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278 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

month or so, output safety margins need to be set more right atrium and then steered back upwards to engage
generously and patients are typically sent home with the atrial appendage. Both ventricular and atrial leads
outputs set high (e.g. 3.5–5 Volts) even when thresholds are tested for performance following placement. Leads
at implantation may have been only 0.5–1 Volts. Chronic are then secured within the pacemaker pocket and the
output settings will then be established at the first post- pulse generator is attached to the leads and secured in
operative visit to the doctor in 6–8 weeks. 37 the pocket. The pocket is closed and testing is repeated to
confirm secure connections of the leads to the pacemaker.
Implantation Activities Device and lead testing is repeated on day 1, weeks 6–8
Devices are inserted under light conscious sedation and and then every 12 months to confirm operation. 38
local anaesthesia. Analgesia may also be administered at
the outset of the case, and antibiotics are commenced Pacemaker Parameters: Programming
before skin incision. An anaesthetist is usually only and Status Reports
present if judged necessary by the implanting doctor.
Knowing how a patient’s pacemaker is programmed is
Passage of leads into the heart during insertion may result crucial to interpreting pacemaker behaviour in the clini-
in endocardial contact, causing AV block or bundle cal setting. This has become increasingly important to
branch block. Therefore a femoral temporary pacing wire enable determination of whether a change in behaviour
may be inserted before progressing to placement of the is a problem or simply an automated behaviour. Device
permanent pacing leads, particularly to ensure reliable printouts are available whenever a device is interrogated
ventricular rhythm during the insertion procedure. His- or reprogrammed. The following section is a guide to
torically, ventricular leads were implanted at the apex of how to interpret device printouts to access key informa-
the right ventricle, a position easily accessed and thought tion about pacemaker programming, highlighting some
well tolerated. However recent trends have moved to of the features of the modern permanent pacemaker,
ventricular lead placement in the right ventricular outflow as well as some of the clinical and diagnostic value of
tract (RVOT), 66,73 to produce a more normal contractile the information provided. Device printouts contain an
pattern than from the apex and to prevent the ventricular enormous amount of information, but of immediate
remodelling seen in chronic RV apical pacing. 66,73 Atrial importance are the summary pages that outline all of the
lead insertion is most commonly at the right atrial operating parameters, active automated features, results
appendage, i.e. in the roof of the right atrium. The from recent tests and battery status (see Figure 11.48 for
atrial lead is passed down the superior vena cava into the an example). Important elements include:

page 1 of 3
Accent TM DR RF 2210 (DEMO prB.E.60) FastPath TM Summary 9 Nov 2010. 17:35
Alerts Note Current Paramenters
Mode DDDR
Base Rate 60 min –1
Max Track Rate 130 min –1
Paced/Sensed AV Delay 200/150 ms
A/V Pulse Amp 2.0/1.25 V
Battery Information A/V Pulse Width 0.4/0.4 ms
Longevity: 11.1–12.2 yrs Episodes
Voltage: 3.13 V
New EGMs: 3
~ERI Most Recent: Entry Into AMS

Magnet Rate 100.0 ppm
Battery Current 9 uA Events
Text Results (Last Session: 8 Sep 2010) AP: 11% VP: 24%
100
A Automatic
Atrium Ventricle %
Time
Capture Today: 1.0 V A Today: 1.0 V A
Last Session: 1.0 V Last Session: 1.0 V
AS-VP AS-VS AP-VP AP-VS PVC
Sense Today: 4.2 mV A Today: >12.0 mV A 21% 68% 3.0% 8.0% 0%
Last Session: 4.2 mV Last Session: >12.0 mV
Lead Today: 530 Ω A Today: 530 Ω A
Impedance Last Session: 530 Ω Last Session: 530 Ω
Mode Switch
Mode Switch: 2%
AMS Episodes: 5
FIGURE 11.48 FastPath Summary from a St Jude Medical Accent™ dual chamber pacemaker (St Jude Medical Sylmar CA), highlighting basic parameters,
events, and test results recorded during pacemaker interrogation. See text for details.

Cardiac Rhythm Assessment and Management 279

● Patient/device details: patient name, type of device, However, in LBBB septal depolarisation occurs well in
date and time of the printout. advance of the delayed conduction to the lateral left ven-
● Battery information: a bar graph displays the progress tricular wall. The impact on contraction is to create ven-
of the battery towards the Elective Replacement Indi- tricular dyssynchrony, with the septum contracting before
cator (ERI); the Magnet Rate (i.e. the rate that asyn- the lateral wall, rather than synchronously with it.
chronous pacing will occur at if a magnet is placed Similarly, ventricular relaxation becomes dyssynchronous
over the device); the longevity (indicating the which may lessen myocardial perfusion and limit ven-
minimum remaining longevity of the device if the tricular filling, both of which can become contributors to
26
patient was to be paced 100% of the time in the severity of heart failure. Whilst the majority of
the current settings). patients with LBBB have dyssnchrony and systolic dys-
● Current Parameters: basic pacemaker set up including function, the impact may not be of note for those with
base rate, maximum rate at which the atrial rhythm otherwise normal hearts, but becomes much more pro-
will be tracked, AV delay, output settings and pulse nounced when there is existing myocardial disease and/
widths for both chambers. or heart failure. 26,81 With very wide LBBB (e.g. >0.14 sec)
● Episodes: summary of any arrhythmia episodes that the impact is greater, as the dyssynchrony between the
have been recorded since the last interrogation, any septal and free wall contraction is exaggerated. 26,75,81,82
Automatic Mode Switching events that have occurred. In CRT, pacing leads on both the right ventricular (RV)
● Events: an event in pacing terms is a beat, rather than septum and the left ventricular (LV) lateral wall are used
a clinical event; every atrial beat (sensed or paced) and to stimulate both muscle masses at the same time, with
every ventricular beat (sensed or paced) is recorded the aim of improving heart failure in patients with sig-
allowing the calculation of the percentage of atrial and nificant dyssynchrony. LV and RV pacing stimuli may
83
ventricular pacing since the last interrogation; this can be delivered simultaneously, although programming of
be compared to previous reports to assess whether either LV or RV stimulation first by 10–80 msec is seen
pacemaker dependence is increasing or decreasing. more often. The aim is that a reduction in QRS duration
● Test Results: the results of device and lead testing per- can be seen electrocardiographically, preferably with the
formed during the current interrogation as well as QRS returning to normal duration (<0.12 sec). Expected
83
testing from the last session performed, including outcomes of CRT include: 76-83,84
graphic trends of all tests over time shown in a sepa-
rate section of the report. ● improvement in NYHA functional class
● Sense Results: the results of the sensing tests carried ● improvement in quality of life
out in the current interrogation, the last session’s ● improvement in physical function
values are also shown, and graphic trends of sensing ● improvement in ejection fraction and reduction in
over time can be viewed in a separate section of the ventricular size
report. ● reduced hospitalisation for heart failure
● Lead Impedance: the results of impedance measure- ● cardiovascular mortality reduction.
ments from the current interrogation and the last The right ventricular septal lead is implanted in standard
session; this provides information about the integrity fashion, positioned either at the RV apex or outflow tract.
of the pacing leads, connections, and their interface Most commonly the left ventricular lead is also posi-
with the myocardium; impedance is the resistance to tioned transvenously, with the lead advanced through the
current provided by the electrical circuit. Variations in coronary sinus into a coronary vein on the lateral LV wall.
impedance may be seen if the pacing lead is being In a minority of cases a separate mini-thoracotomy may
degraded, the pacing circuit is interrupted or not prop- be necessary for secure positioning of an epicardial
erly connected or the pacing lead becomes dislodged. LV lead. Two types of devices currently exist: CRT-P
Generally, measured impedances do not vary by more (Pacemaker) which is a pacemaker achieving resynchro-
than 100 Ohms between sessions.
nisation, and CRT-D (Defibrillator) which adds resyn-
CARDIAC RESYNCHRONISATION THERAPY chronisation to an implantable cardioverter defibrillator.
These latter devices are implanted more commonly as the
Cardiac resynchronisation therapy (CRT) involves the use combination of severe heart failure and ventricular
of pacing to improve the performance of the left ventricle tachyarrhythmias is frequently present. 85,86
in heart failure patients. Initially CRT was undertaken
only in patients with severe heart failure (NYHA Class Non Responders to CRT
III–IV with ejection fraction <30%) due to dilated cardio-
myopathy with left bundle branch block (LBBB) 74,75 but Disappointingly, up to 25 % of patients who receive CRT
its proven efficacy in all major randomised controlled devices fail to gain the expected benefits of improved
78,80
studies 76-80 has seen the range of indications expand to heart function and are termed non-responders. Failure
include patients with less severe heart failure (NYHA to respond may be due to device- or lead-related factors,
Class I and II). CRT is typically only undertaken after or because of cardiac factors which contribute to worsen-
25
demonstrating failure to respond to optimal pharmaco- ing heart failure, especially myocardial ischaemia, atrial
84
logical therapy. fibrillation , and diminishing responses to adjunctive
pharmacological therapy. It should be noted that the
Optimum systolic performance requires all segments of preference in CRT is to see paced ventricular rhythms
the ventricles to contract more or less synchronously. rather than the patient’s own QRS complexes as pacing

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
84
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-
88
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
88
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
89
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-
89
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)
90
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

Cardiac Rhythm Assessment and Management 281










Bi-V RV only









RV Bi-V











Bi-V LV only









LV Bi-V

FIGURE 11.49 The appearance of lead V1 during alternation of pacing sites with a CRT system. In the top strip there is Bi-V pacing with a narrow QRS
which is negative in V1. In the same strip, loss of LV capture results in RV-only pacing. The QRS widens to beyond 0.12s and becomes more deeply negative
in V1. In the second strip RV-only becomes Bi-V pacing after re-establishing LV capture. The QRS returns to its initial morphology as in strip 1. In the 3rd
strip Bi-V pacing is present initially followed by loss of RV capture, resulting in LV-only pacing. Note that the QRS becomes upright in V1 and again widens
to well beyond 0.12 s. In the lower strip LV-only pacing precedes the return to the previous Bi-V morphology as RV capture is restored.



arrhythmias. For patients who have survived previous may initially demonstrate stability, only to decompensate
arrhythmic cardiac arrest, immediate cardioversion or later without warning.
defibrillation at any time or location may be necessary.
Such patients may require an implantable cardioverter Unlike emergency defibrillation, cardioversion shocks are
defibrillator. Emergency defibrillation, biphasic and synchronised to the cardiac cycle so that they are deliv-
monophasic waveforms, electrical principles and equip- ered into the QRS complex. Unsynchronised shocks, if
ment management are discussed more completely in delivered into the T wave, can cause immediate degenera-
Chapter 24. tion into ventricular fibrillation. When synchronisation
is selected (ON) on the defibrillator control panel, a
ELECTIVE CARDIOVERSION marker is inscribed on each detected QRS complex on the
Elective direct current reversion (DCR, or cardioversion) monitor screen to confirm successful synchronisation.
applied under short-acting sedation or anaesthesia is When time permits the patient should be thoroughly
90
undertaken for non-cardiac arrest arrhythmias. These investigated, including physical examination, neurologi-
include atrial fibrillation, tachycardia or flutter, conscious cal assessment, palpation of peripheral pulses, electrocar-
ventricular tachycardia, AV nodal reentry tachycardia, diograph, biochemistry, and serum drug levels where
91
and conscious tachyarrhythmias complicating Wolff– necessary. Fasting should be ensured where possible. If
Parkinson–White syndrome. The time available for prep- atrial fibrillation is present transthoracic echocardiogra-
aration is variable and depends on the haemodynamic phy is undertaken to rule out atrial thrombus, as restor-
impact of the arrhythmia. Patients admitted for reversion ation of atrial contraction may cause pulmonary or
of atrial fibrillation or flutter may be stable throughout systemic arterial embolisation. The patient should be
their hospitalisation, whereas patients with conscious VT fully informed of the rationale for and nature of the

282 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

procedure and have all necessary preparatory tasks including patients with and without non sustained
explained to them. VT. 99,100 In these contexts patients may receive pure ICDs,
or ICDs coupled with cardiac resynchronisation therapy
The cardioversion team should include a minimum of
one medical officer, skilled in emergency rhythm man- capabilities to also combat their heart failure (CRT-D
agement and airway management including intubation, devices).
and two critical care nurses, who usually prepare the The modern ICD features both antibradycardia and anti-
patient and equipment, assist in sedation, perform the tachycardia capabilities. As antibradycardia devices they
cardioversion, document events and manage aftercare. possess all the characteristics of standard dual chamber
Often there is a cardiologist and anaesthetist present for pacemakers, increasingly in the DDD mode. However, if
the separate roles. All team members should confirm there is no history of bradycardia then they may be pro-
readiness, confirm synchronisation selection, and correct grammed at low base pacing rates (e.g. 40/min). If there
defibrillator energy settings (in joules). The patient is is significant heart failure the antibradycardia arm may
sedated (e.g. midazolam) or anaesthetised (e.g. propo- be provided as biventricular pacing (to achieve cardiac
fol), preoxygenated on 100% oxygen delivered by bag resynchronisation). Antitachycardia features are those
and mask, and cardioverted under ECG and oximetry therapies provided to treat ventricular tachyarrhythmias
monitoring. Electrical safety, and ensuring that all per- and include antitachycardia pacing (ATP), also termed
sonnel are clear of the bed, is the primary responsibility overdrive pacing, as well as cardioversion (for VT) and
of the nurse delivering cardioversion, whether via paddles defibrillation (for very fast VT or VF).
or hands-free electrodes.
Devices are inserted in a similar fashion to the pacemaker
After the procedure the patient should be closely moni- (see above on permanent pacemakers). However, ICDs
tored for return to wakefulness, airway protection capa- are most commonly positioned in the left subclavian/
bility, effective respiration and gas exchange, rhythm pectoral location, leaving the right side available for
stability, blood pressure, and for any changes in neuro- conventional placement of external defibrillator paddles
logical status or peripheral pulses. Pain and inflamma- should they ever become necessary. Atrial and ventricular
tion at cardioversion discharge sites may be lessened by leads are placed transvenously via the left subclavian vein.
application of topical ibuprofen 5% cream 2 hours before Atrial leads are normal atrial pacing leads, but the ven-
92
elective DCR, where this is feasible. Energy require- tricular ICD lead differs from a standard pacing lead. ICD
ments for reversion of atrial tachycardia or flutter may be leads are slightly larger and carry the normal ventricular
93
as little as to 50 J. The 2010 recommendations of the pacing circuitry, as well as coils encircling the lead that
European Resuscitation Council are for initial shocks at emit the high energy shock discharges. Single coil systems
70–120 J (biphasic) for atrial flutter, and 120–150 J for have one coil positioned on the lead at the level of the
cardioversion of atrial fibrillation and ventricular tachy- right ventricular cavity, and shocks travel from this coil to
46
cardia. In any of the arrhythmias, if initial shocks are the metal casing of the ICD. Dual coil leads feature this
unsuccessful, repeat attempts at higher energy settings same right ventricular coil as well as a second coil in the
(up to 360 J) may be undertaken. Prior to discharge, superior vena cava. In these systems, shocks can be con-
patients and their families should be informed of the figured to travel from the RV coil to the superior vena cava
potential for post-procedural chest wall discomfort and (SVC) coil, from the RV coil to the ICD, or from the RV
topical and oral analgesic advice provided. Relevant coil to both the SVC coil and the ICD. Configurations can
contact information in the event of redevelopment of impact significantly on the defibrillation threshold, and
arrhythmia symptoms or other health concerns should changes to the shock vector may be undertaken for
also be provided. patients with high defibrillation thresholds.
All modern ICDs provide biphasic shock waveforms only.
IMPLANTABLE CARDIOVERTER Arrhythmia detection and classification usually requires
DEFIBRILLATORS only a few seconds, and charging to maximum joules
Implantable cardioverter defibrillators (ICDs) may be in a new device takes up to 10 seconds. As the battery
implanted for survivors of sudden cardiac death (SCD) declines charge time may increase to 15–20 seconds or
or haemodynamically significant, potentially lethal, ven- longer. Maximum energy delivery capabilities vary
94
tricular arrhythmias. They have been repeatedly demon- between manufacturers but are all in the range of 30–40
strated in large clinical trials to provide significantly J. Typically, shocks for ventricular fibrillation are pro-
improved survival compared with conventional or phar- vided at the maximum available capability of the device,
macological treatment. 95-97 This ‘secondary prevention’ but for ventricular tachycardia, lower ‘cardioversion’
application of ICDs dominated the early indications for shocks may be attempted first (e.g. 15–25 J). If initial
devices, with trial meta analysis demonstrating a mean shocks are unsuccessful, devices are usually programmed
94
98
27% mortality reduction compared to antiarrhythmics. to increase to maximum joules for subsequent shocks.
However, more recently indications have expanded to Defibrillation thresholds may be measured at the time of
‘primary prevention’ in patients without prior cardiac implantation of the ICD. It is desirable that a 10 J safety
arrest, as it has become clear that heart failure patients margin exists, i.e. for a device that can deliver 30 J, it is
with ejection fractions <30% (including both ischaemic preferred that successful defibrillation can be achieved
and non-ischaemic cardiomyopathies) have a high risk at 20 J or less so that there can be confidence that the
of sudden cardiac death due to ventricular arrhythmias, device will revert clinical arrhythmias, and to cover any

Cardiac Rhythm Assessment and Management 283


403400 11/11/02 13:20:12 BASELINE 25 mm/sec 0.40
I


II



III




FIGURE 11.50 Successful antitachycardia pacing delivered by an implantable cardioverter defibrillator. Three simultaneous strips show the presence of
sustained ventricular tachycardia (VT). After the first eight beats, pacing is applied at a rate slightly faster than the tachycardia. Entrainment, or capture,
by the pacemaker is best seen in lead II, where the QRS morphology clearly changes. After 11 paced beats, ATP is ceased, revealing interruption of the VT.



threshold increases in the future. Intraoperative defi- sinus) tachycardias (SVTs) using a variety of criteria, as
101
brillation testing has become less common with time, shown in Figure 11.51. SVT discrimination by a device is
partly because of risks associated with inducing ventricu- similar to criteria a clinician would use when deciding
lar fibrillation, and partly because of evidence that clini- between VT and SVT and includes regularity or irregular-
cal fibrillation has different characteristics to induced ity of the rhythm, sudden or gradual onset, similar or
fibrillation. However, VF induction and defibrillation different morphology to the previous sinus rhythm and
102
testing remains the only way to demonstrate whether a atrioventricular relationships. If these discriminators
device has successfully interrupted VF. If testing is to be indicate that a tachyarrhythmia is supraventricular, then
performed the patient is prepared for external defibrilla- therapy can be withheld, avoiding inappropriate therapy.
tion with all safety precautions and subsequent care as The major device capabilities and programming options
outlined above in the section on cardioversion. of an ICD are shown in Figure 11.51.
ICDs are usually programmed to deliver up to six ‘thera- Patients receiving ICDs require particular education and
pies’ during a tachyarrhythmia episode. For VF, this support, as the experience of shocks can be painful and
usually means six attempts at defibrillation at maximum disturbing and the anticipation of shocks is a cause of
joules and then further antitachycardia therapies are anxiety and/or depression. 70,103 This is especially true of
aborted. No more shocks will be delivered. Antibradycar- shocks delivered to the conscious patient. Inappropriate
dia pacing operation will continue. If the tachyarrhyth- therapy delivery remains a significant problem, and as
mia is interrupted at any point and then recurs, the many as 25% of ICD therapies have been reported as
6-therapy counter will recommence. For ventricular tachy- inappropriate, delivered due either to supraventricular
cardia, attempts may first be made to overdrive pace. arrhythmias or oversensing of electromagnetic inter-
So-called antitachycardia pacing (ATP) aims to interrupt ference. 103,104 The avoidance of strong electrical fields
VT by pacing the ventricles slightly faster than the VT (welding, magnetic resonance imaging, generators)
rate so as to interrupt reentry, the major cause of VT should be stressed, as well as direct contact with devices
70
(see Figure 11.50 for example of reversion). A number of such as TENS machines or electrocautery devices. If
attempts at ATP may be programmed, often with each at surgery requiring diathermy becomes necessary, anti-
slightly more aggressive rates at each successive attempt. tachycardia therapies are usually programmed to OFF to
This is especially true if the patient is known to tolerate avoid inappropriate detection and treatment.
their VT reasonably well. Persistence of VT after ATP will Patients should be encouraged to rest after any therapy
see the device attempt first low energy cardioversion (15– delivery, and where multiple or inappropriate discharges
25 J) and then progress to 30–40 J if unsuccessful. The occur they should report to a healthcare facility for assess-
same limit of six therapies usually applies for an episode. ment. If repeated inappropriate therapy continues, it
105
may be suspended by the placement of a ring magnet over
70
Tachyarrhythmia Detection and Classification the device. This suspends the antitachycardia features of
ICDs are configured to classify and treat arrhythmias first the device while the magnet is in place – no therapy will
be delivered by the device. Removal of the magnet will
on the basis of rate. Defibrillation algorithms using high- immediately reactivate antitachycardia therapies. Back-up
energy settings (30–40 J) are followed when the rate is (antibradycardia) pacing functions remain active and
very fast (e.g. >200/min), as syncope is likely even if the unaffected during magnet application.
rhythm is not ventricular fibrillation (e.g. very fast VT).
At slower rates, other antitachycardia options may first In the event of unsuccessful reversion of a ventricular
be attempted as described above. Additionally, at slower arrhythmia by ICD therapy, standard advanced life
rates of tachycardia, attempts are made to discriminate support protocols should be applied. External defibrilla-
between ventricular and supraventricular (including tion can be undertaken with paddles in normal positions,

