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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
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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