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Toronto Notes 2019 Arrhythmias
2 . Premature Beats
• prematureatrialcontraction
■ ectopic supraventricular beat originating in the atria
■ P wave morphology of the PAC usually differs from that of a normal sinus beat
• junctionalprematurebeat
■ ectopic supraventricular beat that originates in the vicinity of the AV node
■ P wave is usually not seen or an inverted P wave is seen and may be before or closely follow the QRS
complex (referred to as a retrograde, or “traveling backward” P wave) • treatmentusuallynotrequired
3 . Atrial Flutter
• rapid,regularatrialdepolarizationfromamacrore-entrycircuitwithintheatrium(mostcommonly the right atrium)
• atrialrate250-350bpm,usually300bpm
• AVblockusuallyoccurs;itmaybefixed(2:1,3:1,4:1,etc.)orvariable
• etiology:CAD,thyrotoxicosis,mitralvalvedisease,cardiacsurgery,COPD,PE,pericarditis
• ECG:sawtoothflutterwaves(mostcommontypeofflutter)ininferiorleads(II,III,aVF);narrowQRS
(unless aberrancy); commonly seen as 2:1 block with HR of 150
• inatrialflutterwith2:1block,carotidsinusmassage(firstcheckforbruits),Valsalvamaneuver,or
adenosine may decrease AV conduction and bring out flutter waves
• treatmentofacuteatrialflutter
■ acute and if unstable (e.g. hypotension, CHF, angina): electrical cardioversion ■ if unstable (e.g. hypotension, CHF, angina): electrical cardioversion
■ if stable:
1. rate control: β-blocker, diltiazem, verapamil, or digoxin
2. chemical cardioversion: sotalol, amiodarone, type I antiarrhythmics, or electrical cardioversion ■ anticoagulation guidelines same as for patients with AFib
• treatmentoflong-termatrialflutter:antiarrhythmics,catheterradiofrequency(RF)ablation(success rate dependent on site of origin of atrial flutter – i.e. whether right-sided isthmus-dependent or left- sided origin)
4 . Multifocal Atrial Tachycardia (MAT)
• irregularrhythmcausedbypresenceof3ormoreatrialfoci(maymimicAFib)
• atrialrate100-200bpm–3ormoredistinctPwavemorphologiesandPRintervalsvary,somePwaves
may not be conducted
• occursmorecommonlyinpatientswithCOPD,andhypoxemia;lesscommonlyinpatientswith
hypokalemia, hypomagnesemia, sepsis, theophylline, or digitalis toxicity
• treatment:treattheunderlyingcause;calciumchannelblockersmaybeused(e.g.diltiazem,verapamil),
β-blockers may be contraindicated because of severe pulmonary disease
• noroleforelectricalcardioversion,antiarrhythmics,orablation
5 . Atrial Fibrillation
• seeCCSAtrialFibrillationGuidelines2016fordetails(freemobileapp–iCCSavailableoniOSand Android)
• mostcommonsustainedarrhythmia
• incidenceincreaseswithage(10%ofpopulation>80yrold)
• symptoms:palpitations,fatigue,syncope,mayprecipitateorworsenheartfailure
• classification
■ lone: occurs in persons younger than 60 yr and in whom no clinical or echocardiographic causes are found
■ nonvalvular: not caused by valvular disease, prosthetic heart valves, or valve repair
■ paroxysmal: episodes that terminate spontaneously
■ persistent: AFib sustained for more than 7 d or AFib that terminates only with cardioversion
■ permanent/chronic: continuous AFib that is unresponsive to cardioversion or in which clinical
judgement has led to a decision not to pursue cardioversion
■ recurrent: two or more episodes of AFib
■ secondary: caused by a separate underlying condition or event (e.g. MI, cardiac surgery, pulmonary
disease, hyperthyroidism)
■ may be associated with thromboembolic events (stroke risk can be assessed by CHADS2 score in
nonvalvular AFib; CHADS2-VASc if the former gives a score of 0 or 1)
• initiation
■ single circuit re-entry and/or ectopic foci act as aberrant generators producing atrial tachycardia (350-600 bpm)
■ impulses conduct irregularly across the atrial myocardium to give rise to fibrillation
■ in some cases, ectopic foci have also been mapped to the pulmonary vein ostia and can be ablated
• maintenance
■ thetachycardiacausesatrialstructuralandelectrophysiologicalremodellingchangesthatfurther promote AFib; the longer the patient is in AFib the more difficult it is to convert back to sinus rhythm
• consequences
■ the AV node irregularly filters incoming atrial impulses producing an irregular ventricular response
of <200 bpm and the tachycardia leads to suboptimal cardiac output
■ fibrillatoryconductionoftheatriapromotesbloodstasisincreasingtheriskofthrombusformation–
Cardiology and Cardiac Surgery C19
Figure 25. Atrial flutter with variable block
AFib is an important risk factor for stroke
Atrial Fibrillation – AFFIRM Trial
NEJM 2002;347:1825-1833
Study: Randomized, multicentre trial with mean follow-up of 3.5 yr.
Population: 4,060 patients (mean age 70 yr,
61% male, 89% white) with AF and a high risk of stroke or death.
Intervention: Rate control (β-blockers, calcium channel blockers, or digoxin alone or in combination) vs. rhythm control (antiarrhythmic drug chosen by the treating physician).
Primary Outcome: All cause mortality.
Results: There was no difference in mortality
or disabling stroke, anoxic encephalopathy,
major bleeding, and cardiac arrest between
the two groups. There were more incidents of hospitalizations (80.1% vs. 73%, p<0.001) and adverse events (Torsades de Pointes (12 vs. 2, p=0.007), pulseless or bradycardic arrest (9 vs. 1, p=0.01), pulmonary event (108 vs. 24, p<0.001), gastrointestinal event (127 vs. 35, p<0.001), prolonged QT interval (31 vs. 4, p≤0.001), bradycardia (105 vs. 64, p=0.001) in the rhythm- control group.
Conclusion: Rate-control was as effective as rhythm-control in AF and was better tolerated. There were more hospitalization incidents in the rhythm-control group.