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Cardiac Arrhythmias-Tachycardia

Cardiac Arrhythmia-- Tachycardia

1. Supraventricular Tachycardia

A. Atrioventricular (AV) nodal re-entrant tachycardia
1) Most common cause of paroxysmal tachycardia
B. Wolff-Parkinson-White Syndrome (WPW)
C. Accessory atrioventricular (AV) conduction pathways(Kent bundles)
D. Atrial flutter
E. Atrial fibrillation
F. Ectopic atrial tachycardia

2. WPW characteristics

A. short PR interval wide QRS- delta wave accessory pathway
B. Free wall Left Atrium- Type A
C. Right Atrium: anterior superior- Type B Tricuspid
D. annulus: anterior ventricular septum- Tricuspid or Mitral
E. posterior ventricular septum
Reciprocating tachycardia
F. AV conduction- anterograde
G. Accessory bypass- retrograde
Atrial fibrillation
H. Life-threatening
I. Rapid conduction via accessory pathway

3. WPW Treatment

A. Surgical ablation- historical significance
B. Catheter ablation- successful in 80-99% of patients
'C. Drug treatment- often dangerous

4. Atrioventricular nodal re-entrant

A. Successfully treated with catheter ablation
1) Ectopic atrial tachycardia
a) Often multiple ectopic foci
b) Treated with catheter ablation

5. Atrial flutter- fibrillation

A. Mechanism
1) Multiple macro re-entrant circuits
2) Atrial refractory period
3) Structural, fibrosis, SVC, IVC, ASD
B. Effects
1) Irregular heart beats
2) Loss of AV synchrony
3) Risk of thromboembolism

6. Treatment– Pharmagologic

A. Rate Control
1) Digitalis, Beta-blockers, calcium channel blockers
2) Prevention
3) IA- Quinidine, procainamide, disoprymadine,
4) IC- Flecanide, propafenone
5) III- Solatol, amiodarone

7. Antiarrhythmic Drugs

Antiarrhythmic Drugs
I. Membrane StabilizersSodium ion inhibition
IAreduction in upstroke velocity; prolongs repolarizationQRS lengthen, QT lengthenQuinidine, Procainamide, Disoprymadine
IBNo change in upstroke velocity or repolarizationNoneLignocaine, Mexitiline
ICReduction in upstroke velocity; no change in upstroke velocityQRS widenEncainide, Flecainide, Propafenone
II Beta blockersBlock catacholamine actionBradycardia, PR increase, QT decreasePropranalol, Acebutolol, Atenolol
III Anti-arrhythmicsBlock patassium efflux; prolong repolarizationQT increaseAmiodarone, Sotalol
IV Ca-Channel blockersBlocks calcium channelsPR increaseVerapamil, Diltiazem

8. Treatment- Surgical

A. His bundle ablation
1) Pacemaker insertion (contols rate only)
B. "Corridor" procedure
1) Controls rate only
C. "Maze" procedure
1) Controls rate
2) Preserves AV synchrony
3) Reduces risk of thromboembolism

9. Atrial Fibrillation Incidence

Incidence of Atrial Fibrillation
Age (years)LVAD
Overall incidence = 0.4% of populaitonApproximately 1.5 million people in U.S
Ventricular Tachycardia

10. Etiology

A. Idiopathic
B. Non-ischemic Cardiomyopathy
C. RV Dysplasia
D. UHL's Syndrome (Parchment Heart)
E. Long QT syndrome
F. Ischemic Ventricular Tachycardia

12. I. Idiopathic

A. Usually normal ventricles although occasionally dilated

13. II. Non-ischemic Cardiomyopathy

A. Diffuse dilatation or both ventricles
B. patchy fibrosis

14. III. Arrhythmogenic RV Dysplasia

A. Congenital cardiomyopathy
B. Surgical Rx- RV free wall isolation

15. IV. UHL's Syndrome (Parchment heart)

A. No myocardial layer

16. V. Long QT syndrome

A. Criteria
1) Congenital deafness
2) Long QT
3) Syncopal episode- VF
4) Abnormal Repolarization
5) Torsades de pointes
6) Aggravated by Quinidine

17. Ischemic Ventricular Tachycardia

A. Periphery of scar
1) Endocardium and Subendocardium
2) Re-entrant problem
3) Non-uniform repolarization
4) Surgical Treatment
5) Mapping and endocardial resection
6) Endocardial cryoablation
7) Aneurysm repair

