Supraventricular Arrhythmias PDF

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Gold Coast University Hospital

Dr Matthew Rowe

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supraventricular arrhythmias cardiac arrhythmias cardiology medical lectures

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Dr Matthew Rowe's lecture notes on supraventricular arrhythmias, covering topics like syncope, palpitations, and bradycardia. The lecture notes also touch on associated conditions and tests in case studies.

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College Learning Series Supraventricular Arrhythmias Dr Matthew Rowe [Title] [Presenter name] Cardiologist & Electrophysiologist Gold Coast University Hospital College Learning Series Page 1 Content outline 1. Syncope and palpitations 2. Supraventricular tachycardias 3. Atrial fibrillation...

College Learning Series Supraventricular Arrhythmias Dr Matthew Rowe [Title] [Presenter name] Cardiologist & Electrophysiologist Gold Coast University Hospital College Learning Series Page 1 Content outline 1. Syncope and palpitations 2. Supraventricular tachycardias 3. Atrial fibrillation 4. Bradycardia and pacing Curricula standards Knowledge guide: Cardiac arrhythmias: • Atrial fibrillation • Atrial flutter • Atrioventricular node conduction block • Bundle-branch and fascicular block • Sinus node dysfunction • Supraventricular tachycardia • Wolff–Parkinson–White syndrome Know indications for: • Pacemakers • Cardiac resynchronisation therapy College Learning Series Page 2 Syncope Definition: • Transient loss of consciousness • Rapid onset, short duration • Spontaneous complete recovery Pre-syncope resembles the prodrome prior to loss of consciousness. The mechanism/s involved may not be the same. Things that are not syncope: Strokes, seizures, hypoglycaemia, hypoxia, intoxication etc. Things that very rarely cause syncope: • Ischemia (via Bezold-Jarisch reflex) • Vertebrobasilar TIA • Supraventricular tachycardia (via vasovagal or in the elderly) College Learning Series Page 3 Incidence of syncope Incidence of 11% in the Framingham Heart Study cohort over 17 years of follow-up Soteriades ES et al., NEJM 2002;347:878 College Learning Series Page 4 Syncope - Classification and causes Syncope Reflex syncope Orthostatic Hypotension Cardiac Situational Primary autonomic Bradycardia Carotid sinus syncope Secondary autonomic Tachycardia Vasovagal Drug induced Structural disease Cause (%) Vasovagal 65 Cardiac 13 Orthostatic hypotension 10 Other 6 Unknown 5 *from referrals to a hospital syncope unit Volume depletion College Learning Series Page 5 Syncope - Prognosis Soteriades ES et al., NEJM 2002;347:878 College Learning Series Page 6 Syncope - Assessment Other ECG Position Warning Triggers Duration Recovery Injury Exam History Witnesses Prior Episodes Medications Hydration Tongue Biting Nausea College Learning Series Page 7 Syncope - Utility of investigations Test Yield Notes Bloodwork 0.8% Hypoglycemia, anaemia Echocardiogram 0% If baseline ECG normal and no known cardiac disease CT Head 0-4% When no focal neurology, severe headache, anticoagulation and age <65 years EEG 20-50% sensitivity, >90% specificity Sleep deprived EEG increases yield 20-40% Inpatient telemetry 16% In high risk patients Holter monitor 4% Prolonged ECG monitoring 9% Implantable loop recorder 35% Invasive / Expensive 1. Brignole M et.al doi:10.1093/europace/eup097 2. Brignole M, doi:10.1016/j.jacc.2011.11.056 3. Sarasin FP et.al. Am J Med. 2001;111(3):177-184. College Learning Series Page 8 Cardiac syncope Suggestive features: Syncope at rest or during exertion No prodrome Brief (<5mins) Rapid recovery Known structural heart disease Family history SCD/channelopathy Suggestive ECG Findings: • Bifascicular block • QRS >120ms • Mobitz II 2˚ AV Block • Sinus bradycardia <50bpm, pauses >3sec (5sec in AF) • NSVT • Pre-excitation • Features of channelopathy or cardiomyopathy (long/short QT, Brugada, HOCM, ARVC) • Pathological Q waves (old MI) College Learning Series Page 9 Vasovagal syncope Reflex / neurally mediated / neurocardiogenic Normal baroreceptor reflex: 1. On standing 300-800mL of blood shifts from thorax to peripheries 2. Reduced venous return and cardiac output leads to reduced stimulation of baroreceptors in carotid sinus and aortic arch and mechanoreceptors in wall of LV 3. These usually inhibit sympathetic activity and promote parasympathetic activity 4. Therefore reduction in baroreceptor activity increases sympathetic tone and maintains blood pressure. College Learning Series Page 10 Vasovagal Syncope 1430ms PR Prolongation 1600ms 1800ms Slowing of sinus rate College Learning Series Page 11 Vasovagal syncope - Treatment Lifestyle Medications Reassurance Hydration Physical counterpressure manoeuvres (RCT) Midodrine (1 small RCT) 78-95% reported response rate Compression stockings Salt loading Fludrocortisone (weak evidence / modest effect) SSRI (1 RCT – paroxetine) 18% vs 53% recurrent syncope NOT Beta blockers (4 RCTs) Permanent Pacing: Rarely, in select patients over 40 with refractory symptoms and: Prolonged pauses on ambulatory cardiac monitoring (e.g. Loop recorder) No significant vasodepressor (BP) response at tilt-table *See ISSUE-3 trial College Learning Series Page 12 Risk scoring for syncope Many systems e.g. San Francisco Syncope rule Quoted sensitivity 98% In external validation 90% 10% (60 patients) adverse outcome at 7 days • 9 patients recurrent unexplained syncope • 36 arrhythmia (21 subsequent pacemaker) • Stroke, SAH, pneumothorax • 1 death None of these 60 patients were actually discharged Scoring systems = good, clinical evaluation = better? College Learning Series Page 13 Implantable loop recorders Recurrent unexplained syncope where a diagnosis has not been achieved through all other cardiac investigations including: • A complete history and examination • ECG • Echocardiography • Ambulatory ECG • Tilt Table Test And • A neurogenic cause is not suspected • It has been determined the patient does not have structural heart disease associated with high risk of sudden death College Learning Series Page 14 Syncope and driving Private Commercial Clear vasovagal 24 hours 24 hours Cardiac syncope (cause identified and treated) 4 weeks 3 months Unexplained blackout (single) 6 months* 5 years* Unexplained blackout (2 or more) 12 months* 10 years* * Conditional license subject to annual review Austroads Assessing Fitness to Drive 2017. College Learning Series Page 15 Palpitations Importance of history Palpitations - regular or irregular, sustained or brief (e.g. ectopics) Sudden onset and offset – more likely to be AVNRT/AVRT (c.f sinus tachycardia) Number of episodes, duration, frequency, mode of onset, and possible triggers. ‘Neck pounding’ – Contraction of atrial against closed valve AVNRT/AVRT Syncope infrequent - either initial rapid tach or pause on termination – consider pre-excited AF. Also any other pathology leading to poorly tolerated tachycardia – AS, HCM, elderly etc. College Learning Series Page 16 Evaluation of palpitations • Holter monitoring most often normal due to paroxysmal nature • Prolonged ECG monitoring (7-30 days) – 66-75% diagnostic • Echo – Limited value, usually normal • Exercise testing only useful if the arrhythmia is triggered by exertion • Implantable loop recorder – 73% *not Medicare reimbursed Brignole et.al. doi:10.1093/europace/eup097 College Learning Series Page 17 Supraventricular tachycardias Sinus Tachycardia Atrial flutter Atrial fibrillation “SVTs” AVNRT (60%) AVRT (30%) Atrial tachycardia (10%) Junctional tachycardia (1%) College Learning Series Page 18 Mechanisms of arrhythmia Abnormal impulse conduction Re-entry • Flutter, AVNRT, AVRT Abnormal impulse formation Abnormal automaticity • Sinus tach, atrial