CARDIAC ANAESTHESIA
Postoperative care of the
adult cardiac surgical patient
Jonathan H Rosser
Alison D Parnell
Nicholas J Massey
Abstract
Most patients are ready to be transferred to a ward after 24e48 hours on
a cardiac intensive care unit (CICU); however, several potential complica-
tions can occur during this period. The risks during transfer from theatre
to CICU increase if a long distance is involved. A thorough handover to
nursing staff is mandatory. Problems with blood pressure and arrhythmias
are common on the CICU. Patients undergoing hypothermic cardiopulmo-
nary bypass are at greater risk of hypothermia postoperatively. Multiple
factors can cause postoperative cardiac surgical bleeding. Despite efforts
to correct clotting abnormalities, patients occasionally need to return to
theatre because of mediastinal bleeding or cardiac tamponade. The
avoidance of multiorgan failure by maintaining good tissue perfusion
and oxygenation is the main aim of perioperative care and through the
initial postoperative period. Avoidance or treatment of a low cardiac
output state often necessitates cardiac output monitoring and the use
of inotropes, vasoactive drugs or mechanical assist devices such as an
intra-aortic balloon pump. Established organ failure leads to a longer
stay on a CICU, a growing proportion of patients having a protracted crit-
ical care stay.
Keywords Cardiac; cardiac intensive care unit; cardiac output moni-
toring; care; critical; intensive; postoperative; resuscitation; surgery
Royal College of Anaesthetists CPD Matrix: 2A07, 3G00
First 24 hours after cardiac surgery
Transfer and handover
Transfer from theatre to a cardiac intensive care unit (CICU) can
be a period of instability. The distance can be lengthy with the
risk of airway, ventilatory or cardiovascular problems. Infusions
Jonathan H Rosser MBChB FRCA is a Speciality Registrar (ST5) in
Anaesthesia and Intensive Care Medicine (ICM) at Sheffield Teaching
Hospitals, South Yorkshire, United Kingdom. Conflicts of interest: none
declared.
Alison D Parnell BSc MBBS FRCA is a Consultant Anaesthetist at the
Sheffield Teaching Hospitals Cardiothoracic Centre, South Yorkshire,
United Kingdom. Conflicts of interest: none declared.
Nicholas J Massey MBBS FRCA is a Consultant Anaesthetist at the
Sheffield Teaching Hospitals Cardiothoracic Centre, South Yorkshire,
United Kingdom. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 13:10
Learning objectives
After reading this article, you should:
C know five causes of hypotension after cardiac surgery
C be able to list the cardinal symptoms and signs of cardiac
tamponade
C understand the difference in resuscitation if cardiac arrest
occurs immediately after cardiac surgery
of vasoactive drugs continue on battery power. Ventilation and
oxygen are required. The minimum monitoring needed is ECG,
mean arterial pressure (MAP) and pulse oximetry with an
adequately charged transfer monitor. Changing from volatile
anaesthesia to total intravenous anaesthesia (usually propofol)
for transfer can lead to inadvertent hypotension or hypertension.
The following should be carried with the patient: (1) atropine, (2)
a vasoconstrictor, and (3) a bag of colloid.
On arrival at CICU, it is the anaesthetists responsibility to
transfer the patient onto a checked ventilator set up to deliver
lung protective ventilation. Correct tube position should be
confirmed clinically and with capnography. Palpation of a pulse
is sensible while monitoring is transferred and an early blood gas
is desirable.
Important handover information to nursing staff includes:

operation performed and the intraoperative course

premorbid conditions

important medications, for example antiplatelet drugs

left ventricular (LV) function (good, moderate, poor)

