1 full minute prior to dosing patient (hold for pulse

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes.When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia. Medical conditions & medications that can cause potassium imbalance. ECG changes seen in hypo and hyperkalemia.Critical lab values that would indicate a need for treatment.Emergent, ACLS interventions for hypokalemia and hyperkalemia.Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerd podcast. 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!

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes. When a patient's potassium levels get too low or too high, hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia include the patient's medical history and changes to the T wave on the ECG.Medical conditions & medications that can cause potassium imbalance. ECG changes seen in hypo and hyperkalemia. Critical lab values that would indicate a need for treatment. Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on causes of hypo and hyperkalemia can be found on Ninja Nerd podcast. 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!

Case Discussion 70: Management of mild to moderate Hypokalemia

Dr. Samira Farouk, transplant nephrologist at the Mount Sinai Hospital in New York, continues our nephrology series with a discussion of hypokalemia. She and Dr. Emily Gutowski, RTL host, cover the potential causes of low potassium and important concepts to keep in mind while treating this electrolyte disturbance.

In this episode, we review the management of a patient with hypokalemia, including both inpatient and outpatient supplementation with potassium chloride supplements and what dosage forms are available for potassium repletion. Key Concepts Most diets will provide sufficient potassium to avoid hypokalemia. Hypokalemia usually occurs due to drug therapy (such as diuretics) or GI losses from severe vomiting or diarrhea. In patients with chronically low potassium, supplements are dosed to increase dietary intake of potassium by about 20-40 mEq per day. For acute repletion, 10 mEq of potassium should increase serum potassium by about 0.1 mEq/L. Over-the-counter potassium (as potassium gluconate) contains a very small amount of potassium (2.5 mEq). Potassium chloride powders and liquids (like salt substitutes) taste terrible and are poorly tolerated. Most patients will replete potassium via slow-release tablets (Klor-Con or Klor-Con M) or via potassium chloride IV infusions. Most IV fluids do not contain any potassium at all (or very little potassium). Patients receiving these IV fluids who are NPO will eventually become hypokalemic. Certain maintenance fluids do contain potassium – most patients will receive about 40 mEq of potassium per day with these IV fluids.

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes.When a patient's potassium levels get too low or too high hypokalemia or hyperkalemia results respectively.Two things that may lead us to suspect hypo or hyperkalemia include:the patient's medical history; and changes to the T wave on the ECG.Medical conditions that cause potassium imbalance.ECG changes seen in hypo and hyperkalemia.Critical lab values that would indicate a need for treatment.Emergent, ACLS interventions for hypokalemia and hyperkalemia.Additional information on hypo and hyperkalemia can be found on Ninja Nerd podcast. 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!

Ann Marie, Jack and Dan discuss and delve deeper into hypokalemia and hypophosphatemia schemas based on a case presented by Sharmin.   Schemas Hypokalemia Hypokalemia a practical approach Hypophosphatemia     Download CPSolvers App here RLRCPSOLVERS

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Episode 16: MNT Tips, Kidney Disease, and Fall Carrot Soup This week, Zak gives you tips on how to learn MNT concepts, lacing this together with all the kidney diseases you need to know for the RD Exam. We finish off talking Pureed Carrot Soup with a creamy finish. 1. Which of the following would be an appropriate diet for a patient with an acute kidney injury is not on dialysis? A. High Protein, High Sodium Diet B. Low Sodium, High Potassium diet C. Fluid restricted diet with Protein Controlled D. High Calorie High Phosphorus Diet 2. Which of the following is the most likely cause of chronic kidney disease? A. Diabetes B. Hypotension C. GERD D. Low-Sodium Diet 3. If a client goes on hemodialysis, which conditions should the dietitian consider in the long term? A. Hypokalemia and hyperphosphatemia B. Dyslipidemia and osteodystrophy C. Hyperkalemia and hypophosphatemia D. Hypotension and diabetes DM for your RD Exam tutoring needs! Instagram: @zak_snacks Youtube: Zak Kaesberg MS, RDN

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes. When a patient's potassium levels get too low or too high hypokalemia or hyperkalemia results respectively. Two things that may lead us to suspect hypo or hyperkalemia include the patient's medical history and changes to the T wave on the ECG. Medical conditions that cause potassium imbalance. ECG changes seen in hypo and hyperkalemia. Critical lab values that would indicate a need for treatment. Emergent, ACLS interventions for hypokalemia and hyperkalemia. Additional information on hypo and hyperkalemia can be found on Ninja Nerd podcast. Check out the pod resources page at passacls.com. **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!

Download the cheat: https://bit.ly/50-meds  View the lesson: https://bit.ly/HydrochlorothiazideHydrodiurilNursingConsiderations    Generic Name hydrochlorothiazide Trade Name HydroDiuril Indication Hypertension, CHF, renal dysfunction, cirrhosis, glucocorticoid therapy Action Increases sodium and water excretion and produces arterial vasodilation Therapeutic Class antihypertensives, diuretics Pharmacologic Class thiazide diuretics Nursing Considerations • May cause dizziness, hypokalemia, hyponatremia, hypophosphatemia, hypomagnesemia, dehydration • Hypokalemia can increase risk for digoxin toxicity • Monitor blood pressure and intake and output • Monitor electrolyte levels • Patient should take medication at the same time each day even if feeling better • Instruct patient on how to take blood pressure

Download the cheat: https://bit.ly/50-meds  View the lesson: https://bit.ly/FurosemideLasixNursingConsiderations    Generic Name Furosemide Trade Name Lasix Indication Edema, hypertension Action Prevents reabsorption of sodium and chloride in the kidneys, increase excretion of water, sodium, chloride, magnesium, potassium Therapeutic Class Diuretics Pharmacologic Class Loop diuretics Nursing Considerations • Use caution with liver disease • May cause hypotension, dry mouth, excessive urination, dehydration, electrolyte abnormalities, metabolic alkalosis • Hypokalemia may lead to increase risk of digoxin toxicity • Monitor renal panel • Use caution with other antihypertensives • Causes arthritic symptoms/do not administer with aminoglycosides due to ototoxicity

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat coming to you from Children's Healthcare of Atlanta/Emory University School of Medicine. I'm Rahul Damania from Cleveland Clinic Children's Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let's get into our episode: Here's the case presented by Rahul: A 21-month-old girl was brought to an OSH ED for somnolence and difficulty breathing, which developed after she accidentally ingested an unknown amount of liquid medicine that was used by her grandfather. Per the mother, the patient's grandfather was given the liquid medication for the treatment of his opioid addiction. The patient took some unknown amount from the open bottle that was left on the counter by the grandfather. Immediately after ingestion of the medicine, the patient initially became irritable and had some generalized pruritus. The patient subsequently became sleepy followed by difficulty breathing and her lips turned grey. The patient was rushed to an outside hospital ED for evaluation. OSH ED: The patient arrived unresponsive and blue, she was noted to be sleepy and difficult to arouse on arrival, with pinpoint pupils and hypoxic to 88%. , but After receiving Naloxone, however, she became awake and interactive. Her glucose on presentation was 58 mg/dL and Her initial VBG resulted 7.3/49.6/+2. She continued to have intermittent episodes of somnolence without apnea. Poison control called and recommend starting a naloxone infusion; she was also given dextrose bolus. The patient was admitted to the PICU. To summarize key elements from this case, this patient has: Accidental ingestion of an unknown medication Altered mental status Difficulty breathing—with grey lips suggestive of hypoventilation/hypoxia All of which brings up a concern for a toxidrome which is our topic of discussion for today The typical symptoms seen in our patient of pinpoint pupils, respiratory depression, and a decreased level of consciousness is known as the “opioid overdose triad” Given the history of opioid addiction in the grandfather, the liquid medicine given to him is most likely methadone.In fact, in this case, the mother brought the bottle of medicine, which was subsequently confirmed to be prescription methadone given to prevent opioid withdrawal in the grandfather.   To dive deeper into this episode, let's start with a multiple choice question: Which of the following opioids carries the greatest risk of QTc prolongation? A. Methadone B. Morphine C. Fentanyl D. Dilaudid The correct answer is methadone. Methadone prolongs QT interval due to its interactions with the cardiac potassium channel (KCNH2) and increases the risk for Torsades in a dose-dependent manner. Besides the effect on cardiac repolarization, methadone is also associated with the development of bradycardia mediated via its anticholinesterase properties and through its action as a calcium channel antagonist. Hypokalemia, hypocalcemia, hypomagnesemia, and concomitant use of other drugs belonging to the family of CYP3A4 system inhibitors such as erythromycin can prolong Qtc. Even in absence of these risk factors, methadone alone can prolong QTc.   Thanks for that, I think it is very important to involve your Pediatric Pharmacy team to also help with management as children may be concurrent qt prolonging meds. Rahul, what are some of the pharmacological and clinical features of methadone poisoning? Methadone is a synthetic opioid analgesic made of a racemic mixture of two enantiomers d-methadone and l-methadone. besides its action on mu and kappa receptors, it is also an NMDA receptor antagonist. Due to its long action, methadone is useful as an analgesic and to suppress opioid withdrawal symptoms (hence used for opioid...

Hypokalemia is LOW potassium, which starts with L. So the 6 L's can help you recognize the signs and symptoms of LOW potassium or hypokalemia

Download the cheat: https://bit.ly/50-meds  View the lesson: https://bit.ly/DigoxinLanoxinNursingConsiderations    Generic Name Digoxin Trade Name Lanoxin Indication CHF, AFib, A-flutter Action Positive inotropic effect (increases force of myocardial contraction), prolongs refractory period, ↓ conduction through SA and AV nodes. Essentially digoxin is given to increase cardiac output and slow the rate. Therapeutic Class Antiarrhythmic, inotropics Pharmacologic Class Digitalis glycosides Nursing Considerations • Excreted by kidneys • Assess patient for hypersensitivity • Contraindicated with uncontrolled ventricular arrhythmias • Hypokalemia increase risk for toxicity • Hypercalcemia ↑ risk for toxicity • Use caution with diuretic use as they may cause electrolyte abnormalities that can lead to toxicity • Assess patient for cardiac arrhythmias including bradycardia • Signs of toxicity include vision changes (blurred vision, yellow, green vision disturbances) • Monitor pulse rate for 1 full minute prior to dosing patient (hold for pulse

Along with sodium, calcium, & magnesium; potassium is one of the ions necessary for cardiac contraction. A low potassium (hypokalemia) or high potassium (hyperkalemia) should be considered while reviewing the H & T reversible causes of cardiac arrest. Two things that may aid us in identifying hypo or hyperkalemia include the patient's medical history and changes to the T wave on the ECG. Review of conditions and medications that may result in potassium imbalance. A serum potassium less than 3 or greater than 6 should be treated. Emergency treatment of hypokalemia and hyperkalemia. 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!

Hypokalemia and hyperkalemia is one of the Hs in our H & T reversible causes of cardiac arrest. Potassium is one of the electrolytes involved in the cardiac cycle. A serum potassium less than 3 or greater than 6 is significant and should be treated. The patient's medical history and T waves on the ECG can clue us in to possible potassium imbalances. Review of common causes of hypo & hyperkalemia. ACLS treatment for hypo or hyperkalemia. 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!