tach, junctional, ectopy Triggered activity • Early and late afterdepolarization • Ectopy, torsade de pointes, digoxin toxicity Klabunde, R. Cardiovascular Physiology Concepts 2nd Ed. College Learning Series Page 19 SVT diagnostic algorithm Short R-P Long R-P HRS Clinical Practice Guideline. Heart Rhythm 2016;13;e136–e221 College Learning Series Page 20 Diagnostic tips ECG recording during vagal manoeuvres, carotid sinus massage or adenosine Termination with adenosine – AVNRT or AVRT or AT (30%) Termination with a p wave favours AVNRT/AVRT Termination with QRS not as helpful Continuation of p waves with AV block – Flutter or atrial tachycardia College Learning Series Page 21 Narrow complex tachycardia - Acute treatment General approach: Haemodynamically unstable → DC Cardioversion Stable: Vagal manoeuvres Modified Valsalva, carotid massage, facial immersion IV adenosine Contraindicated in severe asthma If on theophylline will need higher dose, potentiated by dipyradimole (Asasantin) IV Calcium channel blocker / Beta blocker Not with broad complexes or known WPW 1. 2. 1. HRS Clinical Practice Guideline. Heart Rhythm 2016;13;e136–e221 2. Appelboam et.al Lancet 2015;386;p1747-1753. College Learning Series Page 22 Atrioventricular Reciprocating Tachycardia (AVRT) Terminology Accessory pathway/bypass tract Manifest vs concealed Pre-excitation Pre-excitation (‘Delta wave’) + tachyarrhythmia = WolffParkinson-White syndrome 95% of arrhythmias in this group are AVRT but they are capable of having other SVTs (e.g. AF) conducted down the accessory pathway Sudden Death Risk Due to pre-excited AF → VF 1:1000 Can be further risk stratified at EP study Link, MS, N Engl J Med 2012;367:1438-48. Obeyesekere MN, Circulation. 2012 May;125(19):2308-15 College Learning Series Page 23 Delta wave in asymptomatic patients Occasionally a delta wave is found incidentally without any history or symptoms of arrhythmia 1/3rd of patients under 40yrs eventually developed symptoms, no patients over 40yrs went on to develop symptoms (or die) Routine EP study is not thought to be of net benefit Consider in cases of high-risk occupation Use of treadmill testing to show abrupt loss of delta wave is reasonable but must be interpreted carefully College Learning Series Page 24 College Learning Series Page 25 College Learning Series Page 26 College Learning Series Page 27 Pseudo R’ Sinus AVNRT College Learning Series Page 28 AV Node Re-entry Tachycardia (AVNRT) Most common of the SVTs Excellent prognosis but can be very symptomatic Typical (Slow-fast, short R-P) and atypical (fast-slow, long R-P) Atrium “Fast” pathway AV Node “Slow” pathway Ventricle College Learning Series Page 29 Focal atrial tachycardia Automaticity, triggered activity or micro-reentry Can originate from right of left atrium Most responsive to beta blocker or calcium channel blocker Often resistant to DC cardioversion HR 100-250bpm ‘Warm-up’ or bursts College Learning Series Page 30 SVT - Long term management Sometimes nothing if symptoms infrequent Excellent prognosis but can be a nuisance Vagal Manoeuvres Catheter ablation – Class I indication Approximately 1% complication rate 90-95% success rate Pill in the pocket Long-term oral therapy (30-50% success) Calcium channel blocker, B-blocker or digoxin Flecainide (in combination with above) Rarely sotalol or amiodarone College Learning Series Page 31 Typical atrial flutter Macro-reentrant circuit, dependent on cavo-tricuspid isthmus Atrial rate typically 250-350bpm and classically 300bpm with 2:1 AV block -> HR 150bpm Associated with HTN, coronary disease, valvulopathy, COPD, cardiomyopathies 10-20% of patients without risk factors 30% of patients with atrial flutter alone will go on to develop atrial fibrillation Can be an initiator of atrial fibrillation or vice-versa College Learning Series Page 32 Typical atrial flutter Anticoagulation = Same as AFib Rate Control Harder to Achieve