Extended Outline

Surgery for Supraventricular Arrhythmias

1. Introduction

A. Radiofrequency (RF) ablation has replaced surgery as treatment of choice for certain re-entrant arrhythmias.
1) Accessory pathways-- Wolff-Parkinson-White Syndrome
2) AV nodal pathways from perinodal pathways
3) Ectopic atrial tachycardias
4) Certain Type I atrial flutte
B. Surgery for RF ablation failures
C. Maze procedure for chronic paroxysmal or sustained atrial fibrillation/flutter

2. Accessory atrioventricular connections

A. Anatomy
1) Divide heart into four "spaces" (LV free wall, RV free wall, posterior, anterior septal).
2) RF ablation of right sided pathways from septum above TV, left sided from beneath MV annulus
3) No accessory pathways exist between the left and right fibrous trigone- the only area in A-V groove where atrial muscle is not in contact with ventricular muscle
4) Majority of L-sided pathways are juxta-annular
5) Right sided pathways are more variable
6) Anterior and posterior septal pathways are variable-unsuccessful RF ablation is likely due to pathways disparate from the true annulus
7) Pathways can cross horizontal and vertical planes
B. Complications of RF catheter ablation (RFCA) (may impact surgical technique)
1) Scarring and fibrosing relate directly to the amount of energy delivered
2) Direct RF ablation to LA side of A-V groove has resulted in the destruction of planes, injury to Cx, CA and CS
3) Excessive energy to RA planes has resulted in destruction of planes
C. Surgical Treatment
1) Indications
a) Recurrent reciprocating tachycardia
b) Poorly controlled (?refractory?) or toxic on medical treatment
c) failed RF ablation or require surgery for concommitant disease
d) Symptomatic, atrio-His, nodoventricular, fasiculoventricular fibers
2) Locating pathways
a) Locate preoperatively with EP studies and epicardial mapping
b) Activation sequence mapping on atrial and ventricular sides of A-V groove
c) Accessory pathways are located in: left free wall> posterior septal> right free wall> anterior septal
3) Surgical approach
a) Endocardial technique- divides ventricular end of accessory pathways
(1) localize pathway to one of four areas
(2) location in vertical plane may vary
(3) endocardial dissection does nothing for atrial end of pathway
(4) complete dissection of anatomical space (s) in every patient, regardless or localization
(5) "Broad-Bands" may necessitate dissection in two anatomic areas
(6) isolation of atrial rim of tissue required to retrograde conduction via juxta-annular pathway
b) Epicardial technique- divides atrial end of accessory pathways
4) Surgical Results
a) 100% success in correction of rhythm- no early or late recurrences
b) 0.5% operative mortality
c) Majority of RFCA failure secondary to anatomical abnormalities
d) Inappropriately aggressive RFCA may render patients surgically incurable due to tissue destruction in the A-V groove

3. AV Nodal reentrant tachycardia

A. Dual A-V conduction pathways, one fast, one slow through AV node or perinodal tissues
B. Anatomy
1) Triangle of Koch
a) Tendon of Todaro superiorly
b) Tricuspid annulus inferiorly
c) Coronary sinus posteriorly
d) Apex in central fibrous body and atrial portion of membranous septum
2) Exact position of AV node in triangle may be variable
C. Surgical treatment
1) Surgery for failure of RFCA or concomitant disease
2) Monitor A-V conduction time during application of cryolesions
3) Apply lesions to boundries of Triangle of Koch
4) Impending heart block signaled by an A-V interval of 200-300ms-"reversible knife"
5) A-V nodal reentrant tachycardia and accessory A-V connections should undergo treatment together
6) Nodoventricular and nodo-His corrections can be concurrently performed
D. Surgical Results
1) Only a single pathway remains
2) No early or late recurrence
3) Dissection of tissue anterior or posterior to A-V node has resulted in A-V block plus late recurrence

4. Ectopic or automatic atrial tachycardias

A. More common on right than left, may be multifocal
B. Surgical treatment
1) Preoperative localization necessary
a) GA may suppress ectopic focus
b) Intraoperative mapping without sophisticated computerized system is difficult
c) Ectopic tachyarrhythmias not inducible by standard programmed stimulation techniques
2) Options
a) Cryoablation
b) Wide excision with pericardial patch
c) Ablation and pericardial patch
d) Isolation
3) Left atrial focus isolation (left atrium remains tachycardic)
a) Option is to ablate His bundle, place pacemaker
4) Right atrial foci if circuit or focus cannot be localized
a) Option is to isolate
C. Surgical Results
1) No recurrence
2) No sequelae

