Search results “Differene between verapamil and diltiazem”
Calcium Channel Blockers - Nifedipine, Verapamil, Diltiazem & Amlodipine
http://usmlefasttrack.com/?p=431 voltage, L type channels, vascular smooth muscles, heart, hypertension, angina, prinzmetal's angina, raynauds, cardiac depression, dizziness, First Aid, for, USMLE, Step 1, wiki, define, wikipedia,
Views: 21831 USMLEFastTrack
Calcium channel blockers are usually well absorbed through the git which means that they go through first pass metabolism . However once entered into the blood stream calcium channel blockers are highly bound to plasma proteins, after doing their action calcium channel blockers are then metabolized by the liver and excreted renally.
Views: 22065 Pill Whiteboard
Calcium Channel Blockers - For Nursing Students and Nurses!
EmpoweRN.com Here is the link for the additional NCLEX style questions! http://empowern.com/2015/02/calcium-channel-blockers/ Also, at the bottom of the page, there is a link to download the audio version of this video with & without music. Please also visit the references & recommended resources links... which you can find at the bottom of the page :) If this video has helped you in any way & you would like to see more videos like it: please give the video a "thumbs up" & also subscribe to the channel. I would like to thank the talented & intelligent contributes of this video: Rizalyn Joy Gadugdug Maria Salvacion Gonzales Yasmin Hashmi Artem Shestakov And Babar Hayatrana Disclaimer: These videos are intended for entertainment purposes only. Please follow the policy and procedures that your institution requires. Please note that the views, ideas & opinions expressed on this channel and in the videos on this channel are not necessarily of those of my employer or institution. The views expressed on this channel and in the videos channel do not represent medical advice. If you have specific medical concerns, please contact your physician. In order to protect patient privacy, all patient identifiers in all videos have been deleted or altered. The views expressed on this channel and in the videos on this channel are personal opinions. I am not an expert nor do I dispense medical advice or procedural specifications. The information I present is for general knowledge and entertainment purposes only. You need to refer to your own medical director, teachers and protocols for specific treatment information. It is your responsibility to know how best to treat your patient in your jurisdiction. Calcium Channel Blockers, as the name suggests, prevents or reduces the opening of these channels. There are different classes of Calcium channel blockers, but almost of all of them acts on the L-type voltage-gated calcium channel. Therefore, blocking or reducing calcium entry into these cells, means inhibiting calcium effects, and thus causes the following reaction: Vasodilation – by acting on vascular smooth muscle, Calcium channel blockers reduces contraction of the arteries which causes an increase in arterial diameter. This drugs primarily affect arteries, with minimal effects on venous vessels. Calcium Channel Blockers also have a Negative Inotropic effect – by acting on cardiac muscle, Calcium channel blockers therefore can reduce the force of the contraction in the heart. Calcium channel blockers also have a Negative Chrono-tropic – effect – by slowing down the conduction of electrical activity within the heart, therefore Calcium channel blockers may affect the rate of the heartbeat. They also can exhibit a Negative Dromo-tropic effect – by slowing down the conduction of the electrical activity of the heart, thus the conduction of velocity also decreases, particularly at the atrioventricular node. Which can ultimately slow the heart rate. Therapeutic Use Calcium Channel Blockers are used to control a variety of medical condition such as high blood pressure, chest pain, and tachyarrhythmia. As anti-hypertensive drug – The effects of calcium in the heart muscles, is that it causes the muscle to act aggressively, by contracting more forcefully. Calcium also stimulates vascular smooth muscle contraction resulting in narrow blood vessels. This series of events many times can result in high blood pressure. By preventing the entry of calcium into the heart muscle and vascular smooth muscles (particularly in the arteries), the heart muscle contraction will not be too strong and arterial vessels are able to relax and dilate, leading to lower blood pressure. As anti-anginal drug – The word angina is one that you will hear a lot as a nursing student and nurse. This is a fancy word for “chest pain.”
Views: 148948 EmpoweRN
Antiarrhythmics (Lesson 5 - Calcium Channel Blockers)
An overview of the mechanism, indications, and side effects of calcium channel blockers.
Views: 8182 Strong Medicine
Calcium Channel Blockers made Simple
I created this video with the YouTube Video Editor (http://www.youtube.com/editor)
Views: 83453 100lyric
Support us on Patreon: https://www.patreon.com/speedpharmacology Follow us on Facebook: https://www.facebook.com/SpeedPharmacology/ Get Speed Pharmacology Merch Here: https://teespring.com/stores/speed-pharmacology **************************************************************************************************** Topics covered include: basic pathophysiology of hypertension, regulation of blood pressure, cardiac output, systemic vascular resistance, baroreceptors, alpha & beta receptors, vasoconstriction, vasodilation, renin-angiotensin-aldosterone system, bradykinin, nitric oxide. Mechanism of action of antihypertensive drugs and their side effects; adrenergic antagonists; alpha & beta blockers, centrally acting adrenergic agents, dihydropyridine & nondihydropyridine calcium channel blockers, loop, thiazide, potassium-sparing diuretics, renin inhibitors, angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor type 1 blockers (ARBs), endothelin receptor antagonist, dopamine-1 receptor agonist, peripheral vasodilators. Drugs mentioned include; Doxazosin, Prazosin, Clonidine, Methyldopa, Amlodipine, Felodipine, Nicardipine, Nifedipine, Diltiazem, Verapamil, Furosemide, Hydrochlorothiazide, Triamterene, Spironolactone, Aliskiren, Benazepril, Captopril, Enalapril, Lisinopril, Quinapril, Ramipril, Candesartan, Irbesartan, Losartan, Olmesartan, Valsartan, Bosentan, Fenoldopam, Sodium Nitroprusside, Nitroglycerin, Hydralazine, and Minoxidil.
