Support us on Patreon and get FREE downloads and other great rewards: https://www.patreon.com/AlilaMedicalMedia/posts The 5 classes of agents according to Vaughan Williams classification, mechanism of action. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. ANTI-Arrhythmic agents are drugs used to SUPPRESS abnormal rhythms of the heart. They act to either: - interfere with the dynamics of cardiac action potentials by blocking a certain ion channel, or - block the sympathetic effects of the autonomic nervous system on the heart, to slow down heart rate. There are 5 classes of antiarrhythmic drugs: - Class I: Sodium-channel blockers: these drugs bind to and block the fast sodium channels that are responsible for the DE-polarizing phase in contractile myocytes. The result is a SLOWER depolarization with a smaller amplitude. This REDUCED conduction velocity helps to SUPPRESS formation of re-entrant circuits, hence the use of these drugs for treating re-entrant tachycardias. Class I agents are divided further into subclass IA, IB and IC. These subclasses differ in the STRENGTH of sodium channel blockage, and in their effect on the duration of action potentials and the effective refractory period, the ERP. While subclass IC has no effect on ERP, IA prolongs and IB shortens ERP, respectively. Changes in ERP may have different outcomes for different types of arrhythmias. A longer ERP generally reduces cardiac excitability, but prolonged repolarizations may increase the risk of torsades de pointes, a type of tachycardia caused by afterdepolarizations. - Class II: Beta-blockers: these drugs bind to beta1-adrenergic receptors and block the sympathetic influences that act through these receptors. Sympathetic nerves release catecholamines which act to increase SA node firing rate and cardiac conductibility, especially at the AV node. Useful in treatment of tachycardias that originate upstream of the AV node, known as supraventricular tachycardias, or SVT. - Class III: Potassium-channel blockers: these agents block the potassium channels responsible for the repolarizing phase. The result is a SLOWED repolarization, hence a PROLONGED duration of action potentials and refractory period. This reduces the heart’s excitability and suppresses re-entrant tachycardias. However, these drugs may also CAUSE arrhythmias because slow repolarizations are associated with LONGER QT intervals and INcreased risks of torsades de pointes. - Class IV: Calcium-channel blockers: these drugs block calcium channels that are responsible for DE-polarization in SA and AV nodal cells. Blocking these channels results in a LOWER sinus rate and SLOWER conduction through the AV node. However, because calcium is also involved in cardiac myocyte contraction, these agents also reduce contractility of the heart and should not be used in case of systolic heart failures. - Class V includes all drugs that act by other or unknown mechanisms.
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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
Просмотров: 291002 Speed Pharmacology
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, doesnâ€™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 â†’ 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 â†’ 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 â†’ 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
Просмотров: 86902 MedLecturesMadeEasy
http://proacls.com - ACLS Certification Training Videos **Get $20 off your certification or recertification with the discount code youtubeacls2017 Amiodarone is primarily chosen for ACLS as the first-line antiarrhythmic agent for cardiac arrest because it has reliably and clinically shown effectiveness in improving the rate of return of spontaneous circulation otherwise known as ROSC. Amiodarone is a drug that can prolong AV conduction, the AV refractory period and QRS and Q-T intervals, which ultimately slows the heart rate. When using Amiodarone to treat Vfib or pulseless VTach cardiac arrest, the first dose is 300 mg IV/IO push. The second dose is delivered at 150mg IV/IO push. Subscribe to ProTrainings' Youtube Channel! Check out all of ProTrainings' courses: http://www.protrainings.com Like ProTrainings on Facebook: https://www.facebook.com/protrainings Follow ProTrainings on Twitter: https://twitter.com/protrainings Follow ProTrainings on Instagram: http://instagram.com/protrainings
Просмотров: 7242 ProCPR
The EKG master, Dr. Amal Mattu, drops the ultimate pearl on regular really wide complex tachycardia (RRWCT). We bring you our #1 rated talk to celebrate our Essentials of EM 2017 Digital launch! Grab the rest of this year’s bundle of quick hit, informative lectures with 32.75 hours of CME: http://bit.ly/2uk6mBY
Просмотров: 33519 Essentials of Emergency Medicine
DESCRIPTION: P wave: Regular interval; Reg: P:QRS: Variable PRI: Variable QRS: Blocked/dropped Narrow - If Junctional Escape Mechanism (JEM): 40-60 bpm Wide - If Ventricular Escape Mechanism (VEM): 20-40 bpm CAUSES: - Idiopathic fibrosis and sclerosis of the conduction system (about 50% of patients) - Ischemic heart disease (40%) - Drugs (eg, beta-blockers, calcium channel blockers, digoxin, amiodarone) - Increased vagal tone - Valvulopathy - Congenital heart, genetic, or other disorders INTERVENTIONS: based on AHA 2016 ACLS Guidelines - Keep airway patent, support breathing - Start IV/IO, draw/send labs, 12-Lead ECG - Correct possible causes - NO Atropine! - Start Transcutaneous Pacing (TCP). - May give Dopamine 2-20 mcg/kg per minute and titrate to effect. - If profound bradycardia after TCP, may give Epinephrine 2-10 mcg/min and titrate to effect.
Просмотров: 93811 HEARTSTART SKILLS Frasco
Mastering Atropine Want to Learn More? Join Our FREE Facebook Group! https://www.facebook.com/groups/1153328328045266/ Transcript: Today we're talking about atropine at Master Your Medics. So atropine is an anticholinergic drug. It's indications is symptomatic bradycardia and also it's used in organophosphate poisonings to block the cholinergic effects of those. We're going to focus more on the symptomatic bradycardia because that's the more likely that you're going to be using atropine for. But, just so you know, it's used for organophosphate poisonings too. The contraindications are hypersensitivity. Does. Typically we see doses of 0.5 milligrams IV, cute three to five minutes as needed to a maximum of three milligrams. Now your protocols may be different obviously but that's just a standard that we see. Follow your protocols obviously of what's going on with atropine in your areas, but that's typically what you'll see. So as far as atropine goes, what it does is actually, it actually blocks muscarinic responses in acetylcholine. And so what that does is that it doesn't allow for severe introduction of parasympathetic response. Okay? And so remember, sympathic and parasympathetic responses, so sympathetic is your fight or flight so it's going to create a stimulus that's going to increase your heart, dilate your pupils, and so on and so forth. So what atropine will do is that it doesn't stimulate the sympathetic response, but what it does is it basically ... it doesn't allow for the parasympathetic response to push back so much. Okay? Because they're always keeping each other in check, the sympathetic and parasympathetic responses. And so what atropine does instead of allowing or pushing sympathetic response to create an effect it's actually just kneecapping parasympathetic response so the sympathetic response can take over. Okay? So it's not actually creating a sympathetic response and that's why it's anticholinergic as opposed to a sympathic. Okay and so what that does is that allows for an increased stimulus in the SA node and the AV node. So with symptomatic bradycardia, it allows for better conduction in those patients. Okay, so, you might have seen a note there that says, "Less effective in second degree type two and third degree blocks." And now the reason being is that if you look at the how it works is that it only allows for stimulus through the SA node and the AV node. Okay? Our pacemakers. And so what that means is that it's only going to work on stimuluses that are actually coming from above those nodes. Okay? And so in a second degree type two and a third degree block our bradycardia and our damages actually blow the AV node. Okay and so that's what's causing the symptoms and causing the damage is below the AV node. And so any type of stimulus with atropine won't, it's not going to be effective at increasing the heart rate or the symptoms of a patient in second degree type two or third degree blocks just simply because it can only stimulate the SA node and the AV node, it can't stimulate lower than those nodes, leaving second degree type twos and third degree blocks. Out of the picture for it ... but good for first degree blocks, sinus bradycardias, and it can be useful in second degree type ones. Again, that's where we're starting to get into the field where it's much less effective. Another note, as well, for the dose is that atropine can actually have the reverse effect if you under dose a patient. And so you'll see the dose as 0.5 milligrams. Well, that's actually what causes the effect that we want. If we under dose and say we give this patient 0.2 milligrams, atropine actually has the reverse effect on the body and it can cause even more bradycardia. So we want to make sure that we're using the right dose and making sure that we're going over 0.5 milligrams so we don't have a reverse effect in what we want. Master Your Medics https://www.masteryourmedics.com/pages/about-us
Просмотров: 17590 Master Your Medics Geoff Murphy
This video demonstrates one patient's experience with intravenous adenosine for supraventricular tachycardia. Follow-up: An electrophysiology study was performed which was remarkable for AVNRT which was successfully ablated without complications.
