EMS Medical Control Rounds Feb 9, 2012

1. EMS Medical Control RoundsFeb 9, 2012 Brought to you by Anna-Jaques Hospital Domenic Martinello, MD And Brenda Painchaud

2. Agenda • Old Business • New Business • Case 1 • Didactic Portion • Closing Remarks

3. Old Business • Multiple new policies and protocols in regard to transfer of two special patients have been successfully implemented • Anna-Jaques currently in process of securing another ACS verification for its Level III Trauma Center designation • Other old business?

4. New Business • Welcome to 2012 • According to the Myan calendar none of this will matter after December 21, 2012. • But it matters now! • New EKG exam will be out soon • Required to maintain your organizations relationship with AJH • This year will be shorter, multiple choice exam to help decrease the time it takes for you to complete (and for me to grade!) • New protocols from the state will be enacted soon, keep an eye out for them • Anyone have any other new business?

5. For Compliance… • All lectures must have clearly stated goals. • Therefore, Goals of this lecture: • I Teach Something • You Learn Something • We all get better at what we do

6. So… without further adieu Lets talk about…

7. Case 1 • Paramedic unit dispatched to private residence for a 65 year old male with syncope • Patient awake and alert per the dispatch and has no complaints at this time • On arrival patient and wife are in the living room, patient is sitting on couch in no distress.

8. History • You arrive and patient is communicating without difficulty • Patient has been having one week of intermittently feeling tired, weak, with decreased exercise tolerance • No medication changes recently, pacemaker interrogated several weeks ago without any problems noted (patient has several years of battery life left) • Medical history: MI age 55, family history of MI, former smoker. PPM/AICD placed for sick-sinus syndrome.

9. History (2) • Patients medications include lisinopril, lasix, spiriva, potassium, multivitamin, plavix, aspirin, albuterol (and PRN combivent) • None of these medications recently changed or added (no recent meds removed) • Patient states has been well until past week (believes he has “the flu”)

10. Physical Exam • Age appropriate adult male sitting on chair • Examination of the HEENT system is normal • Auscultation of lungs show very faint crackles at bases • Heart sounds show increased rate, no murmur • Abdomen soft, non-tender, no masses • Extremity exam is normal, no oedema • Skin is pink, warm, dry. No bruising or other findings • Neuro exam is unremarkable • VS: BP 110/68; HR 130 (regular); RR 12; O2 100%

11. Based on this… What do you do?

12. Rhythm Strip • As your partner is starting an IV, your initial rhythm strip is as follows:

13. After a change of trousers… • Patient was noted as having stable sustained monomorphic Ventricular Tachycardia • Pads were applied • Amiodarone administered • Patient’s defibrillator has occasional firing with this rhythm, often with short periods of termination • Patient had no prolonged termination of rhythm despite these interventions

14. Further Care • Patient arrived, second dose of amiodarone started • Followed by infusion • Lidocaine administered • No effect except for short terminations • AICD likely ran out of charge from firing as patient remained in VT without any further shocks • Defibrillation attempts began and patient required at least 20 defibrillations during ED stay and transfer to tertiary care • Patient provided procainamide at tertiary hospital where rhythm resolved • Patient suffered no long term consequences of his dysrhythmia

15. We all love a happy ending  Lets discuss the interesting pathophysiology of ventricular tachydysrhythmias!

16. Quick Terminology Primer • Fusion Beats • Combination of beats originating in the atria and following the His-Purkinje system which meets with a ventricular beat causing a fusion tracing of both. • Should appear unique to other beats • Capture Beat • Occasionally the atria conducts an impulse that generates a normal cardiac cycle without meeting a ventricular ectopic beat, thus, you may see a normal beat amidst VT • A-V dissociation • Loss of coordination between the atria and ventricles in which the ventricular pacemaker(s) do not wait for impulses from the atria to fire. Synchronicity is lost.