@Kidney_Boy returns to school us on metabolic alkalosis and hypokalemia! What do diuretics, hyperaldosteronism, black licorice, and milk-alkali have in common? Our Chief of Nephrology, Dr. Joel Topf, talks through the pathophysiology of metabolic alkalosis, the utility of urine chloride and pH measurements, why normal saline is sometimes better than balanced solutions, when to reach for acetazolamide, and more! Urine for a good time ; ) Claim free CME for this episode at curbsiders.vcuhealth.org! Episodes | Subscribe | Spotify | Swag! | Top Picks | Mailing List | thecurbsiders@gmail.com | Free CME! Credits Written and Produced by: Matthew Watto MD, FACP Show Notes, CME, Infographic and Cover Art by: Matthew Watto MD, FACP Hosts: Matthew Watto MD, FACP; Paul Williams MD, FACP, Beth Garbitelli   Reviewer: Emi Okamoto MD Executive Producer: Beth Garbitelli Showrunner: Matthew Watto MD, FACP Editor: Clair Morgan of nodderly.com Guest: Joel Topf MD Sponsor: ACP Join the American College of Physicians today! U.S. based post-training physicians can take advantage of a limited-time 20% membership discount. Visit acponline.org/ACPdiscount and use the code ACP20. Membership discount is available only through December 31, 2021.   Sponsor: Grammarly Take the stress out of getting the words right with Grammarly. Our listeners get 20% off Grammarly Premium at grammarly.com/CURB CME Partner: VCU Health CE The Curbsiders are partnering with VCU Health Continuing Education to offer FREE continuing education credits for physicians and other healthcare professionals. Visit curbsiders.vcuhealth.org and search for this episode to claim credit.  Show Segments Intro, disclaimer, guest bio Guest one-liner, Picks of the Week* Case from Kashlak; Definitions Case of Al Kaline - metabolic alkalosis from vomiting Pathophysiology of metabolic alkalosis Case of Mike Arbonate - hypokalemic, metabolic alkalosis from aggressive IV diuresis and therapies to mitigate Case of Fracture Franny - milk-alkali syndrome Case of Hyper Al - metabolic alkalosis from excess mineralocorticoid receptor activation Outro

The post The Management of Hypokalemia in Cardiac Arrest by Jimmy Pruitt appeared first on The Pharm So Hard Podcast.

Show notes at pharmacyjoe.com/episode632. In this episode, I'll discuss how correction of hypokalemia in a hyponatremic patient makes inadvertent overcorrection of hyponatremia more likely. The post 632: Correction of hypokalemia in a hyponatremic patient makes inadvertent overcorrection of hyponatremia more likely appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode632. In this episode, I ll discuss how correction of hypokalemia in a hyponatremic patient makes inadvertent overcorrection of hyponatremia more likely. The post 632: Correction of hypokalemia in a hyponatremic patient makes inadvertent overcorrection of hyponatremia more likely appeared first on Pharmacy Joe.

There are two most commonly used versions of potassium. Potassium chloride (supplementation) or potassium citrate (alkalinizing agent). Potassium chloride, also known as K-Tab or Klor-Con, is an electrolyte supplementation used in treating and preventing Hypokalemia (low potassium). Potassium is an essential cation that is needed for the conduction of nerve impulses in the heart, brain, and muscle. Unlike most drugs, potassium is not measured in “mg'' and is measured in “mEq” or milliequivalents. Potassium chloride comes in multiple dosage forms such as an ER capsule and tablet, a powdered packet, oral solution, and also as an intravenous solution. When the IV solution is used a major concern is for extravasation, which is when plasma escapes from the extracellular space and forms blisters on the patient. If this occurs the drug hyaluronidase is injected as 5 separate 0.2-0.3 mL injections along with applying a cold compress and elevating the extremity. Another important note for the IV solution is that it is never administered as IV push and the solution must be diluted prior to administration. Go to DrugCardsDaily.com for my episode show notes which will contain a drug summary, quiz, and a link to FREE drug card sheets. SUBSCRIBE on Spotify or Apple Podcasts or search for us on your favorite place to listen to podcasts. I will go over the Top 100-200 Drugs as well as throwing in some recently released drugs that peak my interest. Also, if you'd like to say hello, suggest a drug, or leave any constructive feedback on the show I'd really appreciate it! Leave a voice message at anchor.fm/drugcardsdaily or message us through twitter @drugcardsdaily --- Send in a voice message: https://anchor.fm/drugcardsdaily/message

On this episode, I discuss furosemide pharmacology and its ability to promote fluid loss. I discuss conversion to other diuretics and between IV and oral furosemide. Drug interactions are possible with furosemide and the most common interaction is an increased risk of renal impairment with drugs like NSAIDs. Hypokalemia can be dramatic with furosemide and potassium supplementation is often necessary.

Electrolytes are among the drugs we use in the hospital setting. And like any drug, we're better when we truly understand what we are using them to treat. In this episode, we tackle one of the most common electrolyte abnormalities in hospitalized patients....hypokalemia, and we discuss why it makes no sense to say that we treated our patients hypokalemia with 40 mEq of potassium. Understanding why requires understanding how our body shifts around and stores potassium. Join me in this podcast as we figure it out and learn why it makes no sense to say, "I repleted my hypokalemic patient with 40 mEq of potassium."

On this episode, we discuss HYPOKALEMIA, as in low potassium. This is the first of our ELECTROLYTE series! It may seem like a simple topic, but we talk about this electrolyte's role in the body, normal ranges, symptoms, causes, and how to treat this issue. This includes some practical tips to use inside of the hospital and we cover some important nursing considerations.  I would love to answer ANY questions you have about this (or any other) topic! Message me @ashley_nursingcoop or shoot me an email at thenursingcoop@gmail.com with any questions, feedback, or comments. Happy Nursing!

Show notes at pharmacyjoe.com/episode582. In this episode, I’ll discuss why hypokalemia can result from digoxin immune fab fragment administration. The post 582: Why hypokalemia can result from digoxin immune fab fragment administration appeared first on Pharmacy Joe.

This session talks about the basics of the different electrolyte imbalance for POTASSIUM i.e. Hypokalemia & Hyperkalemia with its pathophysiology, investigation to perform, treatment offered in Modern Medicine. Do Listen podcast, will help to increase the overall knowledge and better understanding of disease condition. I am here to spread a bit of knowledge that I have gained regards to MEDICINE. Do share my podcasts with your friends and colleagues, and join in to spread this knowledge and learn. Thank you for listening.

This episode and I talk about my recent experience in the ER and a new word I learned. I apologize for background noise. I was recording while driving. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/kevin-michael31/message

This episode covers hypokalemia!

This episode covers hypokalemia!

