Arrhythmias Flashcards

Question

What is the treatment for stable >48hr AF?

Answer 1

Rate control: bisoprolol/diltiazem Rhythm control: anticoagulated 3-4 weeks prior to DC cardioversion

Answer 2

CHADS-VASc: HF, HTN, Age (65-74, >74), DM, Stroke Hx, Vascular disease, Sex Maximum score = 9

Answer 3

Due to re-entry in a circuit involving AV node and its 2 right atrial input pathways: a superior ‘fast’ pathway and an inferior ‘slow’ pathway Regular tachycardia – 120-240/min Often in absence of structural heart disease Episodes may last few secs – many hours Presentation: - Aware of rapid, very forceful, regular heartbeat - May have chest discomfort, lightheadedness, breathlessness - May have polyuria due to release of atrial natriuretic peptide ECG - Tachycardia with normal QRS complexes - May have rate-dependent bundle branch block Management - Do not always need to treat - Can stop episode by carotid sinus pressure or valsalva manoeuvre - Adenosine (3–12 mg rapidly IV in incremental doses until tachycardia stops) or verapamil (5 mg IV over 1 min) will restore sinus rhythm in most cases. - Intravenous β-blocker or flecainide can also be used. In rare cases, if have severe haemodynamic compromise, tachycardia should be terminated by DC cardioversion. In patients with recurrent SVT, catheter ablation = most effective therapy and will permanently prevent SVT in more than 90% of cases. Alternatively, prophylaxis with oral β-blocker, verapamil or flecainide may be used but commits predominantly young patients to long-term drug therapy and can create difficulty in female patients, as these drugs are normally avoided during pregnancy.

Answer 4

Abnormal band of conducting tissue connects atria and ventricles = ‘accessory pathway’ - Comprises rapidly conducting fibres - resemble Purkinje tissue - conduct very rapidly & rich in sodium channels. - Initiation of contraction by accessory pathway → tachycardia 50% - only conducts in retrograde direction (from ventricles to atria) → no change in ECG in sinus rhythm 50% - also conducts antegradely (from atria to ventricles) → AV conduction in sinus rhythm is mediated via both AV node and accessory pathway, → distorting QRS complex. Premature ventricular activation via pathway: - Shortens PR interval - ‘Slurred’ initial deflection of QRS complex = delta wave This is known as a manifest accessory pathway. As AV node & accessory pathway have different conduction speeds and refractory periods → a re-entry circuit can develop, causing tachycardia When associated with symptoms = Wolff–Parkinson–White syndrome. ECG almost indistinguishable from AVNRT Carotid sinus pressure or IV adenosine can terminate the tachycardia. If atrial fibrillation occurs, it may produce a dangerously rapid ventricular rate because accessory pathway lacks the rate-limiting properties of the AV node - This is known as pre-excited atrial fibrillation - May cause collapse, syncope and sudden death. - Should be treated as emergency, usually with DC cardioversion. Symptomatic patients → 1st line treatment = Catheter ablation - Nearly always curative. Alternatively, prophylactic anti-arrhythmic drugs, such as flecainide or propafenone, can be used to slow conduction in, and prolong the refractory period of, the accessory pathway. Long-term drug therapy is not the preferred treatment for most patients NO Amiodarone – due to SE & ablation is safer and more effective. Digoxin and verapamil shorten the refractory period of the accessory pathway and should not be used.

Answer 5

Ventricular ectopic beats (extrasystoles, premature beats) • QRS complexes in sinus rhythm narrow as ventricles are activated rapidly and simultaneously via the His–Purkinje system. • Complexes of ventricular ectopic beats (VEBs) - premature, broad and bizarre because ventricles are activated sequentially rather than simultaneously. • The complexes may be unifocal (identical beats arising from a single ectopic focus) or multifocal (varying morphology with multiple foci). • ‘Couplet’ and ‘triplet’ = two or three successive ectopic beats. • A run of alternating sinus and ventricular ectopic beats is known as ventricular ‘bigeminy’. • Ectopic beats produce low stroke volume because left ventricular contraction occurs before filling is complete. • Pulse → irregular, with weak or missed beats ( • Usually asymptomatic but may have irregular heart beat, missed beats or abnormally strong beats (due to increased output of post-ectopic sinus beat). • Significance of VEBs depends on presence/absence of underlying heart disease.

