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280 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

produces a synchronised contraction of the LV compared are capturing the QRS will become narrower (usually
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to the patient’s native, dyssynchronous contraction. <0.12 sec) and the axis is either reasonably normal
The aim is for >90% of ventricular beats to be paced to or may be deviated leftward or rightward. Morpho-
achieve the desired benefit from CRT. Amongst device/ logies are usually somewhere between those seen
lead-related factors are loss of capture by either the LV or with RV-only or LV-only pacing. A uniform ECG
RV lead, resulting effectively in loss of resynchronisation. pattern cannot be described, but in a given patient
Recognition of this can be difficult because loss of capture there should be consistency between their ECGs
by only one of the ventricular leads will still appear as (see Figure 11.49).
capture from the remaining ventricular lead (see below).

Optimisation of Device Programming Practice tip
Device programming can have a significant impact on the
benefit conferred by CRT and had historically been con- For the patient with a CRT device whose heart failure is worsen-
ducted under echocardiographic assessment of the impact ing, investigate whether there are device-related factors which
on ventricular filling and contraction. It is not practical may be correctable:
for all patients to undergo regular echocardiography and ● Is the patient being ventricularly paced >90% of the
so alternative approaches to optimisation are being devel- time? If not, they will be losing the potential benefit of
oped. The critical timing factors which should be opti- resynchronisation.
mised are the atrioventricular (AV) delay and the delay ● Can you determine whether there is capture from both the
between stimulation of the left and right ventricles (V–V LV and RV leads? Compare with old ECGs where available.
delay). Recent developments allow ‘electronic optimisa-
tion’ whereby CRT devices themselves can calculate
optimum settings based on automated measurements of
intracardiac events 87,88 , but are not available on all devices. CARDIOVERSION
The impact of effective optimisation may be sufficient to
convert non-responders to responders. Electrical cardioversion can be applied as an alternative
or adjunct to pharmacological therapy in the manage-
Recognising Failure to Capture ment of tachyarrhythmias. By far the most common cause
of tachyarrhythmias is reentry, in which current can con-
in a CRT device tinue to circulate through the heart because of different
Recognising failure to capture in CRT is made difficult by rates of conduction and recovery in different areas of the
the fact that both ventricles are paced. The loss of pacing heart (temporal dispersion). Conduction through reentry
spikes followed by QRS complexes will only occur if there circuits can continue as long as the circulating stimulus
is failure to capture from both the LV lead and the RV encounters non-refractory tissue. The aim of cardiover-
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lead. The ECG during failure to capture by just the LV sion is to excite all myocardial cells at the same time with
lead will still show capture from the RV lead. Instead of the result that all of the heart will also be refractory at
loss of the QRS, to identify loss of capture it is necessary the same time. If this is achieved, the circulating stimulus
to look more closely at QRS morphology and vectors to dies out for lack of non-refractory tissue to conduct
confirm capture or loss of capture from either the left or through. If the applied shock does not depolarise the
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right ventricular lead. A 12-lead ECG is helpful, but if greater bulk of myocardium, then non-depolarised cells
not available, lead V1 (or MCL1) and lead I are the most are still available for conduction and the arrhythmia may
helpful in confirming RV, LV or Bi-ventricular (Bi-V) persist. External shocks of 100–200 Joules (biphasic) are
capture. Specific changes include: required for sufficient current density to reach the myo-
cardium and depolarise the greater bulk of cells, thus
● RV capture only: the QRS will be wide (>0.12 sec) extinguishing available pathways. Drugs or biochemical
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with left axis deviation, lead V1 (or MCL1) will be a correction may be necessary to prevent recurrence. Success
negative complex, most commonly as a QS complex, rates from cardioversion range from 70–95% depending
QRS in lead I will be upright, as an R wave or some- on the rhythm. Arrhythmias due to increased automa-
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times rSR (see Figure 11.49) ticity are less amenable to cardioversion, as there is a
● LV capture only: the QRS will be wide (>0.12 sec) high chance of early arrhythmia recurrence; and for
with right axis deviation, lead V1 (or MCL1) will be arrhythmias occurring as a complication of digitalis
an upright complex, either as an R wave, or less toxicity, cardioversion (but not defibrillation) is
commonly as an rSR, QRS in Lead I will be a negative contraindicated. 89
complex, either as a QS or rS complex (see
Figure 11.49). Early defibrillation increases survival from ventricular
● Bi-Ventricular capture: the ECG is less predictable fibrillation. The success of public-access defibrillator
depending upon the timing of the left and right ven- schemes (in airports, shopping and sporting venues)
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tricular stimuli. If LV stimulation occurs well ahead of has warranted their increased availability. Automatic
RV then the ECG will look more like LV capture only, external defibrillators (AEDs) in the home or community
whereas if RV stimulation occurs well ahead of LV simplify the task of applying defibrillation by non-
then the ECG will look more like RV capture only. healthcare responders and increase access to definitive
Nevertheless, the expectation is that when both leads electrical management for patients suffering ventricular