BRADYARRHYTHMIAS; Disorders of SA node , AV node and Intraventricular conduction system.

BRADYARRHYTHMIAS; Disorders of SA node , AV node and Intraventricular conduction system.

1. PRESENTED BY :- DR.AKASH WARDIYA PG 1 st YEAR DEPARTMENT OF GENERAL MEDICINE RKDF MCH & RC BHOPAL BRADYARRHYTHMIAS

2. CONTENTS Normal physiology of cardiac impulse conduction Introduction: Bradyarrhythmia Bradyarrhythmia: Disorder of SA node Bradyarrhythmia: Disorder of AV node Bradyarrhythmia: Disorder of VENTRICULAR CONDUCTION Diagnostics Management

3. CONDUCTION SYSTEM OF HEART SA NODE (60-100bpm) AV NODE (40-60bpm) BUNDLE OF HIS BUNDLE BRANCHES (LEFT AND RIGHT) PURKINJE FIBRES (30-35bpm)

4. Normal Physiology of Cardiac conduction system Electrical impulse originates in the SA node, which is located in Right atrium in the sulcus terminals. These cells possess automaticity, which is the ability to depolarize spontaneously. The sinus node depolarization spreads through the atria to the atrioventricular (AV) node which transmits the impulse to the ventricular myocardium via His bundle, the right bundle branch and left bundle branch. His bundle travels from the AV node to the muscular septum via the membraneous septum. His bundle divides into a smaller anterior fascicle and a larger posterior fascicle. SYMPATHETIC AND PARASYMPATHETIC NERVES CONTROL HEART RHYTHMICITY AND IMPULSE CONDUCTION BY THE CARDIAC NERVES.

5. situated in the right atrium at the posterior part of the interatrial septum close to the opening of the coronary sinus. The AV junction has distinct regions including a transitional cell zone ( atrionodal cells ), the compact AV node , and the cells of the penetrating part of the His bundle. The atrial muscle fiber is connected with the ventricular muscle fiber only through the bundle of His because a fibrous tissue ring keeps the atrial muscle separated from the ventricular muscle. Damage of bundle of His causes dissociation of atrial and ventricular rhythm. Although the AV node has the potential for pacemaker activity, the normal automaticity rate is 20–60 beats/min, which is overridden by the higher intrinsic rate of the SA node. Therefore, the AV node can provide backup heart rate when the SA node fails to depolarize. Arrangement of gap junctions, along with extracellular matrix and fibroblasts, and a lack of conductance in adjacent valvular tissue allow the AV node to slow conduction and serve as the electrical “gatekeeper” to the ventricle. AV NODE

6. INTRAVENTRICULAR CONDUCTION bundle of His, the left and right bundle branches and the anterior and posterior fascicles of the left bundle branch. The interventricular septum obtains Purkinje fibers from the left bundle branch. The right bundle branch does not give off any Purkinje fibers during its passage through the septum. Purkinje fibers are branched off from the right bundle branch at the level of the origin of the anterior papillary muscle. A network of Purkinje fibers sprouts out from the bundle branches and fascicles and spread through the ventricular endocardium. Impulse conduction through the Purkinje network is very fast (4 m/s) which enables the vast majority of ventricular myocardium to be depolarized approximately simultaneously.

7. Association of ventricular conduction with the ECG

8. Cellular ion currents involved in depolarization and automaticity of SA nodal pacemaker cells Leakiness of Sinus Nodal Fibers to Sodium and Calcium Causes Self-Excitation Phase 4 spontaneous depolarization results from if (funny) current, along with T- and L-type calcium channels. Phase 0 is the depolarization phase of the action potential. This is followed by phase 3 repolarization, which results from the outward-directed hyperpolarizing K+ currents. Cells in the SA node exhibit the most rapid phase 4 depolarization and thus are the dominant pacemakers in a normal heart. Sinus Nodal Fibers Ventricular myocyte