Answer 6

* VEBs frequently found in healthy people * Prevalence increases with age. * Ectopic beats in patients with otherwise normal hearts - more prominent at rest and disappear with exercise. * Treatment not necessary, unless patient is highly symptomatic (β-blockers or, in some situations, catheter ablation). * Sometimes manifestation of otherwise subclinical heart disease - coronary artery disease or cardiomyopathy. * No evidence that anti-arrhythmic therapy improves prognosis but always investigate very frequent VEBs → ECHO (?structural heart disease) & exercise stress test (?underlying ischaemic heart disease).

Answer 7

* Frequent VEBs often occur during acute MI but need no treatment. * Persistent, frequent (over 10/hr) VEBs in patients who have survived acute phase of MI indicate poorer long-term outcome. * Other than β-blockers, anti-arrhythmic drugs do not improve & may worsen prognosis. * Common in patients with heart failure of any cause, including cardiomyopathy. * Associated with adverse prognosis, but this is not improved by anti-arrhythmic drugs. * Effective treatment of the heart failure may suppress ectopic beats. * Also feature of digoxin toxicity, and may occur as ‘escape beats’ in patients with bradycardia. * Treatment = treat underlying condition.

Answer 8

• Occurs most commonly in settings of: acute MI, chronic coronary artery disease, cardiomyopathy • Occurs when there is extensive ventricular disease - impaired left ventricular function or a left ventricular aneurysm. o VT may cause haemodynamic compromise or degenerate into ventricular fibrillation • Caused by abnormal automaticity or triggered activity in ischaemic tissue, or by re-entry within scarred ventricular tissue. • Presentation: palpitation or symptoms of low cardiac output, e.g. dizziness, dyspnoea or syncope. • ECG – tachycardia, broad, abnormal QRS complexes, rate > 120/min ( • May be difficult to distinguish from SVT with bundle branch block or pre-excitation (WPW syndrome). o Features in favour of VT: • History of MI • AV dissociation (pathognomonic) • Capture/ fusion beats (pathogonomic) • Extreme left axis deviation • Very broad QRS complexes (>140 ms) • No response to carotid sinus massage or IV adenosine • Patients recovering from MI sometimes have periods of idioventricular rhythm (‘slow’ VT) at a rate only slightly above preceding sinus rate & <120/min. o Reflect reperfusion of infarct territory → may be good sign. o Usually self-limiting & asymptomatic, & do not require treatment. o Other forms of sustained VT will require treatment, often as an emergency. • VT occasionally occurs in patients with otherwise healthy hearts (‘normal heart VT’), usually because of abnormal automaticity in the right ventricular outflow tract or one of the fascicles of the left bundle branch. o Prognosis is good and catheter ablation can be curative. • Management o Prompt action to restore sinus rhythm is required and should usually be followed by prophylactic therapy. o Synchronised DC cardioversion = treatment of choice if systolic BP is <90 mmHg. o If arrhythmia well tolerated, IV amiodarone may be given as a bolus, followed by a continuous infusion. o IV lidocaine can be used but may depress left ventricular function, → hypotension or acute heart failure. o Hypokalaemia, hypomagnesae- mia, acidosis and hypoxaemia should be corrected. o Beta-blockers effective at preventing VT by reducing ventricular automaticity. o Amiodarone can be added if additional control is needed. o Class Ic anti-arrhythmic drugs should not be used for prevention of VT in patients with coronary artery disease or heart failure because they depress myocardial function and can be pro-arrhythmic (increase likelihood of a dangerous arrhythmia). o In patients at high risk of arrhythmic death (e.g. those with poor left ventricular function, or where VT is associated with haemodynamic compromise), use of an implantable cardiac defibrillator is recommended. o Rarely, surgery (e.g. aneurysm resection) or catheter ablation can be used to interrupt the arrhythmia focus or circuit in patients with VT associated with a myocardial infarct scar.