pre-existing renal function

intravenous infusions, especially cardiovascular system
support

presence of pacing wires

suitability for fast-track pathway/early extubation.
Routine fluid management
Traditionally, cardiac surgical patients were aggressively fluid
restricted and diuresed on the CICU following the haemodilution
associated with cardiopulmonary bypass (CPB) and fluid
received in theatre. After CPB, the systemic inflammatory
response syndrome (SIRS) causes capillary leak and vasodilata-
tion. Despite a positive balance, patients may still have intra-
vascular hypovolaemia and fluid therapy should be targeted to
optimize cardiac output whilst avoiding fluid overload and its
associated problems. Central venous pressure (CVP) trends,
pulmonary artery catheter (PAC) measurements and cardiac
output (CO) monitoring are used to guide fluid requirement. As
with any surgery, fluid administration should then be more
conservative in the following days and oral diuretics may be
introduced.
Colloid is used in preference to crystalloid when volume
replacement alone is required. A total colloid administration
greater than 2000 ml in the absence of overt bleeding should
prompt consideration of other investigations and treatment. Most
centres practise a conservative transfusion strategy following the
association between blood transfusion and worse outcome.
503 2012 Published by Elsevier Ltd.
 CARDIAC ANAESTHESIA
However, in patients with residual cardiac disease, red blood cell
transfusion should be used to maintain a haemoglobin concen-
tration of 8e10 g/dl,1 rather than the 7 g/dl trigger used for
critically ill patients without significant cardiorespiratory disease.
Patients may receive autologous blood from the CPB circuit via
a cell saver or direct from the pump. The pump blood contains
residual heparin which may necessitate the use of further prot-
amine (50e100 mg).
Maintenance intravenous infusion of crystalloid such as 5%
glucose to balance with drugs and other infusions to a total input of
1 ml/kg/hour is indicated, unless there are reasons to limit the
input (e.g. pulmonary oedema, pre-existing end-stage renal
failure). Serum K levels should be maintained in the upper normal
range of 4.5e5.5 mmol/litre to avoid arrhythmias. Insulin therapy
should be instituted if the blood sugar rises above 10 mmol/litre2
whilst bearing in mind that this will lower serum potassium levels.
Hypotension
Hypotension on arrival on the CICU is most commonly due to
hypovolaemia caused by venous pooling on transfer. There are
a number of more serious causes that must be sought and treated
if a fluid challenge, for example 250 ml of colloid over 5 minutes,
does not improve matters. A quick test to confirm that hypo-
volaemia is the cause of hypotension is to raise the patients legs,
which should raise the blood pressure in seconds.
The causes of hypotension immediately after cardiac surgery
to be considered are:

circulatory
 hypovolaemia
 massive mediastinal bleeding
 SIRS response to CPB

cardiac
 myocardial ischaemia
 myocardial dysfunction
 Kinking of a venous graft
 arrhythmias
 cardiac tamponade
 systolic anterior motion of the mitral valve

respiratory
 tension pneumothorax
 overventilation

pharmacological
 propofol or glyceryl trinitrate (GTN)
 inadvertent cessation of inotropes or vasopressors

technical error
 incorrect calibration of arterial pressure transducer
 malposition of arterial pressure transducer.
Hypertension
Hypertension can occur on arrival on the CICU or later on
waking. Increasing the dose of intravenous GTN is rapidly
effective but not always correct. Many of the following causes of
hypertension can co-exist and must be addressed:

anaesthetic
 inadequate sedation/need to extubate
 ongoing muscle relaxation without anaesthesia
 pain

temperature
 hypothermia
ANAESTHESIA AND INTENSIVE CARE MEDICINE 13:10

cardiovascular
 sympathetic vasoconstriction
 hypertrophic ventricle, for example secondary to aortic
stenosis or hypertension
 cerebrovascular accident

