BRADYARRYHTHMIAS

DR.R.PRABHU CHARAN

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

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.

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

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

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

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

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.

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

. Chronotropic incompetence may be secondary to intrinsic sinus node dysfunction or secondary to drugs with negative chronotropic effects.

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

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, 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

TREATMENT Pharmacological- atropine ,b agonists,

theophylline Pacemaker therapy

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

Etiologies of Atrioventricular Block

Autonomic    Carotid sinus hypersensitivity   Vasovagal Metabolic/endocrine     Hyperkalemia   Hypothyroidism    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

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  Emery-Dreifuss MD,)   Myotonic dystrophy   Progressive familial heart block

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).

Most commonly seen CAD, Acute rheumatic carditis, digitalis , Bblockers

First degree AV block

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

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

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 complete AV block

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 preceding T wave

High grade AV block intermittent block of two or

more consecutive supraventricular rythms

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

Two rhythms are independent & asynchronous

P waves bear no relation with QRS complexes

QRS complex morphology is useful to locate level of block

There is no assosciation of P wave with QRS complexes

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

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

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

Treatment To treat in symptomatic or

progressive blocks or physiological unresponsiveness

. Atropine .pacemakers ( temporary/

permanent) . To treat reversible causes

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