Mechanisms of Bradyarrhythmias Flashcards
2 basic ways can have bradyarrhythmia
- SA node disease = impulse formation problem
2. AV node or his/purkinje disease = impulse transmission problem
3 categories of sinus node dysfunction
- sinus bradycardia = heart rate too slow at rest
- chronotropic incompetenece =heart rate fails to augment with increasing metabolic demand
- tachy-brady syndrome/sick sinus syndrome = atrial fibrillation with sinus bradycardia
Clinical manifestation of chronotropic incompetence
fatigue, lightheadedness with exertion –> max sinus rate< 100bmp, failure to reach 70% of max predicted hr with exercise (220-age)
Why not treat tachy brady syndrome with typical anti-arrhythmics
b/c leads to more bradycardia –> use a pacemaker instead
What is SNRT
sinus node recovery time –> how long it takes SA node to recover pacing after being taken off external pacer
1st degree AV block
every p wave conducts to ventricle but slowly –> pr interval>200
2nd degree AV block
some pwaves conduct to ventricle (Mobitz type 1 and 2)
3rd degree AV block
no pwaves conduct to the ventricle
Difference between Mobitz type 1 and 2 second degree heart block
type 1- AV node = benign (aka wenckebach)
type 2-his/purkinje = malignant
EKG features of Wenckebach/Mobitz 1 2nd degree heart block
not all p waves have a narrow qrs, grouped beating AND pr interval gets progressively longer and then drops
EKG features of Mobitz 2 2nd degree heart block
not all p waves have a wider qrs, unpredictable blocked beating AND pr intervals are the same
EKG features of right bundle branch block
rabbit ear v1 (slow right side conduction) –> small R and tall R’
EKG features of left bundle branch block
small r wave and slow downward complex in v1
EKG features of 3rd degree heart block
p waves are dissociated from qrs
EKG features of vasovagal syncope
sinus bradycardia with interspersed complete heart block due to vagal ps effects on SA and AV node
