What is the QRS axis? Is it normal or abnormal?

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 )

Rate and Rhythm?

Rate and Rhythm?

Rate and Rhythm?

Rate and Rhythm?

Rate and Rhythm?

Rate and Rhythm?

Rate and Rhythm?

Scott E. Ewing DO Lecture #4 ECG 101 - Rhythm II - Scott E. Ewing DO Lecture #4

8-Step Method ECG Interpretation Rate Rhythm Axis P wave PR interval QRS complex QT interval ST segment and T wave

Rhythm Atrial Junctional Ventricular Pacemaker Last but not least

Premature Ventricular Contraction

Interpolated PVC’s

Multifocal PVC’s

PVC Couplet

PVC Triplet

Ventricular Bigeminy

Ventricular Trigeminy

Ventricular Escape Rhythm

Accelerated Idioventricular Rhythm

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

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

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

Axis Shift Favoring VT

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

AV Dissociation with VT

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

Capture Beat

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

Fusion Beat

Fusion Beat

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

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

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

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)

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

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

Torsades de pointes

Torsades de pointes 62 yo woman on diuretics with syncope Syncope recurred during this ECG recording Serum potassium concentration was 2.3 mEq/L

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

Pacemakers

Atrial Pacemaker

Ventricular Pacemaker

Pacemaker Failure to Sense

Pacemaker Failure to Capture

Pacemaker Output Failure

Pacemaker Fusion Beat

Last But Not Least

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

Ventricular Fibrillation

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)

Asystole