Views: 226241 Speed Pharmacology
Calcium Channel Blockers
In this video Dr. Mahmudul Hoque Jassy discusses about following topics 1. Classification of Calcium Channel Blocker 2. Indication of amlodipine , nifedipine SR, Larcanidipine, clinidipine and nimodipine 3. Mechanism of contration of vascular smooth muscle and role of voltage sensitive L-type calcium channel in contraction of vascular smooth muscle ( with details intracellular events). 4. How does Amlodipine / Nifedipine SR/ Larcanidipine/ Clinidipine lower BP? 5. Why Nifedipine is used in Raynaud phenomenon in COLD, in EMOTIONAL stress , in SLE and in Scleroderma. ( this indication is confirmed from professor Azizul kahhar sir) 6. Why CCB is used in preterm labor? What is the problem of preterm labour? 7. What is the role of nimodipine in Subaracnoid Hemorrhage and intracerebral hemorrhage with ventricular extension ( Many mechanisms are proposed in different books. but the most acceptable mechanism is discussed with approval of Professor Azizul Kahhar sir) 8. Common adverse effects of CCB( including ankle edema). 9. how Nifedipine and Felodipine produce reflex tachycardia? This video will be useful for medical and nursing students all over the world. Students who take preparation for USMLE, AMC, MRCP, MBBS may find this video helpful
Views: 10456 Pharmacology Videos
Confused about DILTIAZEM Formulations?
Learn different formulation about diltiazem hydrochloride
Views: 390 SomaliMedicine
Paraneoplastic Syndrome - high levels of PTHrH, Calcitriol, Erythropoietin & Lambert Eaton Syndrome
http://usmlefasttrack.com/?p=5360 Paraneoplastic, Syndrome, -, Increased, levels, of, PTHrH,, Calcitriol,, Erythropoietin, &, Lambert, Eaton, Syndrome, Findings, symptoms, findings, causes, mnemonics, review, what is, video, study, Rapid Review, Clinical presenation, First Aid, for, USMLE, Step 1, images, wiki, define, wikipedia, 2013, videos, exam, prep, easy, What is usmle, mnemonic, causes,
Views: 3417 USMLEFastTrack
How does Amlodipine work?
Amlodipine is a medication used to treat high blood pressure. It is classified as a calcium channel blocker. This video explains the mechanism of action of calcium channel blockers. This short video is designed for the average person to understand. This video is intended for personal use. Unauthorized reproduction and distribution without the author's consent is prohibited. The contents of this video are not intended to substitute for professional expertise and judgement of health care professionals.
Views: 99871 Betty Huang
If You’re On Any Of These Medications, DO NOT Use Apple Cider Vinegar
Although ACV is best known for its many health benefits, it is also very important to know that this amazing vinegar can cause side effects http://healthyfoodspot.com/2016/09/11/if-youre-on-any-of-these-medications-do-not-use-apple-cider-vinegar/
Views: 2126204 Article-TUBE2
Diltiazem - New Medication Administration Set
A basic review of Diltiazem (Cardizem) and the new powdered administration set. Please keep comments constructive and respectful.
Views: 18739 BlueJFilms
Verapamil for Cluster Headache (Day 5) - IT'S WORKING!!!
Hey YouTube, this vlog is my experience with Verapamil and Cluster Headache. If you would like to donate, please follow this link... www.PayPal.Me/DougThaHead Yesterday I skipped my dose in the morning as I'm on 120 mg once a day, I skipped it in the morning so I could take it at night. I wanted to try this because my worst headaches are at night. After 5 days I'm SO happy to announce I'm Cluster Headache free for the last 24 hours! I wish peace and comfort in your journey with this disorder, if you have any questions please ask below and subscribe to keep up with the series!
Views: 613 Our Little LIfe
Human clinical trial reveals verapamil as an effective Type 1 diabetes therapy
Researchers at the University of Alabama at Birmingham Comprehensive Diabetes Center have discovered a safe and effective novel therapy to reduce insulin requirements and hypoglycemic episodes in adult subjects with recent onset Type 1 diabetes by promoting the patient’s own beta cell function and insulin production — the first such discovery to target diabetes in this manner.
The Treatment Of High Blood Pressure II
As was discussed in a previous vignette, there are several types of blood pressure medications to lower high blood pressure. Diuretics, ACE inhibitors and beta blockers were all discussed. All have a role to play, and all attack high blood pressure at different places in the body’s process of maintaining blood pressure. Often, combinations must be used to control high blood pressure. This vignette will further discuss different types of medications that are available to control high blood pressure. The next kind of medicine to control high blood pressure is the calcium channel blockers. They are further divided into two different groups: one that opens up the arteries of that lowering the blood pressure inside such as nifedipine and amlodipine, and one that lowers the heart rate such as Verapamil or Diltiazem. These medications are not really considered first-line therapies, but at times they do have a role to play in lowering blood pressure. Verapamil and Diltiazem are also used in certain heart rhythms when the heart rhythm is too fast. The good news with these medications is that there is increasing evidence that they may reduce stroke and heart attacks. However, they do have side effects including headache and swelling in the legs, and of course there’s always a chance that the heart rate can be lowered too much, causing heart failure or just general fatigue. Angiotensin II receptor blockers (ARBs) are a new kind of blood pressure medicine that are being used more and more. They work in a similar way to the ACE inhibitors. They differ in that they do not cause a cough, and so many physicians use this type of medication when the ACE inhibitors cause a cough. This kind of medication includes Losartan, Olmesartan, Eprosartan, Telmisartan, Candesartan, Valsartan, and Irbesartan. It is now thought that they have similar effects on heart failure, kidney disease and heart attacks that ACE inhibitors have, although there are not as many studies done on ARBs as there are on the ACE inhibitors. On a more personal note, I very rarely use these medications because of their high costs and to me personally, they just don’t seem very strong in actually reducing high blood pressure. There are several other classes of medication that are used less frequently. For instance, in very high blood pressures, some doctors use a medication called hydralazine that helps open the arteries up a bit allowing the pressure inside the artery to decrease. This medication is used three times a day, and often causes lots of swelling in the legs. Furthermore, not everyone responds to it. There is also a class of high blood pressure medicines called alpha blockers, such as doxazosin, that actually increase the risk of stroke and heart failure when used. Finally, there probably needs to be a special word given to the medication called clonidine. Clonidine or Catapress is available as a pill or a patch. It’s considered a pretty strong medication, and is one that used a lot when blood pressures are very high, especially if we think somebody is at or near a stroke or kidney failure. It is not used very often long-term because of its two main side effects: it’s very sedating, and it gives a very dry mouth. Both of these symptoms get a little better over time, but for most people they never completely get used to them, either. As one can see, there are a lot of choices out there for high blood pressure, and this vignette just scratches the surface. If you have high blood pressure, please consult your physician as to what to do, but we hope that the information above gives you a little bit more information as to how we approach and treat high blood pressure.