Answer 9

• Form of polymorphic VT is a complication of prolonged ventricular repolarisation (prolonged QT interval). • ECG - rapid irregular complexes that oscillate from an upright to an inverted position and seem to twist around the baseline as the mean QRS axis changes • Usually non-sustained and repetitive, but may degenerate into ventricular fibrillation. • During periods of sinus rhythm, ECG will usually show a prolonged QT interval (> 0.43 s in men, > 0.45 s in women when corrected to a heart rate of 60/min). • Common causes (long QT interval): o Bradycardia o Electrolyte disturbance • Hypokalaemia • Hypomagnesaemia • Hypocalcaemia o Drugs • Disopyramide, flexainide (other class Ia, Ic anti-arrhythmic drugs) • Sotalol, amiodarone (and other class III anti-arrhythmic drugs) • Amitripytline (and other tricyclic antidepressants) • Chlorpromazine (and other phenothiazines) • Erythromycin (other macrolides…) o Congenital syndromes – K and Na channels • Long QT1: gene affected KCNQI: K+ channel (30-35%) • Long QT2: gene affected HERG: K+ channel (25-30%) • Long QT3: gene affected SCNSA: Na+ channel (5-10%) • Long QT4-12: rare • Long QT syndrome subtypes have different triggers, which are important when counselling patients. o Adrenergic stimulation (e.g. exercise) -long QT type 1 o Sudden noise (e.g. an alarm clock) - long QT type 2. o During sleep – type 3 • Treatment should be directed at underlying cause. • Intravenous Mg (8 mmol over 15 mins, then 72 mmol over 24 hrs) should be given in all cases. • Atrial pacing will usually suppress arrhythmia through rate-dependent shortening of QT interval. • Intravenous isoprenaline is a reasonable alternative to pacing but should be avoided in patients with the congenital long QT syndromes. • Long-term therapy may not be necessary if underlying cause can be removed. • Beta-blockers effective at preventing syncope in patients with congenital long QT syndrome. • Some, particularly those with extreme QT interval prolongation (> 500 ms) or certain high-risk genotypes should be considered for implantation of a defibrillator. • Left stellate ganglion block may be of value in patients with resistant arrhythmias. • Brugada syndrome - related genetic disorder that may present with polymorphic VT or sudden death. o Defect in Na channel function o Abnormal ECG (right bundle branch block and ST elevation in V1 and V2 but not usually prolongation of the QT interval). o Implantable defibrillator.

Answer 10

• AV conduction influenced by autonomic activity • Causes: fibrosis, CAD, AV nodal blocking agents (beta-blockers, Ca channel blockers, digoxin, adenosine), anti-arrthymic (Na channel blockers, Class III agents e.g. amiodarone, sotalol) • Other aetiologies o High vagal tone in athletes o Cardiomyopathy e.g. hypertrophic, sarcoid, amyloid, haemochromatosis o Adjacent valvular calcification o Poster catheter ablation for arrhythmia o Electrolyte imbalance o Neuromuscular disorders e.g. myotonic dystrophy, Kearns-Sayre syndrome (mitochondrial disease with progressive external opthalmoplegia), Erb dystrophy, peroneal muscular atrophy o Transient vagotonia: endotracheal suction, micturition, inferior MI • Presentation: fatigue, dyspnoea, junctional escape rhythm • May be intermittent and only evident when conducting tissue is stressed by rapid atrial rate o → Atrial tachyarrhythmias often associated with AV block • 1st degree o AV conduction delayed → PR interval prolonged (>0.20s) o Rarely causes symptoms • 2nd degree o Dropped beats occur as some impulses from atria fail to conduct to ventricles o Mobitz type 1 • Progressive lengthening of successive P intervals → dropped beat • Cycle repeats itself → Wenckebach phenomenon (due to impaired conduction in AV node; may be physiological; sometimes observed at rest/during sleep in athletic young adults with high vagal tone) o Mobits type 2 • PR interval of conducted impulses remain constant but some P waves not conducted • Usually caused by disease of His-Purkinje system • Risk of asystole (flat line on ECG) o 2:1 AV block • Alternate P waves conducted → impossible to distinguish between Mobitz type I and type II block • 3rd degree (complete AV block) o AV conduction fails completely – atria and ventricles beat independently (AV dissociation) o Ventricular activity maintained by escape rhythm arising in AV node or bundle of His (narrow QRS complexes) or distal Purkine tissues (broad QRS complexes) o Distal escape rhythm tend to be slower and less reliable o Slow (25-50/min), regular pulse • Only varies with exercise in case of congenital complex AV block o Compensatory increase in stroke volume → large volume pulse o Cannon waves visible in neck o Intensity of first heart sound varies due to loss of AV synchrony o Aetiology • Congenital • Acquired • Idiopathic fibrosis • MI/ischaemia • Inflammation – acute (aortic root abscess in infective endocarditis); chronic (sarcoidosis, Chagas’ disease) • Trauma – cardiac surgery • Drugs – digoxin, beta-blocker • Stoke-Adams attacks o Recurrent syncope • Caused by episodes of ventricular asystole in complete heart block or Mobitz type II 2nd degree AV block • Or due to sinoatrial disease o Sudden loss of consciousness – occurs without warning & results in collapse o Brief anoxic seizure (due to cerebral ischaemia) may occur if prolonged asystole o Pallor and death-like appearance during attack → once heart starts beating again, have characteristic flush o Recovery rapid • Epilepsy → slow recovery o Similar symptoms to sinoatrial disease and neurocardiogenic syncope • Management o AV block complicating acute myocardial infarction • Common in acute inferior MI – usually transient • As right coronary artery supplies AV node • Usually have reliable escape rhythm • If remains well – no treatment required • Symptomatic 2nd/3rd degree AV blocks – may respond to atropine (0.6mg IV, repeated as required), or temporary pacemaker • Most will resolve in 7-10 days o 2nd/3rd degree AV heart block complicating acute anterior MI • Indicates extensive ventricular damage involving both bundle branches • Poor prognosis • May go into asystole → temporary pacemarker • If present with asystole → IV atropine or IV isoprenaline – help to maintain circulation until temporary pacing electrode can be inserted • External (transcutaneous) pacing can provide effective temporary rhythm support o Chronic AV block • Symptomatic bradyarythmias → permanent pacemaker • Asymptomatic 1st degree or Mobitz type 1 2nd degree block (Wenckebach phenomenon) → no treatment but may indicate serious underlying heart disease • Asymptomatic Mobitz type 2 2nd or 3rd degree AV heart block – due to risk of asystole and sudden death

