(1) atrial sensing of a ventricular spike -> interpreted as an endogenous atrial depolarisation -> another ventricular impulse
can switch to VVI or DVI (but may lose AV synchrony). Also known as endless-loop tachycardia or pacemaker circus movement tachycardia. ⇒ reduce mA delivered to the ventricular or pacing wire ⇒ reduce sensitivity in atrial or ventricular channel > inhibits ventricular pacemaker output (ventricular standstill) 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. ⇒ increase sensitivity threshold or switch to an asynchronous mode (AOO, VOO) in DDD external electrical impulses can also be misinterpreted as atrial activity causing pacemaker mediated tachycardia. ⇒ increase absolute value of sensitivity (making it harder to inhibit) usually due to settings on the pacemaker. Reduced pacemaker output / output failure may be seen on ECG monitoring if the patient contracts their rectus or pectoral muscles (due to oversensing of muscle activity). Abnormal signals may not be evident on ECG. These inappropriate signals may be large P or T waves, skeletal muscle activity or lead contact problems. produces inappropriate/excessive inhibition of atrial pacing -> confuses pacemaker into thinking that there has been a return to spontaneous atrial activity. Oversensing occurs when electrical signal are inappropriately recognised as native cardiac activity and pacing is inhibited. ⇒ decrease absolute value of sensitivity (making it easier to inhibit) ⇒ same mechanisms as failure to capture and pace due to specific setting of sensitivity (including AOO mode). produces atrial pacing when not appropriate. ⇒ 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) ⇒ bipolar leads may be tried in reverse positions or can try convert to unipolar pacing 
⇒ tight and confirm all external connections other causes: fibrosis at wire-myocardium interface, MI, electrolyte imbalance, post-defibrillation, drugs (flecanide, sotalol, betablockers, lignocaine, verapamil).usually due to some specific mechanical problem (wires no longer connected to heart, wires not tightly connected to cable, cable not connected to correct port, output setting to low).visible pacing spikes are seen on ECG but no electrical capture on ECG or cardiac contraction seen in arterial line or SpO2 waveform.⇒ connect the pacemaker directly to the pacing lead (occasionally the connecting wires may be faulty) ⇒ switch to an asynchronous mode to prevent oversensing (AOO, VOO) ⇒ increase output to maximum (20mA atrial and 25mA ventricular) causes: lead malfunction, unstable connection, insufficient power, cross-talk inhibition, oversensing (see below), apparent failure to pace.no electrical output at the pacing wire tips (pacing spikes absent on ECG).back up plan in emergency: transcutaneous or tranvenous pacing, atropine, adrenaline, isoprenaline, ephedrine, electrolyte correction.
fixes: change patient position, reverse bipolar pacing leads, convert to unipolar pacing, replace pacing equipment, return to OT for reinsertion of epicardial wires.check sensitivity (normal = 2-5mV) – changes with position.check capture threshold (find threshold and double it for safety).
check integrity of circuit (start at patient -> pacing box): lead placement, polarity, integrity, tightly connected to correct port of pacing box (atrial/ventricular), battery, settings.
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