9. BRADYARRHYTHMIAS:- Bradyarrhythmia (Brady = slow, arrhythmia = abnormal rhythm) is arbitrarily defined as a heart rate less than 60 beats/min. Normally, the resting heart rate ranges from 60-100 bpm, and this is determined by the pacemaker cells of the Sinoatrial node (SA node). If the sinus node is dysfunctional or suppressed a subsidiary Pacemaker in the atrioventricular node or specialized conduction System will take over leading to a slower junctional or ventricular Rhythm (<60bpm). B radyarrhythmias can be categorized on the basis of the level of disturbance in the hierarchy of the normal impulse generation and conduction system (from sinus node to AV node to His-Purkinje system). SA Node disorders AV Node disorders Intraventricular conduction disorders Sinus pause / arrest Sinoatrial exit block Sick sinus syndrome Chronotropic incompetence Tachy-Brady Syndrome First degree AV block Second degree AV block – Mobitz I Second degree AV block – Mobitz II Third degree AV block Junctional rythm Right bundle branch block (RBBB) Left bundle branch block (LBBB) Incomplete blocks Nonspecific Intraventricular conduction delays Left anterior fascicular block (LAFB) Left posterior fascicular block (LPFB)

10. Sinus arrest/pause:- “Sinus arrest” results from failure of impulse formation within the sinus node. Prolonged absence of sinus node activity (absent P waves) > 3 seconds. The SA node consists of two main groups of cells: A central core of  pacemaking cells ( P cells ) that produce the sinus impulses. An outer layer of transitional cells ( T cells ) that transmit the sinus impulses out into the right atrium. Sinus node dysfunction can result from either: Failure of the P cells to produce an impulse. This leads to sinus pauses and sinus arrest. Failure of the T cells to transmit the impulse. This leads to sino -atrial exit block. SA nodal dysfunction types:-

11. Sinoatrial exit block:- results from failure of sinus node activity to propagate to the atrium and can have similar pattern characteristics of types of AV node block.

12. Sinus bradycardia:- Sinus bradycardia is diagnosed in an adult when the sinus node discharges at a rate less than 60 beats/min. Tachy-Brady Syndrome:- Most commonly AF with alternating symptomatic bradycardia or offset pauses. It is often a reason for pacemaker implantation.

13. Sinus arrhythmia:- Sinus arrhythmia usually occurs in the young, especially those with slower heart rates or after enhanced vagal tone, such as following the administration of digitalis or morphine or athletic training, and decreases with age or with autonomic dysfunction, such as in diabetic neuropathy. Sinus node fibrosis :- m/c in elderly. SA nodal Ischemia and infarction:- m/c in pt with acute inferior & post MI and can be exacerbated by increased vagal tone and drugs like morphine and beta-blockers. Chronotropic incompetence :- Inability of the heart to increase its rate to meet activity or demand and is associated with severe exercise intolerance and increased cardiovascular events and overall morality. Carotid Sinus Hypersensitivity and Neurally mediated Bradycardia :- associated with vaso -vagal syncope. Baroreceptor is senstive to external pressure, so that pressure over carotid a. causes an inappropriate & intense vagal discharge.Syncope related to head turning, shaving, wearing a tight collar. Pathophysiology :- Carotid sinus pressure causes a reflex decrease in heart rate and blood pressure. CSH predominantly affects older males

14. CONDITIONS ASSOCIATED WITH BRADYCARDIA AND CONDUCTION DISORDERS

15. Medications That Can Induce/Exacerbate Bradycardia or Conduction Disorders

16. Transient AV conduction block is common in the young and is most likely the result of high vagal tone found in up to 10% of young adults. Acquired and persistent failure of AV conduction can be due to myocardial ischemia, aging and fibrosis, or cardiac infiltrative diseases. Conduction block in the AV node is classified based on the appearance on electrocardiography (ECG), which may also be a reflection of the location of block along the AV conduction axis. Bradyarrhythmia: Disorder of AV node AV Conduction Blocks First-Degree AV Block Second-Degree AV Block :- Two subtypes Type I/Mobitz I/Wenckebach block Type II/Mobitz II Third-Degree AV Block (complete heart block)