284 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


Configuration
Configuration Defib with Single Tach Arrhythmia Sensing Dual Chamber
Detection Criteria SVT Criteria
Fib Detection 330 ms/182 bpm V < A Rate Branch
Tach Detection 375 ms/160 bpm for 12 intervals Morphology Off
SVT Upper Limit Same as Fib Interval Stability On (80 ms), (60 ms), 12 intervals
V = A Rate Branch
1 Morphology Off
Sudden Onset On (100 ms)
2

MTD 2 min (Fib Therapy)
MTF Same as Tach for 40 sec
Tachyarrhythmia Therapy Tach ATP
Fib/MTF: [1] Defib 36.0 J (801 V) Output 7.5 V, 1.0 ms
85%
[2] Defib 36.0 J (801 V) BCL 200 ms
Min BCL
[3] Defib × 4 36.0 J (801 V) 4 No. Bursts 3
Tach: [1] ATP Stimuli 10 stimuli
[2] CVRT 10.0 J (429 V) Scanning 12 ms
[3] CVRT 20.0 J (605 V) Ramp Off
[4] CVRT × 2 36.0 J (801 V) Shock Waveform Stored EGM
A Sense/Pace, ± 3.0 mV
3 Biphasic, Fixed Tilt EGM #1 V Sense/Pace, ± 8.9 mV
EGM #2
RV (+) to SVC/Can (–)
Defib: 65 % / 65 % Events Fib, MTD, Tach
CVRT: Same as Defib Settings Detection, 16 sec Pre, 1 min Max
TM
FIGURE 11.51 Implantable cardioverter defibrillator (ICD) programmed parameter summary report from St Jude Medical ICD Atlas DR Model V-240
(Courtesy St Jude Medical, St Paul, MN): box 1, detection criteria. Arrhythmias are classified first on the basis of ventricular rate as detected by
sensing circuitry. Defining rates for each rhythm classification are programmable. In the example shown above a rate of >182/min or greater is the
cut-off for ‘Fib Detection’, which then initiates treatment following the steps for fibrillation (Fib/MTF) (box 3). ‘Tach Detection’ is classified when the
rate is between 160 and 182, then further information can be sought to differentiate between supraventricular and ventricular arrhythmias and
initiate appropriate treatment (box 2); box 2, SVT criteria. When rhythms fall into the ‘Tach Detection’ rate (here 160–182/min), treatment is momen-
tarily suspended to allow classification as SVT. If ventricular rate >atrial rate, then the rhythm is classified as VT and therapy applied according to
‘Tach’ (box 3). When ventricular rate <atrial rate (V<A in box 2), the rhythm could be either SVT or VT and an assessment of interval stability is
made (with marked irregularity supporting AF and the withholding of treatment). ECG morphology distinction can also be enabled (although here
is OFF) that compares morphology prior to and during tachycardia. If the ventricular and atrial rates are the same (V=A), again the rhythm could
be either VT or SVT and further discrimination is made on morphology and on whether onset was sudden or gradual. This process of rhythm
detection is extremely rapid and does not unnecessarily delay therapy. Additionally, even when SVT criteria are met, they are usually subordinate
to sustained rate in the ‘Tach Detection’ algorithm; thus, if the tachycardia persists for a set qualifying period, therapy is initiated according to the
‘Tach’ algorithm in box 3; box 3, tachyarrhythmia therapy. Usually two treatment arms, each with six steps, are prescribed and are independently
programmable. Tachyarrhythmias in the ‘Fib’ range are managed more aggressively than those in the ‘Tach’ range. Escalating energy settings for
defibrillation may be described, but here all six attempts at defibrillation are at maximum (36 J). Treatment in the ‘Tach’ range usually commences
with one or more attempts at antitachycardia pacing (ATP), progressing to cardioversion; box 4, tach ATP. This describes the parameter setting
during antitachycardia pacing. In this example 7.5 V is delivered to the ventricles at a basic cycle length (BCL), which is 85% of the cycle length
of the tachycardia (pacing is delivered slightly faster than the tachycardia). It will provide up to three ‘bursts’ of pacing, each of 10 beats or ‘stimuli’.
Ramping is turned off in this case, but if ON it permits the pacing rate to increase progressively after each unsuccessful attempt at overdrive.


taking care to avoid positioning paddles over the ICD. This will disable tachycardia therapies so that if the
105
External chest compressions can safely be undertaken by terminal rhythm is VT or VF, therapies will not be
rescuers, including during device therapy. 70 delivered.
Terminal Care and Mechanisms of Death Other than by disabling therapy, cardiac death may occur
by normal mechanisms. Cardiac arrest in the acute
in the Patient with an ICD context, as well as when it occurs as the endpoint of ter-
ICDs often create uncertainty amongst health care minal illness, ultimately occurs when cardiac metabolism
workers as to how death may occur. In the palliative fails or systemic factors cause cardiac depression or
patient, where active resuscitation for cardiac death is arrhythmic irritability. The same remains true of the
not to be pursued, the decision to disable antitachy- patient with an ICD. However, cardiac depressive factors
cardia therapies is often taken. This can be achieved will not cause bradycardia or asystole because of the
by reprogramming the ICD, and there is often sufficient pacemaker function. What would otherwise be a
time to incorporate this step into palliative planning. bradyarrhythmic death will instead become eventual
Alternatively, when active treatment is being withdrawn failure to capture by the pacemaker. Similarly, if the
as a patient progresses more rapidly towards an unex- cardiac impact of acute or terminal illness produce
pected (acute) death, there may be a need to disable tachyarrhythmias, then these same influences will increase
therapy before the availability of personnel to reprogram the defibrillation threshold and antitachycardia therapies
the device. In this context it may be appropriate to will become unsuccessful. Devices offer no protection
secure a ring magnet over the ICD (tape it in place). against pulseless electrical activity.

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.

286 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











FIGURE 11.52 12 : 34 hours. Ventricular failure to capture, but only a single beat. It could easily have gone undetected. There appears to be complete
atrial failure to capture also.













FIGURE 11.53 12 : 38 hours. After restoring 1 : 1 capture by increasing output to 20 mA (max), there is again worsening failure to capture, every second
beat fails with ventricular rate now 40/min.



II 1 mV






FIGURE 11.54 12 : 46 hours. Further worsening of failure to capture, now with up to 3 consecutive beats of non capture. The strip is at maximum output
(20 mA) and with pulse width at 1.0 ms.





Case study, Continued
Events and treatment steps that followed included: polarity quickly (given underlying asystole), this is best performed
● Ventricular output was increased to 20 mA but single beat not by disconnecting each of the wires from the bridging cable
failure to capture continued intermittently (every 20–30 sec). and reversing polarity (negative lead into positive pole, positive
Whilst seeking medical agreement for atropine administration, into negative) but instead by disconnecting the bridging cable
the following, as shown in Figure 11.53, occurred (12 : 38 hours). from the pacemaker and simply reversing that connection. This
● Intravenous Atropine Sulphate 1.0 mg was administered with must be undertaken cautiously as pacing will be interrupted
prompt restoration of 1 : 1 ventricular (but not atrial) capture. temporarily (2–3 beats if the procedure has been rehearsed),
● Biochemistry and arterial blood gases were normal. and also because it cannot be known whether capture will be
● After 7 minutes of 1 : 1 capture, intermittent single-beat failure achieved in the reversed polarity configuration. After reversal,
to capture recommenced and at 12 : 46, capture again deterio- pacing achieved 1 : 1 capture, but still with the device at maximum
rated and Figure 11.54 was recorded. output and pulse width. To determine whether a better safety
margin in the new configuration was present, or whether another
The ventricular pulse width was increased from 1.0 to 2.0 ms pacing wire would need to be inserted, a threshold test needed
(remembering that capture is influenced not just by the selected to be performed.
current, but also by the duration over which the current is
applied [pulse width]). One-to-one ventricular capture was again Threshold testing in the polarity-reversed configuration revealed a
restored. superior capture threshold of 11 mA at 2.0 ms pulse width. A safety
margin of 9 mA could be achieved (not quite double the threshold,
It was clear that the pacing electrode (the negative terminal) but enough to avert positioning another pacing lead). Repeat
did not have good capture performance, and it was possible thresholds were then performed hourly until 6 pm at which time
that the alternate wire (connected to the positive terminal) might the surgeon and anaesthetist would be leaving the hospital,
be in contact with more responsive tissue. Agreement was reached and then twice overnight. Thresholds remained unchanged and
to attempt reversing polarity of the wires. If better performance the patient’s recovery was uneventful. Spontaneous rhythm
could not be achieved in the polarity-reversed configuration, a re-emerged on day 1 and a permanent pacemaker was not
temporary transvenous pacing wire would be necessary. To reverse necessary.

Cardiac Rhythm Assessment and Management 287



Research vignette
Pickham D, Helfenbein E, Shinn J, Chan G, Funk M, Drew B. How significant corrected QT interval of 500 msecs or greater, with high
many patients need QT interval monitoring in critical care units? risk drug administration the most prevalent indicator and the pro-
Preliminary report of the QT in practice study. Journal of Electro- longation incidence increasing with the number of separate crite-
cardiography, 2010; 43: 572–6. ria present. Within the entire sample population, 8.7% of patients
who did not possess any of the monitoring indicators had devel-
Abstract oped a prolonged QT. This later finding differed significantly from
Recent Scientific Statement from the American Heart Association the AHA research outcomes, which reported a QT prolongation
(AHA) recommends that hospital patients should receive QT inter- incidence of 2.7% in patients not meeting any AHA monitoring
val monitoring if certain conditions are present: QT-prolonging indicators. The authors note that they were broader in their appli-
drug administration or admission for drug overdose, electrolyte cation of the AHA criteria than the original recommendations and
disturbances (K, Mg), and bradycardia. No studies have quantified for the purpose of measurement accuracy they excluded patients
the proportion of critical care patients that meet the AHA’s indica- with atrial fibrillation, significant artefact and a widened QRS dura-
tions for QT interval monitoring. This is a prospective study of 1039 tion. The number of patients excluded on this basis was not speci-
critical care patients to determine the proportion of patients that fied, but it can be assumed that this represented a significant
meet the AHA’s indications for QT interval monitoring. Secondary proportion of the reference population, given the high incidence
aim is to evaluate the predictive value of the AHA’s indications of such electrocardiographic abnormalities in critically ill patients.
in identifying patients who actually develop QT interval Improved methods for accurately determining QT measurement in
prolongation. these patients would lead to a more precise understanding of the
Methods prevalence of repolarisation delay in the wider critical care patient
Continuous QT interval monitoring software was installed in all population.
monitored beds (n = 154) across five critical care units. This system Polymorphic ventricular tachyarrhythmias, particularly torsades de
uses outlier rejection and median filtering in all available leads to pointes, are associated with the prior presence of pathological or
construct a root-mean-squared wave from which the QT measure- acquired ventricular repolarisation delay, as measured by QT inter-
ment is made. Fridericia formula was used for heart rate correction. val prolongation on the surface electrocardiograph. Whilst the
A QT interval greater than 500 milliseconds for 15 minutes or development of such arrhythmias is a relatively uncommon phe-
longer was considered prolonged for analyses. To minimise false nomenon, their occurrence can be potentially catastrophic, par-
positives all episodes of QT prolongation were manually over read. ticularly in patients with significant underlying cardiovascular
Clinical data was abstracted from the medical record. dysfunction.
Results Continuous bedside QT interval monitoring is not universally avail-
Overall 69% of patients had 1 or more AHA indications for QT able in all critical care settings, however the above findings, and its
interval monitoring. More women (74%) had indications than men associated AHA recommendations highlight the need for closer
(64%, P = 0.001). One quarter (24%) had QT interval prolongation bedside vigilance of the electrocardiographic repolarisation status
(>500 ms for ≥15 minutes). The odds for QT interval prolongation of critically ill patients, including its specific evaluation from routine
increased with the number of AHA indications present; 1 indica- 12 lead ECG recordings. Early detection of established or evolving
tion, odds ratio (OR) = 3.2 (2.1–5); 2 indications, OR = 7.3 (4.6–11.7); QT interval prolongation can prompt pre-emptive measures to
and 3 or more indications OR = 9.2 (4.8–17.4). Positive predictive reduce its associated risk, such as the reappraisal and possible
value of the AHA indications for QT interval prolongation was modification of causative drug therapies such as the Class IA and
31.2%; negative predictive value was 91.3%. III antiarrhythmic drugs and some antipsychotic agents, amongst
Conclusion others. Similarly, patients found to have QT prolongation should be
Most critically ill patients (69%) have AHA indications for QT inter- subjected to close serum electrolyte monitoring and control and
val monitoring. One quarter of critically ill patients (24%) devel- enhanced clinical vigilance if bradycardiac or experiencing chronic
oped QT interval prolongation. The AHA indications for QT interval or increasing ventricular ectopic activity. Whilst it was beyond the
monitoring successfully captured the majority of critically ill stated aims of this study to measure the actual incidence of tors-
patients developing QT interval prolongation. ades de pointes or other polymorphic ventricular tachyarrhythmias
in those patients with QT prolongation, this broader risk-benefit
Critique factor remains the key question when assessing the ultimate clini-
The aims of this study were to identify the number of critical care cal worth of implementing continuous repolarisation interval
patients who met the American Heart Association (AHA) clinical monitoring in critical care patients. This is a particularly important
indicators for continuous QT monitoring and to assess the predic- consideration given the additional cost, training and focus required
tive value of these indicators to the development of a prolonged in undertaking such an initiative. Subfactor analysis of the QT pro-
QT interval. It was found that a significant proportion (69%) of the longation risk indicators, e.g. anti-arrhythmic vs other QT prolong-
sampled population had one or more of the AHA continuous QT ing drugs, will further add to the understanding of this evolving
monitoring criteria and that of this subgroup, 31.2% had a clinically area of arrhythmogenic risk monitoring.

288 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



Learning activities
1. List the major ECG criteria for each of the major arrhythmias 4. Discuss the antiarrhythmic therapies available for the treat-
described in this chapter ment of atrial and ventricular arrhythmias.
2. Describe the general approaches to management of bradyar- 5. Describe the indications, mechanisms of action, dose and side
rhythmias, tachyarrhythmias and AV block effect of the major antiarrhythmics in classes I – IV.
3. Describe the ECG features which would allow differentiation of
the various supraventricular and atrial arrhythmias.





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55. Kay GN, Shepard RB. Cardiac electrical stimulation. In Ellenbogen KA, Kay tion and implantable cardioverter defibrillation in advanced chronic heart
GN, Lau CP et al., eds. Clinical cardiac pacing, defibrillation, and resynchroniza- failure: the MIRACLE ICD trial. JAMA 2003; 289: 2685–94.
tion therapy, 3rd edn. Philadelphia. Elsevier Saunders; 2007. 80. Bristow MR, Saxon LA, Boehmer J et al. Comparison of Medical Therapy,
56. Bernstein AD, Camm AJ, Fletcher RD et al. The NASPE/BPEG generic Pacing, Defibrillation in Heart Failure (COMPANION) Investigators. Cardiac
pacemaker code for antibradyarrhythmic and adaptive rate pacing and resynchronization therapy with or without an implantable defibrillator in
antitachyarrhythmic devices. PACE 1987; 10: 794–99. advanced chronic heart failure. N Engl J Med 2004; 350: 2140–50.
57. Sgarbossa EB, Pinski SL, Gates KB et al. Early diagnosis of acute myocardial 81. Verrnooy K, Verbeek XAAM, Peschar M et al. Left bundle branch block
infarction in the presence of ventricular paced rhythm. Am J Cardiol 1996; induces ventricular remodelling and functional septal hypoperfusion. Eur
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58. Schuchert A, Frese J, Stammwitz E et al. Low settings of the ventricular pacing 82. Sundell J, Engblom E, Koistinen J et al. The effects of cardiac resynchroniza-
output in patients dependent on a pacemaker: are they really safe? Am Heart tion therapy on left ventricular function, myocardial energetics and meta-
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60. Tommaso C, Belic N, Brandfonbrener M. Asynchronous ventricular pacing: conduction abnormalities in patients eligible for cardiac resynchronization
a rare cause of ventricular tachycardia. PACE 1982; 5(4): 561–3. therapy. Pacing Clin Electrophysiol 2004; 27(8): 1105–12.
61. Gimbel JR, Bailey SM, Tchou PJ et al. Strategies for the safe magnetic reso- 84. Alonso C, Leclercq C, Victor F et al. Electrocardiographic predictive factors
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1041–6. advanced heart failure. Am J Cardiol 1998; 84: 1417–21.
62. Hayes DL, Zipes DP. Cardiac pacemakers and cardioverter-defibrillators. In 85. Abraham WT, Fisher WG, Smith AL et al. MIRACLE Study Group. Multicenter
Braunwald E, Dipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular InSync Randomized Clinical Evaluation: Cardiac resynchronization in
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63. Vardas PE, Auricchio A, Blanc JJ et al. Guidelines for cardiac pacing and 86. Daubert JC. Atrial fibrillation and heart failure: a mutually noxious associa-
cardiac resynchronization therapy. The task force for cardiac pacing and tion. Europace 2004; 5: S1–S4.
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Europace 2007; 9: 959–98. resynchronization therapy. Heart Rhythm J 2006; 3: AB30–35.
64. Kristensen L, Nielsen JC, Pedersen AK, et al. AV block and changes in pacing 88. Kenny T. The nuts and bolts of cardiac resynchronization therapy. Massachusetts:
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89. Miller JM, Zipes DP. Management of the patient with cardiac arrhythmias. studies. Antiarrhythmics vs Implantable Defibrillator Study, Cardiac Arrest
In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovas- Study Hamburg, Canadian Implantable Defibrillator Study. Eur Heart J 2000;
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2010; 81: 1293–304. lar arrhythmias. New Engl J Med 1996; 335(26): 1933–40.
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cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS S52–8.

Cardiac Surgery and

Transplantation 12





Judy Currey
Michael Graan





Learning objectives Key words

After reading this chapter, you should be able to: cardiac surgery
● outline cardiac surgical procedures including coronary cardiopulmonary bypass
artery bypass graft surgery and valve repair and valve replacement, repair
replacement arrhythmia
● describe the indications, advantages and disadvantages of intra-aortic balloon pump
using cardiopulmonary bypass heart transplant
● outline methods of myocardial preservation during cardiac denervation
surgery ischaemic reperfusion injury
● outline immediate postoperative management of cardiac
surgical patients including haemodynamic, rhythm
monitoring, ventilatory support, postoperative bleeding
including pericardial tamponade, postoperative pain, fluid
and electrolyte and emotional and family support
● outline the principles of counterpulsation in intra-aortic cardiac surgery for coronary artery disease or valvular
disease will be discussed, including the use of cardiopul-
balloon pumping monary bypass. In addition, the use and management of
● outline the benefits and timing of balloon inflation and intra-aortic balloon pumping in cardiac surgical and
deflation, conventional and real timing, management and medical patients will be outlined. The management of
assessment of timing and timing errors patients following heart transplantation will be identified
● describe the nursing management of IABP complications, including the immediate postoperative complications
including limb perfusion, bleeding and immobility-related and their prevention and management.
complications
● discuss methods of weaning IABP and management of IABP CARDIAC SURGERY
removal
● discuss the immediate postoperative care of heart Cardiac surgery includes repair of structural abnormali-
transplant recipients ties, repair or replacement of stenotic or regurgitant
● describe the clinical manifestations of postoperative valves, and bypass of lesions within the coronary arteries
complications in heart transplant recipients that are reducing blood flow to the myocardial tissue.
● identify signs and symptoms of rejection in heart transplant
recipients STRUCTURAL ABNORMALITIES
● evaluate the effectiveness of nursing interventions in the Some structural abnormalities result from myocardial
postoperative management of heart transplant recipients. infarction, and have been described in Chapter 10. Other
structural abnormalities result in valvular disease (mitral,
aortic, tricuspid, pulmonic) and ventricular defects.


