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)

UnidirectionalBlock

Recovery of Excitability & Reentry

BidirectionalConduction

Mechanism of 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 preferentiallyvia the fast pathway

Initiation of AV Nodal Reentrant Tachycardia

PAC = premature atrial complex (beat)

PAC

PAC

Sustainment of AV Nodal Reentrant Tachycardia

Rate 150-250beats per min

P waves generatedretrogradely(AV node atria) andfall within orat tail of QRS

P P P P

Sustained AV Nodal Reentrant Tachycardia

Note fixed, short RP interval mimicking r’ deflection of QRS

V1

Orthodromic AV Reentrant Tachycardia

AP

Anterogadeconduction via normal pathwayRetrograde

conductionvia accessorypathway (AP)

Initiation of Orthodromic AV ReentrantTachycardia

AVN

Ventricles

Atria

AP

PAC = premature atrial complex (beat)

PAC

Sustainment of Orthodromic AV Reciprocating Tachycardia

Atria

AP

AVN

Ventricles

Retrograde P’s fall in the ST segmentwith fixed, short RP

Rate 150-250beats per min

Accessory Pathway with Ventricular Preexcitation(Wolff-Parkinson-White Syndrome)

Fusion activation of the ventricles

“Delta” Wave

APPR < .12 s

QRS .12 s

Sinusbeat

Hybrid QRS shape

Varying Degrees of Ventricular Preexcitation

Normal synchronousoverlapping activationof both ventricles:

On timeAsynchronous

scenario I:

Late

Head startOn time(or late)

Asynchronous scenario II:

QRS

Narrow

Wide

Wide

QRS Width: Synchronous vs. Asynchronous Ventricular Activation

Intermittent Accessory Pathway Conduction

NormalConduction

V Preex V Preex

Note “all-or-none” nature of AP conduction

Orthodromic AV Reentrant Tachycardia

NSR with V Preex

SVT:V Preex gone

Note retrograde P wavesin the ST segment

Concealed Accessory Pathway

No Delta wave during NSR(but AP capable of retrogradeconduction)

Sinusbeat

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)

V5

P P P P’ P

Timing of Expected P

Premature Atrial Complex (PAC)

Non-Compensatory Pause

Premature Atrial Complex (PAC): Alternative Terminology

• Premature atrial contraction

• Atrial extrasystole

• Atrial premature beat

• Atrial ectopic beat

• Atrial premature depolarization

PACs: Bigeminal Pattern

P P’ P P’ P P’

• Note deformation of T wave by the PAC• “Regularly Irregular” Rhythm

PACs with Conduction Delay/Block

Physiologic AV Block

PhysiologicAV Delay

Recovered AV Conduction

P

P

P

P’

P’

P’

PAC with “Aberrant Conduction”(Physiologic Delay in the His Purkinje System)

V1

P P P’ P

RBBB

V1

PACs with Aberrant Conduction(Physiologic RBBB and LBBB)

RBBB LBBB Normalconduction

PACs with Physiologic LBBB and His-Purkinje System Block

V1

Non-conductedPAC

Non-Conducted PAC

P P PP’

V5

V1

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

• RP intervals can be variable • RP often > PR• (Example slower than more common rate mof 150-250 beats per min)

Atrial Tachycardia

V1

Differs fromAV nodal or AV reentrantSVT

Clinical Significance of Atrial Tachycardia

• Similar to sequela of AV junctional reentrant tachycardias

• Must be differentiated from them diagnostically

Atrial Flutter (“Typical,” Counterclockwise)

Reentrant mechanism

II

V1

Atrial Flutter

4:1 2:1

Classicinverted “sawtooth”flutter wavesat 300 min-1 (best seen inII, III and AVF)

Note variableventricularresponse

Atrial Flutter

2:1Conduction(common)

2:1 & 3:2Conduction

1:1Conduction(rare but dangerous)

V. rate 140-160beats/min

Atrial Fibrillation

Focal firingormultiplewavelets Chaotic, rapid

atrial rate at400-600beats per min

V5

Atrial Fibrillation

• Rapid, undulating baseline (best seen in V1)• Most impulses block in AV node Erratic conduction

V1

Atrial Fibrillation: Characteristic “Irregularly Irregular” Ventricular Response

II

Atrial Fibrillation with Rapid Ventricular Response

II

Irregularity may be subtle

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

Varying Degrees of Ventricular Preexcitation

Atrial Fibrillation with Rapid Conduction Via Accessory Pathway

Atrial Fibrillation with Third Degree AV Block

V1

V5

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 baroreceptorreflex and increased vagaltone, affectingSA and AV nodes

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

Normal synchronousoverlapping activationof both ventricles:

On timeAsynchronous

scenario I:

Late

Head startOn time(or late)

Asynchronous scenario II:

QRS

Narrow

Wide

Wide

QRS Width: Synchronous vs. Asynchronous Ventricular Activation

PVCs: Bigeminal Pattern

“Regularly Irregular” Rhythm

Ectopic ventricular activation

Normal ventricular activation

Fusionbeat

Accelerated Idioventricular Rhythm ( Ventricular Escape Rate, but 100 bpm)

Sinus acceleration

SANode

Ventricular Focus

ATRIA AND VENTRICLESACT INDEPENDENTLY

AV Dissociation

V1

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 retrogradelywithin the AV conduction system

Monomorphic VT

V1

Polymorphic VT

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

“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

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

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

More R-Waves Than P-Waves Implies VT!

II

Artifact Mimicking “Ventricular Tachycardia”

Artifact precedes“VT”

QRS complexes “march through”the pseudo-tachyarrhythmia