NONINVASIVE AND INVASIVE ASSESMENT OF SA NODE AND AV NODE AND ITS CLINICAL RELEVANCE

I.TAMMI RAJU

OVERVIEW OF TOPIC SA NODE INTRODUCTION SYMPTOMS DIAGNOSTIC ALGORYTHM

NONINVASIVE ASSESMENT

ECG

EXCERSICE

DRUGS

INVASIVE ASSESMENT

SNRT

SACT TREATMENT

AV NODE INTRODUCTION

CLINICAL FEATURESNON-INVASIVEINVASIVE

ATRIAL EXTRA STIMULI

TREATMENT

INTRODUCTION OF SA NODE

SA NODE:- Located laterally in the epicardial grove of the sulcus terminalis, near the junction of the right atrium and the superior vena cava

ANATOMY

Blood Supply

Right coronary artery in 59 percent,

Left circumflex artery in 38 percent,

Dual blood supply in 3 percent.

Kyrialikdis MK, Kouraouklis CB, Papaioannou JT, et al.. Am J Cardiol 1983;51:749–750

INNERVATION

Both the parasympathetic and sympathetic.

The sinus node is richly innervated with postganglionic adrenergic and cholinergic nerve terminals.

Vagal stimulation-- slows the sinus node discharge rate and increases the intranodal conduction time.

Adrenergic stimulation increases the sinus node discharge rate

SINUS NODE DYSFUNCTIONDisorders of automaticity, conduction, or both.

Abnormal automaticity, / sinus arrest--failure of sinus impulse

generation.

Abnormal conduction, or sinoatrial delay or block- failure of impulse transmission.

SYMPTOMSStokes-Adams attacks, which is a case of

fainting due to insufficient blood to the brain. It is caused by improper contraction of the ventricles.

Dizziness or feeling light headed.Angina or chest pain Fatigue Headache Nausea Palpitations Shortness of Breath.

DIAGNOSTIC ALGORITHM

symptoms of SA NODE dysfunction

Surface ECG

Excersice testing

Drugs-atropine+/-propronolol

Long Term ECG Recording

EPS (INVASIVE)

ECGA routine ECG may provide information in

such patients.

However, the symptoms are nonspecific

and the ECG changes may not be diagnostic.

variants of sinus node dysfunction(sss)

Asystole

Sinustachycardia (>100 beats per minute)

Sinusbradycardia (<60 beats per minute)

Sinus arrest or pause

Sino-atrial exit block

Atrial fibrillation with slow ventricular

response

Atrial frequency < 60 bpm

Ventricular frequency same

Regularityregular

Originsinus node

P-wavenormal

INAPPROPRIATE SINUS BRADYCARDIA

INAPPROPRIATE SINUS TACHYCARDIA

Atrial frequency 100-180 bpm

Ventricular frequency Same

Regularity regular

Originsinus node

P-wave positive in II, AVF

BRADYCARDIA-TACHYCARDIA SYN

SINUS ARREST

The sinus node stops firing resulting in a pause in heart beat

SINO-ATRIAL EXIT BLOCK

The depolarizations that occur in the sinus node cannot leave the node towards the atria. They are blocked.

On the ECG this is expressed as a pause.

SA exit block can be destinguished from sinusarrest because the pause in SA exit block is a multiple of the P-P interval that preceded the pause.

Three subtypes can be distinguished

Type I second degree (Wenkebach) SA exit block:

the P-P interval progressively shortens prior to the

pause

Type II second degree SA exit block:

the pause equals approximately 2-4 times the

preceding PP interval

Third degree SA exit block:

absence of P waves (diagnosed with an sinus node

electrode, during electrophysiological evaluation)

Type I second degree (Wenkebach) SA exit block

SA BLOCK TYPE 2

Exercise testingCHRONOTROPIC INCOMPETENCE

Inability of the sinus node to achieve at least 80 percent of the

age predicted heart rate. Astrand's formula (220- age) at

peak exercise.