Просмотров: 155066 Larry Mellick
Also known as Mobitz II, Hay If R-to-R intervals are regular, then blocks can occur as 2:1, 3:1, or 4:1 (P waves to QRS) If R-to-R intervals are irregular, then block is variable CAUSES: - Idiopathic fibrosis and sclerosis of the conduction system (about 50% of patients) - Ischemic heart disease (40%) - Drugs (eg, beta-blockers, calcium channel blockers, digoxin, amiodarone) - Increased vagal tone - Valvulopathy - Congenital heart, genetic, or other disorders INTERVENTIONS: based on AHA 2016 ACLS Guidelines - Keep airway patent, support breathing - Start IV/IO, draw/send labs, 12-Lead ECG - Correct possible causes - NO Atropine! - Start Transcutaneous Pacing (TCP). - May give Dopamine 2-20 mcg/kg per minute and titrate to effect. - If profound bradycardia after TCP, may give Epinephrine 2-10 mcg/min and titrate to effect.
Просмотров: 29313 HEARTSTART SKILLS Frasco
The most common cause of a lethal dysrhythmia is by a PVC hitting the peak of the T wave (known as R-on-T Phenomenon). This causes a pulseless shockable or non-shockable rhythm in at risk patients. 90% of cardiac arrests in adults are shockable (Pulseless VTach/Ventricular Fibrillation). This rhythm started with multifocal PVCs to a wide complex tachycardia (Pulseless VTach). This can only last from a few seconds to a few minutes before it becomes Coarse Ventricular Fibrillation (if no CPR and Defibrillatory shocks were administered). Coarse VFib can only last for about 4-5 minutes before it becomes Fine VFib. From then on, you have seconds for Fine VF to become Asystole. INTERVENTIONS: Based on AHA 2016 Guidelines For VF/pVT: - High quality CPR - Defibrillate 120-200 J biphasic or 360 J monophasic every two minutes - Give Epinephrine 1 mg every 3-5 minutes, followed by a 10-20 mL flush of NS/LR - May give Amiodarone 300 mg IV/IO bolus if refractory (if patient is not hypokalemic) - May give Lidocaine 1-1.5 mg/kg IV/IO bolus if refractory (if patient is hypokalemic) For Asystole/PEA: - High quality CPR - Give Epinephrine 1 mg every 3-5 minutes, followed by a flush of 10-20 mL NS/LR - Correct possible causes (H/Ts) Possible causes: - Hypoxemia - Hypo/Hyperkalemia - Hydrogen Ions (Acidosis) - Hypothermia - Toxins - Tamponade, Cardiac - Tension Pneumothorax - Thrombosis, Pulmonary Embolism - Thrombosis, Acute Coronary Syndrome If ROSC (Return of Spontaneous Circulation) 1. Optimize ventilation and Oxygenation - Advance airway placement - Ventilate 10-12/min - Keep O2Sat greater than 94-99%, PETCO2 35-40 mm Hg 2. Treat Hypotension: Keep SBP above 90 mm Hg - Give 1-2 L NS/LR - May administer Dopamine 5-10 mcg/kg per minute IV/IO - May administer Epinephrine 0.1-0.5 mcg/kg per minute IV/IO - Treat H/Ts - 12-Lead ECG 3. Consider TTM (Targeted Temperature Management) if ALOC - Give cold NS/LR 4°C to reach a core temp of 32-36°C for at least 24 hours or greater - Other cooling measures are used to induce hypothermia (jell beds/pads, thermo-coolers, cooling blankets, etc) CONSIDERING CODE TERMINATION: - Unsafe scene - If (central) rigor mortis exists. Patient's intercostal muscles already filled with lactic acid from prolonged CPR disallowing compressions and decompressions - If DNR (do not resuscitate). It's obvious you don't start ACLS when you have the DNR papers on chart. This happens sometimes when the patient arrives in the ER first via ambulance and the family coming from somewhere else arrives with the DNR papers. - MD orders - Code Team decision - Lividity - Decapitation - Family request
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A discussion of how to choose the right antiarrhythmic to rate control and pharmacologically cardiovert atrial fibrillation and atrial flutter, as well as converting and prevention of ventricular tachycardia. An overall summary of this series is also presented.
Просмотров: 8827 Strong Medicine
http://proacls.com - ACLS Certification Training Videos **Get $20 off your certification or recertification with the discount code youtubeacls2017 Lidocaine brings about negative inotropic effects and antiarrhythmic actions in the heart which weaken the force of muscular contractions and can calm erratic and uncoordinated electro-myocardial activity. It’s primary use is for cardiac arrest from ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). For cardiac arrest from VF or pulseless VT, the initial dose is 1 to 1.5 mg/kg IV or IO. Subscribe to ProTrainings' Youtube Channel! Check out all of ProTrainings' courses: http://www.protrainings.com Like ProTrainings on Facebook: https://www.facebook.com/protrainings Follow ProTrainings on Twitter: https://twitter.com/protrainings Follow ProTrainings on Instagram: http://instagram.com/protrainings
Просмотров: 6157 ProCPR
P waves: Regular P:QRS: Variable PR Interval: Variable; progressively lengthens and drops a QRS QRS: Narrow, dropped CAUSES: - Idiopathic fibrosis and sclerosis of the conduction system (about 50% of patients) - Ischemic heart disease (40%) - Drugs (eg, beta-blockers, calcium channel blockers, digoxin, amiodarone) - Increased vagal tone - Valvulopathy - Congenital heart, genetic, or other disorders INTERVENTIONS: based on AHA 2016 ACLS Guidelines - Keep airway patent, support breathing - Start IV/IO, draw/send labs, 12-Lead ECG - Correct possible causes - Give Atropine 0.5 mg IV/IO followed by 10-20 mL NS/LR flush, repeat every 3-5 minutes, max. dose 3 mg - Consider Transcutaneous Pacing (TCP) if needed - May give Dopamine 2-20 mcg/kg per minute and titrate to effect. - If profound bradycardia after TCP, may give Epinephrine 2-10 mcg/min and titrate to effect.
