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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
Table 4. Potentially reversible causes of cardiac arrest post-cardiotomy.
BT shunt = Blalock-Taussig shunt; PICU = paediatric intensive care unit;
ECMO = extracorporeal membrane oxygenation; CVP = central venous
pressure; CO
ventricular tachycardia.
= carbon dioxide; VF = ventricular fibrillation; VT =
2
320
oЙоЙклбДдЙ=Е~млЙ=зС=
Е~кЗб~Е=~ккЙлн
H Hypoxia
H Hypovolaemia
H Hypothermia
oЙдЙо~еЕЙ=нз=йзлнJЕ~кЗбзнзгу=й~нбЙенл
Hypoxia can be caused by airway or ventilation
issues. Hypoxia can also be due to a residual
lesion or blockage to pulmonary blood flow (e.g.
clot in the modified BT shunt). Whilst correction
with an FiO2of 1.0 via an endotracheal tube
should correct the majority of issues, consider
the underlying anatomy and surgery carried out.
Blood loss is common following cardiac surgery
and there may be bleeding ongoing that needs
volume replacement. Children can also become
hypovolaemic via 3rd space losses with the
systemic inflammatory response.
Rewarming from bypass should occur prior to
return to the PICU so this should not be a
significant cause, but if on extracorporeal
circuits (e.g. haemofiltration, ECMO) ensure
that the temperature is set correctly and avoid
pyrexia post-cardiac arrest.
H Hyper/hypokalaemia/
metabolic disturbances
T Tension pneumothorax
This will be an unlikely cause in this scenario,
but can be quickly excluded with a blood gas,
checking the potassium, calcium and glucose.
Correct as needed.
Many children will have pleural drains on return
from theatre. Whilst a tension pneumothorax is
unlikely, ensure the drains are not blocked and
use clinical assessment to ensure that the
pleural drain remains
áå=ëáíì
. Ultrasound can
help during the arrest.
8 Paediatric cardiac intensive care
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Table 4 continued. Potentially reversible causes of cardiac arrest post-
cardiotomy. BT shunt = Blalock-Taussig shunt; PICU = paediatric intensive
care unit; ECMO = extracorporeal membrane oxygenation; CVP = central
venous pressure; CO
ventricular tachycardia.
= carbon dioxide; VF = ventricular fibrillation; VT =
2
T Tamponade (cardiac)
T Thromboembolic
T Toxins
This is a common cause of post-cardiotomy
cardiac arrest. Typical features of hypotension,
raised CVP, tachycardia and echocardiographic
evidence prior to the arrest can suggest this. In
neonates/smaller children, however, tamponade
can occur in the absence of pericardial fluid and
occurs due to the myocardial swelling against
the posterior aspect of the sternum. This should
be assumed in all post-cardiotomy cardiac
arrests. Tamponade is not an echo diagnosis
and emergency chest re-opening may be
necessary even in the absence of echo findings.
321
Consideration should be given to
thromboembolic events in children with known
coagulation disorders, or those who have had
shunt insertion, placing them at risk of
thrombosis. Venous thromboembolism (VTE)
prophylaxis should be considered to prevent
this.
This is unlikely to occur as the cause of the
cardiac arrest; however, it is essential to ensure
any infusions or drugs that have been given
were administered correctly.
!!! Pulmonary hypertension
This is more common in neonates/smaller
infants or those with previous left-to-right shunts.
It can be triggered by rising CO2, acidosis,
pain/agitation or waking up. Without a residual
shunt the CVP will increase, followed by
hypotension and signs of low cardiac output.
Without intervention, cardiac arrest can quickly
occur. See question 29.
Key Questions in CONGENITAL CARDIAC SURGERY
Table 4 continued. Potentially reversible causes of cardiac arrest post-
cardiotomy. BT shunt = Blalock-Taussig shunt; PICU = paediatric intensive
care unit; ECMO = extracorporeal membrane oxygenation; CVP = central
venous pressure; CO
ventricular tachycardia.