Answer 11

Due to AV block Recurrent syncope • Caused by episodes of ventricular asystole in complete heart block or Mobitz type II 2nd degree AV block • Or due to sinoatrial disease o Sudden loss of consciousness – occurs without warning & results in collapse o Brief anoxic seizure (due to cerebral ischaemia) may occur if prolonged asystole o Pallor and death-like appearance during attack → once heart starts beating again, have characteristic flush o Recovery rapid • Epilepsy → slow recovery o Similar symptoms to sinoatrial disease and neurocardiogenic syncope

Answer 12

• Conduction block in right or left bundle branch can occur due to many pathologies: o Ischaemic or hypertensive heart disease o Cardiomyopathies • Depolarisation proceeds through a slow myocardial route in affected ventricle rather than through rapidly conducting Purkinje tissues that constitute the bundle branches. → delayed conduction into LV or RV → broadens QRS complex (≥ 0.12 s) → produces characteristic alterations in QRS morphology

Answer 13

can occur in healthy people o Normal variant o Right ventricular hypertrophy or strain – e.g. pulmonary embolism o Congenital heart disease - e.g. atrial septal defect o Coronary artery disease o Activation of right ventricle is delayed as depolarisation has to spread across the septum from LV o Delayed RV→secondary R wave in right precordial leads (V1-3) and wide slurred S wave in lateral waves o Abnormal secondary repolarisation with ST depression/ T wave inversion in right precordial leads o Normal axis

Answer 14

o Often signifies important underlying heart disease. • Coronary artery disease • Hypertension • Aortic valve disease – aortic stenosis • Cardiomyopathy • IHD • Anterior MI • Lenegre disease • Hyperkalaemia • Digoxin toxicity o Normally, the septum is activated from left to right, producing Q waves in lateral waves o In LBBB, septal depolarisation becomes right to left due to the block→ eliminates q wave in lateral leads o Right to left depolarisation produces tall R wave (I,V5-6) and deep S waves in right precordial leads (V1-3)→left axis deviation

Answer 15

VF (IHD) Pulseless ventricular tachycardia (IHD) - Torsades de pointes in patients with underlying prolonged QT interval - ma be related to hypomagesaemia Asystole

Answer 16

Shockable rhythms - adrenaline 1mg IV every 3-5 mins Non-shockable rhythms - adrenaline 1mg IV every 3-5 mins, consider reversible causes - hypoxia, hypovolemia, potassium status

Arrhythmias Flashcards

(40 cards)