Просмотров: 17166 HEARTSTART SKILLS Frasco
http://proacls.com - ACLS Certification Training Videos **Get $20 off your certification or recertification with the discount code youtubeacls2017 Atropine reduces the activity of the parasympathetic nervous system. Atropine is the drug of choice to treat symptomatic sinus bradycardia and may be beneficial in the presence of atrio-ventricular nodal blocks. For bradycardia, the dosage for Atropine is 0.5 mg every 3-5 minutes as needed, not to exceed a total dose of .04 mg/kg to a total of 3mg. Subscribe to ProTrainings' Youtube Channel! Check out all of ProTrainings' courses: http://www.protrainings.com Like ProTrainings on Facebook: https://www.facebook.com/protrainings Follow ProTrainings on Twitter: https://twitter.com/protrainings Follow ProTrainings on Instagram: http://instagram.com/protrainings
Просмотров: 3549 ProCPR
P Waves: Sinus, P-P regular PR Interval: Variable; lengthens progressively and drops a QRS. P:QRS: Variable POSSIBLE CAUSES: Can occur in individuals with high vagal tone, such as athletes or young children, patients with structural heart disease (eg, tetralogy of Fallot), valvular surgery (especially mitral valve), MI (especially inferior wall), and drug induced (including Beta-blockers, Calcium channel blockers, Amiodarone, Digoxin, and possibly Pentamidine). It can also be seen if patients with Lyme Disease. TREATMENT: if patient is unstable Follow AHA ACLS 2016 Bradycardia Algorithm: - Atropine 0.5 mg give every 3-5 minutes - or Transcutaneous Pacing - or Dopamine 2-10 mcg/kg per minute - or Epinephrine 2-10 mcg/kg per minute - cardiac consult
Просмотров: 122595 HEARTSTART SKILLS Frasco
Welcome to LY Med, where I go over everything you need to know for the USMLE STEP 1, with new videos every day. Follow along with First Aid, or with my notes which can be found here: https://www.dropbox.com/sh/xisbr5u8reifaqk/AAAEWF-Ho2r0OJMooCYN_bG-a?dl=0 Finally some pharmacology! Let's talk about anti-Arrhythmia! There are four classes of anti-Arrhythmia drugs. Two work on your nodal tissue. Let's quickly recap on how nodes depolarize! Hopefully you remember all the little details of the L-ca channels and funny sodium channels. Some new things to know, the more sodium channels you have the quicker your heart rate! This explains how sympathetic and parasympathetic stimulation can increase or decrease heart rate. With this background information in hand, let's talk about some pharm. Class II Beta-blockers: These b-blockers will block the B1 adrenergic receptors of the heart and lower the heart rate and contractility. Class IV: These are your calcium channel blockers. This slows phase 0, the further depolarization of the cell. There are two types, dihydropyridines and non-dihydropyridines. All these work on your SA node as well as your AV node, which prolongs your PR interval and ERP. Now what are the two types of drugs that work on non-nodal tissue? Well before we do that, we'll recap it how it depolarize in the first place. These are tissues like the Purkinje fibers, Bundle of His, and ventricular myocytes. The first class that works here are class I Na sodium channel blockers. When you block sodum, you prolong phase 0. However you have three different classes because they also work on potassium K+ to different degrees. Type 1a prolongs K+ efflux and include drugs like procainamide (known for it's drug induced lupus), as well as quinidine. Ib hasten K+ efflux and is best used post-MI. Lastly you have class Ic which has no effect on potassium. This is contraindicated post-MI. Second class that works on these cells are class III, which work on your K+ mainly. This prolongs your action potential and QT, which predisposes you to long qt syndrome and torsades! You need to know the drug amiodarone, a very toxic drug that can cause thyroiditis, pulmonary fibrosis, and hepatotoxicity. The last drug we'll talk about is adenosine. Adenosine increases potassium efflux and stops your heart. Know some adenosine antagonists like caffeine and theophylline. Done with pharm!
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Created by Bianca Yoo. Watch the next lesson: https://www.khanacademy.org/test-prep/nclex-rn/rn-cardiovascular-diseases/rn-dysrhythmia-and-tachycardia/v/ablation?utm_source=YT&utm_medium=Desc&utm_campaign=Nclex-rn Missed the previous lesson? https://www.khanacademy.org/test-prep/nclex-rn/rn-cardiovascular-diseases/rn-dysrhythmia-and-tachycardia/v/pacemakers?utm_source=YT&utm_medium=Desc&utm_campaign=Nclex-rn NCLEX-RN on Khan Academy: A collection of questions from content covered on the NCLEX-RN. These questions are available under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 United States License (available at http://creativecommons.org/licenses/by-nc-sa/3.0/us/). About Khan Academy: Khan Academy offers practice exercises, instructional videos, and a personalized learning dashboard that empower learners to study at their own pace in and outside of the classroom. We tackle math, science, computer programming, history, art history, economics, and more. Our math missions guide learners from kindergarten to calculus using state-of-the-art, adaptive technology that identifies strengths and learning gaps. We've also partnered with institutions like NASA, The Museum of Modern Art, The California Academy of Sciences, and MIT to offer specialized content. For free. For everyone. Forever. #YouCanLearnAnything Subscribe to Khan Academy’s NCLEX-RN channel: https://www.youtube.com/channel/UCDx5cTeADCvKWgF9x_Qjz3g?sub_confirmation=1 Subscribe to Khan Academy: https://www.youtube.com/subscription_center?add_user=khanacademy
Просмотров: 282543 khanacademymedicine
Subject : Pharmacology Thursday - 12th, December 2013 Contents :- - Pathophysiology of Cardiac Dysrythmia - Phases of Cardiac Action Potential - Classification of Anti-arrythmic Drugs - Quinidine - Lidocaine - Phenytoin - Amiodarone
Просмотров: 6795 Kasr Al-Ainy - 3rd Year (2011-2017) Channel
http://proacls.com - ACLS Certification Training Videos **Get $20 off your certification or recertification with the discount code youtubeacls2017 Epinephrine, commonly known as Adrenaline, is a drug that narrows blood vessels and opens airways in the lungs. These effects can reverse severe low blood pressure. Epinephrine is used in Cardiac arrest arrhythmias such as VF, pulseless VT, Asystole and PEA. It can also be used in symptomatic bradycardia. In addition, Epinephrine is an effective treatment for Anaphylaxis. Epinephrine is available in 1:10,000 or 1:1,000 concentrations. For cardiac arrest, Epinephrine should be delivered IV/IO at 1 mg which is 10 ML of 1:10,000 solution administered every 3 to 5 minutes during resuscitation. For treatment of anaphylactic shock Epinephrine 1:1,000 is given to a 30 kg or greater patient: 0.3 mg IM or subcutaneously. Subscribe to ProTrainings' Youtube Channel! Check out all of ProTrainings' courses: http://www.protrainings.com Like ProTrainings on Facebook: https://www.facebook.com/protrainings Follow ProTrainings on Twitter: https://twitter.com/protrainings Follow ProTrainings on Instagram: http://instagram.com/protrainings
Просмотров: 8967 ProCPR
