bradyarrhythmias

1. BRADYARRHYTHMIAS

3. • 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.
• 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 OR 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 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 PP 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.

11. • 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

13. 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, 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.

15. WANDERING ATRIAL PACEMAKER RHYTHM
• Shift of PM activity temporarily from SA node to other atrial or
AV node sites
• Changing P morphology, P-R, R-R intervals
• Heart rate < 100 bpm

17. SINUS ARRHYTHMIA
• Alternating periods of slow and rapid heart rates
• Max R-R interval- minimum R-R interval in the same lead
exceeds 0.12 sec
• Max R-R – min R-R ÷ minimum R-R interval > 10 % in the
same lead
• Resp SA- R-R interval  inspiration, expiration

19. 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.
• 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.

20. 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,
thromboembolism.

21. TREATMENT
• Pharmacological- atropine ,b agonists, theophylline
• Pacemaker therapy

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

27. 1°AVBLOCK
• conductiontime prolonged,butallimpulsesprolonged
• prolonged PR interval(>0.20sec)&allpwavesfollowedby QRScomplex
• mayarisedueto defectinA
Vnode(normal QRS),orinbundleofHIS ,Bundlebranch(
abnormalQRS).
• Mostcommonlyseen CAD, Acuterheumatic carditis,digitalis,B-blockers

28. 1°AVBLOCK

29. 2°AVBLOCK
• Intermittentfailureof A
Vconduction
• Someofsinusimpulsesornottransmitted throughAvnode
• Twotypes,Mobitztype1&2

30. 2°AVBLOCK (MOBITZTYPE-1)
9MOBITZTYPE-1

31. TYPE2
• PRintervalremainsconstant.
• missedbeatsseeninbetween.(pwave followedbyabsentQRS)
• Can be 2:1,3:1,4:1
• lesionusuallysituatedinbundleofHIS frequentlyprogressesto completeA
Vblock

32. ⬥ 2nd degreeAVblock ,2:1AVblock ,dangerousAVblock
⬥ Only one Pwave is conducting.the subsequent Pwave is not conducting and is just
behind the precedingTwave
TYPE2

34. 3°AVBLOCK
• complete interruption of A
Vconduction
• All supraventricular impulsesareblocked ventriclesare
then activated by ectopic pacemakersituatedin inA
V
nodeor below.
• Thus both atria & ventriclesareactivated by two
different pacemakers

35. • 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

37. INVESTIGATIONS
• Routine investigations, mainly serumelectrolytes, ECG,2D ECHO
• Owing to the differencesin innervationof theAV nodeandinfranodal
conductionsystem,
vagal stimulation andcarotid sinusmassageslow conductionintheA
V
nodebut havelessof aneffect oninfranodaltissueandmayevenimprove
conductiondueto areducedrate of activationof distaltissues.
Conversely,atropine, isoproterenol, andexerciseimproveconduction
through theAV node andimpair infranodal conduction

38. • Inpatientswith congenitalCHBandanarrow QRScomplex,exercisetypically
increasesheart rate
• bycontrast,thosewith acquiredCHB, particularlywith wideQRS,donot respond
to exercisewith anincreaseinheartrate
• Electrophysiologicalstudies

39. TREATMENT
Totreatinsymptomaticorprogressiveblocks orphysiologicalunresponsiveness
• Atropine
• pacemakers(temporary/permanent)
• Totreatreversiblecauses