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Cardiac Rhythm Assessment and Management 285

ABLATION studies are well tolerated as long as patients can remain
supine for the sometimes extended periods. The applica-
Ablation therapies are aimed at destroying tissues that (a) tion of radiofrequency and the consequent tissue injury
generate or sustain haemodynamically significant or is painless in most cases. 105,106
potentially lethal arrhythmias (arrhythmic foci or reentry
pathways), or (b) permit uncontrollable atrial arrhyth- Success rates for ablation therapies have been reported
mias to conduct at rapid rates to the ventricles (the acces- at 82–92% for accessory pathway ablation (depending
sory pathways of the Wolff–Parkinson–White syndrome, on pathway location), 90–96% for AV nodal reentry
107
or at times the AV node itself). Tissue destruction is tachycardia, and 75% for atrial tachycardia and flutter.
106
achieved by the application of radiofrequency (RF) energy Complication rates, mostly AV block, have been reported
to very localised areas of the endocardium, which results at 2.1–4.4%, with procedure-related mortality below
in excessive tissue heating, cellular damage and eventual 0.2%. 106,108 When applied to patients with ideopathic
106
tissue death. Unlike preventive or episode-terminating ventricular tachycardia, procedural success has been
108
pharmacological or electrical arrhythmia therapies, reported at 85–100%. Complications, including death
107
successful ablation is curative and can therefore spare from ventricular wall perforation, have occurred,
patients a lifetime of careful medication compliance, self- but major complication rates of less than 1% are gener-
monitoring for complications, and living under the ally seen. 108
uncertainty of arrhythmic threat and/or the delivery of For ablation of ventricular tachycardia, it is necessary to
therapy from an implantable cardioverter defibrillator. first perform pace mapping to locate the focus. Endocar-
The use of percutaneous catheter ablation therapies has dial pacing is applied from many sites until a paced
expanded rapidly as technology and familiarity have rhythm with the same 12-lead ECG morphology as the
developed, and they have been used to treat atrial, ven- ventricular tachycardia is achieved. This confirms the
tricular and AV nodal reentry tachyarrhythmias, as well as focus, thus identifying the location(s) to which radio
the abnormal atrioventricular connections of Wolff– freqency needs to be applied. Generally, ablation is
Parkinson–White Syndrome. For incessant atrial fibrilla- undertaken for monomorphic VT only. 106
tion, it is sometimes necessary to ablate the AV node to
control the ventricular rate. Since this causes complete SUMMARY
heart block, a pacemaker must first be implanted. Iden-
tification of the pulmonary veins as the culprit arrhyth- Alteration to the heart’s electrophysiological function is
mic foci for many patients with atrial fibrillation has seen very common in patients admitted to critical care settings.
the development of ablation techniques to prevent con- Arrhythmia detection is largely the responsibility of the
duction from the pulmonary veins to the atria (pulmo- critical care nurse, who must maintain accurate monitor-
nary vein isolation). ing, constantly observe for the development of arrhyth-
mias, assess their clinical impact, and assist in identifying
For arrhythmia ablation, electrophysiological studies are causative factors. The critical care nurse must also deliver
undertaken to closely map the location of abnormal foci, the care and management of arrhythmias, including
reentry circuits or accessory pathways, and radiofrequency pharmacological and electrical therapies, being aware of
catheters are then guided to these sites to deliver therapy. complications and management of complications of
The search for arrhythmic sites may take some time, but these treatments.

Case study

A 63-year-old woman was admitted to intensive care at 12 : 28 on A unit-based emergency response was activated, including recall
a Friday afternoon following Aortic Valve Replacement. Surgery of the surgeon and anaesthetist, for the following reasons:
was uneventful, however, post-operative asystole required place- ● The patient was known to have underlying asystole. Failure to
ment of two atrial and two ventricular epicardial pacing wires. capture, even on a single beat, could progress to complete loss
Six minutes after admission the following rhythm, as seen in of capture.
Figure 11.52, was observed. ● The ventricular output was already at 18 mA and still losing
● Initial pacemaker settings: DDD mode; Rate 80/min; AV delay capture. An adequate safety margin could not be provided,
160 ms and there was very little scope for increasing output if failure
● Atrial output: 20 mA (maximum) with atrial pulse width to capture recurred (maximum output 20 mA on this device).
@ 1 ms ● Atrial output was already at maximum (20 mA) and not
● Ventricular output: 18 mA (maximum 20 mA) with ventricular capturing.
pulse width @ 1 ms ● It was Friday afternoon. Ideal resources were available now, but
this would change soon, with the resource limitations that
Before continuing, reflect on the following: would you call this a night duty or weekend staffing pose.
genuine emergency; what are the implications of a single non- ● Simultaneous atrial and ventricular failure to capture could
capture beat in this context; and what steps you would take to point to a severe systemic abnormality requiring investigation
manage the situation? and management.