17. Fusion and Capture Beats • Often see both!

18. So… What are Ventricular Tachydysrhythmias?

19. Ventricular Tachydysrhythmiasare BAD…

20. But what are they? • A series of rhythm disturbances which are unified by a rapid heart rate which is focused in the ventricle • Are wide complex (like all ventricular rhythms) • They must have a rate greater than 100 to be considered a tachydysrhythmia • QRS wider than 100ms and MUST have AV dissociation • May have fusion and/or capture beats • Fall essentially into 2 types: • Monomorphic Ventricular Tachycardia (all beats look the same) • Polymorphic Ventricular Tachycardia (different kinds of beats) • Torsades de pointes is a special type of polymorphic VT • Ventricular Fibrillation is essentially a subset of polymorphic VT

21. Symptoms of VT • Weakness • Fatigue • Shortness of breath and dyspnea on exertion • Syncope or near-syncope • Palpitations • Chest pain • Dizziness • Death

22. Monomorphic VT • Typically just referred to as VT • Has uniform appearance on EKG • May be tolerated for a period of time, especially in otherwise healthy people • Causes extreme oxygen and nutrient demand by the heart • Can not be met with diseases such as CAD • Sometimes self terminates (non-sustained VT)

23. Polymorphic VT • 2 Flavours • Ventricular Fibrillation (VF) • Torsades de Pointes (TdP) • Ventricular Fibrillation is, by its nature, a chaotic, nonperfusing rhythm in which many ectopic foci of the ventricle fire in rapid succession and do not generate a coordinated contraction • Is a common fatal pathway of other dysrhythmias • Never spontaneously resolves

24. Polymorphic VT (Part 2) • TdP • A unique polymorphic VT in which the axis of electrical conduction changes over time, typically 180 degrees • Has a very unique appearance, and is very rare

25. Now that we know what they look like… what causes them? • Short list of problems can cause these life threatening dysrhythmias • Structural heart disease • Coronary artery disease • Scarring from prior MI • Ventricular hypertrophy • Acute conditions • Myocardial infarction • Sympathetic induced polymorphic VT • Seen often with cocaine use • Medications • Electrolytes • Potassium and Magnesium most common • Rare disorders • Too many to list, but Right Ventricular Dysplasia, long QT, Brugada syndrome, and HOCM (through the mechanism of ventricular hypertrophy)

26. Structural Heart Disease • VT caused by structural heart disease is by far the most common cause • Is the end result of the breakdown or damage to the conducting system • May take place years after the initial hypoxic insult • Scarring can cause insulated groups of cells which can act as a re-entry circuit that can predispose to VT • Re-entry VT is typically monomorphic

27. Structural Heart Disease (2) • Right Ventricular Dysplasia • Rare condition that is poorly understood • Mostly in adolescent males • Myocardium replaced by fatty and/or fibrous material • Is another cause of sudden death in young (otherwise healthy) adults • symptoms: syncope, fatigue, sudden death

28. Medications and Long QT • ANY medication that can prolong the QT interval can cause VT • Especially polymorphic VT (TdP) • Common drugs: • Almost any antiarrhythmic (ironic?) • Fluroquinolone antibiotics • Antipsychotics / antiemetics (droperidol, Haldol, prochlorperazine, promethazine) • Many many more • Hereditary forms of long QT are now widely recognized

29. Sympathetic Induced PVT • Unusual cause of VT but should be discussed • Often seen in cocaine users • Cocaine sensitizes the ventricular myocardium’s adrenergic and beta receptors • Cocaine also poisons the sodium pumps to an extent • Usually in the context of fleeing from law enforcement • Increased levels of adrenaline and noradrenaline (epinephrine and norepinephrine) precipitate sudden dysrhythmia • Usually VF

30. Rare Conditions of Importance • Brugada • HOCM

31. Brugada Syndrome • Genetic disease with classic EKG presentation • Often causes sudden, unexpected, cardiac death via VF arrest • Most common cause of sudden death in young males in Thailand and Laos • Autosomal Dominant inheritance pattern • Genetic variation of a single sodium channel • Causes repolarization abnormalities (thus the classic EKG) • RBBB with J-point elevation and downsloping of the ST segment • See next slide • Treatment is placement of AICD

32. Brugada EKG • Note leads V1 –V3 especially

33. Treatment of Ventricular Tachydysrhythmias • Monomorphic VT • Stable • Unstable • VF • Torsades • WPW Wide Complex SVT

34. Tx of STABLE Monomorphic VT • Some VT episodes may be stable and relatively well tolerated • Normal BP • No signs of shock • Awake and alert • First line treatment is currently Amiodarone (med control option of Lidocaine) • Consideration of adenosine now provided to determine nature of arrhythmia • Synchronized cardioversion • Please premedicate your patients!

