ATRIO-VENTRICULAR BLOCKS

DR AHMAD USMAN
CONSULTANT INTERVENTIONAL CARDIOLOGIST
OBJECTIVES
• Review heart blocks, their clinical significance and
management
• Provide an overview of pacemaker components,
nomenclature and functions
• Discuss complications of pacemaker implantation
• Talk about pacemaker malfunction
• Touch on ED management and disposition of pacemaker
patients
• Offer a precis of temporary pacing modalities.
• ICDs not covered in this talk.
CASE

• 85 y.o. F complaining of feeling “off” and being “just so tired”

• Denies CP, SOB
• Vaguely recalls feeling a bit “unsteady” on a couple of occasions
• PMHx: osteoporosis, hypothyroidism and depression
• Meds: Calcium, Vit D, Celexa, Synthroid
CASE CONT’D

• Vitals:
• HR 45, regular
• RR 16
• BP 108/75
• 02 sats 97% on RA
• Afebrile
Granny’s ECG
ATRIOVENTRICULAR BLOCKS

• Definition:
• Delay or interruption in the transmission of an impulse from the
atria to the ventricles
• Conduction may be delayed, intermittent or absent.
• Duration
• Transient
• Permanent
• Causes may be:
• Anatomical
• Functional
ETIOLOGY

• Fibrosis and sclerosis of the conduction system

• Ischemic heart disease
• Drugs
• Increased vasovagal tone
• Valvular disease
• Congenital heart disease
• Other:
• Cardiomyopathies, myocarditis, hyperkalemia, infiltrating
malignancies, miscellaneous
• Surgery – CABG, valve replacement
SCLEROSIS AND FIBROSIS OF THE
CONDUCTION SYSTEM
• Account for 50% of AV block
• 2 idiopathic entities:
1. Lev’s Disease:
– “sclerosis of left side of the heart”
– Affects older people
– Associated with calcific aortic and mitral valves that extends into the adjacent
conduction system
2. Lenegre’s Disease:
• Progressive fibrotic, sclerodegenerative disease
• Affects younger people
• May be hereditary
• Slow progression to complete heart block
• Presents with bradycardia and some degree of AVB
ISCHEMIC HEART DISEASE

• Accounts for 40% of AV block

• Chronic or acute ischemic changes can disrupt conduction
• With AMI:
• 20% will develop AVB
• 8% 1st degree AVB
• 5% 2nd degree AVB
• 6% 3rd degree AVB
• Up to 20% increased mortality with bradycardia and/or
blocks post AMI
DRUGS

• Cardiac medications: Digitalis, CCB (especially

verapamil), B-blockers
• Class Ia: Quinidine, procainamide, disopyramide
• Cholinergics: cholinesterase inhibitors
• Opioids and sedatives
• Drugs with Class IA type effects:
• TCAs, carbamazepine, quinine, chloroquine
• Cocaine
INCREASED VAGAL TONE

• Vasovagal
• Pain
• Occulocardiac reflex
• Diving reflex
• Carotid sinus massage
• Hypersensitive carotid sinus syndrome
• Stimulation of carotid sinus leads to bradyasystole and then to
pre/syncope
• Cardioinhibitory: >3s of asystole with carotid stimulation
• Vasodepressor effects
VALVULAR DISEASE

• Due to extension of calcification into conduction system

• Associated with AV and MV repair
• Repair of VSD: including transcoronary ablation of septal hypertrophy
INFECTIOUS

• AVB with the following usually indicates poor prognosis:

• Myocarditis:
• Viral: Cocksackie B
• Bacterial: Diptheria
• Protozoal: Chagas disease
• Spirochetal: Lyme disease
• Syphilis, toxoplasmosis
OTHER
• Congenital heart disease, neonatal SLE syndrome
• Familial heart disease: cardiac sodium channel SCN5A linked mutations
• Cardiomyopathies: HOCM, amyloidosis, sarcoidosis
• Endocrine causes:
• Hyperthyroidism
• hypoadrenalism
• Hyperparathyroidism
• Acromegaly
• Electrolyte abnormalities:
• Hyperkalemia: >6.3 meq/L
• Hypercalcemia
• Hypermagnesemia
• Infiltrative malignancies: lymphoma, multiple myelomas
• Neuromuscular degenerative diseases
• Cardiac tumours
FIRST DEGREE HEART BLOCK

