Temporary Pacemaker Troubleshooting

Reviewed and revised 18 August 2014


Problems with pacing

  • output failure
  • failure to capture

Problems with sensing

  • oversensing
  • undersensing

Pacemaker syndromes

  • Cross-talk
  • Pacemaker syndrome
  • Pacemaker-mediated tachycardia
  • Sensor-induced tachycardia
  • Runaway pacemaker
  • Lead displacement dysrhythmia
  • Twiddler’s syndrome


Systematic approach is essential

  • review rhythm strip and 12 lead ECG
  • 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
  • check mode
  • check rate
  • check capture threshold (find threshold and double it for safety)
  • check sensitivity (normal = 2-5mV) – changes with position
  • fixes: change patient position, reverse bipolar pacing leads, convert to unipolar pacing, replace pacing equipment, return to OT for reinsertion of epicardial wires
  • back up plan in emergency: transcutaneous or tranvenous pacing, atropine, adrenaline, isoprenaline, ephedrine, electrolyte correction


  • no electrical output at the pacing wire tips (pacing spikes absent on ECG)
  • 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


  • visible pacing spikes are seen on ECG but no electrical capture on ECG or cardiac contraction seen in arterial line or SpO2 waveform
  • 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)
  • other causes: fibrosis at wire-myocardium interface, MI, electrolyte imbalance, post-defibrillation, drugs (flecanide, sotalol, betablockers, lignocaine, verapamil)
  • approach:
    ⇒ correct exacerbating causes
    ⇒ tight and confirm all external connections
    ⇒ increase output if possible
    ⇒ bipolar leads may be tried in reverse positions or can try convert to unipolar pacing
    ⇒ 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


  • produces atrial pacing when not appropriate
  • due to specific setting of sensitivity (including AOO mode)
    ⇒ same mechanisms as failure to capture and pace
    ⇒ decrease absolute value of sensitivity (making it easier to inhibit)


  • Oversensing occurs when electrical signal are inappropriately recognised as native cardiac activity and pacing is inhibited
  • produces inappropriate/excessive inhibition of atrial pacing -> confuses pacemaker into thinking that there has been a return to spontaneous atrial activity
  • These inappropriate signals may be large P or T waves, skeletal muscle activity or lead contact problems
  • Abnormal signals may not be evident on ECG
  • 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)
  • usually due to settings on the pacemaker
    ⇒ increase absolute value of sensitivity (making it harder to inhibit)
  • in DDD external electrical impulses can also be misinterpreted as atrial activity causing pacemaker mediated tachycardia
    ⇒ increase sensitivity threshold or switch to an asynchronous mode (AOO, VOO)


  • 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


  • Also known as endless-loop tachycardia or pacemaker circus movement tachycardia
  • VDD or DDD pacing problem
  • can switch to VVI or DVI (but may lose AV synchrony)
  • Mechanisms:

(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)

(2) retrograde conduction between ventricle and atrium through AV node or accessory pathway -> retrograde p waves being sensed as native atrial activity with subsequent ventricular pacing -> paced ventricular complex results in further retrograde conduction with retrograde p wave generation ->  ‘endless’ loop of periodicity -> re-entry tachycardia
⇒ adjustable post ventricular (pacing spike) atrial refractory period (PVARP) or slowing AV conduction e.g. adenosine or activation of magnet mode.

  • Results in a paced tachycardia with the maximum rate limited by the pacemaker programming
  • Newer pacemakers contain programmed algorithms designed to terminate PMT
  • May result in rate-related ischaemia in the presence of IHD


  • Caused by improper timing of atrial and ventricular contractions resulting in AV dyssynchrony and loss of atrial “kick”
  • Variety of clinical symptoms including fatigue, dizziness, palpations, pre-syncope
  • Associated decrease in systolic blood pressure > 20 mmHg during change from native rhythm to paced rhythm


  • Patient manipulation of the pulse generator (accidentally or deliberately)
  • The pacemaker rotates on its long axis, resulting in dislodgement of pacing leads
  • Can result in diaphragmatic or brachial plexus pacing (e.g. arm twitching) depending on extent of lead migration


  • A dislodged pacing wire may float around inside the right ventricle intermittently “tickling” the myocardium and causing ventricular ectopics or runs of VT alternating with failure of capture.
  • If the paced QRS morphology changes from a LBBB pattern (indicating RV placement) to a RBBB pattern (indicating LV placement), this suggests that the electrode has eroded through the interventricular septum.
  • A chest x-ray will usually help to confirm the diagnosis.


  • This potentially life-threatening malfunction of older-generation pacemakers is related to low battery voltage (e.g. overdue pacemaker replacement)
  • The pacemaker delivers paroxysms of pacing spikes at 2000 bpm, which may provoke ventricular fibrillation
  • Paradoxically, there may be failure to capture — causing bradycardia — because the pacing spikes are very low in amplitude (due to the depleted battery voltage) and because at very high rates the ventricle may become refractory to stimulation
  • Application of a magnet can be life saving but definitive treatment requires replacement of the pacemaker


  • Modern pacemakers are programmed to allow increased heart rates in response to physiological stimuli such as exercise, tachypnoea, hypercapnia or acidaemia
  • Sensors may “misfire” in the presence of distracting stimuli such as vibrations, loud noises, fever, limb movement, hyperventilation or electrocautery (e.g. during surgery)
  • This misfiring leads to pacing at an inappropriately fast rate
  • The ventricular rate cannot exceed the pacemaker’s upper rate limit (usually 160-180 bpm)
  • These will also usually terminate with application of a magnet



Journal articles

  • Reade MC. Temporary epicardial pacing after cardiac surgery: a practical review. Part 2: Selection of epicardial pacing modes and troubleshooting. Anaesthesia. 2007 Apr;62(4):364-73. Review. PubMed PMID: 17381573. [Free Full Text]

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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