Approach To Arrythmias

Approach to Arrythmia’s Dan Merrick, MD 10/23/01

Basic to Understanding Arrhythmias is the understanding of their mechanism
Problems with impulse formation
Automaticity
Triggered impulses
2) Problems of impulse conduction
Reentry
Block

Arrythmias caused by problems of automaticity can originate in any cell in the pacemaking and conduction systems that is capable of spontaneous depolarization.

Arrythmias caused by problems of automaticity can originate in any cell in the pacemaking and conduction systems that is capable of spontaneous depolarization. Such cells, termed pacemaker cells, are present in the:
Sinus Node
Purkinje cells scattered through the atria
Common (His) bundle.
Right and left bundle branches
Purkinje system in the fascicles and peripheral network

The Action Potential

Fast Action Potentials Phase 0 is generated by inward sodium current. Duration…… Atrial cells < Ventricular < Purkinje Duration and contours of repolarization are determined largely by outgoing potassium currents and to a lesser degree inward calcium currents. Resting membrane potential = - 80 to - 90 mV. Activation threshold from - 60 to - 70 mV. V max = 300 to 900 V/s Action Potential amplitude = 90 – 130 mV

Slow Action Potentials Phase 0 is generated by inward calcium current. Rates of activation and inactivation are slower. Resting membrane potential = - 40 to - 70 mV. Activation threshold from - 30 to - 40 mV. Vmax is typically slow (< 15 V/s) The action potential amplitude is 35 to 75 mV

All cardiac tissue is innervated by both sympathetic and parasympathetic nerves.

All cardiac tissue is innervated by both sympathetic and parasympathetic nerves.
Both sets of fibers enter the ventricles in the region of the AV groove.
Sympathetic fibers initially course in a subendocardial location then penetrate the ventricular wall location to course along the epicardial surface.
The opposite occurs with the parasympathetic fibers.

Left panel, Intraventricular route of sympathetic and vagal nerves to the left ventricle. Right panel, Schematic of the transverse views of the right ventricular (RV) wall showing functional pathways of the efferent sympathetic and vagal nerves. Top right, Transverse view of the RV outflow tract at the upper horizontal line on the left. Bottom right, Transverse view of the anterolateral wall at the lower horizontal line on the left. The vertical solid line indicates the center of the RV anterolateral wall. Closed circles indicate positions of plunge electrodes labeled 1 to 6. IVS = interventricular septum; LAD = left anterior descending coronary artery; RA = right atrium; RCA = right coronary artery.

Atrial Innervation
Parasympathetic stimulation produces shortening of the duration of the action potential and slowing of conduction
Sympathetic stimulation also may shorten the duration of the action potential but, it accelerates conduction.

AV Node Innervation
Parasympathetic stimulation (as mediated by acetylcholine) results in slowing of condution and prolongation of refractoriness.
Sympathetic stimulation does the opposite.

Ventricular Innervation
Refractoriness is typically decreased by sympathetic stimulation and increased by parasympathetic stimulation.
Conduction is minimally affected by sympathetic or parasympathetic stimulation.

Schematic action potentials of a pacemaking cell. Sinus rhythm is shown in A. Excess sympathetic activity increases the slope of the slow spontaneous depolarization, creating an accelerated rhythm in B. Excess parasympathetic activity decreases the slope of the slow spontaneous depolarization, creating a decelerated rhythm in C. Arrows indicate the slow spontaneous depolarization in all three conditions.

Tonic vagal stimulation produces a greater absolute reduction in sinus rate in the presence of tonic background sympathetic stimulation, a sympathetic-parasympathetic interaction termed accentuated antagonism . The peak vagal effects on sinus rate and AV nodal conduction occur at different times in the cardiac cycle, a brief vagal burst can slow the sinus rate without affecting the AV nodal conduction or can prolong AV nodal conduction time and not slow the sinus rate.

The complex interplay of the Sympathetic and Parasympathetic system can be the cause of arrhythmias in disease states.
This complex interplay can also be used to advantage in the diagnosis and treatment of arrhythmias, e.g. carotid sinus massage.

A 12-lead ECG and lead-II rhythm strip from a 53-year-old woman with severe pulmonary emphysema. Arrows indicate marked variation in P-wave morphology in the rhythm strip.