Grab our free cheatsheet covering the 50 most commonly prescribed medications right here: http://www.NRSNG.com/50meds View the blog post here: https://www.nrsng.com/atropine-atro-pen/ Listen to all the episodes at: https://www.nrsng.com/medmaster-podcast/ Atropine Generic Name: atropine Trade Name: Atro-pen Indication: decreases oral and respiratory secretions, treats sinus bradycardia and heart block, treatment of bronchospasm Action: Atropine is an anticholinergic which means that it inhibits the effects of the parasympathetic nervous system, specifically acetylcholine. This inhibition causes increase in HR, bronchodilation, decreased GI and respiratory secretions. Therapeutic Class: antiarrhythmic Pharmacologic Class: anticholinergic, antimuscarinic Nursing Considerations: avoid in acute hemorrhage, tachycardia, and angle closure glaucoma monitor patient for tachycardia and palpitations may cause urinary retention in elderly patients patients may experience constipation due to slowed GI motility
Просмотров: 27831 NRSNG
Beta blockers for heart disease healthline. Heart rhythm changes (arrhythmias) managing side effects palpitations how are treated? Arrhythmia, the heart can beat too fast, slow, or with an irregular. Beta blockers decrease the heart rate and cardiac output, which lowers blood pressure by blocking effects of adrenalin 21 beta for high pressure; Street drugs such as cocaine, advance can help people whether it has harmful side are often first line medications used in treatment arrhythmias. A url? Q medicalnewstoday articles 173068. A pacemaker also can help a person who has abnormal heart rhythms resume more you need to take certain medicines, such as beta blockers we would like add some specific comments about ventricular arrhythmias. Antiarrhythmics drugs to treat heart disease webmd. Arrhythmias can present as palpitations or with the symptoms of reduced cardiac outflow chest pain, afib patients have a five fold increased risk stroke. Arrhythmia american heart association. Treatments for irregular heartbeats netdoctormodern medicine. Beta blockers in arrhythmias when and where to use? Ncbi. Beta blockers can help to relieve the 'fight or flight' reactions that fuel anxiety 26 webmd helps you understand how antiarrhythmic drugs be used are other types of heart treat arrhythmias, including beta such as metoprolol toprol xl, which reduce for, hypertensionarrhythmiasanxiety symptoms; Propranolol also protect following a attack. Their role has been established in treatment of supraventricular tachycardia (svt) and ventricular tachyarrhythmias (vt). Beta blockers types, side effects, and interactions. 14 besides being used to treat high blood pressure, they're also used to treat angina (chest pain) and or some arrhythmias (abnormal heart rhythms). Prevention & treatment of arrhythmia american heart association. Beta blockers work by making your heart beat more slowly and with less force; They also allow the electrical 1 2002 types of arrhythmias induced drugs vary widely, as do agents obviously, that block beta adrenergic receptors blockers, such administering sodium bicarbonate to induce alkalemia can help rhythm changes (arrhythmias) chemotherapy side effects, causes, symptom walking, swimming, or light aerobic activity you lose weight, be used slow down rate, improve 23 in most people, palpitations not indicate underlying disease, treatment are due an arrhythmia (irregular heartbeat) warrants medical. This can help to reduce blood pressure and alleviate irregular the ability of beta blockers prevent ventricular arrhythmias further emphasizes your doctor will you decide whether taking amiodarone is right for 30 are medications that slow heartbeat. Beta blockers stop the arrhythmia occurring but, more often, are useful for slowing down heart rate digoxin is also commonly prescribed af to help control beta drugs used treat angina, lowering blood pressure, protecting against recurrent attacks and helping people with failure live anyhow, i will see what test shows but am wondering if can lose their knowing exact nature of treatment class ii antiarrhythmic medicines blockers, which work by blocking medicine cause arrhythmias or make your worse doctors clarify type best patient have been extensively in cardiovascular well as digitalis calcium channel do not block accessory amiodarone, prevent recurrence such vts 17 beat slower less forcefully when working. A pacemaker also can help a person who has abnormal heart rhythms resume more you need to take certain medicines, such as beta blockers. They help to regulate and restore disturbances in the heart rhythm. Php&sa u&ved 0ahukewj usxsw43wahwjo5qkhsvlcti4chawcbkwaq&usg afqjcng7mwpcbcacqxg4lsuiw2wdjkxuiq" target "_blank"beta blockers types, side effects, and interactions. Drug cabinet anti arrhythmics british heart foundation. Find the most popular drugs, view ratings, user reviews, and more drugs for treatment of arrhythmias. Beta blockers tiredness, coldness of hands and feet, low blood pressure, nightmares arrhythmia alliance atrial fibrillation association bhf living with 19 can manifest when the heart beats very fast these agents also help prevent cardiotoxicity beta certain 13 tachycardia be observed in persons normal hearts those if fact is a reentrant tachycardia, may, to some extent, decrease frequency are sometimes prescribed control rapid heartbeat there many available, your doctor will evaluate most common type cardiac causes an diagnosed by as premature ventricular since generally well tolerated do not make worse, they Medications for american. Beta blockers to prevent ventricular arrhythmias further emphasizes your doctor will help you decide whether taking amiodarone is right for. Decreasing conduction velocity can help to abolish tachyarrhythmias caused by reentry circuits. Jsp url? Q webcache. Propranolol (beta blocker) uses and side effects anti arrhythmic drugs patient uk. 2&sa u&ved 0ahukewiqrersw43wahugkpqkha7lbb04fbawcbkwaq&usg afqjcnebgfrmkkonuh
Просмотров: 958 BEST HEALTH Answers
Led by John Bielinksi, Jr. PA-C, CME4Life offers a wide variety of CME/CE credit opportunities through live events, online video programs, and take home materials. CME4Life is also the nation’s fastest growing PANCE/PANRE Review Course in the nation! CME Conferences: https://conferences.cme4life.com Shop CME Products: https://www.cme4life.com/shop PA Board Review Conferences - 30 hours of AAPA Category 1 CME Credit Orlando, FL (April 11-14), Nashville, TN (May 23-26), Myrtle Beach, SC (July 24-27), Pensacola, FL (September 12-15), San Antonio, TX (September 26-29), Orlando, FL (October 18-21), Las Vegas, NV (November 7-10), Buffalo, NY (Nov. 30-Dec. 3). Heart of Cardiology Conference - 22 hours of AAPA Category 1 CME Credit Marco Island, FL (April 26-29) IMPACT Emergency Medicine Conferences - 22 hours of AAPA Category 1 CME Credit West Palm Beach, FL (May 11-14), Hilton Head, SC (August 3-6), Park City, UT (December 6-9)
Просмотров: 3581 John Bielinski
http://proacls.com - ACLS Certification Training Videos **Get $20 off your certification or recertification with the discount code youtubeacls2017 The key steps to treating V-Fib are a rapid assessment to confirm cardiac arrest, starting CPR, applying the defibrillator and delivering the first shock as soon as possible. High quality CPR needs to be performed with as few interruptions as possible by giving cycles of 30 compressions at a depth of 2 to 2.4 inches deep at a rate of 100 to 120 per minute followed by 2 breaths. The compressor needs to be changed every 2 minutes to avoid fatigue. After the initial shock an IV or IO needs to be established in order to give medications. The first medication would be epinephrine, 1 mg 1:10,000 IV or IO push every 3-5 minutes. After the initial dose of epinephrine and a second shock is given, you should consider placing an advanced airway with capnography. Remember that once an advanced airway is in place, CPR compressions become continuous at 100 to 120 compressions a minute, and one breath is given every 6 seconds. The next medication to give is amiodarone, 300 mg via rapid IV or IO push. A 150 mg dose of Amiodarone may repeated one time in 3-5 minutes. Subscribe to ProTrainings' Youtube Channel! Check out all of ProTrainings' courses: http://www.protrainings.com Like ProTrainings on Facebook: https://www.facebook.com/protrainings Follow ProTrainings on Twitter: https://twitter.com/protrainings Follow ProTrainings on Instagram: http://instagram.com/protrainings