INTRODUCTION Valvular Disease
The incidence and types of valvular disease have changed
1
Many critically ill patients experience compromised over the past 50 years. Valvular disorders, such as mitral
cardiac function, as either a primary or secondary condi- stenosis and aortic regurgitation, often arise from infec-
tion. This chapter follows on from those situations exam- tious diseases like rheumatic fever and syphilis, which are
ined in Chapter 10, and reviews patients with conditions much less common today. Conversely, there has been a
that tend to be cared for in specialised critical care units. rise in the rate of aortic stenosis, which is due to degen-
In this chapter, the management of a patient who requires erative disease common in ageing. In contrast to these 291

292 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



Fused cusps
Cusp Cusp




Orifice Orifice

Normal valve Normal valve Stenosed valve Regurgitant valve
(open) (closed) (open) (closed) B
A









Stenosed
mitral
valve

Mitral
valve does
not close
properly

C D


FIGURE 12.1 Valvular stenosis and regurgitation: (A) normal position of valve leaflets (cusps) when the valve is open and closed; (B) open position of a
stenosed valve (left) and closed position of a regurgitant valve (right); (C) haemodynamic effect of mitral stenosis shows the mitral valve is unable to open
completely during left atrial systole, limiting left ventricular filling; (D) haemodynamic effect of mitral regurgitation shows the mitral valve does not close
completely during left ventricular systole, allowing blood to re-enter the left atrium.
43


trends, the prevalence of rheumatic fever and rheumatic Aortic valve disease
heart disease among Indigenous Australians is one of the Aortic stenosis is a narrowing of the opening of the valve
highest in the world. Also, Pacific Islanders living in New between the left ventricle and aorta (Figure 12.1). This
2
Zealand have much higher rates of rheumatic fever than stenosis often results from degenerative changes that
the general population. As a result, valvular disorders are occur with age or as a result of congenital abnormalities
3
much more common in these groups. Rheumatic fever is such as a bicuspid aortic valve (prevalence of bicuspid
discussed under infective endocarditis in Chapter 10. aortic valve in the general population is 0.5% and may
cause aortic stenosis or regurgitation). Aortic stenosis is
Stenotic valves have a tightened, restricted orifice, so that usually associated with left ventricular hypertrophy in
blood must be forced through at higher pressure response to the high pressure needed to push blood into
(Figure 12.1). In regurgitation, also called valvular incom- the aorta. Increased myocardial oxygen demands from
petence or insufficiency, incomplete closure of the valve the hypertrophied muscle also mean that angina is
leaflets results in backflow of blood. Valvular conditions common. Often the first sign of aortic stenosis is left heart
can result from congenital deformities, but also from the failure, which is a culmination of these two effects and
degenerative changes associated with ageing, from infec- adaptive dilation. On auscultation, additional heart
4
tion and rheumatic diseases. When a valve is stenosed, sounds are heard as a systolic murmur and a loud S4.
higher pressure is required to push blood through the
narrow opening and the heart compensates by hypertro- Aortic regurgitation may occur acutely when the aortic
phy and dilation. When a valve is incompetent the heart valve is damaged by endocarditis, trauma or aortic dis-
does not empty sufficiently, so again the heart compen- section, and presents as a life-threatening emergency.
sates by hypertrophy and dilation. In both these condi- Chronic aortic regurgitation usually results from rheu-
tions heart failure may result; however, in regurgitation, matic heart disease, syphilis, chronic rheumatic condi-
pressure in the ventricles and atrium grows and this pres- tions or congenital conditions. Again the left ventricle
sure is reflected back into the pulmonary or venous compensates by hypertrophy and dilation, which ulti-
system. Although the heart contains four valves, the mately can result in left heart failure. When left heart
majority of disorders affect the mitral and aortic valves in failure occurs, left atrial pressure rises and may cause
the left side of the heart. pulmonary hypertension. In the acute situation, the

Cardiac Surgery and Transplantation 293

patient presents with collapse, severe hypotension and
4
dyspnoea. Patients with chronic regurgitation may
remain asymptomatic for years, finally presenting with
signs of left heart failure. On auscultation, a diastolic
murmur can be heard.
Left subclavian
Mitral valve disease artery

Mitral valve stenosis often occurs as a result of rheumatic
heart disease and less often from systemic lupus erythro- Internal mammary
(internal thoracic) artery
matosus. These diseases cause damage to the leaflets
and chordae tendineae, so that during healing the scars
contract and seal, restricting the aperture. Left atrial
pressure rises with resultant pulmonary hypertension.
In chronic conditions, this pressure may also affect the
5
right ven tricle. Lung compliance is also reduced,
causing dyspnoea. On auscultation a low-pitched
diastolic murmur and an opening snap can be heard.
Mitral valve regurgitation results when the mitral valve Anterior descending
and chordae tendineae are damaged, often due to myo- branch of the left
coronary artery
cardial infarction, rheumatic disease and infectious endo-
carditis. Backflow into the left atrium during systole
creates elevated atrial and pulmonary pressures, and
5
pulmonary oedema can result. On auscultation, a third
heart sound and a pansystolic murmur can be heard.
Ischaemic Heart Disease
Site of graft
The pathophysiology and implications of ischaemic heart
5
disease are explained in detail in Chapter 10. Single FIGURE 12.2 Internal mammary artery graft .
lesions can be treated by angioplasty and stent; however,
multiple, longer lesions may need coronary artery bypass
surgery. 5 (Figure 12.2). If the radial artery is being harvested for
grafting, the collateral circulation in the forearm is
SURGICAL PROCEDURES assessed. Echo colour Doppler provides best accuracy of
The most common cardiac surgical procedures include forearm circulation, although the clinical Allen test is
coronary artery bypass graft (CABG) surgery, to bypass quite commonly used. The disadvantage of the Allen test
7
lesions within the coronary arteries, and repair or replace- is that it has around 5% false patency result. A selection
ment of stenotic or regurgitant valves. During these pro- of IMA, SVG and radial artery grafts may be necessary over
cedures preservation of systemic circulation, ventilation time as repeat procedures are needed or in patients with
and the myocardium is required and is often achieved extensive disease requiring multiple grafts.
with the aid of cardiopulmonary bypass (CPB). Over recent years a new approach to CABG – minimally
invasive direct coronary artery bypass grafting (MIDCABG)
Coronary Artery Bypass Graft Surgery – has been used. This procedure uses intercostal incisions
CABG uses a section of vein or artery to bypass a blockage and a thorascope instead of a sternotomy to access the
in the patient’s coronary artery. The vessels used for graft- heart and coronary arteries. MIDCABG is also often per-
ing arise from the internal mammary artery, or are taken formed without cardiopulmonary bypass (off pump cor-
from the saphenous vein or radial artery. Saphenous veins onary artery bypass, OPCAB); instead, the heart is slowed
are removed from the legs, and the radial artery from the with beta-blockers to allow the surgery to be performed
8
forearm and used as a free graft with anastomoses at the on a beating heart. OPCAB procedures may also be per-
ascending aorta and distally to one or more coronary formed using full or partial sternotomy to provide access
arteries. When saphenous veins are used as grafts (SVG), for multiple vessels grafting. Both procedures have been
they often develop diffuse intimal hyperplasia, which successful responses to the drive to reduce recovery times,
8
ultimately contributes to restenosis. Patency rates are patient stays in hospital and costs. MIDCABG is cur-
lowest in saphenous vein grafts attached to small coro- rently only used in single-vessel disease, particularly the
nary arteries or coronary arteries supplying myocardial left anterior descending (LAD) artery. More recently,
scars. Consequently, arterial grafts are used more often, robotically-assisted cardiac surgery has been performed
as they are more resistant to intimal hyperplasia. Internal in America and Europe and has been introduced at a
mammary arteries (IMAs) and radial artery grafts may small number of Australian hospitals for CABG and
6
be used. The IMA remains attached to the subclavian mitral valve surgery. This technique has further reduced
artery and is mobilised from the chest wall and anasto- the invasiveness of cardiac surgery, as little more than stab
mosed to the coronary artery distal to the occlusion wounds are required in the right chest for thoroscopy and

294 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

the robotic instruments. Avoiding true thoracotomy or from porcine, bovine or human cardiac tissue. Mechani-
sternotomy improves postoperative pain experiences and cal valves are more durable but have an increased risk
shortens length of stay. 9 of thromboembolism, so lifelong anticoagulation is
required. Biological valves suffer from the same problems
Although CABG is the most common cardiac surgical
procedure undertaken in Australia, the incidence has as the patient’s valve (i.e. calcification and degeneration).
declined since 2005/06 to be 61 procedures/100,000 The choice of valve depends on the age of the patient and
10
population in 2007–08. The decline in surgery rates is potential difficulties with taking anticoagulants.
due to changes in the treatment of CHD, including the Mortality for valvular surgery is higher than for CABG,
advent of percutaneous coronary intervention (PCI). reflecting the underlying loss of ventricular function and
More procedures are now being performed in older additional procedures that are common. Risk stratifica-
patients, with 73% of current patients aged over 60 years. tion models have been developed to help determine the
1
CABG is used to relieve the symptoms of angina by patients that are most likely to have poor recovery and
14
increasing coronary blood flow distal to occlusive coro- outcomes. The major factors that contribute to poor
nary lesions. It is a palliative, not curative, treatment as outcomes are worse left ventricular function and age over
11
the underlying disease process continues. CABG is more 70 years old.
effective than PTCA in patients with extensive, multi-
vessel disease. 9,11 CABG is also used in left main vessel
lesions due to the high risk of extensive infarction associ- Cardiopulmonary Bypass
ated with PTCA in this area. Women do not appear to CPB was developed to enable surgery to be performed on
have the same access to CABG surgery, as men are three a still, relatively-bloodless heart, while preserving the
times more likely to have surgery, although only twice as patient’s circulation. CPB temporarily performs the func-
12
likely as women to have CHD. CABG surgery is com- tions of the heart in circulating blood and of the lungs
monplace, and many cardiothoracic centres have highly by enabling gas exchange with the blood. Silicone can-
efficient, effective systems in place with mortality rates as nulae are inserted into the venae cavae and venous blood
low as 2%.
circulated through a circuit outside the body. In this
circuit the blood is oxygenated, carbon dioxide removed
and blood temperature controlled. Drugs and anaesthet-
Valve Repair and Replacement ics may be added. A roller pump is generally used to
Valve surgery is usually undertaken to repair the patient’s provide the pressure to create blood flow in the circuit
valve or, more often, to replace the valve with either a and back to the patient’s aorta.
mechanical or tissue prosthesis. The clinical decision for Adverse effects of CPB are diverse, and include the
valve surgery is primarily based on the clinical state of the following: 15
patient using the New York Heart Association (NYHA)
classification system and echocardiographic findings. ● Haematological effects due to exposure of the blood
5
The type of surgery used will depend on the valves to tubing and gas exchange surfaces, which initiates
involved, the valvular pathology, the severity of the surface activation of the clotting cycle. Also blood
condition and the patient’s clinical condition. Often component damage due to shear stress from the roller
valve surgery is not a single procedure, and it may action of the pump, which reduces haematocrit, leu-
involve multiple valves, CABG and implantable cardio- cocyte and platelet counts.
verter defribillator (ICD). Valve surgery is palliative, not ● Pulmonary effects due to activation of systemic inflam-
curative, and patients will require lifelong health care. matory response syndrome (SIRS) that increases capil-
lary leakage, and lung deflation during surgery leading
Valve repair may involve resecting and/or suturing pro- to post-operative atelectasis.
lapsed or torn leaflets (valvuloplasty) and repairing the ● Cardiovascular effects due to volume changes, fluid
ring of collagen the valve sits in (annuloplasty), and is shifts and decreased myocardial contractility, which
commonly used for mitral and tricuspid regurgitation. decreases cardiac output. This is most severe during
Commissurotomy (incising valve leaflets and debriding the first 6 hours, but usually resolves within 48–72
calcification) is the treatment of choice for mitral steno- hours.
sis. Both repair processes have demonstrated lower opera- ● Neurological effects due to poor cerebral perfusion
tive mortality than replacement, although complete valve and generation of thromboemboli from aortic
competence may not be able to be achieved. Open pro- cannulation, which can lead to cerebrovascular
cedures are preferred because thrombi and calcification accidents.
can thereby be removed.
● Renal effects due to decreases in cardiac output during
Valve replacement may be necessary, but could be associ- initiation of CPB, which decreases renal perfusion.
ated with higher risks due to long-term disease process ● Post-pump delirium or psychosis, which occurs in
and poor underlying left ventricular function. The most 32% of CPB patients although the cause has not been
common indication for valve replacement is aortic steno- identified. Symptoms include short-term memory
sis, and accounts for 60–70% of valve surgery. Prosthetic deficit, decreased attention, and inability to respond
13
valves may be mechanical or biological. Mechanical to and integrate sensory information.
valves are made of metal alloys, pyrolite carbon and ● Activation of a systemic inflammatory response, which
Dacron (Figure 12.3). Biological valves are constructed may cause vasodilation and increased cardiac output.

Cardiac Surgery and Transplantation 295






















A B










FIGURE 12.3 Prosthetic valves: (A) the Bjork-Shiley valve,
with a pyrolyte-carbon disc that opens to 60 degrees;
(B) the Starr-Edwards caged-ball valve model 6320, with
satellite ball; (C) the St Jude Medical mechanical heart
valve, with a mechano-central flow disc; (D) the Hancock II
porcine aortic valve, with stent and sewing ring covered in C D
Dacron cloth. 5


These effects are well documented, and routine CPB man- NURSING MANAGEMENT
agement and postoperative care are designed to minimise The often-rapid turnaround from complete dependence
and treat the complications. Heparin is added at the com- to intensive care to discharge in post cardiothoracic sur-
mencement of CPB and is reversed with protamine (1 mg gical patients can provide particularly rewarding nursing
of protamine for every 100 units of heparin) when CPB experiences. However, this rapid progression is also often
ceases; activated clotting times are monitored throughout marked by haemodynamic instability, arrhythmias, and
and after CPB. Blood returning to circulation is filtered, biochemical and haematological changes. The increased
and surgical procedures proceed carefully to reduce emphasis on rapid weaning and extubation, often occur-
microemboli. Monitoring and maintenance of adequate ring during turbulent anaesthetic recovery, presents one
arterial flow rates are used to prevent low perfusion. of the more volatile periods in ventilatory support, requir-
Temperature gradients and a rewarming process are insti- ing knowledgeable and skilled nursing and medical
tuted slowly so that cardiac output can meet metabolic management. In addition, the management of ventila-
demands.
tion, temporary pacemaker therapies, and mechanical
cir culatory assist (intra-aortic balloon pumping and
Myocardial Preservation ventricular assist) devices provides opportunity for the
One of the processes involved in CPB is that the aorta is development of broad and detailed expertise.
clamped where a cannula is inserted to return blood to Patients usually return to the intensive care unit for 1–2
the circulation. This clamp prevents blood flow into the days, although where early extubation is undertaken, they
coronary arteries; therefore, the myocardium must be may spend only hours in a recovery unit before progress-
protected from ischaemia. This protection is achieved ing to a cardiothoracic high-dependency area, where
through several mechanisms directed towards reducing nurse to patient ratios may be 1 : 2 to 1 : 3.
oxygen demand: first, oxygen demand is reduced by mild
to moderate hypothermia (28–32°C); second, by reduc-
ing myocardial temperature (0–4°C), through infusing The Immediate Postoperative Period
cold fluids directly into the coronary arteries; and third, Patients should be transported to intensive care accom-
by preventing normal conduction by arresting the heart panied by at least an anaesthetist, an appropriately quali-
during diastole, through infusing a concentrated potas- fied nurse and transport personnel under continuous
sium solution into the coronary arteries. Return to normal cardiac monitoring and assisted ventilation. It is prudent
rhythm is usually achieved by circulation of warm blood, to include capnography during patient transport to detect
though defibrillation may be necessary. ventilator disconnection, dysfunction, or endotracheal

296 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

tube migration. Intensive care or theatre nursing staff may thorough monitoring and interpretation of variables, and
be a component of the transport team. The admission to managed according to specific needs. During the initial
intensive care requires a team approach, with the partici- two hours of recovery period, 95% of patients will experi-
pation of intensive care nursing and medical staff and/or ence haemodynamic instability. 18
technician input. The immediate postoperative decision
making on patient management is influenced by hand-
over from anaesthetists, settling in procedures and col- Hypertension
16
legial assistance. Admission activities are commonly Hypertension is present in up to 30% of patients
19
divided between nurses, with one nurse taking responsi- initially, as hypothermia, stress responses, pain and
bility for establishing monitoring and haemodynamic hypovolaemia contribute to vasoconstriction. 19-21 When
assessment and management, and a second nurse manag- the systemic vascular resistance is excessive, the high after-
19
ing ventilation and endotracheal tube security, as well as load may contribute to low cardiac output. Rewarming
managing chest drains, gastric tube and urinary catheter. to normothermia with space blankets or heated air
If staffing permits, additional nurses may take responsi- blankets, fluid administration, administration of seda-
bility for documentation, performing arterial blood gases, tion or analgesics, and infusion of IV vasodilators (glyc-
12-lead ECG and providing assistance as required. eryl trinitrate or sodium nitroprusside) are all commonly
used to overcome vasoconstriction when contribut-
The objectives of immediate post operative management 19-21
of cardiac surgical patients may include: ing to hypertension. Occasionally beta-blockers are
used. Hypertension increases myocardial workload and
● optimisation of cardiovascular performance contributes to bleeding.
● reestablishment and/or maintenance of normo-
thermia
● promotion of haemostasis Hypotension
● ventilatory support and management Transient hypotension requiring treatment is common
● prevention and management of arrhythmias at some stage during the postoperative period. Contribut-
● optimisation of organ perfusion ing factors to hypotension include hypovolaemia and
decreased venous return (from polyuria, bleeding, venti-
lation and positive end-expiratory pressure, and excess
Haemodynamic Monitoring and Support vasodilation), contractile impairment (from ischaemia or
Typical haemodynamic monitoring includes an intra- infarction, hypothermia, and negative inotropic influ-
arterial catheter for continuous blood pressure monitor- ences), pericardial tamponade, and vasodilation (from
ing and arterial blood sampling. Cardiac output and excess vasodilator therapy, or as part of an inflammatory
22
preload measurement are achieved most commonly with response to cardiopulmonary bypass).
either a pulmonary artery or central venous catheter Hypotension may present with reduced or elevated
configured for pulse contour cardiac output (PiCCO) preload, reduced or elevated cardiac output, and reduced
monitoring (see Chapter 9). or elevated systemic vascular resistance (SVR). When
hypovolaemia is present, cardiac output will be low and
Preload measures provided by the pulmonary artery
catheter include right atrial pressure (RAP) to approxi- SVR usually high. Hypovolaemia is diagnosed by measur-
mate right ventricular filling, and pulmonary artery pres- ing preload indicators, as pressure (RAP, PAP, PCWP) or
17,19
sure (PAP) to approximate right ventricular systole and volume (ITBVI, GEDVI). Colloids (e.g. normal serum
provide insight into pulmonary vascular resistance and albumin) are generally preferred for volume restoration
18
left heart function. The pulmonary capillary wedge pres- in the postoperative period. Blood returned from the
sure (PCWP) is available to approximate left ventricular cardiopulmonary bypass circuit (‘pump blood’) usually
filling and left heart function. Alternatively, the PiCCO accompanies the patient to ICU, and this should be read-
monitoring system represents preload by intrathoracic ministered at a rate suitable to filling indices and blood
blood volume index (ITBVI) and global end-diastolic pressure.
volume index (GEDVI). In addition, the extravascular Hypotension accompanied by elevated preload and low
lung water index (EVLWI) can demonstrate the accu- cardiac output usually represents cardiac dysfunction or
mulation of interstitial lung water. 17 pericardial tamponade, and the distinction should be
quickly sought. 20,23 When such left ventricular dysfunc-
Cardiac output is measured by either intermittent or
continuous thermodilution via pulmonary artery cathe- tion is present, there is usually compensatory vasocon-
ters, or measured intermittently and then approxi- striction and tachycardia, although heart rate responses
mated continuously on a beat-to-beat interpretation of may be unreliable due to cardioplegia, cold, conduction
21
pulse contour by the PiCCO monitoring system. Cardiac disease and preoperative beta-blocking agents. Inotro-
output measurement can be combined with other pic agents, including milrinone hydrochloride, adrena-
pressure variables to calculate systemic and pulmonary line, dopamine or dobutamine, may become necessary
vascular resistance, stroke volume and measures of ven- (these are covered more completely in Table 20.7 and its
tricular work. accompanying text). When the profile of severe left ven-
tricular dysfunction is persistent (either at the time of
Certain common haemodynamic patterns are seen in the coming off bypass or later in intensive care), intra-aortic
early postoperative phase. These must be detected through balloon pumping may be instituted. ECG assessment for

Cardiac Surgery and Transplantation 297

new ischaemia or infarction should be made, which if of Rhythm monitoring and postoperative
significant size, may warrant surgical re-exploration arrhythmias
or angiographic investigation. Pericardial tamponade Continuous rhythm monitoring is necessary while in
is also a cause of hypotension (covered later in this intensive care, and telemetry monitoring is usually con-
chapter).
tinued until discharge from hospital. Lead selection is
A fourth common postoperative profile is hypotension often haphazard, but a chest lead in the V1 position (or
with normal or elevated cardiac output in the presence lead MCL1) generally provides best information on atrial
27
of low SVR. This may occur with excess vasodilator and ventricular activity. Unlike many leads, these two
administration, the use of postoperative epidural infu- leads reliably demonstrate normal rhythms, bundle
27
sions, and vasodilation from a systemic inflammatory branch block and ventricular rhythms, and may be
response to cardiopulmonary bypass and other factors useful in confirming pulmonary artery catheter irritation
such as reinfusion of collected operative site blood. The as the cause of ventricular arrhythmias. 28
24
inotrope milrinone hydrochloride is popular in the post- A 12-lead ECG is performed on admission to the ICU
operative phase because of its dilating effect on radial and should be compared with the preoperative ECG. It
artery grafts, but often contributes to hypotension should be assessed for signs of new ischaemia or infarc-
25
through its systemic vasodilator properties. When hypo- tion, new bundle branch block and arrhythmias or con-
tension is attributable to vasodilation, metaraminol or duction disturbances. Pericarditis, a frequent complication
19
noradrenaline may be used. Arginine vasopressin, by of surgery, appears as ST segment elevation (often, but
infusion, has more recently emerged as an effective alter- not always, in many leads), and may mask or mimic
native vasoconstrictor for cardiac surgical patients. 26 myocardial infarction. The nurse should look for the
classic concave upward, or ‘saddle-shaped’ ST segment, to
A mean arterial pressure of 70–80 mmHg is generally
21
targeted in the postoperative period. This can some- distinguish pericardial changes from the more convex
times be reduced if there has been ventriculotomy or if upward ST segment of infarction. Worsening of pain on
20
there is concern about the status of the aorta. The cardiac inspiration and a pericardial rub help to confirm
27
2
index should be maintained above 2.2 L/min/m , as pericarditis.
hypoperfusion develops below these values. When at Atrial fibrillation is the most common postoperative
these levels, additional assessments are often undertaken, arrhythmia and contributes significantly to postoperative
29
such as mixed venous oxygen saturation measurement morbidity and hospital length of stay. It occurs in up
(to assess oxygen delivery deficits) and arterial pH and to 30–50% of patients, most often on days 2 to 3 post-
lactate measurements (to detect metabolic acidosis from operatively. 15,29 Many patients revert without treatment,
19
anaerobic metabolism). but when treatment becomes necessary beta-blockers and
amiodarone appear the most successful agents for cor-
In addition to assessment of preload, contractility and rection. Digitalis is effective for rate control and IV
29
afterload, heart rate and rhythm should be assessed for magnesium is often used, although further evidence for
their input into cardiac output and blood pressure. its use is needed. Atrial pacing to prevent atrial fibrilla-
Extremes of rate and arrhythmias alter ventricular filling tion is being increasingly explored but a clear recom-
and may need correction. If temporary pacing wires are mendation on pacing sites and protocols has yet to
present, pacing strategies for haemodynamic improve- emerge. By contrast, atrial overdrive pacing can be an
ment include rate rises (even if already in the normal effective means to immediately and safely interrupt atrial
range) and the provision of dual-chamber or atrial flutter. 29
21
pacing as alternatives to just ventricular pacing. Alterna-
tively, if ventricular pacing is present, reducing the rate to Ventricular ectopic beats are common and by themselves
permit expression of a slower sinus rhythm may, with the do not require treatment unless they accompany isch-
19
provision of atrial kick, improve cardiac output and aemia or biochemical disturbance, in which case they
blood pressure (refer to Chapter 11 for more information may progress to more complex arrhythmias. Consider-
on pacing). ation should always be given to the pulmonary artery
catheter as the cause (including both correctly and
malpositioned catheters), as this is an easily corrected
28
influence. Ventricular tachycardia and fibrillation are
uncommon and usually denote myocardial disturbance
Practice tip such as ischaemia or infarction, shock, electrolyte distur-
bance, hypoxia, or increased excitation by high circulat-
Be aware of an apparent paradox: hypertension may occur even ing catecholamine levels. Standard approaches to
17
if there is hypovolaemia. The intense vasoconstriction often resuscitation according to protocols in Chapter 24 apply,
seen postoperatively not only raises blood pressure but aids including standard CPR over the recent sternotomy.
venous return so that right atrial pressure is normal. It may not When ventricular fibrillation cannot be corrected, consid-
be until the patient has warmed and dilated that the true filling eration is often given to re-exploration of the chest to
status becomes revealed. When the patient is cold and with examine graft patency and/or provide internal cardiac
normal filling pressures, be prepared for possible hypotension, massage. The cardiac surgical intensive care unit should
and the need for significant fluid resuscitation, on rewarming. be equipped to enable emergency re-exploration for such
purposes.