!!! Arrhythmias Any arrhythmia can occur post-cardiotomy. The
= carbon dioxide; VF = ventricular fibrillation; VT =
2
development of profound sinus bradycardia or
heart block can cause a low cardiac output
state. Tachyarrhythmia can lead to loss of
cardiac output. Ventricular arrhythmias (e.g.
VF/VT) should raise the question about
coronary artery pathology. Junctional ectopic
tachycardia can cause all degrees of
cardiovascular compromise and may require
ECMO whilst it resolves. See question 14.
322
d) attempting to pace any bradycardia using the epicardial pacing
wires attached;
e) fixing any cardiac lesions, such as a bolus of heparin in cases
of a blocked shunt;
f) low threshold for early diagnostic interventions, including a
computed tomography scan or cardiac catheterisation, once
stability has been obtained.
27 What are the outcomes for children admitted to the
paediatric intensive care unit following congenital
heart disease surgery?
Survival outcomes for children undergoing congenital heart surgery
•
are generally very good.
Outcomes relate to the severity of the lesion, development of
•
postoperative acute kidney injury with the need for renal replacement
therapy, the association of other comorbidities and the age of the
child.
Recent data published in the National Congenital Heart Disease
•
Audit (NCHDA) by the National Institute for Cardiovascular
Outcomes Research (NICOR) from the United Kingdom and
Republic of Ireland shows a 30-day aggregate postoperative survival
of approximately 98%. This does not take into account deaths after
30 days, and some of the more complex lesions, such as hypoplastic
left heart syndrome, are known to have an inter-stage mortality.
8 Paediatric cardiac intensive care
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The ‘Risk Adjustment for Congenital Heart Surgery’ (RACHS-1) was
•
created to help identify risk and understand differences in mortality
amongst children undergoing congenital cardiac surgery. Whilst this
has been modified and adapted by more recent stratification
methods, it remains a simple, helpful tool to understand risk and for
research purposes (Table 5).
Table 5. Risk adjustment for congenital heart surgery categories of risk of
mortality (1 — low risk; 6 — very high risk).
o^`epJN=Е~нЙЦзку
bс~гйдЙ=лмкЦЙкбЙл
N
O
P
Q
Increasing severity
R
S
Repair of ASD, PAPVD and PDA or coarctation of aorta
repair >30 days old
Repair of VSD, tetralogy of Fallot, vascular ring, Glenn
shunt, AP window, coarctation of aorta repair <30 days
old
323
Ross procedure, aortic/mitral/tricuspid valve
replacement, ALCAPA repair, RV-PA conduit, Fontan, PA
band, DORV repair, arterial switch (only), systemic to PA
shunt
Arterial switch (with any other surgery, such as VSD
closure), TAPVD repair <30 days old, Rastelli, truncus
arteriosus repair, hypoplastic aortic arch repair
Truncus arteriosus repair with interrupted aortic arch,
Ebstein’s anomaly repair <30 days
Norwood operation
Multidisciplinary team care at the different stages of the patient
•
pathway is paramount to optimise outcomes:
a) pre-operative care — identify the diagnosis and commence
medical management, nutritional support, management of noncardiac issues and psychological support;
324
Key Questions in CONGENITAL CARDIAC SURGERY
b) peri- and intra-operative care — provide a good anaesthetic
assessment and management, full surgical planning and
appropriate techniques, and expert cardiopulmonary bypass
management;
c) immediate postoperative care — provide excellent PICU care,
with early recognition and management of complications;
d) longer-term postoperative care — ongoing cardiology
management and follow-up, psychological support,
neurodevelopmental care and nutritional support.
Many studies have looked at the longer-term outcomes for children
•
with congenital heart disease and they have found a spectrum of
morbidity related to neurodevelopment, including:
a) impaired communication, such as autism;
b) cognitive impairment;
c) behavioural difficulties;
d) motor developmental delay;
e) seizure disorders.
There are also functional outcomes relating to any underlying cardiac
•
lesions and ventricular function, such as reduced exercise tolerance.
28 What are the effects of positive pressure ventilation on
the cardiovascular system?
The use of ventilators on the PICU changes the respiration from a
•
negative pressure-based mechanism (spontaneous breathing) to a
positive pressure mechanism (mechanical ventilation).
