Brady arryhthmias


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  • It can be seen that this was summerized by the doctor that have been deeply understood the essence of heart conduction procceses and etiopathology. Which is not at all easy even for the cardilogist that are doing it for the life time. VERY nice job. Congratulations
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Brady arryhthmias

  1. 1.  Bradyarrhythmias  Bradyarrhythmias are most commonly caused by failure of impulse formation (sinus node dysfunction) or by failure of impulse conduction over the atrioventricular (AV) node/His-Purkinje system. Bradyarrhythmias may be caused by disease processes that directly alter the structural and functional integrity of the sinus node, atria, AV node, and His-Purkinje system or by extrinsic factors (autonomic disturbances, drugs, etc.) without causing structural abnormalities
  2. 2.  Sinus Node Dysfunction  Sinus node dysfunction is a common clinical syndrome, comprising a wide range of electrophysiologic abnormalities from failure of impulse generation, failure of impulse transmission to the atria, inadequate subsidiary pacemaker activity, and increased susceptibility to atrial tachyarrhythmias.6,7 This disorder has also been variably termed the sick sinus syndrome, tachycardia-bradycardia syndrome, SA disease, and SA dysfunction.
  3. 3.  Sinus bradycardia H.R <60 Normal P-QRS-T complexes Normal phenomenon in athletes , sleep, myxoedema ,obs jaundice, uraemia, raised ICT, glaucomas ,drugs like b blockers,structural nodal disease , carotid sinus hypersenstivity, M.I
  4. 4.  Sinus Pause and Sinus Arrest  Sinus pause or arrest means failure of sinus node discharge with lack of atrial activation of sinus origin.This results in absence of P waves and periods of ventricular asystole if lower pacemakers (junctional or ventricular) do not initiate escape beats (Fig. 40–2).The resulting pause in sinus activity should not be in multiples of preceding sinus cycle length (P-P interval). Asymptomatic sinus pauses of up to 3 sec in duration are not uncommon in trained athletes.15 Pauses longer than 3 sec need careful clinical correlation with symptoms and warrant
  5. 5.  Sinoatrial Exit Block  In SA exit block, as the name implies, the impulse is formed in the sinus node but fails to conduct to the atria, unlike sinus arrest.This particular arrhythmia is recognized on ECG by pauses resulting from the absence of normal P waves and the duration of the pause measuring an exact multiple of the preceding P- P interval.  In first-degree SA block, there is significant prolongation of the time for the sinus impulse to exit into the atria (SA conduction time). This cannot be identified clinically or electrocardiographically. Similar to AV block, second- degree SA block can be type I (Wenckebach) or type II.  In type I there is progressive prolongation of SA conduction, manifested on surface ECG as progressive shortening of P-P interval, prior to the pause created by loss of a P wave.  In type II SA exit block, the P-P intervals remain constant before the pause. Third-degree or complete SA block will manifest as absence of P waves, with long pauses resulting in lower pacemaker escape rhythm; it is impossible to diagnose with certainty without invasive sinus node recordings
  6. 6.  Tachycardia-Bradycardia Syndrome  Sinus bradycardia interspersed with periods of atrial tachyarrhythmias is a common manifestation of sinus node dysfunction  The atrial tachyarrhythmias usually range from paroxysmal atrial tachycardia to atrial flutter and atrial fibrillation. Apart from underlying sinus bradycardia of varying severity, these patients often experience prolonged sinus arrest and asystole upon termination of the atrial tachyarrhythmias, resulting from suppression of sinus node and secondary pacemakers
  7. 7.  These patients are at increased risk for thromboembolism,16 and the issue of long-term anticoagulation should be addressed to prevent strokes.  Therapeutic strategies to control tachyarrhythmias often result in the need for pacemaker therapy.
  8. 8.  Chronotropic Incompetence  Chronotropic incompetence is the inability of the sinus node to achieve at least 80 percent of the age predicted heart rate. .It is present in approximately 20 to 60 percent of patients with sinus node dysfunction.1 .Although the resting heart rates may be normal, these patients may have either the inability to increase their heart rate during exercise or have unpredictable fluctuations in heart rate during activity. .Some patients may initially experience a normal increase in heart rate with exercise, which then plateaus or decreases inappropriately
  9. 9.  . Chronotropic incompetence may be secondary to intrinsic sinus node dysfunction or secondary to drugs with negative chronotropic effects.
