Pacemaker Flashcards
Common PM implanted in vet practice
- Single transvenous lead pacing in RV apex most commonly
o Easy to place
o Alternative sites: bundle of His, biventricular - Single epicardial lead pacing on LV apex
o Alternative for unsuitable to transvenous pacing - Dual chamber may provide superior performance → DDD mode
o Favorize AV synchrony → improve hemodynamics
Risk epicardial pacing
↑ risk for bacteremia, thrombosis, embolism
Consequences of long term RV pacing
Asynchronous ventricular contraction
Impaired cardiac performance
Deleterious myocardial remodeling
Advantage of Dual ch
o Favorize AV synchrony → improve hemodynamics
CO depends on
o Ventricular rate and physiologic HR variation
o Synchrony of atrial/ventricular contraction
Can be attained by
* Pacing atrium
* Endogenous atrial depol → AV delay → ventricular pacing
Hu: improve CO, BP, quality of life
o Ventricular activation sequence
Modes of dual chamber pacing
- DDD mode: 2 leads (1 atrial, 1 ventricular)
- VDD mode: 1 lead in RV with floating electrodes
Disadvantages of dual pacing
o Complex programming,
o ↑ expense, ↑ implantation time
o Technical challenge of placing atrial lead in small patiens
o ↑ complications post op
Define the NASPE/BPEG classification.
1- Chamber paced
O none
A atrium
V ventricle
D dual
2- Chamber sensed
O none
A atrium
V ventricle
D dual
3- response to sensing
O none
T triggered
I inhibited
D dual
4- rate modulation
O non
R rate modulation
5- multisite pacing
O none
A atrium
V ventricle
D dual
What are the typical modes used in veterinary practice?
Most commons: VVI and VVIR
AAI/AAIR
VDD
DDD
VVI modality
- Ventricular depolarization in absence of inherent beat
- Sensing ventricular signal → inhibit PM output
o Important feature to prevent competitive rhythms and trigger arrhythmias if pacing during vulnerable period of cardiac cycle
Disadvantages
o Preset pacing rate (non physiological pacing)
o Asynchronous contraction of A and V → can lead to PM syndrome
VVIR
- Similar to VVI + rate responsiveness (chronotropic competence)
- Stimulation frequency ↑ in response to physical activity/respiration
o Sensors: motion, minute ventilation - AV asynchrony persists
AAI/AAIR
- Single chamber, atrial inhibited +/- rate responsiveness
o Stimulus delivered to atrium
o PM output inhibited by atrial events
AAI/AAIR pacing indications
SSS and normal AV node function
AAI/AAIR pacing advantages
o Maintain AV synchrony
o Synchronous ventricular contraction
o Avoid retrograde conduction through AV node and echo beats
AAI/AAIR pacing disadvantages
lack of depol if AVB occurs
o 24h Holter and Weckenbach testing recommended
VDD
- Atrial synchronous pacing
o Single pacing lead w sensing electrodes in atrial portion of lead
Pacing in ventricle
Sensing in atria and ventricle → input inhibited by ventricular beat but stimulated by atrial beat
o Sensed atrial events → AV delay
Intrinsic ventricular beat during AV delay → inhibit pacing, reset timing cycle
No intrinsic ventricular beat → paced beat at end of AV delay
No intrinsic atrial event → PM escape w paced ventricular depol at lower rate
Upper tracking rate
upper limit of atrial depol permitted to trigger ventricular depol
Requirement for VDD pacing
- Need normal SA node function
DDD
- Dual chamber pacing + sensing with inhibition and tracking → fully automatic PM
- Similar to VDD but atrium is paced
o No intrinsic atrial depol → atrial paced beat → tracked → ventricular paced beat - ECG can vary → normal sinus rhythm, atrial pacing only, AV sequential pacing, atrial synchronous pacing
DDD pacing advantages
preserve AV synchrony
PM refractory periodq
- Pacemaker is refractory for specific (pragrammable) period after paced or sensed depol
o Ventricular events during refractory period = will not reset PM
o Ventricular event after refractory period → sensed and inhibit output
Restart timing cycle
Pacemaker syndrome c/s
- Vasovagal syncope, pre-syncope, shortness of breath, dyspnea with exertion
Mechanism of c/s w/ PM syndrome
o ↑LAP/RAP with atrial contraction against closed AV valve during ventricular contraction
Release of ANP → vasodilation and diuresis
o Stretch of atrial baroR → vagally mediated hypotension
o Stimulation of cardiopulmonary baroR from canon V wave