Episode 19: Bartter and Gitelman  The sun rises over the San Joaquin Valley, California, today is July 10, 2020. In case you did not notice, we did not have an episode last week. We were very busy in our residency. We started a new rotation and a new academic year. We welcomed a new group of PGY1s, along with 3rd-year medical students, and Sub-Is. We also said good bye to our dear graduates: Greg Fernandez, Ronald Gavilan, Yunior Martinez, and Steven Saito. “Spread your wings, it’s time to fly. Make the leap. Own the sky.”(1) Good luck in your careers! Those activities kept us busy, and, as if that wasn’t enough, we saw an increase in incidence of COVID-19 across the nation. In Clinica Sierra Vista, we went from 270 positive cases in May to 700 positive cases in June, we also increased the total tests performed from 1200 in May to 2800 in June. Our positivity rate increased from 21% to 25%. In the county of Kern we have had 5,500 cases and 82 deaths. In California, the total of cases is 260,000 with total deaths of 6,500(2), which may have changed by the time you listen to this episode (numbers were rounded up for easy listening).Also, on a positive note, last weekend we celebrated Independence Day. We hope you had a Happy 4th of July! Especially during these tumultuous times, may America continue to be “the land of the free and the home of the brave.”Welcome to Rio Bravo qWeek, the podcast of the Rio Bravo Family Medicine Residency Program, recorded weekly from Bakersfield, California, the land where growing is happening everywhere.The Rio Bravo Family Medicine Residency Program trains residents and students to prevent illnesses and bring health and hope to our community. Our mission: To Seek, Teach and Serve. Sponsored by Clinica Sierra Vista, Providing compassionate and affordable care to patients throughout Kern and Fresno counties since 1971.“All our dreams can come true, if we have the courage to pursue them.” Walt DisneyWhen you want to reach a goal, dreaming is not enough. At some point, you have to start working to make that dream come true. You may need a little dose of faith, and a big dose of action. What dreams do you have? What kind of doctor do you want to become? Your training in residency is the time to prepare to live that dream. Today we have a resident who is working to reach his goals. Dr Sin is a diligent, trustworthy resident and will participate today for the first time in this podcast. QUESTION NUMBER 1: Who are you?My name is Hasaney and I am a second-year resident at Rio Bravo Family Medicine residency program. I was born and raised in Long Beach, California, to parents who emigrated from Cambodia. I went to Long Beach Polytechnic High School, and continued my studies at UC Irvine majoring in Biological Sciences. I worked in Quality Assurance for a healthcare manufacturing company for a few years, before deciding to pursue a career in Medicine. I enrolled at Ross University School of Medicine in Dominica where I received my medical degree.I’m a pretty simple guy. I love spending time with my girlfriend, my family, and my friends. I love to go camping, especially in Mammoth, California. I love watching and rooting for the Dodgers. QUESTION NUMBER 2: What did you learn this week? I had Nephrology clinic for the first time this past Wednesday and Dr. Moreno gave some little teaching points about different syndromes we may see as family physicians, a couple of them being Bartter Syndrome and Gitelman Syndrome.Bartter SyndromeBartter syndrome is an autosomal recessive disorder associated with metabolic abnormalities: hypokalemia, metabolic alkalosis, hyperreninemia and hyperplasia of the juxtaglomerular apparatus, and hyperaldosteronism; There may also be associated hypomagnesemia. It is a fairly rare disease occurring 1 in 1,000,000, however the similar but milder Gitelman syndrome is more common with a prevalence rate of 1 to 10 in 40,000.In short, Hypokalemia, metabolic alkalosis, and hyperaldosteronism. PathophysiologyThe primary defect in both syndromes is an impairment of the sodium chloride reabsorption in the loop of Henle or distal tubule. The impaired sodium chloride reabsorption leads to volume depletion and activation of the renin-angiotensin-aldosterone system. This increased distal flow of sodium enhances potassium and hydrogen secretion at the secretory sites in the connecting tubules and collecting tubules which leads to hypokalemiaand metabolic alkalosis. Patients generally have a lower blood pressure than the general population in Bartter syndrome but normal blood pressure in Gitelman syndrome. Bartter syndrome mimics chronic ingestion of a loop diuretic, while Gitelman syndrome mimics chronic ingestion of a thiazide diuretic.Presentation and TypesClinical manifestations of Bartter syndrome, besides the metabolic abnormalities we have mentioned, are growth and mental retardation, polyuria and polydipsia. There are four types of Bartter syndrome. Types 1 and 2 are usually severe disorders that cause polyhydramnios during pregnancy and prematurity. They develop hypokalemia, metabolic alkalosis, polyuria and hypocalciuria. Nephrocalcinosis is common and probably contributes to development of kidney dysfunction, sometimes end stage renal disease. Nephrocalcinosis is the deposition of calcium salts in the renal parenchyma. Nephrocalcinosis is related to, but not the same as, kidney stones (nephrolithiasis).Bartter syndrome Type 3 is the classic form, less severe, and presents later in life with the metabolic abnormalities. Late manifestations of Bartter syndrome include proteinuria and a decline in GFR. Bartter syndrome Type 4 causes severe disease, with antenatal presentation and congenital hearing loss.  Gitelman syndromeClinical manifestations of Gitelman are similar to Bartter, except for having normal blood pressure. Patients may develop cramps of arms and legs due to the metabolic abnormalities, as well as fatigue. Hypertension may develop later in life.Both syndromes are usually a diagnosis of exclusion. Patients will present with unexplained hypokalemia, metabolic alkalosis and normal to low blood pressure. Surreptitious vomiting and diuretic use must be ruled out as these could present in a similar way. DiagnosisSurreptitious vomiting is ruled out by measuring urine chloride excretion, with Bartter and Gitelman syndrome showing a urine chloride concentration greater than 25mEq/L, whereas vomiting would show a urine chloride concentration that is less than 25 mEq/L.Suspicion of diuretic use would be ruled out with a urine diuretic screening. Plasma renin and aldosterone levels will be elevated; however, these are not required for diagnosis.TreatmentTreatment requires ad lib NaCl intake with supplements of KCl and if needed magnesium salts. Most patients will require a drug that blocks distal tubule Na-K exchange such as spironolactone. QUESTION NUMBER 3: Why is this knowledge important?As family physicians, we see the full spectrum of Medicine. If we see low blood pressure in a pediatric patient, with the metabolic abnormalities akin to these two syndromes an urgent nephrology referral should be placed. QUESTION NUMBER 4: How did you get that knowledge?Initially, some of it was taught to me by Dr. Moreno. He did not have time to go through most of the details of each syndrome in clinic, so I decided to read a little more about it on Up to Date. Some of the details on Up to Date are very thorough, so I liked to cross reference it with Pocket Pediatrics. QUESTION NUMBER 5: Where did you get that knowledge?The majority of the information were points that I thought were most important from the Up to Date article “Bartter and Gitelman syndromes”.   Speaking Medical: Nephronia by Manpreet Kaur, MS3Nephronia. It may sound like the sister planet of Neptune, but what exactly is it and when would you diagnose a patient with it? Well, on the spectrum of upper UTIs, nephronia would fall at the midpoint between acute pyelonephritis and an intrarenal abscess. It forms when a patient has an acute bacterial infection that results in a renal mass without liquefaction. We usually see this disorder in the pediatric population but there are case reports of this presentation in adults as well. While it sounds rare, it may just be an underdiagnosed disorder. However, with advancements in noninvasive imaging, this diagnosis is being made at an increasing frequency. Acute lobar nephronia (ALN) is similar to acute pyelonephritis (APN). ALN is similar to APN. A few differences are that acute lobar nephronia (ALN) is associated with a longer clinical course, longer fever duration even with treatment, and higher inflammatory markers like CRP and WBC count. A CT is the most sensitive and accurate modality of making the diagnosis but risks of exposure to radiation and possible sedation have to be weighed in small children. Some studies indicate that about 25% of children with ALN can go on to develop renal abscesses and have a higher incidence of renal scarring. Once nephronia has been diagnosed, these patients will require a minimum of 2 weeks of IV antibiotics, followed with 1 week of oral antibiotics. They will show slow improvement with fevers sometimes persisting until the end of the 1st week of treatment.Now you now the medical word of the week: Nephronia. Espanish Por Favor: OrinaOrinaisthat yellowish-colored liquid that comes out of the urethra with a characteristic smell, which in normal circumstances is sterile. Yes, you guessed it, orina is urine in Spanish. Orina can be easily turned into a verb:Orinar. Just like in English, there are several terms to refer to urine (pee, piss, pee-pee), orina can also be called meados(vulgar), orín, pis, pichi, and my favorite: pipí (pronounce pee-pee), normally used with pediatric patients. Now you know the Spanish word of this week: Orina. For your Sanity: A wet noseby Steven SaitoWhat do a puppy and a near-sighted OB doctor have in common? A wet nose.  ConclusionNow we conclude our episode number 19, “Bartter and Gitelman”. Dr Sin briefly shared the highlights of these rare syndromes. Hypokalemia and hypotension may have a long list of differential diagnoses, but keep Bartter and Gitelman on your list. Ms Kaur explained that nephronia is not a planet, but an intermediate state between pyelonephritis and a renal abscess; and we could not leave the word urine out of this renal episode, so we learned the Spanish word orina.This is the end of Rio Bravo qWeek. We say good bye from Bakersfield, a special place in the beautiful Central Valley of California, United States, a land where growing is happening everywhere.If you have any feedback about this podcast, contact us by email RBresidency@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. This podcast was created with educational purposes only. Visit your primary care physician for additional medical advice. Our podcast team for this episode is Hector Arreaza, Hasaney Sin, Manpreet Kaur, and Steven Saito, Audio edition: Suraj Amrutia. See you soon! _____________________References:Ms Moem, http://msmoem.com/2014/poetry-2/spread-your-wings/California Coronovirus Update, https://update.covid19.ca.gov/Emmett M, Ellison DH. Barrter and Gitelman syndromes. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on July 5, 2020)

The hypokalemia chapter is here.The COVID resources are here.

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Talk to a Dr. Berg Keto Consultant today and get the help you need on your journey (free consultation). Call 1-540-299-1557 with your questions about Keto, Intermittent Fasting or the use of Dr. Berg products. Consultants are available Monday through Friday from 8:30 am to 9 pm EST. Saturday & Sunday 9 am to 5 pm EST. USA Only. Take Dr. Berg's Free Keto Mini-Course! Today, we're going to talk about carbs and energy. Many people think they need carbs for energy, but they don't. When you eat carbs, you lose potassium. Low potassium can cause symptoms such as: • Fatigue • Weakness • Paralysis • Leg cramps • Abnormal heart rhythm • High blood pressure • Tremors There is something called insulin-induced hypokalemia. Hypokalemia is low potassium. When you stimulate insulin because your carbs are high, you block an enzyme, which is a pump. You have millions of these in all of your cells. This pump basically keeps the potassium inside of the cell and the sodium outside of the cell to form an electrical gradient so it can act as a battery. 30% of all of the energy in the body is allocated to this pump. If you inhibit this pump, more potassium stays outside of the cell, and you start losing potassium. There are more causes of a potassium deficiency such as: • A spike in insulin • Not consuming enough potassium foods • Loss of fluid • Steroids • Alkalosis • Diuretics • A decrease in magnesium Dr. Eric Berg DC Bio: Dr. Berg, 51 years of age is a chiropractor who specializes in weight loss through nutritional & natural methods. His private practice is located in Alexandria, Virginia. His clients include senior officials in the U.S. government & the Justice Department, ambassadors, medical doctors, high-level executives of prominent corporations, scientists, engineers, professors, and other clients from all walks of life. He is the author of The 7 Principles of Fat Burning. FACEBOOK: fb.me/DrEricBerg?utm_source=Podcast&utm_medium=Anchor TWITTER: http://twitter.com/DrBergDC?utm_source=Podcast&utm_medium=Post&utm_campaign=Daily%20Post YOUTUBE: http://www.youtube.com/user/drericberg123?utm_source=Podcast&utm_medium=Anchor DR. BERG'S SHOP: https://shop.drberg.com/?utm_source=Podcast&utm_medium=Anchor MESSENGER: https://www.messenger.com/t/drericberg?utm_source=Podcast&utm_medium=Anchor DR. BERG'S VIDEO BLOG: https://www.drberg.com/blog?utm_source=Podcast&utm_medium=Anchor

Patricia Westmoreland, MD, returns to the Psychcast to conduct a Masterclass on treating bulimia. Dr. Westmoreland, an attending psychiatrist at the Eating Recovery Center in Denver, previously discussed eating disorders. She is an adjunct assistant professor in the department of psychiatry at the University of Colorado at Denver, Aurora, and has a private forensic psychiatry practice in Denver. Takeaway points Anorexia nervosa and bulimia nervosa can have life-threatening medical complications. All medical complications can resolve with consistent nutrition and full weight restoration. Eating disorders must be treated and associated behaviors stopped to prevent complications from returning. Anorexia-related medical complications usually are attributable to weight loss and malnutrition. Bulimia-related medical complications can occur at any weight, and are related to the mode and frequency of purging. Complications include metabolic abnormalities, such as electrolyte and acid-base disturbances, volume depletion, and damage to the colon. Patients with bulimia have a lower mortality rate than do those with anorexia. However, the mortality of patients with bulimia is two times higher than that of age-matched healthy controls because of acid-base disturbances and severe electrolyte abnormalities. The weight of the patients with bulimia does not matter. Acid-based disturbances and severe electrolyte abnormalities can kill patients at any time without warning and at any weight. Summary About 90% of purging behaviors consists of self-induced vomiting and/or laxative abuse. Self-induced vomiting can cause local complications such as gastric reflux, which can lead to dysphagia and dyspepsia; hematemesis from Mallory-Weiss tears in the esophagus; nosebleeds and subconjunctival hemorrhages; and parotid gland enlargement, known as sialadenosis, which is a chronic, noninflammatory cause of swelling of the major salivary glands. Systemic complications of self-induced vomiting include metabolic derangements, such as hypokalemia, metabolic alkalosis, and volume depletion, which can lead to pseudo-Bartter syndrome from chronic aldosterone secretion as the body attempts to maintain blood pressure; the syndrome is characterized by hyperaldosteronism, metabolic alkalosis, hypokalemia, and normal blood pressure. Treatment of local complications: Gastric reflux can be treated with proton pump inhibitors, and the patient should be screened for Barrett’s esophagus with esophagogastroduodenoscopy. Dental complications such as erosion of the enamel should be addressed with fluoride-based mouthwashes and toothpastes, and gentle toothbrushing. Parotid gland enlargement is treated by sucking on sour candies, applying hot packs, and using anti-inflammatory medications. Treatment of systemic complications: Hypokalemia, which is diagnosed on a basic metabolic panel, needs immediate repletion orally or intravenously. Depending on the severity of the hypokalemia, the patient may need cardiac monitoring in the hospital or ICU to prevent mortality from a lethal arrhythmia. In pseudo-Bartter syndrome, the elevated aldosterone does not normalize until a few weeks after purging stops, so individuals can develop edema and the other electrolyte abnormalities. Treatment is spironolactone, 25-200 mg/day. Complications from laxative abuse occur primarily from stimulant laxatives, which stimulate the myenteric plexus, the nerves of the intestines, and increase intestinal secretions and motility. Cathartic colon syndrome occurs from continued use of stimulant laxatives, which damage the nerves of the colon by rendering it incapable of peristalsis without continued use of laxatives. Individuals who abuse laxatives more than three times per week for at least 1 year are at risk of cathartic colon syndrome and need to stop laxatives immediately. References Westmoreland P et al. Medical complications of anorexia nervosa and bulimia. Am J Med. 2016;129(1):30-7. Mehler PS, Walsh K. Electrolyte and acid-base abnormalities associated with purging behaviors. Int J Eat Disord. 2016 Mar;49(3):311-8. Gibson D et al. Medical complications of anorexia nervosa and bulimia nervosa. Psychiatr Clin North Am. 2019 Jun;42:263-74. Sato Y, Fukado S. Gastrointestinal symptoms and disorders in patients with eating disorders. Clin J Gastroenterol. 2015 Oct;8(5):255-63. *  *  * For more MDedge Podcasts, go to mdedge.com/podcasts Email the show: podcasts@mdedge.com