Просмотров: 22211 ProCPR
As part of the Medical Music project - this song was one of the 5 songs on the M.D.M.C.'s demo album: "One Third Of One Percent... the EP" from 2010. After which this song was one of 2 out of 5 tracks that were picked up by Kaplan Medical's professor of pathology, John Barone, M.D. and is now featured in a collective work of 11 songs in the album "Barone Medical Hip Hop Project. Coming soon. www.baronerocks.com www.themdmc.com Anti-Arrhythmic Drug Sickness Lyrics H Class 1 – Sodium channel blockers Class 2 – Gotta be the Beta Blockers Class 3 – Like Sotalol and Amiodarone Class 4 – Calcium Channel Blockers Class 1 – Sodium channel blockers Class 2 – Gotta be the Beta Blockers Class 3 – Potassium block like Amiodarone Class 4 – Calcium Channel Blockers V1 Quinidine and Procainamide both Class Ia Blocks activated sodium influx one way Pro-cain- amide - making the runway Class I one day - Class III another day Another way - to say it, it's acetylated in the liver prolongs the refractory period Got some serious side effects – anti-histones Sort of like Lupus - SLE-like Syndrome Diso – pyramide – is not really perfect cause of side effects that are anti-cholinergic Quinidine - slowing the rise of phase Zero Prolongs refractory period as well ditto Toxicities - includes a wide QRS The twisting of points – Torsades – you are correct! ANS side effects – we call it Cinchonism Medicine and Music – we call it synergism Fight the pain - Class Ib - is lidocaine Decreased duration of the action potential For ventricular arrhythmias post-MI or cardiac surgery for abnormal re-entry It'll take me a century - to get all these words But if I know one thing - Lidocaine affects the nerves 1a lengthens – 1b shortens up the curve you know it’s too much when a patient’s speech is slurred. Let’s go! Hook V2 Propofanone – flecainide – I’m in the zone (1c) Memorize with repetition – etch it in stone (1c) Conduction in cardiac tissue is marked slow Not too excited – got a higher threshold potential But actual, doesn’t effect the action potential Or its duration – understand it – its all mental 1b’s the best post MI – like Tocainide Most pro-arrhythmic is 1C – like Flecainide Class II – keep up now don’t let me pass you Beta-blockade – its like an auditory tattoo Decreases heart rate and con-tractility Prolongs AV conduction – decreases automaticity Automatically – slowing the pacemaker current Decreasing the slope of phase 4 – less of a burden When you treating SVTs – you can’t be uncertain Glucagon to treat its overdose – “Don’t forget to treat the person” Class III – amiodarone – bertylium If you don’t practice than you the one who’s the silly one Dofetilide – ibutilide – sotalol – the protocol Potassium channel blockers – last resort – used overall Amiodarone slows the slope of phase 3 Long half life – you may see toxicities Like papa smurf – blue pigments – restricted lung disease Check the TFTs – PFTs – and LFTs please Hook Bridge Class 1 and 3 affects the muscles of the ventricles 2 and 4 affect the tissue of the AV node 1 and 3 affects the muscles of the ventricles 2 and 4 affect the tissue of the AV node 1 and 3 affects the muscles of the ventricles 2 and 4 affect the tissue of the AV node 1 and 3 affects the muscles of the ventricles 2 and 4 affect the SA and the AV node V3 Yo – lyrical fitness – witness the antiarrhythmic sickness The main objective is to get into heart’s business quickly Slowing it down – making it re-fractory 4 main classes and then there’s one with no category In holy matrimony – how I’m married to this laboratory On the Barony Pony – all the others are mad boring It’s that important – fully knowing all that is mandatory All these drugs are also proarrhythmics, man – end of story Holy macro foley – keep playing this – don’t fast forward Rewind to remind – reinforce and ask for it Class 4 – Calcium channel blockers – that’s all Indicated for SVTs – here’s a crash course Verapamil – Diltiazam – but not nifidepine Never seen an SVT flat line like Adenosine No Class – like magnesium for torsades Ob/gyn – ecclamplsia – prematurity – tocolysis So much knowledge for all you scholars – come on follow it! Hook Bridge Copyright © 2010, Pramanik Bharadwaj, MDMC Copyright © 2011 - 2018. Pramanik Bharadwaj, MDMC & John Barone, MD. All Rights Reserved. www.baronerocks.com www.themdmc.com
Просмотров: 86503 Pramänik MDMC
Pulseless VT is treated the same way as Ventricular Fibrillation would in AHA ACLS 2016 Guidelines. CPR with immediate Defibrillatory shock is recommended. Biphasic Defibrillators: 120 - 200 Joules or recommended. Monophasic Defibrillators: 360 J. Other secondary interventions can be started if IV/IO access has been established. Medications that can be given with pVT given during compressions: - Epinephrine 1mg IVP/IO (1:10,000) every 3-5 mins. - For refractory pVT: Amiodarone 300mg IVP/IO for the 1st dose; 150mg IVP/IO for the 2nd dose - For possible hypokalemia: Lidocaine 1-1.5mg/kg IVP/IO 1st dose; 0.5-0.75mg/kg 2nd dose Based on AHA ACLS 2015 Guidelines
Просмотров: 60011 HEARTSTART SKILLS Frasco
Grab our free cheatsheet covering the 50 most commonly prescribed medications right here: http://NRSNG.com/50meds Listen to all the episodes at: https://www.nrsng.com/medmaster-podcast/ View the blog post here: https://www.nrsng.com/diltiazem-cardizem-antianginal/ Diltiazem Generic Name: diltiazem Trade Name: Cardizem Indication: hypertension, angina, SVT, a-fib, aflutter Action: inhibits calcium transport resulting in inhibition of excitation and contraction, leads to depression of AV and SA node leading to decreased HR, leads to vasodilatation and decreased blood pressure. Therapeutic Class: antianginals, antiarrhythmics, antihypertensive Pharmacologic Class: Ca Channel Blocker (Bezothiazepine) Nursing Considerations: contraindicated in 2nd and 3rd AV block may cause arrhythmias, CHF, bradycardia, peripheral edema, gingival hyperplasia increases digoxin levels don't drink grapefruit juice assess for signs of CHF monitor EKG continuously tell patient to change positions slowly monitor serum potassium instruct pt on how to take blood pressure
Просмотров: 19828 NRSNG
A review of the literature supporting and refuting the utility of common drugs used in ACLS. Specific topics include: Epinephrine, Amiodarone, and Bicarb. If you code patients and you use these meds, you should know where ACLS recs come from, the data supporting these recs, and where the holes are. This lecture is a rapid review of this literature. Disclaimer: The information posted is not intended as medical advice or an endorsement of any product, procedure, company or opinion. Before acting upon any posting or information on this site, obtain medical advice from your healthcare provider.
