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
- Types of pacemakers
- Common pacemaker issues: Failure to capture
- Common pacemaker issues: Undersensing
- Common pacemaker issues: Oversensing
- Troubleshooting with vectors
- Course: Pacemaker Essentials
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]
Critical Care
Compendium
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