A Curbsiders classic with a fresh intro by Hannah Abrams @hannahRabrams (soon to be MD)! Master the management of hyperkalemia with tools, tips and tactics from @kidney_boy, Joel Topf MD, Chief of Nephrology @KashlakHospital. We cover: common causes of hyperkalemia; the U-shaped curve of potassium levels and mortality; albuterol nebs; how to safely use insulin; potassium binding resins and colonic necrosis; Does it make sense to give loop diuretics and fluids?; Should we be using fludrocortisone?; Plus, answers to all your questions about a high potassium diet and oral potassium supplements! Join us for Dr Topf’s masterful insights on hyperkalemia and potassium homeostasis. Get deeper into potassium physiology with a FREE pdf copy of Joel’s book The Fluid Electrolyte and Acid Base Companion here. Show Notes | Subscribe | Spotify | Schwag! | Top Picks | Mailing List | thecurbsiders@gmail.com Sponsor ACP's Internal Medicine Meeting 2020 April 23-25th in Los Angeles, CA at the LA Convention Center. Early bird rates are available through January 31, 2020. Don’t forget to use the code: IMCURB20 Credits Written, edited and produced by: Matthew Watto MD, FACP Intro: Hannah R Abrams Hosts: Matthew Watto MD, FACP; Paul Williams MD, FACP; Stuart Brigham MD Infographic and Cover Art: Matthew Watto MD, FACP Guest: Joel Topf MD Time Stamps 00:00 Sponsor -ACP’s IM Meeting 2020 in LA 00:28 Disclaimer, intro and guest bio 03:00 Guest one-liner Picks of the week* —Peloton indoor bike; The Nice Guys (film) by Shane Black; Forgotten Anne (PS4 videogame), “your local library” 09:00 Sponsor -ACP’s IM Meeting 2020 in LA 09:55 Clinical case of hyperkalemia; discussion of pseudohyperkalemia 17:00 Hyperkalemia and the EKG 20:31 Threshold for treatment of hyperkalemia 24:20 Use of telemetry and the U-shaped curve for potassium and mortality 27:11 Choice of therapy for acute hyperkalemia 30:13 Albuterol for hyperkalemia 31:24 First rule out urinary obstruction and hyperglycemia; Use of IV insulin and dextrose and frequency of monitoring 36:44 Loop diuretics plus fluid; Distal sodium delivery and potassium handling in the nephron 40:10 Fludrocortisone for hyperkalemia 42:05 Calcium for elevated potassium 45:43 SPS, potassium binding resin 49:43 Risks of SPS (sodium polystyrene sulfonate) and colonic necrosis 55:28 Sodium bicarbonate for acute and chronic hyperkalemia 58:00 Back to the case; TMP-SMX, ace inhibitors (or ARBs) and hyperkalemia 60:05 Threshold for admission; Diet and potassium 62:52 Treatment of chronic hyperkalemia and a bit more on high potassium foods 65:45 Patiromer and sodium zirconium 68:51 Loop diuretics and empiric potassium supplementation 71:12 Can diet alone be used to treat HYPOkalemia? 72:26 Take home points 74:40 NephMadness is coming! March 2019 76:53 Outro 78:00 Stuart’s shares a few puns *The Curbsiders participates in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising commissions by linking to Amazon. Simply put, if you click on my Amazon.com links and buy something we earn a (very) small commission, yet you don’t pay any extra. Disclosures Dr Topf’s blog lists the following disclosures “I have an ownership stake in a few Davita run dialysis clinics and a vascular access center. Takeda Oncology made a donation to MM4MM the program that is taking me to Mount Everest in 2018”. The Curbsiders were sponsored by ACP’s Internal Medicine Meeting 2019 for this episode. Citation Topf J, Williams PN, Brigham SK, Watto MF. “#137 Hyperkalemia Master Class with Joel Topf MD.” The Curbsiders Internal Medicine Podcast https://thecurbsiders.com/episode-list. Original air date: January 28, 2019. 

In this episode we cover that low serum potassium, aka Hypokalemia. From the minor repletion to the immediate resuscitation of a patient with VF arrest secondary to severe hypokalemia, we have you covered. So read the post, then come take a listen to review all things hypo K!

How Metabolic Alkalosis results in Hypokalemia | Principal Cells | Basolateral Na+- K+ ATpase | Luminal K+ channel. H+ move from principal cells into blood and K+ move from blood into principal cells and from principal cells into the urinary lumen. Eventual excretion! --- Support this podcast: https://anchor.fm/kamesa-anota/support

Notes on Potassium imbalances: Hyper and Hypokalemia. We go over causes, a tad of patho and nursing interventions

In this episode, Emily Gutowski interviews Dr. Ankit Patel about hypokalemia. They discuss a patient case, as well as the framework for thinking about the potential etiologies of low potassium. www.runthelistpodcast.com/nephrology/#hypokalemia Click here for this episode's handout: http://bit.ly/hypokalemia_pdf

A quick look at serum potassium levels, whats normal and abnormal.

Belajar gelombang T dalam EKG. Gelombang T adalah depleksi (+) atau tinggi gelombang yang terdiri dari Lead (L1,L2, L3, AvR, AvL, dan AvF adalah < 5 kotak kecil dan kemudian Lead V1, V2, V3, V4, V5, V6 adalah < 10 kotak kecil. Kemudian apabila gelombang T < angka normal dinamakan Hyperkalemia, kemudian bila gelombang T tidak terbentuk dinamakan Hypokalemia dan bila gelombang T depleksi (-) dinamakan Iskemik Miokard.

Arsalan, Sharmin, Rabih and Reza share an approach to hypokalemia.

Harrison's PodClass provides engaging, high-yield discussions of key topics commonly found on rotational and board exams in internal and family medicine.

Master the management of hyperkalemia with tools, tips and tactics from @kidney_boy, Joel Topf MD, Chief of Nephrology @KashlakHospital. We cover: common causes of hyperkalemia; the U-shaped curve of potassium levels and mortality; albuterol nebs; how to safely use insulin; potassium binding resins and colonic necrosis; Does it make sense to give loop diuretics and fluids?; Should we be using fludrocortisone?; Plus, answers to all your questions about a high potassium diet and oral potassium supplements! Join us for Dr Topf’s masterful insights on hyperkalemia and potassium homeostasis. Full show notes available at http://thecurbsiders.com/podcast. Join our mailing list and receive a PDF copy of our show notes every Monday. Rate us on iTunes, recommend a guest or topic and give feedback at thecurbsiders@gmail.com. Sponsor Join us at ACP's Internal Medicine Meeting 2019 April 11-13th in Philadelphia, PA . We'll see you there! Credits Written and produced by: Matthew Watto, MD Hosts: Matthew Watto MD, Paul Williams MD, Stuart Brigham MD Infographic: Matthew Watto MD Edited by: Matthew Watto MD Guest: Dr Joel Topf MD   Time Stamps 00:00 Ad disclaimer, intro and guest bio 05:11 Guest one-liner and picks of the week —Peloton indoor cycle, “your local library”, The Nice Guys (film) by Shane Black, and Forgotten Hand (PS4 game) 11:17 ACP Internal Medicine Meeting 2019 details 12:55 Clinical case of hyperkalemia; discussion of pseudohyperkalemia 19:55 Hyperkalemia and the EKG 23:38 Threshold for treatment of hyperkalemia 27:20 Use of telemetry and the U-shaped curve for potassium and mortality 30:11 Choice of therapy for acute hyperkalemia 33:13 Albuterol for hyperkalemia 34:24 First rule out urinary obstruction and hyperglycemia; Use of IV insulin and dextrose and frequency of monitoring 39:44 Loop diuretics plus fluid; Distal sodium delivery and potassium handling in the nephron 43:10 Fludrocortisone for hyperkalemia 45:05 Calcium for elevated potassium 48:43 SPS, potassium binding resin 52:43 Risks of SPS (sodium polystyrene sulfonate) and colonic necrosis 58:28 Sodium bicarbonate for acute and chronic hyperkalemia 61:00 Back to the case; TMP-SMX, ace inhibitors (or ARBs) and hyperkalemia 63:05 Threshold for admission; Diet and potassium 65:52 Treatment of chronic hyperkalemia and a bit more on high potassium foods 68:45 Patiromer and sodium zirconium 71:51 Loop diuretics and empiric potassium supplementation 74:12 Can diet alone be used to treat HYPOkalemia? 75:26 Take home points 77:40 NephMadness is coming! March 2019 79:53 Outro 81:00 More Kidney Boy!

I tried to create even if this medschool life is out of my league. I read from: www.healthline.com Hypokalemia is a disease that related to the current topic I learn in 2nd year course - physiology on ionic equilibria and resting membrane potential. So, if it happens that you are in junior year now, do pay attention on physiology class because all that you learn now will soon be useful in the future venture! Have a good Friday and thank you for tuning in!

Thiazide diuretics are well-known to help with edema and hypertension. Thiazides need to monitored for electrolyte imbalances. Hypokalemia is a real and significant possibility. Thiazide diuretics can also raise uric acid which can impact our patients with gout. Pay attention to use in this patient population. I also cover drug interactions and the mechanism of action of thiazide diuretics on this episode. Enjoy the show!

Author: Dylan Luyten, MD Educational Pearls:   Most important questions to answer with low potassium are 1. What are their symptoms? 2. Can they take potassium by mouth? Oral repletion is faster, cheaper, and more effective than IV repletion. Give IV potassium when patients have K < 2.5 mmol/L or present with arrhythmias and/or characteristic EKG changes (flattened T waves). Most patients who are hypokalemic are hypomagnesemic and require magnesium supplementation.  Checking a level is unnecessary.   References Ashurst J, Sergent SR, Wagner BJ, Kim J. Evidence-based management of potassium disorders in the emergency department. Emerg Med Pract. 2016 Nov 22;18(Suppl Points & Pearls):S1-S2   Whang R, Flink EB, Dyckner T, et al. Magnesium depletion as a cause of refractory potassium repletion. Arch Intern Med 1985; 145:1686.

