<p>Temporary Pacemaker Troubleshooting</p><p>8/11/10 PY Mindmaps Will Young Tutorial on Pacing</p><p>GENERAL MANAGEMENT</p><p>- review rhythm strip and 12 lead ECG - check integrity of circuit (start at patient -> pacing box): lead placement, polarity, integrity, connected to right port of pacing box – atrial/ventricular, battery, settings - check mode - check rate - check capture threshold (find threshold and double it for safety) - check sensitivity (normal = 2-5mV) – changes with position - backup plans = transcutaneous or tranvenous pacing, atropine, adrenaline, isoprenaline, ephedrine, electrolyte replacement</p><p>Failure to Pace</p><p>= no electrical output at the pacing wire tips - causes: lead malfunction, unstable connection, insufficient power, cross-talk inhibition, oversensing (see below), apparent failure to pace.  check power, battery and connections  increase output to maximum (20mA atrial and 25mA ventricular)  switch to an asynchronous mode to prevent oversensing (AOO, VOO)  connect the pacemaker directly to the pacing lead (occasionally the connecting wires may be faulty)  prepare for transcutaneous pacing  prepare for CPR and chronotropic drugs</p><p>Failure to Capture</p><p>= no electrical out at the pacemaker tips (visible pacing spikes on ECG but no cardiac contraction seen in arterial line or SpO2 waveform) - causes: fibrosis at wire-myocardium interface, MI, electrolyte imbalance, post-defibrillation, drugs (flecanide, sotalol, betablockers, lignocaine, verapamil)  correct exacerbating causes  reverse polarity of both unipolar and bipolar systems may help  in bipolar leads, the negative electrodes develop fibrosis first -> use other electrode and plug into negative terminal and insert return electrode in the subcutaneous tissue (create unipolar circuit)  may need temporary transvenous wire</p><p>Failure to Sense</p><p>- produces atrial pacing when not appropriate - due to specific setting of sensitivity (including AOO mode)  same mechanisms as failure to capture and pace</p><p>Jeremy Fernando (2011)  decrease absolute value of sensitivity (making it easier to inhibit)</p><p>Cross talk</p><p>- in dual chamber pacing it is possible that the atrial pacemaker spike will be sensed by the ventricular wire and is misinterpreted as a ventricular depolarisation -> inhibits ventricular pacemaker output (ventricular standstill). - the opposite can happen as well.  reduce sensitivity in atrial or ventricular channel  reduce mA delivered to the ventricular or pacing wire</p><p>Pacemaker mediated tachycardia</p><p>- VDD or DDD pacing problem - can switch to VVI or DVI (but may loose AV synchrony)</p><p>(1) atrial sensing of a ventricular spike -> interpreted as an endogenous atrial depolarisation -> another ventricular impulse  use an atrial blanking period (now preset into box)</p><p>(2) retrograde conduction between ventricle and atrium through AV node or accessory pathway -> ‘endless’ loop of periodicity  adjustable post ventricular (pacing spike) atrial refractory period (PVARP)</p><p>Oversensing</p><p>- in DDD external electrical impulses can also be misinterpreted as atrial activity -> pacemaker mediated tachycardia  increase sensitivity threshold or switch to an asynchronous mode (AOO, VOO)</p><p>Jeremy Fernando (2011)</p>