Temporary Pacemaker Troubleshooting

Reviewed and revised 18 August 2014

OVERVIEW

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

GENERAL MANAGEMENT

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

FAILURE TO PACE DUE TO OUTPUT FAILURE

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

FAILURE TO CAPTURE

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

FAILURE TO SENSE

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

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)

CROSS TALK

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

PACEMAKER MEDIATED TACHYCARDIA

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

PACEMAKER SYNDROME

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

TWIDDLER’S SYNDROME

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

LEAD DISPLACEMENT DYSRHYTHMIA

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.

RUNAWAY PACEMAKER

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

SENSOR INDUCED TACHYCARDIA

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

References and Links

LITFL

CCC — Pacemakers
ECG Library — Pacemaker malfunction
ECG Library — Pacemaker Rhythms – Normal Patterns

Medmastery

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]