17. CAUSES OF AV CONDUCTION DELAY Congenital/genetic Vagotonic-associated with increased vagal tone Congenital AV block (associated with maternal systemic lupus erythematosus) Congenital heart defects (e.g., L-TGA) Genetic (e.g., SCN5A mutations) Sleep, obstructive sleep apnea High-level athletic conditioning Neurocardiogenic Infectious Metabolic/endocrine Lyme carditis Bacterial endocarditis with perivalvar abscess Acute rheumatic fever Chagas disease Toxoplasmosis Acid-base disorders Poisoning/overdose (e.g., mercury, cyanide, carbon monoxide, mad honey) Thyroid disease (both hypothyroidism and hyperthyroidism) Adrenal disease (e.g., pheochromocytoma, hypoaldosteronism) Inflammatory/infiltrative Other diseases Myocarditis Amyloidosis Cardiac sarcoidosis Rheumatologic disease: Systemic sclerosis, SLE, RA, reactive arthritis (Reiter ’ s syndrome) Other cardiomyopathy-idiopathic, valvular Neuromuscular diseases (e.g., myotonic dystrophy, Kearns-Sayre syndrome, Erb ’ s dystrophy) Lymphoma Ischemic Iatrogenic Acute MI Coronary ischemia without infarction—unstable angina, variant angina Chronic ischemic cardiomyopathy Medication related Beta blockers, verapamil, diltiazem, digoxin Antiarrhythmic drugs Neutraceuticals Catheter ablation Cardiac surgery, especially valve surgery TAVR, alcohol septal ablation Degenerative Lev ’ s and Lenegre ’ s diseases

18. First-Degree AV Block All atrial impulses are conducted to the ventricle PR interval is abnormally long (>200 ms ) AV delay usually occurs within the AV node Pacing is not required

19. Second-Degree AV Block (intermittent failure of conduction between atrium and ventricle) Two subtypes Type I/Mobitz I/Wenckebach block: progressive prolongation of the PR interval until loss of conduction occurs.

20. Type II/Mobitz II: fixed PR interval precedes loss of conduction and is Usually associated with QRS widening.

21. Third-degree AV Block (complete heart block) Complete interruption of conduction between atria and ventricles. Complete heart block (third-degree block) involves complete AV dissociation with a ventricular rate that is slower than the atrial rate. In the absence of a preexisting bundle branch block, a wide QRS escape rhythm implies a block in the distal His or bundle branches; in contrast, a narrow QRS rhythm implies a block in the AV node or proximal His and an escape rhythm originating in the AV junction. Narrow QRS escape rhythms are typically faster and more stable than wide QRS escape rhythms and originate more proximally in the AV conduction system.

22. Right Bundle Branch Block (RBBB) Impulses travel through myocardium of left ventricle to right ventricle and depolarise right ventricle. Conduction through myocardium is slower than that of Bundle of His, QRS complex is seen to be widened. Criteria for RBBB :- QRS> 120 ms M shaped or rSR ` pattern or notched R wave in V1 Prominent S wave in I and aVL , V5 & V6.

23. Causes of RBBB :- Normal variant in 0.2% of adults (prevalence increases with age). CAD → Acute anterior MI (occlusion of proximal LAD). Chronic Corpulmonale . Acute pulmonary embolism. Congenital heart disease e.g. Atrial Septal Defect. Brugada syndrome.

24. LEFT BUNDLE BRANCH BLOCK (LBBB) :- Activation of left ventricle is delayed and contract later than right ventricle. Criteria for LBBB:- QRS > 120ms Broad R wave in I, aVL , V5 & V6 Prominent QS wave in V1 Absence of q waves in I and V6. Causes :- CAD Acute AWMI (new onset LBBB) Dilated Cardiomyopathy Aortic stenosis Long-standing hypertension Clinical significance :- New onset LBBB is an indication for thrombolytic therapy. LBBB in the setting of an acute MI worsens the prognosis. Presence of LBBB cannot be used to diagnose LVH or infarct because LBBB itself results in wide QRS complex and changes in ST-T segment consistent with injury/ischemia.

25. Diagnosis of MI in the presence of LBBB Sgarbossa criteria : Age 21 ST segment elevation of ≥1mm in concordant with QRS complex in any lead (score 5) ST depression ≥ 1mm in leads V1-V3 (score 3) ST segment elevation ≥5mm and discordant with QRS complex (score 2) Score more than equal to 3 indicates Acute Myocardial Infarction.

26. Incomplete Blocks Intraventricular conduction abnormalities in which conduction is slowed in bundle, but not completely blocked. Generally manifests as similar morphology to complete right or left bundle branch block but with QRS duration 100 - 120ms. Compared to complete blocks, etiologies are the same, but clinical significance is reduced. Left Anterior Fasicular Block (LAFB) Duration of QRS complex < 120msec Left axis deviation (> -30 degrees) qR morphology in Lead I,aVL rS morphology in Leads II, III, aVF Prolonged R wave peak time in aVL >45 ms

27. LAFB – significance May be normal variant. Occurs in Hypertensive heart disease, Cardiomyopathy. May be seen in acute MI (LAD territory). LAFB can't be diagnosed if old Inferior Wall MI evident on ECG (Q-waves in II, III, and aVF ;extreme LAD). LAFB is more common than LPFB LPFB :- Left Posterior Fasicular Block The duration of the QRS complex is normal (<120msec) Right axis deviation. rS complexes in Leads I, aVL . Prominent Q wave in leads II, III, and aVF .