Sinus Tachycardia

Reentry

The Three Prerequisites for Reentry
An available circuit
A difference in the refractory period of the two pathyways (limbs) in the circuit
Conduction that is sufficiently slow somewhere in the circuit to allow the remainder of the circuit to recover its responsiveness by the time the impulse returns.

The blue arrows reflect signal transmission down the “slow” pathway and the red arrows reflect transmission down the “fast” pathways. This dual depolarization of the channels is the norm.

A PVC initiates a retrograde impulse through the slow channel which sets up a re-entrant tachycardia.

Atrioventricular Bypass Tracts

In the normal heart, there are no muscular connections between the atria and ventricles. In 1893, Kent described the rare occurrence of such connections, but wrongly assumed that they represented pathways of normal conduction.

Schematic illustration of the anatomic relationship between the normal AV conduction system and the accessory AV conduction pathway provided by the Bundle of Kent. The solid bar represents the nonconducting structures (including the coronary arteries and veins, valves, and fibrous and fatty connective tissue) that prevent conduction of electrical impulses from the atrial myocardium to the ventricular myocardium. ( AVN , AV node; HB , His bundle; RBB , right bundle branch; KB , Kent bundle; LBB , left bundle branch.)

Relationship between an anatomic Bundle of Kent and physiologic preexcitation of the ventricular myocardium (top), and the typical ECG changes of ventricular preexcitation (bottom). Normal condition is presented (A) for contrast with the abnormal condition (B).

Top: The presence of a Kent bundle is indicated by the open space between the right atrium and ventricle, and the AV node by the open space at the summit of the interventricular septum. X indicates the site of the pacemaker: in the sinus node (A) and in the right atrium (B). No pacemaking is required in C. The arrows indicate the directions of impulse conduction. Bottom: the corresponding ECG, indicating sinus rhythm with a normal P wave immediately followed by the QRS complex, indicating ventricular preexcitation (A), an inverted P preceding the QRS complex, indicating an atrial premature beat without preexcitation (B), and an inverted P wave following the QRS complex, indicating a reentrant junctional tachycardia (C).

Who Cares ?????

WPW in a patient with Atrial Fibrillation.

• If the tachycardia has a narrow QRS complex (orthodromic AVRT), the antegrade limb (ie, the pathway that conducts the impulse to the ventricle) is the AV node/His-Purkinje system; in this setting, the delta wave seen during sinus rhythm is lost since antegrade conduction is not via the accessory pathway (ie, the ventricle is not preexcited).

A three-lead ECG rhythm strip during sinus rhythm and the abrupt onset of orthodromic AV-bypass tachycardia. Arrows indicate the retrograde P waves visible in lead II.

• If the tachycardia has a wide QRS complex (antidromic AVRT), the antegrade limb is usually the accessory pathway. An orthodromic AVRT may be associated with a wide QRS complex in the presence of a preexisting or rate-related functional bundle branch block.

Continuous two-lead (V1 and II) rhythm strips from a patient who developed a wide-QRS-complex tachycardia (top) that could have been atrial flutter with 1:1 conduction, antidromic AV-bypass tachycardia, or ventricular tachycardia. The slur on the initial QRS waveform suggests either the flutter or the antidromic tachycardia, and this is confirmed by observing return of the prominent delta wave after sinus rhythm (bottom). Arrows indicate delta waves present before, during, and after the tachycardia. Asterisks indicate abnormally appearing P waves preceding each wide QRS complex.

Because of the potential to vary the conduction times and refractoriness of the AV node and the accessory pathways one has to be very careful with the use of many common agents e.g.,
Verapamil
Propranolol
Digitalis
Lidocaine
Lest you precipitate dangerous tachycardias!!!!!!

Acute Termination Vagal Maneuvers (e.g., carotid sinus massage, valsalva) For Orthodromic AVRT (narrow complex tachycardia) Adenosine, calcium channel blockers, beta blockers, and procainamide. CAUTION: Keep a cardioverter/defibrillator at hand….????? Amiodarone For antidromic AVRT (wide complex tachycardia)…avoid CCB’s, B blockers, adenosine, and digoxin. The drug of choice would be Procainamide.