Acutely use AV nodal blockers Pharmacologic cardioversion not as effective Slowing the flutter rate may lead to rapid 1:1 conduction at rapid HR Catheter Ablation – Class I College Learning Series Page 33 Atypical flutter • ECG not meeting criteria for typical flutter • Macro-re-entrant circuit involving other areas of the atrium • Usually structural heart disease or post-surgical (or post-ablation) • Ablation can be substantially more difficult Typical Atypical College Learning Series Page 34 Atrial fibrillation The process of AF involves a combination of initiation by focal atrial triggers (most commonly the pulmonary veins) and maintenance by abnormal atrial tissue which allows wavelets to propagate around the atrium Mechanisms that lead to left atrial strain, fibrosis and enlargement are involved in most cases of AF e.g. Hypertension, sleep apnoea, valvular disease, cardiomyopathies AF itself leads to further remodelling of the left atrium (“AF begets AF”) Chowdhury et.al Cleveland Journal of Clinical Medicine. 2009 College Learning Series Page 35 AF - Anticoagulation Oral anticoagulation is recommended where the CHA2DS2-VA score is 2 or more, unless contraindications exist Should be considered where the score is 1 No anticoagulation (or aspirin) if score is 0 CHA2DS2-VASc score Annual Stroke Risk (%) 0 0.3 1 0.9 2 2.9 3 4.6 4 6.7 5 10.0 6 13.6 7 15.7 8 15.2 9 17.4 Friberg L, Rosenqvist M, Lip G European Heart Journal, 2012. College Learning Series Page 36 AF - Anticoagulation HAS-BLED Yearly major bleeding (%) 0 − 1 0.7 2 1.9 3 2.4 4 3.4 5 5.7 6 15.5 7 − Variable Points Hypertension 1 Renal disease (dialysis, transplant, Cr >2.26 mg/dL or 200 µmol/L) Liver disease (cirrhosis or bilirubin >2x normal with AST/ALT/AP >3x normal) Stroke history 1 Prior major bleeding or predisposition to bleeding 1 Labile INR (unstable/high INRs, time in therapeutic range <60%) Elderly (age >65) 1 Medication usage predisposing to bleeding (aspirin, clopidogrel, NSAIDs) Alcohol usage (≥8 drinks/week) 1 1 1 In most cases the benefit of stroke prevention will outweigh the bleeding risk 1 1 Friberg L, Rosenqvist M, Lip G European Heart Journal, 2012. College Learning Series Page 37 Which anticoagulant in AF? When oral anticoagulation is used in non-valvular AF, a NOAC is recommended over warfarin Ruff et.al. The Lancet, 15 March 2014, Vol.383(9921), pp.955-962 College Learning Series Page 38 What is ‘Non-valvular’ AF? Non-valvular AF – The definition used to determine eligibility of NOAC drugs – Includes everything except: Metallic heart valves Moderate to severe mitral stenosis NHFA CSANZ Atrial Fibrillation Guideline Working Group 2018 https://doi.org/10.1016/j.hlc.2018.06.1043 College Learning Series Page 39 AF – Anticoagulant dosing Steinberg et.al JACC, 68(24) p2597-2604 2016. College Learning Series Page 40 AF - Rate vs. rhythm No difference in mortality or morbidity between rate and rhythm control Therefore individualise to the patient. Consider: • Heart Failure • Presence of symptoms when rate controlled • Medication side effects • Age When using rate remember lenient rate <110bpm is OK AFFIRM Investigators. N Engl J Med 2002; 347:1825-1833 College Learning Series Page 41 NHFA CSANZ Atrial Fibrillation Guideline Working Group 2018 https://doi.org/10.1016/j.hlc.2018.06.1043 College Learning Series Page 42 AF Risk factor modification Weight Loss Alcohol Reduction 1. Middeldorp ME et al. Heart 2020;106:325–332. 