Since the heart, lungs and vascular system are all interdependent,
•
this change in physiology impacts more than just the lungs.
When treating a right-sided cardiac lesion, some principles of
•
management include:
a) limiting the intrathoracic pressure;
b) lowering the peak and mean airway pressures, with lower
PEEP;
c) shortening the inspiratory times;
d) optimising the tidal volumes, aiming to ventilate to the
functional residual capacity;
e) avoiding hypoxia and respiratory acidosis (to control PVR).
8 Paediatric cardiac intensive care
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When treating a left-sided cardiac lesion, some principles of
•
management include using:
a) ventilation to optimise afterload reduction via a reduction in
transmural pressures;
b) higher PEEP;
c) positive pressure to reduce venous return and volume loading.
Positive pressure ventilation has significant effects on the
•
cardiovascular system (Table 6). In parallel, extubation, and return to
negative pressure ventilation, has the opposite effect and is a highrisk period for all children with congenital cardiac disease, as it
essentially increases the systemic afterload and increases the
volume loading of the pulmonary ventricle. This may or may not be
beneficial.
Table 6. Summary of the effect of positive pressure ventilation on the
heart. RAP = right atrial pressure; RVEDV = right ventricular end-diastolic
volume; RVEDP = right ventricular end-diastolic pressure; LAP = left atrial
pressure; LVEDV = left ventricular end-diastolic volume; LVEDP = left
ventricular end-diastolic pressure.
325
mмдгзе~ку=оЙенкбЕдЙ
pулнЙгбЕ=оЙенкбЕдЙ
mêÉäç~Ç
obar`ba
• Reduced venous return
• Decreased RAP
• Decreased RVEDV
obar`ba
• Reduced pulmonary
venous return
• Decreased LAP
^СнЙкдз~З
bibs^qba
• Increased RVEDP
• Decreased pulmonary
blood flow
obar`ba
• Decreased LVEDP
• Decreased aortic
transmural pressure
• Decreased LVEDV
29 What are the principles of management of a child with
a pulmonary hypertensive crisis?
Pulmonary hypertension can be primary (idiopathic) or secondary
•
(such as due to congenital cardiac disease or the effects of
cardiopulmonary bypass).
326
Key Questions in CONGENITAL CARDIAC SURGERY
Secondary pulmonary hypertension is a relatively common problem
•
on the PICU, particularly in the postoperative phases in children who
have previously had an unobstructed large left-to-right shunt prior to
surgery or neonatal patients who have undergone bypass surgery.
The pathophysiology of an acute pulmonary hypertensive crisis is
•
associated with an acute rise in the PA pressure that leads to clinical
deterioration. It is important to break this cycle to prevent cardiac
arrest (Figure 9).
Figure 9. Pathophysiology of a pulmonary hypertensive crisis.
Children with an acute pulmonary hypertensive crisis can be
•
categorised into two groups:
a) with an intracardiac shunt — where increases in PA pressure
causes the RV pressure to rise, producing a right-to-left shunt.
8 Paediatric cardiac intensive care
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This causes significant systemic desaturation, whilst cardiac
output is maintained;
b) without an intracardiac shunt — where increases in PA
pressure causes the preload to the left ventricle to reduce,
while the pressure-overloaded RV distends, altering the
ventricular interdependence.
Features common to both groups include a sharp rise in central
•
venous pressure, reflecting the elevation of the RVEDP and tricuspid
regurgitation. Compensatory tachycardia is a feature of the early
stage of the crisis, but it is often followed by a bradycardia,
associated with the rapid progression of ventricular failure. This
leads to a fall in cardiac output and even cardiac arrest.
The management of an acute pulmonary hypertensive crisis is aimed
•
at quickly and effectively reducing pulmonary vascular resistance,
whilst simultaneously increasing the systemic vascular resistance
ensuring an adequate systemic cardiac output. Manual
hyperventilation is among the first manoeuvres adopted in these
cases to quickly establish hypocapnia and increase oxygenation
(Table 7).