pharmacological
 overdose of vasoconstrictors

technical error
 incorrect calibration of arterial pressure transducer
 malposition of arterial pressure transducer.
A balance is required when selecting a target blood pressure in
the immediate postoperative period. This must incorporate the
risk of potentially fatal bleeding and the need to maintain
adequate organ perfusion. A friable aortic suture line might
require a maximum systolic pressure of 100 mmHg, but the same
patient might be habitually hypertensive and require a pressure
closer to 140 mmHg for renal perfusion. A sensible strategy is to
keep the pressure low during the first few hours only if it has to
be and then to let it rise progressively.
Heart rate, rhythm and pacing
Drugs, cardioplegia and temporary or permanent surgical inter-
ruption of conduction pathways mean that sinus bradycardia or
heart block requiring pharmacological treatment or pacing is
common. A heart rate of 90 is optimal because the ventricle is
relatively stiff while it recovers from the insult of crossclamping.
Infusions of positively chronotropic drugs such as dopamine,
dobutamine, isoprenaline or epinephrine can all be used to increase
heart rate during this period, which usually lasts about 24 hours.
Temporary pacing wires are placed when there is insufficient
response to drugs or when the surgery performed carries a high risk
of conduction problems (e.g. aortic, mitral valve replacement).
Wires are placed in the epicardium and brought out onto the
patients chest wall with atrial wires on the right and ventricular
wires on the left. Pacing can comprise two right atrial wires (AOO
or AAI), two right ventricular wires (VVI) or four atrioventricular
wires (DDD or DVI) depending on the underlying rhythm. Mal-
functioning pacing wires can trigger ventricular tachycardia (VT)
or ventricular fibrillation (VF) and should always be set in the
demand mode to avoid pacing on a T wave. If full recovery of
conduction does not occur then a permanent pacemaker will be
needed.
Atrial fibrillation (AF) occurs commonly. Fibrillating atria (or
ventricles) cannot be paced. Patients with preoperative AF will
usual have pacing set to VVI. Ventricluar wires are safer than
only atrial wires because atrioventricular conduction blockade or
AF will cause atrial pacing to be ineffective. The disadvantage of
solely ventricular wires is the loss of the atrial kick. This
contributes to ventricular preload and improves stroke volume
which can provide 20% improvement in cardiac output.
Prevention and treatment of atrial fibrillation is covered by
current guidance produced by the National Institute for Health
and Clinical Excellence.
Temperature management
Patients frequently arrive on the CICU with core temperatures
around 35 C unless both active and passive measures have been
taken. Patients at increased risk of hypothermia include those
undergoing hypothermic CPB and deep hypothermia with
504 2012 Published by Elsevier Ltd.
 CARDIAC ANAESTHESIA
circulatory arrest (DHCA). Active management of hypothermia
improves outcome and minimizes adverse effects. Methods such
as warmed intravenous fluids or heated humidified ventilation
circuits tend only to prevent further hypothermia but do not
increase core temperature. Forced-air warming systems reduce
the duration of postoperative hypothermia. Vasodilators may
enhance peripheral perfusion, but, in doing so, can decrease core
temperature by redistributing heat to the extremities.
Hypothermia can cause many problems:

increased SVR
 hypertension
 mediastinal bleeding
 increased myocardial O2 demand
 increased filling pressures masking hypovolaemia

increased risk of arrhythmias and VF

shivering causing increased O2 consumption and CO2
production

coagulopathy from decreased platelet function and
impairment of clotting cascade

prolonged time to extubation.
Care should be exercised with rewarming as the associated
vasodilatation may cause the arterial pressure to fall. Hyper-
thermia should also be avoided as this increases the cerebral
metabolic rate of oxygen consumption.
Clotting correction and bleeding
Excess bleeding after surgery can be due to a surgical cause,
a coagulopathy or both (Figure 1).
All of the following factors increase the risk of coagulopathy:

drug therapy
 aspirin
 clopidogrel
 GPIIb/IIIa inhibitors
 warfarin
 heparin

surgical factors: long CPB duration, redo surgery

haematological factors: haemodilution, massive trans-
fusion, blood dyscrasias

temperature management: hypothermic CPB, DHCA

metabolic disturbance: uraemia, hepatic dysfunction.
Figure 1 Closed drainage systems allow monitoring of blood loss, initially
every 15 minutes.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 13:10
Coagulopathy induced by surgery involving CPB is multifac-
torial. Impaired clotting can persist from surgery especially if there
is ongoing bleeding and transfusion. If available, a thromboelas-
togram (TEG) taken at least 10 minutes after protamine admin-
istration in theatre is the preferred test. It allows rapid diagnosis as
the aetiology of the coagulopathy and can guide blood product
administration. Alternatively, blood samples are sent for clotting
screen and full blood count though these laboratory results may
lag behind the clinical picture. A normal coagulation screen and
platelet count plus chest drainage of more than 400 ml/hour in the
first hour would indicate a surgical source of bleeding and that the
patient should return to theatre for exploration.
The action list for management of postoperative mediastinal
bleeding is:

check chest drains are patent

restore normothermia

control any shivering or hypertension

based on results of TEG/full blood count/clotting studies
give:
 protamine
 platelets
 fresh frozen plasma
 cryoprecipitate
 anti-fibrinolytics (e.g. tranexamic acid or aprotinin)

check ionized Ca2 levels; if low give 10 ml 10% CaCl2

consider transoesophageal echocardiography (TOE) or trans-
thoracic echocardiography (TTE) if tamponade suspected