5. Atrial flutter and fibrillation

A. Anatomy and electrophysiology
1) 4-6 wandering, independent "wavelets" with regional entrainment
2) Atrial reentrant circuits can become stable at short (<95ms) refractory periods
3) Critical mass, volume, or area of atrial tissue is required to maintain fibrillation
B. Fibrillation/Flutter is a continuum (Cox)
1) Single, macroreentrant Right sided circuit (flutter) to
2) Multiple, simultaneous macroreentrant circuits over left and right atria
3) Flutter dependent upon mechanical obstacles
4) Fibrillation shows anatomic independence, with transient circuits–not amenable to ablation
C. "Surgical Cure" or Atrial Fibrillation
1) Elimination of clinical arrhythmia
2) Maintenance of SA nodal tissue as driving impulse
3) Maintenance of A-V conduction
4) Restoration of atrial transport function
5) Items 1-4 reduce the risk of thromboembolism
D. Idiopathic Atrial Fibrillation (Maze procedure)
1) Drug resistant, medically refractory, symptomatic idiopathic (non-Rheumatic) fibrillation
2) Mean age = 56 y.o. , concomitant procedure in 28% or patients
3) 40% require postoperative pacemakers- atrial chronotropic incompetence
4) Atrial transport- 100% RA, 81% LA
5) Local effective refractory period (ERP)- shorter in LA than RA
6) RA more susceptible to reentrant atrial flutter
7) LA more susceptible to reentrant atrial fibrillation
E. Atrial fibrillation associated with degenerative mitral valve disease- indications for Maze procedure
1) <70 years old
2) Normal ventricular function
3) History of H/O embolic events secondary to more that one year of atrial fibrillation
4) Medically refractory and severely symptomatic
5) LA dimension >60 mm
6) Easily reparable valve
F. Maze procedure- indications for Rheumatic Mitral valve disease
1) Modifications usually involve LA (forms of LA isolation)
Surgery for Ventricular Tachyarrhythmias

1. Patient population at risk

A. Usually related to some form of cardiac disease
B. Patients most at risk for life-threatening arrhythmias are:
1) Those sustaining sudden cardiac death without identified cardiac disease
2) Those with known cardiac disease (including post-MI)
3) Those with structural heart defects with known arrhythmogenic potential
a) Long QT, arrhythmogenic dysplasia
C. Sudden cardiac death (350,000-400,000 per year)
1) Often during mild-to-moderate exercise
2) More than 30% of survivors are discharged without neurologic deficit
3) 60% chance of recurrence within 2 years
4) Increased risk of: proximal LAD stenosis, regional LV dysfunction, LV failure (CHF)
5) Overall 50% 5 year survival vs. 80% for age matched cohorts
6) ~70% are not MI related
a) Greater risk of recurrence
b) 2/3 will have significant CAD
D. Ventricular tachycardia following MI results in 40-80% mortality
1) Prior infarct with aneurysm yields an even greater risk
E. If CAD present, CABG better than anti-anginal treatment

