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Key Questions in CONGENITAL CARDIAC SURGERY
b) presence of the defect and the direction of the shunting;
c) pressure gradient estimation across the defect — where a high
velocity jet is representative of a high-pressure gradient and
suggestive of a restrictive communication.
Cardiac computed tomography — which may demonstrate:
•
a) chamber dilatation;
b) presence of the defect.
Cardiac magnetic resonance imaging — which may demonstrate:
•
a) chamber dilatation;
b) presence of the defect and the direction of the shunting;
c) flow estimation. A phase contrast imaging sequence allows
direct measurement of the net blood flow through the aortic
and pulmonary valves during the whole cardiac cycle
(mL/cardiac cycle). Qp/Qs represents the ratio of the net flow
90
through the pulmonary and aortic valves (Figure 17).
Aortic
valve
Pulmonary
valve
Aortic
valve
Pulmonary
valve
Net aorta flow:
79mL
Net pulmonary flow:
236mL
Figure 17. Cardiac magnetic resonance imaging calculation of Qp/Qs by
direct measurement of the net blood flow through the aortic and pulmonary
valves during the whole cardiac cycle.
2 Congenital cardiac physiology
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33 Describe how a left-to-right shunt is detected during
cardiac catheterisation
An intracardiac shunt can be detected and localised by measuring
•
the oxygen saturation levels of blood samples obtained at different
sites, including the SVC, IVC, RA, RV, and PA, with an ‘oximetry
run’.
An increase in oxygen saturation levels (‘oxygen step-up’) localises
•
the level of the left-to-right shunt (Figure 18).
AB
91
Figure 18. An ‘oximetry run’ with: A) an atrial septal defect, where the ‘step-
up’ is detected in the right atrium, denoting the left-to-right shunt to be at an
atrial level; and B) a ventricular septal defect, where the ‘step-up’ is detected
in the right ventricle, denoting the left-to-right shunt to be at a ventricular level.
Key Questions in CONGENITAL CARDIAC SURGERY
34 How is the Qp/Qs ratio calculated during cardiac
catheterisation?
Cardiac output is calculated using the Fick principle, where:
•
Flow = O2consumption
Arteriovenous O2concentration difference
Flow = O2consumption
Arteriovenous O2sats difference x Hb x 1.34
Pulmonary flow = O2consumption
(PV O2sats – PA O2sats) x Hb x 1.34
Systemic flow = O2consumption
(Ao O2sats – RA O2sats) x Hb x 1.34)
92
As O
pulmonary blood flow to systemic
as:
Qp = Ao O2sats – RA O2sats
Qs PV O2sats – PA O2sats
In addition, PV O
RA sats = (3 x SVC sats) + (1 x IVC sats)
where PV = pulmonary vein, PA = pulmonary artery, Ao = aorta, RA
= right atrium, SVC = superior vena cava, IVC = inferior vena cava,
Hb = haemoglobin, sats = oxygen saturation levels.
For example:
•
If RA sats are 60%, PA sats 80%, PV sats 100%, Ao sats 100%.
Qp = Ao O2sats – RA O2sats = 100 – 60 = 40 = 2
Qs PV O2sats – PA O2sats 100 – 80 20
consumption and Hb are the same in both equations, the
2
sats are usually assumed to be 100%.
2
4
blood flow ratio can be expressed
therefore the Qp:Qs is 2:1.
In terms of significance:
•
a) Qp/Qs <1 indicates a right-to-left shunt;
2 Congenital cardiac physiology
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b) Qp/Qs >1 indicates a left-to-right shunt;
c) Qp/Qs >1.5 is considered haemodynamically significant.
35 Describe the relationship between arterial oxygen
saturation and Qp/Qs in patients with total mixing
If Qp = 1:
•
Qs
Pulmonary blood flow = Systemic blood flow
Pulmonary venous return = Systemic venous return
(1 x 100%) (1 x 60%)
Oxygen saturation = (1 x 100) + (1 x 60)
2
= 160 = 80%
2
If Qp = 4:
Qs
93
Pulmonary blood flow: Systemic blood flow = 4:1
Pulmonary venous return: Systemic venous return = 4:1
(4 x 100%) (1 x 60%)
Oxygen saturation = (4 x 100) + (1 x 60)
5
= 460 = 92%
5
From these calculations, it can be seen that patients with total mixing:
•
a) are nearly balanced, with a Qp/Qs = 1, when oxygen
saturation is approximately 80%;
b) cannot have oxygen saturations of 100%, even when the
Qp/Qs ratio is very high.
These calculations are based on three assumptions, that:
•
a) pulmonary venous saturation is nearly 100%, which is not valid
in patients with pneumonia and lung collapse;
Key Questions in CONGENITAL CARDIAC SURGERY
b) systemic venous saturation is nearly 60%, which is not valid in
patients with a low cardiac output state;
c) there is total mixing, which is not valid in patients with
intracardiac streaming.
36 What is Eisenmenger syndrome?
Eisenmenger syndrome is defined as an obstructive pulmonary
•
vascular disease that develops as a consequence of a longstanding
large left-to-right shunt causing an irreversible increase in pulmonary
vascular resistance that approaches and at times exceeds systemic
levels.