Seen in 20 to 60 percent of patients with sinus node

dysfunction.

Although the resting heart rates may be normal,

may have inability to increase their heart rate during

exerciseor

have unpredictable fluctuations in heart rate during activity.

-Gwynn N, R, Kratz, et al. Chronotropic incompetence. Am Heart J 1992;123:1216.

Specific sinus node chronotropic incompetence is the inability of the sinus node to accelerate in response to metabolic demands secondary to intrinsic disease or negative chronotropic drugs.

Functional chronotropic incompetence manifests itself either as atrial tachyarrhythmias or as retrograde ventriculoatrial conduction

DRUGS

Atropine/isoproterenoll— Atropine (1 or 2 mg) / isoproterenol (2 to 3

μg/min)

Abnormal response --- increase in the sinus rate of <25 %, or to a

rate below 90 beats/min.

Potential problems.

There has been no standardization of the pharmacologic testing,

No dose ranging has been reported,

The specificity and sensitivity of the tests are uncertain,

SSS may exist even if the response is normal.

Isoproterenol is risky in patients with ischemic and other types of heart

disease.

DRUGS Beta blockers —

Propranolol has been used to assess sinus node function on the assumption that the chronotropic response may differ between patients with a normal and a sick sinus node.

This approach, however, has been disappointing

DRUGS cont…

Adenosine directly inhibits sinus node activity

Due to increased potassium conductance -hyperpolarization of the resting membrane potential.

Adenosine should be considered as an alternative to invasive testing in patients with suspected SSS.

PHARMACOLOGICAL DENERVATION

Intrinsic heart rate — Atropine (0.04 mg/kg) and propranolol (0.2 mg/kg)

Heart rate at 30 minutes is called the (IHR) .

The IHR is a function of age

IHR, in beats/min = 117.2 - [0.53 x age]

IHR separates intrinsic SSS from extrinsic SSS

Intrinsic SSS is presumed to be present if the sinus rate does not exceed the predicted IHR after atropine.

Long-Term Electrocardiographic

Recording

In patients engaged in normal daily activities

document and quantitate the frequency and complexity of an

arrhythmia

correlate the arrhythmia with the patient's symptoms, and

evaluate the effect of antiarrhythmic therapy on spontaneous

arrhythmia.

For example, recording normal sinus rhythm during the

patient's typical symptomatic episode effectively excludes

cardiac arrhythmia as a cause

HOLTER RECORDING

HOLTER RECORDINGIf symptoms are frequent, 24- or 48-hour

ambulatory Holter monitoring can be useful. Documentation of symptoms in a diary by

the patient. Often the sinus pauses recorded are not

associated with symptoms. Several Holter monitor studies demonstrated

the futility of treating asymptomatic pauses, even if they were 3 seconds or longer.

The length of the pause correlated poorly with symptoms and prognosis

EVENT RECORDING.

In many patients, the 24-hour snapshot provided by the Holter recording is incapable of documenting the cause of the patient's symptoms.

These devices are about the size of a pager and are kept by the patient for 30 days.

IMPLANTABLE LOOP RECORDER

For patients with infrequent and transient symptoms, neither Holter recorders nor 30-day event recorders may yield diagnostic information.

In such patients, implantable loop recorders may be used.

This device (about the size of a pack of chewing gum) is inserted under the skin at about the second rib on the left front of the chest and is activated by passing a special magnet over the device.

LOOP RECORDERS

Signal-averaged P wave

fractionated endocardial electrograms in the SSS:-

Long, low amplitude signals early during the signal averaged P wave were found to be characteristic of SSS.

sensitivity-76% specificity-91%In paroxysmal atrial fibrillation the incidence of

SSS was higher in those with low amplitude atrial early potentials on a signal-averaged P wave

- Yamada, et al. J Am Coll Cardiol 1996; 28:738.

EPS

ELECTROPHYSIOLOGICAL TESTING

IndicationsThe symptomatic patient who has no ECG findings suggestive of SSS.

