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  3. 3. 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
  4. 4. • The main cellular elements of the SA node are small, densely packed, round, pale cells with sparse myofibrils and rare gap junctions. • The pacemaker (p) cells are arranged in elongated clusters and make contact with each other but not with the ordinary working myocardium. • The latter communication is maintained via “transitional” cells, which form a narrow zone at the borders of the node, most abundantly in the crista terminalis.
  5. 5. 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
  6. 6. 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
  7. 7. SINUS NODE DYSFUNCTION Disorders 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.
  8. 8. SYMPTOMS  Stokes-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.
  9. 9. variants of sinus node dysfunction(sss) • Asystole • Sinus bradycardia (<60 beats per minute) • Sinus arrest or pause • Sino-atrial exit block • Sinus tachycardia (>100 beats per minute) • Atrial fibrillation with slow ventricular response
  10. 10. Atrial frequency < 60 bpm Ventricular frequency same Regularity regular Origin sinus node P-wave normal SINUS BRADYCARDIA
  11. 11. SINUS TACHYCARDIA Atrial frequency 100-180 bpm Ventricular frequency Same Regularity regular Origin sinus node P-wave positive in II, AVF
  13. 13. SINUS ARREST Sinus pause is the result of transient failure of impulse formation within the SA node or impulse propagation from the SA node When the postulated sinus inactivity, manifested by absent P waves, is prolonged, the condition is called sinus arrest
  14. 14. 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 distinguished from sinus arrest because the pause in SA exit block is a multiple of the P-P interval that preceded the pause.
  15. 15. 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)
  16. 16. DIAGNOSTIC ALGORITHM symptoms of SA NODE dysfunction Surface ECG Excersice testing Drugs-atropine+/-propronolol Long Term ECG Recording EPS (INVASIVE)
  17. 17. ECG •A routine ECG may provide information in such patients. •However, the symptoms are nonspecific and the ECG changes may not be diagnostic.
  18. 18. Exercise testing CHRONOTROPIC 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 exercise or have unpredictable fluctuations in heart rate during activity. -Gwynn N, R, Kratz, et al. Chronotropic incompetence. Am Heart J 1992;123:1216.
  19. 19. • 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
  20. 20. DRUGS Atropine/isoproterenol — 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.
  21. 21. 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 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.
  22. 22. 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.
  23. 23. 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
  25. 25. HOLTER RECORDING • If 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
  26. 26. 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.
  27. 27. 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.
  28. 28. 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.
  29. 29. ELECTROPHYSIOLOGICAL TESTING Indications •The 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.
  30. 30. 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.
  31. 31. 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.
  32. 32. 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.
  33. 33. 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.
  34. 34. SNRT cont….  SNRTc corrected by subtracting the sinus cycle length from the SNRT defined as the recovery interval in excess of the sinus cycle  Total recovery time (TRT) which is the time required to return to the basal sinus rate. Normal values have generally been estimated as follows : •SNRT < 1500 milliseconds •CSNRT < 550 milliseconds •TRT 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.
  35. 35. • 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 • The noninvasive determination of the sinus cycle length, corrected to the basic cycle length, after a bolus of adenosine is also an indicator of SSS. Burnett, D, Abi-Samra, F, Vacek, JL. Use of intravenous adenosine asnoninvasive diagnostic test for sick sinus syndrome. Am Heart J 1999;137:435
  36. 36. Limitations of SNRT  Changes 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
  37. 37. 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.
  38. 38. SACT • Sino Atrial Conduction Time • Can be measured in two ways Indirect Direct
  39. 39. SACT cont… Indirect method;  The usual method  This 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. .
  40. 40. SACT • A1-A1 The interval between each of the normal sinus beat or the stable sequence of paced beats. • A2-paced impulse • A3-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 to as the return interval • Four zones after APD
  41. 41. No reset/collision/Interferance APD IN LAST 20-30% OF SCL
  42. 42. RESET(MAJOR PART) ie, less than compensatory-impulse in earliest third of zone 2(40-50% OF SCL)
  44. 44. SA ECHO’S/RE-ENTRY
  45. 45. SACT  The 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
  46. 46. 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
  47. 47. 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
  50. 50. CORRELATION OF SNRT AND SACT WITH ECG ABNORMALITIES Patients with Symptomatic sinus bradycardia – longer SNRT and SACT Patients with SA block - longer SACT 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.
  51. 51. 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. . .
  52. 52. 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)
  53. 53. TREATMENT OF SSS  Mainly directed at symptoms  Search for remidial causes - Drugs -Ischemia -Autonomic imbalance  Mostly by pace makers.  Drugs-Theopylline  Ablation for AF
  54. 54. 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.
  55. 55. FOLLOW-UP Three 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.