  10. 10.  Clinical Presentation  Even though sinus node dysfunction can occur in any age group, more than half the patients affected are older than 50 years of age at the time of diagnosis  They present with syncope, bradycardia, exercise intolerence fatigue, atrial fibrillation, thromboemboism
  11. 11.  Investigations  ECG( Holter monitoring)  Autonomic testing This can be assessed by observing the response of heart rate and rhythm with carotid sinus massage, head-up tilt testing, andValsalva maneuver. Pharmacologic evaluation of the sinus node can be performed with atropine, isoproterenol, and propranolol. Following injection of atropine 0.04 mg/kg intravenously, the heart rate increases by 15 percent and to more than 90 beats/min. Isoproterenol infusion at 1 to 3 g/min increases heart rate by 25 percent. Patients with sinus node dysfunction show blunted heart rate responses to the preceding infusions .EPS
  12. 12.  TREATMENT  Pharmacological- atropine ,b agonists, theophylline  Pacemaker therapy
  13. 13.  Delay or interruption in conduction of atrial impulse through Av node &bundle of HIS  3TYPES 1st degree 2nd degree 3rd degree
  14. 14.  Etiologies of Atrioventricular Block  Autonomic Carotid sinus hypersensitivity Vasovagal Metabolic/endocrine Hyperkalemia Hypothyroidi sm Hypermagnesemia Adrenal insufficiency Drug-related Beta blockers Adenosine Calcium channel blockers Antiarrhythmics (class I & III) Digitalis Lithium Infectious Endocarditis Tuberculosis Lyme disease Diphtheria Chagas disease Toxoplasmosis Syphilis Inflammatory SLE MCTD Rheumatoid arthritis Scleroderma
  15. 15.  Infiltrative Amyloidosis Hemochromatosis Sa rcoidosis Neoplastic/traumatic Lymphoma Radiation Mesothelioma , Catheter ablation , Melanoma Deg enerative Lev disease Lenègre disease Coronary artery disease Acute MI  Heritable/congenital Congenital heart disease Facioscapulohumeral MD (4q35) Maternal SLE Kearns-Sayre syndrome Emery-Dreifuss MD,) Myotonic dystrophy Progressive familial heart block
  16. 16.  1°heart block conduction time prolonged , but all impulses prolonged prolonged PR interval( >0.20 sec)& all p waves followed by QRS complex may arise due to defect in AV node ( normal QRS) , or in bundle of HIS , Bundle branch ( abnormal QRS).
  17. 17.  Most commonly seen CAD,Acute rheumatic carditis, digitalis , Bblockers
  18. 18.  First degreeAV block
  19. 19.  2°AV block Intermittent failure of AV conduction some of sinus impulses or not transmitted through Avnode ( pwave nt followed by QRS ( dropped beat) Two types , Mobitz type 1&2
  20. 20.  TYPE 1 transmission through conducting system becomes increasingly difficult until it fails completely sequence begins with normal or prolonged P-R INTERVAL , with each beat P-R interval lengthens , until beat is dropped defect usually situated in Avnode It can be physiological or pathological
  21. 21.  TYPE 2 PR interval remains constant . missed beats seen in between.( p wave followed by absent QRS) Can be 2:1, 3:1, 4:1 lesion usually situated in bundle of HIS frequently progresses to completeAV block
  22. 22.  2nd degree AV block ,2:1 AV block ,dangerous AV block  Only one P wave is conducting.the subsequent P wave is not conducting and is just behind the precedingT wave
  23. 23.  High grade AV block intermittent block of two or more consecutive supraventricular rythms
  24. 24.  3°AV block complete interruption of AV conduction All supra ventricular impulses are blocked ventricles are then activated by ectopic pacemaker situated in in AV node or below.Thus both atria & ventricles are activated by two different pacemakers
  25. 25.  Two rhythms are independent & asynchronous  P waves bear no relation with QRS complexes  QRS complex morphology is useful to locate level of block
  26. 26.  There is no assosciation of P wave with QRS complexes
  27. 27.  Clinically pt may be asymptomatic or can present with syncope, hypotension , ventricular flutter, fibrillation  Stokes Adam syndrome syncopal attack due to ventricular asystole occurs when ectopic pacemaker fails to discharge during transition from 2nd to 3rd degree heart block or when 2 or more pacemakers compete
  28. 28.  Investigations routine investigations, mainly serum electrolytes, ecg, 2d echo) bundle of his electrogram. Owing to the differences in innervation of the AV node and infranodal conduction system, vagal stimulation and carotid sinus massage slow conduction in the AV node but have less of an effect on infranodal tissue and may even improve conduction due to a reduced rate of activation of distal tissues. Conversely, atropine, isoproterenol, and exercise improve conduction through the AV nodeand impair infranodal conduction
  29. 29.  In patients with congenital CHB and a narrow QRS complex, exercise typically increases heart rate; by contrast, those with acquired CHB, particularly with wide QRS, do not respond to exercise with an increase in heart rate  Electro physiological studies
  30. 30.  Treatment To treat in symptomatic or progressive blocks or physiological unresponsiveness . Atropine .pacemakers ( temporary/ permanent) .To treat reversible causes