Views: 4792 ChristianWebMD.com
Support us on Patreon: https://www.patreon.com/speedpharmacology Follow us on Facebook: https://www.facebook.com/SpeedPharmacology/ Get Speed Pharmacology Merch Here: https://teespring.com/stores/speed-pharmacology **************************************************************************************************** Topics covered include: cardiac conduction system, SA node, AV node, bundle of His, bundle branches, purkinje fibers, cardiac action potential, pacemaker cells, conducting cells, contractile cells, mechanisms of arrhythmias, bradycardia, tachycardia, abnormal automaticity, triggered activity, Wolff–Parkinson–White syndrome, atrioventricular nodal reentry tachycardia, Vaughan-Williams classification, class I (A, B, C), class II, class III, class IV antiarrhythmic drugs. Antiarrhythmics mentioned include: Procainamide, Quinidine, Disopyramide, Lidocaine, Mexiletine, Flecainide, Propafenone, Propranolol, Metoprolol, Atenolol, Esmolol, Amiodarone, Dronedarone, Sotalol, Dofetilide, Ibutilide, Verapamil, Diltiazem, Digoxin, Adenosine, and Magnesium sulfate. Source of the animation of the cardiac conducting system: http://www.passmyexams.co.uk/GCSE/biology/cardiac-conduction-system.html
Views: 258303 Speed Pharmacology
Calcium Channel Blockers
-- Created using PowToon -- Free sign up at http://www.powtoon.com/youtube/ -- Create animated videos and animated presentations for free. PowToon is a free tool that allows you to develop cool animated clips and animated presentations for your website, office meeting, sales pitch, nonprofit fundraiser, product launch, video resume, or anything else you could use an animated explainer video. PowToon's animation templates help you create animated presentations and animated explainer videos from scratch. Anyone can produce awesome animations quickly with PowToon, without the cost or hassle other professional animation services require.
Views: 26109 Alison Fowler
Cardizem Video
We were faced with the following challenge. Cardizem was added as an optional medication for the region. We opted to use it because of its apparent benefits over Lopressor and the fact that it can be used standing order. The issue is that the only cost effective preparation requires some specific education regarding its use. We felt that there needed to be training beyond what was covered in the CNYEMS rollout before we put this medication on the rigs. We did not have time to put everyone through face-to-face training so we are trying this different approach. We made a video. A bunch of us (who would probably have preferred to remain anonymous if you didn't already know who we are) made the above video. Rescue 911, for those of you who don't recall, was one of the original "reality" TV shows that began its original run in 1989. It is known for being hosted by William Shatner and including rather melodramatic clips of personal interviews during the recreation of each incident. The first part of the video is modeled after the show. Following this are director's comments reminiscent of a late night infomercial. We even have an appearance by our own Air-1 pilot, Sergeant "Lieutenant" Jim. Finally, I would like your feedback. We are implementing training ideas on a trial and error basis (a highly heuristic method, if you will). So far we have received excellent feedback on the rig check reviews. Feedback is imperative to make sure that we provide you with material that is worthwhile and meeting your needs. Special thanks goes out to everyone who participated. I'd especially like to recognize folks behind the scenes including Dan who spent a bunch of time shooting footage, editing and adding effects and my partner in training (and cinematic producer / director) Susie. Thank you. --Dr. Fullagar WAVES Member Specific Information: The first portion of the video contains a number of answers, if you pay close attention, to the quiz you were e-mailed. The second portion has somewhat more direct answers to questions with a demonstration on how to mix and draw up the diltiazem properly. WAVES ALS Providers: Please complete and return the quiz you were e-mailed to Susie. The quiz helps us document that you have an understanding of the content that was trying to be conveyed.
Views: 736 WAVESAmbulance
NCLEX RN Review 2018: Calcium Channel Blockers
*Subscribe for more great NCLEX videos: https://www.goo.gl/8mBXbY Get free help for the NCLEX RN test with our NCLEX RN review video about Calcium Channel Blockers. Find more NCLEX Review Videos Here: Diuretics - https://www.youtube.com/watch?v=xLej3EYEOrw IV Fluids - https://www.youtube.com/watch?v=Xdf7jutmSvg EKG Reading - https://www.youtube.com/watch?v=h9ah8lWXhmQ ...And More Check all of our Nursing Certification Resources: http://www.mometrix.com/academy/nursing-certification/ Get a NCLEX Study Guide: http://www.mometrix.com/studyguides/nclex/ Learn with NCLEX Flash Cards: https://www.flashcardsecrets.com/nclex/ Free NCLEX Practice Questions: http://www.mometrix.com/academy/nclex-exam/ STAY IN TOUCH! Like NCLEX Prep Facebook Page: https://www.facebook.com/MometrixNCLEX/ Follow our NCLEX Twitter Account: https://twitter.com/MometrixNCLEX NCLEX Pinterest Board: https://goo.gl/NbA2CP
Views: 25351 NCLEX Study Guide
Specific Antidotes for Drug Overdose/Poisoning
Drug overdose & Antidotes are enumerated in a simple way for revision. Enjoy & Learn ! ______________________________________________________________ Please Visit & Subscribe Our Channel for Latest Videos: https://www.youtube.com/lastsecondmedicine Visit us on Facebook: https://www.facebook.com/lastsecondmedicine Follow us on Twitter: https://twitter.com/Last_Second_Med Visit Blog www.lastsecondmedicine.blogspot.com Support us on Patreon: https://www.patreon.com/lastsecondmedicine Please Leave you valued suggestion in Comments.
