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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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340
Key Questions in CONGENITAL CARDIAC SURGERY
6 What baseline information regarding cardiopulmonary
anatomy and function is required when assessing an
ACHD patient on arrival in the intensive care unit?
Primary cardiac lesion(s).
•
Surgical or catheter interventions that have been undertaken.
•
Any important residual haemodynamic lesions (static or dynamic).
•
Optimal intra-operative and postoperative haemodynamics and
•
ventilatory settings for the patient.
In cases admitted postoperatively, it is additionally important to know
•
whether the surgeon achieved all they had aimed to, or whether there
were any unexpected intra-operative challenges.
7 What are the minimal baseline investigations for
assessment of a critically ill ACHD patient?
The normal physiological status of the patient may be very abnormal
•
when compared with that of a patient with acquired cardiac disease.
In this patient population, trying to correct what may be adaptive
•
pathophysiological processes can potentially be harmful.
It is important to have knowledge of when the patient was last well,
•
and most recent (prior to admission) values of:
a) haemoglobin;
b) oxygen saturations;
c) systemic and pulmonary pressures;
d) electrocardiogram (beware in patients with massive atrial
enlargement, where atrial tachycardia may mimic sinus
tachycardia);
e) cardiac function on the most recent echocardiogram or cardiac
magnetic resonance imaging scan.
These should be compared with values obtained on admission to the
•
intensive care. Additional investigations that should be undertaken
(depending upon the clinical situation) are:
a) plain chest radiograph;
b) routine laboratory investigations;
c) haematinics (if cyanotic, with automated electronic particle
counts);
d) coagulation screen (citrate adjusted if erythrocytotic with
haematocrit >60);
e) pregnancy test (if female of childbearing age);
9 Adult congenital cardiac intensive care
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f) blood cultures;
g) serum or faecal alpha-1 antitrypsin (Fontan circulation with
ascites).
8 Describe some of the challenging situations when
managing patients with ACHD on the intensive care
unit.
All ACHD patients have the potential to have very abnormal
•
cardiopulmonary physiology; however, any anatomy that leaves a
patient with an effectively univentricular circulation, the presence of
systemic-pulmonary shunts, the potential to shunt bidirectionally, and
the Fontan circulation are particularly challenging in the critical care
setting.
A number of diagnoses and previous interventions may make blood
•
pressure monitoring inaccurate, including patients with:
a) previous or existing classic or modified Blalock-Taussig (BT)
shunt — where blood pressure will under-read, and the
catheter or cuff should be placed on the contralateral arm.
With bilateral shunts, lower body blood pressure readings may
be more accurate;
b) coarctation, previous femoral bypass or multiple cardiac
catheterisation — where lower limb pressure may under-
represent the central pressure;
c) radial line cannulation or surgical cutdown (especially neonatal)
— which may have an ulnar-dominant or absent radial artery.
Cuff pressure is usually accurate however, and ulnar
cannulation should be avoided.
341
Patients with cyanotic congenital heart disease and those with
•
univentricular circulation tolerate hypovolaemia poorly. Assessment
of volaemic status is further complicated by coexisting impairment of
ventricular function and/or atrioventricular valve regurgitation.
Monitoring central venous pressure in patients with Fontan or total
cavo-pulmonary connection (TCPC) circulation is not possible.
The presence of basal crepitations in a patient with pulmonary vein
•
stenosis may not indicate systemic ventricular failure or volume
overload but rather pulmonary vein congestion, and hence, should be
interpreted with caution.
Measuring cardiac output in congenital heart disease (particularly
•
where complex) can be challenging. Pulmonary artery catheterisation
is not possible in the presence of tricuspid or pulmonary atresia, a
342
Key Questions in CONGENITAL CARDIAC SURGERY
Fontan circulation or TCPC. Furthermore, the presence of
intracardiac and extracardiac shunts make pulmonary artery catheter
data unreliable. If non-invasive measures are used, the presence of a
chronically low cardiac output state and correspondingly small aorta
mean that oesophageal Doppler measures may be invalid.
9 What are the differences in pacing in the critically ill
ACHD population compared to patients with acquired
cardiac disease?
When considering the pacing route (transvenous vs. epicardial),
•
certain circulations make traditional transvenous routes impossible,
such as tricuspid atresia. In this situation, alternative access must be
used (Figure 2) or in an emergency, transcutaneous pacing may be
required.
Where cardiac output is borderline, pacing optimisation using
•
echocardiography can be helpful, although there is little evidence in
the literature to date.
Figure 2. Access for pacing in a patient with tricuspid atresia. A = atrial
or proximal pulmonary vein; B = epicardial; C = transaortic access; TA =
tricuspid atresia; AoV = aortic valve; RV = rudimentary right ventricle; LV
= left ventricle; MV = mitral valve.
9 Adult congenital cardiac intensive care
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In patients with restrictive ventricular disease and limited stroke
•
volume, high pacing rates may be required (occasionally up to 120
bpm) in order to maximise cardiac output.
Although indications for biventricular pacing are in general the same
•
as in acquired cardiac disease, where the patient is critically ill due
to limited cardiac output, expert advice should be sought.
10 What are the main differences regarding respiratory
support for a critically ill patient with ACHD and
acquired cardiac disease?
Associated craniofacial abnormalities seen in some syndromes may
•
complicate both the process of intubation and ventilation, and make
non-invasive ventilation impossible.
Tracheostomy may be complicated due to the presence of collateral
•
blood vessels or abnormal airway anatomy.
In patients with associated congenital pulmonary disease, there may
•
be a hypoplastic lung or severe V/Q mismatch. Associated
pulmonary hypertension may or may not need treating. Comparison
with previous investigations is crucial, and interpretation of values
must be in the context of right ventricular function.
Finally, when planning weaning from mechanical ventilation, previous
•
cardiac surgery (possibility of phrenic nerve injury) or associated
congenital musculoskeletal deformities must be taken into
consideration.
343
11 What are the main differences regarding non-
cardiopulmonary organ dysfunction in a critically ill
patient with ACHD and acquired cardiac disease?
Associated gastrointestinal anatomical defects are not uncommon,
•
and may include asplenia/polysplenia, GI or renal dysfunction.
In patients with cyanotic congenital heart disease, associated renal
•
dysfunction is common, and tolerance of intravenous contrast agents
may be poor, with a rapid rise in serum potassium seen postprocedure.
Abnormal liver function tests are common, and may be a reflection of
•
high venous pressure, low cardiac output, or as a result of
medication.
Thyroid dysfunction is common in ACHD patients, and should be
•
managed in the context of critical illness in the standard manner.
In a patient with severe right ventricular heart dysfunction, low rates
•
of enteral feeding may be required to avoid ileus.
344
Key Questions in CONGENITAL CARDIAC SURGERY
12 What are the specific considerations in a patient being
managed postoperatively following coarctation
repair?
Patients following a coarctation repair are closely monitored for
•
rebound arterial hypertension and mesenteric ischaemia.
Spinal neurological damage is a rare but a reported complication.
•
There is literature discussing the use of cerebrospinal fluid drainage
•
following thoracoabdominal aortic surgery and a reduction in the
incidence of neurological injury; however, its role in the ACHD
population is unknown.
13 What are the specific challenges for patients on the
intensive care unit following interventional closure of
an atrial septal defect?
The incidence of arrhythmias, both tachycardia and bradycardia, are
•
high in the immediate post-procedural period. In the more elderly
patient population, there may be significant restrictive left ventricular
(as well as right ventricular) disease. If the cardiac output remains
suboptimal despite pacing, inotrope and volume resuscitation,
fenestration should be considered to maintain cardiac output (but at
the expense of cyanosis).
Pre-operative pulmonary hypertension may take time to resolve post-
•
procedure.
14 What are the principles of managing a patient with an
atrioventricular septal defect with inadequate cardiac
output?
Although atrioventricular septal defects (AVSDs) tend to be repaired
•
in childhood, adults do present with partial defects, which can be
repaired.
If the cardiac output is inadequate postoperatively and particularly in
•
the setting of increasing inotropic support, in addition to exclusion of
tamponade, left and/or right ventricular failure, arrhythmia and left
ventricular outflow tract obstruction should be specifically excluded
using echocardiography.
15 What are the challenges in managing an ACHD patient
following surgery for tetralogy of Fallot?
Adults with tetralogy of Fallot are most likely to have undergone re-do
•
surgery, although primary repair may be undertaken in a small number
of cases.
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Most patients undergoing redo surgery for tetralogy have an
•
uncomplicated postoperative course.
Severe right ventricular dysfunction pre-operatively should be
•
managed in the usual way.
In patients who have had either primary repair, or where there has
•
been relief of significant proximal pulmonary artery stenosis, the
increase in pulmonary blood flow can significantly increase lung
capillary permeability, and acute lung injury can ensue.
16 What specific considerations or concerns should be
addressed following surgery for Ebstein’s anomaly?
The immediate postoperative care strategy for patients with repair of
•
Ebstein’s anomaly is largely driven by their residual right ventricular
function.
In addition, there is a significant incidence of postoperative atrial
•
arrhythmias, and restrictive left as well as right ventricular function.
Care must be taken to:
•
a) maintain sinus rhythm and optimise pacing using
echocardiography;
b) avoid elevation in venous pressure;
c) avoid over-distension of the right ventricle by excessive fluid
administration;
d) measure filling pressure and cardiac output with care — and
when inadequate, take action early;
e) maintain normoxia and normocarbia, whilst avoiding aggressive
ventilation.
345
Worsening liver function tests in such patients are not usually related
•
to a drug reaction but rather an indication of an inadequate cardiac
output in the context of a high venous pressure. Where the cardiac
output is inadequate, interatrial fenestration may be considered (if not
already done) or, alternatively, percutaneous/surgical acute
mechanical circulatory support.
17 What factors should be considered when managing
patients with underlying cyanotic heart disease in the
intensive care unit?
Over years, these patients will have developed adaptive mechanisms
•
to increase oxygenation to tissues, including an increase in cardiac
output and haematocrit, and a rightward shift in the oxyhaemaglobin
dissociation curve.
346
Key Questions in CONGENITAL CARDIAC SURGERY
It is not necessary to try to normalise their oxygen saturations to
•
those of non-cyanotic patients, but rather to those they have when
well, unless the intervention was intended to restore normoxia.
Patients are prone to haemostatic abnormalities, and these correlate
•
with the level of erythrocytosis:
a) abnormalities of prothrombin time, partial thromboplastin time,
factors V, VII, VIII, IX and thrombocytopaenia have been
documented but do not usually need treating;
b) citrate bottles adjusted for the haematocrit must be used when
measuring the INR.
Determining the volaemic status and appropriate level of haemoglobin
•
can be challenging, but certain principles apply. These patients are
intolerant of hypovolaemia and must be kept well hydrated.
Whether the transfusion parameters for intensive care are
•
appropriate for these patients is not clear, and although there is little
or no evidence in the literature, some intensivists will have a lower
threshold for transfusion than in the non-cyanotic patient population.
Routine venesection is not indicated, and iron deficiency is relatively
•
common.
In any patient admitted with abnormal neurology, headache or post-
•
ictal, a high index of suspicion should exist for cerebral abscess or
haemorrhage.
Hyperviscosity and arteriolar vasoconstriction can lead to
•
hypoperfusion of the kidneys and subsequent renal failure. Any
investigation that requires intravenous contrast must be performed
with the patient well hydrated and using appropriate precautions to
prevent further renal injury. Those with significant kidney injury are at
risk of developing marked hyperkalaemia following administration of
intravenous or intra-arterial contrast media.
18 What are the principles of managing a failing right
ventricle on the intensive care unit?
When in the subpulmonary position, the failing right ventricle can be
•
supported using standard inotropic agents whilst avoiding pulmonary
vasoconstrictors.
Although no one positive inotropic agent has been shown to be
•
superior to another, there are theoretical benefits in using
levosimendan, in terms of its effects on VA coupling.
Any potentially treatable underlying cause should be addressed,
•
such as volume overload or arrhythmia, including heart rate and
pacing optimisation, guided by echocardiography.
9 Adult congenital cardiac intensive care
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Cardiac output may be maintained or improved by optimising preload
•
and minimising right ventricular afterload (Table 1).
Table 1. Improving cardiac output by optimising preload and reducing
afterload.
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Diuretics
Pressors
Feeding/nutrition
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Airway pressures
Pleural collections
Airways
Overfilling increases RV filling pressure, size and wall stress,
impairing RV function.
Excessive systemic vasodilatation may reduce RV preload to a
level that is detrimental in particular in the presence of a
restrictive RV. Cautious vasoconstriction (with noradrenaline)
may be indicated, together with volume resuscitation.
Any increase in intra-abdominal pressure potentially reduces
venous return to the right heart. The combination of
postoperative status ± borderline cardiac output and high
venous pressure puts the patient at high risk of gut ischaemia.
Introduction of enteral feeding should therefore be cautious.
Optimising airway pressures (minimising peak, plateau and
positive end-expiratory pressures) should be balanced carefully
against the development of basal atelectasis and hypoxaemia.
Pleural collections should be managed aggressively in the
context of RV failure.
Bronchoconstriction may be treated using bronchodilators.