35. Tx: Unstable monomorphic VT • At first sign of instability you MUST consider cardioversion as your initial treatment • NOTE: If there is no pulse you treat per the VF guidelines (which will follow on the next slide) • DO NOT DELAY CARDIOVERSION • You may end up treating VF or Asystole if you do • EARLY CARDIOVERSION SAVES LIVES • Do not forget the “sync” button! • Pain management is appropriate if IV has already been established • Use fentanyl • DO NOT DELAY CARDIOVERSION FOR IV PLACEMENT!

36. Tx: VF (and pulseless VT) • “At a cardiac arrest the first procedure is to take your own pulse!” • Samuel Shem – The House Of God • (if you haven't read it, you should!) • Immediately initiate ABC therapy • EARLY CARDIOVERSION GIVES YOU THE BEST CHANCE TO RESTORE PERFUSING RHYTHM! • The longer the heart and brain are without blood flow the worse the outcome • Begin CPR immediately • Intubation and IV access are optional • Consider IO use and LMA to save time! • If there is no pulse, there is no sync! Defibrillate! • Drugs come later, and are available in your algorithms but are usually combinations of epinephrine and amiodarone (or lidocaine)

37. Tx: Torsades de Pointes (TdP) • Is a special polymorphic VT • May or may not have a pulse • No Pulse: Start CPR, defibrillate, give Magnesium 1-2g IV • Pulse: IV access give Magnesium 1-2g IV • Consider cardioversion (sync If possible!) or overdrive pacing • Sometimes may self terminate • Class Ia drugs are CONTRAINDICATED • Lidocaine (IIa) only has temporary benefit • Overdrive pacing can treat bradycardia dependant torsades, it overrides the affected ventricles and may restore rhythm; isoproterinol is also used in the hospital

38. Tx: WPW SVT • Hard to diagnose without history • Accessory AV pathway through Mahaim Fibers • May look like VT! • First step in STABLE is adenosine (its nice that its OK to use in VT now, and this was THE reason for making that change!) • May break WPW-SVT (which can be ORT or ART) • Amiodarone is indicated for this purpose (not well studied) • Procainamide is the drug of choice • Unstable patients require immediate cardioversion • Be ready for VF, it is more likely than with other rhythms

39. Cardioversion/Defibrillation (aka “Edison Medicine”) • Highly underutilized treatment • There is a culture of fear around electrical cardioversion yet it is used safely every day in hospitals across the country • Important to remember: • Likely safer than most antidysrhythmic drugs • Faster than drugs • Think about sync • If there is a pulse, there is a sync • If no pulse, no sync • MANAGE PAIN (and provide sedation if able) • If time permits

40. Antidysrhythmic Medications • Classes (Singh Vaughan Williams Classification) • Class I • IA • IB • IC • Class II • Class III • Class IV

41. Class I • All class I agents are sodium channel blockers • Sometimes called “fast channel blockers” • “a” drugs have intermediate association/dissociation with cardiac sodium receptors; also tend to widen the QRS complex • Quinidine, Procainamide • “b” drugs have fast association/dissociation and do not affect the QRS complex • Lidocaine, Phenytoin, Tocainide, • “c” drugs have slow association/dissociation and may affect QRS • Flecanide, Propafenone

42. Class I (part 2) • Ia drugs • Used for ventricular dysrhythmia • Prevention of atrial fibrillation • Procainamide is the drug of choice for WPW syndrome induced tachydysrhythmias • Ib drugs • Used mostly for VT and Afib, lidocaine used to be used peri-MI for prevention of dysrhythmia, but often induced asystole • Ic drugs • Prevention and treatment of paroxysmal atrial fibrillation (often called “pill in the pocket therapy”) • Can also be used for dysrhythmias secondary to abnormal conduction systems