2. Pathophysiology

A. Wide QRS >14 msec is diagnostic of Ventricular- tachycardia (nl=<80 msec)
B. Polymorphic (vs monomorphic)
1) No constant morphology for > 5 complexes, or
2) No clear isoelectric baseline, or
3) QRS complexes asynchronous in multiple leads
4) Frequently degenerates into VF
C. Sustained tachycardia– at least 15 seconds
D. Possible mechanisms:
1) Reentry
2) Normal/abnormal automaticity
3) Triggered activity due to after-depolarization
E. Action potential
1) Resting membrane potential (electrical diastole = -85 mV)
2) Electrical, mechanical or chemical signal reduces membrane potential
3) At threshold, cell will depolarize (phase 0), reversing polarity to +30 mV
F. Automaticity
1) Resting membrane potential (phase 4) is characteristically constant
2) Some specialized cells will automatically depolarize until they reach threshold, depolarize and initiate beat
3) Depolarization is usually most rapid in SA node, which dominates rhythm
4) Peri-MI tachycardias
a) Associated with: hypoxemia, hypocalcemia, catacholamines, drugs (digitalis)
b) Usually responsive to:
(1) lidocaine, procainamide, Beta- blockade, discontinuing sympathomimetics
c) Phase 4 dependent arrhythmias are not induced or terminated by EP testing and are rarely approached surgically
5) Triggered automaticity
a) Arises during repolarization when late after-depolarizations reach threshold
G. Re-entrant arrhythmias
1) Two or more electrically heterogenous pathways of varying conduction or refractoriness
a) Unilateral block
b) Slow conduction over alternative route
c) Delayed excitation just distal to blocked tissue
d) Re-excitation of proximal tissue upon return of the impulse
H. Pathophysiologic substrate for ventricular arrhythmias
1) Chronic CAD (ischemia)
a) Usually gives rise to reentrant arrhythmia
b) Alters conduction and refractoriness
2) Acute infarction
a) Peri-ischemic areas of abnormal, viable tissue
b) Alters conduction and refractoriness
c) Heterogeneous infarcts are more arrhythmogenic than homogenous infarcts
I. Effect of thrombolytic therapy on then arrhythmogenic substrate
1) Canine data would predict increased arrhythmias
2) Clinically, no significant increase in life-threatening arrhythmias
J. Programmed Electrical Stimulation (EPS)
1) Rapid ventricular pacing
a) Burst pacing at 250 bpm
b) Single, double or triple stimulus to terminate arrhythmia
c) Hemodynamic instability may require instability
2) Premature ventricular stimuli
a) Depolarization introduced in late stimuli, then earlier, until no ventricular response is elicited
b) In no VT, double stimuli introduced 50-100ms after refractory period
c) S1 (fixed), S2 (premature stimulus), S1-S2 interval reduced by 10ms
d) When S2 no longer initiates ventricular response, S3 is initiated, S2-S3 interval then decreased
e) Reentrant arrhythmia or refractoriness of S2, S3 occurs
f) Multiple sites studied
g) Ventricular tachycardia secondary to automaticity, not induced my EPS

3. Surgical Treatment

A. Indirect techniques
1) Myocardial revascularization
2) Blind aneurysmectomy (non-directed, without electrophysiological mapping)
3) 50% success, 25% mortality
B. Encircling endocardial ventriculotomy (EEV)
1) Endocardial incision which completely encircles fibrosis (‘twilight zone' around infarct)
2) Isolates arrhythmogenic substrate and reentrant circuit
3) Higher mortality than endocardial resection (incision sparing only epicardial surface induces regional ischemia)
4) Extremely limited application
C. Electrophysiologically directed endocardial resection
1) Intraoperative mapping on CPB, normothermic
2) Endocardial resection
3) Many modifications, each with similar success to endocardial resection
a) Cryoablation
b) Laser
c) Sequential resection (normothemic)
4) Cumulative 14.4% mortality
D. Implantable Cardioverter Defibrillator (ICD)
1) Historical controls- 26% chance of 1-year sudden death
2) ICD implantation– 98-99% one year freedom from sudden cardiac death
3) Endocardial leads have replaced (almost all) epicardial patches
E. Results of non-pharmacological therapy
1) Subendocardial resection
a) 17%- inducible, sustained monomorphic VT post-op
b) 11%- required antiarrhythmic medication
2) ICD
a) 1.5% 30-day mortality
b) 70% 5-year survival

4. Treatment Strategies

A. LVEF is most important determinant of outcome
B. If EPS suggests an arrhythmogenic focus can be ablated– subendocardial resection
C. Inferior LV wall– 41% failure of subendocardial resection (difficult area); therfore, consider ICD
D. Non-ischemic VT– subendocardial resection not applicable
E. Arrhythmogenic events >/= 2 weeks ICD not a good choice
F. Drug requirements following procedure
1) Endocardial resection-- 11%
2) ICD– ~50%
G. ICD– restricted lifestyle
Pacemaker Therapy for Cardiac Arrhythmias

1. Anatomic principles

A. Mature conduction system
1) Sinoatrial (SA) node: spindle-shaped bundle with hear extending toward intra-atrial groove, tail toward IVC
2) Preferential conduction but not anatomic pathway from SA to atrioventricular (AV) node
a) Atrial muscle tract in ant limbus of fossa ovalis, crista terminalis and continuation to atrial septum
3) No gross anatomical landmarks for AV node and bundle of His– located within Triangle of Koch
a) Tendon of Todaro superiorly
b) Tricuspid annulus inferiorly
c) Coronary sinus posteriorly
d) Apex in central fibrous body and atrial portion of membranous septum
e) AV node is usually far removed (anteriorly) from coronary sinus
f) AV node becomes a penetrating bundle at apex of triangle, passes into ventricular septum
g) Branching and non-branching bundles are sandwiched between muscular ventricular and membranous septum
h) Compact node, penetrating bundle and branching bundle form a continuous axis of cells running the length of the ventricular septum
4) Endocardial anatomy
a) Atrial leads are designed for placement in (pectinate muscle) atrial appendage
b) Ventricular leads– apex (trabeculae)

