Cardiac Arrhythmias II: Tachyarrhythmias Michael H. Lehmann, M.D. Clinical Professor of Internal Medicine Director, Electrocardiography Laboratory

Supraventricular Tachycardias (Supraventricular - a rhythm process in which the ventricles are activated from the atria or AV node/His bundle region)

Supraventricular Tachycardia (SVT) Terminology QRS typically narrow (in absence of bundle branch block); thus, also termed narrow QRS tachycardia Usually paroxysmal, i.e, starting and stopping abruptly; in which case, called PSVT “Paroxysmal Atrial Tachycardia (PAT)” - the older term for PSVT - is misleading and should be abandoned

AV Junctional Reentrant Tachycardias (typically incorporate AV nodal tissue)

Mechanism of Reentry Bidirectional Unidirectional Recovery of Conduction Unidirectional Block Recovery of Excitability & Reentry

AV Nodal Reentrant Tachycardia

AV Nodal Reentrant Tachycardia Circuit F = fast AV nodal pathway S = slow AV nodal pathway (His Bundle) During sinus rhythm, impulses conduct preferentially via the fast pathway

Initiation of AV Nodal Reentrant Tachycardia PAC PAC PAC = premature atrial complex (beat)

AV Nodal Reentrant Tachycardia Sustainment of AV Nodal Reentrant Tachycardia Rate 150-250 beats per min P waves generated retrogradely (AV node  atria) and fall within or at tail of QRS

Sustained AV Nodal Reentrant Tachycardia P P P P Note fixed, short RP interval mimicking r’ deflection of QRS

Orthodromic AV Reentrant Tachycardia Anterogade conduction via normal pathway AP Retrograde conduction via accessory pathway (AP)

AV ReentrantTachycardia Initiation of Orthodromic AV ReentrantTachycardia PAC Atria AP AVN Ventricles PAC = premature atrial complex (beat)

AV Reciprocating Tachycardia Sustainment of Orthodromic AV Reciprocating Tachycardia Atria Rate 150-250 beats per min AP AVN Ventricles Retrograde P’s fall in the ST segment with fixed, short RP

Ventricular Preexcitation (Wolff-Parkinson-White Syndrome) Accessory Pathway with Ventricular Preexcitation (Wolff-Parkinson-White Syndrome) Sinus beat Hybrid QRS shape “Delta” Wave PR < .12 s AP Fusion activation of the ventricles QRS  .12 s

Ventricular Preexcitation Varying Degrees of Ventricular Preexcitation

Intermittent Accessory Pathway Conduction V Preex V Preex Normal Conduction Note “all-or-none” nature of AP conduction

Orthodromic AV Reentrant Tachycardia NSR with V Preex Note retrograde P waves in the ST segment SVT: V Preex gone

Concealed Accessory Pathway Sinus beat No Delta wave during NSR (but AP capable of retrograde conduction)

Summary of AV Junctional Reentrant Tachycardias Reentrant circuit incorporates AV nodal tissue P waves generated retrogradely over a fast pathway Short, fixed RP interval

Clinical Significance of AV Junctional Reentrant Tachycardias Rarely life-threatening However, may produce serious symptoms (dizziness or syncope [fainting]) Can be very disruptive to quality of life Involvement of an accessory pathway can carry extra risks

Atrial Tachyarrhythmias

Sinus Tachycardia (100 to 180+ beats/min) P waves oriented normally PR usually shorter than at rest

Causes of Sinus Tachycardia Hypovolemia ( blood loss, dehydration) Fever Respiratory distress Heart failure Hyperthyroidism Certain drugs (e.g., bronchodilators) Physiologic states (exercise, excitement, etc)

Premature Atrial Complex (PAC) V5 Non-Compensatory Pause P P P P’ P Timing of Expected P

Premature Atrial Complex (PAC): Alternative Terminology Premature atrial contraction Atrial extrasystole Atrial premature beat Atrial ectopic beat Atrial premature depolarization

