Downloaded 13 times
Uploaded byPDT DM CARDIOLOGY
Bradyarryhthmias
The document summarizes the intrinsic cardiac conduction system and how it regulates heart rate. It describes the roles of the sinoatrial node, atrioventricular node, bundle of His, bundle branches and Purkinje fibers in initiating and distributing electrical impulses throughout the heart. It also discusses how the sympathetic and parasympathetic nervous systems can respectively increase or decrease heart rate through their effects on these conduction pathways. Various types of bradyarrhythmias and atrioventricular conduction blocks are then outlined.
More Related Content
Similar to Bradyarryhthmias
More from PDT DM CARDIOLOGY
Bradyarryhthmias
- 1. BY DR RAMDHANKUMAR KAMAT SR CARDIOLOGY IGIMS PATNA
- 2. 2 Intrinsic Cardiac ConductionSystem Approximately 1% of cardiac muscle cells are autorhythmic rather than contractile 70-80/min 40-60/min 15-40/min
- 3. 3 Intrinsic Conduction System Function:initiate & distribute impulses so heart depolarizes & contracts in orderly manner from atria to ventricles. SA node AV node Bundle of His Bundle Branches Purkinje fibers
- 9. 9 Regulation of theheart beat • Sympathetic from the cardiac plexus supplies all parts of the heart (atria, ventricle and all parts of the conduction system) • Parasympathetic from Vagus nerves supply mainly the atria, SA and AV nodes, very little supply to ventricles • Sympathetic: increase the permeability of the cardiac cells to Na+ and Ca++ i.e Positive Chronotropic and positive Inotropic action • Parasympathetic: Increase the permeability of the cardiac cells to K+ and decrease its permeability to Na+ and Ca++
- 10. Extrinsic Innervation ofthe Heart
- 11. 11 Autonomic Innervation ofthe Heart
- 12. Effects of SympatheticStimulation . 1. ↑ Rate of rhythm of SA Node → ↑ Heart Rate (Chronotropic Effect) 2. ↑ Excitability of AV Junctional fibers (Bathmotropic Effect) 3. ↑ Conduction Velocity (Dromotropic Effect) 4. ↑ .Force of Contraction (Inotropic effect)
- 13. Effects of ParasympatheticStimulation 1. ↓ Rate of rhythm of SA Node↓ Heart Rate 2. ↓ Excitability of AV Junctional fibers→↓Conduction Velocity 3. ↓ Force of contraction ( By increasing membrane permeability to K+ ions)
- 14. 14 Parasympathetic Effects onHeart Rate • Parasympathetic (vagal) nerves, which release acetylcholine at their endings, innervate S-A node and A-V junctional fibers proximal to A-V node. • Causes hyperpolarization because of increased K+ permeability in response to acetylcholine. • This causes decreased transmission of impulses maybe temporarily stopping heart rate.
- 20. The SA nodeconsists 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.
- 23. • Bradyarrhythmias • Bradyarrhythmiasare 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
- 25. • Sinus NodeDysfunction • 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.
- 27. • 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
- 28. • Sinus Pauseand 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 . • 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. Pauses longer than 3 sec need careful clinical correlation with symptoms.
- 30. • Sinoatrial ExitBlock • 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
- 33. • 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
- 34. • These patientsare 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.
- 37. • 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
- 38. • . Chronotropicincompetence may be secondary to intrinsic sinus node dysfunction or secondary to drugs with negative chronotropic effects.
- 39. • 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
- 40. • Investigations • ECG(Holter monitoring) • Autonomic testing This can be assessed by observing the response of heart rate and rhythm with carotid sinus massage and Valsalva 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
- 41. • TREATMENT • Pharmacological-atropine , b agonists(isoprenaline ,orciprenaline), theophylline • Pacemaker therapy
- 43. AV Conduction defects •Delay or interruption in conduction of atrial impulse through Av node &bundle of HIS • 3 TYPES 1st degree 2nd degree 3rd degree
- 44. • Etiologies ofAtrioventricular Block • Autonomic = Carotid sinus hypersensitivity , Vasovagal Metabolic/endocrine = Hyperkalemia Hypothyroidis m 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
- 45. • Infiltrative =Amyloidosis , Hemochromatosis, Sarcoidosis Neoplastic/traumatic = Lymphoma , Radiation Mesothelioma , Catheter ablation , Melanoma • Degenerative = Lev disease , Lenègre disease Coronary artery disease= Acute MI • Heritable/congenital= Congenital heart disease, Facioscapulohumeral MD (4q35), Maternal SLE , Kearns-Sayre syndrome , Myotonic dystrophy , Progressive familial heart block
- 46. • 1°heart block prolongedPR 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).
- 47. • Most commonlyseen CAD, Acute rheumatic carditis, digitalis , B blockers
- 48. • First degreeAV block
- 49. • 2°AV block Intermittentfailure of AV conduction some of sinus impulses are not transmitted through Av node ( p wave not followed by QRS ( dropped beat) Two types - Mobitz type 1&2
- 50. MOBITZ TYPE I •There is progressive prolongation of PR interval ,shortening of RR and a pause that is less than 2 times the immediately preceding RR interval on ecg. • The ecg complex after pause exhibits shorter PR interval than immediately preceding the pause.
- 51. • TYPE 1 transmissionthrough 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
- 52. • TYPE 2 PRinterval 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 complete AV block
- 53. • 2nd degreeAV 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 preceding T wave
- 54. • High gradeAV block intermittent block of two or more consecutive supraventricular rhythms
- 55. • 3°AV block completeinterruption of AV conduction All supra ventricular impulses are blocked ventricles are then activated by ectopic pacemaker situated in AV node or below. Thus both atria & ventricles are activated by two different pacemakers
- 56. • Two rhythmsare independent & asynchronous • P waves bear no relation with QRS complexes • QRS complex morphology is useful to locate level of block
- 57. • There isno association of P wave with QRS complexes
- 58. • Clinically ptmay 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
- 59. • 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 node and impair infranodal conduction
- 60. • In patientswith 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
- 61. • Treatment 1) Totreat reversible causes 2) To treat in symptomatic or progressive blocks or physiological unresponsiveness . Atropine .pacemakers ( temporary/ permanent)
- 65. TEMPORARY PACEMAKER • Canbe used temporarily either prophylactically or supportively until the condition for rate or conduction resolves.
- 66. Pacemaker code • 5letters- 1st- chamber paced(O:none,A:atrium,V:ventricle,S:single,D:dual) 2nd- chamber sensed(O:none,A:atrium,V:ventricle,S:single,D:dual) 3rd- response to sensing(O:none,I:inhibition,T:triggered,D:I + T) 4th- programmable function or rate response(R) 5th- anti-tachyarrythmia function if present(O:none,P:anti tachycardia pacing, S: shock, D:pace +shock) • Common pace maker mode- VVIR or DDDR