298 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

Ventilatory Support ● pulmonary hypertension from cardiac failure or valve
Ventilation should be approached according to the disease
general principles described in Chapter 15. As anaesthe- ● cardiogenic shock/post-pump failure
sia is not typically reversed at the end of the operation, ● systemic inflammatory response syndrome due to car-
patients are generally admitted apnoeic, and within 1–3 diopulmonary bypass
hours return to wakefulness and spontaneous breathing. ● early or rapid weaning that is undertaken before com-
plete readiness, leading to failure at weaning attempt
Ensuring a secure airway is an initial priority; the follow- ● surgical pain limiting spontaneous effort and poten-
ing should be undertaken: tially leading to atelectasis or sputum retention.
● Confirmation of endotracheal tube position and its
security immediately on admission: Approaches to weaning
● auscultation for equal bilateral air entry to rule out As patients often have no underlying pulmonary pathol-
right main bronchus intubation, ogy, and have been ventilated for brief periods only, rapid
● recording of the ETT insertion length should be weaning phases have become the norm in most centres.
sufficient In many instances, as soon as the patient wakes and
● postoperative chest X-ray, taken within 30 minutes, begins spontaneous breathing activity he/she may be
should also be examined for ETT positioning suitable for at least a trial of spontaneous breathing in
● Initial ETT care: CPAP mode, usually with some modest level of pressure
● assessment for air leak around the cuff (via perfor- support (e.g. 5–10 cm H 2O). If tolerated and the patient
mance of minimal occlusive volume or pressure maintains an adequate minute volume, SpO 2 and PaCO 2 ,
tests) then extubation may be considered within as little as
● ETT is adequately secured and positioned so as not another 30 minutes. Normal demonstrations of airway
to apply undue pressure against soft tissues of the protection capability (e.g. neuromuscular control, gag,
mouth and lips. swallow, cough and patient strength) should be sought
There has been a general trend to more rapid ventilatory before extubation (see Chapter 15 for details).
weaning in recent years, and in some centres ‘fast-track’ These short ventilation times and rapid weaning carry a
cardiac surgical recovery includes extubation at the end greater risk of weaning failure. Patients may initially wake
of the operation before transfer to a recovery unit for and appear to sustain spontaneous ventilation well for
suitable patients. Indices of respiration show no improve- some time, only to lapse back under anaesthetic influ-
ment when intubation is maintained for longer com- ence. A return to greater ventilatory support may be
30
pared with early extubation, and pooled results from necessary. Additionally, demonstrations of spontaneous
randomised early extubation trials show earlier ICU dis- breathing for as little as 30 minutes may be insufficient
charge and shorter lengths of stay (by 1 day) when early for patients to fail, as they have not exceeded reserves.
extubation is undertaken. 31 Failure to wean carries greater significance in the cardiac
Apart from these fast-track approaches, ventilation is surgical patient with existing pulmonary hypertension, as
commonly employed for 2–6 hours in the uncomplicated respiratory acidosis causes pulmonary vasoconstriction,
patient. Reasons for continuing ventilation beyond this abruptly worsening pulmonary hypertension and the risk
time frame may include: of pulmonary oedema and/or right ventricular failure.
● intraoperative neurological event Where ventilation has been more prolonged due to
● gas exchange deficit with unresolved hypoxaemia postoperative pulmonary problems, weaning may be
● ventilatory inadequacy approached more cautiously, as might be applied to the
● significant haemodynamic insufficiency general longer-term ventilated patient. Gradual manda-
● patients returning from theatre late in the evening tory rate reduction or increasing periods of spontaneous
may sometimes continue ventilation overnight to ventilation interspersed with periods of greater assistance
optimise postextubation breathing ability. have been used. 31
For many patients, ventilation is provided purely for
initial airway and apnoea protection rather than for treat- Assessment and Management of
ment of pulmonary deficits. In the absence of pulmonary Postoperative Bleeding
disease, many centres provide fairly uniform approaches The harvest sites for radial arteries or saphenous veins are
to parameter settings that aim at sustaining ventilation uncommon sources of significant blood loss and are gen-
and oxygenation, while limiting traumatic risk to the erally easily managed with dressings or compression.
lungs (see Table 12.1). However, approaches to ventila- Intrathoracic bleeding, however, may be torrential and
tion will need to be tailored in the presence of operative threaten life. Occasionally surgical bleeding from the
complications or coexisting lung disease. aorta, arterial grafts or myomectomy sites may exceed
replacement capabilities, and at times patients succumb
Ventilation challenges specific to the postcardiac surgical to overwhelming haemorrhage. Maintenance of drain
setting include:
patency and strict recording of losses and total fluid
● atelectasis due to operative access balance are paramount, and fluid balance assessments
● pneumothorax (pleural opening for grafts, or over shorter intervals, even every 5–10 minutes, become
ventilation-induced trauma) necessary during active bleeding. Because of the potential

Cardiac Surgery and Transplantation 299



TABLE 12.1 Postoperative ventilation settings

Nominal or generally
acceptable settings Alternatives to nominal settings and reasons for variation
SIMV with volume control ventilation Pressure control suitable. Generally used only if there is significant hypoxaemia or the
need to exert greater control on pulmonary pressure. Hybrid modes such as Autoflow,
pressure-regulated volume control or volume control plus (VC+) are also suitable,
generally for same indications as pressure control.
Tidal volume 8–10 mL/kg Lower tidal volumes (6–8 mL/kg) when there is known compliance disorder (atelectasis,
pulmonary oedema, fibrosis) or unexplained high plateau pressures.
Mandatory rate 10 L/min Faster rates may be necessary if low tidal volume strategies become necessary. Lower rates
if gas trapping risk due to airways disease.
Inspiratory flow 30–50 L/min to provide I : E Slower flows to prolong the inspiratory time may be necessary if there is atelectasis and
ratio of 1 : 2 to 1 : 4 acceptable hypoxaemia, or if there is a desire to lessen inspiratory pressures. Faster flows to enhance
expiratory time necessary only if gas-trapping risk.
PEEP minimum levels of 5 cmH 2 O Higher levels of PEEP according to severity of hypoxaemia.
Pressure support 5–10 cmH 2 O Automated pressure support modes such as automatic tube compensation (autoadjusted
pressure support according to overcome flow resistance of tracheal tubes) or volume
support (autoadjusted pressure support to achieve target tidal volume on spontaneous
breaths) exist. There is no pressing indication for their use in uncomplicated cardiac
surgical patients.
Permissive hypercapnoea rarely necessary Particularly important to avoid if existing pulmonary hypertension, as may worsen acutely
with respiratory acidosis.
FiO 2 initially 1.0 then wean down according According to PaO 2 /SaO 2.
to PaO 2 /SaO 2



rates of bleeding, the cardiac surgical unit must be Chest drainage should be monitored closely, and while
equipped to institute rapid volume replacement, and bleeding is active, volumes should be assessed every 5
have access to adequate blood and blood product minutes and patency of drains ensured to avert tampon-
stores, blood warmers, and all necessary procoagulant ade. Sudden cessation of drainage should always raise the
therapies. In addition, dedicated equipment should be possibility of the loss of tube patency and risk of tam-
available to facilitate emergency resternotomy to control ponade, but tamponade may also occur while drainage
haemorrhage. continues, as collections and compression may occur at
sites isolated from drains, or losses may simply be occur-
One or more chest drains are inserted to remove and ring faster than that able to be removed by patent drains.
monitor blood loss, but the positioning of drains is vari-
able, depending in part on the procedure performed, the Chest drains should also be observed for bubbling, to
surgical route taken, and surgeon preference. Regardless assess for air leaks originating from either system faults
of these considerations there will always be a retrosternal/ or patient leaks. When bubbling can be attributed to the
anterior mediastinal drain, as the sternum is generally the patient, the patency of tubes becomes additionally impor-
major source of bleeding in the absence of complications. tant to avert tension pneumothorax, which may accumu-
Additional drains may be inserted in the pericardial or late rapidly, even over the course of a few breaths in the
pleural spaces. Pericardial drains are more likely to be ventilated patient.
inserted following aortic valve surgery, while pleural Blood transfusions are not aimed at restoring haemoglo-
drains become necessary following mammary artery har- bin to normal levels, and, despite variations in acceptable
vesting or when the pleura is opened for any other reason. levels, relative anaemia is almost universally tolerated.
Pleural drains may be anterior, posterior, or ‘wrap-around’ Haemoglobin levels are thus not routinely treated unless
configurations in which they project over the anterior below 80 g/L, except in the elderly or when there are
lung, following the pleural space first from midline, to significant comorbidities. 19,32 From these levels patients
lateral and then finally the posterior pleural space.
return to normal haemoglobin status within 1 month
Reportable postoperative blood losses vary, but greater postoperatively. 32
than 100 mL/h, or greater than 400 mL in the first 4
hours, would generally be regarded as excessive and
worthy of surgeon notification. Importantly, excessive Contributors to impaired haemostatic capability
bleeding does not always represent a surgical defect that Many factors may contribute to postoperative bleeding by
reoperation might correct, as there are many contributors their influence on coagulation and haemostatic ability.
to impaired haemostatic capability in the cardiac surgical CPB is used in the majority of cardiac surgical cases and
patient (see below). exerts many influences on coagulation, as do additional

300 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

factors such as preoperative medications, anaemia or including full blood examination, clotting profile and
coagulopathies. Contributing factors include: measures of fibrinolytic activity.
● cardiopulmonary bypass influences:
● heparinisation, haemodilution, platelet damage Heparin reversal
and altered function Cardiopulmonary bypass requires full heparinisation
32
● disseminated intravascular coagulation (DIC) (initially 300 IU/kg), which is reversed at end-operation.
following activation of the systemic inflammatory The specific antidote, protamine sulphate, is adminis-
response syndrome post-CPB tered as bypass is ceased, at a dose of 1 mg per 100 units
32
● preoperative anticoagulant/antiplatelet medications heparin used (i.e. 3 mg/kg). If reversal is less than com-
commonly encountered plete, as evidenced by a prolonged ACT, further prot-
● aspirin, coumadin, clopidogrel amine sulphate (at doses of 25–50 mg over 5–10 minutes)
● preoperative anaemia due to aortic valve disease, may be necessary.
autologous blood donation or the various chronic
anaemias Management of bleeding
● clotting factor deficiency Treatment approaches to bleeding once the patient is in
● hypothermia intensive care include further protamine administration
● coexisting coagulopathies if the ACT remains prolonged, blood and blood product
● increased fibrinolytic activity administration (platelets, clotting factors, fresh frozen
● surgical defects such as failure of access site closure, or plasma), procoagulants (desmopressin acetate) and anti-
vascular anastomosis defects. fibrinolytic agents (see Table 12.2 for more details).
Other general measures such as rewarming the patient
and preventing or treating hypertension should be
Bedside assessment of bleeding undertaken.
The activated clotting time (ACT) is the most commonly
used assessment of coagulation and heparin activity Autotransfusion
during cardiac surgery and subsequently in intensive care. Chest drain systems used in cardiothoracic surgery can be
It measures the time to onset of fibrin formation (initial configured for retransfusion of collected blood during
clot development). The ACT has been valuable because it rapid blood loss. If losses are fresh, and are collected with
can be inexpensively and efficiently performed at the reliable sterility, they can be transfused back into the
bedside, providing prompt results and requiring only patient. Blood that has been collected and left standing
modest personnel training. Bleeding patients with a pro- in the drain receptacle rapidly becomes unsuitable for
longed ACT come under consideration for administration retransfusion, and so autotransfusion is generally limited
32
of protamine or other agents. Treatable levels vary from to blood that has collected over 1–2 hours, rarely longer.
greater than 120 sec to greater than 150 sec among dif- Blood filters should always be used for protection against
ferent centres. clots that may have developed in the drain receptacle.
A limitation of ACT measurements is that they provide Assessment and Management of
no information about clotting processes beyond initial
fibrin formation, so clotting deficits such as impaired clot Pericardial Tamponade
strength or the presence of significant fibrinolysis as con- Postoperative pericardial tamponade results from the
33
tributors to bleeding are not revealed by this test. By accumulation of blood or effusion fluid within the peri-
contrast, the thromboelastograph (TEG) measures the cardium. An increasing volume within the pericardial
33
clotting process as it proceeds over time. TEG monitor- space eventually compresses cardiac chambers, impeding
ing not only reveals abnormalities early in the clot process venous return and therefore causing low cardiac output
(time to fibrin formation, as would be demonstrated by and hypotension. Pericardial tamponade is an emergency,
the ACT) but also the subsequent development of clot and varies in severity from shock to pulseless electrical
strength, clot retraction, and finally fibrinolytic activity activity.
33
for each of their contributions in the bleeding patient. Described as one of the extra-cardiac obstructive shocks,
TEG monitoring, although considerably more expensive pericardial tamponade often resembles cardiogenic
than the ACT, is now available as a bedside or operating shock. The low cardiac output and hypotension result in
room technology and offers better insight into bleeding oliguria, altered mentation, peripheral hypoperfusion
causes. In addition, because TEG monitoring identifies and development of lactic acidosis. Compensation
deficiencies at the various stages of clot formation, devel- includes tachycardia and marked vasoconstriction, elevat-
opment of clot strength and the presence of undue ing the systemic vascular resistance. As in cardiogenic
fibrinolytic activity, it may permit better matching of shock, there is usually elevation of the filling pressures
procoagulant, blood product or antifibrinolytic therapy (right atrial, pulmonary artery and pulmonary capillary
to needs. 33
wedge pressures), sometimes with a particularly sugges-
No matter which of the above technologies is used at the tive merging of the pulmonary artery diastolic, right atrial
23
bedside, the patient with significant bleeding should be and pulmonary artery wedge pressures. Additional fea-
evaluated more fully as soon as bleeding develops. Blood tures that may be present include muffled heart sounds,
should be drawn and sent for laboratory assessment, decreased QRS voltage, electrical alternans, narrowing

Cardiac Surgery and Transplantation 301



TABLE 12.2 Management of the bleeding patient post-cardiac surgery 21,22,25,33,34,44

Therapy Dose Comments/issues
Protamine sulphate 25–50 mg slow IV (<10 mg/min); Specific antidote to heparin. May cause hypotension.
may be repeated if ACT prolonged Contraindicated in patient with seafood allergy.
Aprotinin (Trasylol) continuous infusion of 2 million units Antifibrinolytic. Proteinaceous. Anaphylaxis risk on
over 30 min, then 500,000 units re-exposure. Alert should be posted on history.
per hour
Desmopressin acetate (DDAVP) 0.4 mcg/kg IV Promotes factor VIII release; limited evidence for use.
‘Pump blood’ (blood retrieved from often 400–800 mL This is the remaining blood in bypass circuit; usually
bypass circuit at end-operation) centrifuged before returning to patient; note: this
blood contains heparin from CPB.
Whole blood/packed cells as necessary to achieve Hb >80 g/L Autologous blood sometimes available when patients
or more according to needs have donated blood preoperatively.
Fresh frozen plasma as necessary ‘Broad-spectrum’ factor replacement; contains most
factors. Useful adjunct to massive blood transfusion.
Platelet concentrates as necessary Generally ABO and Rh compatible preferred.
Epsilon-aminocaproic acid (Amicar) 100 mg/kg IV followed by 1–2 g/h Antifibrinolytic. Inhibits plasminogen activation.
Cryoprecipitate 10 units IV Contains factor VIII and fibrinogen (factor I).
Calcium chloride or gluconate 10 mL 10% solution Used to offset citrate binding of calcium in stored blood.
Prothrombinex 20–50 IU/kg IV Contains factors II, IX and X.




pulse pressure and pulsus paradoxus, along with features loops, or side-to-side rolling of the patient to possibly
of increasing anxiety and/or dyspnoea in the awake bring collections into proximity of drain tubes. When
patient. tube patency is in doubt, the surgeon may even pass a
suction catheter through the chest drain under aseptic
Echocardiography is the definitive assessment tool to conditions in an attempt to remove clots at the drain tip.
23
reveal the presence of pericardial collections as well as If the above measures do not relieve tamponade, consid-
identifying the impact on relaxation, filling and contrac- eration is given to re-exploring the pericardium, either by
tion of each cardiac chamber. The chest X-ray is of limited returning to the operating theatre or, in an emergency, to
use and may show little, even with significant pericardial the intensive care unit, although this is less preferable.
collections.
Emergency opening of the sternotomy and mediastinal
Importantly, the ‘classic’ or typical haemodynamic profile re-exploration requires a coordinated team response, and
described above is not uniformly seen in tamponade, and where possible operating room staff should be included
tamponade should never be excluded because the hae- to manage the sterile field and assist the surgeon. Equip-
modynamic status does not match this profile. This may ment and disposable materials should be counted and
be because classic tamponade implies uniform compres- documented in the manner normally applied in theatre.
sion of the entire heart, which may not be the case with When the situation has been stabilised, consideration
haemorrhagic tamponade. A clot may develop over just should be given to returning to theatre for final assess-
one chamber rather than occupying the entire pericar- ment and chest closure.
dium, and so there may be compromise to only a single
chamber rather than the whole heart. 21,23

Management of pericardial tamponade
The management of pericardial tamponade includes
limiting further losses into the pericardium, relief of Practice tip
pericardial pressure through evacuation of blood or
clots, and management of the haemodynamic impact Given the variability of presentation of cardiogenic shock, and
of tamponade. the importance of accurate identification, clinicians should
search for tamponade whenever there is haemodynamic insta-
Steps to control bleeding and blood pressure as described bility postoperatively, especially when the haemodynamic
above may limit further losses into the pericardium. All status does not match classic patterns for the major shock
steps should be taken to maintain or re-establish chest states. The management of postoperative cardiac arrest accom-
tube patency (crushing clots within tubing, ‘milking’ panying any arrhythmia, as well as pulseless electrical activity,
when it is truly necessary) and to ensure free flow of should include consideration of tamponade.
blood from the chest by avoiding dependent tubing