Views: 3072 Last Second Medicine
Antiarrhythmic Drugs
This is a brief overview of antiarrhythmic agents, or drugs used to resolve abnormal cardiac rhythms. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS Class IA antiarrhythmic agent Moderate sodium s, which s action potential duration Quinidine side effects blocks hERG , which results long QT and can cause torsades de pointes Procainamide Less prolongation QT segment, less TdP Disopyramide s force contraction heart Side effects: constipation, urinary retention, glaucoma IB antiarrhythmic Mild sodium s, which s action potential duration Lidocaine Intravenous only Mexiletine Can be administered orally IC antiarrhythmic Marked sodium s, doesn’t change action potential duration Flecainide Possibly produces an ventricular arrhythmias Propafenone Some beta er effects (bradycardia and cardiac inotropy) addition to changing AP duration by changing Na influx, Is also: phase 4 depolarization threshold potential sub degree Na+ AP duration change Beta-adrenergic receptor ers (beta ers) catecholamines (norepinephrine, epinephrine, dopamine) Reduces myocardial need for oxygen, can ischemia slope phase 4 depolarization s self-generated rhythmic firing heart (s automaticity) Prolong repolarization AV node → reentry Effectively s refractory period III antiarrhythmic s potassium s (delayed-rectifier potassium (DRK) s) Prolongs repolarization (phase 3) Amiodarone, Sotalol, Ibutilide, D etilide, Dronedarone III: Amiodarone Wide range effects through many mechanisms s sinus node firing s automaticity s reentrant circuits s Na, K, and Ca s ( I, III, IV antiarrhythmics) s alpha and beta ( II) adrenergic receptors → vasodilation and d intropy Treats many tachyarrhythmias: atrial flutter, atrial fibrillation, vtach, ventricular flutter, SVT Pharmacokinetically unique: absorbed slowly, deposits adipose tissue Half life 25-60 days → cannot easily diminish or reverse effects Side effects: pulmonary (pneumonia, pul fibrosis); cardiac (brady, arrhythmias, long QT, TdP); thyroid (due to iodine); GI; CNS Amiodarone Wide range effects through many mechanisms sinus node firing; s automaticity; s reentrant circuits; Na, K, and Ca alpha and beta adrenergic receptors vasodilation and intropy Treats many tachyarrhythmias: atrial flutter, atrial fibrillation, vtach, ventricular flutter, SVT Pharmacokinetically unique: absorbed slowly, deposits adipose tissue Half life 25-60 days Side effects: pulmonary (pneumonia, pul fibrosis); cardiac (brady, arrhythmias, long QT, TdP); thyroid (due to iodine); GI; CNS High rates torsades de pointes Dronedarone (amiodarone analog without iodine) Gastrointestinal side effects but not TdP Sotalol Calcium L-type Ca2+ Most effective cells dependant on Ca (SA, AV nodes) transmission through AV node (for rapid atrial pulses) Terminates reentrant rhythms Treats AV nodal reentrant tachycardia (primary treatment) Side effects: hypotension and heart failure pts taking beta-ers Diltiazem and Verapamil Digoxin Inhibits activity sodium potassium pump (Na+-K+ ATPase inhibitor) Treats heart failure complicated with atrial fibrillation (by decreasing heart rate) s vagal tone; reduces sympa tic activity Opens potassium (K+ activator) Intravenously with saline flush (short 10 s half life) Hyperpolarizes cells Allows for rapid termination reentrant supraventricular tachycardia chemical defibrillator
Views: 83877 MedLecturesMadeEasy
Amlodipine Side Effects
This video is for the website http://www.amlodipinesideeffects.com. It is my testimonial of the use of the hypertension medication, Amlodipine. http://www.hangoutmarketingtrainingreview.net
Views: 39768 Brian Sloan
SVT or Supraventricular Tachycardia
This video demonstrates the treatment of a patient with supraventricular tachycardia (SVT) using adenosine.
