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PROPERTIES Allow user to leave interaction: Show ‘Next Slide’ Button: Completion Button Label: Anytime Show always View Presentation Arrhythmias - Part 1 Karima Sajadi, MD Sarah A. Stahmer MD Cooper University Hospital Objectives • Understand the basic mechanisms that give rise to arrhythmias • Review the basic types of tachy-arrhythmias and their treatment • Review the presentation of wide complex tachycardias and their treatment • Review the basic types of brady-arrhythmias and their treatment Slide 3 Mechanisms • Enhanced automaticity – spontaneous depolarization of the myocytes that are normally not arrhythmogenic • Triggered activity – depolarizations that are triggered by the preceding beat and occur during or after repolarization • Reentry – existence of slow and fast conducting pathways that allow antero- and retrograde conduction Slide 4 Tachydysrhythmias Tachydysrhythmias Regular Irregular Narrow complex Wide complex Narrow complex Wide complex Sinus Tachycardia Atrial Tachycardia Atrial Flutter AVNRT/AVRT Ventricular tachycardia Pacer-mediated tachycardia SVT with pre-existing BBB SVT with rate-dependent BBB MAT Atrial Fibrillation Atrial Flutter with variable block Torsade des Pointes Ventricular fibrillation Slide 5 Regular Narrow-Complex Tachyarrhythmias 1. Sinus tachycardia 2. Atrial tachycardia 3. 3. Atrial flutter 4. 4. Paroxysmal supraventricular tachycardia – A. AVNRT (AV nodal reentry tachycardia) – B. AVRT or ORT (Orthodromic reciprocating tachycardia) Slide 6 Sinus Tachycardia • Physiologic response rather than a pathologic rhythm • Maximal rate = 220 bpm – age (years) Slide 7 Sinus Tachycardia • Causes: – Fever, anxiety, hypovolemia, thyrotoxicosis – Peripheral vasodilatation – Exogenous catecholamines (cocaine, amphetamine, dopamine) – Anticholinergics (TCAs, Benadryl) – LV dysfunction (CHF, myocardial ischemia) – RV dysfunction (PE, RV infarct) Slide 8 Sinus Tachycardia • ECG Recognition: – Discrete P waves before every QRS, constant PR interval – Rate should vary in response to respirations, vagal stimulation, pain, stress – An isolated sinus tachycardia is a potentially life threatening rhythm until the underlying cause is identified and treated! Slide 9 Sinus Tachycardia Slide 10 Atrial Tachycardia • A single ectopic atrial pacemaker • Causes: – Enhanced automaticity – Reentry – patients with a history of cardiac surgery – Triggered activity – think digoxin toxicity • ECG recognition: – Atrial rate 150-250 bpm – slower than atrial flutter, with which it can be confused – Ectopic P wave morphology distinct from baseline sinus node P wave Slide 11 Atrial Tachycardia Slide 12 Atrial Flutter • Mechanism: regular microreentry circuit that rotates counterclockwise around right atrium • Inherently unstable and converts to NSR or atrial fibrillation • Causes: ischemic heart disease, congestive CM, PE, myocarditis, hyperthyroidism, etc Slide 13 Atrial Flutter • ECG recognition: – atrial rate 250-230, ventricular rate 75-150 bpm – if variable ventricular response then it is irregular – sawtooth wave pattern in inferior leads. • Treatment: – depends on time of onset (> or < than 48 hrs) – preserved or impaired heart function – presence of WPW syndrome Slide 14 Atrial Flutter: 1:1 Slide 15 Atrial Flutter 2:1 Slide 16 AVNRT • Mechanism: – reentry at AV node or perinodal tissue. – triggered by premature atrial conduction (PAC) – PAC conduction is blocked down the fast pathway (with a long refractory period) – conducted anterograde through the slow pathway (with a short refractory period) – reenters via recovered fast pathway Slide 17 AVNRT • ECG recognition: – Narrow complex regular tachycardia at 140-280 bpm – P wave not seen due to simultaneous atria/ventricular activation • Causes: – Atrial stretch (ACS, CHF) – irritability (exogenous catecholamines) – inflammation (pericarditis) • Treatment: – Vagal maneuvers, adenosine – beta-blockers, diltiazem, digoxin Slide 18 AVNRT Slide 19 Atypical AVNRT Slide 20 AVRT or ORT • Less common than AVNRT, difficult to distinguish from AVNRT on EKG • Mechanism: – macroreentry through normal conducting system and an accessory AV pathway – impulse conducts anterograde down the AVN – reenters via an accessory pathway, resulting in narrow-complex tachycardia – P wave visible due to delayed activation of the atria • ECG recognition: – P wave follows QRS Slide 21 ORT • Causes: same as AVNRT • Treatment: – AV-nodal blocking agents are usually effective due to antegrade activation of the ventricles via the AVN – Ablation treatment has a 95% success rate Slide 22 AVRT or ORT Slide 23 ORT Slide 24 ORT after Adenosine Slide 25 Irregular Narrow-Complex Tachyarrhythmias 1. Multifocal Atrial Tachycardia (MAT) 2. Atrial fibrillation 3. Atrial flutter with variable block Slide 26 MAT • Mechanism: – absent single dominant pacemaker – multiple atrial foci fire independently • ECG recognition: – at least 3 different P wave morphologies – variable P-R, P-P, R-R intervals – isoelectric baseline present to distinguish from atrial fibrillation Slide 27 MAT • Causes: – – – – COPD, hypoxia Pulmonary Hypertension CHF Theophylline toxicity – Electrolyte abnormalities (low K/Mg) • Treatment: – treat underlying cause – Magnesium, Verapamil may be beneficial Slide 28 MAT Slide 29 Atrial Fibrillation Slide 30 Atrial Fibrillation • Mechanism: – due to multiple reentrant wavelets between left and right atria • ECG recognition: – irregularly irregular rhythm – disorganized atrial activity – no clear P waves between QRS complexes Slide 31 Atrial Fibrillation • Causes: – Ischemic heart disease, HTN – pericarditis – “holiday heart” – thyrotoxicosis, etc • Treatment: – Rate control – Cardioversion (chemical or electrical) – Anticoagulation Slide 32 Atrial Flutter with Variable Block • Mechanism: – Atrial rate up to 300 bpm – not all depolarizations conduct through the AV node – especially in patients on medications that block AV node • ECG recognition: – irregular narrow QRS complexes – the ratio of atrial flutter waves to QRS complexes varies (2:1, 3:1, etc) Slide 33 Atrial Flutter with Variable Block Slide 34 Conclusion • This concludes part 1 of the arrhythmia presentation. • Continue to Arrhythmias Part 2 for the next installment of this lecture. • Cases studies and references for this section are found at the end of Arrhythmias Part 3.