Pacemakers & Pacing in the
ED
Albury Wodonga Education Program 2014
What’s wrong here?
Twiddlers syndrome
follow the link to read
more
Twiddler syndrome
Ventricular
Electrophysiology
Pacemaker cells
Myocytes
Conduction pathways
Ventricular Depolarisation from N Engl J Med 2006;355:28894
Figure 3. Modulation of cardiac electrical activity by activation of ClC-2 channels in cardiac
pacemaker cells and myocytes Changes in action potentials (top panels) and membrane currents
(bottom panels) of cardiac pacemaker cells (A), or atrial and ventricular myocytes
•
•
Slide showing spontaneous decay of membrane potential causing
phase 0 of pacemaker cells
note: myocytes also decay but less quickly hence slower intrinsic
rates
Duan D J Physiol 2009;587:2163-2177
©2009 by The Physiological Society
Why do we need to pace?
Sinuatrial pause/arrest
Atrial Fibrillation
AV block - high degrees which are new
Neurally mediated syncope
Heart failure - severe cardiomyopathy
Cardiac Resynchronisation Therapy -CRT
Overdrive pacing
Permanent Pacemakers
Permanent Pacemakers
only way of knowing
how it operates is by
getting the details from
the patient
can only interrogate the
device if you know what
type it is
Pacing Modes
Chamber paced
O-none, A-atrial, V-ventricular, D-dual
Chamber sensed
O-none, A-atrial, V-ventricular, D-dual
Response to sensing
O-none, T-triggered, I-inhibited, D-dual
Magnets and pacemakers
All pacemakers respond to a magnet by switching to
an asynchronous pacing mode at a programmed
atrioventricular (AV) delay and a fixed magnet rate
depending on the manufacturer, device model, and
the status of the battery.
The programmed mode DDD switches to DOO, VVI
switches to VOO, and AAI switches to AOO
Why pace in ED
Bradycardia
Sinuatrial disease
3rd degree AV block
type 2, second degree block
myocardial infarction causing significant AV block
Why pace in the ED
Profound rhythm disturbance causing
haemodynamic compromise
Slow rates can be tolerated if BP/GCS normal
Failure of chronotropic pharmacotherapies isoprenaline, adrenaline (atropine is a temporary
measure)
When do we pace in ED?
The decision to institute pacing in the ED should be
taken by senior staff or in discussion with a tertiary
centre in Melbourne
Pacing is not technically difficult
The decision to pace is the difficult part
How can we pace?
Transcutaneous
Transvenous
Transcutaneous pacing
Consent
Clean and dry
optimise contact
Analgesia & Sedation
infusions of opiate and
benzodiazepine to relieve
pain/distress but maintain
airway
Transcutaneous pacing
Mode
Fixed or Demand
Demand avoids R on T
Energy
as little as required +10mV
Rate
60-70bpm
enough to maintain
haemodynamics
Transcutaneous Pacing
Confirm Capture
Electrical
Mechanical
check pulse or arterial wave form
Tex
t
Pacing - how to make the Phillips defib. work.
Transvenous pacing
sterile technique
multiple routes
best to avoid L sub
clavian as this route
most commonly used
for permanent
pacemaker
Transvenous pacing
Start 25mA - should be able
to reduce to 5mA
Rate 60-70bpm
adjust sensitivity settings to
consistently detect native R
waves
see:sensitivity setting for a
recommendation on how
to do this
Transvenous pacing
Invasive
Less energy required
safer for transfer
ECG showing atrial pacing
How to tell if the pacemaker
is also a defibrillator.
Shock coils
ICD - Internal Cardioverting
Defibrillator
Shock
coils
What can go wrong?
Failure to capture
Hiccups
Pain
Bleeding
Infection
Links
http://lifeinthefastlane.com/education/ccc/pacemakers/
http://lifeinthefastlane.com/education/ccc/temporarypacemaker-troubleshooting/
http://radiopaedia.org/articles/cardiac-pacemakers
http://www.cardiacengineering.com/pacemakers-wallace.pdf
http://www.modernmedicine.com/modernmedicine/news/temporary-pacemakers