return to theatre if conservative measures fail or evidence
of tamponade.
Postoperative cardiac tamponade
Cardiac tamponade is a clinical diagnosis in which various
physiological parameters are affected by the reduction in cardiac
output due to compression of the heart by a fluid collection
around it.
Mediastinal bleeding immediately postoperatively leads to
a rapidly accumulating collection of pericardial blood, usually
detected within 24 hours of surgery. A delayed presentation can
occur several days postoperatively. It is more common after
valve surgery than after coronary artery bypass graft alone.
Patients with valve replacements, especially mechanical valves,
are often treated with heparin or warfarin soon after surgery to
prevent thrombus formation around the valve.
The classical clinical scenario of Becks triad (increased jugular
venous pressure, hypotension and muffled heart sounds) is
frequently difficult to diagnose in a postoperative sedated and
ventilated patient. A decrease in the hourly urine output is often an
early indicator that cardiac output is compromised. Chest drains
might have precipitously stopped draining if a clot has formed.
Hypotension, tachycardia and a worsening metabolic acidosis can
be the next signs. Increased CVP, pulsus paradoxus and low-
voltage ECG complexes might not occur until later. The presence
of a PA catheter will detect a rising pulmonary artery wedge pres-
sure (PAWP), but falling cardiac index despite fluids and inotropes
or vasoconstrictors. Eventually, there will be equalization of right
atrial pressure, pulmonary artery diastolic pressure and PAWP.
Loss of the y-descent on the CVP trace can be difficult to detect.
As soon as tamponade is suspected, a TOE or TTE should be
considered; however, posterior collections are not visualized
505 2012 Published by Elsevier Ltd.
 CARDIAC ANAESTHESIA
well with TTE. If the patient deteriorates precipitously, imme-
diate chest reopening is indicated. If diagnosed and treated
promptly and correctly, cardiac tamponade should not cause an
increase in mortality. If diagnosed late when multiorgan failure is
established, prognosis worsens considerably.
Low cardiac output
The main aim of management after cardiac surgery is good
haemodynamic performance and, therefore, adequate tissue
perfusion and oxygenation. Even short periods of cardiovascular
dysfunction can lead to multiorgan failure with consequent
increased morbidity and mortality. Myocardial function is
impaired for 6e8 hours after surgery and usually returns to base-
line within 24 hours. During this period of recovery an inotropic
agent is sometimes required to avoid the development of a low
cardiac output state. When compensatory sympathetic mecha-
nisms are exhausted, a low cardiac output will manifest itself
clinically. It is not unusual for the right ventricle (RV) to be
selectively affected. Failure of the RV can be refractory to standard
therapy and difficult to treat.
The clinical features of low cardiac output are:

poor peripheral perfusion: cool, pale extremities and
sweating

pulmonary congestion and poor arterial oxygenation

oliguria from poor renal perfusion

metabolic acidosis from tissue anaerobic metabolism.
In the absence of monitoring, clinical signs of end-organ perfu-
sion are used as an indirect measure of cardiac output. Urine
output is a particularly useful monitor; however, it can be
misleading in renal impairment and when diuretic infusions are
being administered. Persisting clinical signs of low cardiac output
despite fluid resuscitation and clinically guided treatment
warrant the initiation of cardiac output monitoring; elective
cardiac output monitoring is generally reserved for higher-risk
cases. In cardiac surgery, the thermodilution pulmonary artery
flotation catheter (Figure 2) remains the gold standard form of
cardiac output monitoring; the less invasive alternatives involve
oesophageal Doppler or pulse contour analysis (Figure 3). Recent
improvements in the latter might make routine monitoring more
Figure 2 Continuous thermodilution cardiac output monitor (Vigilance II;
Edwards Lifesciences) uses a pulmonary artery flotation catheter and can
also support venous saturation (SvO2) monitoring. Reproduced, with
permission, from Edwards Lifesciences.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 13:10
Figure 3 Pulse contour analysis uses existing arterial cannula (Vigileo;
Edwards Lifesciences). Reproduced, with permission, from Edwards
Lifesciences.
common. Postoperative TOE or TTE can be very informative but
they are intermittent rather than continuous.
Monitoring is used to aid diagnosis of the cause, then
continually to assess and guide treatment. A cardiac index of less
than 2.0 litres/minute/m2 with a PAWP of greater than 20 mmHg
indicates intervention is required; however, trends over time in
haemodynamic parameters are more important than absolute
figures. A higher cardiac index than this is desirable, but it might
not be achievable. Non-cardiac correctable causes should be
excluded (respiratory, acid-base or electrolyte disturbance),
ischaemia and tamponade treated, arrhythmias controlled and
preload and heart rate optimized.
Causes of low cardiac output include:

