Pacemakers & Pacing in the ED Albury Wodonga Education Program 2014

What’s wrong here? Twiddlers syndrome follow the link to read more Twiddler syndrome Twiddler syndrome

Ventricular Electrophysiology Pacemaker cells Myocytes Conduction pathways Ventricular Depolarisation from N Engl J Med 2006;355:

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 Duan D J Physiol 2009;587: ©2009 by The Physiological Society Slide showing spontaneous decay of membrane potential causing phase 0 of pacemaker cells Slide showing spontaneous decay of membrane potential causing phase 0 of pacemaker cells note: myocytes also decay but less quickly hence slower intrinsic rates note: myocytes also decay but less quickly hence slower intrinsic rates

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

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? TranscutaneousTransvenous

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 Rate60-70bpm enough to maintain haemodynamics

Transcutaneous Pacing Confirm Capture ElectricalMechanical 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 sensitivity settingsensitivity setting

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

What can go wrong? Failure to capture HiccupsPainBleedingInfection

Links pacemaker-troubleshooting/ pacemaker-troubleshooting/ medicine/news/temporary-pacemakers medicine/news/temporary-pacemakers