Atrial Fibrillation Electrophysiology

The normal electrical conduction system of the heart allows the impulse that is generated by the sinoatrial node (SA node) of the heart to be propagated to and stimulate the myocardium (muscle of the heart). When the myocardium is stimulated, it contracts. It is the ordered stimulation of the myocardium that allows efficient contraction of the heart, thereby allowing blood to be pumped to the body.

In atrial fibrillation, the regular impulses produced by the sinus node for a normal heartbeat, are overwhelmed by rapid electrical discharges produced in the atria and adjacent parts of the pulmonary veins. Sources of these disturbances are either automatic foci, often localized at one of the pulmonary veins, or a small number of reentrant sources (rotors) harbored by the posterior wall of the left atrium near the junctions with the pulmonary veins. The pathology progresses from paroxysmal to persistent AF as the sources multiply and localize anywhere in the atria. Because recovery of the atria from excitation is heterogeneous, the electrical waves generated by the AF sources undergo repetitive, spatially distributed breakup and fragmentation in a process known as “fibrillatory conduction”.

AF can be distinguished from atrial flutter (AFL), which appears as an organized electrical circuit usually in the right atrium. AFL produces characteristic saw-toothed F-waves of constant amplitude and frequency on an ECG whereas AF does not. In AFL, the discharges circulate rapidly at a rate of 300 beats per minute (bpm) around the atrium. In AF, there is no regularity of this kind, except at the sources where the local activation rate can exceed 500 bpm.

Although the electrical impulses of AF occur at a high rate, most of them do not result in a heart beat. A heart beat results when an electrical impulse from the atria passes through the atrioventricular (AV) node to the ventricles and causes them to contract. During AF, if all of the impulses from the atria passed through the AV node, there would be severe ventricular tachycardia resulting in severe reduction of cardiac output. This dangerous situation is prevented by the AV node since its limited conduction velocity reduces the rate at which impulses reach the ventricles during AF.

Resources: ^ Klabunde, Richard (2005). Cardiovascular Physiology Concepts. Lippincott Williams & Wilkins. pp. 25, 28. ISBN 978-0781750301.

Characteristics

Arrhythmogenic Right Ventricular Dysplasia, also known as arrhythmogenic right ventricular cardiomyopathy, is characterized by replacement of the right ventricular muscle by fatty and fibrous tissue. Patients usually present with arrhythmias of right ventricular origin that range from isolated premature ventricular beats to nonsustained or sustained VT and ventricular fibrillation. Other clinical manifestations include global or regional right ventricular dysfunction, ECG changes, and late evolution to right or biventricular heart failure. Tachycardia is due to reentry and has a LBBB morphology

EKG Characteristics

• Incomplete or complete RBBB
• Inverted T waves in the anterior precordial leads
• Localized prolongation of the QRS complex in leads V1 and V2
• Epsilon waves visible as sharp discrete deflections at the terminal portion of the QRS complex in the anterior precordial leads
• Use QRS width in Lead I which is always <120ms
• Lead III R>S
• S wave upstroke in V1 – V3 >55ms was found in 95 percent of ARVD

Imaging Characteristics

• Abnormal Signal Averaged ECG which is present in 50-80% of cases.
• Echo shows Right Ventricular dysfunction
• Workup with MRI

Criteria for Diagnosis

Family history

• Major
  • Familial disease confirmed at necropsy or surgery
• Minor
  • Family history of premature sudden death (<35 years of age) due to suspected ARVD
  • Family history {clinical diagnosis based on present criteria)

ECG depolarization/conduction abnormalities

• Major
  • Epsilon waves or localized prolongation (>110 ms) of QRS complex in right precordial leads (V1-V3)
• Minor
  • Late potentials on signal-averaged ECG

ECG repolarization abnormalities

• Minor
  • Inverted T waves in right precordial leads (V2 and V3) in people >12 years of age and in absence of right bundle branch block

Arrhythmias

• Minor
  • Sustained or nonsustaincd left bundle branch block-type VT documented on ECG, Holter monitoring or during exercise testing
  • Frequent ventricutar extrasystoles (> 1000/24 h on Holter monitoring}

Global or regional dysfunction and structural alterations

• Major
  • Severe dilatation and reduction ol RV ejection fraction with no or mild LV involvement
  • Localized RV aneurysms (akinetic or dyskinetic areas with diastolic bulgings)
  • Severe segmental dilatation of RV
• Minor
  • Mild global RV dilatation or ejection fraction reduction with normal LV
  • Mild segmental dilatation of RV
  • regional RV hypokincsia

Tissue characteristics of walls

• Major
  • Fibrofatty replacement of myocardium on endomyocardial biopsy

References

Diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy. Br Heart J 71:215, 1994

 RVOT Ventricular Tachycardia: EP Study, Mapping And Ablation

Background

RVOT Ventricular Tachycardia represents up to 10% of all Ventricular Tachycardias. Episodes usually begin between ages 20-40 years old and NSVT is frequent compromising 60-92% of the cases. Associated with no clearly defined structural heart disease. Patients usually present with palpitations that are occur with caffeine intake, stress, exercise (during or in recovery), or Hormonal triggers.