Views: 163215 Larry Mellick
Calcium channel blocker
Calcium channel blockers (CCB), calcium channel antagonists or calcium antagonists are a number of medications that disrupts the movement of calcium (Ca2+) through calcium channels. Calcium channel blockers are used as antihypertensive drugs, i.e. as medications to decrease blood pressure in patients with hypertension. CCBs are particularly effective against large vessel stiffness, one of the common causes of elevated systolic blood pressure in elderly patients. Calcium channel blockers are also frequently used to alter heart rate, to prevent cerebral vasospasm, and to reduce chest pain caused by angina pectoris. Despite their effectiveness, CCB's often have a high mortality rate over extended periods of use, and have been known to have multiple side effects. Potential major risks however were mainly found to be associated with short-acting CCBs. This video is targeted to blind users. Attribution: Article text available under CC-BY-SA Creative Commons image source in video
Views: 24189 Audiopedia
Prinzmetal's angina (Medical Condition)
Symptoms, risk factors and treatments of Prinzmetal's angina (Medical Condition) Variant Angina is a variant form of angina pectoris caused by coronary artery vasospasm, usually occurring spontaneously and frequently associated with ST segment elevation This video contains general medical information If in doubt, always seek professional medical advice. The medical information is not advice and should not be treated as such. The medical information is provided without any representations or warranties, express or implied. We do not warrant or represent that the medical information on this websiteis true, accurate, complete, current or non-misleading Music: 'Undaunted' Kevin Macleod CC-BY-3.0 Source/Images: "Prinzmetal's angina" CC-BY-2.5 https://www.freebase.com/m/08zr95
Nitrovasodilators and Angina Pectoris Part 3
DescriptionIn this video we discuss the mechanism of action of nitrovasodilators and consider why they can be used to treat Angina Pectoris
Views: 619 Ben1994
Support us on Patreon: https://www.patreon.com/speedpharmacology Follow us on Facebook: https://www.facebook.com/SpeedPharmacology/ Get Speed Pharmacology Merch Here: https://teespring.com/stores/speed-pharmacology **************************************************************************************************** Topics covered include: absorption (passive diffusion, facilitated diffusion, active transport, endocytosis), distribution (volume), metabolism (phase I, phase II), elimination (zero, first-order kinetics), steady state, cytochrome P450 (inducers, inhibitors)
Views: 305155 Speed Pharmacology
Calcium Channel Blockers - Clinical Nurse Pharmacology
Learn about Calcium Channel Blockers in a fun and innovative way!
Views: 58703 Cc Cc
Medications for high blood pressure (Calcium channel blockers) interacts with FORSKOLIN Forskolin might decrease blood pressure. Taking forskolin with medication for high blood pressure might cause your blood pressure to go too low. Some medications for high blood pressure include nifedipine (Adalat, Procardia), verapamil (Calan, Isoptin, Verelan), diltiazem (Cardizem), isradipine (DynaCirc), felodipine (Plendil), amlodipine (Norvasc), and others. Medications that increase blood flow to the heart (Nitrates) interacts with FORSKOLIN Forskolin increases blood flow. Taking forskolin with medications that increase blood flow to the heart might increase the chance of dizziness and lightheadedness. Some of these medications that increase blood flow to the heart include nitroglycerin (Nitro-Bid, Nitro-Dur, Nitrostat) and isosorbide (Imdur, Isordil, Sorbitrate). http://www.youtube.com/watch?v=4WI5I6a1E3c http://www.youtube.com/user/MultiHerbalHealth
Views: 5355 Herbal Health
2015 Atrial Fibrillation Patient Conference: Treating Afib w/ Medications: Mintu Turakhia, MD, FHRS
http://www.stopafib.org To be notified when new conference videos are posted, or for the latest afib news, sign up at http://www.stopafib.org 2015 Get in Rhythm. Stay in Rhythm.™ Atrial Fibrillation Patient Conference In his talk about Treating Atrial Fibrillation with Medications at the 2015 Get in Rhythm. Stay in Rhythm.™ Atrial Fibrillation Patient Conference, Dr. Mintu Turakhia of Stanford University covered: • How does the doctor decide what medications to recommend? •Rate control vs. rhythm control [1:15] • Consider restoring sinus rhythm when AF causes symptoms [2:43] • Whether rhythm control should be used without overt symptoms [4:45] • Rapid heart rate may not be obvious [4:55] • Heart failure from AF may not be obvious [5:50] • Mechanisms to see how fast heart rates lead to failure [8:05] • Cycle of AF and heart failure [8:27] • How does doctor decide what to recommend [8:47] • Severity of AF influences decisions [13:16] • Severity defined by behavior, then burden [14:40] • Natural time course of AF [16:00] • Classification of AF [16:30] • What drugs can be used [17:37] • Typical doses of antiarrhythmic drugs [18:33] o Sotalol and dofetilide [18:52] o Amiodarone [19:47] and dronedarone [20:29] o How doctors decide what rate control agents to use first-line [20:53] o Digoxin – TREAT-AF study [21:38] • How structural heart disease vs. no structural heart disease relates to drug choice [18:06] • AF and heart failure Video watching time is approximately 25 minutes. Dr. Turakhia is a cardiac electrophysiologist, outcomes researcher, and Assistant Professor of Medicine and of Health Research and Policy at Stanford University. He is Chief of Cardiac Electrophysiology at the Palo Alto VA Health Care System and is an Associate Investigator at the Center for Innovation to Implementation. In his clinical role, Dr. Turakhia performs complex catheter ablation (primarily for AF), device implantation, and left atrial appendage occlusion. Dr. Turakhia has an active clinical research program, with funding from AHA, VA, NIH, the medical device industry, and foundations. His research program aims to improve the treatment of heart rhythm disorders, with an emphasis on atrial fibrillation, by evaluating quality and variation of care, comparative and cost-effectiveness of therapies, and predicting outcomes such as stroke. Dr. Turakhia has extensive expertise in using large administrative and claims databases for this work. His other research interests include technology assessment of new device based therapies and the impact of changing health policy and reform on the delivery of arrhythmia care. Dr. Turakhia has over 70 publications and is a Fellow of the American Heart Association, American College of Cardiology, and Heart Rhythm Society. Transcript http://www.stopafib.org/newsitem.cfm/NEWSID/549/
Views: 6943 StopAfib
Potassium channel blockers
