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Tachydysrhymias

Tachydysrhymias. Stefan Da Silva Oct 19 th 2006 Special Guest: Dr. Phil Ukrainetz With a little help from Drs. R. Hall and D. Peterson. Tachydysrhythmias. Dysrhythmia: any abnormality in cardiac rhythm Anatomy SA node AV node Bundle Branches. Tachydysrhythmias. Tachydysrhythmias.

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Tachydysrhymias

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  1. Tachydysrhymias Stefan Da Silva Oct 19th 2006 Special Guest: Dr. Phil Ukrainetz With a little help from Drs. R. Hall and D. Peterson

  2. Tachydysrhythmias • Dysrhythmia: any abnormality in cardiac rhythm • Anatomy • SA node • AV node • Bundle Branches

  3. Tachydysrhythmias

  4. Tachydysrhythmias • Cardiac Electrophysiology (the very basics!) • Na/K pump • 3 Na OUT • 2 K IN • This generates approx 10 mV potential across membrane • The flow of K down the concentration gradient toward the ECF generates another 80 mV • Ca is also exchanged for Na along membrane via osmotic gradient = 90 mV membrane resting potential

  5. Tachydysrhythmias

  6. Tachydysrhythmias

  7. Tachydysrhythmias • Mechanisms for Dysrhythmias • Altered Automaticity • Re-entry • Triggered Mechanisms

  8. Tachydysrhythmias • Altered Automaticity • Impulse related • Can occur in multiple settings (ischemia, electrolyte abnormalities, drugs…) • Can be a result of spontaneous phase 4 depolarization in “non-pacemaker” cells (abnormal automaticity) • Eg. VT after MI • Increase in the slope of depolarization causing it to be more positive/closer to threshold (enhanced automaticity) • Eg. Idioventricular rhythm after MI • Enhanced automaticity as a result of catecholamine increase stimulating non-SA nodal pacemakers.

  9. Tachydysrhythmias • Re-entry • Conduction related • Most common cause of narrow complex rhythms (50% - 80%) • Need 3 conditions for re-entry • 1) Pathway  2 paths available • 2) Unequal responsiveness between routes • 3) Decrease in conduction of one route

  10. Tachydysrhythmias • What happens??? • Dysfunction at the junction • Impulse finds one route “dysfunctional” (ie. in refractory phase) therefore travels down alternate route and circles back up towards initial route (retrograde) since it has recovered from refractory period. • Can result in narrow complex tachycardia

  11. Tachydysrhythmias • Triggered • Result of “afterdepolarization”  fluctuations in membrane potential that occur as the resting potential is approached which may precipitate another depolarization • Dependant on heart rate for propagation • Can be either early or late afterdepolarizations. • Late: enhanced by faster heart rates. eg. Intracellular Ca overload in reperfusion therapy post MI can cause dysrhythmias such as VT, bigeminy, junctional rhythms • Early: enhanced by slower heart rates. eg. Torsades de pointes

  12. Triggered Activity(early afterdepolarizations) Early afterdepolar-izations occur during either phase 2 or phase 3 of the action potential, and are seen most commonly in QT prolongation.

  13. Triggered Activity(late afterdepolarizations) Late afterdepolar-izations occur shortly after completion of repolarization, and are seen most commonly in digitalis intoxication and high catecholamine states.

  14. Tachydysrhythmias • Antidysrhythmic Drugs • Class I • Na (fast) channel blockers • “Membrane stabilizing” • Anti-ectopic effects • IA: slows deplolarization and conduction. Prolong repolarization and AP duration • Eg. Procainamide: dosage  20 – 30 mg/min until termination of dysrhythmia, decrease in BP, widening QRS greater than 50% of initial width or total dose of 18 – 20 mg/kg adminstered (can be given up to 50 mg/min in “urgent” situations..) • Maintenance: 1 – 4 mg/min • Can be given orally as outpt.

  15. Tachydysrhythmias • IB: slows depolarization and conduction. Shorten repolarization and action potential duration • Eg. Lidocaine: Dosing • 1.0 - 1.5mg/kg IV single dose (if refractory can repeat dose 0.5 – 0.75 mg/kg IV q 5 – 10mins…max dose 3 mg/kg) • IC: markedly slows depolarization and conduction. Prolongs repolarization and action potential duration • Eg. Propafenone • 1 – 2 mg/kg at 10mg/min….infuse slowly

  16. Tachydysrhythmias • Class II • B-Blockers (all the “ol’s”…propanolol, esmolol, metoprolol) • Slow SA node rate and AV conduction • Prolong action potential • Depress conduction in ischemic myocardial tissues • Class III • Prolong action potential and refractory period • Exhibit antifibrillartory effects • Eg. Amiodarone • Dosing: • Arrest: 300mg IV push then 150 mg IV in 3 to 5 mins..max dose in 24 hrs is 2.2g • Arrhythmias: 150 mg IV over 1st 10 minutes can repeat q 10 min as needed to max dose.