Mechanism

1. Tachycardia is due to cAMP mediated triggered activity.
2. Are usually adenosine sensitive.

Diagnosis

• In more than 80% of the cases, the QRS is LBBB with an inferior axis.
• The diagnosis is one of exclusion and ARVD must be ruled out. Sarcoidosis can also mimic RVOT VT
• MRI abnormalities can be seen in RVOT
• Long term prognosis is excellent and sudden death is rare

EP Evaluation

Pre Ablation

• Be certain to discontinue anti-arrhythmic agents for a minimum of five half lives prior to procedure.

Induction

• You may need up to 10 mcg of Isoproterenol Aminophylline, Phenylephrine or Epinephrine infusion to initiate VT. Also sedation may suppress the VT.
• Only 1/3 initiated with programmed stimulation and may need to use burst pacing.

Mapping

• When VT or PVCs occur record for future reference for pacemapping.
• To map advance the catheter to the Pulmonic Valve (area with no electrograms) most originate at the septal portion of the RVOT.
• Pacemap must be an identical match.

EKG Localization

RVOT Differential ECG

Free Wall Versus Septal

1. To differentiate RV free wall versus septum use the inferior leads which are typically broader (QRS > 140ms)
2. R wave notching in the inferior leads
3. Lead V3 R/S Ratio < 1

Anterior (Leftward) Versus Posterior (Rightward)

• Look at Lead I. Large positive R or qR wave signifies posterior (rightward) location and a negative QS signifies an anterior site. Middle sites are isoelectric.

Caudal (> 2 cm from PV) Versus Cranial

• VT arising with 2 cm of the pulmonary valve near the His bundle virtually always has a negative QRS in lead aVL

Epicardial

• To signifiy epicardial a ratio of time to R wave peak to total QRS duration greater tham 0.54 is a useful indicator

Ablation

• Ablation at successful sites tends to be only moderately early 10-60 msec pre before QRS onset
• Pacemapping adds little additional precision to sites based on 3D activation mapping.
• Fractionated potentials and diatolic potentials are rarely seen.
• The vast majority of RVOT VT, both septal (70-80%) and free wall (20-30%) originates 1-2cm beneath the pulmonary valve. It may also originate from the proximal pulmonary artery above the valve.
• Use 4 mm tip with temp control mode at 40-50W at 55 degrees for 60 seconds.
• Termination at successful sites generally occurs within 10 seconds with acceleration of the tachycardia then general slowing.
• Acute procedural success is 93% with a 5% recurrence rate

Difficult Cases

• Consider prexcited antidromic right sided tachycardias.
• A small number of RVOTs may originate in the epicardium near the AIV.

Medical Treatment

• Beta Blockers
• Calcium Channel Blockers
• Class 1 Anti-Arrhythmics
• Class 3 Anti-Arrhythmics

References

1. Utility of the 12-lead electrocardiogram in localizing the origin of right ventricular outflow tract tachycardia. Ram L. Jadonath, MD, David S. Schwartzman, MD, Mark W. Preminger, MD, Charles D. Gottlieb, MD, and Francis E. Marchlinski, MD. A~ HEART J 1995;130:1107-13.

ACTION POTENTIAL:

Phase o:  Cell is stimulated, cell menbrane is more permeable to sodium ions.

Phase 1:  Brief period of rapid repolarization:  sodium influx ends in fast channels: potassium flows out

Phase 2:   Plateau phase: influx of calcium and sodium through slow channels which sometimes occurs in Phase 0 and Phase 1:   Respondible for the refractory period during whic the depolarized stae is maintained.  Calcium’s role is related to the contractility of the heart.

Phase 3:  Negativity restored due to increased loss of intracellular potassium.

Phase 4:  Return to resting membrane potential (-90 mV).  Normal distribution of Na+ and K+ are restored.

Need a review of cardiac action potentials?  These instructional videos are fabulous!

Definitions of the Properties of Cardiac Function:

Automaticity:  the ability of certain cells in the heart to initiate electrical impulses spontaneously

Excitability:  the ability of the cardiac cells to respond to stimulation

Conductivity:  the ability to transmit an impulse through specialized conduction system and atrial / ventricular muscle

Refractoriness:  the inability to undergo repeat stimulation until after a certain period of time has elapsed

Contractility:  the ability of the fibers to shorten when stimulated, resulting in the contraction of muscle creating a pump action

Depolarization and Repolarization:

Polarized Cell:  The cell at rest.  The interior of the cell has a negative charge with respect to the outside.  Normal distribution of K+ and Na+ is maintained.

Depolarization:  The cardiac cell is stimulated when Na+ enters the cell and an inward electricla current is produced.

Repolarization:  The cell recovers as K+ leaves and outward electrical current is produced

Click Here  for animation of this process.

Refractory Periods:

Absolute Refractory Period (ARP):  a relatively long period following excitation during which cells cannot respond to another stimulus, regardless of its strength.  This period of time is roughly the duration of systole.

Relative Refractory Period (RRP):  a narrow window of time near the beginning of the ARP during which stimulus strength must be above normal and the response from which is less than normal.

Vulnerable Period:  not a refratory period but a window of time during the refractory phase that the heart is prone to develop fibrillation in response to a premature beat delivered at that time; generally corresponds to the top of the T wave.

Supernormal Period (SNP):  also not a refracctory period, but is an interval of time during which it may be possible for a premature stimulus to conduct with better than expected behavior.

A review of the action potential of the heart is appropriate here. You will love these instructional videos!