327
Table 7. Management strategies for an acute pulmonary hypertensive
crisis.
oЙЗмЕЙ=ймдгзе~ку=
о~лЕмд~к=кЙлблн~еЕЙ
• Reduce PaCO
(increase minute volume)
• Maximise FiO
2
1.0
2
• Inhaled nitric oxide
fеЕкЙ~лЙ=лулнЙгбЕ
о~лЕмд~к=кЙлблн~еЕЙ
• Vasopressin/
noradrenaline
• Inotropes
(e.g. adrenaline)
lнЬЙк=ЕзелбЗЙк~нбзел
• Fluid bolus
(increase RV
preload)
• ECMO
• Milrinone
• Sedate and muscle relax
• Avoid/correct acidosis
• Magnesium replacement
Although children on the PICU with pulmonary hypertension may be
•
commenced on oral pulmonary vasodilators, such as sildenafil, to
enable weaning from inhaled nitric oxide and mechanical ventilation,
these are seldom helpful in the acute setting.
328
Key Questions in CONGENITAL CARDIAC SURGERY
30 What is the role of the congenital cardiac surgeon in
the care of the non-cardiac surgical patient on the
paediatric intensive care unit?
The congenital cardiac surgeon may be asked to assist with:
•
a) cannulation and ongoing management of extracorporeal life
support;
b) thoracic trauma in children;
c) drainage of complex pericardial or pleural effusions;
d) pleurectomy in a pleural effusion otherwise difficult to manage;
e) multidisciplinary team discussions on all relevant decision-
making;
f) back-up support for interventional cardiology.
31 What is the role of an interventional paediatric
cardiologist in the paediatric intensive care unit?
The interventional paediatric cardiologist offers a great deal to the
•
PICU, with common interventions including:
a) participating in multidisciplinary team discussions on all
relevant decision-making;
b) balloon atrial septostomy in patients with:
i) transposition of the great arteries with inadequate
mixing;
ii) restrictive atrial septum in single-ventricle anatomy;
c) pericardiocentesis and drain insertion;
d) balloon dilatation procedures, such as:
i) valvuloplasty in critical aortic or pulmonary stenosis;
ii) pulmonary vein stenosis;
e) stent insertion into the:
i) right ventricular outflow tract;
ii) PDA;
f) closure of lesions:
i) coiling of major aortopulmonary collaterals (MAPCAs);
ii) device closure of an ASD or VSD;
g) diagnostic studies, such as:
i) Qp:Qs measurement;
ii) identification of residual lesions;
iii) assessment of pulmonary hypertension;
h) electrophysiology catheterisation, such as:
i) temporary transvenous pacing wire insertion;
ii) diagnostic studies;
iii) arrhythmia ablation;
iv) implantation of a permanent defibrillator or pacemaker.
8 Paediatric cardiac intensive care
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These procedures may be carried out at the patient’s bedside or in
•
the cardiac catheterisation laboratory.
32 What are the potential complications experienced by
long-term patients on the paediatric intensive care
unit?
Long-term patients can experience a number of comorbidities as a
•
consequence of a prolonged stay on the PICU. Consideration of
these factors needs to be a part of their ongoing care plan (Figure
10).
• Anxiety disorder
• Depression
• Post-traumatic stress disorder
• Behaviour disturbances
Psychological
Neurological
• Withdrawal from sedation
• Delirium
• Developmental delay
• Sleep disturbance
• Myopathy
Respiratory
• Subglottic stenosis
• Upper airway oedema
• Respiraory muscle weakness
Mobility
• Pressure ulceration
• Muscle atrophy
• Critical illness myopathy
• Tissue oedema
Figure 10. Potential complications of a prolonged stay on the
paediatric intensive care unit.
Patient
Gastrointestinal
• Feed intolerance
• Poor growth
• Poor nutrition
• Gastric ulceration
• Constipation
Infection
• Ventilator-associated pneumonia
• Line sepsis
• Urosepsis from catheter
• Colonisation (e.g.
• Antibiotic resistance
Vascular
• Difficult vascular access
• Thrombosis
• Line sepsis
mлЙмЗзгзе~л
329
)
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