Vicky Vella is an emergency physician practicing in the United Kingdom with a special interest and expertise in eating disorders. In December of last year, Vicky had a guest post on the St Emlyn’s blog about the MARSIPAN Guidelines. Never heard of them? Neither had pretty much anybody. MARSIPAN is an acronym for Management of Really Sick Patients with Anorexia Nervosa. Anorexia is often viewed as a chronic condition that doesn't really warrant emergency care, but that's not the case. Mortality with anorexia nervosa is high (on the order of 10-20%) and patients can present, as MARSIPAN suggests, really sick.   Consider an eating disorder/anorexia in patients presenting with Self Harm. Up to 70% of patients with anorexia will self harm Diabetic Ketoacidosis.  In the UK around half of 15-25 year olds with type 1 diabetes will withhold insulin to try and lose weight. Not all of them will have an eating disorder, but many will Vasovagal syncope. We often ask if a patient had breakfast or enough to drink today, but there may be an underlying eating disorder   What question(s) to ask Vicky starts with, "What's your relationship with food?" "Do you eat regular meals?" The patient may not disclose that there's a problem. Information may come from a family member   Who has anorexia nervosa Highest risk is 13-17 yo age group, both male and female Can actually affect all ages, races, genders   What's the difference between anorexia nervosa and someone who just doesn't eat much? Anorexia is a mental illness. Sometjing the person doesn't have much control over Less of a desire to be thin than a fear of being obese Guilt associated with eating May restrict intake, exercise to burn off consumed calories Often mood swings, social isolation, can become aggressive toward family DSM 5 Criteria Restriction of energy intake relative to requirements leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal or, for children and adolescents, less than that minimally expected. Intense fear of gaining weight or becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight. Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.   Red Flags in the Anorexia Workup (from the MARSIPAN Guidelines) BMI low risk 15–17.5 medium risk 13–15 high risk

"I find it very gratifying to treat because you can see the effects of your treatment right in front of your eyes. And your patients can go from very sick to well within a matter of hours." - Marc Probst, MD Who is Marc Probst, MD? Courtesy of Marc Probst, MD Marc Probst, MD, MS is an Academic Emergency Physician at The Mount Sinai Hospital in New York City. Dr. Probst is funded by a career development grant from the National Institutes of Health (NIH). His interests include syncope, shared decision-making, and Halloween. Twitter @probstMD   Diabetic Ketoacidosis (DKA) Biochemical Findings Hyperglycemia Ketosis (High anion gap) Metabolic Acidosis Parameters to treat DKA Blood glucose >250mg/dL Elevated anion gap w/albumin adjustment >10 Serum bicarbonate