Potassium Channel Blockers are easy! Check it out! I work hard to make and find the best videos for you to study from (it’s not easy)! You can help by suggesting any good videos you've seen in the comments below! Good luck in school!! Hey, guys. This is Dr. Joel with MedImmersion. You are watching a flash flood review series video where I review the highest yield stuff for your board exams in as little time as possible. In this video, I'm going to be talking about the potassium channel blockers, which are a class of the antiarrhythmic agents. I'll cover some general principles about the class as a whole, and then a few specific drugs in that category, or in this class. It's gonna be awesome, so stick around. If you watch a lot of MedImmersion videos, and they're helpful for you, think about getting an account at medimmersion.com. That will speed you up in your studying because when you're logged into MedImmersion on your browser and use the links in these videos, you will automatically skip past these lengthy introductions on my MedImmersion videos and also on other people's videos that I've linked to. And you'll be able to skip over a lot of the YouTube advertisements on my MedImmersion videos. Okay. Let's jump into it. This lecture is going to cover a subset of the antiarrhythmics, the potassium channel blockers. I'll give you an introduction as to what they are. Then, talk about some general principles that will include the mechanism of action, clinical uses, adverse or side effects, and then I will cover a couple of the highest yield examples in this class. Alright. First of all, if you need to review the entire topic of the antiarrhythmics, with a little bit of cardiac physiology, you should really go over and watch The Antiarrhythmic Agents Lecture first. This lecture, right now, is a little bit more focused, and I assume that you know a couple of things about antiarrhythmics. So, the potassium channel blockers, in the Vaughn Williams Antiarrhythmic Agent Classification, are the Class III antiarrhythmics. You should know that. And we use the potassium channel blockers and the Class I, or sodium channel blockers, for rhythm control. The Class IIs and Class IVs are more rate control. Four drugs that we're gonna talk about amiodarone, ibutilide, dofetilide, and sotalol, which you can remember by the mnemonic AIDS. As for the mechanism of action, these block myocardial potassium channels, and that has its primary effect on the specific potassium channels that are responsible for the delayed rectifier current, which have a very important contribution on the length of the action potential, and thus, the effective refractory period of cardiac myocytes. And to explain that a little bit further. Have you ever wondered why exactly the action potential of a neuron through the spinal cord or a peripheral neuron looks different than the action potential in myocardium. Well, it's built that way on purpose. The plateau phase, or the prolongation of the action potential, or the refractory period, gives cardiac tissue special properties that prevent it or contribute to prevention of arrhythmias. So, the picture on the left is what maybe a bland neuron action potential might look like in the peripheral nervous system. On the right, we have a cardiac action potential. And both of these are pretty bland images. They're not exactly right. But the point here is that there's a plateau where the cell stays in its non-polarized state for a little bit longer, for a period of time. Potassium plays a big part in that. The initial depolarization is caused by a rapid influx of sodium. And then, it's maintained in that depolarized state by both calcium and potassium trading places across the cell membrane in relatively small amounts. In phase three, which is the repolarization phase, finally there's a delayed switch, or a delayed rectifier current of potassium, which finally turns on and allows an efflux of positive ions, allowing the membrane potential to come back down to a very negative number. So, hopefully you can see why if we mess around with the potassium channels that contribute to phase three, we prolong or at least change the shape of the cardiac action potential, which, of course, would have an effect on some kinds of arrhythmias. So, it was pretty easy to see, I think, from that previous picture that delaying the potassium efflux during the repolarization phases increases or stretches out the action potential duration and also the effective refractory period. Also, these do not have any effect on the sodium channels, meaning that the conduction velocity, or phase zero, wouldn't be affected or decreased. And visually, it looks like this, the action potential stretched out and the effective refractory period is increased. Also, that means that the QT interval is prolonged. Okay. Does that make sense? We use the Class III antiarrhythmic agents for rhythm control.
Views: 6850 Med Immersion
What is CARDIOVERSION? What does CARDIOVERSION mean? CARDIOVERSION meaning, definition & explanation
What is CARDIOVERSION? What does CARDIOVERSION mean? CARDIOVERSION meaning - CARDIOVERSION pronunciation - CARDIOVERSION definition - CARDIOVERSION explanation - How to pronounce CARDIOVERSION? Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/by-sa/3.0/ license. Cardioversion is a medical procedure by which an abnormally fast heart rate (tachycardia) or other cardiac arrhythmia is converted to a normal rhythm using electricity or drugs. Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle, restoring the activity of the electrical conduction system of the heart. (Defibrillation uses a therapeutic dose of electric current to the heart at a random moment in the cardiac cycle, and is the most effective resuscitation measure for cardiac arrest associated with ventricular fibrillation and pulseless ventricular tachycardia.) Pharmacologic cardioversion, also called chemical cardioversion, uses antiarrhythmia medication instead of an electrical shock. To perform synchronized electrical cardioversion, two electrode pads are used (or, alternatively, the traditional hand-held "paddles"), each comprising a metallic plate which is faced with a saline based conductive gel. The pads are placed on the chest of the patient, or one is placed on the chest and one on the back. These are connected by cables to a machine which has the combined functions of an ECG display screen and the electrical function of a defibrillator. A synchronizing function (either manually operated or automatic) allows the cardioverter to deliver a reversion shock, by way of the pads, of a selected amount of electric current over a predefined number of milliseconds at the optimal moment in the cardiac cycle which corresponds to the R wave of the QRS complex on the ECG. Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period (or relative refractory period) of the cardiac cycle, which could induce ventricular fibrillation. If the patient is conscious, various drugs are often used to help sedate the patient and make the procedure more tolerable. However, if the patient is hemodynamically unstable or unconscious, the shock is given immediately upon confirmation of the arrhythmia. When synchronized electrical cardioversion is performed as an elective procedure, the shocks can be performed in conjunction with drug therapy until sinus rhythm is attained. After the procedure, the patient is monitored to ensure stability of the sinus rhythm. Synchronized electrical cardioversion is used to treat hemodynamically unstable supraventricular (or narrow complex) tachycardias, including atrial fibrillation and atrial flutter. It is also used in the emergent treatment of wide complex tachycardias, including ventricular tachycardia, when a pulse is present. Pulseless ventricular tachycardia and ventricular fibrillation are treated with unsynchronized shocks referred to as defibrillation. Electrical therapy is inappropriate for sinus tachycardia, which should always be a part of the differential diagnosis. Various antiarrhythmic agents can be used to return the heart to normal sinus rhythm. Pharmacological cardioversion is an especially good option in patients with fibrillation of recent onset. Drugs that are effective at maintaining normal rhythm after electric cardioversion, can also be used for pharmacological cardioversion. Drugs like amiodarone, diltiazem, verapamil and metoprolol are frequently given before cardioversion to decrease the heart rate, stabilize the patient and increase the chance that cardioversion is successful. There are various classes of agents that are most effective for pharmacological cardioversion.