Patients with frequent symptomatic tachyarrhythmias should be referred for EPS studies for evaluation and selection of treatment.
Pharmacologic
Ablation
Surgery

AV Nodal Re-entrant Tachycardia

Schematic diagrams illustrating the contrasting routes of impulse conduction within the slow (alpha) and fast (beta) AV-nodal pathways. The slower conduction is represented by a wavy line . Slow – Fast (Typical) AVNRT

Continuous recordings of simultaneous leads V1 and V5. The slow-fast variety of AV-nodal tachycardia, with its closely following retrograde P waves ( arrows ), is initiated and terminated by APBs. Note the premature P wave following the fourth QRS complex in the top strip that initiates the tachycardia and the premature P wave preceding the fifth QRS complex in the bottom strip that terminates it.

Typical AVNRT (Slow – Fast)

Ventricular Tachycardia

In the ladder diagrams, an X indicates the site of impulse formation, a vertical line indicates normal conduction through the atria or ventricles, a diagonal line indicates conduction through the AV node and conduction around a reentry circuit, and a short perpendicular line indicates the site of block.

Definition: Ventricular tachycardia consist of at least three consecutive QRS complexes originating from the ventricles and recurring at a rapid rate (> 100 bpm). Sustained ventricular tachycardia is arbitrarily defined as lasting > 30 seconds. The rhythm is generally regular or slightly irregular.

In unselected patients presenting with wide complex tachcardias, V. Tach. is the diagnosis in 80% of cases. If the patient has underlying structural heart disease, the occurrence of V. Tach.as the cause of the rhythm increases to 95%. Is it Ventricular Tachycardia or Supraventricular Tachycardia wih aberrancy??????????????????????

Factors favoring Ventricular Tachycardia

AV Dissociation
QRS > 0.14
QRS Axis between – 90 & - 180 degrees
Positive QRS deflection in all precordial leads
LBBB morphology with rightward QRS axis
Capture beats, fusion beats
QRS morphology identical to PVC’s during sinus rhythm
LBBB QRS morphology with one of the following
R in V1 or 2 greater thatn 0.03 sec
Any Q in V6
Onset of QRS to nadir of S in V1 > 0.06 sec
Notching of downstroke of S in V1 or V2
Chou (3 rd ed) Electrocardiography in Clinical Practice

Wellens, et. al.,The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am. J. Med 1978; 64;27-33.

Sustained monomorphic ventricular tachycardia with atrioventricular (AV) dissociation. Note the independence of the atrial (sinus) rate (75 per minute) and ventricular (QRS) rate (140 per minute).

A three-lead rhythm strip from a 62-year-old man who presented with acute shortness of breath 2 months after an inferior-posterior MI. Arrows indicate capture beats and asterisks indicate fusion beats. Fusion and Capture Beats

The six precordial leads of the ECG from a 25-year-old woman with palpitations of sudden onset (A) illustrate VT with no lead (V1 to V6) having an RS morphology and from another patient (B), illustrating VT with a prolonged interval from onset of the QRS complex to the nadir of the S wave. Arrows in B indicate the period of 0.12 second from QRS onset to S nadir in leads V2 and V3.

A continuous recording of lead MCL 1 from a 77-year-old woman with ischemic cardiomyopathy and chronic heart failure. An arrow indicates the onset of the VT and asterisks indicate contrasting narrow and broad initial R waves in lead MCL 1 .

Twelve-lead ECG from a 59-year-old man with chronic heart failure following an extensive anterior myocardial infarction. Arrows indicate the taller first "rabbit ear" in lead V1. Asterisks indicate the QS pattern in lead V6.

Twelve-lead ECG from a 63-year-old man with recurrent VT and heart failure awaiting cardiac transplantation while being maintained on propafenone therapy. Asterisks indicate the QS appearance in lead V6.

A schematic diagram of lead-V1 recordings during LBBB and two varieties of RVT. The brackets indicate the durations from the onsets of the QRS complexes to the nadirs of the maximal negative waveforms: 0.05 second in A and B, and 0.09 second in C and D.