  17. Tachydysrhythmias • Class IV • Slow Ca channel blockers • Depress anterograde conduction through AV node. • Eg. Diltiazem • Dosing: 15 – 20 mg IV over 2 minutes, can repeat at 20 – 25 mg IV after 15 minutes • Can give Calcium prior to decrease hypotensive effects

  18. Tachydysrhythmias • Approach • ABC’s • Stable vs non-stable • ECG • Wide vs Narrow!!! • Regular vs Irregular • P waves vs No P waves • Old Chart (old ECG’s extremely helpful)

  19. Tachydysrhythmias • What do you want to know? • Stable or not stable • Stable…now what? • Have time to do focussed hx and physical • Hx: • timing, palpitations, dizziness, chest pain, SOB, syncope etc • Previous hx of similar • Medications • Physical • Evidence of end-organ perfusion/alteration in cognition • Regular cardio-pulmonary exam. • ECG • Interventions

  20. Tachydysrhythmias • Case #1 • 76 yr old male presenting with 1 day hx of heart “racing” and mild breathless • PMHx: “some heart problems” • Meds: “…half a blue pill for BP and water pill or something like that…” • Vitals: fluctuating HR 120 – 150, BP 160/96, Sat 96% RA, 36.5 temp

  21. CASE #1 Tachydysrhythmias

  22. Tachydysrhythmias • Atrial Fibrillation • “chaos” • Irregularly irregular • No distinct “P” waves • Narrow Complex • Ashman Phenomenon: isolated/repeated aberrant ventricular conduction in RBBB pattern • Atrial rates of ~300 bpm • Ventricular rates ~ 150 – 200 • Can be dangerous in patients with LV dysfunction as high likelihood of going into heart failure if in Afib • If > 200 bpm beware of accessory pathway and predisposition to Vfib

  23. Tachydysrhythmias • Causes: IHD, pericarditis, thyroid dysfunction, cardiomyopathy, PE, CHF • Tx: • Stable vs unstable • Immediate cardioversion if unstable • Rate control • Preserved vs unpreserved ventricular function • Ca++/B-blockers • If in doubt Diltiazem can be used for both normal and impaired LV function (ACLS) • Rhythm control • Duration • Chemical vs Electrical • Amiodarone • Anticoagulation • Anticoag clinics • Afib clinic here in Calgary • Don’t forget to think about cause of atrial fib/flutter and treat!

  24. Tachydysrhythmias • “Convert or Not to Convert”…. • > 48 hrs increased risk of embolic (however Rosen’s mentions can convert up to 72 hrs) • Chemical vs Electrical • Electrical • 50 – 100 J to start • No associated risk of malignant ventricular dysrhythmias on pts with dig unless evidence of toxicity • Can premedicate with rate slowing agent (Ca++) • Chemical • Amiodarone 5mg/kg IV, over 15 – 20 minutes • Other options…procainamide, ibutilide • Don’t forget about Anticoagulation!

  25. Tachydysrhythmias Atrial Flutter • “sawtooth” pattern best seen in II, III, aVF, V1, V2 • Usually 2:1 or 4:1 but any ratio can be seen • Atrial rates ~300/min (classical) • Ventricular rates ~ 150 bpm (classical) • Narrow Complex • Causes: CHF, Underlying heart disease, Valve dysfxn, Metabolic

  26. Tachydysrhythmias • Tx: stable vs unstable • Ca++ (Diltiazem may better b/c of less hypotension and inotropic effect)/B-blocker • Digitalis (0.5mg IV initial and repeat doses q1-2hrs in 0.25mg increments until effect or total dose = 1.5mg) • Magnesium (2 – 4 g IV) • Cardioversion (unstable or recurrent) • Low energy cardioversion 25 – 50 J • Determine cause!! • Pitfalls • Watch out for possibility of accessory pathway (eg. Ventricular rates of > 200 bpm since normal AV nodal pathways are unlikely to allow rates that high) • Avoid primary AV nodal blocking agents in these instances since may precipitate Vfib • Should investigate with EP studies