Views: 3233 The Audiopedia
UAB trial to test promising new treatment approach for diabetes
Anath Shalev, MD, director of the UAB Comprehensive Diabetes Center, explains the “repurposing of verapamil as a beta cell survival therapy in type 1 diabetes” trial, which will test an approach different from any current diabetes treatment. The trial is based on Shalev's research showing that verapamil, a common blood pressure drug, reverses diabetes in animal models. Learn more about the trial, and the research behind it, here: http://www.uab.edu/news/innovation/item/5508-in-human-clinical-trial-uab-to-test-drug-shown-to-completely-reverse-diabetes-in-human-islets-mice Follow the trail of discoveries that led to the new trial here: http://themixuab.blogspot.com/2014/11/discovery-route-path-to-potential.html?+news
Diuretics quick revision in 3 min by DR.VISHWA MEDICAL COACHING
Diuretics quick revision in 3 min by DR.VISHWA MEDICAL COACHING. It includes mechanism of action, classification and different types of diuretics. Diagrammatic presentation.. Contact DR.VISHWA MEDICAL COACHING WhatsApp support for getting similar updates on +919930788955..
Amlodipine Nursing Considerations, Side Effects and Mechanism of Action Pharmacology for Nurses
Grab our free cheatsheet covering the 50 most commonly prescribed medications right here: http://www.nrsng.com/50meds View full post: https://www.nrsng.com/amlodipine-norvasc/ Listen to all the episodes at: https://www.nrsng.com/medmaster-podcast/ Amlodipine Generic Name: Amlodipine Trade Name: Norvasc Indication: hypertension, angina Action: blocks transport of calcium into muscle cells inhibiting excitation and contraction Therapeutic Class: antihypertensive Pharmacologic Class: Ca channel blocker Nursing Considerations  may cause gingival hyperplasia  grapefruit juice may increase drug level  monitor blood pressure and pulse prior to and during therapy  monitor intake and output  assess for signs of CHF  assess characteristics of angina  instruct patient of interventions for hypertension and how to take blood pressure
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Pathology & Remodeling of Heart Failure
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What are the risks or side effects of medications used to manage arrhythmia? (Evgueni Fayn, MD)
Evgueni Fayn, MD, Medical College of Wisconsin electrophysiologist, talks about the risk factors and side effects of drugs used to treat arrhythmia or irregular heartbeat. Dr. Fayn is part of the Arrhythmia Program team at Froedtert & The Medical College of Wisconsin. http://www.froedtert.com/arrhythmia
Amlodipine basic Pharmacology
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Calcium channel blocker Meaning
Video shows what calcium channel blocker means. A class of drug used to treat hypertension and also angina and arrhythmia.. Calcium channel blocker Meaning. How to pronounce, definition audio dictionary. How to say calcium channel blocker. Powered by MaryTTS, Wiktionary
Views: 517 ADictionary
003 - PreRegCentral: Hypertension and its Management Part 2
This video briefly outlines the key points of the role of Calcium channel blockers and Diuretics in the management of Hypertension Please subscribe to our channel and follow us on Facebook and Twitter for regular updates: Facebook: https://www.facebook.com/prereg.central Twitter: https://twitter.com/PreRegCentral All content (visual and audio) was created by PreReg Central
Views: 648 Pre Reg Central
Antiarrhythmic Drug Classes
Learning the Anti-Arrhythmic Agents just got a whole lot easier! ***MedImmersion to the rescue*** Listen guys, I really hope this video helps you in school. I definitely had fun making it! If you have questions, comments, or even criticisms...please, leave a comment. I love teaching and working with students, so your comments mean a lot to me! Good Luck in school! Hey YouTube, this is Dr. Joel. In this video, I'm gonna be covering the antiarrhythmic agents. I'm gonna start with a review of cardiac physiology, and then jump right into the agents themselves. I'll cover the Class I, Class II, Class III, Class IV, Class V, and then just give you some departing thoughts and then I will finish off with a couple of knowledge challenge questions, just to see where you're at. OK? Let's get started. In order to do a really good review of the cardiac antiarrhythmic agents, it's first important important for me to cover a little bit of cardiac physiology, starting first with the cardiac action potential. And that's because this action potential is a little bit different than the action potential that you're going to see in nerves. Also, a solid understanding of this action potential will help you later understand why the drugs work the way they do. So, this picture on the right represents a cardiac action potential. And, one thing that you need to understand is that this action potential is going to be a little bit different depending on which part of the heart you're measuring. However, the principles that I'm about to cover will apply to all of those tissues in the heart. And, if you want to, you can click on this link, which will take you to a picture that I think does a really cool job about showing the differences in the cardiac action potential in the different sections of the heart and that also how all those electrical depolarizations add up to make the electrocardiogram wave form. Anyway, on the X axis, we have time and on the Y axis, we have voltage. In the polarized state, the heart rests at about negative 95 millivolts. An action potential cycle takes about 200 milliseconds. And that number changes depending on which part of the heart you're in or which tissue you're sampling. So, on this graph, you can see that the heart starts at about negative 95 millivolts then it very quickly shoots up to about 20 or so, by this graph, pause at 20 millivolts. It stays there for a bit, and then the cell starts to repolarize itself. And that's the cycle. I'm going to add a cell membrane at the top of this picture and I'm going to walk through the phases of the action potential one at a time and what I want you to do is, I want you to imagine that above this cell membrane is the extracellular space and below this membrane is the intracellular space. OK, starting off with Phase 0, which is the depolarization phase. This is caused by a opening of voltage-gated sodium channels. And these are very fast, rapid-acting channels that allow a large amount of sodium to move very quickly. Sodium is positively charged, so if positive things come into the cell, then the cell becomes more