cardiac arrhythmias ii: tachyarrhythmias michael h. lehmann, m.d. clinical professor of internal...
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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