Просмотров: 51198 Temple EM
Atropine is an anticholinergic and an antimuscarinic that's commonly administered to patients experiencing bradycardia. Learn all about the drug class, indications and contraindications, mechanism of action, and how to administer it. My website http://www.thepracticalparamedic.com/ Let's be Facebook Friends https://www.facebook.com/ThePracticalParamedic/?ref=bookmarks Resources https://acls-algorithms.com/bradycardia/ Atropine http://www.healthline.com/health/anticholinergics#About1 Antimuscarinic Drugs https://www.nursingtimes.net/antimuscarinic-drugs/200030.article Organophosphate Toxicity Clinical Presentation http://emedicine.medscape.com/article/167726-clinical Antimuscarinics (Muscarinic Antagonists) http://tmedweb.tulane.edu/pharmwiki/doku.php/antimuscarinics My local protocols.
Просмотров: 19649 The Practical Paramedic
Wolff Parkinson White Syndrome (WPW) explained clearly by Dr. Seheult of https://www.medcram.com Understand WPW ECG findings, pathophysiology, symptoms, treatment options, common pitfalls, and more. WPW syndrome can cause life-threatening arrhythmias via accessory pathways in the heart. Learn the key EKG findings of Wolff Parkinson White pattern as well as treatment options for WPW. Free quiz (on this video) at the MedCram website: https://www.medcram.com/courses/ekg-ecg-interpretation-explained-clearly This complete ECG/EKG interpretation course provides: - The physiology of the heart - EKG leads and vectors - Leads and EKG paper - The ECG tracing - EKG waves, complexes, and intervals (p waves, QRS complexes, PR interval etc.) - Axis on EKG and precordial leads - The autonomic nervous system and the heart - Heart rate and automaticity on the ECG - The R to R interval - Rhythm, arrhythmias, and escape rhythms, - Premature beats and pauses on EKG - Bigeminy, trigeminy, and tachyarrhythmias - V-tach and torsades de points - Atrial and ventricular flutter - WPW syndrome (Wolff-Parkinson-White) and WPW pattern. - Atrial fibrillation and ventricular fibrillation on ECG - Heart blocks and escape rhythms (1st, 2nd, and 3rd-degree heart block) - Bundle branch blocks, hemiblocks, and fascicular blocks - Hypertrophy (LVH) and atrial enlargement - COPD, PE, Hyperkalemia, Digoxin and the EKG - How to systematically read an EKG (and what a normal ECG looks like) - Many practice EKG strips (that Dr. Seheult interprets step by step) - EKG quizzes follow each video. Visit https://www.MedCram.com for this entire course and over 100 free lectures. This is the home for ALL MedCram.com medical videos (many medical videos, medical lectures, and quizzes are not on YouTube). Speaker: Roger Seheult, MD Co-Founder of MedCram.com (https://www.medcram.com) Clinical and Exam Preparation Instructor Board Certified in Internal Medicine, Pulmonary Disease, Critical Care, and Sleep Medicine. MedCram: Medical education topics explained clearly including: Respiratory lectures such as Asthma and COPD. Renal lectures on Acute Renal Failure and Adrenal Gland. Internal medicine videos on Oxygen Hemoglobin Dissociation Curve and Medical Acid Base. A growing library on critical care topics such as Shock, Diabetic Ketoacidosis (DKA), and Mechanical Ventilation. Cardiology videos on Hypertension, ECG / EKG Interpretation, and heart failure. VQ Mismatch and Hyponatremia lectures have been popular among medical students and physicians. The Pulmonary Function Tests (PFTs) videos and Ventilator associated pneumonia bundles and lectures have been particularly popular with RTs. NPs and PAs have given great feedback on Pneumonia Treatment and Liver Function Tests among many others. Many nursing students have found the Asthma and shock lectures very helpful. Subscribe to the official MedCram.com YouTube Channel: https://www.youtube.com/subscription_center?add_user=medcramvideos Recommended Audience - medical professionals and medical students: including physicians, nurse practitioners, physician assistants, nurses, respiratory therapists, EMT and paramedics, and many others. Review and test prep for USMLE, MCAT, PANCE, NCLEX, NAPLEX, NBDE, RN, RT, MD, DO, PA, NP school and board examinations. More from MedCram.com medical videos: MedCram Website: https://www.medcram.com Facebook: https://www.facebook.com/MedCram Google+: https://plus.google.com/u/1/+Medcram Twitter: https://twitter.com/MedCramVideos Produced by Kyle Allred PA-C Please note: MedCram medical videos, medical lectures, medical illustrations, and medical animations are for medical education and exam preparation purposes, and not intended to replace recommendations by your doctor or health care provider.
Просмотров: 20674 MedCram - Medical Lectures Explained CLEARLY
Nursing educator Michele G. Kunz discusses the new AHA ECC changes for 2011. Here she discusses cardiac arrest algorithms, and the drugs and treatments for this. Some of the subjects covered are antiarrhythmics, amiodarone, asystole, cardioversion, the reversible causes of death (Hs and Ts), and vasopressin. (The next AHA and ECC guidelines changes are expected to be out in 2015.) See all of Michele's publications at http://EmpowermentEducation.com See more about Michele at http://MicheleKunz.com See Michele's nursing blog at http://TheNurseEducator.com Please share this video on Facebook, LinkedIn, and Google+. Thank you very much for your help. Please subscribe to my YouTube channel, and connect with me on Google+. Thank you very much. Send your requests and ideas for videos you would like me to make.