decreased LV preload
 hypovolaemia (rewarming, bleeding, sedatives, vasodi-
lators, analgesics)
 cardiac tamponade
 increased intrathoracic pressure (high airway pressures,
tension pneumothorax)
 RV dysfunction (RV infarction, pulmonary hypertension)

decreased contractility
 pre-existing poor LV function
 myocardial stunning
 inadequate revascularization
 acidebase disturbance

arrhythmias

increased afterload
 vasoconstriction
 fluid overload and ventricular distension
 LV outflow tract obstruction (after mitral valve repair or
replacement)

diastolic dysfunction (especially with hypertrophic
ventricle)

co-existing pathologies
 SIRS and sepsis
 anaphylactic reactions (blood products/drugs)
 adrenal insufficiency (primary or if on preoperative
steroids).
Sometimes mechanical cardiac support is needed. The com-
monest form is the intra-aortic balloon pump (IABP) (Figure 4).
A long balloon is placed in the descending thoracic aorta via the
femoral artery using the Seldinger technique. It is timed to inflate
506 2012 Published by Elsevier Ltd.
 CARDIAC ANAESTHESIA

Typical intra-aortic balloon pump arterial

pressure waveform
D

120 Increased coronary

C artery perfusion

mmHg
100

B B
80
E
A

Reduced myocardial
O2 demand

A, one complete cardiac cycle; B, unassisted aortic end-diastolic

pressure; C, unassisted systolic pressure; D, diastolic augmenta-
tion; E, reduced aortic end-diastolic pressure; F, reduced systolic
pressure.
Reproduced, with permission, from Datascope Medical Co.

Figure 5

though practices vary between units (Figure 6). Appropriate

Figure 4 Intra-aortic balloon pump console. Reproduced, with permission,
from Datascope Medical Co.
in diastole and deflate in systole, so-called counterpulsation.
This displaces blood both proximally and distally, causing an
increase in diastolic pressure and a decrease in systolic pressure
(Figure 5).
The reduced myocardial O2 demand (in contrast to inotropes)
means that this method is particularly useful in:

cardiogenic shock

acute myocardial infarction

mitral regurgitation and ventricular septal defect

refractory ischaemia

weaning from CPB.
It may be helpful while waiting for surgery or coronary inter-
vention and as support during anaesthetic induction.
Aortic regurgitation is a contraindication.
The benefits of IABP counterpulsation are:

decreased afterload and increased preload

decreased myocardial O2 demand

increased coronary artery perfusion

decreased LV end-diastolic pressure

decreased LV wall tension.
A summary of postoperative haemodynamic management is
shown in Table 1.
Fast-track cardiac surgery
It used to be conventional to ventilate patients after cardiac
surgery, partly because of hypothermia and high-dose opioids.
However, extubation in the first few hours is now well accepted
patient selection, an anaesthetic using shorter-acting drugs and
normothermic bypass with active warming methods facilitates
the process. Exclusions include those with severe pulmonary
hypertension and those at high risk of bleeding overnight. There
has never been any clinical detriment demonstrated from this
process, and avoidance of CICU bed usage and decreased length
of inpatient stay are both of clinical and economic benefit. Fast
track has been defined as patient progression from 1:1 intensive
care nursing to 1:2 high-dependency nursing on the same oper-
ative day. Haemodynamics usually improve on extubation. The
criteria for tracheal extubation after cardiac surgery are:

cardiovascular stability
 heart rate 60e110 beats/minute
 MAP 60e95 mmHg
 chest drainage below 100 ml/hour

temperature stability
 not shivering
 core temperature 36 C or greater
 peripheral temperature 30 C or greater

reversal of anaesthesia
 eyes open spontaneously
 obeys commands
 moving all limbs
 comfortable on questioning

ventilation
 respiratory rate greater than 12 and less than 30 breaths/
minute
 FiO2 on T-piece 0.6 or less
 arterial oxygen pressure (Pao2) over 10 kPa, arterial
carbon dioxide pressure (Paco2) under 7 kPa.
Analgesia is provided by intravenous morphine (nurse adminis-
tered or patient-controlled analgesia) or epidural analgesia, with
supplementation from regular intravenous paracetamol.