The symptomatic patient in whom ECG fail to correlate with symptoms.

The patient who develops dysfunction of the SA node on usual doses of drugs.

EPS indications cont…

The patient with syncope or near syncope who has bundle branch or multifascicular block may require electrophysiologic evaluation of the SA node, the AV node, and the infranodal His-bundle branch-Purkinje system.

Electrophysiologic testing that shows SA nodal dysfunction allows the selection of appropriate therapy in up to 50 percent of these patients.

CONTRAINDICATIONS

Unstable angina

Bacteremia or septicemia

Acute decompensated congestive heart

failure not caused by the arrhythmia

Major bleeding diathesis

Acute lower extremity venous thrombosis if

femoral vein cannulation is desired.

SINOATRIAL NODE RECOVERY TIME — The SNRT is perhaps the most

useful test of overall sinus nodal automaticity.

The atria are driven rapidly: a normal SA node will have a recovery

time within certain limits,

while recovery will be delayed in a depressed or sick sinus node.

SNRT cont….It is performed by placing a catheter near the SN.

Overdrive stimulation is performed at a rate higher

than that of the SA node for about one minute (the

range in most published reports is 30 to 180 sec).

Pacing is then stopped, and the time from the last

paced atrial beat to the first spontaneous electrical

beat with a sinus morphology is measured. Pacing

is increased 10 to 20 beats/min up to 200

beats/min, if tolerated.

SNRT cont…. SNRTc corrected by subtracting the sinus

cycle length from the SNRT

SNRTn a function of the cycle length-,

SNRT/sinus cycle length.

Total recovery time (TRT) which is the time required to return to

thebasal sinus rate..

SNRT

Normal values have generally been estimated as follows :SNRT/SCL <150 percentCSNRT < 550 millisecondsTRT less than five seconds.

Josephson, ME. Sinus Node Dysfunction. In: Josephson ME, ed. Clinical Cardiac Electrophysiology. Techniques and Interpretations. Third ed. Philadelphia: Lippincott; 2002:68.

The SNRT or SNRTc is abnormal in more than 50 percent of patients with suspected SSS.

J Am Coll Cardiol 1995; 26:555

Overdrive suppression, used in conjunction with intravenous disopyramide ,may increase the sensitivity of the test and its potential to diagnose a SSS .

Ishikawa, et al.. Sinus node recovery. Europace 2000; 2:54

Limitations of SNRTChanges in autonomic tone due to the effects of pacing

Changes in P-wave morphology suggesting a pacemaker shift

Sinoatrial entrance block

The hemodynamic effects of atrial pacing

Secondary pauses.

In fact, direct SN recordings have demonstrated that the majority of these pauses are due to sinoatrial exit block rather than impaired automaticity.

- Tracy, CM, Akhtar,

M, DiMarco, JP, et al

THE USE OF TRANSESOPHAGEAL ATRIAL PACING

Transesophageal pacing has been used to assess sinus node dysfunction, primarily by assessing SNRT, and has been recommended in the evaluation of patients with syncope.

Brembilla-Perrot, B, Beurrier, D, Houriez, P, et al. Utility oftransesophageal atrial pacing in the diagnostic evaluation of patientswith unexplained syncope associated or not with palpitations. Int JCardiol 2004; 96:347.

SACT

Sino Atrial Conduction Time

Can be measured in two ways

Indirect

Direct

SACT cont…Indirect method; The usual methodThis approach involves the placement of a

catheter near the sinus node. Strauss method

progressively premature atrial extrastimuli (A2) are introduced after every eighth to tenth beat of stable sinus rhythm.

Narula method Brief periods of atrial pacing at rates above sinus.

.

