SYNCOPE ECG CASES Dr Herman Chua Emergency Medicine Consultant Lyell McEwin Hospital
Case 1 92 year old female resident of nursing home found slumped on the chair watching TV
CASE 1
Case 1 Sinus pause (with junctional escape rhythm)
CASE 1
Conduction system of the heart
Sinus node dysfunction SA node fails to function as pacemaker of heart = BRADYCARDIC RHYTHM
Sinus node dysfunction How does it manifest? Inappropriate sinus bradycardia
Sinus node dysfunction How does it manifest? Sinus arrest
Sinus node dysfunction How does it manifest? Escape rhythm
Sinus node dysfunction Causes Intrinsic (irreversible) sick sinus syndrome Extrinsic (reversible) drugs (CCB, β-blocker, digoxin, amiodarone) metabolic (hyperkalaemia) enhanced vagal tone hypoxia, hypercapnia hypothermia hypothyroidism CNS
Sick sinus syndrome Important to exclude extrinsic reversible causes first Treatment : permanent pacemaker
Case 2 86 year old female who collapsed at the shopping mall. Sustained large scalp laceration
CASE 2
Case 2 Complete heart block with ventricular escape rhythm
CASE 2
Conduction system of the heart
AV Block 1 - delay in conduction 2 - intermittent failure in conduction 3 - total interruption of conduction
Complete heart block Complete failure of atrial impulses reaching ventricles = P waves fail to conduct
Complete heart block Usually escape rhythm comes to the rescue
Complete heart block Escape complexes completely independent from P waves (AV dissociation) Origin of escape rhythm depends on location of AV block
Localizing the AV Block AV nodal Infranodal
Localizing the AV Block AV nodal junctional escape rhythm (40-60 bpm) good prognosis Infranodal ventricular escape rhythm (20-40 bpm) bad prognosis
Complete heart block ECG features P waves and QRS complexes completely dissociated Escape rhythm can be narrow or wide Ventricular rate slower than atrial rate
MI Drugs (CCB, β-blocker, digoxin) Metabolic (hyperkalaemia) Congenital Degenerative (Lev, Lenegre) Infiltrative (sarcoid, amyloid) Infective (Lyme) Hypothyroidism Neuromuscular disease Complete heart block Causes
CHB with junctional escape
Inferoposterior MI with CHB
Case 3 74 year old female presents after an episode of collapse. Has been lethargic and unwell for the last few days. PMH x : AF
CASE 3
Case 3 Slow AF with multifocal PVCs = DIGOXIN TOXICITY
CASE 3
Digoxin Toxicity Inhibits Na + -K + -ATPase increase intracellular calcium increase in myocardial contractility (positive ionotropic effect) increase RMP, lowers firing threshold increase in automaticity Enhances vagal tone decrease SA & AV nodal conduction velocity
Digoxin toxicity ECG effects Increased AUTOMATICITY Ectopic beats Tachyarrhythmias Decreased CONDUCTION Bradyarrhythmias
Digoxin toxicity ECG manifestations Almost any dysrhythmia Classic : atrial tachycardia with block bidirectional VT Common : frequent PVCs AV blocks sinus bradycardia / slow AF AF with CHB ( regular AF )
Digoxin toxicity Level = 4.2
Digoxin toxicity Level = 27!!
Digoxin effect
Case 4 24 year old male with recurrent palpitations, who presents with palpitations, dyspnoea and pre-syncope while waiting for bus
CASE 4
Case 4 Wolff-Parkinson-White syndrome
CASE 4
Pre-excitation Syndrome Wolff-Parkinson-White Accessory pathway(s) bypass normal AV conduction Result in ventricular preexcitation Predispose to tachyarrhythmias
Accessory pathway
Pre-excitation Syndrome ECG features Short PR < 0.12s Wide QRS > 0.12s Initial slurring of QRS complex (delta wave) Secondary ST-T changes
WPW
Pre-excitation Syndrome ECG features Can resemble pseudoinfarction pattern negative delta waves secondary ST-T changes (repolarization abnormalities)
Pre-excitation Syndrome Clinical Significance Tachyarrhythmias requiring accessory pathway for initiation & maintenance (re-entry) AVRT Tachyarrhythmias in which accessory pathway acts as bypass route for conduction AF / flutter
Atrio-ventricular reciprocating tachycardia
Orthodromic AVRT
AF in WPW
Post reversion
Case 5 43 year old female presents with unexplained episode of collapse while playing netball
CASE 5
Case 5 Prolonged QT (Congenital LQT1 variant)
CASE 5
Long QT Important cause of SCD Cause of death : torsade de pointes
Long QT QT interval determination measured from beginning of Q wave to end of T wave Corrected QT interval (Bazett formula) QTc = QT / [RR] 0.5 QT c > 450ms abnormal
Measuring QT interval
Long QT Risk of torsades greatest when QT c > 500ms
Long QT Causes Congenital (channelopathy involving mutations in genes encoding K + channel proteins) LQT1, LQT2, LQT3 most common LQT4-7 Acquired electrolytes (hypokalaemia, hypomagnesaemia, hypocalcaemia) drugs (class Ia, Ic, III antiarrhythmics, antipsychotics, macrolides, antifungals) hypothermia ACS CNS event
Torsades de pointes
Torsades in sotalol overdose