302 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

Assessment and Management of Regardless of low mortality rates, the possibility of death
Postoperative Pain and painful wounds can concern patients. Consequently,
As much an art as a science, pain control in the cardiac patients undergoing cardiac surgery often experience
surgical patient remains a major challenge and continues anxiety and depression, which can be distressing for
37–39
to provide uncertainty and opportunities for nursing cli- patient and family. Women appear to be more vulner-
nicians and researchers. Principles are similar to those able to these emotions in relation to cardiac surgery than
40
outlined in Chapter 7. Surgical pain, often complicated men. Although it is normal and potentially protective
by pericardial inflammation, results in differing pain to experience anxiety, higher levels of these emotions can
types, requiring different approaches. These different be destructive. Anxiety and depression are predictive of
34
approaches to pain management must be balanced worse postoperative outcomes, including poorer psycho-
against the promotion of spontaneous breathing, chest social adjustment and quality of life, more cardiac symp-
41
physiotherapy, mobilisation, and participation in educa- toms and readmissions. Therefore, it is essential to
tion and lifestyle modification programs. consider and address anxiety and depression when pro-
viding care for cardiac surgical patients.
Analgesic options include intravenous, oral or rectal anal- Preoperative preparation provided by nurses usually
gesics, antiinflammatories and, less commonly, epidural incorporates information and support, so that patients
therapies and nerve blocks. Intravenous opiates and and their families are familiar with procedures and can
codeine/paracetamol preparations provide the mainstay cooperate during recovery. However, seeing a patient
42
of postoperative analgesia. When insufficient, or when who is successfully recovering from surgery may instil
clinical and electrocardiographic features suggest pericar- more confidence. Patients who have had their surgery
ditis, antiinflammatory agents such as rectal indometha- postponed or who have been operated on in an emer-
cin are appropriate. The place of IV COX-2 inhibitors gency setting may need additional support. For many
such as parecoxib appear uncertain, as analgesic efficacy patients, fast-track procedures, including admission on
now must be weighed against emerging data suggesting day of surgery, early extubation and early discharge pro-
increased thrombotic complications. 35
cesses, decrease the discomfort associated with being
Fluid and Electrolyte Management away from home and surgical costs. For other patients
there is too little time to be informed and understand
Fluid therapy in the postoperative period is aimed at postoperative and post-discharge care. Also, critical path-
maintaining blood volume, replacing recorded and ways for cardiac surgery do not include assessing the
insensible losses, and providing adequate preload to patient’s psychological state, so nurses must take care to
sustain haemodynamic status. Isotonic dextrose solu- consider this aspect. Consequently, family members
tions (5%) or dextrose 4% + saline 0.18% are commonly assume an important role in supporting patients and
used at approximately 1.5 L/day as maintenance fluids. 14
helping them understand recovery requirements. It is
Potassium replenishment is generally necessary accord- vital that family members understand and anticipate a
ing to measured serum potassium. Polyuria is usually certain amount of anxiety and depression, particularly in
evident in the early postoperative period due to deliber- the first week post-discharge. Family members may also
ate haemodilution while on cardiopulmonary bypass. be distressed by seeing their loved one ill and the unfa-
With polyuria comes potassium losses, which must be miliar ICU environment and equipment, so the addi-
treated to avert atrial or ventricular ectopy and tachyar- tional requirement for them to assess and support the
rhythmias. Because of these predictable potassium losses, patient may be onerous. Printed information regarding
protocols for potassium replacement may be instituted, the surgery, recovery and emotions will be useful for the
with standing orders for potassium replacement (e.g. patient and family.
10 mmol over 1 hour if the serum potassium is
<4.5 mmol/L, or 20 mmol over 2 hours if <4.0 mmol/L). INTRA-AORTIC BALLOON PUMPING
Main line hydration infusions may also have added
potassium to avoid hypokalaemia. Hypomagnesaemia Intra-aortic balloon pumping (IABP) is a widely-used cir-
may also develop due to polyuria, and is likewise proar- culatory assist therapy that has become straightforward
rhythmic. Supplementation (magnesium chloride) is in application and relatively free of complications. 43,44
often used for arrhythmia management postoperatively, The primary aim of IABP is to assist restoring an existing
but its effectiveness has been questioned in many trials. 36 imbalance between myocardial oxygen supply and
demand. The main indications are for cardiogenic shock,
Hyperkalaemia occurs less often but is seen particularly myocardial infarction or ischaemia and weaning from
when there is impaired renal function. Additional con- cardiopulmonary bypass. The combined effects of increas-
tributors to a rising potassium level include acidosis, ing cardiac output and mean arterial pressure (increasing
administration of stored blood, haemolysis, inotrope use, oxygen supply) and decreasing myocardial workload
and any postoperative use of depolarising muscle relax- (reducing oxygen demand) make IABP therapy ideal for
ants such as suxamethonium.
the management of infarct-related cardiogenic shock,
45
Emotional Responses and Family Support for which IABP should be regarded as a standard
The experience of being diagnosed with a cardiac disor- management.
der, waiting for surgery, the surgical experience and recov- IABP therapy involves placement of a balloon catheter in
ery is an emotional journey for patients and their families. the descending thoracic aorta. This catheter is most

Cardiac Surgery and Transplantation 303




































FIGURE 12.4 Intra-aortic balloon catheter. On the left the inflated catheter can be seen behind the heart, with its tip below the arch of the aorta and the
left subclavian artery. The balloon cycles between inflated (during diastole), and deflated (during systole) as on the right above. Blood fills the aorta while
the balloon is deflated, and with inflation the balloon almost fills the descending aorta, displacing 40 mL blood from the aorta to the coronary and systemic
circulation. (Courtesy Datascope Corporation, Fairfield, NJ).



which opens at the catheter tip from which the aortic
pressure waveform is monitored; and a helium drive
lumen, through which the helium is shuttled from
the pumping console to the catheter balloon. Balloon
volumes range from 25 mL (paediatric use) and 34–
50 mL in adults (most commonly used is 40 mL balloon)
and selected according to patient height (40 mL balloon
is used for a patient height of 162–183 cm).
PRINCIPLES OF COUNTERPULSATION
When pumping is initiated, the balloon will be
inflated rapidly at the onset of diastole of each cardiac
cycle and then deflated immediately just before the
onset of the next systole; this sequence is referred to as
counterpulsation.
Balloon Inflation

At the onset of diastole, the balloon is rapidly inflated
with (most commonly) 40 mL helium. This inflation
causes a sudden rise in pressure in the aortic root during
FIGURE 12.5 IABP catheter position in CXR, the tip is located in second
intercostal space anterior ribs or fifth intercostal space posterior ribs. diastole, raising mean arterial pressure and, importantly,
coronary perfusion pressure. The blood displaced by
the balloon expansion improves blood flow into the
commonly advanced from a percutaneous femoral artery coronary circulation (which fills largely during diastole),
access until the tip of the catheter is situated just below as well as to the brain and systemic circulation. Thus there
the left subclavian artery (Figure 12.4). A chest X-ray or is improved myocardial oxygen supply, increased mean
46
fluoroscopy should reveal the catheter tip just below the arterial pressure, as well as improved systemic perfusion.
aortic arch, or at the level of the second anterior intercos- The balloon remains inflated for the duration of diastole.
tal space or fifth posterior intercostal space (Figure 12.5). The arterial pressure wave should reveal a sharp rise in
The catheter has two lumens – a monitoring lumen, pressure at the dicrotic notch, with a second pressure

304 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



































FIGURE 12.6 IABP during 1 : 1 assist (counterpulsation on every beat). Balloon inflation at the start of Diastole and deflation just before next systole. IABP
during 1 : 2 assist (counterpulsation on every second beat). Inflation of the balloon rapidly at the inflation point (IP) raises diastolic pressure, producing a
peak diastolic pressure (PDP) that exceeds the systolic pressure (PSP). The balloon remains inflated during diastole. With balloon deflation just prior to the
next systole there is a rapid decline in pressure to the balloon-assisted end-diastolic pressure (BAEDP), which is lower than normal, reducing afterload. The
ensuing systole is achieved with a reduced systolic pressure (the assisted peak systolic pressure, APSP).




peak now appearing on the waveform, described as the Real timing
‘augmented diastolic’ or ‘balloon-assisted peak diastolic’ In contrast to conventional timing, during real timing
pressure. This peak is usually at least 10 mmHg higher (also referred to as R wave deflate) the balloon remains
than the systolic pressure (Figure 12.6). inflated for slightly longer, and is deflated not before but
at the same time as systole. The reduction in aortic end-
Balloon Deflation diastolic pressure is therefore not seen, but deflating
As the inflated balloon largely obstructs the aorta, it must simultaneously with left ventricular contraction still
48
be deflated to permit systolic emptying of the left ven- favourably effects left ventricular emptying. Thus there
tricle. Two separate approaches to the timing of balloon is improved stroke volume, systolic pressure reduction,
deflation have emerged: ‘conventional timing’, and ‘real and decreased ventricular work and oxygen demands as
47,49
timing’. seen during conventional timing. Box 12.1 sum-
marises the impact of balloon inflation and deflation on
haemodynamic status and the oxygen supply:demand
Conventional timing balance.
In conventional timing, the balloon is deflated immedi- The arterial pressure wave reveals the impact of IABP
ately prior to systole. Rapid deflation induces a precipi- therapy on haemodynamic status. Placing the pump into
tous drop in aortic pressure at the end of diastole (a 1 : 2 assist (balloon pumping on only every second beat)
reduced aortic end-diastolic pressure). This reduces the is useful to highlight balloon pump impact and how
duration of the left ventricle isovolumetric contraction assisted beats vary from the normal pressure cycle during
phase of cardiac cycle (most oxygen consuming phase of systole and diastole. Figure 12.6 depicts the impact of
cardiac cycle), left ventricular afterload and improves left IABP on haemodynamic status and the arterial pressure
ventricular emptying, improving stroke volume and waveform.
cardiac output. 46,47 In addition, less pressure is required
for left ventricular emptying, so systolic work and oxygen
demands on the myocardium are reduced. Thus defla- COMPLICATIONS OF INTRA-AORTIC
47
tion during conventional timing should see the aortic BALLOON PUMPING
pressure drop to below normal at end-diastole, just in Serious complications are uncommon during IABP treat-
advance of the subsequent systole. Systolic pressure ment and continue to decrease in frequency in the last
should be lower than during non-assisted beat. decade with advances in pump technology and smaller

Cardiac Surgery and Transplantation 305

usually undertaken if indicated and according to specific
BOX 12.1 Effects of intra-aortic balloon hospital protocol (no literature available to support sys-
counterpulsation temic heparinisation).
Hourly assessments of peripheral perfusion (colour,
Balloon inflation warmth, movement, sensation) should be performed to
● increased aortic diastolic pressure (augmented, or balloon- identify potential deficits. Dorsalis pedis and posterior
assisted peak diastolic pressure, BAEDP) tibialis pulses should be palpated and may sometimes
● increased mean arterial pressure require examination with a Doppler probe. Deficits
● increased myocardial perfusion and oxygen supply should be promptly reported and consideration given
● increased cerebral and systemic perfusion to catheter removal or reinsertion on the contralateral
limb. When pulses cannot be demonstrated, the limb
Balloon deflation should be assessed for the development of compartment
● decreased afterload syndrome. At times the viability of a limb must be
● increased stroke volume and cardiac output weighed against the potential survival benefit of IABP to
● decreased LV congestion, decreased PCWP, decreased the patient.
pulmonary congestion
● decreased left ventricular workload
● decreased systolic pressure Prevention and Treatment of Bleeding
● decreased myocardial oxygen demand Significant bleeding is uncommon, but blood loss may
51
● decreased duration of isovolumetric contraction occur from the femoral arterial access site. In addition
to physical factors at the insertion site, contributors to
bleeding include heparinisation, thrombocytopenia from
the physical effect of the pump on platelets, and/or other
anticoagulants or antiplatelet agents used for the primary
50
catheter size. Limb ischaemia remains the commonest disease. Regular observation should be made of the inser-
serious complication, especially in patients with existing tion site for bruising or external bleeding, as well as
51
vasculopathy, providing impetus to the development of other possible sites of bleeding due to heparinisation.
smaller catheters, which have now reached 7.5 French Treatment includes pressure at the insertion site (includ-
gauge. Additional complications, such as bleeding, ing the use of sandbags), reinforcement of dressings,
catheter migration, thromboembolism, insertion-site and/or topical procoagulant agents. Monitoring of coagu-
vascular damage, thrombocytopenia and device-related lation status and haemoglobin should be undertaken
problems such as timing inaccuracy, device failure and and blood or blood products may (uncommonly) be
gas leaks, also occur but are less common. These are required.
described below.
Prevention of Immobility-related
NURSING MANAGEMENT Complications

Prevention of complications, as well as optimisation of The need for immobilisation of the patient, and in par-
the impact of counterpulsation, form the major compo- ticular the leg, is often overemphasised, and may heighten
nents of nursing care of a patient being treated with IABP. the risk of atelectasis, pressure area development and
Thorough understanding of the impact of the presence of venous stasis and thrombosis. Sensible limitation of leg
the balloon, as well as the beneficial and detrimental movement is advised, but patients can generally still
effects of counterpulsation, is essential. move in bed, and should still be turned 2-hourly for pres-
sure relief as long as the insertion site is adequately pro-
Maintenance of Limb Perfusion tected and supported. The femoral access limits flexion at
The use of smaller-gauge catheters has reduced the poten- the hip beyond 30 degrees, which may also hamper effec-
tial for obstruction of arterial flow past the catheter to the tive chest physiotherapy and increase the risk of atelecta-
lower limbs, as has the trend to sheathless insertion. sis and pneumonia.
Nevertheless, the threat of limb ischaemia remains an Migration of the balloon catheter towards the aortic
important issue in patient care, as IABP is most com- arch or towards the abdominal aorta may cause com-
monly undertaken in patients with atherosclerosis, promised perfusion to left arm (occlusion of left sub-
potentially involving the lower limbs, even in the absence clavian artery), kidneys (renal arteries) or abdominal
of overt peripheral vascular deficits. Identification of viscera (superior mesenteric artery). Therefore, neuro-
patients at risk (known claudication, chronically cold feet vascular observation of upper limbs, urine output and
and peripheral vascular diseases) may be useful to ensure bowel sounds are part of nursing management of patient
appropriate vigilance and prompt intervention where with IABP in situ.
necessary. Peripheral perfusion may also be compromised
by arterial embolisation should thrombi develop on
the catheter. Although catheter materials are non- Weaning of IABP
thrombogenic, the risk of thrombi formation remains Weaning of intra-aortic balloon pumping therapy is gen-
and is heightened if periods of catheter stasis (interrupted erally undertaken once the patient has stabilised, is free
pumping) are encountered. Systemic heparinisation is of ischaemic signs and symptoms and is on minimum or

306 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

no inotropic support. Algorithms have been offered for should be set to ‘earlier’ until the inflation upstroke
52
approaches to weaning therapy, but their impact on emerges smoothly out of the dicrotic notch.
weaning duration or success has not been studied.
Weaning is carried out by either gradual reductions in Early deflation
balloon inflation volume (volume weaning) or gradual Deflating the balloon earlier than necessary shortens the
reductions in assist frequency from 1 : 1 through 1 : 2 and duration for which the balloon remains inflated and
1 : 4 (ratio weaning). Hybrids of the two approaches are therefore limits the benefit of IABP. When deflation is
sometimes used. Support is reduced at intervals while the very early, it may cause harm. Deflation sees the aortic
patient is observed for haemodynamic deterioration, pul- pressure drop markedly but there is now time for blood
monary congestion, or the return of ischaemic signs and to fill the space left by the balloon before systole com-
symptoms. mences. Aortic end-diastolic pressure increases and may
Assessment of Timing and Timing Errors even exceed the normal end-diastolic pressure, increasing
Accurate timing of inflation and deflation in relation to the duration of isovolumetric phase, worsening left
ventricular afterload and increasing myocardial oxygen
the cardiac cycle is required to maximise IABP benefit. demand (Figure 12.9). Correction is achieved by setting
Errors in timing may lessen the potential benefit, or in deflation to later until the pressure drop of deflation
some cases may worsen cardiac performance and increase occurs just in advance of the succeeding systole.
demands on the myocardium. Nurses are required to
continually assess the haemodynamic impact of balloon Late deflation
pumping, the accuracy of timing via inspection of the
arterial pressure waveform, and to adjust timing to opti- When deflation begins too late, systole commences before
mise the impact of balloon pumping. complete emptying of the intra-aortic balloon. The typical
reduction of aortic end-diastolic pressure is not seen.
Early inflation When significantly late, the end-diastolic pressure may
Early inflation will at times be difficult to differentiate even be increased prolonging the duration of the isovolu-
from correct inflation timing but is recognised by the metric contraction phase, and worsening afterload. As
onset of inflation soon after the peak systolic pressure, systole occurs against an incompletely deflated balloon,
before the pressure has declined to the level of the dicrotic the stroke volume and cardiac output suffer and ventricu-
notch (Figure 12.7). Early inflation may limit the stroke lar work and oxygen demand increases (Figure 12.10).
volume and cardiac output, as terminal systole is impeded Deflation should be set to earlier until the systolic
and may result in increased myocardial oxygen demands. upstroke emerges out of the reduced end-diastolic pres-
The inflation point should be adjusted (to later) until the sure dip.
inflation upstroke emerges smoothly out of the dicrotic
notch.
ALARM STATES
Late inflation Alarm functions vary according to manufacturer and
The arterial pressure waveform reveals the onset of model. The main alarm states common to most devices,
diastole (the dicrotic notch) before balloon inflation and their causes and significance, are shown in Table
commences (Figure 12.8). This generally results in a 12.3. Importantly, in most alarm states the pump con-
lower augmented diastolic pressure than could otherwise soles will revert to standby, suspending pumping. The
be achieved. As the duration of balloon inflation is less- balloon is at risk of developing thrombi within the folds
ened, the desired rise in mean arterial pressure and coro- of the balloon while deflated, and these can be liberated
nary perfusion will not be achieved. The inflation marker as arterial emboli on recommencement of pumping. It is























FIGURE 12.7 IABP during 1 : 2 assist. Early inflation. The inflation point (IP) can be seen high in the downstroke of systole, in this case well before the
dicrotic notch (DN).

Cardiac Surgery and Transplantation 307



































FIGURE 12.8 IABP during 1 : 2 assist. Late inflation. Note that the inflation point (IP) occurs well after the dicrotic notch (DN). Late inflation is also obvious
in 1 : 1 assist with balloon inflation well after the dicrotic notch.




































FIGURE 12.9 IABP during 1 : 2 assist. Early deflation. The balloon has been deflated well in advance of the subsequent systole. The aortic pressure does
drop off (not much from non assisted diastole) but then begins to rise again before the next systole gets underway, and may even exceed the normal
end-diastolic pressure. Early deflation is also obvious in 1 : 1 assist.


important to treat alarm states promptly, to limit the Gas loss alarms
duration of balloon stasis. If interruption to pumping is Most devices will determine the severity of gas losses and
prolonged, intermittent manual inflation of the balloon classify them as slow, rapid or disconnect. In all gas loss
with a syringe is recommended (e.g. once every 5–10 states it is imperative that assessments be made to exclude
minutes). balloon rupture and helium leak into the arterial

308 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

















FIGURE 12.10 IABP during 1 : 2 assist. Late deflation. The late deflation is seen here as the sharp drop-off before systole and a balloon assisted end diastole
that does not fall to below the normal patient end-diastolic pressure.