SACTA1-A1 The interval between each of the normal sinus

beat or the stable sequence of paced beats.A2-paced impulseA3-The first spontaneous sinus beat that occurs

after termination of the pacing.A2-A3 The interval between the final paced impulse

(A2) and the first spontaneous beat (A3) is referred toas the return interval

Four zones after APD

No reset/collision/Interferance

APD IN LAST 20-30% OF SCL

RESET(MAJOR PART)

ie, less than compensatory-impulse in earliest third of zone 2(40-50% OF

SCL)

INTERPOLATION

SA ECHO’S/RE-ENTRY

SACTThe A1-A1 interval Time required to generate a sinus impulse.,

conduction time does not contribute to A1-A1.

A2-A3 (Because A2 resets the SN, the return cycle length) =

generation of the next sinus beat (reflecting SNautomaticity) +

conduction of the impulse into and out of SN tissue.

(A2-A3) –(A1-A1) = Total time it takes to enter and exit the

SN tissue. This number represents twice the SACT SACT = [(A2-A3) – (A1-A1)] / 2

Normal SACT times generally range from 40 to 150 milliseconds

Limitations of SACT The assumption that entrance into and exit out of the SN takes the same

amount of time is not necessarily valid

Distance of the stimulation site from the SN is another source of error. The

farther the site is from the SN, the greater the potential for overestimation of

the SACT due to conduction delays in both atrial and perinodal tissues.

Reproducibility of results

sinus arrhythmia

shift in intrinsic pacemaker site

Depression of automaticity, and

sinus entrance block

Direct recording of the sinoatrial conduction time (sinus node electrogram)

Endocardial recordings demonstrate diastolic phase 4 activity followed by a slow upstroke culminating in a rapid atrial EGM.

The directly measured SACT was defined as the interval between the local EGM and the rapid atrial deflection.

Sinoatrial block occurs when the local EGM was seen in the absence of an atrial deflection

SACT-DIRECT METHOD

SENSITIVITY OF SNRT AND SACT70%

SPECIFICITY OF SNRT AND SACT90%

CORRELATION OF SNRT AND SACT WITH ECG ABNORMALITIES

Patients with Symptomatic sinus bradycardia – longer SNRT and SACT

Patients with SA block -longer SACT; and

Patients with the tachycardia-bradycardia syndrome had a longer SNRT

Breithardt, G, Seipel, L, Loogen, F. Sinus node recovery time and calculated sinoatrialconduction time in normal subjects and patients with sinus node dysfunction. Circulation 1977; 56:43.

SINUS NODE AND ATRIAL REFRACTORY PERIOD

SA nodal refractoriness has been determined using both the extrastimulus and pacing train techniques.

Normal subjects having a SNERP of 250 to 350 msec as compared to a value of 500 to 550 msec in patients with the SSS

Kerr, CR, Strauss, HC. The measurement of sinus node refractoriness inman. Circulation 1983; 68:1231.

.

.

COMPLICATIONS DURING EP STUDY

Hematoma at the puncture site in the groin and or neck

Hemorrhage

Infection caused by manipulation of catheters (theoretical risk)

Perforation upon catheter manipulation inside the heart of small patients (most commonly involving the right atrial appendage and the right ventricular outflow tract)

TREATMENT OF SSSMainly directed at symptoms

Search for remidial causes - Drugs

-Ischemia-Autonomic imbalance

Mostly by pace makers.

Drugs-Theopylline

Ablation for AF

A number of additional pacemaker features may be useful in selected patients:

Rate responsive programming

SSS and chronotropic insufficiency and exertional symptoms.

Mode switching

SSS who have paroxysmal atrial tachycardia.

Class I indications

Sinus bradycardia in which symptoms are clearly related to the bradycardia’.

Symptomatic chronotropic incompetence

Class II

Sinus bradycardia (heart rate <40 beats/min) with symptoms suggestive of

bradycardia, but without a clearly demonstrated association.

Sinus node dysfunction in a patient with unexplained syncope.

Chronic heart rates <40 beats/min while awake in a minimally

symptomatic patient.

DRUG-INDUCED SINUS NODE DYSFUNCTION

Some patients will meet the above indications

for pacemaker implantation due to the effects

of medications that are necessary for the

treatment of arrhythmias or other medical

conditions.

