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Published byΦιλοκράτης Αλέξιος Βλαβιανός Modified over 6 years ago
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What is the QRS axis? Is it normal or abnormal?
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Is the QRS axis normal or abnormal. Bonus: What is the rhythm
Is the QRS axis normal or abnormal? Bonus: What is the rhythm? (hint: the axis might help you decide )
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Rate and Rhythm?
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Rate and Rhythm?
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Rate and Rhythm?
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Rate and Rhythm?
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Rate and Rhythm?
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Rate and Rhythm?
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Rate and Rhythm?
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Scott E. Ewing DO Lecture #4
ECG Rhythm II - Scott E. Ewing DO Lecture #4
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8-Step Method ECG Interpretation
Rate Rhythm Axis P wave PR interval QRS complex QT interval ST segment and T wave
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Rhythm Atrial Junctional Ventricular Pacemaker Last but not least
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Premature Ventricular Contraction
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Interpolated PVC’s
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Multifocal PVC’s
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PVC Couplet
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PVC Triplet
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Ventricular Bigeminy
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Ventricular Trigeminy
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Ventricular Escape Rhythm
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Accelerated Idioventricular Rhythm
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Wide Complex Tachycardia
Ventricular - regular Monomorphic ventricular tachycardia Fascicular tachycardia Right ventricular outflow tract tachycardia Ventricular - irregular Torsades de pointes tachycardia Polymorphic ventricular tachycardia Supraventricular Bundle branch block with aberrant conduction Atrial tachycardia with preexcitation
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Ventricular Tachycardia
VT rate normally 120300 bpm Rhythm is regular or almost regular ( < 40 ms beat to beat variation), unless disturbed by the presence of capture or fusion beats If a monomorphic broad complex tachycardia has an obviously irregular rhythm the most likely diagnosis is atrial fibrillation with either aberrant conduction or preexcitation
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Frontal Plane Axis QRS axis normally - 30° to + 90°, with the axis most commonly ~60° With VT mean frontal plane axis changes and often bizarre Axis shift > 40° left or right suggestive of VT Lead aVR is situated in the frontal plane at -210° aVR negative with normal cardiac axis aVR positive extremely abnormal axis to the left or right aVR positive originates close to the apex, with depolarization moving upwards towards base of the heart
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Axis Shift Favoring VT
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Direct Evidence of Independent Atrial Activity
With VT, sinus node continues to initiate atrial contraction P waves are dissociated from the QRS complexes and are positive in leads I and II Atrial rate usually slower than the ventricular rate AV dissociation usually diagnostic for VT, lack of direct evidence of independent P wave activity does not exclude the diagnosis
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AV Dissociation with VT
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Indirect Evidence of Independent Atrial Activity
Capture beat Occasionally an atrial impulse may cause ventricular depolarization via the normal conduction system Resulting QRS complex occurs earlier than expected and is narrow Shows that even at rapid rates the conduction system is able to conduct normally, thus making a diagnosis of SVT with aberrancy unlikely Capture beats are uncommon and their absence does not exclude the diagnosis
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Capture Beat
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Indirect Evidence of Independent Atrial Activity
Fusion beats Occurs when a sinus beat conducts to the ventricles via the AV node and fuses with a beat arising in the ventricles Resulting QRS complex has an appearance intermediate between a normal beat and a tachycardia beat Fusion beats are uncommon and their absence does not exclude the diagnosis
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Fusion Beat
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Fusion Beat
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Indirect Evidence of Independent Atrial Activity
QRS concordance throughout the chest leads QRS complexes in precordial leads are either predominantly positive or predominantly negative Presence of concordance suggests that the tachycardia has a ventricular origin Positive concordance probably indicates that the origin of the tachycardia lies on the posterior ventricular wall; the wave of depolarization moves towards all the chest leads and produces positive complexes Similarly, negative concordance is thought to correlate with a tachycardia originating in the anterior ventricular wall
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Answer: NSVT 28 yo female with palpitations and lightheadedness
Sinus rhythm (normal QTc) with non-sustained monomorphic VT (starting 2nd beat, rate 170 bpm) Ventricular beats have a LBBB pattern and inferior / borderline rightward QRS axis raising consideration of monomorphic VT arising from the RVOT Isolated PVCs and two ventricular couplets with the same morphology Retrograde P waves Patient had an idiopathic cardiomyopathy with global mild ventricular hypokinesis
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Answer: Accelerated Idioventricular Rhythm
67 yo man with previous acute MI with normal QRS duration Most consistent with AIVR, originating from the left ventricle and therefore accounting for the atypical RBBB morphology ST elevations in the precordial leads are likely due to the injury current from underlying acute myocardial infarction AIVR may be marker of reperfusion following acute MI 83 bpm too slow for VT and too fast for complete heart block
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Answer: VT with Rate 170 bpm
RBBB morphology is atypical (monomorphic R, rather than rSR', in V1), and the R:S ratio is less than 1 in V6, both suggestive of ventricular tachycardia Most common underlying diagnosis in adult patients with sustained monomorphic VT is coronary heart disease status post AMI This patient had a non-ischemic cardiomyopathy Morphology of the VT is suggestive of origin from the left side of the heart, near the base (RBBB with inferior/rightward axis)
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Answer: VT with Underlying ST and AV Dissociation
77 yo with CAD Wide complex tachycardia at 165 bpm and RBBB morphology Underlying sinus tachycardia at 136 bpm and AV dissociation confirming the diagnosis of VT (Note the clear sinus P wave just after 5th QRS) QRS morphology and axis are consistent with origin of the VT from the posterior septum Patient had a prior large inferior-posterior MI
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Torsades de pointes Tachycardia
Torsades de pointes (“twisting of points”) a polymorphic VT in which the cardiac axis rotates over a sequence of 520 beats QRS amplitude varies similarly, such that the complexes appear to twist around the baseline Usually associated with conditions that prolong QT interval Usually not sustained Recur unless the underlying cause is corrected May be prolonged May degenerate into ventricular fibrillation Transient prolongation of the QT interval is often seen in AMI and may lead to torsades de pointes Management different from the management of other VTs
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Torsades de pointes
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Torsades de pointes 62 yo woman on diuretics with syncope
Syncope recurred during this ECG recording Serum potassium concentration was 2.3 mEq/L
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Answer: Torsade de pointes
74 yo woman with syncope with life-threatening finding Complex ECG showing Underlying atrial fibrillation Long QT(U) Ventricular pacing with intermittent sensing failure Run of torsade de pointes-type of polymorphic ventricular tachycardia
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Pacemakers
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Atrial Pacemaker
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Ventricular Pacemaker
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Pacemaker Failure to Sense
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Pacemaker Failure to Capture
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Pacemaker Output Failure
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Pacemaker Fusion Beat
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Last But Not Least
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Ventricular Fibrillation
67 yo man at the onset of a cardiac arrest Arrow indicates the early-occurring PVC that initiates the ventricular flutter that rapidly deteriorates into ventricular fibrillation
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Ventricular Fibrillation
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Answer: Ventricular Fibrillation / Ventricular Flutter
51 year male seen in the emergency department Classic ECG obtained during a VF cardiac arrest Findings typical of ventricular fibrillation with more organized ventricular electrical activity in the second half of the strip consistent with ventricular flutter Characteristic systematic variation in QRS axis of torsade is not seen here (although torsade may degenerate terminally into ventricular fibrillation)
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Asystole
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