Page 340 - ACCCN's Critical Care Nursing

Cardiac Surgery and Transplantation 317

or ischaemic injury often involves fluid resuscitation to a hospital discharge is predictive of long-term sinus node
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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
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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
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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,
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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
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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
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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
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ventricular epicardial pacing wires are inserted and atrial of rejection and CAV. Standard use of cyclosporine
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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
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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