As a consequence, pulmonary artery pressures can be systemic or
•
supra-systemic. In patients with supra-systemic pressures, there is
shunting from right to left and resultant cyanosis.
The likelihood for Eisenmenger syndrome to develop in a patient
•
depends on the specific underlying cardiac defect and any operative
interventions that have taken place.
Early development of Eisenmenger syndrome is more commonly
•
94
associated in patients with persistent truncus arteriosus, common
atrioventricular septal defect, VSD, PDA and TGA. Although some
patients with ASD develop Eisenmenger syndrome, the cause-effect
relationship in this patient cohort is less well established.
The high pulmonary vascular resistance is usually established by 2
•
years of age but sometimes may develop earlier.
Eisenmenger syndrome may also develop earlier in patients with
•
Down’s syndrome.
Differential diagnoses for Eisenmenger syndrome include primary
•
pulmonary hypertension and congenital heart disease with cyanosis
and elevated right heart pressures, such as tetralogy of Fallot.
The development of Eisenmenger syndrome seems to correlate with
•
damage to the pulmonary vasculature as a result of longstanding
increased tension on the arterial and capillary walls.
This reactive adaptation produces an increasing amount of fibrous
•
perivascular deposits and a reduction in the production of NO.
Interstitial changes contribute to the stiffness of the lung
parenchyma, which reduces the efficiency of gas exchange and
increases vascular resistance.
Patients that develop Eisenmenger syndrome initially experience an
•
improvement of their symptoms of congestive heart failure, as the
increasing pulmonary vascular resistance reduces the pulmonary
overflow. Ultimately, the pulmonary pressure continues to rise and
becomes supra-systemic, resulting in shunt reversal and cyanosis.
2 Congenital cardiac physiology
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Closure of an intracardiac shunt after the development of
•
Eisenmenger syndrome is associated with RV failure due to the high
RV afterload.
On chest radiograph, the cardiac shadow decreases in size and lung
•
fields become oligaemic, whilst the PA shadow remains enlarged
(Figure 19).
95
Figure 19. Chest radiograph of a patient with
Eisenmenger syndrome demonstrating a decreased
cardiac shadow, oligaemic lung fields and enlarged
pulmonary artery shadows.
Echocardiography may show evidence of RV hypertrophy, a non-
•
dilated LV and a right-to-left shunt across the defect.
On cardiac catheterisation, the Qp/Qs ratio is usually <1.5, with the
•
pulmonary vascular resistance index >8 Wood unit/m2that does not
respond to pulmonary vasodilators.
The median survival of a patient with Eisenmenger syndrome is 20-
•
50 years of age.
Key Questions in CONGENITAL CARDIAC SURGERY
The use of novel pulmonary vasodilators may have some benefits in
•
remodelling the pulmonary vascular bed in the early stages of
pulmonary vascular disease.
37 Describe the principles of measuring oxygen
saturation levels
Oxygen saturation levels represents the percentage of haemoglobin
•
(Hb) binding sites in the blood occupied by oxygen.
Normal arterial oxygen saturation levels (SaO2) are 95-100%, while
•
mixed venous oxygen saturation levels (SvO2) are 65-75%.
Oxygen saturation is measured non-invasively by pulse oximetry,
•
where a sensor device is placed on a thin part of the patient’s body,
usually a fingertip or earlobe. The device emits two wavelengths of
light through the body part to a photodetector, which measures the
changing absorbance at each of the wavelengths, allowing it to
determine the absorbance due to the pulsing arterial blood.
The accuracy of pulse oximetry is best with oxygen saturation levels
•
96
of 70-100%, with reduced accuracy in the range of 50-70% and is
considered inaccurate below 50%.
False pulse oximetry readings can also occur with hypoperfusion,
•
vasoconstriction, cold limbs, dark-coloured skin, excessive
movements (such as shivering) and incorrect sensor application.
In addition, false readings can also occur if the haemoglobin binds to
•
a molecule other than oxygen, such as in carbon monoxide poisoning
and methaemoglobinaemia.
Blood gas analysis can be used to invasively measure the oxygen
•
saturation levels, in addition to the other measurements, such as
oxygen tension (PO2), pH, PCO2, base deficit, blood lactate and
electrolytes.
38 What is cyanosis?
Cyanosis represents a bluish discolouration of the skin and mucous
•
membranes due to presence of at least 5g/dL of deoxyhaemoglobin.
Cyanosis associated with desaturation of arterial blood is termed
•
central cyanosis, while cyanosis with normal arterial oxygen
saturation is termed peripheral cyanosis.
Peripheral cyanosis is caused by increased extraction of oxygen by
•
peripheral tissues, such as in circulatory shock, hypovolaemia or
vasoconstriction from cold.
Blood haemoglobin levels significantly affect the occurrence of
•
cyanosis. Normally, 2g/dL of deoxyhaemoglobin are present at the
venules, so an additional 3g/dL of deoxyhaemoglobin from arterial
blood can produce cyanosis.