In such cases, patients should be considered to

have the same indication for pacemaker

implantation as those with intrinsic sinus node

dysfunction

FOLLOW-UPThree major issues that need to be considered;

1. Ventricular pacing can induce dyssynchrony observe for evidence of heart failure.

2. In patients with an AAI pacemaker, monitoring for progression to high degrees of

AV block is essential as the reported rate varies from 0.6 to as high as 3 percent.

3. Due to the thromboembolic risks associated with unrecognized AF, patients should

be observed for the development of atrial arrhythmias.

AV NODE

ANATOMY OF AV NODE

BLOOD SUPPLY The AV node AV nodal artery ---right coronary artery in 90 percent left circumflex artery in 10 percent .The bundle of His –both the AV nodal artery and branches of the left anterior descending artery.

The left bundle has a rich blood supply AV nodal artery, Posterior descending artery, and Branches of the left anterior descending artery.

Frink RJ, James TN.. Circulation 1973;43:491–502

CLINICAL FEATURES First-degree AV block -long a-c wave

diminished intensity of S1.

type I second-degree AV block- the heart rate may increase

imperceptibly with

gradually diminishing intensity of s1,

widening of the a-c interval

terminated by a pause, and a wave not followed

by a v wave.

type II AV block --Intermittent ventricular pauses and

a waves in the neck not followed by v

waves s1 maintains a constant intensity.

In complete AV block

-variable intensity of s1

-a waves in the jugular venous pulse --lacking a consistent relationship to ventricular contraction.

-Intermittent large (cannon) a waves

may be seen in the jugular venous pulse when atrial and ventricular contractions occur simultaneously.

The second heart sound can split normally or

paradoxically, depending on the manner of ventricular activation.

First-Degree AV Block

During first-degree AV block, every atrial impulse conducts to the ventricles and a regular ventricular rate is produced, but the PR interval exceeds 0.20 second in adults.

PR intervals as long as 1.0 second have been

noted and can at times exceed the P-P interval, a phenomenon known as “skipped” P waves.

can result from a conduction delay in the AV node (A-H interval), in the His-Purkinje system (H-V interval), or at both sites.

First-degree and type I second-degree AV block can occur in normal healthy children, and a Wenckebach AV block can be a normal phenomenon in well-trained athletes, as noted earlier, probably related to an increase in resting vagal tone

Third-Degree (Complete) AV Block No atrial activity is conducted to the

ventricles Atria and ventricles are controlled by

independent pacemakers. A type of complete AV dissociation. The atrial pacemaker can be sinus or

ectopicThe ventricular focus is usually located just

below the region of the block, which can be above or below the His bundle bifurcation.

ventricular pacemaker activitycloser to the His bundle appear to be more stable and a faster escape rate than can those located more distally in the ventricular conduction system.

The ventricular rate in acquired complete heart block is less than 40 beats/min but can be faster in congenital complete AV block

COMPLETE HEART BLOCK

COMPLETE AV BLOCK cont…

Can result from block at

the AV node (usually congenital)

within the bundle of His/intra-hisian or

Infra Hisian/distal to it in the Purkinje system (usually acquired)

Block proximal to the His bundle –escape focus in or near the His bundle.

normal QRS rates of 40 to 60 beats/min

His bundle recording –differentiate AV nodal from

intrahisian block.

High-Grade Atrioventricular Block

When two or more consecutive atrial impulses do not

conduct to the ventricle, it is defined as high-grade

AV block.

It may be associated with a junctional or ventricular

escape rhythm. .

Unless a clearly defined reversible etiology is

identified, permanent pacing is indicated.

EPS IN AV NODE DYSFUNCTIONPatients with AV block without clear

symptom association.

Patients with symptoms suggestive of bradyarrhythmias, but in whom significant AV block has not been documented.

When the site of AV block cannot be determined by surface tracings.( 2: 1 AV block ).

BASE LINE RECORDINGSThe first intracardiac tracing is a recording from

the high right atrium (HRA) close to the sinus node.