• SA node is normal
• Normal P wave
• AV node conducts more slowly than normal
• Prolonged PR interval >0.2s
• PR interval is constant
• Rest of conduction is normal
• Normal QRS
FIRST DEGREE AVB

• Conduction delay can occur in:

• Atrium: 3% of cases
• May be due to intratrial pathology
• EKG findings: widening of P wave and decreased P wave voltage
• AV node:
• Most common site
• Common causes: increased vagal tone, CCB, digoxin, BB
• EKG findings: long PR interval with a narrow or wide P wave and
narrow QRS
• Bundle of His:
• Drugs that block sodium channels can impair depolarization and
slow conduction (Quinidine, procainamide)
FIRST DEGREE AVB

• Clinical significance – none

• Treatment – none
• May progress to 2nd or 3rd degree AVB
SECOND DEGREE AVB

• Some atrial impulses fail to reach the ventricles

• 2 types:
• Mobitz Type I (Wenckebach): progressive PR interval lengthening to a
non-conducted P wave
• Mobitz Type II: PR interval constant prior to P wave that does not conduct
to the ventricles.
SECOND DEGREE A-V BLOCK
(MOBITZ I OR WENCKEBACH)
MOBITZ TYPE I (WENCKEBACH) AVB

• Most often involves AV node

• Benign
• Features:
• Gradually increasing PR interval
• Gradually decreasing R-R interval
• Dropped beat
• Largest delay occurs in the first beat and then decreases
beat to beat until block occurs and cycle is reset
• Group beating: 3:2,4:3 etc.
 Second Degree Heart Block (2º)
Mobitz Type I
(Wenkebach)

PR PR PR DROPPED BEAT
MOBITZ TYPE I

• Clinical implications:
• Often asymptomatic
• May have some symptoms eg lethargy, confusion
• If cardiac output is reduced, patient may experience angina, syncope or heart
failure due to bradycardia and resultant hypoperfusion state.
• Can occur in athletes with high vagal tone
• Elderly: aging prolongs cycle length
FURTHER IMPLICATIONS:

• Underlying IHD:
• Mobitz type I can be complication of inferior MI as:
• RCA supplies inferior and posterior walls and AV and SA nodes
• Associated with increased mortality
• Treatment:
• Removing reversible causes (ischemia, increased vagal tone,
medications
• Pacemaker if symptomatic during day
• No pacemaker is symptoms at night
• May progress to 3rd degree AVB
MOBITZ TYPE II
MOBITZ TYPE II AVB

• Always occurs below the AV node

• 20% within Bundle of His
• 80% in bundle branches
• Widened QRS
• PR interval may be normal or slightly prolonged but
constant
• Non-conducted P wave on EKG
• Clinical implications:
• Dizziness
• Presyncope
• Syncope
MOBITZ TYPE II AVB

• Type II is permanent and may progress to higher levels of block

• Treatment:
• Remove reversible causes
• Potential candidates for pacemaker insertion
SECOND DEGREE AVB 2:1

• Unable to classify as Mobitz type I or II

• Ratio of 2 P waves to 1 QRS
• Clinical significance:
• Will be associated with symptoms (dizziness, lethargy etc.)
• May progress to 3rd degree AVB
• Treatment - pacemaker
THIRD DEGREE A-V BLOCK
THIRD DEGREE (COMPLETE) AVB

• No atrial impulses reach the ventricles due failure of

AV node therefore no P wave conduction
• AV dissociation (Ps marching through…)
• QRS complex:
• Narrow: block at AV node to level of bundle of His
• Wide: block below level of bundle of His
• More distal the block the slower the escape rhythm
• If <40bpm: pacemaker is unreliable causing profound
bradycardia or asystole
• Syncope is very common
CLINICAL SIGNIFICANCE

• Clinical Implications:
• Dizziness
• Presyncope
• Syncope
• Ventricular tachycardia
• Ventricular fibrillation
• Confusion
• Can worsen angina and CHF
• Treatment:
• Pacemaker!