Patients with certain chronic heart, respiratory and lung
diseases may be referred for organ transplantation assess-
,ĞůŝƵŵ ĚƌŝǀĞ ůŝŶĞ ment when their disease state is such that their life expec-
ĨƵůů ŽĨ ďůŽŽĚ tancy is less than 2 years and quality of life intolerable.
Patients who receive organ transplants are commonly
debilitated and may have an acute on chronic presenta-
tion at the time of surgery. The surgical procedure is
lengthy, up to 12 hours, and involves cardiopulmonary
bypass. The duration and nature of the surgery in patients
ZƵƉƚƵƌĞĚ with severely compromised health status serves to com-
ďĂůůŽŽŶ pound the often critical condition of such patients in the
early postoperative period.
FIGURE 12.11 Intra-aortic balloon rupture and presence of blood in
helium drive line. The immediate period following surgery is commonly the
first contact that critical care clinicians have with trans-
plant recipients and their families. The exception may be
patients awaiting heart transplantation who are sup-
ported by an intra-aortic balloon pump or mechanical
circulation. Small gas losses of helium may or may not circulatory support (MCS) also known as a ventricular
be of clinical significance, but the delivery of sizeable assist device (VAD) as a ‘bridge to transplantation’ (see
helium volumes may behave as gas emboli, and if deliv- Figure 12.12). Ideally, patients with MCS are returned to
ered into the coronary circulation may result in lethal a sound physical, mental and nutritional state prior to
arrhythmias or result in neurological complications if receiving a transplant, and, as part of their recovery, await
delivered into the cerebral circulation. In all gas loss transplantation in the ward or home setting. For specific
alarm states, the helium drive line should be inspected management of patients on MCS, readers are referred to
for the presence of blood to indicate loss of integrity of specific resources (e.g. websites and operating manuals
the balloon. If blood is present in the drive line (Figure for individual MCS: HeartMate, Throratec, VentrAssist
12.11), pumping should be suspended and no attempts and DuraHeart).
at recommencing balloon pumping should be made.
Prompt removal and/or replacement, along with thor- Heart transplantation is a life-saving and cost-effective
ough patient assessment, is essential. form of treatment that enhances the quality of life for
many people with chronic heart failure. Legislation that
defined brain death and enabled beating-heart retrieval
HEART TRANSPLANTATION was enacted in Australia from 1982. This legislation her-
alded the establishment of formal transplant programs.
The ultimate goal of organ transplantation is to provide
an improved quality of life and long-term survival for In Australia, the first heart program commenced in
53,54
patients with end-stage heart disease. To optimise patient 1983. The success of transplantation in the current era
outcomes, the early postoperative management of these as a viable option for end-stage organ failure is primarily
patients requires critical care clinicians with specific due to the discovery of the immunosuppression agent
55
expertise to collaborate with a multidisciplinary team cyclosporin A. In this section, heart transplantation as
of health professionals. In the following sections, the a component of critical care nursing is discussed, with
important management issues in the early postoperative reference to evidence-based practices.
period for heart transplant recipients are discussed. The
major long-term complications of heart transplantation HISTORY
are also discussed briefly as survivors may be readmitted Heart transplant surgery for refractory heart failure was
to critical care with life-threatening complications years first performed in Australia in 1968, only months after
after their transplant. the first heart transplant was performed in South Africa

Cardiac Surgery and Transplantation 309



TABLE 12.3 Intra-aortic balloon pump alarm states

Alarm state Causes/significance
Catheter alarm ● Obstruction (complete or subtotal) of the catheter, drive line or balloon
● Device reverts to standby (non-assist); commonly due to catheter flexion at insertion site due to limb position
or excessive surface to vessel depth
Loss of trigger ● ECG trigger: signal disrupted or low in amplitude, or asystole
● Pressure trigger: pulse pressure below threshold for detection
● Pacer trigger: pacing spikes not detected or absent (including demand pacing)
● Device reverts to standby until restoration of trigger; alternative trigger selection may be necessary
Gas loss alarms ● Leak in circuit/drive line or balloon; gas leak may be to the environment or into the patient as
a helium embolus
● Pump reverts to standby; refilling of circuit may be necessary
Low augmentation ● Augmented diastolic pressure is lower than operator-selected alarm level; pumping is not interrupted
Pneumatic drive ● Functional problem with the pump inflation/deflation pneumatic system
● Device reverts to standby; alarm may sometimes be activated during tachycardia; 1 : 2 assist or assist at reduced
augmentation may be possible until a replacement device is accessed
Autofill failure ● Routine 2-hourly refilling of the system with helium may fail if gas tank is incompletely open or if circuit leaks
cause volume loss during the filling attempt
● Device reverts to standby
System failure ● Console self-testing has identified component malfunction
● Device reverts to standby; restarting may be possible but a replacement device should be accessed
Low helium supply ● Helium tank empty or incompletely opened
Low battery ● Reconnect to power and recharge






56
60
in December 1967. However, high mortality rates asso- management of patients and their carers. Advances in
ciated with severe acute rejection and infection within device design and capability, e.g. fully implantable with
months of surgery led to a reduction in the number of internal batteries, are likely to be required for this option
heart transplants performed worldwide, and in effect a to be truly viable.
moratorium occurred with the procedure. Heart trans-
plantation was finally established in the modern era as a
viable treatment option for end-stage heart failure during OUTCOMES FROM HEART TRANSPLANTATION
the early 1980s when cyclosporin A, a then-novel immu- Currently, the top centres around the world achieve
nosuppressive agent, dramatically improved patients’ sur- survival rates for heart transplant patients approaching
vival rates by reducing episodes of acute rejection and 80–90% at one year, with more than 50% of patients
lowering attendant infectious complications. 57 surviving longer than 11 years. In Australia and
61
New Zealand, approximately 85% of heart transplant
INCIDENCE patients survive to 1 year and 75–80% survive more
62,63
Heart transplants in the modern era have been performed than 5 years.
in Australia since 1986 and in New Zealand since 1987.
In 2009, 72 heart transplants were performed in Australia
58
and New Zealand. As the annual number of transplants INDICATIONS
globally is likely to remain relatively stable because of The vast majority of patients referred for heart transplan-
limited organ availability, future routine management of tation have NYHA functional class III or IV symptoms
end-stage heart failure may involve the insertion of a left (see Chapter 10), secondary to ischaemic heart disease or
ventricular assist device (LVAD) designed for long-term some form of dilated cardiomyopathy. 64,65 Commonly,
permanent mechanical circulatory support, so-called patients listed for transplantation have a life expectancy
‘destination therapy’. Indeed, there have been clinical of less than 2 years without transplantation. Accepted
trials that include destination therapy since the success of contraindications for heart transplantation include active
66
67
68
59
LVADs in the REMATCH study. In the past decade, malignancy, complicated diabetes, morbid obesity,
LVADs available have been used primarily as ‘bridge to uncontrolled infection, active substance abuse and an
transplantation’ therapy (i.e. support for a failing native inability to comply with complex medical regimens. 69,70
heart until a suitable heart becomes available), not ‘des- Age has become a relative contraindication, with 16 days
tination therapy’. The implementation of destination old being the youngest and 71 years of age being the
64
therapy will require nurses to gain skills in the long-term oldest. However, the presence of multiple comorbidities

310 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




Left side battery
omitted for clarity



Aorta


Heart


External
battery
pack

A
XVE
LVAD


Skin
line
Vent adapter &
XVE System vent filter
B controller










FIGURE 12.12 Mechanical circulatory support VADs: (A) Thoratec®USA LVAD and
RVAD; (B) HeartMate®USA; (C) VentrAssist ((A) and (B) Courtesy Thoratec Corpora-
tion (C) Courtesy Ventracor Limited).











C



in patients over 70 years of age would be expected to Patients referred for heart transplant assessment must
exclude the majority of such patients from consider- have exhausted all other accepted pharmacological and
ation. 66,71 Other relative contraindications include renal surgical treatment options for end-stage heart failure,
failure and an irreversible high transpulmonary gradient such as optimal therapeutic doses of common heart
(mean pulmonary artery pressure minus pulmonary failure medications; revascularisation via coronary artery
72
artery wedge pressure) of greater than 15 mmHg (see bypass graft surgery or percutaneous transluminal
section on Early allograft dysfunction and failure later in coronary angioplasty; continuous IV infusions of
this chapter). In the context of a rigorous postoperative do butamine in the community/home setting; IV levo-
regimen of polypharmacy, frequent follow-up medical simendan (a calcium sensitiser); antiarrhythmic drugs
appointments and routine cardiac biopsies, a strong to suppress, or an internal cardiac defibrillator to
social support network, absence of psychiatric illnesses treat, potentially lethal arrhythmias; and insertion of
and a willingness to participate actively in the recovery a biventri cular pacemaker (i.e. chronic resynchronisa-
process are highly desirable characteristics of prospective tion therapy) to re-establish atrioventricular synchrony
recipients. 72 (see Chapter 11).

Cardiac Surgery and Transplantation 311

The average costs associated with heart transplantation can be configured to support biventricular function
are high, at approximately $A35,000 for the first year and (BiVAD configuration). The LVAD configuration for
58
$A15,000 for each ongoing year. However, the high heterotopic heart transplantation is illustrated in
incidence of chronic heart failure and associated hospi- Figure 12.15.
talisation costs are also considerable. During 2000, it was
estimated that over half a million Australians had chronic
heart failure (CHF), with 325,000 patients per annum CLINICAL PRACTICE
73
experiencing symptoms. Hospital admissions for heart Postoperative nursing and collaborative management of
failure were estimated at 100,000, totalling more than 1.4 orthotopic heart transplant recipients involves full hae-
million days, figures that represent prevalence rates of modynamic monitoring with a pulmonary artery catheter
73
526 hospitalisations and 7400 days per 100,000/annum. (PAC), a triple- or quad-lumen central venous catheter
The cost of a single hospital admission for CHF in Aus- (CVC), arterial line, indwelling urinary catheter, and
74
tralia is currently approximately $A6000. In 2006, 5-lead cardiac monitoring to assist in dysrhythmia dis-
approximately 263,000 Australians experienced chronic crimination. A 12-lead ECG is also recorded. If the ortho-
heart failure, with 2350 dying from end-stage heart topic transplant is performed with the standard technique,
75
disease. In New Zealand, hospital admissions for heart a remnant P wave from the native heart may be visible
failure consume approximately 1% of the healthcare on the ECG or cardiac monitor (see Figure 12.16). As
76
budget. In the context of a 50% mortality rate within 4 the native sinus node cannot conduct across the right
years of being diagnosed with chronic heart failure, a atrial suture line, the recipient’s heart rate is determined
50% mortality rate within 1 year for patients with severe by the conduction system of the donor heart, not the
77
heart failure, and the burden of care associated with native heart. Of interest, it is possible for the native heart
78
heart failure exceeding that of all types of cancer, trans- to generate a P wave while the donor heart is in atrial
plantation for end-stage heart failure is actually a viable fibrillation or other dysrhythmia. (More detailed discus-
and economical treatment option for individuals and sion of cardiac monitoring and haemodynamic manage-
society; it is, however, a limited resource, available to only ment of patients with a heterotopic heart transplant
a few recipients. is available. 78,86 ) Monitoring data are combined with
physical assessment information from all body systems
to determine nursing and collaborative interventions.
FORMS OF HEART TRANSPLANT SURGERY Intensive continuous monitoring and assessment of
The most common heart transplant surgery is orthotopic haemodynamic parameters according to evidence based
transplantation, with two surgical techniques used: the practices 87-89 and overall clinical status allows nurses to
standard or bicaval approaches. The standard technique detect and subsequently respond to emergent postopera-
has been used since the 1960s and involves anasto moses tive complications.
79
of the donor and native atria. Complications associ- Full ventilatory support is required until the patient’s
ated with the standard technique can include abnormal haemodynamic status is stable. Respiratory status is mon-
atrial contribution to ventricular filling, and tricuspid itored via clinical, radiological and laboratory-derived
and mitral valve insufficiency. 80,81 Since the mid-1990s, data (see Chapter 13). Enteral feeding is usually com-
82
the bicaval technique as described by Dreyfus et al. menced on the day of admission. Renal and neurological
has gained favour. The main advantage of the bicaval function are closely monitored, as cyclosporin has a del-
approach is the maintenance of atrial conducting path- eterious effect on renal function and can lead to failure
90
ways and the likelihood of promoting sinus rhythm as well as neurotoxicity. For the small number of patients
91
82
and its associated superior atrial haemodynamics (see who develop allograft dysfunction requiring mechanical
Figure 12.13). Reported potential disadvantages include circulatory support (i.e. IABP, ECMO or Thoratec LVAD),
stenoses in the inferior and superior vena cava at the or acute renal failure requiring haemofiltration, hospitali-
anastomosis sites. 82
sation in the critical care unit tends to last weeks rather
The second form of heart transplant surgery is hetero- than days.
topic transplantation, although these account for less
83
than 0.5% of heart transplants in Australasia. In this The immediate period after transplantation can be a time
procedure, the donor heart is implanted in the right side of great hope and joy for recipients and their family and
84
of the chest next to the native heart to augment native friends; however, complications and setbacks can make
systolic function. Figure 12.14 illustrates a chest X-ray of the path to recovery prolonged, unpredictable and diffi-
the donor heart next to the native heart. cult. The provision of psychosocial support by all
members of the transplant/critical care team to family
Heterotopic heart transplantation is primarily indicated members and friends is an important part of patients’
in patients with pulmonary hypertension refractory to recovery from organ transplantation. Meetings with
pulmonary vasodilator therapies. It may also be con- family that convey honest and open information about
sidered in patients with a large body surface area that patient progress need to be conducted regularly. Support-
are unlikely to receive a suitably large-sized donor heart ing and managing patient and families following trans-
to enable an orthotopic procedure to take place, 79,85 or plant is consistent with support provided to other critically
when the donated organ is unsuitable as an orthotopic ill patients (see Chapter 8). In addition, there is the issue
85
graft. Heterotopic transplantation is usually performed of dealing with lost hope if the transplant fails; a very
to support the left ventricle (LVAD configuration), but distressing time for all involved. In the immediate

312 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

































FIGURE 12.13 LEFT Completion of bicaval transplant technique, showing the interior vena caval, superior vena caval, aortic, and pulmonary artery anas-
79
tomoses RIGHT Commencement of the left artrial anastomosis.






SVC

SVC
AO AO
RA
PA
PA
RV
LV RA
LV

RV
LA appendage
FIGURE 12.14 Chest X-ray showing heterotopic heart transplant. DONOR RECIPIENT





FIGURE 12.15 Heterotopic heart transplant (LVAD configuration).
85
postoperative period, transplant recipients are at risk of
developing complications that include hyperacute rejec-
tion, acute rejection, infection, haemorrhage and renal
failure. In the immediate postoperative period, heart
transplant recipients may experience morbidity specific to
the heart transplant procedure, such as early allograft
dysfunction (i.e. organ failure due to preservation injury),
bleeding, right ventricular failure and acute rejection.
Long-term complications include chronic renal failure,
hypertension, malignancy and cardiac allograft vascu-
lopathy. The common immediate potential complica-
tions and associated clinical management for heart FIGURE 12.16 Rhythm strip post orthotopic transplant (standard
recipients are discussed below. technique).

Cardiac Surgery and Transplantation 313

Hyperacute Rejection rejection (grade 1) is rarely treated, and only 20–40% of
Hyperacute rejection is now a rare form of humoral rejec- mild cases progress to moderate rejection (grade 3A),
95,98
tion that occurs minutes to hours after transplantation usually requiring treatment. Grades 3B and 4 rejection
and results from ABO blood group incompatibility or the are always treated, as they represent myocyte necrosis.
92
recipient having preformed, donor-specific antibodies. Cellular rejection is usually treated with higher doses of
ABO blood group and panel reactive screening of anti- corticosteroids, such as ‘pulse’ doses of methylpredniso-
human lymphocyte antigen (anti-HLA) antibodies lone (1–3 g IV over 3 days), and antilymphocyte anti-
preoperatively minimises the possibility of hyperacute body agents (ATG, ATGAM or OKT3). Humoral rejection
rejection, particularly in health care systems where blood is treated with plasmapheresis, high-dose corticosteroids,
that has been prospectively cross-matched is routinely cyclosphosphamide therapy and antilymphocyte anti-
99,100
used. If it occurs, hyperacute rejection leads to organ body therapy. It may be judicious to review the
failure and rapid activation of the complement cascade, patient’s medications during periods of rejection to
producing severe damage to endothelial cells, platelet ensure that drugs capable of reducing cyclosporin or
activation, initiation of the clotting cascade, and extensive tacrolimus serum levels such as certain anticonvulsants
microvascular thrombosis. There is no effective treat- and antibiotics have not been taken. In addition to aug-
78
ment for hyperacute rejection apart from mechanical mentation of immunosuppression therapy, fluid, phar-
circulatory support or interim retransplantation. macological and mechanical therapeutic interventions
are instituted to support cardiac function, depending on
the degree of ventricular dysfunction.
Acute Rejection Immunosuppression Therapy
Acute rejection can be classified as either cellular or
93
humoral. Cellular rejection involves T-cell infiltration In this section, a brief discussion of immunosuppression
of the allograft. Cellular rejection occurs much more therapies and associated nursing implications is pro-
commonly than humoral rejection, but both may occur vided. To prevent rejection of the transplanted organ,
94
simultaneously. Humoral or microvascular rejection is recipients receive a triple-therapy regimen of immuno-
thought to be primarily mediated by antibodies. Humoral suppression agents for the remainder of their life. Triple-
rejection may occur due to the presence of a positive therapy usually consists of corticosteroids (prednisolone
donor-specific cross-match, or in a sensitised recipient or prednisone), a calcineurin antagonist (cyclosporine or
with preformed anti-HLA antibodies. 95 tacrolimus [FK506]) and an antiproliferative cytotoxic
agent (mycophenolate mofetil, azathioprine or sirolimus/
Percutaneous transvenous endomyocardial biopsy is con- rapamycin). 101,102 For heart patients, sirolimus or rapamy-
96
sidered the gold standard for detecting cardiac rejection. cin may become the cytotoxic drug of choice following
Grading of cardiac rejection is noted in Table 12.4. findings of a recent study that demonstrated a lower
97
In humoral rejection, endomyocardial biopsy reveals incidence of cardiac allograft vasculopathy at 6 and 24
increased vascular permeability, microvascular thrombo- months, and lower rejection rates with sirolimus com-
sis, interstitial oedema and haemorrhage, and endothelial pared with azathioprine. 103
78
cell swelling and necrosis. An echocardiogram is also
performed to evaluate systolic cardiac function. Immunosuppression therapy is commenced preopera-
tively or in operating theatre. Maintenance immunosup-
Therapeutic interventions for rejection vary between pression regimen is usually instituted within hours of
centres and are based on the grade of rejection, degree admission to ICU, with each patient’s immunosuppres-
of haemodynamic compromise, clinical findings and sive needs individually assessed. For instance, the
time elapsed since transplantation. Asymptomatic mild administration time for introduction of the selected
immunosuppressive agent(s) may be delayed in patients
with preexisting renal dysfunction. When the administra-
tion of the usual regimen of immunosuppression is
TABLE 12.4 Standardised cardiac biopsy grading 98 delayed, induction therapy with anti-lymphocyte agents
(anti-thymocyte globulin (ATG), ATGAM or OKT3) or
Grade Nomenclature interleukin-2 receptor antagonists (basiliximab, dacli-
0 No rejection zumab) may be used in the immediate postoperative
period. 104,105 Induction therapy may be used in circum-
1 A. Focal (perivascular or interstitial) infiltrate stances of primary allograft failure perioperatively, e.g.
without necrosis
B. Diffuse but sparse infiltrate without necrosis HLA mismatch (rare), or early humoral rejection, or to
allow for a delay in initiating cyclosporine in patients at
2 One focus only with aggressive infiltration and/or risk of renal failure. 106,107 The common drugs used to
focal myocyte damage
suppress the immune system and the nursing implica-
3 A. Multifocal aggressive infiltrate and/or myocyte tions are illustrated in Table 12.5. As highlighted in the
damage table, some immunosuppressive agents are cytotoxic
B. Diffuse inflammatory process with necrosis
(e.g. mycophenolate mofetil), requiring safety measures
4 Diffuse, aggressive, polymorphous process with during preparation, delivery and disposal. Likewise, some
necrosis, with or without any of the following: immunosuppressive agents will be given IV (e.g. azathio-
infiltrate, oedema, haemorrhage, vasculitis
prine) until patients can eat and drink as they cannot be

314 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



TABLE 12.5 Immunosuppression table 108

Drug names Typical dose Important side effects Nursing considerations
Calcineurin antagonists Maintenance
Cyclosporin 5–10 mg/kg/day (target Renal impairment Monitor renal and liver function.
blood levels) Hypertension
Tacrolimus 0.2–0.5 mg/kg/day (target Hypercholesterolaemia Mix oral liquid cyclosporin with
blood levels) Abnormal liver function orange juice or milk in glass.
Headaches Do not crush tablets.
Gingival hypertrophy Time sampling of serum drug levels
(cyclosporin only) with dosage times.
Hirsutism (cyclosporin only)
Diabetes (tacrolimus only)
Corticosteroids Maintenance
Prednisolone/prednisone 0.2–0.5 mg/kg/day Mood change Monitor blood glucose levels.
Augmentation for rejection Weight gain
‘Pulse’ of 2 g over 3 days for Glucose intolerance
acute rejection Osteopenia
Muscle weakness
Antiproliferative Maintenance
cytotoxic agents 1–2 mg/kg/day Bone marrow suppression Cytotoxic: take full precautions when
Azathioprine 2–3 g/day (adult) Gastrointestinal tract irritation preparing, administering and
Mycophenolate mofetil (especially mycophenolate disposing of drugs.
mofetil)
Rapamycin Starting at 0.03 mg/kg/day
(target blood levels) Bone marrow suppression Minimise dietary cholesterol.
Hypercholesterolaemia Monitor platelets and serum
Hypokalaemia potassium.
Interleukin-2 receptor Induction of
antagonist immunosuppression: Few and infrequent These drugs are often used in patients
Basiliximab 20 mg/kg preoperatively with preexisting renal dysfunction.
Daclizumab and day 4 Other immunosuppression agents
1 mg/kg preoperatively and may be delayed with the use of
days 14, 28, 42, 56 these agents.
Little information about
compatibilities: avoid concurrent
administration.
Antilymphocyte Induction or augmentation
preparations for rejection Anaphylaxis Premed of paracetamol, promethazine
ATGAM/OKT3 Various, may target T Sterile meningitis and hydrocortisone 30 min prior to
lymphocyte levels Pulmonary oedema slow infusion.
Serum sickness





crushed for naso-gastric administration. In addition, as atrial flutter or fibrillation. 98,107 More severe forms of
blood levels of some immunosuppression agents (e.g. acute rejection are suspected when signs and symptoms
cyclosporine, sirolimus) are taken regularly to assess effi- of varying degrees of heart failure emerge. If patients are
cacy, nurses need to be aware of timing blood sampling awake and alert, they may complain of severe fatigue,
to dosage times in order to obtain accurate data to inform sudden onset of dyspnoea during minimal physical effort,
doses. syncope or orthopnoea. Physical assessment and haemo-
dynamic monitoring will reveal clinical signs of left and
right cardiac failure (see Chapter 9).
Nursing practice
Nurses have an important role in detecting acute rejec-
tion, as it is diagnosed by clinical signs and supported by Infection
histological findings from an endomyocardial biopsy. Infection is a major risk factor for transplant recipients
Low-grade rejection can be suspected when non-specific due to their immunosuppressed state. The periods of
signs such as malaise, lethargy, low-grade fever and mood greatest risk for patients are the first 3 months after trans-
changes are present. Acute rejection causing cardiac irrita- plantation, and after episodes of acute rejection when
tion is revealed by a sinus tachycardia greater than 120 immunosuppression agents are increased. 108,109 In addi-
beats/min; a pericardial friction rub; or new-onset atrial tion to the nosocomial bacterial infections that all surgi-
dysrhythmias such as premature atrial contractions, cal patients are exposed to in critical care (see Chapter 6),