28. Left posterior fascicular block :- Right axis deviation rS complexes in Leads I, aVL Prominent Q wave in leads II, III, and aVF Prolonged R wave peak time in aVF >45 ms (time from onset of QRS till peak R wave) LPHB – significance LPHB may mimic old IWMI due to Q waves in II, III, aVF . Broad nature & dual blood supply of posterior bundle makes isolated LPFB rare.

29. Bifascicular block Two of three fascicles of His / Purkinje system are blocked. Most commonly RBBB + either LAFB OR LPFB. Etiologies : CAD (most common) Hypertension Aortic stenosis Congenital heart diseases Trifasicular Block Presence of conducting disease in all three fascicles. Has three features Prolongation of PR interval (First degree AV block). RBBB. Either LAFB/LPFB.

30. Investigations:- Diagnostic investigations for bradycardia, alongside a focused history and examination, should include: 1 st  line investigations Further investigations 12 lead  ECG Event recorder / loop recorder Full blood screen* Exercise testing 24hr Holter monitor Tilt table testing Echocardiogram Lyme titres and urinary antigen test Chest X-ray Electrophysiology testing

31. Management of sinus node dysfunction. Management of sinus node dysfunction begins with eliminating reversible causes and confirming whether symptoms correlate with bradycardia. If symptoms are clearly correlated, permanent pacing should be offered. If it is unclear, a trial of oral theophylline can be considered diagnostically. If there is no correlation between symptoms and bradycardia, then observation is appropriate. Class I recommendations should be performed or are indicated. Class IIa recommendations are considered reasonable to perform. Class IIb recommendations may be considered. Class III recommendations are associated with harm more than benefit. Class I indications for pacing in SA node dysfunction included documented symptomatic bradycardia, SND-associated long-term drug therapy for which there is no alternative, and symptomatic chronotropic incompetence. Class IIa indications include those outlined previously in which SND is suspected but not documented and for syncope of unexplained origin in the presence of major abnormalities of SA node dysfunction. class IIb indication for pacing Mildly symptomatic individuals with heart rates consistently <40 beats/min. Pacing is not indicated in patients with SA node dysfunction who do not have symptoms and in those in whom bradycardia is associated with the use of nonessential drugs. Because conduction system abnormalities are common after transcatheter aortic valve replacement, recommendations on postprocedure surveillance and pacemaker implantation are recommended.

32. Indications for Permanent Pacing in Sinus Node Dysfunction (SND) • Symptoms that are directly attributable to SND • Symptomatic sinus bradycardia because of essential medication therapy for which there is no alternative treatment • Tachy-brady syndrome and symptoms attributable to bradycardia • Symptomatic chronotropic incompetence • In patients with symptoms that are possibly attributable to SND, a trial of oral theophylline may be considered to increase heart rate and determine if permanent pacing may be beneficial

33. In patients with acquired second-degree Mobitz type II atrioventricular block, high-grade atrioventricular block, or third-degree atrioventricular block not caused by reversible or physiologic causes, permanent pacing is recommended regardless of symptoms. For all other types of atrioventricular block, in the absence of conditions associated with progressive atrioventricular conduction abnormalities, permanent pacing should generally be considered only in the presence of symptoms that correlate with atrioventricular block.

34. Recommendations for General Principles of Chronic Therapy/Management of Bradycardia Attributable to Atrioventricular Block COR LOE Recommendation III: Harm C-LD In patients with first-degree atrioventricular block or second-degree Mobitz type I (Wenckebach) or 2:1 atrioventricular block which is believed to be at the level of the atrioventricular node, with symptoms that do not temporally correspond to the atrioventricular block, permanent pacing should not be performed. III: Harm C-LD In asymptomatic patients with first-degree atrioventricular block or second-degree Mobitz type I (Wenckebach) or 2:1 atrioventricular block which is believed to be at the level of the atrioventricular node, permanent pacing should not be performed.