Dr. Wang:            Welcome to the monthly podcast On The Beat for Circulation, Arrhythmia and Electrophysiology. I'm Dr. Paul Wang, 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.                                 This month's issue of Circulation: Arrhythmia and Electrophysiology has a number of fascinating and important articles. Let's start with the first article by Philip Halbfass and Associates, which describes the use of esophageal endoscopy in patients undergoing atrial fibrillation ablation. Of 1,802 patients undergoing afib ablation, 832 underwent post-procedural esophageal endoscopy. All patients were ablated using a single tip re-circular ablation catheter. Category one lesions described as erythema erosion were seen in 98 out of these 295 patients, while in 52 out of the 295 patients, ulceration was seen. In three of the 832 patients, esophageal perforation occurred, and in two of the 832 patients, atrial-esophageal fistula occurred.                                 Esophageal perforation only occurred in patients with category two lesions with an absolute risk of 9.6%. The authors concluded that post-ablation esophageal endoscopy is able to identify patients with high-risk lesions. One out of 10 patients with post-ablation esophageal ulcers progressed to perforation, while no patients without esophageal ulcers showed evidence of perforating complications.                                 In the next article by Christian Sohns and Associates describes the relationship between atrial fibrosis identified with magnetic resonance imaging and atrial rotor activity identified by noninvasive electrophysiological mapping. Ten patients underwent pulmonary vein isolation for persistent atrial fibrillation. Late gadolinium enhancement using magnetic resonance imaging, which projected onto the anatomy used for noninvasive electrophysiologic mapping.                                 The noninvasive electrophysiologic mapping identified 410 rotors evenly distributed between the left atrium and the right atrium. This study found that there was no statistically significant association between the presence of late gadolinium enhancement and the presence of rotors.                                 In the next article written by Jereon Venlet examines the endocardial unipolar voltage that best identifies abnormal epicardial electrograms. Thirty-three patients underwent endocardial epicardial right ventricular electro-anatomical mapping in ablation of right ventricular scar-related ventricular tachycardia. Eighty-six percent of abnormal epicardial electrograms had corresponding endocardial sites with bipolar electrogram less than 1.5 millivolts.                                 The remaining abnormal epicardial electrograms could be identified by endocardial unipolar voltages of less than 3.7 millivolts. The authors concluded that this use of endocardial unipolar voltage cut off at normal bipolar voltage sites improves the identification of all abnormal epicardial electrograms where there is less than 1 millimeter of fat.                                 The next article by Alan Bulava and Associates examines the outcomes of hybrid epicardial and endocardial radial frequency ablation, a persistent atrial fibrillation. Seventy patients underwent the epicardial thoracoscopic procedure followed by endocardial mapping ablation two to three months later. At the time of catheter ablation, 76% of patients were in sinus rhythm. All four pulmonary veins were found to be isolated in 69% of the patients and the left atrial posterior wall was isolated in 23% of the patients.                                 In the 12 months after the catheter ablation, 77% were arrhythmia-free, off antirrhythmic drugs. The majority of arrhythmia occurrences occur during the first 12 months following catheter ablation. Using previously ineffective antiarrythmics drugs and re-ablation procedures, arrhythmia-free survival increased to 97% during a mean followup of 936 days. Left atrial volume greater than 165 milliliters, the absence of sinus rhythm before catheter ablation and induce-ability of any sustained tachyarrhythmia at the end of catheter ablation predicted atrial fibrillation recurrence.                                 The authors concluded that the majority of patients after epicardial ablation required endocardial catheter ablation to complete the linear ablation or pulmonary vein isolation lesion sets. In the next article, Jason Roberts and Associates studied the clinical phenotype of Type 6 Long QT Syndrome, stemming from mutations in the KCNE2 encoded voltage gated channel beta subunit.                                 The authors examined individuals reported pathogenic KCNE2 mutations collected from inherited arrhythmia clinics in the Rochester LQTS registry as well as previously reported LQT6 cases identified through a med-line database search. Of 44 probands studied, 16 probands had resting QTC intervals and only developed QT prolongation and malignant arrhythmias following exposure to QT prolonging stressors. Ten had other Long QT pathogenic mutations and 10 did not have a Long QT phenotype, with the remaining eight subjects having a Long QT phenotype, but with evidence suggesting that the KCNE2 variant was not the underlying culprit.                                 The authors noted that the collective frequency of KCNE2 variance implicated in Long QT6 syndrome in the exome aggregation consortium database was 1.4%, in comparison with the 0.0005% estimated clinical prevalence of LQT6 syndrome. Thus, the authors concluded that based on clinical phenotype, the high allelic frequencies of LQT6 mutations in the exome consortium database, in absence of prior documentation of genotype phenotype segregation, many KCNE2 variants, and perhaps all have been erroneously designated as long QT syndrome causative mutations.                                 Instead, KCNE2 variants may confer pro-arrhythmic susceptibility when provoked by additional environmental acquired or genetic factors. In the next article, Alexander Quinn and Associates examine how mechanically-induced ectopy may cause ventricular fibrillation, the mechanism of commotio cordis. It is known that the block of stretched sensitive ATP inactivated potassium channels limits ventricular fibrillation occurrence in a porcine model of commotio cordis.                                 In isolated rabbit heart preparations using optical voltage mapping combined with pharmacological block of potassium ATP or stretch activated cation nonselective channels, the authors showed that the mechanical stimulation reliably triggers premature ventricular excitation at the contact site with induce-ability predicted by local tissue indentation. Mechanically-induced premature ventricular excitation induction is decreased by stretch activated cation nonselective channel block.                                 The authors also found that mechanically-induced premature ventricular excitation resulted in ventricular fibrillation only if the mechanical stimulation site overlaps the re-polarization wave edge in hearts where T-waves involve a well-defined re-polarization edge traversing the epicardium. This defines a narrow subject-specific vulnerable window for commotio cordis-induced ventricular fibrillation in both time and space.                                 In the next article Matthias Seidl and Associates examine the gene expression required for development of atrial fibrillation in a transgenic mouse model. Recent studies showed that atrial fibrillation susceptibility is associated with down regularization of target genes of the CREB/CREM family of transcription factors. CREB/CREM refers to cyclic and P-response element binding protein modulator.                                 Short CREM repressor isoforms like CREM-IbΔC-X bind to cyclical A&P responsive elements preventing transcriptional activation. Messenger RNA for CREM-IbΔC-X is up-regulated in atrial biopsies from patients with paroxysmal or chronic atrial fibrillation. The authors examined transgenic mice expressing CREM-IbΔC-X, which spontaneously developed atrial fibrillation proceeding to permanent fibrillation with age.                                 The authors found that the most prominent alterations of the gene program linked to CREM-induced atria modeling were identified in expression of genes related to structure, metabolism, contractility and electrical activity regulation. In the next article by Takumi Yamada and Associates electrophysiologic characteristics of the idiopathic ventricular arrhythmias originating from the parietal band, one of the muscle bands of the right ventricle, were examined.                                  Of 294 consecutive patients with right ventricular origins, 14 patients had ventricular arrhythmia origins in the parietal band. All patients have left bundle block pattern with 12 inferior and two superior axis. All patients had the notch in the middle of the curess in all cases. Seven patients had precordial transition before lead V3 and four patients had a slow curess onset.                                 Far field ventricular electrogram with an early activation was always recorded in His bundle region regardless of the location of the ventricular arrhythmia origin. During the catheter ablation, a mean number of 10.4 radio frequency of applications with a mean duration of 1,099 seconds were delivered. Catheter ablation was successful in 10 patients and ventricular arrhythmias recurred in four with a mean followup of 41 months.                                 In the Advances in Arrhythmia and Electrophysiology section, the Buza and Associates have reviewed cancer treatment-induced arrhythmias. The authors describe ECD advances in arrhythmias associated with individual cancer chemotherapeutic agents. Now here with a review of the highlights from the articles from journals throughout the world in the past month, is Dr. Suraj Kapa. Dr. Kapa:              Hello. Today we're going to be going over several hard hitting articles we have identified that seem to stand out in the electrophysiological literature from the month of July 2017. The first area we will be delving into is that of atrial fibrillation. Specifically related to cardiac mapping and ablation. The first article in this area that we've chosen was published by Samuel et al. in the Journal of Cardiovascular Electrophysiology entitled Catheter Ablation for the Treatment of Atrial Fibrillation Is Associated with a Reduction in Healthcare Resource Utilization.                                 Samuel et al. reviewed data from a large population base cohort in Quebec, Canada including over 1,500 patients undergoing cardiac ablation for atrial fibrillation. They demonstrated that healthcare resource utilization including hospitalizations, emergency room visits and cardioversions were significantly reduced both 12 months as well as 24 months after the next ablation. These findings seem to suggest that catheter ablation has a sustained overall impact on resource utilization amongst patients with atrial fibrillation.                                 While the study was not randomized and was a retrospective evaluation of outcomes, these findings are provocative. Certainly as we wait for the results of the Cabana trial in about one year we hope to see whether or not cardiac ablation carries the weight of potential beneficial impacts both in terms of long-term care as well as long-term outcomes. Of course being a retrospective evaluation, one question that lies with regards to these findings is whether or not the reduction in resource utilization might be a byproduct of improved ambulatory care of these patients or whether it's a byproduct of patients understanding their disease process better, and thus perhaps not seeking emergency room care or hospitalization as frequently.                                 The next publication we'll focus on was published by Anselmino et al. in The International Journal of Cardiology entitled Conduction Recovery Following Catheter Ablation in Patients with Recurrent Atrial Fibrillation and Heart Failure. This publication synergizes with several other publications that have come out in the month of July. Focusing on the publication by Anselmino et al., they reviewed retrospectively patients undergoing redo atrial fibrillation ablation in the setting of underlying heart failure.                                 What they demonstrated was that nearly a third of patients had no pulmonary vein reconnection, but tended to have more persistent forms of atrial fibrillation suggesting more extensive atrial substraights. This study is complimentary to a publication by [inaudible 00:15:23] et al., published in JACC EP. this past month where they evaluated the longterm outcomes of patients who, when presenting for redo atrial fibrillation ablation had persistent pulmonary vein isolation.                                 In that article, they found that nearly 17% of patients presenting for redo ablation had persistent pulmonary vein isolation. Moreover, these patients tended to perform significantly worse in terms of longterm outcomes than those who presented with PV reconnection, with about a 56% freedom from affiliate swipe after we do ablation in the setting of persistent pulmonary vein isolation as opposed to 76% when there was PV reconnection seen.                                 So the question becomes if we see this greater atrial substraight, should we automatically be doing more ablation? Of course as we all know, there have been many studies performed trying to tease out whether additional ablation in patients who might have more significant atrial substraight carries benefits. In this regard, Fink et al. in last month's edition of Circulation, Arrhythmia and Electrophysiology demonstrated that in fact as an index procedure of performing a stepwise concomitant café plus linear ablation on top of pulmonary vein isolation in persistent and long standing persistent atrial fibrillation patients did not necessarily confer an increased likelihood of longterm success over pulmonary vein isolation alone.                                 Thus, the jury continues to still be out as far as what the right strategy is in many of these patients. However, these studies highlight the importance of continued evaluation and understanding of how we can use information about atrial substraight to guide our ablation procedures more successfully. Changing gears, we'll move on the pathophysiology mechanisms of disease within atrial fibrillation.                                 The article we will choose to focus on here was published by Die et al. in The Journal of Cardiovascular Electrophysiology entitled The Effects of Extrinsic Cardiac Nerve Stimulation on Atrial Fibrillation Induce-ability: The Regulatory Role of the Spinal Cord. Over the course of the last several years many investigators have sought to show that modulation of the autonomic nervous system can successfully alter cardiac electrophysiology and provide antiarrythmic benefits.                                 However, when subject to prospective trials such as the recently published Defeat HF Trial, they have not necessarily found clear benefit. Thus, a critical question becomes how we translate our animal models into human treatment. The interesting results from Die et al. lie in the fact that they looked at the effects of spinal cord stimulation and spinal cord block in addition to concomitant stimulation of other centers such as the venous nerve, the stellate ganglion and ganglionated plexi.                                 They demonstrated that spinal cord stimulation enhanced the effects of venial nerve stimulation while attenuating the effects of stimulating the left stellate ganglion or ganglionated plexus. In turn, the combinations of these different levels of stimulation had different effects on affiliate swipe induce-ability, whether significantly increasing or decreasing the potential.                                 The reason this article is important is it highlights the extensive cross linking and synergy that exists within the autonomic nervous system and that attention paid to only a single center of autonomic innovation may not be sufficient for certain paradigms of care. This past month there were also two reviews summarizing the role of the autonomic nervous system and modulation of that nervous system and the treatment of arrhythmias.                                 The first was by Witt et al. and Europace. The other by Schwartz et al. in the International Journal of Cardiology. These articles help the reader understand the extensive crosslinking and cross communication that might occur, that might sometimes defeat our efforts to use a single element of the autonomic nervous system to modulate cardiac arrhythmias. Changing gears yet again, we'll move on to risk stratification and management for atrial fibrillation.                                 Perino et al. in last month's edition of The Journal of the American College of Cardiology published an article entitled Treating Specialty in Outcomes in Newly Diagnosed Atrial Fibrillation from the Treat AF Study. They present data based on a very large cohort of over 180,000 veterans regarding the effect of treating specialty on atrial fibrillation outcome. Interestingly they demonstrated that when a cardiologist was involved in the care of the patient, there was an overall decrease in stroke and mortality.                                 Albeit with a concomitant increase in hospitalization for AF. The stroke reduction seen was also seen to be secondary to better anticoagulation prescription within 90 days of diagnosis when those patients were seen by a cardiologist as compared with a general internist. This earlier prescription anticoagulation however did not mediate the mortality reduction. These data presented by a Perino et al. are provocative in this era of rising healthcare costs.                                 The question is, as atrial fibrillation rates rise, as the general population ages, how quickly and how aggressively we should engage specialty care early on in patient evaluation. The data by Perino et al. suggests that maybe this engagement should occur earlier. Part of the reasons for this might be improved understanding of current evidence regarding treatment of such patients or better systems of care that allow for providers to identify patients who might need alterations and care faster.                                 However, if anything this is hypothesis-generating. Why anticoagulation prescriptions are delayed when patients are not seen by a specialist or why there would be a difference in mortality are important factors to review further. In this past month Hernandez et al. in Stroke published an article discussing the large degree of geographic variation that exists with regards to appropriate anticoagulation prescription in patients with atrial fibrillation.                                 They demonstrated that there's extensive inhomogeneity across the United States in terms of how and in whom anticoagulation gets prescribed. Thus, how much of these outcomes are specialist-driven, geographically-driven or based on elements of access to care or other issues are going to be important features that have to be evaluated.                                 The next article in risk stratification was published by Mostofsky et al. in Heart, entitle Chocolate Intake and Risk of Clinically Apparent Atrial Fibrillation: The Danish Diet, Cancer and Heart Study. In this study they demonstrated in a population of over 55,000 patients that when accounting for as many variables as they could, higher chocolate intake, more than once per month, was associated with a decreased atrial fibrillation risk when compared with those consuming less chocolate than once per month.                                 Of course, they note that despite these attempts to account for multiple confounding variables, residuary confounders cannot be accounted for. The relevance of this article lies in the question of lifestyle choices patients are asked to make when thinking about how to either prevent themselves from having atrial fibrillation or trying to even treat their atrial fibrillation risk.                                 Chocolate has been shown to have multiple potential beneficial effects in multiple areas of cardiology, however, how to counsel patients with data like these becomes very difficult. The questions lies in how chocolate might mediate arrhythmia risk and how it might also modulate other potential risks such as weight gain or other factors.                                 Thus while important to consider this in light of patients often asking what they can and cannot have, it is important to further consider that we don't understand the full story. The other key element to understand is that really when they say that chocolate intake reduces risk of clinically apparent atrial fibrillation they are speaking about moderate chocolate intake and not necessarily having it for three meals a day.                                 Changing gears away from atrial fibrillation, we will next focus on the area of ICDs pacemakers and CRT. Aberi et al. in Nature's Scientific Reports published regarding inductively power wireless pacing via miniature pacemaker and remote stimulation control system. Their approach provides potential novel opportunities beyond currently available both lead-based and leadless pacemakers and improving battery and allowing for further miniaturization of such devices.                                 They noted by creating a very novel inductive power supply they're able to miniaturize the pacing components and also significantly reduce the power requirements. In fact, they suggested that they could create a leadless device that could be as small as being delivered out of the anterior ventricular vein. This is the first report of such an inductively powered miniaturized pacing system with low enough power consumption that may prove viable for ambulatory human use.                                 The desire to create improved pacing and fibrillation systems is further highlighted by an article published by [Kalu 00:25:41] et al. in JACC Clinical Electrophysiology this past month where they demonstrated initial results of percutaneous epicardially delivered partially insulated defibrillator lead. Work like these holds the potential to improve options for patients and in traditional vascular access is not desired, or an identifying new ways of delivering pacing therapy that exists outside the traditional lead base or even somewhat miniaturized leadless approaches.                                 