2 Congenital cardiac physiology
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In a patient with polycythemia who has an Hb level of 20g/dL, 3g/dL
•
of deoxyhaemoglobin, cyanosis will be manifest with an oxygen
saturation of 85% (20-3 = 17; 17/20 = 0.85). Whilst in an anaemic
patient with an Hb level of 6, 3g/dL deoxyhaemoglobin cyanosis will
be manifest with oxygen saturation of 50% (6-3 = 3; 3/6 = 0.5).
Cyanotic congenital heart diseases (Table 3) are associated with
•
central cyanosis, caused by deoxygenated blood passing into the
systemic circulation. This is due to either a right-to-left shunt (such as
tetralogy of Fallot), mixing (such as tricuspid atresia) or parallel
systemic and pulmonary circulations (such as TGA).
Table 3. Common acyanotic and cyanotic congenital heart diseases.
^Еу~езнбЕ=ЬЙ~кн=ЗблЙ~лЙл
Left-to-right shunts:
• ASD
• VSD
• AVSD
• PDA
Obstruction to flow:
• Aortic stenosis
• Pulmonary stenosis
• Coarctation of the aorta
Using the hyperoxia test, which detects the changes of arterial oxygen
•
tension (PaO2) to 100% oxygen inhalation, allows the differentiation of
cyanosis caused by cardiac or pulmonary disease, where:
a) pulmonary causes of cyanosis produce an increase in PaO2to
>100mmHg;
b) cardiac causes of cyanosis only produce a slight rise in PaO
of 10-30mmHg and it does not go above 100mmHg, because
of the deoxygenated blood that continues to bypass the lung.
`у~езнбЕ=ЬЙ~кн=ЗблЙ~лЙл
• Truncus arteriosus
• Transposition of great arteries (TGA)
• Tricuspid atresia
• Tetralogy of Fallot
• Total anomalous pulmonary venous drainage
(TAPVD)
97
2
39 What are the sequelae of chronic cyanosis?
Polycythemia.
•
Clubbing.
•
Key Questions in CONGENITAL CARDIAC SURGERY
Central nervous system complications, such as a brain abscess and
•
cerebrovascular stroke.
Bleeding tendency, as well as increased risk of thromboembolism.
•
Hypercyanotic spells.
•
Hyperuricaemia and gout.
•
40 Describe the oxygen-haemoglobin dissociation curve
(Figure 20)
The oxygen-haemoglobin dissociation curve describes the
•
relationship between the partial pressure of oxygen (PO2) and
98
Oxyhaemoglobin (% saturation)
PaO2 (mmHg)
Figure 20. Oxygen-haemoglobin dissociation curve, where a left shift
represents a greater affinity of haemoglobin for oxygen (blue curve) and
a right shift represents a reduced affinity of haemoglobin for oxygen (red
curve). DPG = disphosphoglycerate.
2 Congenital cardiac physiology
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oxygen saturations (percentage of haemoglobin binding to oxygen),
which is not linear but rather sigmoid.
Above a PO2of 8kPa (60mmHg), changes in the PO2make very little
•
difference to oxygen saturation levels.
Below a PO2of 8kPa (60mmHg), however, a small drop in the PO
•
produces a large fall in the oxygen saturation levels.
The PO2at which 50% of haemoglobin is saturated has been
•
chosen as the reference point, called P50.
The position of the dissociation curve is an expression of the affinity
•
of haemoglobin for oxygen.
Shift of the curve to the left denotes an increased affinity of
•
haemoglobin to oxygen, where the same oxygen saturation levels
occur at a lower PO2and more oxygen is bound to haemoglobin.
Shift to the right denotes decreased affinity of haemoglobin to
•
oxygen.
Foetal haemoglobin has a higher affinity to oxygen (shifting of the
•
curve to the left) to allow better oxygen extraction from the placenta.
Factors that causes the curve to be shifted to the right (less affinity
•
of haemoglobin to oxygen) include low pH, high temperature, high
CO2and high levels of 2,3-disphosphoglycerate (2,3-DPG). These
factors occur at tissue level, so more oxygen is released from
haemoglobin to be taken up by the tissues.
2
99
41 Describe how oxygen content in blood is calculated
Oxygen content represents the actual amount of oxygen present per
•
volume of blood.
Oxygen is carried in blood either bound to haemoglobin or dissolved
•
in plasma. Dissolved oxygen accounts for only 2% of the total oxygen
content in blood.
Dissolved oxygen concentration is rather constant at 0.003mL
•
O2/100mL blood/mmHg but is dependent on its partial pressure.
Thus, with a PO2of 100mmHg, the concentration of dissolved
oxygen will increase to 0.3mL O2/100mL.
The remaining 98% of the total oxygen content of blood is reversibly
•
bound to haemoglobin.
The oxygen-binding capacity of haemoglobin is the maximum amount
•
of oxygen that can be bound to haemoglobin per volume of blood.
Assuming that haemoglobin is 100% saturated, 1g of haemoglobin
can bind 1.34mL oxygen.
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