Pacing at this position allows evaluation of sinoatrial node function and atrioventricular conduction;

Recordings from this site also help determine the direction of atrial activation (eg, high-low versus low-high, and right-left versus left-right).

PA INTERVAL

Atrial electrogra

m

HBE-D

The reported normal range is 20 to 60 msec.

Represent -total atria conduction, reflection of internodal

conduction (sinoatrial to atrioventricular node)

AH INTERVAL

AH INTERVAL

Atrial electrogra

m

HBE-D

This interval is taken to represent AV nodal conduction.

50 to 120 msecmarkedly influenced by the autonomic

nervous system Long AH intervals –drugs,increased vagal

tone,AV node disease

HV INTERVAL

Atrial electrogra

m

HBE-D

conduction time through the distal His-Purkinje . less influenced by the autonomic nervoussystem, Normal, 35 to 55 msecA prolonged HV interval is consistent with diseased

distal conduction in all fascicles .

HBE-D

first-degree AV block

most common EPS finding in patients with P-R prolongation is a long A-H interval because intra- and infra-Hisian conduction compromise only a minor portion of the P-R interval

Second-degree AV block — Type IWenckebach almost always occurs in

the AV node. During EPS, this process is most evident on a

His bundle EGM.

progressively longer A-H interval and a stable H-V interval

until the final beat of the series in which there is an atrial EGM with no ventricular EGM.

True type II second-degree block Mobitz II

almost always, if not always, occurs in the HPS.

His bundle EGM follows the atrial EGM prior to the dropped ventricular EGM confirming the site of block.

Third-degree (complete) AV blockMost patients with complete AV block are

treated with permanent pacemakers EPS is not generally indicated. Among patients with complete AV block,

EPS may be indicatedwhen symptoms are not present,the site of block is not apparent, orthe block is potentially reversible

Findings suggestive of high risk

alternating left bundle branch block (LBBB) and right bundle branch block (RBBB), or those with

RBBB with alternating left anterior and left posterior fascicular block.

Symptomic- prolonged H-V interval (>55 milliseconds)

Asymptomatic -H-Vinterval >100 milliseconds

Highest progression to complete heart block and should receive pacemakers

ATRIAL EXTRASTIMULI

ATRIAL EXTRASTIMULI

Long coupling interval – conduct through the AV node with a constant velocity.

As the coupling intervel becomes shorter the conduction velocity decreases –increased A-H iterval.

Decremental conduction is a property of AV node

AVN REFRACTORY PERIODERP- longest copling intervel between the

basic drive and the premature impulse that fails to propogate through the AVN.

NORMAL-- <450 milliseconds.

Increasing refractory period with shorter cycle lengths indicates abnormal HPS conduction.

PHARMACOLOGIC CHALLENGE

Procainamide normally prolongs the H-V interval by 10 to 20 percent.

After administering procainamide-Doubling of the H-V interval,-an H-V interval >100 milliseconds or

the-development of infra-Hisian block

represent poor HPS reserve. Mandates permanent pacing

TREATMENT OF AV DYSFUNCTION

INDICATIONS OF PACING

Class I

Complete (third-degree) AV blockAdvanced second-degree AV block (block of

two or more consecutive P-waves)Symptomatic Mobitz I or Mobitz II second-

degree AV blockMobitz II second-degree AV block with a

widened QRS or chronic bifascicular block,regardless of symptoms

Exercise-induced second or third degree AV block (in the absence of myocardial ischemia)

Class IIAsymptomatic Mobitz II second-degree AV

block with a narrow QRS intervalFirst-degree AV block when there is

hemodynamic compromise because of effective AV dissociation secondary to a very long PR interval.

Bifascicular or trifascicular block associated with syncope that can be attributed to transient complete heart block

PACING IN CONGENITAL CHBcongestive heart failure

average heart rate of less than 50

beats/min in the awake infant

history of syncope or presyncope

significant ventricular ectopy or

exercise intolerance

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