We'll next focus on the area of sudden death and cardiac arrest. The first article we'll focus on was published by Stecker et al. in The Journal of The American Heart Association entitled Health Insurance Expansion and Incidence of Out of Hospital Cardiac Arrest: A Pilot Study in the US Metropolitan Community. This article looked at the results of The Affordable Care Act, mainly health insurance expansion, on the rate of out of hospital cardiac arrest in a large US metropolitan community of over 600,000 people.                                 They separately studied a middle aged population that might have been affected by healthcare expansion versus an older population, above 65, who would have had relatively stable insurance plans having been covered by Medicare both prior to and after this change in healthcare plans. They demonstrated that there was a significant decrease in overall out of hospital cardiac arrests amongst middle age people without any significant change amongst the more elderly Medicare population in the same time period.                                 The time period studied was relatively short, nearly less than a decade. Of course, whether there were other events that might have occurred to alter this risk such as improvements in care beyond the combination of availability and mandates plus carrying health insurance, it remains to be seen. However, the data is very suggestive. Further evaluation at the national level in varying communities however would be useful, as well as consideration of population level cost benefit analysis.                                 The next article published by Shen et al. in the New England Journal of Medicine entitled Declining Risk of Sudden Death in Heart Failure. They presented data across 40,000 patients from multiple clinical trials over two decades regarding the changing rates of sudden death amongst heart failure patients. Interestingly they noted there was an overall 44% reduction in sudden death rates across these trials over time dating from the 1990s to 2014.                                 In the earliest trials considered, the mortality rate within 90 days after randomization was as high as 2.4% while the most recent trials suggest that that rate is more like 1.0%. This profound decline was attributed to improved usage and prescription of medications early on in the heart failure course, which may modulate outcomes.                                 The relevance of these findings lies in trials that have been published recently and met analysis that we've discussed regarding utility of defibrillators in nonischemic cardiomyopathy or even ischemic cardiomyopathy. The recently published Danish study suggested that ICDs might not confer an equivalent mortality risk as what would have been expected years ago. However, this publication by Shen et al. is particularly provocative because it calls into question whether the same mortality benefit we anticipated from earlier heart failure trials should still be the rubric by which current defibrillator trials are powered.                                 Namely, if we consider that Danish saw the 25% difference in mortality, with a 44% overall reduction in sudden death seen in trials over time for heart failure, seeking a 25% reduction might be excessive. Thus, this highlights the need to potentially power trials for ICDs and the benefit of such ICDs better. This importance of better stratifying better heart failure patients for sudden death risk has been raised in multiple articles this month, including in a review by Holiday et al. in Circulation and in the series of reviews published in Volume 237 of The International Journal of Cardiology.                                 The last article we choose to focus on in the role of sudden death and cardiac arrest was published by Vehmeijer in Circulation: Arrhythmia and Electrophysiology entitled Prevention of Sudden Cardiac Death in Adults with Congenital Heart Disease: Do the Guidelines Fall Short? They reviewed outcomes amongst 26,000 adults with congenital heart disease in light of existing guidelines for risk prediction and prevention of sudden death.                                 They demonstrated that less than half of the patients with sudden cardiac death actually had a guideline basis recommendation for an ICD on the basis of either the 2014 consensus statement on arrhythmias or the 2015 European Society of Cardiology Guidelines. These findings are very provocative in suggesting that we don't really understand who requires treatment amongst adults with congenital heart disease.                                 With improved care paradigms, both with improvements in surgical outcomes as well as ambulatory care of these patients and recognition of need for interventions, arrhythmias are becoming a greater and greater problem amongst patients with adult congenital heart disease. However, large scale studies are limited in stratifying overall risk of arrhythmias. The risk is certainly present as many of these patients have ventricular scar often attributable to cardiac surgeries or have hemodynamic insults that may result in progressive fibrosis of the ventricles.                                 In addition, the basal abnormalities of cardiac formation itself may lend itself to a sudden increased risk of arrhythmias. Thus, the question remains as how to best risk stratify these patients in order to reduce these overall sudden death rates. Changing gears yet again, we'll focus on two articles within the realm of cellular electrophysiology. The first article was published by Cerrone et al. in Nature Communications entitled Plakophilin-2 is Required for Transcription of Genes that Control Calcium Cycling and Cardiac Rhythm.                                 They demonstrated that plakophilin-2, or PKP2, which is known to mediate arrhythmogenic right ventricular cardiomyopathy due to abnormalities in the desmosomes actually has other direct electrical effects independent of substraight effects that are seen. Specifically PKP2 plays a significant role in maintaining gene transcription for several genes that mediate normal electrophysiologic activity, such as the ryanodine receptor, calsequestrin and others.                                 They demonstrated that this reduced expression of other genes secondary to PKP2 absence or abnormality leads to increased isoproterenol or adrenaline-induced arrhythmias that in turn can be suppressed with Flecainide. These findings are provocative in the fact that they suggest that it is possible for patients to have abnormalities of genes such as PKP2 that result in electrical abnormalities independent of the structural abnormalities.                                 Furthermore, it suggests that manifestation of the disease such as catecholaminergic polymorphic ventricular tachycardia may be immediate upstream of typical channels associated with the disease. For example, if PKP2 reduces expression of the ryanodine receptor, this might result in manifestations similar to CPTB in some patients. Along the same lines, Hewitt et al. published in Science Advances regarding deregulated calcium cycling underlies the development of arrhythmia and heart disease due to mutant obscurin.                                 Obscurins are a relatively growing area of interest as these are cytoskeletal proteins that have be associated with both hypertrophic and dilated cardiomyopathy. Similar to the story we just told about PKP2 however, they demonstrated that obscurins, likely through circa 2 and pentameric phospholamban can cause abnormal calcium handling. In fact, they demonstrated that the principle phenotype associated with obscurin abnormalities is one of an electrical abnormality, namely frequent PVCs.                                 In turn, mechanical phenotypes such as cardiomyopathy result in the setting of chronic pathologic stress such as increased afterload, thus these findings demonstrate that genes such as obscurin or PKP2, which are commonly associated with structural or mechanical myopathic processes might have direct independent electrical effects. The story with obscurin raises further question into how this may apply to conditions of PVC-related cardiomyopathy or other such conditions.                                 The other key point about these two areas of interest lie in the fact that it is possible as these genetic abnormalities mediate not just direct substraight elements, but arrhythmogenesis via abnormal channel expression, whether in all patients presenting with such specific genetic abnormalities substraight-based ablation alone will result in reduction of arrhythmia tendency. Of course this remains to be seen and is primarily hypothesis-generating.                                 Next we'll focus on three articles within the area of genetic channelopathies. The first paper was published by Rohatgi et al. in The Journal of the American College of Cardiology entitled Contemporary Outcomes in Patients With Long QT Syndrome. In a large single center practice, they reviewed the results of over 600 patients predominantly affected by LQT1 or LQT2 and demonstrated that after initial evaluation along with treatment based on the individual, done at a highly skilled center, 92% of patients did not experience any breakthrough cardiac events over longterm followup.                                 It was noted however, that the incidence of breakthrough cardiovascular events over longterm followup were far more common in patients who were symptomatic prior to their first evaluation than asymptomatic. In other words, if you were symptomatic prior to your first evaluation, the likelihood of a breakthrough cardiovascular event over longterm followup was as high as 25%, but if you were asymptomatic it was as low as 2%.                                 These data suggest that our overall care of the Long QT patient is improving. However, it also supports that further improvements in care are needed as breakthrough cardiovascular events can continue to occur. It also highlights the importance of close followup of that symptomatic patient in the modern era.                                 The second article was published by Kannenkeril et al. in JAMA Cardiology entitled the Efficacy of Flecainide in the Treatment of Catecholaminergic Polymorphic Ventricular Tachycardia. Flecainide currently carries a class 2A indication according to both the 2015 ENC guidelines and 2013 HRS AHRA APHRS consensus statement for treatment of patients with CPVT who fail max dose beta blockers. A lot of this evaluation however, has been based on retrospective evaluations.                                 Kannenkeril reviewed in a prospective single blind placebo controlled crossover trial the effect of Flecainide on exercise associated arrhythmias in CPTV patients who were already on max tolerated beta blockers and had an ICD. Amongst the 14 patients included of whom 13 completed the study, they showed there was a significant reduction in median ventricular arrhythmia score during exercise and in fact there was complete suppression with Flecainide compared to the placebo of 85%.                                 These findings thus add to the existing literature in terms the potential incremental value of Flecainide in achieving adequate arrhythmia suppression when used in conjunction with maximal tolerated beta blockers. The last article within the realm of genetic channelopathies we'll focus on was published by Yang et al. in The Journal of Physiology entitled A Multi-Scale Computational Modeling Approach Predicts Mechanisms of Female Sex Risk in the Setting of Arousal-Induced Arrhythmias.                                 It is recognized that female gender can increase the risk of Torsades in the setting of both inherited and acquired prolonged QT syndromes. In a combination of experimental and computational approaches, Yang et al. demonstrated that hormone concentrations can partly mediate this risk, specifically as it relates to her-related mutations. They demonstrated testosterone and high progesterone levels provide a protective effect against Torsades. However, estrogen can enhance Torsadogenic potential, particularly in the setting sympathetic stress.                                 They also demonstrated the mechanism by which this likely occurs is due to interaction of estrogen with pore loop or intracavity binding site of the her channel. In fact, on top of this they demonstrated that combined treatment with both estrogen and Dofetilide can simultaneously blockade the pore channel of her. These findings are provocative and hypothesis-generating. In terms of potential future research to further clarify risk for patients, particularly as it may apply to menstruating females who might have varying levels of estrogen, especially when being treated with concomitant QT prolonging agents such as Defetilide.                                 Next we will focus on three articles within the realm of ventricular arrhythmias. The first article was published by Sapp et al. in JACC Clinical Electrophysiology entitled Real Time Localization of Ventricular Tachycardia Origin from the Twelve Lead Electrocardiogram. They presented a methodology for rapidly determining in real time the approximate origin of a ventricular tachycardia using the 12 lead during cardiac ablation.                                 In 38 patients they used a variety of methods that involved multiple linear regression learning methods and demonstrated that a patient-specific regression method using at least 10 training set pacing sites in the individual patient can provide a localization accuracy of the exit site for VT of as much as five millimeters. Furthermore, with additional pacing sites that accuracy could improve further.                                 These findings support the continued utility of the standard 12 lead ECG in localizing the exit site of ventricular tachycardia. Furthermore, it points out the importance of considering that the electrocardiogram can be patient-specific. By using multiple pacing sites, this helps an algorithm learn how a patient-specific heart exists in terms of its electrical propagation potential. Further informing based on a 12 lead of a specific VT approximately where it should be exiting from.                                 The next article we will focus on was published by Muser et al. in again, JACC Clinical Electrophysiology entitled Longterm Outcomes of Catheter Ablation of Electrical Storm in Nonischemic Dilated Cardiomyopathy COMpared with Ischemic Cardiomyopathy. The summary point to this article is in a single center, large volume group of patients including about 267 total, the longterm outcomes of VT recurrence or mortality was no different between nonischemic and ischemic patients.                                 This is important to note as most prospective studies and in fact retrospective studies of the role of ventricular tachycardia ablation have focused on ischemic patients where the substraight is relatively predicable. These findings highlight that ablation may provide a reasonably effective therapy irrespective of the cause of the myopathy. Finally, changing gears within the realm of ventricular arrhythmias, we'll focus on a translational article by Motloch et al. in JACC Basic to Translational Science entitled Increased Afterload Following Myocardial Infarction Promotes Conduction-Dependent Arrhythmias That Are Unmasked by Hypokalemia.                                 They studied the role of increased afterload after myocardial infarction in a listing arrhythmias in a porcine infarct model. They demonstrated that in the setting of increased afterload there was increased widespread interstitial fibrosis. Interestingly, pacing -induced arrhythmias induced by a rapid burst pacing were mediated by hypokalemia associated conduction abnormalities rather than repolarization abnormalities.                                 The reason these findings are potentially important lie in the fact that arrhythmias in the early stages after myocardial infarction, especially in a setting of increased afterload, might be considered to be secondary to either repolarization abnormalities or depolarization abnormalities. These findings suggest that in the setting of concomitant hypertension the primary problem really lies in hypokalemia associated conduction abnormalities.                                 Thus, treatments that impair cardiac excitability, for example, even sodium channel blockade, may similarly confer an increased risk of ventricular arrhythmias when in the presence of increased afterload and myocardial infarction. It also calls into question whether interventions such as antitachycardia pacing in patients with hypertension, in other words increased afterload, might be more prone to acceleration of the ventricular arrhythmias than patients who are relatively better managed as far as afterload.                                 Changing gears yet again, we will focus on EP relevant myopathies. [inaudible 00:44:19] et al. published in JACC Clinical Electrophysiology regarding use of the 12 lead electrocardiogram to localize regions of abnormal electron atomic substraight in arrhythmogenic ventricular cardiomyopathy. There were really two major articles in this regard that have been published both in the same month.                                 The other article was published by Andrews et al. in Circulation, Arrhythmia and Electrophysiology entitled Electrical and Structural Substraight of Arrhythmogenic Right Ventricular Cardiomyopathy Determined Using Noninvasive Electrocardiographic Imaging and Late Gadolinium Magnetic Resonance Imaging.                                 The relevance of both of these articles lies in their statements about the potential utility of noninvasive approaches essentially using electrocardiograms to determine the distribution of substraight in arrhythmogenic right ventricular cardiomyopathy. The article by [inaudible 00:45:16] et al. specifically focused on fractionation of the QRS. They showed that patients with evidence of fractionation in the QRS on a 12 lead ECG had more extensive substraight.                                 Furthermore, distribution of fractionation to specific leads such as inferior, anterior or basal superior leads, was 100% specific, but veritably sensitive for identifying substraight as it localizes to specific cardiac regions. In turn, the publication by Andrews et al. in Circulation, Arrhythmia and Electrophysiology reviewed how the addition of multiple leads by a noninvasive electrocardiographic imaging could be used to even more specifically hone in on the relevant substraights.                                 Their further benefit was in the suggestion that repolarization abnormalities in fact co-localized with origination sites for ventricular ectopy in these patients. In combination, these sites highlight the utility of simple, noninvasive methods of electrocardiographic imaging in identifying and defining the arrhythmogenic substraight in the NRVC.                                 The next article we will review was by Sommariva et al. in Nature's Scientific Reports published just this past month entitled MIR 320A as a Potential Novel Circulating Biomarker of Arrhythmogenic Cardiomyopathy. They did micro RNA analysis on 53 healthy controls, 21 idiopathic VT patients and 36 arrhythmogenic cardiomyopathy patients and demonstrated that the circulating micro RNA 320A was significantly higher in arrhythmogenic cardiomyopathy than in either other cohorts.                                 It is recognized that some patients with idiopathic VT, especially right ventricular [inaudible 00:47:09] VT might reflect a cohort that might have what we call "concealed ARVC." The question thus becomes how to define why a patient has a specific manifestation of disease because longterm outcomes, if there is some underlying ARVC might be worse if the ARVC is not recognized and if cure is assumed based on treatment of the initial presenting rhythm.                                 Thus identifying novel ways of defining the presence of a disease even in the absence of obvious structural abnormalities carries benefit in terms of suggestions on longterm followup. Complimentary to the previously discussed article on the role of PKP2 mutations on mediating electrical instability in the heart, the study by [inaudible 00:48:01] et al. does in fact suggest that there might be methods of distinguishing arrhythmogenic cardiomyopathy from whether it be controls or truly idiopathic ventricular tachycardia using a very specific circulating biomarker.                                 On a completely different route, we'll finish our podcast today with a discussion of Bruner et al. published in European Heart Journal entitled Alcohol Consumption, Sinus Tachycardia and Cardiac Arrhythmias at the Munich Oktoberfest: Results from the Munich Beer-Related Electrocardiogram Workup Study or Munich Brew.                                 Bruner et al. studied over 3,000 voluntary participants with a combination of breath alcohol concentration measurements and electrocardiographic recordings via smartphone throughout the Munich Oktoberfest. In addition, they sought to evaluate chronic alcohol consumption effects on arrhythmias in a separate cord of over 4,000 patients from the Cora S4 study. In the study regarding acute alcohol effects, they demonstrated that in line with increasing BAC, there was a greater occurrence of arrhythmias in particular sinus tachycardia in almost a third of patients.                                 What was even further interesting was that respiratory sinus arrhythmia over the course of higher BAC is from baseline was reduced in the setting of alcohol use. Similarly, with chronic alcohol consumption there was an apparent significant association with the occurrence of sinus tachycardia. The reason these findings are important is in their suggestive element that the effects of alcohol intake in terms of whether it be acute or chronic arrhythmogenesis might somewhat lie in their effects on the basal autonomic states. As demonstrated by the reduction in overall sinus arrhythmia.                                 These findings serve to further elucidate mechanisms by which alcohol may mediate arrhythmias in a large real world patient sample. Thank you for joining us on this edition of On The Beat. Tune in next month again for more articles that might be of interest to the general electrophysiologic community all summarized in a single location.