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 CARDIAC ANAESTHESIA

Management of postoperative haemodynamic problems

BP CO Management

BPY eCOY If empty; give volume then inoconstrictor (may need to add potent
inotrope/inodilator or IABP)
eCO[/ May be oversedated; give vasoconstrictor or inoconstrictor
BP/ eCOY If empty; give volume then inodilator (balanced with constrictor)
eCO[/ Nothing
BP[ eCOY If empty; give volume then inodilator
eCO[/ Review sedation/vasodilator
BP, blood pressure; CO, cardiac output; Y, decreased; [, increased; /, normal.
Inoconstrictors/vasoconstrictors
C Dopamine: no evidence in renal dose but useful drug for dealing with mild vasodilation and myocardial stunning after bypass.
C Epinephrine: good when potent inotrope needed and particularly useful in RV failure but causes tachycardia and lactic acidosis.
C Norepinephrine: alone acts as potent vasoconstrictor causing reflex bradycardia and reduction in cardiac output, but in presence of vasodilation
(anaesthesia, systemic inflammatory response syndrome, phosphodiesterase (PDE) inhibitors), preserves or raises cardiac output because it is
also a b1-agonist. Useful to maintain
mean arterial pressure in well-filled patients with evidence of good cardiac output. Important to wean off when cause of vasodilation resolved.
Inodilators/vasodilators
C Dobutamine: does occasionally have a place but vasodilation and tachycardia make it difficult to use.
C PDE inhibitors (e.g. milrinone, enoximone): excellent when potent inotrope needed and when used together with norepinephrine to balance
systemic vascular resistance. Duration of action lengthy and accumulate in renal failure. Need loading dose, often given on bypass and must be
given very slowly if started postoperatively because these are potent dilators.
C Glyceryl trinitrate: standard venodilator, titratable with rapid onset and offset. Sodium nitroprusside is both a vaso- and venodilator but is rarely
used.
A drug with pure inotropic action without either vasoconstriction or vasodilation side effects is not yet currently available in the UK
(e.g. levosimendan).

Resuscitation after cardiac surgery
Management of cardiac arrest immediately after cardiac surgery
differs from conventional algorithms. Cardiac arrest can be
identified immediately as the patient is highly monitored and
chest reopening is a standard part of resuscitation. A course,
recently endorsed by the European Resuscitation Council,
advocates a standardized cardiac surgery arrest protocol.3 If all
traces on the monitor are flat and there is no carotid or femoral
pulse after 10 seconds, commence basic life support for non-VF/
VT arrests only. In contrast, VF/VT arrests e because external
Figure 6 Early extubation is beneficial for many patients.
massage can cause injury e are treated with three consecutive
attempts at defibrillation (150e360 J biphasic) before basic life
support and emergency re-sternotomy. While waiting for chest
opening, cardiopulmonary resuscitation is performed at 30:2
with a single shock every 2 minutes. Amiodarone 300 mg is
administered into a central vein after the third failed shock.
Reversible causes are treated. Internal cardiac massage and
internal defibrillation can be commenced once the chest is open
and, if unsuccessful, CPB can be initiated. Severe bradycardia or
asystole is treated with immediate pacing e set to DDD at 90
e100 bpm at maximum amplitude e if pacing wires are in situ.
Atropine is administered only if epicardial pacing is either
unavailable or unsuccessful. Again, if no immediately reversible
causes are identified for non-VF/VT arrests, emergency re-
sternotomy is indicated. For both the shockable and non-
shockable sides of the protocol, vasopressors are used with
caution and only as instructed by a senior doctor.
Arrhythmias can severely compromise cardiac output.
Atrial arrhythmias such as atrial fibrillation do not usually occur
until 24e48 hours postoperatively, unless there is pre-existing
atrial fibrillation. Ventricular arrhythmias are uncommon unless
K levels are abnormal. They can be a signal of ischaemia or
impending cardiac arrest. External defibrillator pads should be
connected immediately. Amiodarone is the drug of choice for the
most tachyarrhythmias. VT that severely compromises blood
pressure is treated with sedation and DC cardioversion followed by
intravenous amiodarone 150 mg over 20 minutes, repeated if
necessary.

