Pacemaker Failure
Pacemaker failure has three causes: generator failure, lead failure,
or failure of capture. Generator failure is rare in a device that has been previously
evaluated and not near the end of useful battery life, unless the generator (or leads)
is struck directly by ESU. Lead failure, also unusual, but reported during patient
repositioning,[55]
can result in undersensing (intrinsic
activity is not detected); oversensing ("detection" of events unrelated to intrinsic
activity); or failure to deliver sufficient energy to the myocardium to produce a
depolarization (i.e., loss of capture). Myocardial changes that lengthen the refractory
period or increase the energy requirement for depolarization (failure to capture)
can result from myocardial ischemia/infarction, acid-base disturbance, electrolyte
abnormalities, or abnormal antiarrhythmic drug levels.
The response to a pacemaker failure depends on the clinical situation:
the patient with a perfusing rhythm and stable vital signs can be observed while
a plan is made to correct the problem. For the patient with inadequate perfusion,
the following steps can be tried (while cardiopulmonary resuscitation is in progress
where appropriate):
- A magnet can be applied if the pacemaker is known to revert to an asynchronous
mode, which will also eliminate sensing behavior in these devices. For many of the
Autocapture devices with magnet mode enabled, magnet application might increase pacing
amplitude and restore capture. Devices from ELA medical typically increase their
pacing amplitude when a magnet is applied. Some pacemakers perform threshold margin
testing upon magnet placement, which can further reduce pacing.[24]
- Temporary pacing can be initiated, and it can be transthoracic (transcutaneous),
transvenous, or transesophageal. Transesophageal (atrial) pacing generally requires
a functional atrium and AV node for ventricular activation, and it will likely be
unsuccessful in the presence of atrial fibrillation or AV nodal disease. In the
setting of external pacing, the electrocardiogram is often misinterpreted, since
the pacemaker artifacts are large compared to the QRS complexes ( Fig.
35-7
). Successful ventricular pacing has been reported with transesophageal
pacemakers, but it is not reliable at this time.[65]
Note that any external pacing might further inhibit pacemaker output at energies
that will not produce myocardial capture.[66]
[67]
- Sympathomimetic drugs can be administered to decrease depolarization threshold
and/or increase chronotropicity. Epinephrine (0.5 to 1 µg/min) or dopamine
(5 to 20 µg/kg/min) should be considered. Isoproterenol (0.5 µg/min)
is often recommended, but this drug is not widely available and its use is complicated
by hypotension. Antimuscarinic drugs (atropine, glycopyrrolate) might be helpful.
- Causes of myocardial ischemia should be sought and corrected. Myocardial
ischemia can substantially increase the energy required for ventricular capture.
[68]
- Disturbances of electrolyte balance, antiarrhythmic drug levels, and acid-base
equilibrium should be investigated and corrected. Potassium, calcium, and
*Gimbel
JR: Implantable pacemaker and defibrillator safety in the MR environment: New thoughts
for the new millenium. In 2001 Syllabus, Special Cross-Specialty Categorical Course
in Diagnostic Radiology: Practical MR Safety Considerations for Physicians, Physicists,
and Technologists. Oak Lawn, IL, Radiological Society of North America, pp. 69–76,
2001.
magnesium abnormalities can raise depolarization thresholds. Potassium flux, ionized
calcium level, and acid-base equilibrium can be affected by hyperventilation and
hypoventilation.
- If none of the above measures succeeds, consideration should be given to
placement of epicardial leads by the surgical staff.
Figure 35-7
Improper placement of a transesophageal pacemaker. The
top recording is electrocardiographic (ECG) lead
II, the middle recording is ECG lead III, and the
bottom recording is the invasive arterial pressure
waveform. This 72-year-old man developed a sinus bradycardia with evidence of tissue
underperfusion. A transesophageal pacemaker was placed, and the large electrocardiographic
artifacts at 75 beats/min were misinterpreted as ventricular systoles (i.e., capture).
They were the pacing stimuli as represented on the ECG monitor. This patient has
a sinus rate of 50 beats/min with a first-degree atrioventricular block (PR interval
of 280 msec). The patient's native atrial (P) and ventricular (R) depolarizations
are identified. The arterial pressure waveform confirms pacing noncapture.