Podcast summary of articles from the May 2017 edition of Journal of Emergency Medicine from the American Academy of Emergency Medicine.  Topics include Ketamine for acute pain, qSOFA vs SIRS for sepsis, hypokalemia in  Cushing Syndrome, elevated liver enzymes, outpatient management of pulmonary embolisms, FEIBA for anticoagulation reversal, and board review on concussions.  Guest speakers include Dr. Courtney Smalley of the Cleveland Clinic Emergency Services Institute, and Dr. Allison Lane of the Banner University Medical Center in Tucson, Arizona

The blood sugar is NOT the emergency- Acidosis, Hypokalemia, and Dehydration are!!! Signs and Symptoms Vomiting Abdominal pain Polydipsia Polyuria Step 1: Test for DIABETIC-KETO-ACIDOSIS Diabetes Blood sugar Typically notably elevated (>250 mg/dL) Can be normal in certain circumstances Ketones Easiest test is a urinalysis Serum ketones also can be obtained Acidosis Blood gas (arterial […]

This week we discuss the presentation and treatment of hypokalemia. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_61_0_Final_Cut.m4a Download Leave a Comment Show Notes Take Home Points Hypokalemia has a wide variety of presentations ranging from generalized weakness, to paralysis, to cardiac arrhythmia or cardiac arrest. When you discover hypokalemia, be sure to check and EKG. Think about underlying causes of hypokalemia, because it is rarely a solo event. Treat with oral potassium supplementation of 40-60 orally every 4-6 hours for mild hypokalemia and 10-20 mEq/hour IV for severe or symptomatic hypokalemia. Additional Reading LITFL: Hypokalemia LITFL: Hypokalemic Periodic Paralysis Core EM: Hypokalemia Read More

This week we discuss the presentation and treatment of hypokalemia. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_61_0_Final_Cut.m4a Download Leave a Comment Show Notes Take Home Points Hypokalemia has a wide variety of presentations ranging from generalized weakness, to paralysis, to cardiac arrhythmia or cardiac arrest. When you discover hypokalemia, be sure to check and EKG. Think about underlying causes of hypokalemia, because it is rarely a solo event. Treat with oral potassium supplementation of 40-60 orally every 4-6 hours for mild hypokalemia and 10-20 mEq/hour IV for severe or symptomatic hypokalemia. Additional Reading LITFL: Hypokalemia LITFL: Hypokalemic Periodic Paralysis Core EM: Hypokalemia Read More

This week we discuss the presentation and treatment of hypokalemia. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_61_0_Final_Cut.m4a Download Leave a Comment Show Notes Take Home Points Hypokalemia has a wide variety of presentations ranging from generalized weakness, to paralysis, to cardiac arrhythmia or cardiac arrest. When you discover hypokalemia, be sure to check and EKG. Think about underlying causes of hypokalemia, because it is rarely a solo event. Treat with oral potassium supplementation of 40-60 orally every 4-6 hours for mild hypokalemia and 10-20 mEq/hour IV for severe or symptomatic hypokalemia. Additional Reading LITFL: Hypokalemia LITFL: Hypokalemic Periodic Paralysis Core EM: Hypokalemia Read More

This week we discuss how to aggressively resuscitate patients with DKA as well as dispelling some dogmatic teachings on the topic. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_60_0_Final_Cut.m4a Download Leave a Comment Tags: Cerebral Edema, DKA, Hypokalemia, Insulin, Resuscitation Show Notes Take Home Points DKA should be suspected in any patient with altered mental status and hyperglycemia. Get a VBG (ABG not necessary) to confirm the diagnosis. Hypokalemia kills in DKA. Aggresively replete potassium and consider holding insulin, which drops serum potassium, until K is greater than 3.5 The insulin bolus isn't necessary and appears to cause more episodes of hypokalemia. Just start insulin as an infusion at 0.14 units/kg Be vigilant about cerebral edema. Any change or deterioration in mental status should prompt treatment and evaluation. Mannitol in the euvolemic, normotensive patient and 3% hypertonic saline in the hypotensive/hypovolemic patient Finally, don't forge to always hunt down the underlying cause of the DKA. Infection and non-compliance is the most common so liberally administer broad spectrum antibiotics if you've got even a hint of infection brewing

This week we discuss how to aggressively resuscitate patients with DKA as well as dispelling some dogmatic teachings on the topic. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_60_0_Final_Cut.m4a Download Leave a Comment Tags: Cerebral Edema, DKA, Hypokalemia, Insulin, Resuscitation Show Notes Take Home Points DKA should be suspected in any patient with altered mental status and hyperglycemia. Get a VBG (ABG not necessary) to confirm the diagnosis. Hypokalemia kills in DKA. Aggresively replete potassium and consider holding insulin, which drops serum potassium, until K is greater than 3.5 The insulin bolus isn't necessary and appears to cause more episodes of hypokalemia. Just start insulin as an infusion at 0.14 units/kg Be vigilant about cerebral edema. Any change or deterioration in mental status should prompt treatment and evaluation. Mannitol in the euvolemic, normotensive patient and 3% hypertonic saline in the hypotensive/hypovolemic patient Finally, don't forge to always hunt down the underlying cause of the DKA. Infection and non-compliance is the most common so liberally administer broad spectrum antibiotics if you've got even a hint of infection brewing

This week we discuss how to aggressively resuscitate patients with DKA as well as dispelling some dogmatic teachings on the topic. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_60_0_Final_Cut.m4a Download Leave a Comment Tags: Cerebral Edema, DKA, Hypokalemia, Insulin, Resuscitation Show Notes Take Home Points DKA should be suspected in any patient with altered mental status and hyperglycemia. Get a VBG (ABG not necessary) to confirm the diagnosis. Hypokalemia kills in DKA. Aggresively replete potassium and consider holding insulin, which drops serum potassium, until K is greater than 3.5 The insulin bolus isn’t necessary and appears to cause more episodes of hypokalemia. Just start insulin as an infusion at 0.14 units/kg Be vigilant about cerebral edema. Any change or deterioration in mental status should prompt treatment and evaluation. Mannitol in the euvolemic, normotensive patient and 3% hypertonic saline in the hypotensive/hypovolemic patient Finally, don’t forge to always hunt down the underlying cause of the DKA. Infection and non-compliance is the most common so liberally administer broad spectrum antibiotics if you’ve got even a hint of infection brewing

6 L’s Lethargy Leg cramps Limp muscles Low, shallow respirations Lethal cardiac dysrythmias Lots of urine (polyuria)   The post Ep6: Hypokalemia (6 L’s) appeared first on NURSING.com.

Question: A patient who has been suffering from severe diarrhea has developed hypokalemia and cardiac arrhythmias as a result. Which of the following treatments would most likely be ordered for this patient to correct the situation? Answer: A. IV administration of potassium Rationale:  Hypokalemia occurs when there is not enough potassium; this decrease in potassium can […] The post QOD 2: Hypokalemia and Cardiac Arrhythmias (Labs/Basic Care and Comfort) appeared first on NURSING.com.

Question: A patient who has been suffering from severe diarrhea has developed hypokalemia and cardiac arrhythmias as a result. Which of the following treatments would most likely be ordered for this patient to correct the situation? Answer: A. IV administration of… The post QOD 2: Hypokalemia and Cardiac Arrhythmias (Labs/Basic Care and Comfort) appeared first on NURSING.com.

What is the evidence behind K+ repletion? What is a framework to think through for hypokalemia? What are the different repletion formulations and what else can you do to mitigate hypokalemia? Stepping back, do we really need to get labs every single day?!Sponsor: Hellofresh (50% off + free shopping with code: 50COREIM)CME : http://bit.ly/CIMCME || Show Notes & TranscriptTimestamp01:45 Pearl 1: Evidence for potassium repletion 09:10 Pearl 2: Framework for hypokalemia17:09 Pearl 3: Repletion goals23:00 Pearl 4: Options for hypokalemia treatment29:13 Pearl 5: Frequency of lab checks and repletionTags: IMCore, CoreIM, nephrology, hospital medicine, potassium diet, interprofessional educationFind the best disability insurance for you: https://www.patternlife.com/disability-insurance?campid=497840Our Sponsors:* Get a great deal on HelloFresh (use code 50COREIM): http://hellofresh.comAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy