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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3612_Библиотеки_им_академика_М_И_Перельмана
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Key Questions in CONGENITAL CARDIAC SURGERY
Many precipitants, such as infection, pulmonary hypertension
or systemic vasodilatation, acutely disrupt this equilibrium,
exacerbating cyanosis or congestive heart failure.
9 What are the principles of anaesthesia for patients with
congenital heart disease?
The circulation may be destabilised by many events that occur during
•
anaesthesia, including:
a) reduced venous return to the right ventricle;
b) reduced myocardial function;
c) increased pulmonary vascular resistance — with subsequent
reduced venous return to the left ventricle;
d) decreased systemic vascular resistance — with reduced aortic
root pressure, potentially impairing coronary artery blood flow;
e) abnormal temperature or glucose availability — altering
enzyme function in the myocardium and other tissues.
250
As patients are usually hypovolaemic, secondary to pre-operative
•
starvation and vasodilatation caused by anaesthetic agents, venous
return must be carefully monitored.
Excess bleeding, potentially due to failed haemostatic management,
•
may cause reduced preload and circulatory instability.
Many anaesthetic agents suppress myocardial function. These
•
effects are minimised by balanced anaesthetic techniques, typically
utilising opioids, sedatives and a muscle relaxant.
Induction and extubation are high-risk periods, requiring extra
•
vigilance, as both hypoventilation and positive intrathoracic pressure
causing hypercapnia can increase pulmonary vascular resistance
(PVR).
Hypothermia and hyperthermia are a hazard to the circulation and
•
metabolic homeostasis. Effective temperature control includes active
warming or cooling, both off and on cardiopulmonary bypass.
Adequate temperature control helps to minimise coagulation
abnormalities.
Neonates have minimal ability to store glycogen and glucose-
•
containing fluids may be required.
Endocarditis is a risk and prophylactic antibiotics should always be
•
considered.
Patients with abnormal connections between the left and right heart
•
are at risk of paradoxical emboli from intravenous injections.
7 Anaesthesia and congenital heart disease
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10 What are the principles of anaesthesia in the presence
of a cyanotic lesion?
Cyanosis occurs when arterial blood contains deoxyhaemoglobin at
•
concentrations greater than 20g/L. In cyanotic lesions, it can worsen
when:
a) oxygen saturation in the pulmonary veins is reduced due to a
ventilation-perfusion mismatch, such as with ventilatory failure,
pulmonary oedema or pneumonia;
b) excessive right-to-left shunting.
Management of cyanosis involves manipulation of ventilation and
•
vascular resistance.
Right-to-left shunting is encouraged by a rise in PVR, a fall in
•
systemic vascular resistance (SVR) or a combination of both.
PVR elevation may be caused by hypoxia, hypercarbia or acidosis.
•
Positive end-expiratory pressure (PEEP) during intermittent positive
pressure ventilation (IPPV) directly increases PVR but may indirectly
decrease it by avoiding alveolar collapse and subsequent hypoxia.
Poor fluid resuscitation results in acidosis and increased PVR,
•
whereas fluid overload causes pulmonary oedema, hypoxia and
increased PVR.
Extubation is a particularly challenging period. Although early
•
extubation avoids coughing and increased PVR, due to irritation from
the endotracheal tube, it risks hypoxia and hypercarbia.
Anaesthetic agents frequently reduce SVR and systemic
•
vasopressors may be needed to maintain the balance between PVR
and SVR.
251
11 What are the principles of management in a patient
undergoing repair of an Ebstein’s anomaly?
Ebstein’s anomaly occurs when the tricuspid valve leaflets fail to
•
delaminate from the myocardium. The functional annulus is displaced
into the right ventricle with varying degrees of ‘atrialisation’ of the
right ventricle, tricuspid regurgitation and right atrial dilatation.
Cardiac output may fall due to increased regurgitant flow.
The main anaesthetic risks include:
•
a) poor cardiac output;
b) right-to-left shunting through an interatrial communication;
c) increased susceptibility to arrhythmias.
252
Key Questions in CONGENITAL CARDIAC SURGERY
The goals are to minimise PVR, optimise preload and maintain
•
myocardial contractility.
Maintaining sinus rhythm and right ventricular preload more
•
effectively supports cardiac output than using inotropes or
vasopressors.
Some authors advocate the use of a small dose of a vasopressor
•
agent to maintain adequate systemic perfusion pressure and avoid
the administration of a large amount of fluid, thus preventing further
dilatation of the right ventricle.
12 What are the principles of managing a neonate with
hypoplastic left heart syndrome?
Neonates with HLHS have a single functional (right) ventricle. Mixed
•
pulmonary and systemic venous blood is ejected into systemic and
pulmonary circulations (Figure 5). Flow distribution to the two
circulations is dependent on PVR and SVR.
In these patients, neonatal PVR is too high to allow passive
•
pulmonary flow, making conversion to a parallel circulation
impossible.
The first operation is usually a Norwood procedure with a neo-aorta
•
constructed from pulmonary artery and is performed within the first
week of life. The pulmonary circulation is provided by a BlalockTaussig shunt or a RV-to-PA conduit (Sano modification, Figure 6).
Pre-operatively, the goals are to optimise:
•
a) pulmonary function, especially to avoid infection;
b) systemic perfusion, by:
i) maintaining a patent ductus arteriosus using
prostaglandin E
ii) keeping the SVR low and PVR high to maintain balance;
iii) using inotropes.
The peri-operative challenges include:
•
a) balancing pulmonary and systemic perfusion in the context of
pulmonary hyper-reactivity. This can potentially be achieved by
modifying ventilation parameters;
b) managing myocardial dysfunction and ischaemia;
c) minimising cerebral hypoxia during circulatory arrest — which
can be improved by increasing the:
i) perfusion pressure;
;
2
7 Anaesthesia and congenital heart disease
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253
Figure 5. Hypoplastic left heart syndrome, characterised by hypoplasia
of the mitral valve, aortic valve, left ventricle and ascending aorta. The
systemic circulation is maintained by flow across a large patent ductus
arteriosus. Blood circulates both antegradely in the descending aorta
and retrogradely into the aortic arch and coronary arteries. A drop in
pulmonary vascular resistance will favour circulation into the lungs and
reduce flow into the systemic circulation. RA = right atrium; RV = right
ventricle; LA = left atrium; LV = left ventricle; IVC = inferior vena cava; SVC
= superior vena cava; Asc Ao = ascending aorta; PDA = patent ductus
arteriosus; MPA = main pulmonary artery.
ii) haemoglobin;
iii) arterial carbon dioxide tension.
Near-infrared spectroscopy (NIRS) is useful to monitor cerebral
•
saturations.
254
Key Questions in CONGENITAL CARDIAC SURGERY
Figure 6. Circulation following the Norwood procedure, where
pulmonary venous (red) and systemic venous (blue) blood mix in the
atria via an atrial septal defect, resulting in mixed blood ejected into
common outflow with a balanced circulation. RA = right atrium; RV = right
ventricle; LA = left atrium; LV = left ventricle; IVC = inferior vena cava; SVC
= superior vena cava; Neo-Ao = neo-aorta; BTS = Blalock-Taussig shunt.
13 What are the anaesthetic considerations for a patient
with a single ventricle?
Single ventricles provide flow to both the pulmonary and systemic
•
circulations, acting as systems in parallel, with flow depending on the
relative resistances in the circuits.
A bidirectional Glenn procedure (Figure 7) can usually be performed
•
by the age of 6 months. Pressure monitoring from internal jugular
lines then reflects pulmonary artery pressures.
7 Anaesthesia and congenital heart disease
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255
Figure 7. Bidirectional Glenn procedure, where the superior vena cava
is anastomosed to the pulmonary artery. Oxygenated blood (red) enters
the right atrium through an atrial septal defect and mixed blood (purple)
is ejected into the systemic circulation. BTS = Blalock-Taussig shunt; PA =
pulmonary artery; SVC = superior vena cava.
Total cavopulmonary connection (TCPC) is usually achieved by 4
•
years. As blood flow through the lungs is then entirely passive,
minimising the PVR is vital (Figure 8).
When managing a TCPC circulation, it is important to avoid an
•
elevation in PVR due to:
a) hypoxia;
b) hypercarbia;
c) acidosis;
d) drugs (e.g. ketamine).
256
Key Questions in CONGENITAL CARDIAC SURGERY
Figure 8. Total cavopulmonary connection (TCPC) circulation, where
venous blood (blue) flows passively from the superior and inferior vena
cavae into the pulmonary circulation. Oxygenated blood (red) returns to
the right ventricle via an atrial septal defect and is ejected into the
systemic circulation. PA = pulmonary artery; IVC = inferior vena cava;
SVC = superior vena cava.
Hypovolaemia is poorly tolerated in passive circulations.
•
As the risk of arrhythmias is increased in this patient population and
•
is poorly tolerated, maintenance of sinus rhythm is paramount. This
is particularly problematic where the whole right atrium is within the
circuit (classical Fontan) rather than only the vena cavae (TCPC).
Often the function of the systemic ventricle, which is a morphological
•
right ventricle, is impaired and responds poorly to increased
metabolic demand. Over time, hypertrophy and dilatation occur and
response to inotropes is poor.
7 Anaesthesia and congenital heart disease
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Central venous lines are a very significant risk, especially for
•
thrombosis or post-surgical line obstruction to venous drainage.
14 What are the principles of anaesthesia in a patient
undergoing repair of coarctation of the aorta with poor
left ventricular function?
All obstructions to systemic blood flow causing a severe increase in
•
afterload lead to upper body hypertension and congestive heart
failure. In patients with coarctation of the aorta, the obstruction can
cause severe impairment of left ventricular function in the early days,
especially when the PDA spontaneously closes.
When preparing for surgery in these patients, the blood pressure
•
may be monitored above and below the coarctation via the right
radial and femoral arteries.
Pre-operative inotropes may be required to support ventricular
•
contractility and cardiac output.
Significant proximal hypertension with cross-clamping of the aorta
•
may require vasodilators.
Some centres use a small dose of heparin during the procedure to
•
prevent stasis-related clotting in the proximity of the vascular clamps.
Hyperventilation should be avoided throughout, as it causes
•
vasoconstriction with reduced cerebral and spinal perfusion.
Postoperative analgesia provides comfort and control of
•
hypertension. Intercostal blocks can be sited under direct vision
intra-operatively to effect this.
257
15 What are the principles of anaesthesia for a patient
with pulmonary atresia and an intact ventricular
septum?
Pulmonary atresia with intact ventricular septum (PA-IVS) is one of
•
the most challenging conditions that an anaesthetist might need to
face (Figure 9).
It is characterised by right ventricular hypertrophy and hypoplasia,
•
capable of generating supra-systemic pressures, and varying
degrees of tricuspid valve hypoplasia.
The degree of hypoplasia of the tricuspid valve is directly linked to the
•
presence of coronary sinusoids. These ventriculo-coronary fistulae
render myocardial perfusion dependent on intracavitary pressures.
As a result, any change in preload, central venous pressure and
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systemic vascular resistance, can affect myocardial perfusion,
especially when coronary arteries present with significant stenoses.
258
Key Questions in CONGENITAL CARDIAC SURGERY
Figure 9. Pulmonary atresia with intact ventricular septum. As blood
cannot be ejected from the right ventricle, all pulmonary flow occurs
through a patent ductus arteriosus. Venous blood (blue) enters the left
atrium via an atrial septal defect, mixing with oxygenated blood (red)
from the pulmonary veins. Note the right ventricular dependent sinusoids
feeding the coronary circulation. ASD = atrial septal defect; PDA = patent
ductus arteriosus.
Pulmonary flow is PDA-dependent, requiring pre-operative
•
prostaglandin E2.
Although radiofrequency perforation and dilatation of the valve may
•
be possible, tamponade is a recognised risk and adequate vascular
access is required pre-procedure.
Total atresia of the infundibulum requires a modified Blalock-Taussig
•
shunt (BTS) to produce a balanced circulation.
Inotropes are associated with an increased subpulmonary gradient
•
and should be avoided where possible.
7 Anaesthesia and congenital heart disease
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16 What are the principles of anaesthesia for ligation of a
patent ductus arteriosus in a preterm neonate?
Patency of the ductus arteriosus in preterm infants is inversely
•
proportional to gestational age. Approximately 50% of preterm
infants <1200g will have a PDA.
Preterm neonates are challenging to anaesthetise and full cardiac
•
assessment is necessary, as PDA is associated with other
conditions, such as coarctation of the aorta, ventricular septal defect,
pulmonary stenosis and aortic stenosis.
Respiratory disease and intermittent positive pressure ventilation
•
(IPPV) elevate PVR, inhibiting closure of the PDA.
Although PDA ligation is usually a short procedure with minimal
•
blood loss, significant bleeding may occur if the pulmonary artery,
aorta or ductus are torn. Sufficient vascular access should be in
place.
Although retraction of the lung during surgical exposure is
•
unavoidable, it further impairs ventilation and is poorly tolerated.
Inotropic support may be necessary postoperatively.
•
Recurrent laryngeal nerve injury may cause stridor following
•
extubation.
Some cases can now be undertaken in the cardiac catheter
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laboratory.
259
17 What are the principles of anaesthesia for a patient
with an obstructed total anomalous pulmonary venous
connection?
In obstructed TAPVC, the pulmonary venous return is limited by the
•
severity of the obstruction. Significant stenosis has several
catastrophic consequences, including:
a) low cardiac output and shock, due to a lack of LV preload;
b) pulmonary oedema due to pulmonary venous hypertension;
c) right heart failure and systemic venous congestion due to
pulmonary arterial hypertension.
Presenting features include cyanosis, tachypnoea, acidosis,
•
pulmonary oedema, pulmonary hypertension and right heart failure.
Management of pulmonary hypertension by IPPV to improve
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oxygenation may be necessary pre-operatively.
Arterial access is required for monitoring of both cardiovascular and
•
metabolic status.
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