43. Class II • Beta Blockers • Block effects of epinephrine and norepinephrine on the Beta 1 receptor (primary mechanism of interest as Beta-1 receptors are found mostly in the heart and kidney) • Also affects Beta-2 receptors in the lungs and muscles, beta-3 receptors in adipose cells, and even alpha-1 receptors in blood vessels in some of this class • Side effects include bradycardia, hypotension, complete heart block, syncope • Are broken down by selectivity • All are used to control heart rate (decrease myocardial O2 demand); prevent ventricular dysrhythmias (through decreased excitation and catecholamine blockade); and all decrease mortality from MI if given in the first 12-24 hours (not acutely!)

44. Class II (part 2) • Class II drugs are categorized further by their selectivity • Nonselective Beta Blockers (B1, B2, B3 Effect) • Nadolol, Propranalol, Sotalol, Timolol, Eucommia Bark (herbal) • Nonselective Beta Blockers with Alpha-1 Blocking properties • Carvedilol and Labetalol • Nonselective Beta Blockers with sympathomimetic activity • Note: these drugs at higher doses cause TACHYCARDIA and HYPERTENSION! • Penbutolol and Pindolol (Pindolol also acts on the 5-HT1a receptor) • Beta-1 Selective Blocking Agents • Atenolol, Esmolol, Metoprolol, • Beta-2 Selective Blocking Agents (no clinical utility, experiments) • Butaxamine and ICI-118,551 • Beta-3 Selective Blocking agents (no clinical use, experimental) • SR59230A

45. Class III • Potassium Channel Blockers • Do not affect sodium channels, increase the action potential and refractory period • Help prevent reentry dysrhythmias • Can CAUSE TdP! • All have some use in WPW (though procainamide is preferred) • Some specific uses and special notes: • Ibutilide – only FDA approved drug for chemical cardioversion of Afib • Sotolol – used for treatment of atrial and ventricular tachydysrhythmias • Amiodarone – used in ventricular dysrhythmias, atrialtachydysrhythmias, SVT, and others • Note: Amiodarone is “class III” but also has actions similar to Class I and Class II drugs, possibly some Class IV activity • Bretylium is a Class III drug for VF/VT but currently unavailable

46. Class IV • Called “slow channel blockers” • Are all calcium channel blockers • Used for prevention of recurrent (non WPW) SVT • Also have uses in controlling rate of atrialtachydysrhythmias such as atrial fibrillation and atrial flutter • Side effects: dizziness, bradycardia, hypotension, dizziness, complete heart block • Classes: • Dihydripyridine class (the “-dipine” drugs, mostly vascular effects) • Felodipine, Nicardipine, Nimodipine, Nifedipine • Phenylalkylamine (more cardiac selective, less hypotention) • Verapamil • Benzothiazepine (intermediate between above 2 classes) • Diltiazem • Nonseletive • Fendiline, mibefradil, fluspiriline

47. Class V • The obligatory “Other” class • Adenosine • Naturally occurring purine molecule with extremely short half-life • In high doses can transiently cause complete AV block • Useful for treatment of SVT but can also transiently unmask underlying rhythms and help distinguish VT and Afib/Flutter • Caffeine is a direct antagonist of adenosine as they are chemically similary • Digoxin • Purified cardiac glycoside • Second line drug for afib and aflutter as well as CHF • Poisons the Na/K/ATPase pumps • Is highly toxic with narrow therapeutic • Nurse Charles Cullen killed at least 40 patients with Digoxin over 16 years • Magnesium Sulfate • Naturally occuring mineral that is treatment of TdP

48. So… Got all that?

49. Take Home Messages • Get good at reading the monitor and 12-leads • Get to know your antidysrhythmics • Early cardioversion saves lives • Pulse = sync; no pulse = no sync • Fear not the electricity! • Consider IO and LMA for vascular access and airway management in arrest situations to save precious time • WPW SVT is confusing and hard to determine on initial presentation, treat it like VT or SVT w/ aberrancy

50. Question and Answer Time! • Any questions?