PACs: Bigeminal Pattern Note deformation of T wave by the PAC “Regularly Irregular” Rhythm

PACs with Conduction Delay/Block Physiologic AV Block P P’ Physiologic AV Delay P P’ Recovered AV Conduction P P’

(Physiologic Delay in the His Purkinje System) PAC with “Aberrant Conduction” (Physiologic Delay in the His Purkinje System) V1 P P P’ P RBBB

PACs with Aberrant Conduction (Physiologic RBBB and LBBB) V1 RBBB LBBB Normal conduction

PACs with Physiologic LBBB and His-Purkinje System Block V1 Non-conducted PAC

Non-Conducted PAC V5 V1 P P P’ P Note deformation of T wave by the PAC

Bigeminal/Blocked PACs Mimicking Sinus Bradycardia V1 Only the 4th bigeminal PAC conducts

Clinical Significance PAC’s Common in the general population May be associated with heart disease Can be a precursor to atrial tachyarrhythmias

Atrial Tachycardia V1 RP intervals can be variable Differs from RP often > PR (Example slower than more common rate mof 150-250 beats per min) Differs from AV nodal or AV reentrant SVT

Clinical Significance of Atrial Tachycardia Similar to sequela of AV junctional reentrant tachycardias Must be differentiated from them diagnostically

(“Typical,” Counterclockwise) Atrial Flutter (“Typical,” Counterclockwise) Reentrant mechanism

Atrial Flutter Classic inverted II “sawtooth” flutter waves at 300 min-1 (best seen in II, III and AVF) II 4:1 2:1 V1 Note variable ventricular response

Atrial Flutter V. rate 2:1 140-160 Conduction beats/min (common) 2:1 & 3:2 Conduction 1:1 Conduction (rare but dangerous)

Atrial Fibrillation Focal firing or multiple wavelets Chaotic, rapid atrial rate at 400-600 beats per min

Atrial Fibrillation V5 V1 Rapid, undulating baseline (best seen in V1) Most impulses block in AV node  Erratic conduction

Atrial Fibrillation: Characteristic “Irregularly Irregular” Ventricular Response II

Rapid Ventricular Response Atrial Fibrillation with Rapid Ventricular Response II Irregularity may be subtle

of Ventricular Response Atrial Fibrillation: Autonomic Modulation of Ventricular Response Baseline Immediately after exercise

Clinical Significance of Atrial Flutter and Fibrillation Causes Usually occur in setting of heart disease; but sometimes see “lone “ atrial fibrillation Hyperthyroidism (atrial fibrillation) May acutely precipitate myocardial ischemia or heart failure Chronic uncontolled rates may induce cardiomyopathy and heart failure Both can predispose to thromboembolic stroke, etc

Ventricular Preexcitation Varying Degrees of Ventricular Preexcitation

Atrial Fibrillation with Rapid Conduction Via Accessory Pathway

Atrial Fibrillation with Third Degree AV Block Regular ventricular rate reflects dissociated slow junctional escape rhythm

Regular Narrow QRS Tachycardias

Differential Diagnosis of Regular Narrow QRS (Supraventricular) Tachycardia Reentrant SVT incorporating AV nodal tissue AV nodal reentrant tachycardia Orthodromic AV reentrant tachycardia SVT mechanism confined to the atria Sinus tachycardia Atrial flutter Other regular atrial tachycardias Short-RP favors AV node-dependent reentrant SVT

Determining AV Nodal Participation in SVT by Transiently Depressing AV Nodal Conduction Vagotonic Maneuvers Carotid sinus massage Valsalva maneuver (bearing down) Facial ice pack (“diving reflex;” for kids) Adenosine (6-12 mg I.V.) If SVT “breaks,” a reentrant mechanism involving the AV node is likely If atrial rate unchanged, but ventricular rate slows (#P’s > #QRS’s), SVT is atrial in origin

SVT Responses to AV Nodal Depressant Maneuvers SVT termination AV nodal reentrant tachycardia Orthodromic AV reentrant tachycardia No SVT termination (despite maximal attempts) Sinus tachycardia Atrial flutter or fibrillation Most atrial tachycardias (a minority are “adenosine-sensitive”)