347
Pulmonary vascular
resistance
Arterial blood gases
Positive pressure
ventilation
Evidence of elevated pulmonary vascular resistance should be
countered by the use of inhaled or systemic pulmonary
vasodilators.
Hypoxia and/or hypercarbia result in pulmonary vasoconstriction.
Normoxia and normocarbia should be aimed for.
Positive pressure ventilation will reduce venous return, and
generally early extubation is recommended; however, this must
be balanced against the risk of basal atelectasis and abnormal
arterial blood gases.
348
Key Questions in CONGENITAL CARDIAC SURGERY
Pulmonary arterial hypertension, even if only moderate, should be
•
treated if the cardiac output is inadequate in the context of
subpulmonary right heart failure. Additional treatment options include:
a) inhaled nitric oxide;
b) nebulised prostacyclin;
c) oral or intravenous sildenafil (care — may have systemic
effects).
In the event of progressive or worsening haemodynamic status, early
•
implementation of acute mechanical circulatory support should be
considered.
19 What are the principles of managing a failing systemic
morphologically right ventricle in the intensive care
unit?
This may be seen in a number of conditions, including congenitally
•
corrected transposition of the great arteries (ccTGA) or TGA
repaired with an atrial switch procedure.
Reversible causes (arrhythmia, volume overload) should be sought
•
and treated.
In these patients, the coronary arteries are usually angiographically
•
unobstructed. If an electrocardiogram suggests ischaemia, however,
coronary angiography is indicated.
Interventions used for systemic ventricular failure in the non-congenital
•
patient (pharmacological and mechanical support) may be less useful
in this patient population, although intra-aortic balloon counterpulsation
can be helpful (taking care to use an appropriately sized balloon for the
individual patient aortic diameter) in older patients.
The role of newer inodilators, such as levosimendan, is uncertain.
•
In some centres, multi-site pacing has been used with good effect;
•
however, even simple heart rate optimisation and modification of
atrioventricular (AV) delay may significantly alter haemodynamics.
In the event of progressive or worsening haemodynamic status, early
•
implementation of acute mechanical circulatory support should be
considered.
20 What considerations should be made when managing
patients with a Fontan circulation in the intensive care
unit?
The combination of univentricular circulation and systemic venous
•
hypertension in a Fontan circulation is challenging to manage.
9 Adult congenital cardiac intensive care
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The passive flow of blood from the systemic venous circulation to the
•
pulmonary circulation depends upon adequate preload and
avoidance of pulmonary hypertension.
The positive pressure involved in mechanical ventilation does
•
considerably reduce the systemic cardiac output and can cause
significant haemodynamic instability. If mechanical ventilation is
unavoidable, the cardiac output should be optimised by keeping
intrathoracic pressure low, draining pleural effusions, avoiding
pulmonary vasoconstrictors and treating bronchoconstriction.
Ventilator settings should be titrated accordingly, aiming for early
•
extubation, if possible.
Patients with Fontan circulation have very poor tolerance of
•
hypovolaemia, are at high risk of atrial arrhythmias (which can be
lethal) and at risk of thrombi.
Atrial arrhythmias should be prevented and standard practice, such
•
as optimisation of electrolytes, should not be underestimated.
It is important to remember that some patients may not have
•
transvenous access to the heart if pacing is indicated, such as those
with a TCPC; in this case, external pacing should be available. It is
essential to always involve an expert in the care of such patients.
349
21 What considerations should be made for managing a
univentricular heart (non-Fontan) on the intensive care
unit?
When considering the use of inotropic and vasoactive agents, the
•
nature of the pulmonary connections must be considered.
The unprotected pulmonary circulation with or without Eisenmenger
•
physiology should be managed, so as to minimise any further
increase in pulmonary artery pressures.
Where the pulmonary vasculature is protected by pulmonary artery
•
stenosis/banding, the relative effects of pulmonary versus systemic
constriction or dilatation may be different when compared with cases
where there is an absent pulmonary connection with systemicpulmonary collaterals or shunts.
In the patient with absent pulmonary connection and systemic-
•
pulmonary collaterals/shunts, a small increase in pulmonary vascular
resistance (PVR) may result in a significant reduction in pulmonary
blood flow and dramatic desaturation. In contrast, an increase in
systemic vascular resistance (SVR) and/or a fall in PVR may result in
an increase in systemic-pulmonary shunting with a fall in cardiac
output.
Attention should also be paid to oxygen administration, as this may
•
itself alter the balance between pulmonary and systemic circulations.
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