Page 420 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

290 PART 3: Cardiovascular Disorders

three positions but a fourth letter describes rate adaptive feature and In recent years CRT (cardiac resynchronization therapy) has been
the fifth letter denotes multisite pacing (which may become more com- used in patients on optimal medication still symptomatic with heart
monly used in the future with alternative pacing sites). The coding is failure and ventricular conduction delay to improve their symptoms
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summarized in Table 36-10. The first three letters must always be and offer a mortality reduction. 69,70 CRT therapy includes biventricular
specified but the fourth and fifth may only be necessary in some situa- pacing, usually RV site plus an LV site (Fig. 36-9). LV pacing
tions. AAI indicates that the pacemaker paces and senses in the atrium is usually via lead position in the coronary sinus but in some cases
and inhibits if an intrinsic cardiac signal is sensed in the atrium. DDD the LV lead may be epicardial. The indications for these devices are
indicates that the pacemaker paces and senses in both atrium and expanding, hence will increase in usage. The CRT system can be a
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ventricle and there are dual responses to sensed events, for example, pacemaker only system (CRT-P) or can incorporate a defibrillator
the system inhibits in response to sensed events in both chambers but (CRT-D).
a sensed or paced event in the atrium will trigger a paced event in the
ventricle after a programmed delay. VVIR indicates that the pacemaker
paces and senses in the ventricle, inhibits if an intrinsic cardiac signal is CARDIOVERSION/DEFIBRILLATION
sensed in the ventricle and has the ability to vary the pacing rate within a Electrical shocks delivered transcutaneously, transvenously or epicardi-
programmed range, for example, 60 to 130 based on the programmable ally induce changes in the transmembrane potential of myocardial cells.
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rate sensor settings. These stimuli may interrupt reentrant circuits by prolonging tissue
■ CHOICE OF PACING MODALITY refractoriness and/or by producing new excitation waves. Synchronized
cardioversion effectively terminates most supraventricular tachyar-
Atrial or dual chamber pacing systems have been shown to prevent the rhythmias and monomorphic sustained V T. Biphasic waveforms have
development of paroxysmal and permanent AF compared to ventricular been incorporated into ICDs and the latest generations of external defi-
pacing systems. 44,62-64 In patients with sinus node dysfunction, atrial- brillators. These biphasic waveforms have been demonstrated to reduce
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based pacing has been reported to reduce development of symptomatic cardioversion and defibrillation energy requirements. If an electrical
heart failure compared to ventricular pacing. Atrial-based pacing shock is not synchronized to the QRS, the shock may be delivered
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optimizes cardiac hemodynamics by preserving the atrial contribution during the vulnerable repolarization phase and initiate VF. External
to cardiac output which is particularly important in patients with heart pads rather than handheld paddles improve tissue contact, reduce over-
failure and patients with diastolic dysfunction, for example, secondary all system impedance and reduce the energy required for cardioversion
to left ventricular hypertrophy. However, atrial-based pacing therapies or defibrillation.
have not been shown to be associated with substantial improvements
in quality of life, exercise tolerance or overall survival when compared IMPLANTABLE CARDIOVERTER DEFIBRILLATORS
to ventricular pacing in several large prospective randomized clinical
trials. 44,63,65 Thus, the choice of pacing modality should be individualized Three major secondary prevention trials have demonstrated the superi-
based on the patient’s long-term prognosis, associated comorbidities and ority of the ICD compared to pharmacologic therapy for the prevention
expected functional status. of sudden cardiac death in patients presenting with a life-threatening
■ CARDIAC PACING ISSUES IN THE ICU episode of ventricular tachycardia (V T) or ventricular fibrillation (VF)
in the absence of a reversible cause.
In several clinical trials, the
34,35,39
The pacing system consists of the implantable pulse generator, which ICD has also been shown to prevent sudden cardiac death in patients
with severe left ventricular dysfunction and no history of spontaneous
contains the battery and integrated circuits that control pacing/sensing sustained V T/VF. 31-33,73,74 Consequently, more and more patients will
function, and one or more leads. The programming of a pacemaker is receive ICDs and knowledge of their functioning is important to the
determined by the patient’s underlying intrinsic rhythm and diagnosis. critical care physician.
If the patient has only transient episodes of bradycardia, the pacemaker
If the patient has complete heart block, the pacemaker is usually pro- ■ ICD THERAPIES
may be programmed to ventricular pacing at a low backup rate of 40 bpm.
grammed to a lower physiologic rate of 60 to 70 bpm and an upper rate of ICDs provide antitachycardia pacing therapies for termination of sus-
120 to 150 bpm depending on age, type of heart disease and activity level. tained V T, internal cardioversion therapies for V T if pacing therapies
The most common problems encountered, related to a pacing system, are ineffective and defibrillation therapies for VF and very rapid V T.
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are capture failure, undersensing, oversensing, or triggered pacing. 66,67 In addition, pacing therapy for bradycardia may be programmed.
Capture failure may be due to pacing lead dislodgement, lead perfora- The ICD is usually programmed to backup VVI pacing at 40 bpm
tion, lead fracture, disconnection of the pacing lead from the power unless the patient has significant bradycardia and pacing needs. V T
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source, power source failure or pacing thresholds higher than pro- detection is based on rate and sometimes on onset characteristics,
grammed. Pacing threshold may increase secondary to myocardial regularity of rhythm and/or duration of the intracardiac electrogram.
infarction, fibrosis, antiarrhythmic drug use, electrolyte abnormalities An example of effective antitachycardia pacing therapy for sustained
(hyperkalemia), and acidosis. Failure to sense may occur due to lead V T is shown in Figure 36-10. Occasionally, the antitachycardia pacing
dislodgment or perforation, changes in intracardiac electrograms due to therapy accelerates the V T to a more rapid V T or VF for which a shock
underlying disease state, electromagnetic interference causing reversion is delivered (Fig. 36-11). One of the most frequent complications asso-
to asynchronous pacing or spontaneous occurrence of a spontaneous ciated with the ICD is the delivery of an inappropriate shock for sinus
ventricular event in the pacemaker blanking period. Oversensing may tachycardia or a rapid atrial tachyarrhythmia, such as AF or atrial
occur due to myopotential inhibition (more common with unipolar flutter. This can be minimized by programming a high tachycardia
leads) or sensing extraneous signals (usually due to lead insulation detection interval (the rate that the device classifies as V T), program-
failure) or P- or T-wave oversensing. Triggered pacing may occur inap- ming a sudden rate onset feature to eliminate detection of sinus tachy-
propriately when the patient with a dual chamber pacemaker develops cardia which is rarely abrupt in onset or programming a rate regularity
AF/flutter or the pacemaker senses retrograde P waves causing pace- feature to prevent AF being detected as V T. Some ICDs discriminate
maker-mediated tachycardia (Fig. 36-8). Most of these problems can between V T and atrial tachyarrhythmias using ventricular electrogram
be identified by interrogation and evaluation of the pacing system using morphology changes. Dual chamber ICDs enhance discrimination
the pacemaker programmer. Many of these problems can be solved by of AF or SVT from V T by comparing atrial activity relationships to
reprogramming the pacemaker. 68 ventricular activity.

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