Cardiac Surgery and Transplantation 315

immunosuppressed transplant recipients are at risk of Nursing practice
acquiring opportunistic bacterial, viral or fungal infec- Early detection of haemorrhage is achieved by close mon-
tions; latent infections acquired from the donor organ itoring of the following: haematological status; chest tube
such as cytomegalovirus (CMV); or reactivation of their patency, drainage volume and drainage consistency;
own latent infections (e.g. CMV or Pneumocystis carinii). and trends in haemodynamic data that suggest cardiac
To combat Pneumocystis carinii, patients receive trime- tamponade (see earlier in this chapter). Our clinical expe-
110
thoprim with sulfamethoxazole twice weekly. Despite rience suggests that if patients are hypotensive sporadi-
preoperative screening for CMV, the shortage of donor cally for no readily apparent reason, efforts should be
organs often necessitates CMV mismatching. Effective made to eliminate the existence of cardiac tamponade.
prophylaxis for CMV infection is provided by administer- Suspicion of cardiac tamponade may be confirmed
ing CMV hyperimmune globulin to CMV-positive and by chest X-ray or echocardiogram if the patient’s haemo-
CMV-negative recipients who receive a heart from a sero- dynamic status is stable. Sudden cardiac arrest or haemo-
111
positive donor. This commences within 24–48 hours of dynamic collapse secondary to cardiac tamponade
105
surgery. For CMV-negative recipients of organs from warrants an immediate return to theatre or a sternotomy
seropositive donors, ganciclovir for 1–2 weeks followed in critical care.
by oral therapy for 3 months is required in addition to
CMV hyperimmune globulin. 111-113
Acute Renal Failure
Nursing practice Acute renal failure or varying degrees of renal dysfunction
can occur in the initial postoperative period due to pre-
To prevent infection, standard precautions and meticu- existing renal dysfunction, cyclosporin, nephrotoxic anti-
lous hand-washing (see Chapter 6) are performed, rather biotics, or sustained periods of hypotension secondary to
114
than isolation procedures. Mandatory measures to cardiopulmonary bypass or allograft dysfunction. Diuretic
prevent overwhelming sepsis are a high level of vigilance therapy is invariably needed in the initial postoperative
by clinicians for signs of infection; obtaining empirical period due to these factors, as well as the fluid retention
evidence from blood, sputum, urine, wound and catheter- effects of corticosteroids and raised filling pressures
tip cultures; and aggressive and prompt treatment for secondary to a transient loss of right and/or left ventricu-
specific organisms. Although typical signs and symptoms lar compliance. High doses or continuous infusions
119
of infection are blunted in transplant recipients, clini- of diuretics may be required in patients who were on
cians should suspect infections when patients have a diuretic therapy preoperatively. Close monitoring of
low-grade fever, hypotension, tachycardia, a high cardiac serum electrolyte levels will indicate the need for any
output/index, a decrease in systemic vascular resistance supplements.
(SVR), changes in mentation, a new cough or dys-
pnoea. 115,116 Elevated white cell count, the presence of Nursing practice
dysuria, purulent discharge from wounds, infiltrates on
chest X-ray, sputum production or pain also indicate In addition to all the usual nursing and collaborative
infection. measures that are taken to prevent, detect and support
renal dysfunction/failure in patients following cardiac
Prior to administering blood products, nurses must ascer- surgery on cardiopulmonary bypass (see earlier in this
tain the CMV status of the patient and donor. Recipients chapter and Chapter 18), the type and dose of immuno-
who are seronegative for CMV and who receive a heart suppressive agents in the postoperative period are care-
from a seronegative donor must receive whole blood, fully selected and initiated according to individual risk
packed/red cells or platelets that are CMV-negative, leuco- factors and clinical status. Experience suggests that early
depleted or both in order to avoid development of a intervention with haemofiltration to support renal func-
primary CMV infection. 79,112,117 tion is preferable to continued use of high-dose diuretics
and deferred haemofiltration. This is because there is
Haemorrhage/Cardiac Tamponade little scope to maintain low doses of renal toxic immuno-
The risk of haemorrhage or cardiac tamponade is greater suppressants for weeks given the imminent risk of rejec-
for heart transplant recipients than for patients undergo- tion and resultant allograft failure.
ing coronary artery bypass graft or valvular surgery. Pre-
operative anticoagulation for end-stage heart failure or Early Allograft Dysfunction and Failure
atrial fibrillation, impairment of hepatic function second- Primary allograft failure is the leading cause of death in
ary to right heart failure, redo surgery, surgical suture the first month and year after surgery. 120,121 In the immedi-
lines connecting major vessels and atria, and a larger ate postoperative period, myocardial performance is
than usual pericardium are all contributing factors. depressed due to the clinical sequelae of cardiopulmo-
Good surgical technique is mandatory in preventing post- nary bypass and ischaemic injury associated with surgical
operative bleeding. As the promotion of haemostasis is a retrieval, hypothermic storage, prolonged ischaemic
major therapeutic goal postoperatively, blood products, times, and reperfusion. Despite a preferred time period
procoagulants and antifibrinolytics are commonly between organ retrieval and reimplantation of 2–6 hours,
administered according to laboratory and clinical data. the vast distances between capital cities (up to 3000 km)
Postoperative mortality from bleeding has been reported over which donor hearts may be transported, and a
to occur in up to 6.7% of cases. 118 decision to accept marginal, suboptimal organs, led

316 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

Australian researchers and transplant teams to pioneer unsustainably high cardiac index. In severe cases, vaso-
prolonged ischaemic times of up to 8 hours (New pressin may be infused at doses of 0.04–0.1 units/min
Zealand, 7 hours). 122 concurrently with noradrenaline. 128 Experience suggests
that the dose of adrenaline should be minimised in the
Heart transplants have been, and are likely to continue
to be, performed in Australia and New Zealand and presenceof metabolic acidosis, and the noradrenaline
other countries that encompass long distances with infusion increased to achieve normotension, a calculated
-5
ischaemic periods beyond 6 hours, as excellent short- SVR higher than 900 dynes/sec/cm and a sustainable
term (30-day mortality) and long-term (ejection fraction cardiac index.
at 1 year) outcomes have been reported. These out- Nursing practice
122
comes were achieved by using innovative preservation
techniques and postoperative mechanical assistance in Depressed left ventricular compliance and contractility
the form of intra-aortic balloon counterpulsation and/ due to cardiac dysfunction presents clinically with reduced
or a right ventricular assist device. 122,123 Adrenaline is cardiac index, bradycardia, reduced tissue and end-organ
invariably commenced intraoperatively, irrespective of perfusion (decreased mental status, oliguria, poor peri-
ischaemic time, to provide inotropic support to the pheral perfusion, slow capillary refill and raised serum
transplanted heart. lactate), low systemic venous oxygenation (SvO 2 ), and
dyspnoea. Bradycardia may not be evident due to
Early allograft dysfunction can present as left, right or chronotropic support of the denervated heart with atrial
biventricular dysfunction. Management of cardiac dys- pacing and/or isoprenaline. The following discussion
function is dependent on clinical signs and underlying focuses on management of right heart dysfunction/
aetiologies that include pulmonary hypertension, acute failure and left heart dysfunction/failure (see also
rejection, and ischaemic injury. Right ventricular dysfunc- Chapter 10).
tion is usually secondary to pulmonary hypertension,
whereas left ventricular or biventricular dysfunction Right heart dysfunction/failure is suspected in patients
results from acute rejection and ischaemic injury. with preexisting pulmonary hypertension or a haemody-
namic profile in the intra- or postoperative context that
To prevent right ventricular dysfunction and failure includes a rising CVP, low-to-normal PAWP, high calcu-
secondary to raised pulmonary pressures, prospective lated pulmonary vascular resistance, raised pulmonary
heart transplant recipients are screened preoperatively artery pressures, systemic hypotension, and oliguria. The
for the degree and reversibility of pulmonary hyperten- haemodynamic management of patients with right ven-
sion. Reversible pulmonary hypertension is a transpul- tricular dysfunction/failure involves optimising right
monary gradient less than 15 mmHg that responds to ventricular preload and afterload by titrating fluid and
pulmonary vasodilator therapies, such as prostaglandin pharmacological therapies to achieve adequate tissue and
124
E1, prostacyclin or inhaled nitric oxide (NO). Right end-organ perfusion. Fluid resuscitation to a CVP between
ventricular dysfunction or failure can also occur in the 14 and 20 mmHg and inotropic therapy is necessary to
postoperative context due to ischaemic injury, an under- ensure that the failing right ventricle continues to act as
sized heart (greater than 20% difference in body surface a conduit for the left ventricle. Nitric oxide by inhalation
area between donor and recipient), or hypoxic pulmo- is the therapy of choice, as it provides selective pulmo-
nary vasoconstriction. Isoprenaline or milronine, nary vasodilation at doses of 20–40 ppm, thereby reduc-
79
dobutamine and adrenaline are administered in this ing right ventricular afterload without producing systemic
situation. 112 hypotension. 124,129 A secondary benefit of inhaled NO is
improved oxygenation due to reduced mismatching of
Left ventricular dysfunction cannot be anticipated pre- 130
operatively, so when signs first emerge peri- or post- ventilation/perfusion. If inhaled NO is not available,
o peratively, fluid management strategies (filling or IV prostaglandin E1 or prostacyclin may be used to reduce
diuresis as deemed appropriate) and inotropic agents are right ventricular afterload when pulmonary pressures
131
112
commenced immediately. In patients with prolonged exceed 50 mmHg.
ischaemic times, mechanical assistance in the form of
an IABP is invariably instituted perioperatively. Mild right ventricular dysfunction may be treated with
milrinone at doses of 0.375–0.750 µg/kg/min or drug
In the initial postoperative period, cardiac dysfunction combinations that provide afterload reduction and ino-
can also occur as a result of a low systemic vascular tropic support (e.g. sodium nitroprusside and adrena-
resistance (SVR) syndrome, characterised by a calculated line). Appropriate respiratory management is essential, as
−5
SVR of less than 750 dynes/sec/cm in the presence of hypoxaemia and metabolic or respiratory acidosis can
an unsustainable high cardiac output. 125,126 The cause of exacerbate right ventricular failure. If pharmacological,
low SVR syndrome is not fully understood, although it fluid and inhaled NO therapies do not produce sustained
has been linked with systemic inflammatory response improvement in right ventricular performance, a right
syndrome (SIRS) associated with cardiopulmonary VAD (e.g. Biomedicus centrifugal pump or Abiomed BVS
bypass (see Chapter 20), the chronic use of angiotensin- 5000) is indicated to provide temporary support for the
converting enzyme inhibitors for end-stage heart failing right ventricle.
failure (see Chapter 10), and a deficiency of vasopres-
sin. 125,127 Noradrenaline is titrated to achieve a calculated The immediate haemodynamic management of left ven-
SVR within normal parameters and to lower the tricular dysfunction/failure secondary to acute rejection

Cardiac Surgery and Transplantation 317

or ischaemic injury often involves fluid resuscitation to a hospital discharge is predictive of long-term sinus node
79
PAWP of 14–18 mmHg, high-dose inotropes, vasodilator dysfunction. Insertion of a permanent pacemaker for
agents and insertion of an IABP to achieve a cardiac index long-term heart rate control is rarely required. Isoprena-
2
greater than 2.2 L/min/m and adequate end-organ per- line infusions at doses of 0.5–2 µg/min may be used
fusion. The insertion of an LVAD (e.g. Biomedicus cen- for chronotropy in combination with atrial pacing. As
trifugal pump) or full mechanical circulatory support noted earlier, atrial dysrhythmias such as atrial flutter
with extracorporeal membrane oxygenation (ECMO) is may be an early indication of acute rejection. Ventricular
indicated when aggressive therapeutic regimens fail to arrhythmias are rare and often lethal in spite of aggres-
produce a cardiac output that provides adequate end- sive resuscitation attempts. Persistent arrhythmias should
organ perfusion. 112,132 As noted earlier, augmentation of always prompt investigation of the patient’s rejection
the immunosuppression regimen may also be necessary level. 112
to manage the acute rejection.
Third, as patients rely on circulating catecholamines,
orthostatic hypotension is common. Patients are edu-
Denervation cated to sit up slowly from a lying position. Fourth,

Donor heart implantation severs both afferent and effer- patients rarely feel anginal pain after surgery; however,
ent nervous system connections to the heart. Hence, the there are some reports of patients regaining feelings of
transplanted heart has no direct autonomic nervous angina pectoris. 136 The inability of patients to feel angina
system innervation but is responsive to circulating cate- pectoris is important, because all heart transplant recipi-
cholamines. Denervation impairs circulatory system ents are at risk of developing accelerated allograft coro-
homeostasis, as evidenced by: a volume-expanded state; nary artery disease. 137 As part of discharge education,
a tendency to hypertension; no sensation of angina patients are taught to identify clinical signs of angina
pectoris; a high resting heart rate; a slow or absent baro- other than chest pain, such as shortness of breath and
receptor reflex (to increase heart rate/cardiac output in sweating. A summary of the main clinical manifestations
response to hypotension); and no rises in heart rate and and nursing practice issues for patients following heart
79
contractility due to hypovolaemia or vasodilation. As transplantation is included in Table 12.6.
the cardiac allograft is dependent on an adequate preload,
the effects of postural changes in recipients are important.
(A detailed discussion of physiology of the transplanted Practice tip
79
heart is provided elsewhere. )
Heart transplant patients have a denervated heart, so carotid
Nursing practice sinus massage will not slow a tachyarrhythmia and atropine will
not increase sinus node firing or atrioventricular conduction.
There are four important clinical manifestations of dener-
vation in the early postoperative period. First, drugs that
act directly on the autonomic nervous system to modify MEDIUM- TO LONG-TERM COMPLICATIONS
heart rate (e.g. atropine, digoxin) and vagal manoeuvres There are four long-term complications associated with
(carotid sinus massage) are ineffective. Amiodarone and heart transplantation: (1) cardiac allograft vasculopathy;
adenosine are effective antiarrhythmic agents. Neither (2) malignancy; (3) renal dysfunction; and (4) hyperten-
amiodarone nor sotalol interact with immunosuppres- sion. 138 Cardiac allograft vasculopathy (CAV) is a diffuse,
112
sive agents. However, as the denervated donor sinus proliferative form of obliterative coronary arteriosclerosis
node is more sensitive to exogenous adenosine than a that affects 30–60% of heart transplant recipients in the
sinus node innervated in the normal way, 133 it has been first 5 years after surgery. 139 Sudden death, ventricular
79
suggested that adenosine be avoided. That is, a usual arrhythmias and symptoms of congestive heart failure
adenosine dose may produce toxic-like effects in the may be the first signs of significant CAV. The aetiology
context of a denervated heart. Overdrive atrial pacing is of CAV is multifactorial, including immunological factors
a viable alternative to drug therapy to treat a tachyar- (e.g. episodes of acute rejection and anti-HLA antibod-
rhythmia such as atrial flutter. 134
ies), non-immunological cardiovascular risk factors (e.g.
Second, although a high resting heart rate is possible hypertension, hyperlipidaemia, preexisting diabetes and
from efferent cardiac denervation, sinus or junctional new-onset diabetes), the surgical procedure (e.g. donor
bradycardias may occur in the early postoperative period age, ischaemic time and reperfusion injury), and side
due to transient sinus node dysfunction or preoperative effects of immunosuppression drugs such as cyclosporin
amiodarone. Studies suggest that sinus node dysfunc- and corticosteroids (e.g. CMV infection and nephro-
tion occurs in about 20% of cases, although anecdotal toxicity). 112,139-141 Statins at doses less than that prescribed
135
experience suggests a higher percentage. To prevent low for hyperlipidaemia are commenced within 2 weeks of
cardiac output secondary to bradycardias, atrial and surgery irrespective of cholesterol levels to reduce episodes
112
ventricular epicardial pacing wires are inserted and atrial of rejection and CAV. Standard use of cyclosporine
112
pacing of >90 beats/min, and often at 110 beats/ may be augmented by mycophenolate mofetil, everoli-
min, is commenced. Atrial pacing at 110 beats/min mus or sirolimus as they have been shown to reduce
112
appears to ‘train’ the sinus node to conduct at rates the onset and progression of CAV. Diagnosis of CAV
of 70–100 beats/min in the long term. A resting sinus is difficult, due to allograft denervation, and because
or junctional heart rate below 70 beats/min prior to coronary angiogram underestimates the extent of the

318 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



TABLE 12.6 Summary of nursing practice for patients after heart transplantation

Clinical manifestation Nursing practice considerations
Acute rejection ● Detect acute rejection by clinical signs and endomyocardial biopsy.
● Suspect low-grade rejection when malaise, lethargy, low-grade fever and mood changes are present.
● Acute rejection is manifested by a sinus tachycardia >120 beats/min, a pericardial friction rub, or
new-onset atrial dysrhythmias.
● Suspect severe acute rejection with manifestations of left and right heart failure; awake patients may
complain of severe fatigue, sudden onset of dyspnoea during minimal physical effort, syncope or
orthopnoea.
Infection ● Standard infection control precautions and meticulous hand-washing is required.
● Observe for signs of infection: low-grade fever, hypotension, tachycardia, a high cardiac output/index,
a decrease in systemic vascular resistance, changes in mentation, a new cough, dyspnoea, dysuria,
sputum production, or pain.
● Monitor blood, sputum, urine, wound and catheter-tip cultures, infiltrates on chest X-ray, and institute
aggressive and prompt treatment for specific infective organisms.
● Check CMV status before administering blood products.
Haemorrhage/cardiac ● Monitor haematological status; chest tube patency, drainage volume and drainage consistency; and
tamponade trends in haemodynamic data that suggest cardiac tamponade.
● Patients who are hypotensive sporadically should be assessed to eliminate cardiac tamponade as a
cause.
Acute renal failure ● Support renal function, including titration of immunosuppressive agents to individual risk factors and
clinical status, and early haemofiltration.
Early allograft dysfunction ● Augment the immunosuppression regimen to manage the acute rejection.
Left heart failure ● Observe for depressed left ventricular compliance and contractility: reduced cardiac index, possible
bradycardia (may not be evident due to atrial pacing and/or isoprenaline), decreased mental status,
oliguria, poor peripheral perfusion, slow capillary refill and raised serum lactate, low systemic venous
oxygenation, and dyspnoea.
● Fluid resuscitate to a PAWP of 14–18 mmHg, high-dose inotropes, vasodilator agents, IABP to achieve
2
a cardiac index >2.2 L/min/m with adequate end-organ perfusion.
● Insertion of full mechanical circulatory support (ECMO or LVAD) is indicated when other interventions
do not provide adequate end-organ perfusion.
Right heart failure ● Observe for right heart dysfunction/failure: rising CVP, low to normal PAWP, high calculated
pulmonary vascular resistance, raised pulmonary artery pressures, systemic hypotension, and oliguria.
● Optimise right ventricular preload and afterload: titrate fluid and medications to achieve adequate
end-organ perfusion; fluid resuscitate to a CVP of 14–20 mmHg; consider inhaled NO (selective
pulmonary vasodilation and improved oxygenation from reduced ventilation/perfusion mismatch),
prostaglandin E1 or prostacyclin, milrinone, or drug combinations with afterload reduction and
inotropic support (e.g. sodium nitroprusside and adrenaline).
● Institute appropriate respiratory management to minimise hypoxaemia and metabolic or respiratory
acidosis.
● If no sustained improvement in right ventricular performance, a right VAD is indicated for temporary
support.
Denervation ● Drugs with direct autonomic nervous system actions on heart rate (e.g. atropine, digoxin) and vagal
manoeuvres (carotid sinus massage) are ineffective.
● Use overdrive atrial pacing to treat tachyarrhythmias.
● Sinus or junctional bradycardias may occur, and atrial/ventricular epicardial pacing is used to ‘train’
the sinus node.
● Orthostatic hypotension is common: patients should sit up slowly from a lying position.
● Patients rarely feel anginal pain after surgery: they need to identify other clinical signs of angina, such
as shortness of breath and sweating.




disease and is insensitive to early lesions. Currently, disorders 147,148 as a consequence of long-term immuno-
142
intravascular ultrasound (IVUS) provides the most reli- suppression therapy. 149,150 Nurses play an important role
112
able quantitative information about the degree of CAV. in educating patients about how to avoid and reduce the
As the definitive treatment for CAV is retransplantation, risks of sun exposure. Treatment options in transplant
143
ongoing research into the prevention of CAV will be recipients are the same as for the general population (e.g.
the most important factor in reducing the incidence and chemotherapy, radiation therapy and surgical excision),
associated mortality. in addition to a reduction in immunosuppression therapy;
however, outcomes remain poor. 146
All heart transplant recipients are at a greater risk of devel-
oping malignancies than the general population, particu- Long-term renal dysfunction occurs primarily post-
larly carcinoma of the skin 144-146 and lympho-proliferative transplantation due to cyclosporin nephrotoxicity. Careful

Cardiac Surgery and Transplantation 319

monitoring of cyclosporin levels, and avoidance of hypo- ● Haemodynamic stability constitutes the most
volaemia and other nephrotoxic drugs are important common challenge in the postoperative period and
measures in reducing progression to renal failure. Impor- may be managed with fluids, cardiovascular medica-
tantly, findings from recent research indicate that chronic tions, cardiac pacing and intra-aortic balloon
cyclosporin nephrotoxicity can be reversed by eliminat- pumping.
92
ing cyclosporin from immunosuppression regimens. ● Bleeding in the postoperative period may be due
End-stage renal failure requiring dialysis or renal trans- to inadequate reversal or heparin, coagulopathy or
plantation has been reported in 3–10% of patients. 151 surgical bleeding; therefore, appropriate diagnosis
must occur before relevant treatment is instigated.
Systemic hypertension following transplantation has
been linked with cyclosporin-induced tubular nephrotox-
icity, peripheral vasoconstriction and fluid retention. 152
Lifestyle modifications such as weight loss, low sodium INTRA-AORTIC BALLOON PUMPING
diet and exercise are recommended along with optimal ● Major benefits include increasing cardiac output,
therapeutic doses of cyclosporin, and combinations of increasing myocardial oxygen supply and decreasing
calcium channel blockers and angiotensin-converting myocardial oxygen demand.
enzyme inhibitors and blockers. Such approaches have ● Appropriate timing is essential to obtain maximum
112
been reported to achieve blood pressure control in up to benefits, so correction of timing errors forms a central
65% of patients. 153 component of care.
● Assessment of limb perfusion, with timely interven-
tion when perfusion is inadequate, is essential to
LIFESTYLE ISSUES prevent limb ischaemia.
Following such momentous surgery, patients require
sound advice regarding returning to driving, work,
exercise and sexual activity. Cardiac rehabilitation with HEART TRANSPLANT
aerobic and resistance exercise is recommended to prevent ● A triple-therapy regimen consisting of corticosteroids,
short-term weight gain and glucose intolerance, as well a calcineurin antagonist and an antiproliferative
as adverse effects of immunosuppressive therapy on skel- cytotoxic agent is used to suppress the immune
etal muscle. Return to work or education is expected system after organ transplantation. All cytotoxic
113
and encouraged after surgery. Driving a vehicle can be agents necessitate specific administration and dis-
considered once the patient’s gait, tremor and other posal procedures.
neurological issues are normalised, and any bradycardia ● Indications for heart transplantation include end-
managed by pacemaker implantation. Pregnancy is stage heart failure secondary to ischaemic heart disease
113
possible after one year following transplantation; but and cardiomyopathy. Possible complications in the
only under the management of the multidisciplinary early postoperative period include acute rejection,
team who will explain the considerable risks involved. 113 infection, haemorrhage, renal failure, right ventricular
failure and allograft dysfunction (left ventricular
dysfunction/failure).
SUMMARY ● Although early signs of low-grade rejection can be
Primary compromise of the cardiovascular system causes non-specific, signs of moderate rejection usually
patients to require admission to a critical care area and present as organ dysfunction/failure.
the need for specialised care including intra-aortic balloon ● The CMV status of the donor and recipient must be
pumping, and post cardiac surgery management. Appro- known so that blood products with an appropriate
priate assessment and management is essential to prevent CMV status are administered.
secondary complications arising. Important principles of ● Denervation of the heart renders vagal manoeuvres
care are summarised below. (e.g. carotid sinus massage), and drugs that act directly
on the autonomic system (e.g. atropine, digoxin) to
CARDIAC SURGERY modify heart rate, ineffective.

