Bradyarrhythmias are caused by problems with impulse formation in the sinus node or impulse conduction through the AV node. Sinus node dysfunction can cause sinus bradycardia, sinus pause/arrest, or chronotropic incompetence. Atrioventricular block is classified as first, second, or third degree and may be caused by conditions like CAD, drugs, or infiltrative diseases. Second degree AV block is further classified as Mobitz type I or II based on PR interval characteristics. Third degree AV block causes complete dissociation between atrial and ventricular rhythms.

3.  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

5.  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.

7.  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

8.  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

10.  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

12.  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

13.  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.

16.  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

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

18.  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

19.  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

20.  TREATMENT
 Pharmacological- atropine ,b agonists,
theophylline
 Pacemaker therapy

22.  Delay or interruption in conduction of atrial
impulse through Av node &bundle of HIS
 3TYPES
1st degree
2nd degree
3rd degree

23.  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

24.  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

25.  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).

26.  Most commonly seen CAD,Acute rheumatic
carditis, digitalis , Bblockers

27.  First degreeAV block

28.  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

29.  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

30.  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

31.  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

32.  High grade AV block
intermittent block of two or more
consecutive supraventricular rythms

33.  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

34.  Two rhythms are independent & asynchronous
 P waves bear no relation with QRS complexes
 QRS complex morphology is useful to locate
level of block

35.  There is no assosciation of P wave with QRS complexes

36.  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

37.  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

38.  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

39.  Treatment
To treat in symptomatic or progressive blocks
or physiological unresponsiveness
. Atropine
.pacemakers ( temporary/ permanent)
.To treat reversible causes