Просмотров: 34293 michelekunz
A geeky rendition of Nicki Minaj's "Super Bass," created for my UCSD BIPN105 Student Project (Sciatic Nerve experiment testing Verapamil, Amiodarone, and high [Ca2+]. ==== Lyrics: This one's for the drug Verapamil The doc gives it out when you're feelin' ill When you feel that your heart be actin' up It'll find ion channels and plug 'em up The ion, Ca2+, wants to flow in the cell To depolarize the heart when all is well But Verapamil acts as a channel blocker Just beats out the Ca2+ like a big fat bouncer Your heart's goin' fast, fast; it's never gonna last, last So you took the drug, drug, took it with a shrug, shrug Then your heart started slowin' down Doc said that's right, you're on the rebound I said, that's cool but what about a nerve? I mean, how would it work, would the pathway preserve? No Ca2+ channels so what's up with that Is it cool if I stick my nerve in a Verapamil bath? No its not, no its not It's gonna block the potassium channel like a dried snot Now the cell can't really repolarize So the action potential's gonna grow lengthwise BOY YOU GOT MY HEARTBEAT RUNNIN' AWAY BEATING LIKE A DRUM AND ITS RUNNIN' ASTRAY CAN'T YOU HEAR THAT BOOM BADOOM BOOM BOOM BADOOM BOOM BASS? (Its arrhythmia) BOOM BADOOM BOOM BOOM BADOOM BOOM BASS ITS ARRHYTHMIA Boom, badoom, boom Boom, badoom, boom, he's got arrythmia Boom, badoom, boom Boom, badoom, boom, he's got arrythmia This one is for the drug Amiodarone This one won't stop at potassium alone It can block K+ channels, it can block Na2+ Be it heart or nerve, it works the same way Like Verapamil this drug is used for arrhythmia Depolarization slows like in a coma Repolarization ain't gonna work, and when it don't work The AP won't take off, off, uh Excuse me, this is really awesome But what about high extracellular calcium I mean, sigh, I really like milk If I put my nerve in it will I start to feel ill? Yes you are, yes you are Those calcium ions are way too large They're gonna block up, they're gonna get stuck in the sodium channels and wreak havoc! Now you know what all these drug treatments do Prolonging those CAPs in nervous tissue We can't hear that boom, badoom, boom boom, badoom boom bass Our hearts won't race Cause now, now we know what to take, take Yeah what to take
Просмотров: 3466 cookiexguru
Tachycardia rapid algorithm review by the ACLS Certification Institute. To view more videos, check out the ACLS Certification Institute at http://www.aclscertification.com or subscribe to our channel at https://www.youtube.com/user/aclsinstitute.
Просмотров: 97504 ACLS Certification Institute
Table of Contents: 00:10 - Normal Conduction 01:48 - 01:49 - Sinoatrial Node (SA Node) 02:14 - Atrioventricular Node (AV Node) 02:32 - The QRS Complex 02:45 - The T Wave 03:10 - Waves, Intervals and Segments (Oh My!) 06:19 - Determining the Rate (Regular Rhythm) 06:28 - Method Two 06:29 - Determining the Rate (Regular Rhythm) 07:41 - Method Two 08:41 - Method Three 09:01 - Steps to Interpreting Rhythm 09:48 - Most Common Dysrhythmias 11:20 - Sinus Tachycardia and Sinus Bradycardia 12:23 - Premature Atrial Contraction 13:40 - Premature Ventricular Contraction 14:47 - Sinus Tachycardia and Sinus Bradycardia 14:47 - Premature Atrial Contraction 14:48 - Premature Ventricular Contraction 14:48 - Supraventricular Tachycardia 14:48 - Ventricular Tachycardia 14:49 - Amiodarone(Cordarone) 14:49 - IV Amiodarone 14:49 - Sivaram CA, Beckman KJ. N Engl J Med 1997;337:1813-1813. 14:50 - IV Amiodarone 14:50 - Diltiazem (Cardizem) 14:50 - Diltiazem IV 14:50 - Devices 14:50 - Pacemakers 14:50 - Heart Block 14:51 - What Are the Types of Pacemakers? 14:51 - NASPE Nomenclature 14:51 - Dual Chamber Pacemaker 14:51 - 14:51 - Single Chamber Pacemaker 14:52 - Wenkebach Phenomenon 14:52 - Devices 14:52 - Diltiazem (Cardizem) 14:52 - IV Amiodarone 14:52 - Sivaram CA, Beckman KJ. N Engl J Med 1997;337:1813-1813. 14:52 - Amiodarone(Cordarone) 14:53 - Sivaram CA, Beckman KJ. N Engl J Med 1997;337:1813-1813. 14:53 - Antiarrhythmic Drugs 14:53 - Supraventricular Tachycardia 14:53 - Premature Ventricular Contraction 14:53 - Sinus Tachycardia and Sinus Bradycardia 14:53 - Most Common Dysrhythmias 14:53 - Steps to Interpreting Rhythm 14:54 - Most Common Dysrhythmias 14:55 - Sinus Tachycardia and Sinus Bradycardia 14:55 - Premature Atrial Contraction 14:55 - Premature Ventricular Contraction 15:37 - Atrial Fibrillation 17:27 - Supraventricular Tachycardia 18:56 - Ventricular Tachycardia 19:13 - Supraventricular Tachycardia 19:44 - Ventricular Tachycardia 20:04 - Antiarrhythmic Drugs 21:59 - Sivaram CA, Beckman KJ. N Engl J Med 1997;337:1813-1813. 22:00 - Amiodarone(Cordarone) 22:01 - Antiarrhythmic Drugs 27:09 - Amiodarone(Cordarone) 29:42 - Sivaram CA, Beckman KJ. N Engl J Med 1997;337:1813-1813. 30:20 - Chan TC, Jhanji V. N Engl J Med 2015;372:1656-1656. 31:00 - IV Amiodarone 32:19 - PO Amiodarone 32:27 - IV Amiodarone 32:28 - PO Amiodarone 32:56 - Diltiazem (Cardizem) 35:21 - Diltiazem IV 36:18 - Devices 36:59 - Pacemakers 37:35 - Rhythms Treated with Pacing 38:30 - Heart Block 39:57 - Wenkebach Phenomenon 40:34 - Mobitz II 40:54 - NASPE Nomenclature 40:54 - Dual Chamber Pacemaker 40:55 - Single Chamber Pacemaker 40:55 - Let’s Talk About These 40:55 - NASPE Nomenclature 40:55 - What Are the Types of Pacemakers? 40:56 - Mobitz II 40:57 - What Are the Types of Pacemakers? 41:15 - NASPE Nomenclature 43:06 - Single Chamber Pacemaker 45:33 - Dual Chamber Pacemaker 47:24 - 47:59 - Pacemaker Hardware 48:34 - Pacemaker Programming 49:06 - Pacemaker Problems 51:49 - Tachyarrhythmias 52:08 - What are the Tachyarrhythmias? 52:10 - No one ever died from acute ventricular fibrillation. They only die when it becomes chronic. 52:10 - Tachyarrhythmias 52:34 - No one ever died from acute ventricular fibrillation. They only die when it becomes chronic. 52:34 - What are the Tachyarrhythmias? 53:11 - What Makes Tachyarrhythmias Dangerous? 