● Surgical procedures may be performed as treatment ● Nursing practices for managing patients with heart
for structural abnormalities, ischaemic lesions within transplantation focus on prevention and management
coronary arteries, and repair or replacement of cardiac of complications, maintenance of comfort and pro-
valves. motion of long term recovery.

320 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



Case study
Mr Martin is a 59-year-old patient admitted for elective aortic, On the basis of the PaCO 2 the SIMV rate was increased to 13 breaths
mitral and tricuspid valves surgery. His past history includes rheu- per minute, which corrected the PaCO 2 and pH. FiO 2 was progres-
matic heart diseases (severe mitral valve regurgitation, aortic ste- sively decreased from FiO 2 1.00 to 0.40 over the next hour while
nosis and aortic regurgitation, and moderate to severe tricuspid pulse oximetry revealed a SpO 2 greater than 98%.
valve regurgitation) and gout. He has had those valve problems Mr Martin was switched to CPAP/PS after 30 minutes of spontane-
for many years, but recently has developed exertional dyspnoea. ous ventilation on waking, where he sustained adequate ventila-
Coronary angiography was normal but left ventriculogram tion. He was assessed as suitable and extubated six hours post
reveals severe left ventricle systolic dysfunction. Preoperative tran- admission. After extubation supplemental face mask oxygen was
soesophageal echocardiography report reveals dilated left ventri- applied at 8 LPM to keep SaO 2 >97% and changed to nasal prong
cle with severe global systolic dysfunction, dilated right ventricle oxygen at 3LPM three hour post extubation. Lung recovery pro-
with moderately reduced systolic function, severe pulmonary gressed uneventfully, aided by twice-daily physiotherapy and
hypertension and confirmation of pathology of three valves.
mobilisation. Oxygen was discontinued on day 3.
Surgery was reported as uncomplicated. Aortic and mitral valves
were replaced with new mechanical valves and tricuspid valve was Cardiovascular
repaired with an annuloplasty ring. Cardiopulmonary bypass had Rhythm: Epicardial dual-chamber pacing wires were in place, but
been used for 180 minutes and aortic cross-clamp time was 149 pacing was provided in the AAI mode (demand atrial pacing) at 80
minutes. An intra-aortic balloon pump catheter was inserted at the beats/min, with no evidence of AV block. Pacing continued for 24
end of the case to assist with post operative left ventricle recovery. hours before sinus rhythm emerged above 80 beats/min, inhibiting
An infusion of glyceryl trinitrate (GTN) 20 mcg/min was the only the pacing. After 48 hours of sinus rhythm, the back-up pacing was
drug infusion in progress. turned off and the pacing wires isolated. These wires were removed
on day 5 without problems. Initially Mr Martin was normotensive
On admission to the ICU the patient was intubated and ventilated. with assistance of IABP (augmented diastolic pressure of 120, sys-
He had left radial arterial and pulmonary artery catheters (PAC) in tolic pressure of 110, diastolic pressure of 55 and mean arterial
situ. Two mediastinal and a pericardial drain tube had been placed pressure of 80 mmHg), with a cardiac index of 3.1L/min/m . Filling
2
and had drained 140 mL of blood to the time of admission. There pressures were kept at upper normal range with colloid administra-
was no air leak. A urinary catheter was also present. Early chest tion as he was vasodilated, with a SVR of 716 dynes/sec/cm . His
−5
X-rays confirmed ETT, PAC, chest tube and IABP catheter place- core temperature on admission was 36.3°C, not requiring active
ment. Lung fields were mildly congested and cardiomegaly was warming. Chest drainage remained modest, with total blood loss
present. of 150 mL in the first hour. Blood pressure and cardiac output
The main dimensions of Mr Martin’s progress, care and manage- remained within normal limits in first 24 hours. IABP was weaned
ment follow. (ratio wean) on day 1 post operative over a period of 6 hours
without any compromise, and the IABP catheter was removed 24
Neurological status hours post ICU admission.
Began to wake at 2 hours postoperatively, and was obeying com-
mands, able to move all limbs with equal strength. Pupils were Fluid balance
normal size and reactive to light. Pain was managed with regular Chest drainage for the first 4 hours was 400 mL and total drainage
intravenous tramadol, morphine (boluses) and paracetamol at 48 hours was 750 mL, at which time drains were removed. Mr
suppositories in initial phase and continued with IV tramadol for Martin’s urine output remained within 0.5–1 mL/kg/hr with normal
48 hours and oral paracetamol for 4 days post operative. serum urea and creatinine. Hourly fluid assessment was main-
Ventilation tained for the duration of ICU stay and a positive fluid balance was
Initial parameters: ETT secured at lip level 25 cm, equal air entry recorded on both days (1100 mL and 480 mL respectively). Oral
bilaterally. SIMV mode, tidal volume (VT) 720 mL (80 kg), rate fluids were commenced 3 hours post extubation and within 24
10/min, inspiratory flow 40 L/min, PEEP 5 cmH 2 O, FiO 2 1.00, pres- hours a light diet was being tolerated according to local practice,
sure support 10 cmH 2 O, producing acceptable peak inspiratory Mr Martin remained in the ICU until the second postoperative
pressures of 22–26 cmH 2 O. morning and was then discharged to the step-down unit after
removal of all lines and tubes. Mr Martin was started on warfarin
Admission ABG (after 20 minutes) revealed the following: tablets for his mechanical valves on day one post operative and the
● PaO 2 366 mmHg dosage was titrated by the cardiac team according to his INR
● PaCO 2 52 mmHg results. DVT prophylaxis (heparin) and gastric ulcer prophylaxis
● pH 7.34 (omeprazole) were continued up to day 7 postoperative when Mr
● HCO 3 25 mmol/L Martin was discharged from hospital with cardiac rehabilitation
−
● SaO 2 99.9%. program.

Cardiac Surgery and Transplantation 321



Research vignette
Bauer, BA, Cutshall SM, Wentworth LJ et al. Effect of massage interventions were set out in a very distinct way that minimised
therapy on pain, anxiety, and tension after cardiac surgery: A the chance of bias in collecting data. Nonetheless, two sets of data
randomized study. Complementary Therapies in Clinical Practice were collected; subjective data that could produce bias results;
2010 16(4): 70–75. and, objective data such as heart rate, blood pressure and respira-
Abstract tory rate that were not significantly different between the groups.
Integrative therapies such as massage have gained support as The subjective data such as pain, anxiety and tension, were signifi-
interventions that improve the overall patient experience during cantly different between the groups, with massage group patients
hospitalisation. Cardiac surgery patients undergo long procedures reporting less tension on day 2 compared with the control group
and commonly have postoperative back and shoulder pain, patients. At day 4 massage group patients reported lower levels of
anxiety, and tension. Given the promising effects of massage tension, pain and anxiety than the control group patients. Of note,
therapy for alleviation of pain, tension, and anxiety, we studied the when day-3 data were compared with day-2 posttreatment values,
efficacy and feasibility of massage therapy delivered in the post- patients who had received a massage had significant worsening of
operative cardiovascular surgery setting. Patients were randomised pain, anxiety, and tension, although when the change from day 2
to receive a massage or to have quiet relaxation time (control). In to day 3 was compared for the 2 groups the difference was not
total, 113 patients completed the study (massage, n = 62; control, significant.
n = 51). Patients receiving massage therapy had significantly Based on these results, massage as one specific complementary
decreased pain, anxiety and tension. Patients were highly satisfied and alternative therapy, is recommended in postoperative cardiac
with the intervention, and no major barriers to implementing patients, but mainly to start after day three postoperation for
massage therapy were identified. Massage therapy may be an maximum effects as patients have fewer invasive lines and are
important component of the healing experience for patients after more mobile. The study was conducted in a single centre and for
cardiovascular surgery. very specific surgical group (cardiac patient); hence results may not
be generalised to all surgical populations. The question of rele-
Critique vance and effect of complementary and alternative medicine
Pain, anxiety and tension management post cardiac surgery is vital earlier in the postoperative course has not been answered by this
for complete and on time recovery, and to prevent undesirable study but should be explored as a potential area for improvement
complications. Complementary and alternative medicine therapies in care.
such as massage have been used to alleviate pain and anxiety in
various clinical settings, including post operatively without proper This article gives an insight into a bigger picture in critical care
study design. The efficacy of these therapies needs to be proven in area; that is, critical care nursing is not just about haemodynamic
a randomised control research with appropriate scientific rigour. monitoring, ventilation and other advanced mechanical and tech-
The sample of patients in this study was stable, fairly uncompli- nical modalities. The provision of critical care nursing must com-
cated cardiac surgical patients without history of chronic pain syn- prise holistic, complete and all-rounded nursing practices. Critical
dromes. The study was designed to be credible with large enough care nurses should always think outside the square to find ways
sample size powered to detect a significant difference between the to improve outcomes of critically ill patients and should pass
two randomised groups. Randomisation was well controlled using these skills to novice nurses; skills such as complementary and
randomised block design to keep the difference in patient numbers alternative medicine therapies are one such skill to develop and
in each group less than or equal to two at all times. The share.










Learning activities

1. Discuss initial assessment of IABP timing and alarms with a 5. Describe the assessment needed throughout a ventilation
senior colleague. weaning process, in preparation for extubation and post-
2. Outline nursing assessment and management of patient with extubation. Identify any factors that would identify a patient
IABP in situ, including measures to prevent complications. that is not ready for extubation.
3. Identify the model of IABP that your critical care unit uses, and 6. Identify the possible causes of hypotension and low cardiac
review the alarms that are present, the causes of those alarms output in the postoperative cardiac surgical patient. Outline
and the response of the pump when it senses an alarm situa- the management options for each of these causes.
tion. With one of the senior staff, discuss the mechanisms that 7. Consider the possible causes of bleeding in the postoperative
you should undertake to correct each of the alarm situations. cardiac surgical patient and outline the appropriate assess-
4. Identify any abnormalities on the ABGs in the case study and ment and management for each of these causes.
discuss corrective treatment.

322 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

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Respiratory Assessment


and Monitoring 13






Amanda Corley
Mona Ringdal


assess critically ill patients and monitor for responses to
Learning objectives treatment or early signs of deterioration.
This chapter provides a comprehensive description of the
After reading this chapter, you should be able to: principles and practice of respiratory assessment, moni-
● demonstrate an understanding of respiratory anatomy and toring, and diagnostics. This knowledge is important in
normal physiology providing timely and effective interventions for critically
● describe the mechanisms that contribute to altered ill patients with respiratory dysfunction. The following
respiratory function two chapters then discuss the management of respiratory
● examine the key principles underpinning assessment and alterations (Chapter 14) and oxygenation and ventilation
monitoring of respiratory function interventions (Chapter 15).
● discuss nursing assessment and monitoring activities for
critically ill patients with respiratory dysfunction RELATED ANATOMY AND
● explain the importance of patient assessment skills, and the PHYSIOLOGY
contribution of diagnostic and laboratory findings to
ongoing clinical management The thorax cavity contains the trachea and bronchial tree,
● justify the physiological bases for different types of the two lungs, pleura and diaphragm. The mediastinum,
monitoring located between the lungs, houses and protects the heart,
● discuss some common forms of diagnostic procedures used great vessels and the oesophagus. Twelve pairs of ribs
in critical care cover the lungs, ten of which are connected to the spine
posteriorly, and to the sternum or to the cartilage of the
rib above anteriorly (ribs 8–10). The 11th and 12th ribs
have no anterior attachment (see Figure 13.1). 1
Key words The respiratory system is divided into upper and lower
respiratory tracts: the upper airways consist of the nose,
work of breathing nasal conchae, sinus and pharynx; the lower respiratory
2
gas exchange tract includes the larynx, trachea, bronchi and lungs.
Larger airways are lined with stratified epithelial tissue,
oxygen delivery which have a relatively high cellular turnover rate; these
hypoxaemia cells protect and clear these large airways. There are also
pulse oximetry additional specialised features of this tissue including an
capnography extensive distribution of mucus/goblet cells and cilia,
arterial blood gases which facilitate the mucociliary clearance system and aid
diagnostic imaging airway clearance.

UPPER RESPIRATORY TRACT
INTRODUCTION The nasal cavities contain an extremely vascular and
mucoid environment for warming and humidifying
The respiratory system ensures adequate tissue and cel- inhaled gases. To maximise exposure to this surface area,
lular oxygenation for the body. It is responsible for gas the nasal conchae create turbulent gas flow. Cilia at the
exchange through the uptake of oxygen and excretion of top of the epithelial cells and mucus provide filtration
carbon dioxide; assists in optimal organ function; con- and cleaning of the inhaled air. Mucus is moved by the
tributes to acid–base balance; and therefore plays a large cilia lining the conducting airways towards the pharynx
role in maintaining homeostasis. A thorough under- at a rate of 1–2 cm per minute. One litre of mucus is
standing of the anatomy, physiology and pathophysio- produced every day with only a small part not reabsorbed
logy of this complex body system is required to accurately by the body. 3,4 325

326 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


Thyroid cartilage bronchi. Further divisions within these conducting
Cricoid cartilage airways end with the terminal bronchioles, the smallest
Trachea Upper lobe airways without alveoli. These conducting airways do not
Clavicle of left lung
Upper lobe participate in gas exchange but form the anatomical dead
7
of right lung space (approximately 150 mL).
Scapula 1 1 Larger airways have a greater proportion of supporting
cartilage, ciliated epithelium, goblet and serous cells and
2 2 hence a mucous layer. As the airways become smaller,
cartilage becomes irregularly dispersed, the number of
3 3
goblet cells and amount of mucus decreases until, at the
Sternum 4 4 alveolar level, there is only a single layer of squamous
epithelial cells. Alveolar macrophages are present in these
5 5 epithelial cells, and phagocytose any small particles that
6 6 may enter the alveolar area. Smooth muscle surrounds
Lower lobe and supports the bronchioles, enabling airway diameter
Middle lobe 7 7 of left lung change and subsequent changes in airway resistance to
Lower lobe 8 8 gas flow. 8
9 9
Rib cartilages
10 10 THORAX/LUNGS
The lungs and heart are protected within the thoracic
FIGURE 13.1 Ventilatory structures of the chest wall and lungs, showing cage. Expansion of the thorax enables the lungs to fill
1
the ribs and lobes of the lungs. with air during inspiration when respiration is triggered,
and to passively compress to expel air from the lungs
during expiration. The diaphragm separates the thorax
The pharynx is a muscular tube that transports food and from the abdomen and actively participates in the venti-
air to the oesophagus and larynx, respectively. Inferior lation process. The diaphragm is the most important
to the pharynx, the larynx consists mostly of cartilage inspiratory muscle, performing approximately 80% of
attached to other cartilage and surrounding structures, the work of breathing. Inspiration is initiated from the
and houses the vestibular (false) vocal folds and the true medulla, sending impulses through the phrenic nerve to
5
vocal cords (see Figure 13.2). An important pair of car- stimulate the diaphragm to contract and flatten. The
tilages within the larynx is the pyramid-shaped aryte- phrenic nerve originates in the cervical plexus and involves
noids, which act as attachment points for the vocal cords. the third to fifth cervical nerves. It splits into two parts,
This area is easily damaged by pressure from endotra- passing to the left and right side of the heart before it
cheal tubes; the most significant independent risk factor reaches the diaphragm. For this reason, patients can have
for injury to the arytenoids is the length of intubation ventilation difficulties if phrenic nerve damage is due to
8,9
6
time. The thyroid cartilage (‘Adam’s apple’) and the C3–C5 trauma.
cricoid cartilage protect the glottis and the entrance to the The conducting airways move inspired air towards the
4
trachea. Another cartilage in the larynx is the triangular- respiratory unit, ending in the terminal bronchioles. The
shaped elastic epiglottis which protects the lower airways respiratory bronchioles, the alveolar ducts and alveolar
from aspiration of food and fluids into the lungs. The sacs form the respiratory unit where the diffusion of gas
epiglottis usually occludes the inlet to the larynx during molecules, or gas exchange, occurs. The respiratory unit
swallowing. The primitive cough, swallow and gag reflexes makes up most of the lung with a volume of 2.5–3 L
further protect the airway. 4 during rest (see Figure 13.3).
7
LOWER RESPIRATORY TRACT Surfactant
The trachea is a hollow tube approximately 11 cm long Of particular importance to the structure and function
and 2.5 cm in diameter, and marks the beginning of the of the respiratory system are the type I and II alveolar
lower respiratory tract. The trachea is supported by 16–20 epithelial cells. Type I cells provide support of the wall
C-shaped cartilages, and is another area at risk of pressure within the alveolar unit. Type II cells produce an impor-
damage from artificial airways. The trachea divides at the tant lipoprotein, surfactant, that lines the inner alveolar
carina into the left and right main bronchi. The bronchial surface, and lowers surface tension of the alveoli, stabilis-
tree has two main stem bronchi that are structurally dif- ing the alveoli to optimise lung compliance and facilitate
ferent. The right bronchus is wider and angles slightly expansion during inspiration. If surfactant synthesis is
7
where it divides further into the three lobes of the right reduced due to pulmonary disease, lung compliance
lung. The most common site of aspiration of foreign decreases and the work of breathing increases. 10
objects is the right bronchus because of its anatomical
position. The acutely angled left main bronchus divides Pleura
further into the two main lobes of the left lung. Each lung is contained within a continuous thin mem-
The airways within each lung branch out further into brane called the pleura, and thus each lung is surrounded
secondary (or lobar) bronchi then tertiary (or segmental) by a pleural sac. The two pleura sacs, one on each side of

Respiratory Assessment and Monitoring 327


Epiglottis
Hyoid bone

Thyrohyoid membrane

Thyroid cartilage
Corniculate cartilage
Arytenoid cartilage
Cricohyoid ligament
Cricoid cartilage
Trachea


Corniculate cartilage
Muscular process
of arytenoid cartilage
Vocal process of
arytenoid cartilage
Cricoid cartilage
Vocal cords
Thyroid cartilage
Digastric
anterior belly
Epiglottis Mylohyoid Mastoid process
Hyoid bone Stylohyoid Digastric
Levator scapulae posterior belly
Superior horn of Longus capitis Scalenus medius
thyroid cartilage Omohyoid Thyrohyoid
Cricothyroid Thyroid cartilage
Thyroid cartilage Sternothyroid Sternohyoid
Corniculate cartilage Sternocleido-
Arytenoid cartilage Trapezius mastoid
Inferior horn of
thyroid cartilage
Cricoid cartilage
Clavicle
Trachea
A B Sternum Trachea
5
FIGURE 13.2 Larynx. (A) Cartilages and ligaments; (B) Neck muscles.

CONDUCTING AIRWAYS RESPIRATORY UNIT

BRONCHI, SUB- BRONCHIOLES ALVEOLAR
TRACHEA SEGMENTAL SEGMENTAL DUCTS,
BRONCHI BRONCHI Non- Respiratory ALVEOLI
respiratory




















GENERATIONS 8 15 21-22 24 28

FIGURE 13.3 Lower airway branches. 5