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 CARDIAC ANAESTHESIA
Long-term care of the postoperative cardiac patient
Although some patients are fast tracked and most of the rest
leave CICU within 48 hours, some experience organ failure and
a longer length of stay or a readmission. Although relative results
have improved, the proportion of long-term patients is
increasing, probably because of the sicker and older patient
population now considered for cardiac surgery.
The common complications seen in CICU patients are:

respiratory failure

renal failure

stroke

sternal dehiscence/wound infection

sepsis

heparin-induced thrombocytopenia

chronic cardiac failure.
Maintenance of good tissue perfusion perioperatively is good
preventative medicine.
The factors leading to organ failure include:

pre-existing co-morbidities

cardiopulmonary bypass

exaggerated systemic inflammatory response

excessive bleeding

major blood product transfusion

cardiac tamponade

poor cardiac function after bypass.
Respiratory failure
Many patients are ex- or current smokers and many have chronic
obstructive airways disease. Postoperative basal collapse or
consolidation is almost universal, even when the left pleura has
not been opened to harvest the left internal mammary artery.
Widespread alveolar collapse can occur because of sputum
retention or intraoperative lung collapse. There might be a collec-
tion of blood in opened pleural spaces. Acute lung injury/acute
respiratory distress syndrome can occur alone (pump lung) or as
part of multiorgan failure. In the early phase, this results in alveolar
oedema and poor gas exchange. Pleural effusions due to water
overload, cardiac failure and low plasma albumin concentration
are common in long-term patients following cardiac surgery. The
management of these patients should comprise lung protective
ventilation strategies and aiming to achieve negative fluid balance.
General intensive care medicine measures including oral hygiene,
stress ulcer prophylaxis and 30 head up tilt should be instituted.
Patients with limited cardiac reserve or with tight left internal
mammary artery grafts might not tolerate high positive end-expi-
ratory pressure levels.
Renal failure
Acute renal failure is a recognized complication of cardiac
surgery. Oliguria with a serum creatinine of approximately 200
mmol/litre is relatively common. Most patients recover before
renal failure is established. A sensible strategy is to monitor and to
maintain cardiac index at or above 2.5 litres/minute/m2 and
a MAP of 70 mmHg, or higher in a previously hypertensive
patient, if these are achievable. Hydration should be as liberal as is
tolerated by filling pressures and by respiratory function. Liberal
use of colloids and crystalloids containing sodium chloride often
leads to a hyperchloraemic acidosis for which a change to 1.4%
sodium bicarbonate as maintenance fluid might help.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 13:10
The opportunity to place a double-lumen central venous
cannula ready for RRT should be taken early. This will allow
prompt institution of RRT as soon as there is an indication:
acidosis, hyperkalaemia, problematic fluid overload or uraemia.
The only reason to use diuretics is if the sole problem is fluid
overload, in which case a bolus of up to 1 mg/kg frusemide
followed by an infusion of 1e4 mg/hour can maintain adequate
urine output in a patient destined for early renal recovery.
Neurological impairment
During the perioperative period cerebral hypoperfusion, macro-
or micro-embolization may result in varying degrees of neuro-
logical injury ranging from subclinical changes detected only by
magnetic resonance imaging, through subtle deficits (up to 40%)
to debilitating stroke (1e5%). Slow waking, confusion or focal
neurological deficits are common presenting signs. Primary
haemorrhagic stroke is uncommon.
Invasive ventilation should be continued until good sponta-
neous respiration and airway reflexes return. A reduced
conscious level may prolong the requirement for ventilation and
tracheostomy may be indicated. Impaired swallowing and loss of
pharyngeal reflexes make aspiration a serious risk.
Urgent intervention such as thrombolysis is usually contra-
indicated, and the need for antiplatelet therapy or anti-
coagulation is usually guided by the surgery. Ischaemic stroke
can take 48 hours to develop signs on computed tomography
scans though some patients are scanned earlier to exclude bleeds
if anticoagulation is planned. The prognosis is often difficult to
predict and variable, though many patients with severe deficits
make significant improvements.
Stroke is a devastating complication and is feared by many
patients and their families. It is important that patients and their
families are warned about this potential complication. Good
communication and an honest guide to the likely prognosis and
further management are needed. Full assessment by a neurolo-
gist or stroke specialist and involvement of the multidisciplinary
team are beneficial. A
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FURTHER READING
Bojar RM. Manual of perioperative care in adult cardiac surgery. 4th edn.
Blackwell: Massachusetts, 2004.
Klein A, Vuylsteke A, Nashef SAM. Core topics in cardiothoracic critical
care. Cambridge: Cambridge University Press, 2008.
Mackay JH, Arrowsmith JE, eds. Core topics in cardiac anaesthesia.
Cambridge: Greenwich Medical Media, 2004.
509 2012 Published by Elsevier Ltd.