2. Voskoboinik et.al N Engl J Med 2020; 382:20-28 College Learning Series Page 43 AF ablation Aim To isolate the most common source of triggers for AF (the pulmonary veins) from the rest of the left atrium Indication: • Symptomatic paroxysmal or persistent AF refractory or intolerant to at least one Class I or III antiarrhythmic medication • Catheter ablation can be considered for symptomatic paroxysmal or persistent AF in selected patients with heart failure with reduced ejection fraction Predictors of failure: • Older age • Long standing persistent (vs. paroxysmal) • Increasing left atrial size • Female* • Valvular or structural heart disease LA Complication Rate: 3-4% Winkle et.al. Heart Rhythm 2016;13:2119–2125 College Learning Series Page 44 AF ablation outcomes No mortality benefit Significant reduction in AF burden and particularly symptomatic AF One RCT showing reduced death and HF hospitalisation in EF <35% and failed medical therapy (CASTLE-AF) College Learning Series Page 45 AF ablation improves symptoms and QOL Yao, Andrade et.al. JACC EP 2020 College Learning Series Page 46 Bradycardias 1˚ AV “block” (PR prolongation) 2˚ AVB Mobitz I (PR prolongation) 2˚ AVB Mobitz II (No PR prolongation) 3˚ AVB (Complete Heart Block) Regular R-R and P-P. More P than QRS College Learning Series Page 47 Bradycardia – 2:1 AV Block 2:1 AV Block Mobitz II AV Block Question: Is the block at the level of the AV node (benign) or at/below the His (pathological)? Feature Suggests AV node Suggests Infra/Hisian QRS duration Narrow Wide PR interval Long Short Response to exercise Block improves Block worsens During acute MI Inferior MI Anterior MI Other Type I Mobitz elsewhere Syncope Go back to the history - is there syncope, is there symptom rhythm correlation? Observe for longer and take serial ECGs or rhythm strips College Learning Series Page 48 Bradycardia – Sinus node dysfunction Sinus node dysfunction (SND) is most often related to age-dependent progressive fibrosis of the sinus nodal tissue and surrounding atrial myocardium Most common in 70s and 80s Can co-exist with atrial tachyarrhythmias (“tachybrady syndrome”) Diagnosis: • • Sinus rate <50bpm and sinus pauses >3 seconds Chronotropic incompetence – Failure to reach 80% predicted HR The sole reason to consider treatment of SND is the presence of symptoms Sleep apnoea is a common, treatable cause of sinus node dysfunction College Learning Series Page 49 Permanent pacing for bradycardia Indications Any patients, in the absence of reversible causes, with: • Mobitz II 2nd degree, high-grade or 3rd degree AV block Symptomatic patients, in the absence of reversible causes with: 1. Sinus node dysfunction (Class I) 2. Atrial fibrillation and bradycardia (Class I) 3. Bradycardia due to goal directed medical therapy (e.g. beta blocker in HF – Class I) 4. Mobitz I or marked PR prolongation with clear correlation with symptoms (Class IIa) College Learning Series Page 50 Cardiac resynchronisation therapy • 25% of heart failure patients have dyssynchronous myocardial contraction – evidenced by broad QRS on ECG • This is mechanically inefficient and over time exacerbates pathological remodelling • Leads to worsening symptoms and increased mortality • CRT aims to correct this by activating both the right and left ventricle simultaneously • Unlike a standard pacemaker the aim is to pace every beat (target >98% paced) College Learning Series Page 51 CRT reduces mortality COMPANION MIRACLE (CRT-P) MADIT-CRT CARE-HF College Learning Series Page 52 CRT - Predictors of benefit Cleland JG, Eur Heart J 2013;34:3547–56. College Learning Series Page 53 2012 ACCF/AHA/HRS Focused Update. JACC College Learning Series Page 54 Key learning points Resources 1. Syncope and Palpitations • Importance of history SVT Link, MS, N Engl J Med 2012;367:1438-48. https://doi.org/10.1056/NEJMcp1111259 2. Supraventricular Tachycardias • Differential diagnosis using R-P interval 3. Atrial fibrillation • Anticoagulation • Rate control • Rhythm control • Risk factor modification 4. Bradycardia and Pacing • Importance of symptoms AF CSANZ Atrial Fibrillation Guideline https://doi.org/10.1016/j.hlc.2018.06.1043 Pacing 2018 AHA Guidelines https://doi.org/10.1161/CIR.0000000000000628 [email protected] College Learning Series Page 55 College Learning Series Page 56

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