  27. Tachydysrhythmias

  28. Tachydysrhythmias • Case # 2 • 40 yr old male “feeling funny in chest”. • PMHx: Healthy • Meds: none • Vitals: HR 200, BP 130/80, Sats 98% RA,

  29. Tachydysrhythmias

  30. Tachydysrhythmias • Narrow Complex Tachycardias (that are not Afib/Aflutter) • QRS < 0.12 sec and ventricular rate of > 100 • P waves usually “hidden” due to fast rate • Regular • Stable vs Unstable

  31. Tachydysrhythmias • Sinus Tachycardia • Don’t forget to think about the cause!!! • Response to physiological stress due to body trying to increase cardiac output • Eg. Sepsis, PE, shock… • Tx: treat the cause!!

  32. Tachydysrhythmias • Atrial Tachycardia • Tachycardia originating above nonsinus focus above the AV node • Gradual or abrupt • Hallmark: narrow complex tachycardia with each QRS preceded by a P wave that is morphologically different from the sinus P wave

  33. Tachydysrhythmias • Case #3 • 75 yr old male sent in by GP because of lightheadedness and dizziness following progressive SOB and productive cough for 2 days. • PMHx: COPD • Meds: “Damm oxygen at home…makes me feel like a dog on a leash…AND I can’t smoke with it on!!” • Vitals: 120 HR irregular, 160/90, O2 88% on 1 L

  34. ECG Tachydysrhythmias

  35. Tachydysrhythmias • Multifocal Atrial Tachycardia • “wandering atrial pacemaker” • ECG findings • At least 3 morphologically distinct P waves • Changing P-P, P-R, and R-R intervals • Atrial rhythm usually b/w 100 – 180 bpm • Most commonly in elderly patients • Causes: chronic lung problems, pulmonary disease • TX: treat underlying problem (usually resp) • Mg 2 g IV over 60 secs then 1 – 2 g/h infusion • Verapamil 5 – 10 mg IV • B-blockers (watch out for theroretical risk of increasing pulmonary issues)

  36. Tachydysrhythmias • Supraventricular Tachycardia • SVT: any tachycardia originating above the ventricles; includes sinus tach, Afib, aflut, PSVT, junctional tach • PSVT: a type of SVT; two causes……. • AVNRT: AV node Re-entrant Tachycardia (also called Paroxysmal Junctional Tach) - AV node reentry • HR usually less than 200 • P wave usually buried • AVRT: AV Re-entrant Tachycardia - re-entry b/w atria and ventricle due to accessory pathway • Suspect if HR > 200 • WPW most common

  37. Tachydysrhythmias • Tx: • Stable vs Unstable • Vagal maneuvers • Adenosine • Cardioversion • Other options: Amio, CCB, procainamide…

  38. Tachydysrhythmias • Case # 3 • 17 yr old male with episodic “racing heart” for years. No parents with him. States he has had this before and sees a cardiologist but can’t remember who. • Vitals: HR 60, BP 110/60, Sats 98% RA

  39. Tachydysrhythmias

  40. Tachydysrhythmias • WPW • Most common accessory pathway syndrome • Hallmark: PSVT at 150 – 300 bpm • Loss of normal AV conduction restraint • 70 % of pts have no underlying heart disease • Classic 3 features • Short PR interval ( < 0.12 sec) • QRS > 0.10 • “Delta” wave (early activation of myocardium)

  41. Orthodromic Narrow QRS Delta wave absent Down through AV node Up through accessory pathway Antidromic Wide QRS Delta wave present Down through accessory pathway Up through AV node Tachydysrhythmias

  42. Tachydysrhythmias • WPW • Treatment • Stable vs Unstable • Depends on 3 observations: • Symptoms of instability • QRS duration or Delta wave presence • QRS regularity or irregularity • Regular Orthodromic • Most common • Treat same as SVT • Regular Antidromic or any irregular rhythm • High risk of Vfib (esp when RR interval < 0.20) • Avoid AV nodal blocking drugs (CCB, BB, dig, adenosine) • Procainamide is drug of choice or cardioversion if > 250 bpm • Amiodarone can also be considered

  43. Tachydysrhythmias • Wide Complex Tachycardias • > 100 bpm and QRS > 0.12 sec • 2 groups • Ventricular • SVT with aberrancy • Must determine difference in order to treat properly • Use focused hx, physical exam, and ECG tracing

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