53:50 - Treatment of Tachycardia 54:36 - Classifying Tachycardia 55:47 - Differentiating Wide Complex Tachycardias 57:07 - Supraventricular Tachycardia 57:08 - Differentiating Wide Complex Tachycardias 57:15 - Supraventricular Tachycardia 57:20 - Supraventricular Tachycardia 57:40 - AF in Presence of WPW 57:42 - Wolf Parkinson WhitePre-excitation 57:42 - Supraventricular Tachycardia 58:05 - Wolf Parkinson WhitePre-excitation 58:39 - AF in Presence of WPW 58:44 - Wolf Parkinson WhitePre-excitation 59:12 - AF in Presence of WPW 59:34 - Treating SVT 01:00:33 - Ablation 01:01:30 - Ventricular Tachycardia 01:01:33 - Ventricular Tachycardia 01:02:21 - Ventricular Tachycardia 01:02:44 - Ventricular Tachycardia 01:02:53 - Acute Treatment 01:02:59 - Chronic Treatment of VT 01:03:00 - Electrophysiology Study 01:03:00 - Internal Cardioverter Defibrillator 01:03:00 - 01:03:01 - Internal Cardioverter Defibrillator 01:03:01 - Electrophysiology Study 01:03:01 - The Workup 01:03:01 - KNOW THE LV FUNCTION! 01:03:02 - Chronic Treatment of VT 01:03:02 - Acute Treatment 01:03:03 - Ventricular Tachycardia 01:03:03 - Acute Treatment 01:03:24 - Chronic Treatment of VT 01:03:28 - KNOW THE LV FUNCTION! 01:04:02 - The Workup 01:04:12 - KNOW THE LV FUNCTION! 01:04:12 - Chronic Treatment of VT 01:04:14 - KNOW THE LV FUNCTION! 01:04:14 - The Workup 01:04:52 - Electrophysiology Study 01:06:21 - Internal Cardioverter Defibrillator 01:06:50 - 01:07:35 - Defibrillator Problems 01:08:26 - Some Specific Examples 01:08:29 - Atrial Fibrillation 01:08:43 - Treatment of Atrial Fibrillation 01:10:50 - Atrial Flutter 01:11:10 - Mr. Tachy
Просмотров: 1722 Paul Logan
http://proacls.com - ACLS Certification Training Videos - This video is the latest version based on the latest 2017 guideline updates. **Get $20 off your certification or recertification with the discount code youtubeacls2017 The key steps to treating V-Fib are a rapid assessment to confirm cardiac arrest, starting CPR, applying the defibrillator and delivering the first shock as soon as possible. High quality CPR needs to be performed with as few interruptions as possible by giving cycles of 30 compressions at a depth of 2 to 2.4 inches deep at a rate of 100 to 120 per minute followed by 2 breaths. The compressor needs to be changed every 2 minutes to avoid fatigue. After the initial shock an IV or IO needs to be established in order to give medications. The first medication would be epinephrine, 1 mg 1:10,000 IV or IO push every 3-5 minutes. After the initial dose of epinephrine and a second shock is given, you should consider placing an advanced airway with capnography. Remember that once an advanced airway is in place, CPR compressions become continuous at 100 to 120 compressions a minute, and one breath is given every 6 seconds. The next medication to give is amiodarone, 300 mg via rapid IV or IO push. A 150 mg dose of Amiodarone may repeated one time in 3-5 minutes. Subscribe to ProTrainings' Youtube Channel! Check out all of ProTrainings' courses: http://www.protrainings.com Like ProTrainings on Facebook: https://www.facebook.com/protrainings Follow ProTrainings on Twitter: https://twitter.com/protrainings Follow ProTrainings on Instagram: http://instagram.com/protrainings
Просмотров: 1835 ProCPR
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.
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http://proacls.com - ACLS Certification Training Videos **Get $20 off your certification or recertification with the discount code youtubeacls2017 Adenosine is indicated for narrow-complex supraventricular tachycardia or SVT, unstable narrow-complex reentry tachycardia, regular and monomorphic wide-complex tachycardia, and as a diagnostic maneuver for stable narrow-complex SVT. Adenosine is effective in terminating narrow complex SVT due to reentry involving the AV node or Sinus node. It’s important to note that Adenosine does not convert atrial fibrillation, atrial flutter or ventricular Tachycardia known as V-tach. The initial bolus of 6mg is given rapidly over 1 to 3 seconds followed by a normal saline bolus of 20ml. A second dose of 12mg can be given in 1 to 2 minutes if needed. Subscribe to ProTrainings' Youtube Channel! Check out all of ProTrainings' courses: http://www.protrainings.com Like ProTrainings on Facebook: https://www.facebook.com/protrainings Follow ProTrainings on Twitter: https://twitter.com/protrainings Follow ProTrainings on Instagram: http://instagram.com/protrainings
Просмотров: 3724 ProCPR
http://proacls.com - ACLS Certification Training Videos **Get $20 off your certification or recertification with the discount code youtubeacls2017 When a patient has no pulse, no breathing, and shows a flat line on the ECG monitor, asystole is present. CPR needs to be initiated first. Asystole is not a shockable rhythm and treatment for Asystole involves high quality CPR, airway management, IV or IO therapy, and medication therapy which is 1mg epinephrine 1:10,000 every 3-5 minutes rapid IV or IO push. Remember, CPR should not be stopped for the delivery of medications. Unless there are special circumstances like hypothermia or drug overdose, prolonged resuscitative efforts beyond 20 minutes are usually unnecessary and futile. The team leader may consider stopping resuscitation if ETCo2 is less than 10 after 20 minutes of high quality CPR and all treatments have been exhausted. Subscribe to ProTrainings' Youtube Channel! Check out all of ProTrainings' courses: http://www.protrainings.com Like ProTrainings on Facebook: https://www.facebook.com/protrainings Follow ProTrainings on Twitter: https://twitter.com/protrainings Follow ProTrainings on Instagram: http://instagram.com/protrainings
Просмотров: 6065 ProCPR
he ECG master, Amal Mattu (@amalmattu), wowed the Essentials 2015 crowd with his practice-changing ECG pearl to catch STEMIs before they happen, looking at only ONE lead! https://www.essentialsofem.com/course/2015
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The big baddie, asystole. It's reassuring to know we ALL end up in asystole sooner or later, but let's hope no time soon.
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