Atrial Tachycardia - Thomas Jefferson University

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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 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 Narrow complex

MAT Atrial Fibrillation Atrial Flutter with variable block

Irregular Wide complex

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.