2. Electrophysiology of cardiac pacing

A. Myocardial cells can be depolarized by artificial electrical stimulation
B. Impulse initiation and propagation
1) Resting potential (-90 mV in ventricular tissue, -50 mV in SA and AV nodal tissue
a) Function of intracellular and extracellular K+
b) At rest, Na and Ca channels are closed, small number of K channels open
c) With depolarizing stimulus, Na channels open and K channels close
2) Na-dependent (fast response) action potential (normal atrial and ventricular myocardial cells and conduction tissue outside SA and AV nodes)
a) Phase 0– cell depolarized to +20 millivolts
b) Phase 1– Na influx causes Ca and K channels to open (repolarization)
c) Phase 2– inward Ca current and persistent outward K current cause plateau
d) Phase 3– increased outward K flow and decreased inward Ca (and Na) flow– repolarization
3) Slow response action potential
a) Na channels are voltage-inactivated, Ca channels carry inward current
b) Action potential with slow rate of rise
c) Can be seen in pathologic states
4) Propagation of cardiac impulse
a) Nexal junction provide low-resistance intercellular pathway
b) Anistrophy- propigation along fibers is much faster than across fibers
c) Automaticity- the ability to generate an action potential de novo
d) Overdrive suppression
(1) stimulation of a cell at a rate above its intrinsic rate
(2) suppression of the cell's pacemaker ability results
(3) cells with lower (less negative) resting potentials and less Na entry during phase 0 have a lower degree of overdrive supression– thus the SA node is the primary pacemaker
C. Physics/Engineering
1) V=IR; where V= voltage, I= current (mAmps) and R= resistence (Kohms)
2) E=VIt; where E= energy ( Joules), t=time (pulsewidth PW in msec)
3) E= (V)2 x PW/R [??is that V squared or x2?]
4) The size of the distal tip is inversely proportional to the concentration of the electrical charge, and therefore the amount of energy required to capture myocardium
D. Sensing intra-myocardial electrical activity
1) Circuitry includes: sensing amplifier, bandpass filter, threshold comparator
2) Factors affecting sensing
a) Electrode size,
b) Unipolar/ bipolar configuration
c) Lead position

3. Current pacemaker technology

A. Permanent leads
1) Endocardial unipolar or bipolar
a) Active fixation leads–more stable, higher pacing thresholds
b) Passive fixation leads- lower chronic pacing leads
2) Epicardial- historically poorer performance
B. Pulse genterator

4. Clinical cardiac pacing

A. Terminology
1) Blanking period- turning off of sensor to avoid saturation by an anticipated high-voltage signal
2) Refractory periods- incorporated into pacing cycle to avoid resetting pacer in response to an appropriate signal (e.g. T-wave being interpreted as R-wave)
3) Lower rate interval- longest interval between consecutive ventricular paced events
4) A-V interval
5) Atrial escape interval- interval from ventricular pacing stimulus (or sensed beat) following atrial stimulus
B. Modes
1) VOO- risk of ventricular arrhythmia due to pacing on T-wave of intrinsic depolarization
2) VVI- lose of A-V synchrony
3) AAI- infrequently used, for chronotropic support normal AV conduction
4) DVI
a) Committed- delivers ventricular pacing stimulus at A-V interval regardless of sensed ventricular event
b) Noncommitted- inhibits ventricular output if ventricular activity is sensed
5) DDD- incorporates AAI, DVI and VDD modes
C. Rate responsiveness
1) Patient- improved sense of well being at rest, less tendency to develop CHF
D. Acute electrophysiologic testing of leads
1) Pacing threshold energy requirement
2) Atrial and ventricular electrogram amplitudes
3) Slew rates (if necessary)
4) P, R wave amplitude
5) Lead resistence
6) Current at the threshold level for capture of chamber paced
7) Threshold will increase in first 2-3 weeks then decrease to 2-3x initial measured level

5. Complications

A. Implantation
1) Venous access
2) Wire trauma
3) Generator
B. Post-surgical
1) Late perforation
2) Venous thrombosis
3) Loss of capture in a lead
a) Lead fracture- high impedence
b) Insulation break- low impedence
c) Exit block- fibrosis around electrode inhibits conduction
4) Pacemaker mediated tachycardia- macroreentrant circuit
5) Infection- treat with generator/ lead removal