positive. OK, does that make sense? Basically, that's why you see this huge skyrocketing here of the voltage from negative 95 to positive 20. It's because those positive sodium ions are moving in very quickly. Next is Phase 1, which is the initial repolarization phase, which is basically caused by the rapid inactivation of those sodium channels. Almost as quickly as they open, they start to close again. At the same time, voltage-gated potassium channels start to open allowing potassium to efflux or exit the cell. Potassium is also positively charged. So if you have positive things leaving the cell, then the cell becomes more negative, right? And that's why there's a little dip there in the voltage. Next, with Phase 2, you get calcium channels and they begin to open. Calcium, again, also positive. Positive things coming into the cell would make the cell more positive. But potassium is still moving out, so that would make the cell more negative, and hence you get this plateau phase. It kind of balances out for a little bit. It's not exactly flat, but it's close. We still call it the plateau phase. And, as you know, the calcium plays an effect on how the muscle cells contract. So that's important as well for contraction. Next is the rapid repolarization phase, which is Phase 3. More of the voltage-gated slow potassium channels are opening and they allow more potassium to rush out and the calcium channels begin to close so the cell starts to move back down to a negative value, a strong negative value. And you have to remember, the sodium-potassium ATPase pump is also chugging along this whole time. It's still working, it's still pumping potassium in and sodium out, which is just another factor that is driving that cell back down to its polarized state. Lastly is the fourth phase, which is the resting potential phase.
Views: 79706 Med Immersion
Medical vocabulary: What does Amlodipine mean
What does Amlodipine mean in English?
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ESC 2015: Dual antiplatelet therapy in unstable angina - Prof Gislasen
Professor Gunnar Gislasen, Gentofte University Hospital, Denmark, talks to Cardio Debate about his recent study that investigates the differences in dual anti-platelet treatment for acute coronary syndrome in patients undergoing PCI or not. For more in-depth insight and analysis on issues in cardiology visit the Cardio Debate website: www.cardio-debate.com TRANSCRIPT Well this is a register-based nationwide study from Denmark. We wanted to look at the persistence with dual antiplatelet therapy in patients with acute coronary syndrome. We know that the guidelines recommended at least 12 months period of dual antiplatelet therapy for all patients after acute coronary syndrome. We have done a similar study in the early clodipogrel period, where we found that especially patients not undergoing revascularization, had no persistence on dual antiplatelet therapy, shorter treatment duration and less often started on therapy. Now we have three different ADP receptor blockers available – clopidogrel, prasugrel and ticagrelor. So what we did, we identified all patients admitted with acute coronary syndrome – that is myocardial infarction and unstable angina – and we included in total 9700 patients, mainly patients with myocardial infarction, 90 per cent (8700 patients), and 1100 patients with unstable angina. What we found, that patients not undergoing revascularization were less seldom started on dual antiplatelet therapy, especially among patients with unstable angina. And in total 30 per cent of patients were not started on dual antiplatelet therapy. When we looked at the persistence we found that approximately 30 per cent of patients stopped dual antiplatelet therapy after the first 60 days of treatment, especially among patients not undergoing revascularization. So the conclusion of the study is that we need to be more focused on using dual antiplatelet therapy, starting patients on treatment and improving persistence, especially among patients not undergoing revascularization. How will these findings impact on clinical practice? Well the impact is that this is a treatment that we know prevents recurrent vascular events. We need to focus on patients where they are more likely to start treatment. We also need to focus on the individuals that we are not starting on therapy, and identify the reasons among doctors and health care personnel why they are not starting treatment. And then to secure long-term treatment – at least for most patients 12 months of treatment – we now need to focus on those patients that are most likely to discontinue treatment prematurely.
Views: 136 Cardio Debate
Acid Reflux / GERD
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Antihypertensive Drug|| Metoprolol +Amlodipine 25/5 mg|| by Guruji with Ashraf
Antihypertensives are a class of drugs that are used to treat hypertension (high blood pressure).Antihypertensive therapy seeks to prevent the complications of high blood pressure, such as stroke and myocardial infarction. Evidence suggests that reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34%, of ischaemic heart disease by 21%, and reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease. There are many classes of antihypertensives, which lower blood pressure by different means. Among the most important and most widely used drugs are thiazide diuretics, calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists (ARBs), and beta blockers. Which type of medication to use initially for hypertension has been the subject of several large studies and resulting national guidelines. The fundamental goal of treatment should be the prevention of the important endpoints of hypertension, such as heart attack, stroke and heart failure. Patient age, associated clinical conditions and end-organ damage also play a part in determining dosage and type of medication administered. The several classes of antihypertensives differ in side effect profiles, ability to prevent endpoints, and cost. The choice of more expensive agents, where cheaper ones would be equally effective, may have negative impacts on national healthcare budgets. As of 2009, the best available evidence favors the thiazide diuretics as the first-line treatment of choice for high blood pressure when drugs are necessary. Although clinical evidence shows calcium channel blockers and thiazide-type diuretics are preferred first-line treatments for most people (from both efficacy and cost points of view), an ACE inhibitor is recommended by NICE in the UK for those under 55 years old.
Views: 71 Guruji with Ashraf