The schematic diagram of lead V6, indicating the method for measuring the duration from the onset of the QRS complex to the peak to the R or S wave, and the recordings of the ECG in leads V4 to V6 from two patients illustrate the slow rise of the R wave (A) and the slow descent of the S wave (B).

Right sided versus Left Sided Ventricular Tachycardia

Twelve-lead ECG from a 63-year-old man with recurrent VT and heart failure awaiting cardiac transplantation while being maintained on propafenone therapy. Asterisks indicate the QS appearance in lead V6 ( A) are contrasted with those from a 62-year-old man who returned with acute chest pain 1 month after a posterolateral MI (B). Concordant Negativity = RVT Concordant Positivity = LVT

A . Electrophysiologic mapping and ablation confirmed an origin of VT in the RV outflow area. Arrows indicate the negativity of right-axis deviation in lead I. This RVOT V.Tach can usually be cured with radiofrequency catheter ablation.

Simultaneous recording of leads V1, II, and V5 from a 32-year-old woman who presented with palpitations but no other evidence of heart disease. Arrows indicate initiation of the episodes of palpitation by VPBs

A new approach to the differential diagnosis of a Regular Tachycardia with a Wide QRS complex. Brugada et.al.; CIRC v 83#5; May 1991: 1649 - 1659

Brugada’s Criteria for Ventricular Tachycardia
Absence or RS complex in all precordial leads
R to S interval > 100ms in one precordial lead
Atrioventricular Dissociation
Morphologic criteria for VT present in precordial leads V1-2 and V6
Any Q in V6 V1 or 2 R > 30 ms V1 or 2 onset to S Nadir > 60 ms V1 or 2 S notching SVT c aberrancy VT YES NO VT YES NO VT YES NO VT YES NO

Aberration

Stripes of Aberration 1) Triphasic morphology a) rsR in V1 b) qRs in V6 2) Initial deflection identical to normal beat (if RBBB) 3) Immediately preceding atrial activity 4) Second in a row phenomenon 5) Alternating BBB pattern separated by single normal beat 6) Identical wide QRS pattern previously diagnosed as aberrancy

Triphasic morphology a) rsR in V1 b) qRs in V6 Initial Deflection of the Abnormal Beat is Identical to Normal Beat

Immediately preceding atrial activity. rsR’ variant in V1

Alternating BBB pattern separated by single normal beat

The refractory period of the cardiac conducting pathways is proportional to the length of the preceding cycle (RR interval). Thus, the longer the cycle and slower the rate, the longer the ensuing refractory period, and vice versa. Ventricular aberration can therefore result from a shortened immediate cycle, an extended preceding cycle, or a combination of both. . In the case of two regular cycles with normal conduction, as shown above the conduction in the third beat (beat 3) is also normal. However, the conduction in the third beat may become aberrant (lower two diagrams) if either the second cycle is shortened ( B ) or the first cycle is lengthened ( C ). In the diagrams, 1 , 2 , and 3 are consecutive beats and the stippled area represents the refractory period of some part of the conducting system during the second cycle.

Gouaux and Ashman first drew attention to the fact that aberrant conduction was likely to complicate atrial flutter/fibrillation when a longer cycle was followed by a shorter cycle. Aberration produced by a long-short sequence is sometimes referred to as the Ashman phenomenon. It is important to keep in mind that this cycle sequence cannot be used to differentiate aberration from ectopy because, by the rule of bigeminy , a lengthened cycle also tends to precipitate a ventricular extrasystole.

If a wide QRS complex ends a longer-shorter cycle sequence, we have seen that differentiation between aberration and ectopy may be difficult. If an even longer cycle followed by an even shorter cycle ends with a normally conducted beat, the evidence against aberration is strong, and the diagnosis of ectopy is favored.

http://www.cardiologylinks.org	224
http://ecg-experts.blogspot.com	72
http://cardiologylinks.webs.com	56
http://www.slideshare.net	18
http://www.medpedia.com	1
http://translate.googleusercontent.com	1

Approach To Arrythmias

by Mari Caban on Mar 18, 2008

Accessibility

Categories

Tags

Upload Details

Usage Rights

6 Embeds 372

Statistics

Approach To Arrythmias — Presentation Transcript