Carotid Sinus Massage Stimulation of carotid sinus triggers baroreceptor reflex and increased vagal tone, affecting SA and AV nodes

Vagotonic Maneuver (Carotid Sinus Massage) Termination of SVT by Vagotonic Maneuver (Carotid Sinus Massage)

SVT Carotid Sinus Massage

SVT Adenosine 6 mg P P P P

Ventricular Tachyarrhythmias

Premature Ventricular Complex (PVC): Alternative Terminology Premature ventricular contraction Ventricular extrasystole Ventricular premature beat Ventricular ectopic beat Ventricular premature depolarization

Premature Ventricular Complex (PVC) Compensatory Pause

PVCs: Bigeminal Pattern “Regularly Irregular” Rhythm

Accelerated Idioventricular Rhythm ( Ventricular Escape Rate, but  100 bpm) Fusion beat Ectopic ventricular activation Sinus acceleration Normal ventricular activation

AV Dissociation ATRIA AND VENTRICLES ACT INDEPENDENTLY SA Node Ventricular Focus

Ventricular Tachycardia (VT) Rates range from 100-250 beats/min Non-sustained or sustained P waves often dissociated (as seen here)

Ladder Diagram of AV Dissociation During Ventricular Tachycardia Slower atrial rate Faster ventricular rate Impulses invade the AV node retrogradely and anterogradely, creating physiologic “interference” and block. Under the right conditions, some anterograde impulses may slip through. This phenomenon is not equivalent to third degree AV block

Ladder Diagram of AV Dissociation During Third Degree AV Block Faster atrial rate Slower ventricular (escape) rhythm Note that impulses block anterogradely and retrogradely within the AV conduction system

Monomorphic VT

Polymorphic VT V1

Causes of PVC’s and VT PVC’s are fairly common in normals but are also seen in the setting of heart disease Monomorphic VT often implies heart disease, but can sometimes be seen in structurally “normal” hearts Polymorphic VT can result from myoardial ischemia or conditions that prolong ventricular repolarization Electrolyte derangements, hypoxemia and drug toxicity can cause PVC’s and VT

MI Scar-Related Sustained Monomorphic VT Circuit

(Polymorphic VT Associated with Prolonged Repolarization) “Torsade de Pointes” (Polymorphic VT Associated with Prolonged Repolarization)

Clinical Significance of PVC’s and VT Can be a tip-off to underlying cardiac, respiratory or metabolic disorder VT may (but need not invariably) lead to hemodynamic collapse or more life-threatening ventricular tachyarrhythmias, increasing the risk of cardiac arrest

Ventricular Flutter VT  250 beats/min, without clear isoelectric line Note “sine wave”-like appearance

Ventricular Fibrillation (VF) Totally chaotic rapid ventricular rhythm Often precipitated by VT Fatal unless promptly terminated (DC shock)

Sustained VT: Degeneration to VF

Atrial Fibrillation with Rapid Conduction Via Accessory Pathway: Degeneration to VF

Diagnosing Regular Wide QRS Tachycardia

VT or SVT with Aberrant Conduction? Regular Wide QRS Tachycardia: VT or SVT with Aberrant Conduction? V1

Sustained Aberrant Conduction V1

Clinical Clues to Basis for Regular Wide QRS Tachycardia REMEMBER: VT does not invariably cause hemodynamic collapse; patients may be conscious and stable History of heart disease, especially prior myocardial infarction, suggests VT Occurrence in a young patient with no known heart disease suggests SVT 12-lead EKG (if patient stable) should be obtained

VT or SVT with Aberrant Conduction? Regular Wide QRS Tachycardia: VT or SVT with Aberrant Conduction?

More R-Waves Than P-Waves Implies VT! II

Artifact Mimicking “Ventricular Tachycardia” QRS complexes “march through” the pseudo-tachyarrhythmia Artifact precedes “VT”